tag:blogger.com,1999:blog-81253003293827868922024-03-18T22:18:42.866-07:00iAgegerontology, aging, geriatrics, science, old age, ageing,old people, retirement, death, "Mario Garrett"Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.comBlogger223125tag:blogger.com,1999:blog-8125300329382786892.post-13939112423587628282024-03-18T22:18:00.000-07:002024-03-18T22:18:03.633-07:00Growing up in Malta<p><span style="font-size: medium;">Walk through any Mediterranean city and the fast food on sale has nothing to compare with the ideal diet that academics think we eat. </span></p><p><span style="font-size: medium;">Fast foods are accessible to everyone: kebabs, burgers, butter and lard pastries, sweets, ice cream, donuts, fried chicken, and sodas are all the opposite of traditional diets. But the world is changing again. The growth of traditional food, inspired by our neighbors the Italians' "slow food" movement has brought back some of the local dishes, mostly from the Arabs. Food based on legumes cooked with garlic and chilies, roasted vegetables, and lean rabbit cooked in garlic and red wine. We ate fish pie nearly twice a week in summer when the fishermen came back to shore with their boats brimming with the local catch of Mahi Mahi (Lampuki). Before the popularity of fridges, everything had to be eaten fresh. The Mahi Mahi were so cheap that we had fish for a month and the housewives got creative in how to cook it. Fried, roasted, or in soup with lemon and rice ("aliota"). But the pie won favor as it included fish, spinach, and ricotta in a flour pastry shell. </span></p><p><span style="font-size: medium;">Then came the sweet pastries made without baking using leftover cake and biscuits mixed with nuts and candied fruits and drenched in evaporated condensed milk. Some fruits that only grow in Malta are also making a comeback. A small sweet pear called a "Bambinella" (from the Italian meaning a small girl) is still a popular indigenous fruit. We had lots of healthy soups, such as minestrone made with squash that had been harvested and then left on top of the roofs of the farms to mature in the sun. When cut open and a slice is purchased it gives the soup a mellow rich body with that traditional orange color. But the absolute favorite foods have never left the island. The local "pastizzi" of filo pastry filled with ricotta or peas. And there is always the local bread baked in a traditional wood-fired oven that is rare to find nowadays, but you can still find it. </span></p><p><span style="font-size: medium;">Our memories of the past are tied to the foods we ate at the time. When I visit my parents, which I try and do every year, I go and look for these wonderful foods. Some restaurants cater to this new demographic. Food has become a time portal for me as it is the best way to transport myself to the past. I have a secret pleasure of going away on my own to the city and in some of the local shops that still make traditional "pastizzi" I order 6 and walk to the garden overlooking the harbor and watch the ships as I devour these small pastries. Such fleeting escapades remind me of who I am and where I came from. It anchors me to my culture and my foundation. Food has a way of transporting me across time and mostly good times.</span></p><p><span style="font-size: medium;"><br /></span></p><p><span style="font-size: medium;">Now, living in the United States, the food tastes like plastic. I try to capture the taste by buying organic and local produce, which is an improvement, but I cannot capture the same flavor of my past. Only when I travel back to Europe, especially Turkey and Sicily do I taste some of those flavors again. Perhaps that is why I like traveling so much. But it is more than food. It is how I felt as a young boy. That feeling of hope, of having a whole world to explore. The hunger was not just for food but for the excitement of all those opportunities that I believed existed for me, all I had to do was be adventurous. Perhaps by trying to capture the foods of my past, I am trying to capture that feeling of hope, that the world is full of opportunities. </span></p><p><span style="font-size: medium;">Perhaps that is the secret, being able to meditate and enjoy the world around us, and food certainly helps.</span></p><p><span style="font-size: medium;">It is that feeling of belonging that we are trying to capture. As a child, I felt close to my family. I used to rush home from school and I knew that I had a safe place and that mum would be cooking and we get to eat together and maybe dad would tell us stories about his work. There were always the vendors that came pulling their carts selling "bigilla" (bean chili paste) or just fresh stalks of chickpeas still on their branch. </span></p><p><span style="font-size: medium;">My favorite was the vendor who sold romance novels. Mum who never went to school could read in Maltese, English, and Italian. I used to go and buy the sheet from the vendor. It measured something like 4 by 4 feet. I will take it to the kitchen table fold it and very carefully, using the only knife we had, a serrated bread knife, cut the paper into individual pages. Mum would then sew the pages together to make a book. She used to follow these romance novels religiously, and every month another chapter was added and I had my job, cutting the pages. </span></p><p><span style="font-size: medium;">There was always something happening and I belonged with this family. Sharing the food was not so much about sharing, as we devoured our food like stray cats. Sharing meant being together. We cannot recapture that now as we rarely see each other as a family. Like most of us, we have our own families now. My mum has severe dementia and my dad is angry at the world. He did not expect his life to end like this. We, the children are lost, despite having our own families our parents still remain our foundation and how we knew we belonged. Now we offer this belonging to our children even though we seem to have lost it for ourselves.</span></p><div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-86894876424505648472024-03-18T22:10:00.000-07:002024-03-18T22:10:41.899-07:00 Medicine and Long Life<blockquote style="background-color: white; color: #26282a; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 13px; margin: 0px; outline: none !important; padding: 8px;" type="cite"><div style="outline: none !important;"><div class="yiv7157549675ydp43300893yiv9845642538yqt1776473636" id="yiv7157549675ydp43300893yiv9845642538yqt09254" style="outline: none !important;"><div style="outline: none !important;"><div class="yiv7157549675ydp43300893yiv9845642538ydp506912feyahoo-style-wrap" style="font-size: 18px; outline: none !important;"><div style="outline: none !important;"><div dir="ltr" style="outline: none !important;"><div style="outline: none !important;"><p class="yiv7157549675ydp43300893yiv9845642538ydp32a257c1MsoNormal" style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;"><span style="font-size: 10pt;">Why do we have medicine?</span></p><div style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;">The answer is obvious that a child can answer. It is to help people. To help them live long and healthy lives.</div><p class="yiv7157549675ydp43300893yiv9845642538ydp32a257c1MsoNormal" style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;"> </p><div style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;">But does medicine help us live long?</div><div style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;">Some medicines do, like some vaccines, and most interventions help people live slightly longer.</div><p class="yiv7157549675ydp43300893yiv9845642538ydp32a257c1MsoNormal" style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;"> </p><div style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;">But people still die. In the last hundred years, we have only improved life expectancy at older age by 6 years. The great improvement in medicine has been in helping children survive childhood. And this was not just medicine it was because of public health. We made great progress in getting clean fresh water to communities and an efficient sewage system. Laws that protect the air we breathe, the hours worked, and age restrictions. It is these factors that have improved life the most rather than medicine.</div><p class="yiv7157549675ydp43300893yiv9845642538ydp32a257c1MsoNormal" style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;"> </p><div style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;">For older people medicine performs invasive treatment like heart operations, setting bone fractures, and through medication like controlling blood pressure, cholesterol, and diabetes. These help some older people live slightly longer and in better health. But only slightly.</div><p class="yiv7157549675ydp43300893yiv9845642538ydp32a257c1MsoNormal" style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;"> </p><div style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;">Two researchers examined what happens if we completely cure some chronic diseases.</div><div style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;">Like a magician with their magic wand, they eliminate all diseases. This can only be done statistically. Kenneth Manton eliminated one disease at a time. By eliminating all of these killer diseases at 87 years of age, people live an additional 5.7 years for males and 6.5 years for females.</div><p class="yiv7157549675ydp43300893yiv9845642538ydp32a257c1MsoNormal" style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;"> </p><div style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;">Another researcher eliminated one disease at a time and saw the effect this had on people’s lives. Again, they did this using statistics. Douglas G. Manuel reported that by eliminating cancer they predicted that one fifth of the years of life gained would be spent in poor health—and increased cost. This is because living longer results in these people getting dementia or other chronic disease such as atherosclerosis. On the other hand, eliminating musculoskeletal conditions would result in a year of good health for women and under half a year for men.</div><p class="yiv7157549675ydp43300893yiv9845642538ydp32a257c1MsoNormal" style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;"> </p><div style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;">Many diseases are waiting for us in older age. The healthiest people on earth, like the Blue Zone people, one of which is in Okinawa, tend to live a long life. They only get sick for a few days before they die. There is no long period of sickness. In the end, it is best to be healthy as death comes quickly and our bodies seem to know how to shut down effectively when we are healthy.</div><p class="yiv7157549675ydp43300893yiv9845642538ydp32a257c1MsoNormal" style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;"> </p><div style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;">We need to understand why our bodies are designed to shut down. We need to study aging not just specific diseases.</div><p class="yiv7157549675ydp43300893yiv9845642538ydp32a257c1MsoNormal" style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;"> </p><div style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;">Then I return the question. Does medicine help people live long and healthy lives?</div><p class="yiv7157549675ydp43300893yiv9845642538ydp32a257c1MsoNormal" style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;"> </p><div style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;">The answer might be that medicine allows us to believe we can change our nature. But as yet we do not understand “aging” enough to be able to change very much, but we all take what we can get right now.</div><p class="yiv7157549675ydp43300893yiv9845642538ydp32a257c1MsoNormal" style="font-family: Garamond, serif; font-size: 10pt; margin: 0in; outline: none !important; text-align: justify;"> </p></div></div></div></div></div></div></div></blockquote><div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-19788382042213997782023-11-23T18:52:00.000-08:002023-11-23T18:52:57.517-08:00 Don’t Blame the Chickens or the Foxes<p><span style="background-color: white; font-family: Garamond, serif; text-align: justify;"><span style="font-size: medium;">I have been teaching a university course on programs for older people for ten years. Every year I get some of my bright students come back to tell me that the program does not run as it was intended. The program that they interned in (clinical experience) operated differently from how it should have operated. Most reduced their services to make a larger profit. At first, I thought that this was an anomaly, infrequent events. But it happened with many of my students across a broad range of services. At one time one of my students, an ex-military intelligence in his previous life, wrote a critique of hospice services. I thought it was intriguing so I followed up and did my own research. What I found was that not only was he right, but there were other ways that he missed that hospices use to increase their profit and unfortunately reduce their care to older adults that are dying. How can this be?</span></span></p><p class="yiv1081640464ydpc5a31301MsoNormal" style="background-color: white; font-family: Garamond, serif; margin: 0in; outline: none !important; text-align: justify;"><span style="font-size: medium;">I then decided to research all services to older adults. The results were devastating but informative. In the United States, every service that is provided for older adults is designed to increase profit generation. Every single one and it did not matter if they were “for-profit”, or “not-for-profit.” There are only two ways to increase your profit, you either increase prices for your services, reduce the number of services, and/or reduce their costs. What I found is that across a broad range of services, the preferred method was to reduce services. This had the direct effect of causing harm to the older client. It is predictable institutional abuse at a level that is difficult to comprehend in a developed and rich country. But my task was not simply to document these abuses, but to find a solution. That is when I came up with a parable.</span></p><p class="yiv1081640464ydpc5a31301MsoNormal" style="background-color: white; font-family: Garamond, serif; margin: 0in; outline: none !important; text-align: justify;"><span style="font-size: medium;">A farmer has a brood of hens, he sells their eggs. Next to the farm there were a couple of foxes with their own small family to feed. They often got into the chicken coop and helped themselves to some of the chickens. This continued to happen year after year. I ask my students, who is at fault? Are the chickens at fault as they remain defenseless? Are the foxes at fault since they attempt to feed themselves and their families? Or is it the farmer who is incompetent at protecting the chickens? You cannot blame the chickens or the foxes which is what the media does. They blame people for not doing their homework and checking up on nursing homes, or hospices when they are at their most vulnerable stage in their life. Others blame the medical and pharmaceutical companies for their greedy behavior as they need to make a profit to survive. No one seems to blame the farmer, the government. We have regulatory agencies that are designed to safeguard our citizens, but they are not doing their job. Like the farmer they are incompetent, but unlike the farmer who loses the sale of his eggs, these administrators still get a hefty paycheck every month. When I figured that the solution was to enhance and strengthen government regulatory agencies, I formulated a theory that explains all of this and predicts that these abuses will continue to increase unless we enhance oversight. The book was published as Critical Age Theory on Kindle an Amazon company. It was generating some interest, but not a blockbuster, but then one day my account on Kindle was deleted. No explanation was given and no apology for deleting more than 12 books I had online.</span></p><p class="yiv1081640464ydpc5a31301MsoNormal" style="background-color: white; font-family: Garamond, serif; margin: 0in; outline: none !important; text-align: justify;"><span style="font-size: medium;">I remember a friend of mine Allen Smith, a Professor of Economics at Eastern Illinois University, who published about similar institutional abuse this time on social security. He published The Alleged Budget Surplus, Social Security, and Voodoo Economics and in 2000, The Looting of Social Security. All of these books were critical of what the government was doing. Strangely, the last of these books was stopped from being published. Someone bought the rights and stopped printing it. At the end of his life Professor Smith bought the rights back and made it public again. I distribute it free to my students.</span></p><p class="yiv1081640464ydpc5a31301MsoNormal" style="background-color: white; font-family: Garamond, serif; margin: 0in; outline: none !important; text-align: justify;"><span style="font-size: medium;">Basically, he is saying the same thing, don’t blame the chickens or the foxes.</span></p><p class="yiv1081640464ydpc5a31301MsoNormal" style="background-color: white; font-family: Garamond, serif; margin: 0in; outline: none !important; text-align: justify;"><span style="font-size: medium;">We must hold our government to a higher standard as their only job, their sole reason for existing, is to better the lives of its constituents, the chickens. If they are not doing that then they have relinquished their right to govern. Most radical governments now, the populists, want to overthrow all our institutions and start again. But that is wrong; these institutions developed for a reason. Just because they are not functioning properly does not mean that they cannot be fixed. Look at the motive for their inception and you will find the answer of how to fix them. Perhaps we can regain a system of care that promotes health and dignity in our last stages of life.</span></p><div><br /></div><div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-38756502453796100572023-11-23T17:06:00.000-08:002023-11-23T18:42:42.528-08:00Many Dementias<p></p><div class="separator" style="clear: both; text-align: center;"><p class="MsoNormal" style="background-color: white; margin: 0in; text-align: justify;"><span style="font-family: Garamond, serif; font-size: large;">My mother, of 86 years of age, has dementia. But we do not really know what that means. At first, she was slow and fragile; her short-term memory was shot. The doctors found high calcium in her blood and diagnosed a benign tumor in the hyperthyroid. They operated and she came back energetic, hyperactive, and hallucinating and talking with her dead mother and sister. Then she stopped eating and only drank when directed. She shrank in weight and became nearly catatonic. I met with the family as I predicted a quick death. I made the family take uncomfortable decisions. We admitted her to a nursing home, and when my sister visited her four hours later and saw how anxious she was, mum came back home. She had an infection, ended up in hospital, and came back with a bloody nose. This abuse further solidified the</span><span style="font-family: Garamond, serif; font-size: x-large;"> primary caregiver, </span><span style="font-family: Garamond, serif; font-size: x-large;">my younger brother's determination to protect mum by keeping her home. Then she started independently eating and drinking and while still looking for her dead relatives, she was getting more exercise than anyone else. She was physically getting stronger. She is in constant motion and repeats nonsensical words as though she is praying. From the moment she wakes up to the last breath at night she is in motion and vocal.</span></p><p class="MsoNormal" style="background-color: white; margin: 0in; text-align: justify;"><span style="font-family: Garamond, serif; font-size: large;"><br /></span></p><p class="MsoNormal" style="background-color: white; margin: 0in; text-align: justify;"><span style="font-family: Garamond, serif; font-size: large;">It seems there are layers of diseases, one waiting for the other to emerge and take priority, or both acting at the same time. Our categorization of diseases is not designed for older people with multiple diseases. Especially in psychiatric nosology, the idea of identifying specific diseases as distinct and independent diseases is nonsensical. As we get older the body ages across the board. A weaker heart, lung, muscles, skeleton, joints, everything is diminished, some more than others. An emerging disease is not independent but can be an expression of all of these small deteriorations. My mother had a hyperthyroid tumor that created a calcium imbalance that slowed her cognition and body down, and she also had Lewy Bodies Dementia that created the hallucinations, and ontop of these she also must have Vascular dementia or Alzheimer’s disease that destroyed her memory. All of these were acting upon her at the same time. Then there are other neurological diseases that we still have not identified. Her improved eating habits cannot be explained by the dementia diagnosis alone. There are other changes that are hidden from us. Among 90-year-olds half of the cause of their dementia is unknown as there are so many other biological changes happening. When there are neurological deficits you can be certain that other diseases will emerge at the same time. Aging might be the most obvious factor, but that does not inform us on how to prevent or delay dementias as we cannot stop aging, but we can improve how we age. Psychiatric nosology will eventually be dragged kicking and screaming through this terrain of older patients’ maladies until we finally admit that unless we start looking at the whole person, studying aging and not just diseases, we will never get a handle on dementia.</span></p><p class="MsoNormal" style="background-color: white; font-family: Garamond, serif; font-size: 10pt; margin: 0in; text-align: justify;"> </p><p class="MsoNormal" style="background-color: white; font-family: Garamond, serif; font-size: 10pt; margin: 0in; text-align: justify;"> </p></div><br /><p></p><div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-57762482979703843042023-08-01T21:35:00.000-07:002023-08-01T21:35:06.867-07:00The Sixth Scientific Revolution Transforming Humans as Context Bound<p>All scientific discoveries contribute towards a better understanding of the universe that we live in. All of this knowledge reinforces our belief that the universe is orderly and that we are at the center. In contrast, there are some scientific revolutions that change how we think about ourselves, as humans. There are some discoveries that shake up our complacency about our importance in the grand scheme of the universe. Such scientific revolutions deserve special merit since by removing our self-centered bias, we get closer to a more universal truth about us and the universe we inhabit. Since our bias for self-centeredness is strong, so are these scientific revolutions. This paper examined five such scientific revolutions and postulates a sixth one that is emerging.</p><div><br /></div><div>It is easy to define the first of such revolutionary thinking. Thales of Miletus 6th century BCE argued that we should observe physical events without assigning the cause to "god." He argued that there is an underlying process that causes the world to behave the way it does and that we need to work out these hidden processes rather than simply call it the will of god. This revolutionary thinking caused the birth of science. </div><div><br /></div><div>The second scientific revolution was by the 16th century Nicolaus Copernicus., who in astronomy, removed the earth from the center of the universe and placed it among other planets revolving around the sun. By doing this Copernicus also moved humankind, and not just Earth, from being at the center of the universe and we attained a more peripheral place in the universe.</div><div><br /></div><div>The third revolution that continued to move humans away from being the center of the universe was by the 19th century Charles Darwin. By publishing his The Origin of Species, Darwin pushed humans off the throne of superior beings and back into our mammalian lineage. The theory asserts that like all other beings, we evolved and share lineage with lower primates and other living things. Like all other animals, we are a work in progress. </div><div><br /></div><div>The 20th century brought the fourth revolution with Sigmund Freud who emphasized the concept of an unconscious mind. The notion of the unconscious can be traced back to ancient civilizations when dreams were considered to be messages from the gods. Even early philosophers like Plato and Aristotle explored the idea of unconscious mental processes. At the turn of the century, scientists such as Franz Anton Mesmer, Pierre Janet, Alfred Adler, and Carl Jung all worked on this unconscious mind that hid thoughts and decisions from consciousness and therefore from us. But it was Freud that took this concept further and developed a theory of the mind that argued that the unconscious mind is the primary motivator for behavior. The theory put forward the interpretation that we are not in conscious control of our actions.</div><div><br /></div><div>The later part of the 20th century brought us the fifth revolution with Albert Einstein and his colleagues who developed the idea that the matter is relative. This theory of relativity postulated that gravity and acceleration are indistinguishable, that mass and energy cause gravity and time to curve, and that the acceleration of massive objects causes ripples in spacetime. All of this makes our natural world less rigid, and our reality is determined by context by the locality of the event. </div><div><br /></div><div>These theories have one thing in common, what we believe about who we are, as humans on Earth, is not true. That we are part of a larger universe, that we evolved from other life forms, and that how we see the world is relative to our position in the universe. There is a locality in our reality. Where we are is important. The sixth revolution takes all these concepts of moving humankind away from being to the center of the universe as it argues that even our body is part of such a locality. That the biological and chemical context that we reside in determines how we function and behave. This environmental physiology, where the environment changes our physiology proposes that although we see ourselves as sovereign entities we are in reality a conglomerate of different processes that are influenced by the world we live in. As such, under this environmental physiology, there is no “us” and “them”, no “me” and the “environment”, as both converge. Environmental physiology highlights the malleability of our physiology. Richard Rorty said this beautifully: “…had physiology been more obvious psychology would never have arisen…if the body had been easier to understand, nobody would have thought that we had a mind.” (p 239). </div><div><br /></div><div>Most of the developments in environmental physiology highlight human intervention in modifying the body. However, equally impressive, and more instructive, is the evidence showing how nature itself manipulates our bodies. By observing how nature manipulates and modifies our bodies, scientists have learned new techniques that emulate nature. Despite the impressive nature of these technological advances, the underlying theme is how nature has such a powerful force on us by constantly changing and modifying our bodies. </div><div><br /></div><div>Technological advancements include: </div><div>Genetic Engineering and Recombinant DNA technology led to the creation of genetically modified organisms (GMOs); </div><div>Polymerase Chain Reaction (PCR) amplified specific DNA segments, making it possible to study and analyze genes and their functions more easily;</div><div>Gene Sequencing has led to insights into genetic variations, disease mechanisms, and personalized medicine; Stem Cell Research that promoted regenerative medicine, and tissue engineering; </div><div>CRISPR-Cas9 Gene Editing technology allows precise modification of DNA sequences, making gene editing faster, and more accessible; </div><div>Synthetic Biology of new biological components, systems, and even entire organisms, with varied applications; </div><div>Omics Technologies advancements in how molecules interact within living organisms resulting in contributions to genomics, proteomics, and metabolomics; </div><div>Human Embryonic Stem Cells that repair specific damaged organs; </div><div>Induced Pluripotent Stem Cells (iPSCs) takes adult cells and reprogram them to an embryonic stem cell-like state; Immunotherapy such as immune checkpoint inhibitors and CAR-T cell therapy, harness the immune system to target and eliminate cancer cells; </div><div>Microbiome Research that evaluates the bacterial makeup of the stomach enabling the development of probiotics; </div><div>Nanobiotechnology that promotes targeted drug delivery, biosensors, and imaging technologies; </div><div>Neuroscience and Brain Imaging such as functional MRI (fMRI), provide insights into the brain's structure and function; and </div><div>Artificial Intelligence and Machine Learning in Biology accelerate data analysis, drug repurposing, protein folding predictions, and diagnostics.</div><div><br /></div><div>Such advancements, impressive as they may seem, are just a small insight into the way that nature itself behaves. Scientists have used this limited knowledge about what we know about how the environment influences our bodies to experiment with coming up with technologies in a short span of time. But it would express a special kind of hubris if we forget to add how nature itself manipulates “us.” There is a vast number of unknown-unknowns, but what we have learned provides enough substantiating evidence to affirm that our context, our environment, changes us. This knowledge has taught us that we are more malleable and receptive than we believe. Nature manipulates our bodies on a daily basis. The sixth revolution in science is knowledge about how nature influences and changes our genes, how genes are expressed, how our body processes food, how we uptake nutrients, how we age, how we think, and how we behave.</div><div><br /></div><div>Natural influences on the body include: </div><div>Epigenetic modifications that determine the expression of specific genes, subdue some and excite others without altering the underlying genetic sequence. Environmental factors, such as diet, stress, and exposure to toxins, can lead to epigenetic modifications, influencing health outcomes; </div><div>Plasmids, are small, circular DNA molecules in humans that come from bacteria and archaea and become inserted in human cells. They often carry genes that provide selective advantages, such as antibiotic resistance, leading to the spread of antibiotic resistance genes; </div><div>Horizontal Gene Transfer (HGT) is the transfer of genetic material between different organisms, typically bacteria can exchange genetic material-- share beneficial genes, such as antibiotic resistance genes--through processes like conjugation, transformation, and transduction; </div><div>Jumping Genes (Transposons) are segments of DNA capable of moving within a genome. They can "jump" from one location to another, potentially affecting gene regulation and function, playing a significant role in shaping the human genome's evolution and diversity; </div><div>Retroviruses are individual strands of RNA viruses that can multiply into human cell DNA by integrating their genetic material into the host genome; </div><div>Human endogenous retroviruses (HERVs) are remnants of ancient retroviral infections in our ancestors' germ cells; MicroRNAs (miRNAs) play a crucial role in post-transcriptional gene regulation by binding to messenger RNAs (mRNAs) and either degrade them or inhibit their translation into proteins;</div><div>Dysregulation of miRNAs has also been linked to the progression of diseases, such as cancer and neurodegenerative disorders; </div><div>Prions are misfolded proteins that can induce the misfolding of other normal proteins, leading to a chain reaction that can propagate disease in the brain and nervous system, such as Creutzfeldt-Jakob disease in humans and bovine spongiform encephalopathy (mad cow disease) in cattle; </div><div>Endocrine Disruptors such as Bisphenol A (BPA) are chemicals that can interfere with the endocrine system, disrupting hormonal regulation reproductive and developmental abnormalities; </div><div>Gut bacteria break down complex carbohydrates, producing essential vitamins, and regulating immune responses affecting weight, inflammatory bowel disease, and allergies. which can influence our metabolism, immune system, and overall health; </div><div>RNA editing such as Adenosine-to-inosine (A-to-I), is a process that alters the nucleotide sequence of RNA after transcription. It is modified by enzymes called ADARs (adenosine deaminases acting on RNA and can impact gene expression, particularly in the nervous system, and is essential for normal brain function;</div><div>Genetic recombination is the process of exchanging genetic material between two DNA molecules during meiosis (cell division), homologous chromosomes exchange genetic material through crossing over. It occurs during sexual reproduction and contributes to genetic diversity; </div><div>DNA Repair Mechanisms correct errors that arise during replication or as a result of external factors. For example, Nucleotide excision repair (NER) is a DNA repair pathway that removes and replaces damaged nucleotides caused by exposure to ultraviolet radiation;</div><div>Hormesis where exposure to low or moderate levels of a stressor or toxin can result in a beneficial or stimulatory response, leading to improved health, resilience, or longevity. In other words, "What doesn't kill you makes you stronger." Hormesis can occur in various biological contexts such as Radiation Hormesis, Exercise Hormesis, Caloric Restriction Hormesis, and Phytochemical Hormesis.</div><div><br /></div><div><br /></div><div>All of these processes, and many others that we still have not discovered, interact. For example, exposure to low or moderate stressors that trigger hormetic responses may lead to epigenetic modifications. A hormetic response could activate specific cellular pathways that, in turn, influence epigenetic modification that changes how some genes are expressed (Vaiserman, 2011). The relationship can also be reciprocal where epigenetic modifications can regulate genes involved in stress response pathways or cellular repair mechanisms. Specific epigenetic changes may enhance or dampen hormetic responses, affecting the magnitude of the beneficial effect elicited by the stressor. In some cases, epigenetic changes induced by hormetic responses may be heritable. Offspring could inherit the altered epigenetic marks from their parents, potentially passing on the beneficial effects of hormesis to subsequent generations (Xavier, et al, 2019). Both hormesis and epigenetics have been linked to aging and longevity (Vaiserman, 2011). Moderate stressors that induce hormetic responses are believed to contribute to lifespan extension in various organisms. Epigenetic changes, on the other hand, can influence the aging process by regulating genes involved in cellular senescence and age-related diseases.</div><div><br /></div><div>The Sixth Revolution in science moves humans from a homo-centric view of the world to one that places humans as more malleable and porous, allowing for the context, and the environment, to influence and change us.</div><div><br /></div><div><br /></div><div>REFERENCES</div><div><br /></div><div>Rorty, R. (1979). Transcendental arguments, self-reference, and pragmatism. Transcendental arguments and science: Essays in epistemology, 77-103.</div><div><br /></div><div>Vaiserman, A. M. (2011). Hormesis and epigenetics: is there a link?. Ageing research reviews, 10(4), 413-421.</div><div><br /></div><div>Xavier, M. J., Roman, S. D., Aitken, R. J., & Nixon, B. (2019). Transgenerational inheritance: how impacts to the epigenetic and genetic information of parents affect offspring health. Human reproduction update, 25(5), 519-541.</div><div><br /></div><div>TECHNOLOGICAL INNOVATIONS</div><div>Genetic Engineering and Recombinant DNA Technology:</div><div>Watson, J. D., & Crick, F. H. (1953). Molecular structure of nucleic acids: A structure for deoxyribose nucleic acid. Nature, 171(4356), 737-738.</div><div>Cohen, S. N., Chang, A. C., Boyer, H. W., & Helling, R. B. (1973). Construction of biologically functional bacterial plasmids in vitro. Proceedings of the National Academy of Sciences, 70(11), 3240-3244.</div><div><br /></div><div>Polymerase Chain Reaction (PCR):</div><div>Mullis, K. B. (1986). The unusual origin of the polymerase chain reaction. Scientific American, 262(4), 56-61.</div><div>Saiki, R. K., Scharf, S., Faloona, F., Mullis, K. B., Horn, G. T., Erlich, H. A., & Arnheim, N. (1985). Enzymatic amplification of beta-globin genomic sequences and restriction site analysis for diagnosis of sickle cell anemia. Science, 230(4732), 1350-1354.</div><div><br /></div><div>Gene Sequencing:</div><div>Sanger, F., Nicklen, S., & Coulson, A. R. (1977). DNA sequencing with chain-terminating inhibitors. Proceedings of the National Academy of Sciences, 74(12), 5463-5467.</div><div>Venter, J. C., Adams, M. D., Myers, E. W., Li, P. W., Mural, R. J., Sutton, G. G., ... & Zhu, X. (2001). The sequence of the human genome. Science, 291(5507), 1304-1351.</div><div><br /></div><div>Stem Cell Research:</div><div>Evans, M. J., & Kaufman, M. H. (1981). Establishment in culture of pluripotential cells from mouse embryos. Nature, 292(5819), 154-156.</div><div>Takahashi, K., & Yamanaka, S. (2006). Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors. Cell, 126(4), 663-676.</div><div><br /></div><div>CRISPR-Cas9 Gene Editing:</div><div>Doudna, J. A., & Charpentier, E. (2014). Genome editing. The new frontier of genome engineering with CRISPR-Cas9. Science, 346(6213), 1258096.</div><div>Jinek, M., Chylinski, K., Fonfara, I., Hauer, M., Doudna, J. A., & Charpentier, E. (2012). A programmable dual-RNA–guided DNA endonuclease in adaptive bacterial immunity. Science, 337(6096), 816-821.</div><div><br /></div><div>Synthetic Biology:</div><div>Gibson, D. G., Glass, J. I., Lartigue, C., Noskov, V. N., Chuang, R. Y., Algire, M. A., ... & Venter, J. C. (2010). Creation of a bacterial cell controlled by a chemically synthesized genome. Science, 329(5987), 52-56.</div><div>Khalil, A. S., & Collins, J. J. (2010). Synthetic biology: applications come of age. Nature Reviews Genetics, 11(5), 367-379.</div><div><br /></div><div>Omics Technologies:</div><div>Aebersold, R., & Mann, M. (2003). Mass spectrometry-based proteomics. Nature, 422(6928), 198-207.</div><div>Lander, E. S., Linton, L. M., Birren, B., Nusbaum, C., Zody, M. C., Baldwin, J., ... & Bouvrette, S. (2001). Initial sequencing and analysis of the human genome. Nature, 409(6822), 860-921.</div><div><br /></div><div>Human Embryonic Stem Cell Research:</div><div>Thomson, J. A., Itskovitz-Eldor, J., Shapiro, S. S., Waknitz, M. A., Swiergiel, J. J., Marshall, V. S., & Jones, J. M. (1998). Embryonic stem cell lines derived from human blastocysts. Science, 282(5391), 1145-1147.</div><div>Yu, J., Vodyanik, M. A., Smuga-Otto, K., Antosiewicz-Bourget, J., Frane, J. L., Tian, S., ... & Thomson, J. A. (2007). Induced pluripotent stem cell lines derived from human somatic cells. Science, 318(5858), 1917-1920.</div><div><br /></div><div>Immunotherapy:</div><div>Hodi, F. S., O'Day, S. J., McDermott, D. F., Weber, R. W., Sosman, J. A., Haanen, J. B., ... & Urba, W. J. (2010). Improved survival with ipilimumab in patients with metastatic melanoma. New England Journal of Medicine, 363(8), 711-723.</div><div>Maude, S. L., Laetsch, T. W., Buechner, J., Rives, S., Boyer, M., Bittencourt, H., ... & Wood, P. (2018). Tisagenlecleucel in children and young adults with B-cell lymphoblastic leukemia. New England Journal of Medicine, 378(5), 439-448.</div><div><br /></div><div>Microbiome Research:</div><div>Turnbaugh, P. J., Ley, R. E., Hamady, M., Fraser-Liggett, C. M., Knight, R., & Gordon, J. I. (2007). The human microbiome project. Nature, 449(7164), 804-810.</div><div>Qin, J., Li, R., Raes, J., Arumugam, M., Burgdorf, K. S., Manichanh, C., ... & Wang, J. (2010). A human gut microbial gene catalogue established by metagenomic sequencing. Nature, 464(7285), 59-65.</div><div><br /></div><div>Nanobiotechnology:</div><div>Farokhzad, O. C., & Langer, R. (2009). Impact of nanotechnology on drug delivery. ACS Nano, 3(1), 16-20.</div><div>Sweeney, S. M., & Wooley, K. L. (2005). Self-assembling polymers for gene delivery: from laboratory to clinical trial. Advanced Drug Delivery Reviews, 57(15), 2075-2087.</div><div><br /></div><div>Neuroscience and Brain Imaging:</div><div>Ogawa, S., Lee, T. M., Nayak, A. S., & Glynn, P. (1990). Oxygenation-sensitive contrast in magnetic resonance image of rodent brain at high magnetic fields. Magnetic Resonance in Medicine, 14(1), 68-78.</div><div>Kandel, E. R., Schwartz, J. H., & Jessell, T. M. (2000). Principles of neural science (Vol. 4). McGraw-Hill, Health Professions Division.</div><div><br /></div><div>Artificial Intelligence and Machine Learning in Biology:</div><div>Alipanahi, B., Delong, A., Weirauch, M. T., & Frey, B. J. (2015). Predicting the sequence specificities of DNA- and RNA-binding proteins by deep learning. Nature Biotechnology, 33(8), 831-838.</div><div>Topol, E. J. (2019). High-performance medicine: the convergence of human and artificial intelligence. Nature Medicine, 25(1), 44-56.</div><div><br /></div><div>NATURAL INFLUENCES</div><div>Epigenetics</div><div>Jirtle, R. L., & Skinner, M. K. (2007). Environmental epigenomics and disease susceptibility. Nature Reviews Genetics, 8(4), 253-262.</div><div><br /></div><div>Plasmid </div><div>Modi, S. R., Lee, H. H., Spina, C. S., & Collins, J. J. (2013). Antibiotic treatment expands the resistance reservoir and ecological network of the phage metagenome. Nature, 499(7457), 219-222.</div><div><br /></div><div>Horizontal Gene Transfer</div><div>Thomas, C. M., & Nielsen, K. M. (2005). Mechanisms of, and barriers to, horizontal gene transfer between bacteria. Nature Reviews Molecular Cell Biology, 6(9), 711-721.</div><div><br /></div><div>Jumping Genes</div><div>Chuong, E. B., Elde, N. C., & Feschotte, C. (2017). Regulatory evolution of innate immunity through co-option of endogenous retroviruses. Science, 351(6277), 1083-1087.</div><div><br /></div><div>Retroviruses</div><div>Grandi, N., & Tramontano, E. (2018). Human endogenous retroviruses are ancient acquired elements still shaping innate immune responses. Frontiers in Immunology, 9, 2039.</div><div><br /></div><div>MicroRNAs</div><div>Bartel, D. P. (2009). MicroRNAs: target recognition and regulatory functions. Cell, 136(2), 215-233.</div><div><br /></div><div>Prions</div><div>Prusiner, S. B. (1998). Prions. Proceedings of the National Academy of Sciences, 95(23), 13363-13383.</div><div><br /></div><div>Endocrine Disruptors</div><div>Diamanti-Kandarakis, E., Bourguignon, J. P., Giudice, L. C., Hauser, R., Prins, G. S., Soto, A. M., ... & Zoeller, R. T. (2009). Endocrine-disrupting chemicals: an Endocrine Society scientific statement. Endocrine Reviews, 30(4), 293-342.</div><div><br /></div><div>Gut Bacteria</div><div>Sender, R., Fuchs, S., & Milo, R. (2016). Revised estimates for the number of human and bacteria cells in the body. PLOS Biology, 14(8), e1002533.</div><div><br /></div><div>RNA Editing</div><div>Nishikura, K. (2010). Functions and regulation of RNA editing by ADAR deaminases. Annual Review of Biochemistry, 79, 321-349.</div><div><br /></div><div>Genetic Recombination</div><div>Hunter, N. (2015). Meiotic recombination: The essence of heredity. Cold Spring Harbor Perspectives in Biology, 7(12), a016618.</div><div><br /></div><div>DNA Repair</div><div>Lehmann, A. R., & McGibbon, D. (2006). Xeroderma pigmentosum. Orphanet Journal of Rare Diseases, 1(1), 27.</div><div><br /></div><div>Radiation Hormesis, </div><div>Macklis, R. M., & Beresford, B. (1991). Radiation hormesis. Journal of Nuclear Medicine, 32(2), 350-359.</div><div><br /></div><div>Exercise Hormesis, </div><div>Ji, L. L., Kang, C., & Zhang, Y. (2016). Exercise-induced hormesis and skeletal muscle health. Free Radical Biology and Medicine, 98, 113-122.</div><div><br /></div><div>Caloric Restriction Hormesis, </div><div>Turturro, A., Hass, B. S., & Hart, R. W. (2000). Does caloric restriction induce hormesis?. Human & experimental toxicology, 19(6), 320-329. </div><div><br /></div><div>Phytochemical Hormesis</div><div>Son, T. G., Camandola, S., & Mattson, M. P. (2008). Hormetic dietary phytochemicals. Neuromolecular medicine, 10, 236-246.</div><div><br /></div><p></p><div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-67228172546431952612022-08-23T13:55:00.002-07:002022-08-23T13:55:32.589-07:00Summary of "Politics of Anguish" (book)<p><span style="font-family: Calibri, sans-serif; font-size: 12pt; text-align: justify; white-space: pre-wrap;">Chapter 1 : The Creation of a New Disease</span></p><span id="docs-internal-guid-db57d7ce-7fff-98ad-3fdb-32610cafe145"><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Feared more than cancer or heart attack, Alzheimer’s disease has now capture people’s fears and worries. But finding how the disease develops and then progresses has eluded scientists. Going back in time when Dr. Alois Alzheimer observed the new disease provides some evidence and clues to why we have failed to control this disease. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Finding that there were some clamping of neurons, plaques and tangles, in the brain was not a new discovery. But the creation of this new disease relied on other issues at the time. It relied on a belief that certain people are inferior, that politically it was beneficial for the Munich clinic to define this new disease to compete with the Prague clinic, and the belief that old age is a dustbin of medical problems. The motivation for creating this new disease was not only scientific but also political in 1900 Germany.</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Alzheimer’s disease stayed dormant until the 1950s when American scientists started looking at diseases of older age and searching for cures. By the 1970’s the zeal of searching for a pill to cure all maladies, including Alzheimer’s disease, blinded researchers and they lost focus on how the disease develops and progresses.</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">The foundation of the science is however unstable. The initial observations that Alzheimer observed, the plaques and the tangles, were common, not just for Alzheimer’s disease but also for many other diseases including neurosyphilis (Dr. Alzheimer’s speciiality.) The plaques and the tangles did not directly cause the disease as many people had these in their brain but never developed the disease. This is a story of how the most frightening disease in the world was created by a perfect storm. Today we are left with disorganized research and a 100% failure of finding a cure or a way of slowing the disease. The future looks bleak and we can only understand this present situation by looking back in history. </span></p><br /><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Chapter 1: The Creation of a New Disease </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">What Alois Alzheimer identified more than a century ago was an early onset dementia that was important, but not for the reasons he and his clinic director Emil Kraepelin presumed. Initially Alzheimer saw a pattern that fit the biological proof in support of the clinical observations—plaques and tangles and early-age of onset. Subsequent researchers fell into the same pattern: a habitual research method of finding proof. We now know that these criteria are not discrete enough to both define and predict Alzheimer’s disease. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">And we know this because of the ambivalence of the neurobiology, of how the plaques and tangles relate to the disease. Questions arose from the beginning, which to this day we still cannot answer, because there is a problem with what we are trying to explain. Other than familial Alzheimer’s disease, the remaining paths of the disease are random and cannot be measured reliably. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Clinicians remain dependent on prognostic tools that are unreliable. There remains a healthy discussion about the validity of the diagnosis. Research on the clinical features of Alzheimer’s disease is based on combining many short–term, specific, small, cross-sectional study samples. As a result research is fragmented and confusing. Whether by choice or chance we are told that the salvation to this disease will come from a cure. But this construct contains a falsehood. A similar search for laboratory proof is currently being undertaken for Alzheimer’s disease. But how did this state of disorganization in research come about? To find an answer we have to move away from science and look closer at the politics of the disease.</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Chapter 2: Politics </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Only tenuous evidence existed that separate Alzheimer’s disease from senile dementia. The current consensus among researchers is that Alzheimer’s disease and senile dementia are indistinguishable in contrast to Alzheimer’s belief. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">The imperative to promote a more biological psychiatry was a paradigm-changing endeavor in the 20th century. Alzheimer’s disease played a major role in contributing to psychiatry’s reliance on neurobiology, biology, chemistry and genetics. Because of its prominence, Alzheimer’s disease will likely play a large role in the future of psychiatry. This prediction is being realized with the introduction in 2010 of the NIH-sponsored Research and Domain Criteria (RDoC) which integrates biomarkers, genomics and clinical observations to define both normal and abnormal behavior. Alzheimer’s disease is the proving concept for this new U.S. federally-funded nosology.</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">The fact that in the 1900s the Munich laboratory competed with the Prague laboratory was also a factor. Even today, biomedical research remains a highly competitive field. Nowadays biomedical research seems particularly prone to fraud because of the level of competition among clinics. Back in the 1900s Kraepelin understood this competition which played a significant role in the scramble to be the first to define Alzheimer’s disease. The belief that some people are different from others because of genetics may have also helped Kraepelin assert the distinction between Alzheimer’s disease and senile dementia. The eugenics argument is rarely mentioned in the literature despite the importance of the philosophy in academic circles at the turn of the 20th century. The fact that most of Kraepelin’s perceived competitors were Jewish—at a time when Jews were considered inferior by some groups—could not have been a small consideration. As an example, Fischer’s obscurity and his early demise in prison because of his Jewish beliefs, is another indication of the strong undercurrent of racist beliefs at the time. Although Fischer’s insights into dementia have now been vindicated his legacy remains obscured. But of all these factors, the central issue was—and still is—ageism. If Alzheimer could not argue that this new disease was not just for older people, there would be no classification of a new disease. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Diseases of old age are not news. For most of the past century, it was assumed that old age is a stage of dying and therefore associated with decrepitude. Older adults were meant to have diseases and die. No medical interest exists to subvert such inevitability. The reason why Alzheimer’s disease gained traction is because, for the first time, the disease was affecting younger people. The importance of these prejudices are present with us today. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">The birth of Alzheimer’s disease as we know it today, was more than simply a new clinical observation it also had political overtones. It reflected the stereotypes of the time. In 2011, the NIA changed the definition of Alzheimer’s disease to allow the pharmaceutical industry to experiment with a clinical disease before it becomes diagnosed (pre-clincial). But this is creating costly and divergent research. After a century of research we are still unclear about the diseases that come under Alzheimer’s diseases and sadly, we are not closer to understand what causes Alzheimer’s disease or its many variants. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Chapter 3: Disorganized research</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Several major sources of confusion remain in Alzheimer’s disease research. The primary confounder comes from the fact that we do not know what Alzheimer’s disease is, and even if we did, we cannot reliably diagnose it, either clinically or neurobiologically. Even if we accept the NIA’s pre-clinical stage of Alzheimer’s disease, the validity and reliability of pre-clinical data is poor at best, and contradictory at worst. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">The varied causes of cognitive diseases are not well understood. Gaining knowledge about chemical, neurological and biological pathways and processes does not directly contribute to our understanding of behavioral or clinical disorders. After more than a hundred years of research, there remains a lack of understanding of whether one disease has different expressions—Alzheimer’s disease, Lewy Body Dementia, Vascular dementia—or whether different disease processes lead to the same pathway of expression—Alzheimer’s disease caused by physical trauma, bacteria, virus or vascular disease. Therefore, it is difficult to make distinct and accurate diagnoses. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">The concept that Alzheimer’s disease is not a disease but a syndrome provides an impetus for more research by examining the process of the disease, rather than investing all research efforts in finding a cure. The cause/s of the disease are still unknown. Correlational studies might imply causation but this is psychology, not science. Researchers need to admit that the results are puzzling because we are working from an incomplete theory—one that we need to update.</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">The second source of confusion comes from the great variance among older adults—heteroscidasticity. Even among identical twins, this drift can result in one twin getting Alzheimer’s while the other escapes. This relates to epigenetic changes that influence both brain plasticity and neurogenesis. This variance, that increases among individuals as they age, will continue to dilute the linear association between a specific neuropathology and its expression, especially among older adults. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Although researchers look for genetic markers that will eliminate all these epigenetic or environmental factors, so far The Alzheimer’s forum has identified more than 1,395 studies working on 695 genes that account for up to 0.5 percent of Alzheimer’s disease. If 695 genes account for half of one percent of Alzheimer’s disease, then even if researchers can identify and manipulate all of these genes the disease will not be cured. This criticism, that genetic studies cannot explain all the variance of Alzheimer’s disease, can be applied to the search for biomarkers, both biological and chemical. The only challenge to the current expression of biological determinism is the fact that there is no competing paradigm to guide research. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">The deduction is that confusion becomes a ploy, not a failure or an expression of incompetence. Confusion as a method allows a small research group connected with the NIA to dictate and continuously change the meaning of the disease. Regardless of the intention, the result is obvious. Confusion and uncertainty have created great fear. This confusion unfortunately spills over into clinical practice as well, affecting patients, their families and their rights as citizens. Alzheimer’s disease is over-registered and over-diagnosed with consequential wasted health care costs and undue stress to the family. Perhaps the confusion is that we did not understand that our fear of Alzheimer’s disease has become a neurobiolgical playground where we have feverishly worked ourselves into a research cul de sac. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Chapter 4: Research cul de sac</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">The inductive method of observing a disease to learn what people have in common creates a false syllogism—a fallacy. Just because everyone with dementia has the neuropathology, we cannot logically argue that everyone with the neuropathology will have dementia. Because science should also be based on a deductive model, where theory directs the line of investigation, researchers need to conduct more theory-driven hypothesis testing. A mounting body of evidence does not support the theoretical construct that a linear causal pathway exists between a biomarker, causing MCI that then matures into a dementing illness. Infact a systematic review of the literature agues for broad use of techniques to counter MCI. Partly for this reason, we see very little deductive reasoning in research on Alzheimer’s disease, although it is evident in neurobiological studies. The two worlds of neuroscience and clinical services that are evident in Alzheimer’s disease remain distinct, separate and divorced. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">The lack of validity, across a whole spectrum of issues in Alzheimer’s disease research is a negative statement. The anomalies point to the necessity of expanding the concept of biomarkers to explain how they might be moderated or mediated by other, as of yet unexplored factors. It could be that the plaques and tangles are like scarring on a wound—indicative of a trauma but serving as a protective feature. Clearing the scab will not change the underlying trauma and might even be detrimental to the healing process. We are leading to potential situations where despite being competent and having normal memory and behavior, a patient might still be diagnosed with dementia. Such is the mission of the Research Domain Criteria. We need to resist this biological determinism mode of thinking, which is becoming more and more prevalent, and which has negative repercussions on our relationship with our medical and legal institutions. Alzheimer’s disease is playing a major role in persuading researchers to adopt such a system of biological determinism. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">The relationship between Alzheimer’s disease and changes in the normal aging processes need to be distinguished. One possible clue could be the speed of attrition. Even though we still do not know enough about normal aging processes, sudden attrition might be indicative more of disease pathology. A longitudinal perspective is crucial for elucidating such a distinction. Despite all the ambiguity surrounding the disease, we see the disease as very real and very frightening. We remain fixated on it because it feeds a very personal and intimate fear. We accept a fanciful process of causation because it is safe to assume that we know how to approach the problem and possibly find a cure. But if we reinterpret the philosophy behind our fear of Alzheimer’s disease we might arrive at some basic understanding that might help in defining a new, badly-needed research paradigm. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Chapter 5: Philosophy of Alzheimer’s disease</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">People need a consistent, stable sense of self throughout their lifetimes, including when they self-project into future situations. This is the essence of being, of Dasein. A purely neurobiological model of cognition cannot explain some basic anomalies in research. For example, a woman misdiagnosed with Alzheimer’s disease nevertheless makes herself believe that she has the disease; men who pretend to be 20 years younger become younger; and clusters of people who have very long lives age well without Alzheimer’s disease but these clusters are found only in small geographic areas. All these events can help us understand the dynamics of our reality, our being. This is the study of ontology. Such preoccupations have also received validation from neurological studies. The next frontier involves accepting a broader definition of being—of Dasein—that includes others, the environment and our geography. It is not biological determinism, because the biology/genetics is determined by the environment and our interpretation of that environment. We own the biology as well as the environment.</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">There is a cultural condition of the fear of Alzheimer’s disease. That there is an element of self–limitation, of a self-fulfilling prophecy and it may be time to question our own mindsets. Older adults report that their fear of Alzheimer’s disease has increased from the second most feared disease to the most feared disease. Fear of dementia is now so strong that there is a new term: “Dementiaphobia”. This alone represents significant condition of our Dasein—both in terms of what we care about (gaining ownership of beliefs and ideas), the Facticity (we have no control over whether we get Alzheimer’s disease), and also in our personal projections of the future (the likelihood that we are going to get Alzheimer’s disease). </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">In this context, fear has already limited our ability to deal with negative cognitive episodes. This is a constant in our lives. Many opportunities exist to misinterpret cognitive decline as both long-term and Alzheimer’s disease-related. Fear is nuanced. A family member suffering Alzheimer’s disease creates a template for us to follow, a mindset, especially if we provide care for them. There is significant deterioration in the health of caregivers when compared to a similar group of non-caregivers. Caregiving becomes more stressful the longer one does it. The stress does not stop when the care recipient dies. Also seen in the “widowhood effect”—where the surviving spouse dies soon after their partner—exemplifies how intimate relationships define what is important in life. Death following spousal death among older adults has been estimated at between 30 percent and 90 percent in the short term, and around 15 percent in the long term. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Not only are we led to believe that Alzheimer’s disease is random without any control, caring for a loved one with Alzheimer’s disease magnifies this as a likelihood in our future. This association might contribute more to familial dementia then genetic factors. Because we learn by experience we are sensitized to look for “signs” of the disease that we then use to promote the likelihood that we will get the disease. “We have nothing to fear but fear itself” is the new watchword for Alzheimer’s disease. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Chapter 6: Complexity Theory of Dementias</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">The brain is the most complex organ in the universe. Nothing else is more complex. The simple theory that two misfolded proteins by themselves create a breakdown of thinking is not accurate. Theories based on the Amyloid Cascade hypothesis are incomplete. Emerging evidence points to a more complex process. There are many possible causes of dementia. The initial injury might or might not progress. The neurological disease might or might not affect cognition. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">These considerations are valid and have been left out of the new research agenda. Our conventional reliance on genetic causes is similarly simplistic. Accepting the evidence that external injury (viral, bacterial, biological, chemical, environmental, behavioral) can initiate dementia reframes the disease as a public health issue. In this case, we can alleviate or minimize some of these causes. We are already doing this with head trauma in sports with new protocols for diagnosis and treatment. Other injuries that are shown to contribute to dementias should be similarly addressed. By addressing potential traumas, perhaps we could eventually prevent most of the initial causes of the disease. Such an approach opens the door to positive, creative prevention. Adjusting the focus to include the study of multiple causes also brings the disease squarely into the public health field. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">A central puzzle of dementias is the penumbra. Also, a feature of stroke, the penumbra or shadow that accompanies the surrounding dead tissue in the brain might explain why some stroke victims experience the growth of the penumbra that eventually leads to dementia. The process of penumbra raises radical scientific questions about the progression of dementias and whether or not the neuropathology can be contained. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Perfusion (blood circulation) and the role of vascular conditions play a major role in dementias. Emphasizing the roles of an active lifestyle, healthy diet, and awareness of vascular issues moves the discussion further into the public health realm. Within Complexity Theory, the concept of the brain functioning as a machine is incorrect. Even dementia patients learn new things, and they sometimes forget things then remember them, or have episodes of clarity. How can we explain this fluctuation through neuronal death? Appreciating that parts of the brain can continue to grow, switch capacity from left to right and back to front, and vice versa, and acknowledging that cognition might be an assimilation of different systems within the same brain, will help researchers ask more incisive questions about the role of the brain. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Acknowledging that the brain is always changing, neurons and glial cells constantly die and get replaced, where more than 30,000 proteins constantly misfold and get degraded, where constant injuries to the brain are accommodated, where memories are constantly re-imaged and prioritized, where cognitive functions are shifted from one area of the brain to another, all of these events define the daily functioning of our brain. The question that needs to be asked is why does this constant maintenance stops or becomes overwhelmed?</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Science will benefit from a resurgence of sociological and philosophical discussion about the role of cognition in the mind, the distinction between mind and brain, and the concept of self. All these broad discussions have been rejected in preference for the more simplistic explanation. So far, after a century of confusion, it is time to stop repeating the same mistakes in the hope of coming up with new results. We need a new methodology that might provide different results. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Chapter 7: Synthesis</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">A more inclusive approach allows diverse literature to be included rather than ignored. The body as a sovereign entity a self-willed, independent, exclusive and free agent is an illusion. Ample evidence now shows that our body—meaning our brain and body—not only respond to external activity but also mirrors these activities. External influences—of which we are unaware most of the time—affect how we think, behave and feel. Social constructs, memes, and stereotypes affect us because we internalize and operationalize them within us. There is no impermeable barrier between our external environment and our body; an illusion of the mind creates this duality. No better example exposes this illusion than dementias and aging. The crescendo of fear of dementias affects us. We often live trapped in a world where fear dictates our future. Fear of dementia as represented by Alzheimer’s disease now represents perhaps the penultimate disease meme of the 21st century. To combat this we need to expand our study of dementias to include social and psychological factors, otherwise, we will remain in our current research cul de sac. We need to shift from a hypercognitive model to a caring model. Care might lead to a cure. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Chapter 8: Epilogue</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">This is as far as science can take us. Criticism of dementia research dictates a number of changes that need to be made at the Federal level to promote a healthier and more inclusive scientific debate. Scientists need to be very sure of what they are studying and to emphasize the validity and reliability of their subject matter. Such recommendations are necessarily abstract, nuanced, and academic. But on a more personal level, I can identify the basic parameters of the data and conjecture how I see this Complexity Theory apply at an individual level. This is not prescriptive in any way but the start of a discussion away from the neurobiology. </span></p><br /><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Recommendation for self-help</span></p><br /><p dir="ltr" style="line-height: 1.2; margin-bottom: 10pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Calibri, sans-serif; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Summary and Class Discussion Points</span></p><br /><br /><br /></span><div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-56997132787621326732022-08-23T13:43:00.001-07:002022-08-23T13:43:19.145-07:00 Older Smell <span id="docs-internal-guid-efd618f1-7fff-f27d-f13d-5f1bd72290c5"><p dir="ltr" style="background-color: white; line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify; text-indent: 22.5pt;"><span style="background-color: transparent; font-size: 13pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span style="font-family: arial;">On their return from visiting a nursing home, my children when we were in kindergarten happily shared with me their impression that the residents “smell.” A nursing home is not the best place to get to know older adults, but the stereotype remains. There are even some fancy scientific theories to explain why this is so. We know that taste and smell diminish with age, but that older people also have a distinct odor is worth exploring.</span></span></p><p dir="ltr" style="background-color: white; line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify; text-indent: 22.5pt;"><span style="font-family: arial;"><span style="background-color: transparent; font-size: 13pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Visiting Japan, one is immediately faced with the strict culture of washing and bad odor is frowned upon. The Japanese even have a distinct name for the body odor of older people </span><span style="background-color: transparent; font-size: 13pt; font-style: italic; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Kareishu</span><span style="background-color: transparent; font-size: 13pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">. After conducting a poll of 150 men and women, the Japanese Shiseido Group found that odor from older people is the second most offensive scent behind bad breath. We will return to this study later on. </span></span></p><p dir="ltr" style="background-color: white; line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify; text-indent: 22.5pt;"><span style="background-color: transparent; font-size: 13pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span style="font-family: arial;">Body odor in humans is determined by various factors, including genetic background, physiological conditions, behavioral patterns, food ingestion, and disease types, but most often there is a stereotype that it relates to getting old. The theory is that older people smell because of their aging biology. One theory suggests that aging causes hormonal imbalances resulting in more lipid acid in our skin. And as skin matures, its natural antioxidant protection decreases, resulting in greater oxidation of this lipid acid resulting in Nonenal. The smell of this chemical compound is similar to oil that goes rancid when left out. This chemical is more common among people over 40 years of age. Another biological theory is that the major contributor is the bacterial activity in skin gland secretions. Numerous skin bacteria help produce smelly substances and as we get older this bacteria seems to be more common. </span></span></p><p dir="ltr" style="background-color: white; line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify; text-indent: 22.5pt;"><span style="font-family: arial;"><span style="background-color: transparent; font-size: 13pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">It could also be related to diet. In 2017 Jun Nishihira with Hokkaido Information University and his colleagues reported that eating a mushroom extract (Champignon) was found to improve body smell, as well as bad breath and smelly poo. The idea that perhaps we can counteract this </span><span style="background-color: transparent; font-size: 13pt; font-style: italic; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Kareishu </span><span style="background-color: transparent; font-size: 13pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">was explored by Dae Youn Hwang with Pusan National University, Republic of Korea, and his colleagues. They found that extracts of Spiraea Japonica—a deciduous, perennial shrub native to Japan—reduced the odor of older adults. </span></span></p><p dir="ltr" style="background-color: white; line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify; text-indent: 22.5pt;"><span style="font-family: arial;"><span style="background-color: transparent; font-size: 13pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Developing products to counteract </span><span style="background-color: transparent; font-size: 13pt; font-style: italic; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Kareishu </span><span style="background-color: transparent; font-size: 13pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">opens the market to businesses making money off older people’s fears and stereotypes. Shiseido Group at one point developed a perfume "Harmonage Fragrance" specifically formulated to neutralize older people’s body odor. Then there is the line of anti-age-stench soaps by Mirai Clinical that this time uses persimmon extract as a natural deodorizer. The issue is not that body odor changes with age, it does, the issue is whether this smell is bad. </span></span></p><p dir="ltr" style="background-color: white; line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify; text-indent: 22.5pt;"><span style="background-color: transparent; font-size: 13pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span style="font-family: arial;">Researchers have shown that the body odors of some animals—including mice, black-tailed deer, otters, owls, and rabbits—change with age and that animals can distinguish their young and old peers by smell. Even people can tell the difference between old and young otters and rabbits by how they smell. </span></span></p><p dir="ltr" style="background-color: white; line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify; text-indent: 22.5pt;"><span style="background-color: transparent; font-size: 13pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span style="font-family: arial;">Older people might smell differently from younger people, but this is not always a bad smell. We know for example, that some frail older people experience difficulties in mobility and getting washed, but those that are still functional and maintain good hygiene might be different.</span></span></p><p dir="ltr" style="background-color: white; line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify; text-indent: 22.5pt;"><span style="background-color: transparent; font-size: 13pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span style="font-family: arial;">Johan Lundström and his colleagues at the University of Pennsylvania stitched absorbent pads into the armpits of T-shirts and asked volunteers of different ages to sleep in the shirts for five consecutive nights. During the day, the volunteers stored the T-shirts in sealed plastic bags; avoided spicy foods, cigarettes, and alcohol; and showered with odorless shampoo and soap. After the fifth night, blindfolded volunteers rated the pads and found elderly people's odors both less intense and less unpleasant than odors from young and middle-aged people. Middle-aged men had the most unpleasant odor while the odors of middle-aged women were judged to be the most pleasant. Old people's smell was often instantly recognizable and not necessarily in a bad way. The result from this study is different from the earlier study by the Shiseido Group. But then again if I am selling a fragrance I want to create a market of smelly older adults so that they will buy my fragrance. In reality, older adults might smell differently but not in a bad way. The lesson is how easily we accept the negative stereotype of older people smelling.</span></span></p><span style="font-family: arial;"><div><span><span style="font-family: arial;"><br /></span></span></div></span><b>Kenkou to Yoi Tomodachi 4</b><span style="font-family: arial;"><br /><br /><br /></span><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt;"><span style="background-color: white; color: #222222; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span style="font-family: arial;">References</span></span></p><span style="font-family: arial;"><br /></span><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt;"><span style="font-family: arial;"><span style="background-color: white; color: #222222; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Nishihira, J., Nishimura, M., Tanaka, A., Yamaguchi, A., & Taira, T. (2017). Effects of 4-week continuous ingestion of champignon extract on halitosis and body and fecal odor. </span><span style="background-color: white; color: #222222; font-size: 12pt; font-style: italic; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Journal of Traditional and Complementary Medicine</span><span style="background-color: white; color: #222222; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">, </span><span style="background-color: white; color: #222222; font-size: 12pt; font-style: italic; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">7</span><span style="background-color: white; color: #222222; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">(1), 110-116.</span></span></p><span style="font-family: arial;"><br /></span><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt;"><span style="font-family: arial;"><span style="background-color: white; color: #222222; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Kim, J. E., Choi, Y. J., Lee, S. J., Gong, J. E., Seong, J. E., Park, S. H., & Hwang, D. Y. (2022). Evaluation of Deodorizing Effects of Saccharina japonica in 10-Month-Old ICR Mice Using a Novel Odor Marker Associated with Aging. </span><span style="background-color: white; color: #222222; font-size: 12pt; font-style: italic; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Evidence-Based Complementary and Alternative Medicine</span><span style="background-color: white; color: #222222; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">, </span><span style="background-color: white; color: #222222; font-size: 12pt; font-style: italic; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">2022</span><span style="background-color: white; color: #222222; font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">.</span></span></p><span style="font-family: arial;"><br /><br /></span><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt;"><a href="https://www.scientificamerican.com/article/old-person-smell/" style="text-decoration-line: none;"><span style="color: blue; font-size: 13pt; font-variant-east-asian: normal; font-variant-numeric: normal; text-decoration-line: underline; text-decoration-skip-ink: none; vertical-align: baseline; white-space: pre-wrap;"><span style="font-family: arial;">https://www.scientificamerican.com/article/old-person-smell/</span></span></a></p><span style="font-family: arial;"><br /></span><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt;"><span style="font-family: arial;"><span style="background-color: white; color: #222222; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Mitro, S., Gordon, A. R., Olsson, M. J., & Lundström, J. N. (2012). The smell of age: perception and discrimination of body odors of different ages. </span><span style="background-color: white; color: #222222; font-size: 10pt; font-style: italic; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">PloS one</span><span style="background-color: white; color: #222222; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">, </span><span style="background-color: white; color: #222222; font-size: 10pt; font-style: italic; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">7</span><span style="background-color: white; color: #222222; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">(5), e38110.</span></span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt;"><span style="font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span style="font-family: arial;">https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0038110</span></span></p><div><span style="font-size: 12pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><br /></span></div></span><div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-65824033054216851212022-08-23T13:38:00.004-07:002022-08-23T13:38:39.150-07:00Hospice<p><span style="font-family: arial; font-size: 10pt; text-align: justify; white-space: pre-wrap;">When talking about gerontology—the study of older people—most people assume that it is a new study as they have not heard of it. The same goes for hospice. If you bring it up in a conversation most people will know of someone who went through hospice, but again they think that this is a current trend, something new. So, it comes as a bit of a shock when people learn that gerontology is as old as writing itself. The first known record of writing is the Sumerian Saga of Gilgamesh about 4,000 years ago. The most famous of the five poems is "Gilgamesh, Enkidu, and the Netherworld." a poem that describes the love that King Gilgamesh has for Enkidu, a half-god when he tragically dies. An event that sets Gilgamesh on a search to find a cure for aging and to death in order to bring his friend back from the dead. The story has spawned many others, and there are traces of this story everywhere, including in the bible. It is important to understand that the first evidence we have of literature dealt with getting old and dying. </span></p><span id="docs-internal-guid-96d7165e-7fff-1a77-4424-84208b0e8fdc"><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span style="font-family: arial;">Even the term “gerontology” was used in 1903 by Ilya Mechnikov, an immunologist who with Paul Ehrlich was jointly awarded the 1908 Nobel Prize in Physiology or Medicine. Gerontology even fathered the discipline of endocrinology (the study of hormones) and transplantation (transplanting organs). A hundred and twenty years later, people still think that gerontology is new because they do not want to think about aging and about dying. This is very much true in Japan as well. In 2016 Mitsunori Miyashita with the University of Tokyo asked Japanese people about a ‘good death’ and showed that they tended to avoid thinking about it. The study also found that they gave their family a large say in how they should die. We do not want to think about death. </span></span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span style="font-family: arial;">Hospice provides care for people who are dying. Such care was first established during the Crusades in the years after 1000 and became widespread in the Middle Ages. It formally became a branch of medicine when Cicely Saunders founded St. Christopher’s Hospice in London in 1967. This first hospice set the stage for other hospices throughout the world. In Japan, the first systematic palliative care service was launched at Yodogawa Christian Hospital, Osaka, in 1973, and then in 1981, the first palliative care unit (PCU) was opened at Seirei Mikatahara General Hospital, Shizuoka. After 1990 when insurance started covering PCU treatment, hospice grew into a national service that covered all of Japan. By 2017, there were 394 PCUs with 8,068 beds. All of the designated cancer hospitals have PCUs. </span></span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span style="font-family: arial;">In Japan, like in every other country, most people want to die at home and a third want to die at PCUs. However, the reality is that most die in hospitals. Masanori Mori and Tatsuya Morita have identified the need for more training and better specialization in Japan to promote better and more accessible care for the dying. And there have been great advances. By 2015 there were more than 50,000 physicians trained in palliative care. While a study that started in 2008 to monitor palliative care in Japan called the Outreach Palliative Care Trial of Integrated Regional Model (OPTIM) has recently found that Nurses' palliative care knowledge, and practice improved with more training. </span></span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span style="font-family: arial;">The fundamental problem with hospice relates to what we discussed earlier in the introduction, people do not want to talk about it, and that includes physicians and nurses. Health care workers do not want to go into hospice. If you are part of a profession of saving people’s lives then helping them to die seems contradictory. Most people leave hospice till the very end. Others shy away from contacting hospice, even though most hospice services can be delivered to your home. The only way to change this is to accept death as part of the cycle of life. Talking about death does not have to be sad as it can highlight the privilege of being alive. By appreciating that having a good death needs to be planned. We have known this for centuries perhaps now is the time to accept it for ourselves.</span></span></p><span style="font-family: arial;"><br /></span><b>Kenkou to Yoi Tomodach 3</b><span style="font-family: arial;"><br /><br /></span><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span style="font-family: arial;">References</span></span></p><span style="font-family: arial;"><br /></span><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt;"><span style="font-family: arial;"><span style="background-color: white; color: #222222; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Mori, M., & Morita, T. (2016). Advances in hospice and palliative care in Japan: A review paper. </span><span style="background-color: white; color: #222222; font-size: 10pt; font-style: italic; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">The Korean Journal of Hospice and Palliative Care</span><span style="background-color: white; color: #222222; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">, </span><span style="background-color: white; color: #222222; font-size: 10pt; font-style: italic; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">19</span><span style="background-color: white; color: #222222; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">(4), 283-291.</span></span></p><span style="font-family: arial;"><br /></span><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span style="font-family: arial;">Nakazawa, Y., Kato, M., Miyashita, M., Morita, T., & Kizawa, Y. (2018). Changes in nurses' knowledge, difficulties, and self-reported practices toward palliative care for cancer patients in Japan: an analysis of two nationwide representative surveys in 2008 and 2015. Journal of pain and symptom management, 55(2), 402-412.</span></span></p><span style="font-family: arial;"><br /></span><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span style="font-family: arial;">What are the main challenges facing palliative/end-of-life care today in relation to Japan’s ageing society</span></span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span style="font-family: arial;">Posted on January 31, 2018 by pallcare</span></span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span style="font-family: arial;">Mariko Masujima, Principal Investigator, and Zaiya Takahashi, Core Promoter, the Center of Excellence for End-of-Life Care at Chiba University, describe the present situation, policy and cultures about end-of-life care in Japan.</span></span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span style="font-family: arial;">Accessed: https://eapcnet.wordpress.com/2018/01/31/what-are-the-main-challenges-facing-palliative-end-of-life-care-today-in-relation-to-japans-ageing-society/</span></span></p><div><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><br /></span></div></span><div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-49921594096957917102022-08-23T13:36:00.001-07:002022-08-23T13:36:14.752-07:00 Drugs and Older Adults<p><span style="font-family: Garamond, serif; font-size: 10pt; text-align: justify; white-space: pre-wrap;">America is the country for sex, drugs, and rock and roll….well maybe just drugs and rock & roll. Americans can be very traditional when it comes to discussing sex, but as for drugs we use medication as much as the Japanese. Most Americans are on some kind of medication or illicit drug. During 2015–2016, almost half of the U.S. population, including children, used one or more prescription drugs. If you include recreational drugs, alcohol, and tobacco then you can assume that nearly everyone is on some kind of mood-altering drug. In addition, nearly everyone takes caffeine, either from coffee, soft drinks, or tea. Drugs are everywhere and they are differentiated only by whether they are legal or not and whether they are prescribed by a doctor or self-administered.</span></p><span id="docs-internal-guid-3a1dc5c9-7fff-db8a-bfe3-6feffc7f49a3"><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">When discussing the problem of drugs, most people fall into the habit of automatically blaming recreational drugs. There is a long-standing myth that drug abuse is rare among older adults. The belief was that long-term drug addicts either recovered or died, and that addiction and use of illegal drugs by older adults were restricted to a small group of older criminals. But when we look at reality a different picture emerges. It is prescription medication among older people that is a primary concern. It is legal medications that cause more harm--those prescribed by your doctor--or those that you can buy from a pharmacy off-the-shelf. Prescription drugs are more popular with older people, especially older women. Pain relievers remain the most popular drug for the last two decades. Nearly a third of adults over 65 are on prescription medication. Most of these are not addictive, but the most popular medicines are, especially those for pain relievers.</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">While we see older men being addicted to alcohol and illicit drugs, older women are more likely to be addicted to pain medication like sedatives, hypnotics, and anxiolytics for anxiety. One type of anxiolytics is Benzodiazepines, which treat anxiety, pain, or insomnia, and are highly addictive and common. There are also common medications that older adults should not be taking. These drugs are updated every year under the BEERS criteria. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Some medications might also be used inappropriately either intentionally or through forgetfulness. Older adults forget what medications they are on, and when and how to take them. Even though the US spends more on medications than any other country—mainly because we pay more for drugs than most countries—Japan leads the world in prescribing medications for older adults. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">When the world saw a decline in life expectancy for the first time this century in 2014, that was not due to wars, in the US this was attributed to the over-prescription of opioid medication. Promoted by big pharma, opioids were sold with the lie that they were not addictive. There was a fivefold increase in prescription opioid overdose deaths from 1996 to 2016 in the US. While newspapers focused on younger adults who misused prescription opioids, it was middle-aged and older adults between 50-64 years and older that use prescription opioids at a higher rate than any other group.</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Combined with alcohol, prescription drug abuse among older adults is one of the fastest-growing health problems in the US. Alcohol and prescription drug abuse affect up to one in six older adults. Since older adults have a decreased ability to metabolize chemicals, the drugs stay in the body longer and our brains seem to get more sensitive to these drugs. This makes it dangerous for older adults to use any drug, even if the person is not addicted. On top of this, there is self-abuse. One-tenth of all older adults are also binge drinkers—five or more drinks at a time. Binge drinkers were more likely to be male and more likely to also use tobacco and/or cannabis. In the US cannabis use among older adults increased to one in twenty people, especially among older men younger than 69. Prescription medication combined with other drugs does not mix well. With increasing access to geriatric doctors, nurses, and gerontologists we see a reduction in prescriptions and an overall improvement in life. In a complex world, having someone help you to navigate around these many drug options will benefit you to get the most from medications.</span></p><br /><i style="background-color: white; font-family: Arial, Tahoma, Helvetica, FreeSans, sans-serif; font-size: 13.2px;">Kenkou to Yoi Tomodachi 2</i></span><div><span><span style="font-family: Arial, Tahoma, Helvetica, FreeSans, sans-serif;"><span style="font-size: 13.2px;"><i><br /></i></span></span></span></div><div><span><span style="font-family: Arial, Tahoma, Helvetica, FreeSans, sans-serif;"><span style="font-size: 13.2px;"><i><br /></i></span></span><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">References</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Han, B. H., Moore, A. A., Ferris, R., & Palamar, J. J. (2019). Binge drinking among older adults in the United States, 2015 to 2017. Journal of the American Geriatrics Society, 67(10), 2139-2144.</span></p><br /><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Han, B. H., Sherman, S. E., & Palamar, J. J. (2019). Prescription opioid misuse among middle-aged and older adults in the United States, 2015–2016. Preventive medicine, 121, 94-98.</span></p><br /><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Tsuji</span><span style="font-family: "Cambria Math", serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">‐</span><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Hayashi, Y., Fukuhara, S., Green, J., & Kurokawa, K. (1999). Use of prescribed drugs among older people in Japan: association with not having a regular physician. Journal of the American Geriatrics Society, 47(12), 1425-1429.</span></p><br /><br /><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">https://www.addictioncenter.com/addiction/elderly/</span></p><br /><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">https://acpinternist.org/archives/2021/03/cannabis-use-increasing-among-older-adults.htm</span></p><br /><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">https://www.verywellmind.com/us-has-highest-levels-of-illegal-drug-use-67909</span></p><br /><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">https://www.cdc.gov/nchs/products/databriefs/db334.htm#:~:text=During%202015%E2%80%932016%2C%20almost%20one,the%20pattern%20varied%20by%20age.</span></p><br /><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">https://rehabs.com/blog/most-popular-drug-in-us-by-decade/</span></p><br /></span></div><div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-75584745219009726642022-08-23T13:10:00.001-07:002022-08-23T13:36:32.306-07:00 Ending our Story <p><span style="font-family: Garamond, serif; font-size: 10pt; text-align: justify; white-space: pre-wrap;">We have an image in our minds of how our life will progress. This is usually formed when we were children, so it is simplistic. It goes something like this: we grow up, make lots of money, get married, have kids, and live happily ever after. We quickly find that this story might not be true for us. But even though we might be disillusioned, what this tells us is that with these stories we like to predict. We like to tell a coherent story about our lives. It is part of how we are designed and we like to guess what will happen in the future, and we seem to do it for our own death as well.</span></p><span id="docs-internal-guid-b3487045-7fff-03bc-8555-03113cb6f4e2"><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">When we ask people how long they expect to live they will be surprised to learn that they are fairly accurate. We tend to underestimate how long we live but otherwise, it is fairly accurate. It is so accurate that statisticians who work with life insurance (actuaries) use this to adjust how long they expect us to live and therefore adjust how much we pay for life insurance.</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">David Phillips, with the University of California San Diego, has been looking at this phenomenon. In 1992 Phillips and his colleagues examined three million deaths from natural causes. Women are more likely to die in the week following their birthdays than in any other week of the year. It seems that females are able to prolong life enough it seems until they have reached a positive, symbolically meaningful occasion—their birthday. For women a birthday seems to function as a “lifeline.” In contrast, male deaths peak shortly before their birthday, suggesting that their birthday functions as a “deadline” for males. Older men are more likely to experience their looming birthday as a negative sign. The importance of a “lifeline” or a “deadline” also works for other significant days.</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">In 2016 Andrew Stickley and his colleagues looked at over 27,000 suicides in Japan between 2001–2010. What they found was that males were more likely to commit suicide around their birthday—5 days before and a week after their birthday. While females, they committed suicide 7–11 days before their birthday. In Japan, birthdays seem to be a deadline for both males and females. We find cultural variations throughout the world.</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">David Phillips and Elliot King showed that in a small Jewish group death declines by about a third below normal before the Jewish holiday of Passover and then peaks by the same amount the week after. It seems that Jewish people hold on to life a little bit longer to celebrate Passover. In contrast, non-Jewish deaths showed no such pattern around the same period.</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">The same is found for the Chinese who are less likely to die the week before the Harvest Moon Festival but peak the week after. In the West deaths spike during Christmas and New Year’s holiday period possibly because these periods are both stressful and indulgent. Also, people might delay seeking medical treatment during the festive season. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">Another interesting observation centers around Tetraphobia, the fear of the number “4” that is common in Japan, as well as in China, Taiwan, Singapore, Malaysia, Korea, and Vietnam. This superstition seems to have arisen from the similarity of the pronunciation of the word “four” and “death” in Japanese as well as in Mandarin and Cantonese. When looking at death from heart disease among Japanese and Chinese Americans we find that there are extra deaths on the fourth of the month. No such increases showed up among other populations. </span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">It is difficult to make any conclusions. Certain days such as our birthdate can have significance. We might see it as an accomplishment (for women) or as a deadline (for men), or as evidence of loneliness among suicidal Japanese. Some festivities which are stressful likely to hasten our demise (Christmas and New Year) while other holidays we might withstand till after they pass (Passover for Jews and Harvest Moon Festival for Chinese.) Then there are days that we fear that act as a self-fulfilling prophecy (the 4</span><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span style="font-size: 0.6em; vertical-align: super;">th</span></span><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"> of each month). What seems to emerge is that how we think about death influences when we die, at a minimum by a few days and at a maximum by some years.</span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><br /></span></p><p dir="ltr" style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt; text-align: justify;"><span style="font-family: Garamond, serif; font-size: 10pt; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><i style="background-color: white; font-family: Arial, Tahoma, Helvetica, FreeSans, sans-serif; font-size: 13.2px; text-align: start; white-space: normal;">Kenkou to Yoi Tomodachi 1</i></span></p><br /></span><div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-49549233567765822152022-08-22T17:23:00.008-07:002022-08-22T17:23:53.927-07:00Long Hiatus<p> After a long hiatus, more than two years off this blog post, I have decided to return to this medium. It is not that I have not been writing. I have published three books during this break from blogging, but I realize that my blogs reach more people that need to read about these advances in gerontology. </p><p>I have also been writing blogs for a Japanese newspaper called the <i>Kenkou to Yoi Tomodachi. </i>I have been writing monthly editorials, so I should start by reproducing them here first.</p><div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-31872027332800051042022-08-22T16:55:00.006-07:002022-08-22T16:57:33.451-07:00Most Popular Gerontology Professor in the USA according to Authority.org<p></p><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiOYmpSKwNwfA7VMhiDMBcAIe8flY2s3ZbfIDyGZ7l6j35gmtaSTmDVB_qa47RKgrEnfRMhKv7EkJvbk0JMbMCNDyL_hMi4xqeakHZTIz0_8KbrnSTAn1J44PG68-i5S8AcWXFLJIWJg24y96PO9EpoLVT8uJSFKaWRfjk2XdbXiCALJ3OmWvbzpnhLJA/s2048/Screen%20Shot%202022-08-21%20at%208.38.04%20PM.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1218" data-original-width="2048" height="307" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiOYmpSKwNwfA7VMhiDMBcAIe8flY2s3ZbfIDyGZ7l6j35gmtaSTmDVB_qa47RKgrEnfRMhKv7EkJvbk0JMbMCNDyL_hMi4xqeakHZTIz0_8KbrnSTAn1J44PG68-i5S8AcWXFLJIWJg24y96PO9EpoLVT8uJSFKaWRfjk2XdbXiCALJ3OmWvbzpnhLJA/w517-h307/Screen%20Shot%202022-08-21%20at%208.38.04%20PM.png" width="517" /></a></div><br /> https://www.authority.org/rankings/best-colleges-for-gerontology/professors<p></p><div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-39393218549258238582020-10-17T15:13:00.000-07:002020-10-17T15:13:29.971-07:00 Do older people have a chance of escaping COVID-19?<p>Everyone wants a simple answer to this 2020 COVID-19 pandemic. We have politicians forecasting that a vaccine is on its way that will save us. We are told that this is the only answer. But such predictions are misguided and wrong, especially for older people. A vaccine will not end the threat posed by COVID-19 or other viruses following. To appreciate this view, we need to understand how vaccines work.</p><p>We have a lot of experience with flu vaccines. The flu is much simpler than a cold virus (COVID-19 is a cold virus.)</p><p>Although there are four types of influenza (flu) viruses—A, B, C, and D—influenza A and B viruses are the only ones that cause flu pandemics. A-type viruses have two proteins called H and N. Since there are 18 types of H and 11 types of N there can 198 different A-viruses. B viruses have two types—Victoria and Yamagata—with sub-types. Every year we check what is happening in Asia and then we select a few flu viruses from there and develop vaccines. Vaccines usually include inactive viruses, dead viruses. In some cases, however, attenuated viruses (weakened live viruses) are used. </p><p>Vaccines work by pretending to infect the body and then the body reacts in three ways. It is best to see the body's reaction as a war with different types of defense: soldiers, mercenaries, and intelligence units. </p><p>The first line of attack are antibodies produced by B cells. Antibodies are soldiers, that either go out into the bloodstream to fight the viruses or stick close to the fort on the B cells. Antibodies have five methods of killing the virus and are therefore effective soldiers. Newly infected people are unlikely to have detectable antibodies during the first few days, but most develop them after one to three weeks. In the meantime, the second cell type that fights infections is T cells. One type of T cell is mercenaries that inject the virus with a lethal poison. Unlike antibodies, these T cells only fight one specific type of virus. They are very specific. Another type of T cell calls for help, especially from antibodies. In the absence of antibodies, T cells can control infection by themselves. What is interesting is that T cell responses are found in most COVID-19 patients that may last longer than antibodies. The third way the body reacts is through Natural Killer (NK) cells. If B-cells are soldiers, and T-cells are mercenaries, then NK-cells are the CIA, the intelligence unit. They kill viruses, cancer and they play an important role in pregnancy by differentiating the fetus as a special foreign body. Aging reduces the number and effectiveness of NK cells. Taken together, with reduced efficiency at generating antibodies due to reduced B- and T-cells, aging brings about a reduced resilience to infections in general and specifically to COVID-19.</p><p>Even with an effective vaccine, sometimes the vaccines completely miss the viruses that are around. The U.S. Centers for Disease Control and Prevention found that in 2018-2019 vaccines were effective between 12%-16%. with older adults having the lowest effectiveness despite having the highest vaccination rates. Meaning that on average the vaccines do not work in seven out of eight cases among older adults. Older adults do not produce enough antibodies even if they take the right vaccine. Most older adults are inefficient at producing antibodies. This is why even though older people take a flu vaccine they still get infected and some eventually still die from the flu. Flu deaths are higher among older people. Also, as Asim Biswas just discovered in 2020, because older adults have had many different colds and flu infections, these earlier antibodies may conflict with current vaccination. Our memory of infections reduces our ability to generate new antibodies. As a result, older adults are not only at greater risk of death and sickness from influenza than younger people, but they also have greater difficulty in developing protection when given the vaccine. </p><p>What is surprising is that sometimes it looks like the vaccines not only do not help but they might be detrimental. When the Canadian researcher Melissa Andrew and her colleagues in 2017 compared older adults who were vaccinated with those who were not vaccinated, they found that infections were higher among those who were vaccinated. The argument is that those that get vaccinated are more likely to be frail and prone to get infections in the first place. Most of the time there are other viruses that cause similar symptoms, but they are missed by the vaccines for that year. Tom Jefferson and his colleagues looked at many studies and found no evidence of a benefit of influenza vaccination in older adults. Meaning that it does not matter whether you take the vaccine or not. This is because there are many other viruses floating around at any one time, and that older adults, with or without a vaccine, do not cope well with these other viruses. </p><p>The complexity of flu is nothing compared to the complexity of the cold viruses. In addition, cold viruses persist in the environment and are resistant to most household disinfectants—which is why washing our hands is so important as we wash the viruses off our skin, but washing does not destroy them. Some cold viruses are lethal, killing more than a third of those infected, such as MERS-CoV, and some are inconvenient but harmless, such as the common cold. </p><p>There are two types of cold viruses either Adenovirus or Coronavirus. Each type has many, many subsets with a lot of variabilities. For example, there are 57 Adenovirus types (and hundreds, or maybe thousands, of sub-types). Then there are seven types of human Coronaviruses with many sub-types and mutations. With flu having two proteins in comparison cold viruses have many: COVID-19 for example has 29 proteins.</p><p>Because the T-cells are too specific and the COVID-19 mutates quickly—already in three months Los Alamos National labs found 14 strains—it is unlikely that T cells will be effective. Antibodies are still the best attack, except for older people who are not efficient at producing them, even with a vaccine. The Natural Killer cells are still an unknown in this fight and might be another avenue for controlling COVID-19 but we know older adults have fewer of these cells as well. Overall the only sure way we have of combating this disease is through social measures of reducing the probability of infection and reducing the infection load. Both can be achieved through the well-known drill of distancing, hand washing, wearing masks, and most importantly, not to gather. The world is going to be a distinctly different place. </p><p>The activity by drug companies is to develop therapies rather than vaccines. Therapies that address some of the effects of the disease, in particular, the lung infections that leave some of the COVID-19 victims scarred for life. But there is another side of the infection that is more worrisome, the infection to the brain. Recent studies showing that COVID-19 causes dementia takes us back to an awareness of how few tools we have to combat this disease. We know how difficult it is to treat the brain, as research on dementia has taught us, so this will be a challenge to address. In the end, we need to rely on preventing rather than attacking. The world has changed for all, but it will be especially different for older adults.</p><p><br /></p><p>Further Readings</p><p>Andrew, M. K., Shinde, V., Ye, L., Hatchette, T., Haguinet, F., Dos Santos, G., ... & Chit, A. (2017). The importance of frailty in the assessment of influenza vaccine effectiveness against influenza-related hospitalization in elderly people. The Journal of infectious diseases, 216(4), 405-414.</p><p>Bernstein, E., Kaye, D., Abrutyn, E., Gross, P., Dorfman, M., & Murasko, D. M. (1999). Immune response to influenza vaccination in a large healthy elderly population. Vaccine, 17(1), 82-94.</p><p>Biswas, A., Chakrabarti, A. K., & Dutta, S. (2020). Current challenges: from the path of “original antigenic sin” towards the development of universal flu vaccines: Flu vaccine efficacy encounters significant hurdles from pre-existing immunity of the host suggesting assessment of host immunity before vaccination. International Reviews of Immunology, 39(1), 21-36.</p><p>Centers for Disease Control and Prevention; Seasonal Influenza (Flu) (2017) Seasonal influenza vaccine effectiveness 2018-2019. Available at https://www.cdc.gov/flu/vaccines-work/2018-2019.html Accessed June 25, 2020</p><p>Jefferson, T., Di Pietrantonj, C., Al‐Ansary, L. A., Ferroni, E., Thorning, S., & Thomas, R. E. (2010). Vaccines for preventing influenza in the elderly. Cochrane database of systematic reviews, (2).</p><p>Varatharaj, A., Thomas, N., Ellul, M., Davies, N. W., Pollak, T., Tenorio, E. L., ... & Coles, J. P. (2020). UK-wide surveillance of neurological and neuropsychiatric complications of COVID-19: The first 153 patients. The Lancet Psychiatry.</p><p><br /></p><p><br /></p><div class="separator" style="clear: both; text-align: center;"><img alt="" border="0" class="placeholder" height="240" id="d54019470156" src="https://www.blogger.com/img/transparent.gif" style="background-color: #d8d8d8; background-image: url('https://fonts.gstatic.com/s/i/materialiconsextended/insert_photo/v6/grey600-24dp/1x/baseline_insert_photo_grey600_24dp.png'); background-position: center; background-repeat: no-repeat; opacity: 0.6;" width="320" /></div><br /><p></p><div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-32960439173883625452019-11-01T03:55:00.003-07:002019-11-01T03:55:20.033-07:00INDEX<div class="widget BlogArchive" data-version="1" id="BlogArchive1" style="background-color: white; font-family: Arial, Tahoma, Helvetica, FreeSans, sans-serif; font-size: 12px; line-height: 1.4; margin: 30px 0px; min-height: 0px; position: relative;">
<h2 style="font-size: 11px; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal; margin: 0px 0px 1em; position: relative;">
iAge Archive over 200 Blogs</h2>
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<li class="archivedate expanded" style="background: none; border-width: 0px; list-style: outside none none; margin: 0.25em 0px; padding: 0.25em 0px 0.25em 15px; text-indent: -15px;"><a class="toggle" href="https://www.blogger.com/null" style="color: inherit; cursor: pointer; font-family: Arial, sans-serif;"><span class="zippy toggle-open" style="color: #898989; line-height: 0.6em; text-shadow: rgba(0, 0, 0, 0.1) 2px 2px 1px;">▼ </span></a><a class="post-count-link" href="https://iage-marius.blogspot.com/2019/" style="color: #737373; text-decoration-line: none;">2019 </a><span class="post-count" dir="ltr">(2)</span><ul class="hierarchy" style="border-width: 0px; line-height: 1.2; list-style: none none; margin: 0px; padding: 0px;">
<li class="archivedate expanded" style="background: none; border-width: 0px; list-style: outside none none; margin: 0.25em 0px; padding: 0.25em 0px 0.25em 1.2em;"><a class="toggle" href="https://www.blogger.com/null" style="color: inherit; cursor: pointer; font-family: Arial, sans-serif;"><span class="zippy toggle-open" style="color: #898989; line-height: 0.6em; text-shadow: rgba(0, 0, 0, 0.1) 2px 2px 1px;">▼ </span></a><a class="post-count-link" href="https://iage-marius.blogspot.com/2019/10/" style="color: #737373; text-decoration-line: none;">October 2019 </a><span class="post-count" dir="ltr">(1)</span><ul class="posts" style="border-width: 0px; line-height: 1.2; list-style: none none; margin: 0px; padding: 0px;">
<li style="background: none; border-width: 0px; list-style: outside none none; margin: 0.25em 0px; padding: 0.25em 0px 0.25em 1.3em;"><a href="https://iage-marius.blogspot.com/2018/05/cartographer-of-mind.html" style="color: #737373; text-decoration-line: none;">Cartographer of the Mind</a></li>
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<li class="archivedate expanded" style="background: none; border-width: 0px; list-style: outside none none; margin: 0.25em 0px; padding: 0.25em 0px 0.25em 1.2em;"><a class="toggle" href="https://www.blogger.com/null" style="color: inherit; cursor: pointer; font-family: Arial, sans-serif;"><span class="zippy toggle-open" style="color: #898989; line-height: 0.6em; text-shadow: rgba(0, 0, 0, 0.1) 2px 2px 1px;">▼ </span> </a><a class="post-count-link" href="https://iage-marius.blogspot.com/2018/08/" style="color: #737373; text-decoration-line: none;">August 2018 </a><span class="post-count" dir="ltr">(2)</span><ul class="posts" style="border-width: 0px; line-height: 1.2; list-style: none none; margin: 0px; padding: 0px;">
<li style="background: none; border-width: 0px; list-style: outside none none; margin: 0.25em 0px; padding: 0.25em 0px 0.25em 1.3em;"><a href="https://iage-marius.blogspot.com/2018/08/the-san-diego-union-tribune.html" style="color: #737373; text-decoration-line: none;">THE SAN DIEGO UNION-TRIBUNE</a></li>
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<h2 style="font-size: 11px; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal; margin: 0px 0px 1em; position: relative;">
About Me</h2>
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<div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-5814495759140721262019-10-20T08:55:00.000-07:002019-10-20T08:55:04.706-07:00Cartographer of the MindThe exploration of the physical world would not have been possible without the skills of the map makers. There has not been any great discovery without a map that might have formed the basis for the exploration. In 2013, Jerry Brotton published <i>A History of the World in 12 Maps</i>, which described why specific maps were important in making history. Maps not only represent it, but they also determine our world. In 2017 following her GPS, a 23-year-old woman drove her Toyota Yaris straight into a lake in Ontario, Canada. Following in the path of Columbus who followed a similarly flawed map made around 1491 by Henricus Martellus, a German cartographers which had Japan straight ahead to the east of Spain. It was also third smaller, but compensated by using Arabian miles (1830 meters) rather than about 1,480 meters for Italian miles and which led Columbus to expect the voyage to Asia to be much shorter. He came across America by using a flawed map. Maps are the spring board to exploration, and in todays information overload, gaining a reference map helps in knowing where you are trying to get.<br />
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Today we need maps to navigate the information morass. We used to refer to this as the information highway, but there are no rules, no lanes, no order, different speed, erratic direction, unseen drivers, no drivers and many hope for sales. Everyone is selling. This is the Memorial Day sale of information, every imaginable interest pushing across their ideas. Fake news, fake science, conspiracy theories, shoddy research, pet theories and the awareness of relative truth presented together with the scientific and the spiritual.<div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-9116419546235608172019-09-16T06:38:00.000-07:002019-10-20T08:58:02.781-07:00Preparing for Death The Final FrontierOne in five Americans still die while using emergency services. One in seven of these emergency room deaths occur among patients 85 years and older. Although death is our only exit strategy in life, few of us are preparing for it. Ask any person how they want to die and they will have a definitive response, “quick and painless.” Yet despite this authoritative choice, we remain shy when planning to achieve such an exit--which is why many of us will end up in an emergency room to die. <br />
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A classic study conducted in Oregon—which has a state law for physician assisted suicide—found that twice the number of terminally ill hospice patients choose to speed their deaths by refusing food and drink rather than by physician assisted suicide. Their nurses reported that these patients, who typically died within two weeks, died more serenely than those who chose other methods.<br />
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Planning for death might involve a number of formal decisions, such as advance directives, living wills, powers of attorney, and Do Not Resuscitate orders, and hospice. However these options remain underutilized. An analysis of a random sample of all U.S. deaths in 1986 found that about 10% of decedents had living wills. In addition, when they were completed, it is not uncommon to find that the attending clinical staff ignored them. <br />
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In addition, although hospice is an increasingly-accepted choice, often considered to be the "gold standard" of optimal end-of-life care, less than half of eligible patients utilize these services, and when they do, most start hospice too late. Hospice care is not just for the dying patient, but also for the family. Caregivers of the dying are twice as likely to have depressive symptoms as the dying themselves. This is why the hospice setting is more likely to be at home than at a hospital, and involves the family. <br />
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Communication is especially important. One of the ways to initiate an end of life discussion is to start with “Five Wishes.” This document meets the legal requirements for an advance directive in California and in 41 other states. Answers to the following questions will start the discussion of how you can die with dignity: <br />
The Person I Want to Make Care Decisions for Me When I Can't;<br />
The Kind of Medical Treatment I Want or Don't Want;<br />
How Comfortable I Want to Be;<br />
How I Want People to Treat Me;<br />
What I Want My Loved Ones to Know.<br />
<br />
Dying quickly and painlessly means that we are willing to discuss these final details with those around us. This level of dignity implores us to communicate about our eventual death and to design a course of action that reflects our wishes and desires. This is a difficult and uncomfortable topic. But no one said that aging is easy.<br />
<br />
Mario Garrett PhD is a professor of gerontology at San Diego State University can be reached mariusgarrett@yahoo.com <br />
© Mario Garrett 2010<div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com1tag:blogger.com,1999:blog-8125300329382786892.post-30577958825594865682018-08-26T21:40:00.005-07:002018-08-26T21:40:59.628-07:00THE SAN DIEGO UNION-TRIBUNE<div class="g" style="background-color: white; color: #222222; font-family: Roboto, arial, sans-serif; font-size: small; line-height: 1.2; margin-bottom: 26px; margin-top: 0px;">
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<span class="st" style="line-height: 1.4; word-wrap: break-word;"><span class="f" style="color: grey;">Jan 7, 2012 - </span>Directed by SDSU professor <span style="color: #6a6a6a; font-weight: bold;">Mario Garrett</span>, the festival's purpose is to offer positive images of aging. All films are free of charge and screen at ...</span></div>
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<span class="st" style="line-height: 1.4; word-wrap: break-word;"><span style="color: #6a6a6a; font-weight: bold;">Mario Garrett</span>. Sometimes we joke about how other civilizations or other ages looked upon old age. Since we have “medicalized” aging and death, we have ...</span></div>
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<span class="st" style="line-height: 1.4; word-wrap: break-word;"><span style="color: #6a6a6a; font-weight: bold;">Mario Garrett</span>. Volunteerism has long been one of America's traditions. Since Benjamin Franklin's founding of Philadelphia's first volunteer firefighter company in ...</span></div>
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<span class="st" style="line-height: 1.4; word-wrap: break-word;">Life span is a moving target. <span style="color: #6a6a6a; font-weight: bold;">Mario Garrett</span>. Not all immortal beings are the creation of Hollywood. In the same league as Peter Pan, Dracula and the Highlander, ...</span></div>
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<span class="st" style="line-height: 1.4; word-wrap: break-word;"><span style="color: #6a6a6a; font-weight: bold;">Mario Garrett</span>. The state of well-being among older adults does not seem to be improving. A recent AARP report compared sex and well-being in 1999, 2004, ...</span></div>
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<span class="st" style="line-height: 1.4; word-wrap: break-word;"><span class="f" style="color: grey;">Sep 6, 2011 - </span>By <span style="color: #6a6a6a; font-weight: bold;">Mario Garrett</span> ... Copyright 2011 The <span style="color: #6a6a6a; font-weight: bold;">San Diego Union-Tribune</span> LLC. ... <span style="color: #6a6a6a; font-weight: bold;">Mario Garrett</span>, Ph.D., is a professor of gerontology at San Diego State</span></div>
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<span class="st" style="line-height: 1.4; word-wrap: break-word;">Letter to the <span style="color: #6a6a6a; font-weight: bold;">San Diego Union-Tribune</span> about "Suicide Kits" -- by Faye Girsh ... the Living - by Dr. <span style="color: #6a6a6a; font-weight: bold;">Mario Garrett</span> in the <span style="color: #6a6a6a; font-weight: bold;">San Diego Union Tribune</span> -- July 12, 2011</span></div>
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<span class="st" style="line-height: 1.4; word-wrap: break-word;">"New Insights in Aging" by <span style="color: #6a6a6a; font-weight: bold;">Mario Garrett</span> This is a book, taken from a series of 500 ... from September, 2010 to November, 2011, in the <span style="color: #6a6a6a; font-weight: bold;">San Diego Union Tribune</span>.</span></div>
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<span class="st" style="line-height: 1.4; word-wrap: break-word;">San Diego State University gerontology professor <span style="color: #6a6a6a; font-weight: bold;">Mario Garrett</span> writes more surprising facts in the <span style="color: #6a6a6a; font-weight: bold;">San Diego Union Tribune</span>: Americans 55 and older had 3.3<wbr></wbr> ...</span></div>
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<span class="st" style="line-height: 1.4; word-wrap: break-word;"><span class="f" style="color: grey;">Apr 25, 2011 - </span>The <span style="color: #6a6a6a; font-weight: bold;">San Diego Union-Tribune</span>, March 13, 2011. ―Florist proves irresistible in La Jolla ... to emotion and, perhaps, longevity‖. By <span style="color: #6a6a6a; font-weight: bold;">Mario Garrett</span>.</span></div>
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<span class="st" style="line-height: 1.4; word-wrap: break-word;">State becoming equal parts Hispanic and white. <span style="color: #6a6a6a; font-weight: bold;">San Diego Union Tribune</span>. Retrieved from .... Angelica Garcia. B5. Diversity in Dementia. <span style="color: #6a6a6a; font-weight: bold;">Mario Garrett</span>, PhD.</span></div>
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<span class="st" style="line-height: 1.4; word-wrap: break-word;">Join us for the next public lecture as we welcome <span style="color: #6a6a6a; font-weight: bold;">Mario Garrett</span>, PhD, professor of ... The <span style="color: #6a6a6a; font-weight: bold;">San Diego Union-Tribune</span> · ETC: Spy Camp, Brain Fitness, Songwriters' ...</span></div>
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<div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-67598573868308053522018-08-26T21:09:00.003-07:002019-09-16T06:37:41.845-07:00TIMES OF MALTA <div style="background-color: white;">
<a href="https://www.timesofmalta.com/articles/view/20180107/health-fitness/Stop-looking-for-a-pill-to-cure-dementia.667400" ping="/url?sa=t&source=web&rct=j&url=https://www.timesofmalta.com/articles/view/20180107/health-fitness/Stop-looking-for-a-pill-to-cure-dementia.667400&ved=2ahUKEwiS1MP6rYzdAhUMGKwKHa5ZCWEQFjAAegQIEhAB" style="color: #660099; cursor: pointer; font-family: roboto, arial, sans-serif; font-size: small;">Stop looking for a pill to cure dementia - Times of Malta</a><br />
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<a href="https://www.timesofmalta.com/articles/view/20180812/life-features/the-pain-of-ageing.686640" ping="/url?sa=t&source=web&rct=j&url=https://www.timesofmalta.com/articles/view/20180812/life-features/the-pain-of-ageing.686640&ved=2ahUKEwiS1MP6rYzdAhUMGKwKHa5ZCWEQFjABegQIEBAB" style="color: #660099; cursor: pointer; font-family: roboto, arial, sans-serif; font-size: small;">The pain of ageing - Times of Malta</a><br />
<span style="color: grey; font-family: "arial" , sans-serif;"><span style="font-size: 11px;"><b><br /></b></span></span><a href="https://www.timesofmalta.com/articles/view/20180819/health-fitness/vent-farms-for-people-who-dont-wake-up.687026" ping="/url?sa=t&source=web&rct=j&url=https://www.timesofmalta.com/articles/view/20180819/health-fitness/vent-farms-for-people-who-dont-wake-up.687026&ved=2ahUKEwiS1MP6rYzdAhUMGKwKHa5ZCWEQFjACegQIERAB" style="color: #660099; cursor: pointer; font-family: roboto, arial, sans-serif; font-size: small;">Vent farms for people who don't wake up - Times of Malta</a><br />
<span style="color: grey; font-family: "arial" , sans-serif;"><span style="font-size: 11px;"><b><br /></b></span></span><a href="https://www.timesofmalta.com/articles/view/20171217/life-features/Fear-of-death-and-purpose-of-living.665886" ping="/url?sa=t&source=web&rct=j&url=https://www.timesofmalta.com/articles/view/20171217/life-features/Fear-of-death-and-purpose-of-living.665886&ved=2ahUKEwiS1MP6rYzdAhUMGKwKHa5ZCWEQFjADegQICxAB" style="color: #660099; cursor: pointer; font-family: roboto, arial, sans-serif; font-size: small;">Fear of death and purpose of living - Times of Malta</a><br />
<span style="color: grey; font-family: "arial" , sans-serif;"><span style="font-size: 11px;"><b><br /></b></span></span><a href="https://www.timesofmalta.com/articles/view/20180325/life-features/we-need-a-big-brain-to-age.674341" ping="/url?sa=t&source=web&rct=j&url=https://www.timesofmalta.com/articles/view/20180325/life-features/we-need-a-big-brain-to-age.674341&ved=2ahUKEwiS1MP6rYzdAhUMGKwKHa5ZCWEQFjAEegQIDxAB" style="color: #660099; cursor: pointer; font-family: roboto, arial, sans-serif; font-size: small;">We need a big brain to age - Times of Malta</a><br />
<span style="color: grey; font-family: "arial" , sans-serif;"><span style="font-size: 11px;"><b><br /></b></span></span><a href="https://www.timesofmalta.com/articles/view/20180722/health-fitness/can-we-stay-alive-longer.684938" ping="/url?sa=t&source=web&rct=j&url=https://www.timesofmalta.com/articles/view/20180722/health-fitness/can-we-stay-alive-longer.684938&ved=2ahUKEwiS1MP6rYzdAhUMGKwKHa5ZCWEQFjAFegQIDhAB" style="color: #660099; cursor: pointer; font-family: roboto, arial, sans-serif; font-size: small;">Can we stay alive longer? - Times of Malta</a><br />
<span style="color: grey; font-family: "arial" , sans-serif;"><span style="font-size: 11px;"><b><br /></b></span></span><a href="https://www.timesofmalta.com/articles/view/20180527/life-features/all-demented-sinners.680150" ping="/url?sa=t&source=web&rct=j&url=https://www.timesofmalta.com/articles/view/20180527/life-features/all-demented-sinners.680150&ved=2ahUKEwiS1MP6rYzdAhUMGKwKHa5ZCWEQFjAGegQIDRAB" style="color: #660099; cursor: pointer; font-family: roboto, arial, sans-serif; font-size: small;">All demented sinners - Times of Malta</a><br />
<span style="color: grey; font-family: "arial" , sans-serif;"><span style="font-size: 11px;"><b><br /></b></span></span><a href="https://www.timesofmalta.com/articles/view/20180610/life-features/how-films-portray-ageing.681330" ping="/url?sa=t&source=web&rct=j&url=https://www.timesofmalta.com/articles/view/20180610/life-features/how-films-portray-ageing.681330&ved=2ahUKEwiS1MP6rYzdAhUMGKwKHa5ZCWEQFjAHegQIDBAB" style="color: #660099; cursor: pointer; font-family: roboto, arial, sans-serif; font-size: small;">How films portray ageing - Times of Malta</a><br />
<span style="color: grey; font-family: "arial" , sans-serif;"><span style="font-size: 11px;"><b><br /></b></span></span><a href="https://www.timesofmalta.com/articles/view/20170528/health-fitness/dementia-deaths-are-on-the-rise.649262" ping="/url?sa=t&source=web&rct=j&url=https://www.timesofmalta.com/articles/view/20170528/health-fitness/dementia-deaths-are-on-the-rise.649262&ved=2ahUKEwiS1MP6rYzdAhUMGKwKHa5ZCWEQFjAIegQIARAB" style="color: #660099; cursor: pointer; font-family: roboto, arial, sans-serif; font-size: small;">Dementia deaths are on the rise - Times of Malta</a><br />
<span style="color: grey; font-family: "arial" , sans-serif;"><span style="font-size: 11px;"><b><br /></b></span></span><a href="https://www.bc-legal.co.uk/bcdn/446-220-does-stress-cause-dementia" ping="/url?sa=t&source=web&rct=j&url=https://www.bc-legal.co.uk/bcdn/446-220-does-stress-cause-dementia&ved=2ahUKEwiS1MP6rYzdAhUMGKwKHa5ZCWEQFjAKegQICRAB" style="color: #660099; cursor: pointer; font-family: roboto, arial, sans-serif; font-size: small;">Does Stress Cause Dementia? - BC Legal</a><br />
<span style="color: grey; font-family: "arial" , sans-serif;"><span style="font-size: 11px;"><b><br /></b></span></span><a href="http://exivo.com/l/141938" ping="/url?sa=t&source=web&rct=j&url=http://exivo.com/l/141938&ved=2ahUKEwiS1MP6rYzdAhUMGKwKHa5ZCWEQFjAMegQIBxAB" style="color: #660099; cursor: pointer; font-family: roboto, arial, sans-serif; font-size: small;">How much does your soul weigh? - Times of Malta - exivo</a><br />
<span style="color: grey; font-family: "arial" , sans-serif;"><span style="font-size: 11px;"><b><br /></b></span></span><a href="http://malta.latestnews365.com/social.html" ping="/url?sa=t&source=web&rct=j&url=http://malta.latestnews365.com/social.html&ved=2ahUKEwiS1MP6rYzdAhUMGKwKHa5ZCWEQFjANegQIBRAB" style="color: #660099; cursor: pointer; font-family: roboto, arial, sans-serif; font-size: small;">Latest and breaking news from Malta, Social | Latest News Malta</a><br />
<span style="color: grey; font-family: "arial" , sans-serif;"><span style="font-size: 11px;"><b><br /></b></span></span><a href="http://internationalpsychoanalysis-net.ipbooks.net/category/general-news/page/10/" ping="/url?sa=t&source=web&rct=j&url=http://internationalpsychoanalysis-net.ipbooks.net/category/general-news/page/10/&ved=2ahUKEwiS1MP6rYzdAhUMGKwKHa5ZCWEQFjAPegQIAxAB" style="color: #660099; cursor: pointer; font-family: roboto, arial, sans-serif; font-size: small;">International Psychoanalysis » General News</a><br />
<span style="color: grey; font-family: "arial" , sans-serif;"><span style="font-size: 11px;"><b><br /></b></span></span><a href="https://theworldnews.net/mt-news/we-truly-have-social-bodies" ping="/url?sa=t&source=web&rct=j&url=https://theworldnews.net/mt-news/we-truly-have-social-bodies&ved=2ahUKEwiS1MP6rYzdAhUMGKwKHa5ZCWEQFjAQegQIAhAB" style="color: #660099; cursor: pointer; font-family: roboto, arial, sans-serif; font-size: small;">We truly have social bodies - TheWorldNews.net</a><br />
<span style="color: grey; font-family: "arial" , sans-serif;"><span style="font-size: 11px;"><b><br /></b></span></span><a href="https://theworldnews.net/mt-news/aliens-in-our-body" ping="/url?sa=t&source=web&rct=j&url=https://theworldnews.net/mt-news/aliens-in-our-body&ved=2ahUKEwiS1MP6rYzdAhUMGKwKHa5ZCWEQFjARegQIABAB" style="color: #660099; cursor: pointer; font-family: roboto, arial, sans-serif; font-size: small;">Aliens in our body</a></div>
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<span style="color: #006621; font-family: "roboto" , "arial" , sans-serif; font-size: 14px;">https://www.timesofmalta.com/.../Stop-looking-for-a-pill-to-cure-dementia.667400</span><br />
<span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"><br /></span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">Sunday, January 7, 2018, 16:10 by </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> ... </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> was born in Malta and is currently a professor of gerontology at San Diego State University in</span><wbr style="color: #222222; font-family: roboto, arial, sans-serif; font-size: small;"></wbr><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> ...</span><br />
<span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">You visited this page on 8/25/18.</span><br />
<span style="color: #006621; font-family: "roboto" , "arial" , sans-serif; font-size: 14px;">https://www.timesofmalta.com/articles/view/20180812/.../the-pain-of-ageing.686640</span><br />
<span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"><br /></span><span class="f" style="color: grey; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">Aug 12, 2018 - </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> was born in Malta and is currently a professor of gerontology at San Diego State University in California, US. ?Share. Black day ...</span><br />
<span style="color: #006621; font-family: "roboto" , "arial" , sans-serif; font-size: 14px;">https://www.timesofmalta.com/.../vent-farms-for-people-who-dont-wake-up.687026</span><br />
<span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"><br /></span><span class="f" style="color: grey; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">Aug 19, 2018 - </span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">We can always stay alive even when dead, until pneumonia or some other bacteria, fungi, virus or parasite gets us. </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> was born in ...</span><br />
<span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">You've visited this page 2 times. Last visit: 8/25/18</span><br />
<span style="color: #006621; font-family: "roboto" , "arial" , sans-serif; font-size: 14px;">https://www.timesofmalta.com/articles/.../Fear-of-death-and-purpose-of-living.665886</span><br />
<span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"><br /></span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">Sunday, December 17, 2017, 10:21 by </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> ... </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> was born in Malta and is currently a professor of gerontology at San Diego State University ...</span><br />
<span style="color: #006621; font-family: "roboto" , "arial" , sans-serif; font-size: 14px;">https://www.timesofmalta.com/articles/view/.../we-need-a-big-brain-to-age.674341</span><br />
<span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"><br /></span><span class="f" style="color: grey; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">Mar 25, 2018 - </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> was born in Malta and is currently a professor of gerontology at San Diego State University in California, US. ?Share. Advert ...</span><br />
<span style="color: #006621; font-family: "roboto" , "arial" , sans-serif; font-size: 14px;">https://www.timesofmalta.com/articles/view/.../can-we-stay-alive-longer.684938</span><br />
<span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"><br /></span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">Sunday, July 22, 2018, 08:42 by </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> .... </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> was born in Malta and is currently a professor of gerontology at San Diego State University in ...</span><br />
<span style="color: #006621; font-family: "roboto" , "arial" , sans-serif; font-size: 14px;">https://www.timesofmalta.com/articles/view/20180527/.../all-demented-sinners.68015...</span><br />
<span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"><br /></span><span class="f" style="color: grey; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">May 27, 2018 - </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> was born in Malta and is currently a professor of gerontology at San Diego State University in California, US. He will be the ...</span><br />
<span style="color: #006621; font-family: "roboto" , "arial" , sans-serif; font-size: 14px;">https://www.timesofmalta.com/articles/view/.../life.../how-films-portray-ageing.68133...</span><br />
<span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"><br /></span><span class="f" style="color: grey; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">Jun 10, 2018 - </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> was born in Malta and is currently a professor of gerontology at San Diego State University in California, US. He will be publishing ...</span><br />
<span style="color: #006621; font-family: "roboto" , "arial" , sans-serif; font-size: 14px;">https://www.timesofmalta.com/articles/view/.../dementia-deaths-are-on-the-rise.64926...</span><br />
<span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"><br /></span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">Sunday, May 28, 2017, 10:58 by </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> ... </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> was born in Malta and is currently a professor of gerontology at San Diego State University in ...</span><br />
<span style="color: #006621; font-family: "roboto" , "arial" , sans-serif; font-size: 14px;">https://www.bc-legal.co.uk › BC Disease News</span><br />
<span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"><br /></span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">... see how stress can cause dementia, but not all dementia is caused by stress.' [i</span><wbr style="color: #222222; font-family: roboto, arial, sans-serif; font-size: small;"></wbr><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">] </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> 'Does stress cause dementia' (January 2018 </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Times of Malta</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">) ...</span><br />
<span style="color: #006621; font-family: "roboto" , "arial" , sans-serif; font-size: 14px;">exivo.com/l/141938</span><br />
<span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"><br /></span><span class="f" style="color: grey; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">Dec 31, 2017 - </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> was born in Malta and is currently a professor of gerontology at San Diego State University in California, US. ?Share. Advert ...</span><br />
<span style="color: #006621; font-family: "roboto" , "arial" , sans-serif; font-size: 14px;">malta.latestnews365.com/social.html</span><br />
<span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"><br /></span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> was born in Malta and is currently a professor of gerontology at San Diego State .... Malta to execute EU-Japan partnership - </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Times of Malta</span><br />
<span style="color: #006621; font-family: "roboto" , "arial" , sans-serif; font-size: 14px;">internationalpsychoanalysis-net.ipbooks.net/category/general-news/page/10/</span><br />
<span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"><br /></span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">Click Here to Read: Fear of death and purpose of living by </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> on the </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Times of Malta</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> website on December 17, 2017. Graham Crumb. Public Domain ...</span><br />
<span style="color: #006621; font-family: "roboto" , "arial" , sans-serif; font-size: 14px;">https://theworldnews.net/mt-news/we-truly-have-social-bodies</span><br />
<span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"><br /></span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">4:18 / 05.08.2018 </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Times of Malta</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> .... </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> was born in Malta and is currently a professor of gerontology at San Diego State University in California, US.</span><br />
<span style="color: #006621; font-family: "roboto" , "arial" , sans-serif; font-size: 14px;">https://theworldnews.net/mt-news/aliens-in-our-body</span><br />
<span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;">2:16 / 25.02.2018 </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Times of Malta</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> ... </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold;">Mario Garrett</span><span style="color: #222222; font-family: "roboto" , "arial" , sans-serif; font-size: x-small;"> was born in Malta and is currently a professor of gerontology at San Diego State University in California, US.</span></div>
<div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-30809022748935055652018-05-20T17:14:00.003-07:002018-08-26T20:28:37.362-07:00Slowing Down Aging<div class="MsoNormal" style="font-family: "Times New Roman", serif; margin: 0in 0in 0.0001pt;">
<span style="font-family: "garamond" , serif;">Do ugly older people die younger?</span></div>
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<span style="font-family: "garamond" , serif;">In 2012 Ian Deary and his colleagues with the University of Edinburgh, tested whether older adults who looked less attractive died before their more attractive peers. The authors asked people to rate the photographs of 292 older adults aged 83 years of age. They rated the photographs on how old healthy, attractive intelligent and happy they looked. They also looked at how symmetrical the faces are (the left side of the face is proportionally similar to the right). Then the authors followed the people in the photographs over a 7-year period to see which ones died first. They were trying to see if we can predict who dies first. What they found is that the main predictor was how old they were judged to be. After accounting for how old they looked, this was followed by how healthy they were rated from the photographs. Looking more attractive did not have any advantage after accounting for how old they looked. It seems, looking older rather than looking less attractive predicted an early death. But the two are related—looking attractive is also related to looking younger. Age determines how we judge people as attractive.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">Look around and you see people that look better than others—and by better of course, I mean younger. We naturally assume that looking younger is healthier and more attractive. That dress that takes 10 years off, or a haircut that makes you look younger are all compliments. And we can easily speed up aging by stress for example. We know of people that have gone through a trauma in their life and they “aged” quickly. We have this idea of the process of aging that can speed up or slow down. One of the main stressors in our modern lives is money, and lack of it. We know that rich people live longer, but are they also more attractive? Such a relationship could work from both sides with attractive people getting more preferential treatment and becoming more successful which in turn allows them to make their life better.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">Susanne Huber and Martin Fieder 2014 found rich your parents predict facial attractiveness in their children at young adulthood (17-20 years old). Of course, attractiveness is mainly due to the symmetry of the face. In 2001 Deborah Hume and Robert Montgomerie with Queen's University, Canada, examined this symmetry. What they found is that women symmetry was best predicted by how fat they are and by previous health problems. For men, facial attractiveness was best predicted by how rich they are and their how comfortable their environment is. Attractiveness seems to be positively related to the degree to which an individual cope with stress growing up. For women it is mainly their weight and health, for men it is mainly money.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">The economics of beauty has been written about extensively. Daniel Hamermesh in 2011 consolidated some of these thoughts in his book <i>Beauty Pays</i>. There is no age limit for vanity. In the US single women aged seventy years and older spend over forty-three minutes a day in grooming. From archeological sites we can see that grooming behavior extends across the world and throughout human history. Of course, what we think of beautiful differs by country, culture and across time, but there are certain constants and being younger is one of them. There are no older Venuses nor older Davids. Old age is not paraded as examples of beauty. Never was across any culture.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">Which is why women are judged more harshly for their looks than men, we also see ageing as being more determinantal to women in how they are treated by others. For people who weren’t born to have attractive features or have been in an accident, Hamermesh mentions that cosmetic surgery has been a solution for many older adults including increasingly for older men. In 2016 the US spent $16.4 billion on cosmetic procedures. This is one and a half times more than the total economic productivity of Malta ($10.95 billion in 2016). Americans spend more on having body parts modified than Malta’s total economy. And one of the main group is those entering into older age, 55 years and older.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">In 2016, those over 55 years and older had 4.1 million total cosmetic procedures, an increase of 3-4% in procedures since the previous year. Of these 387,000 were surgical procedures, and 3.7 million were minimally-invasive procedures (injections and friction). For middle aged adults the main surgical procedures were eyelid surgery, facelift, dermabrasion, liposuction and forehead lift. Minimal invasive surgery included in order of popularity; Botox, soft tissue fillers, chemical peel, laser skin resurfacing and microdermabrasion. While most popular procedures among young adults focus on their bodies, older adults are apparently more concerned about more visible features, such as their faces. Older adults know that they are being judged by how old they look and their faces are their calling cards.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">For these older adults who have had cosmetic surgery, regardless of how young they look, they will not prolong their time of death. What they are fighting is not death but being judged. In a world that judges attractiveness by how old we look older adults are in greater and increasing numbers resorting to fighting it b attempting to look younger. But it is the judgment that needs to change. Such vanity discrimination draws striking parallels with ageism, racism and sexism. The only way to confront these is not by becoming the “other” but by eliminating the category of other altogether.<o:p></o:p></span></div>
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<em style="background-color: white; box-sizing: border-box; color: #2c2d30; font-family: "proxima nova regular", arial, sans-serif; font-size: 18px;"><span style="box-sizing: border-box; font-family: "proxima nova bold" , "arial" , sans-serif;">© USA Copyrighted 2018 Mario D. Garrett</span></em></div>
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<span style="font-family: "garamond" , serif;">References<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">Dykiert, D., Bates, T. C., Gow, A. J., Penke, L., Starr, J. M., & Deary, I. J. (2012). Predicting mortality from human faces. Psychosomatic medicine, 74(6), 560-566.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">Huber, S., & Fieder, M. (2014). Effects of parental socio-economic conditions on facial attractiveness. Evolutionary Psychology, 12(5), 147470491401200514.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">Hume, D. K., & Montgomerie, R. (2001). Facial attractiveness signals different aspects of “quality” in women and men. Evolution and human behavior, 22(2), 93-112.<o:p></o:p></span></div>
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<div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-68272515196444296512018-05-20T17:13:00.005-07:002018-08-26T20:28:37.604-07:00How Films Portray Aging<div class="MsoNormal" style="font-family: "Times New Roman", serif; margin: 0in 0in 0.0001pt;">
<span style="font-family: "garamond" , serif;">In our increasingly digital world, we get an enormous amount of information from films. Our imagination has always been fired up by films. A relationship that has endured since the first films.</span><span style="font-family: "garamond" , serif;"> </span><span style="font-family: "garamond" , serif;"> </span><span style="font-family: "garamond" , serif;">How older people are portrayed in film is best described through the interpretation of a narrative arc. An arc is the linear development of a story—a beginning, a middle and an end.</span><span style="font-family: "garamond" , serif;"> </span></div>
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<span style="font-family: "garamond" , serif;">One of the first films describing a simple story about older people is the 1952 Japanese film Ikiru by the acclaimed director Akira Kurosawa—acclaimed for the Seven Samurai, Rashomon, and Ran. Ikiru has a fairly simple narrative arc. An older man who worked in an office all his life, on the cusp of retirement, is informed that he has terminal cancer. The narrative arc focusses on the main character in the film attempting to find meaning and leaving behind a legacy in his life before he dies. This simple story highlights that after one’s entire life spent doing what you are supposed to do—work, maybe family—that at the end what is important is relationships. At the end, he finds some solace among his younger mates, where he finds friendship.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">This narrative arc of an older man at the end of life, was further developed by another seminal director, Ingmar Bergman who in 1957 wrote and directed Wild Strawberries. Filmed in black and white, perhaps in homage to Ikiru, the film goes further in search of the meaning of one’s life. Following a fairly similar story of an accomplished professor, Wild Strawberries explores the question of what was it all about? We do not have ambitions for getting old, and once we get there, we remain without a plan. Admired but not loved, the professor starts to explore what the continuation of his story in older age should be. Like Ikiru, relationships seem to be the answer. Such a conclusion is not far-fetched from what we observe at the end of life.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">In 2012 Bronnie Ware, an Australian palliative care nurse, wrote The Top Five Regrets of the Dying: A Life Transformed by the Dearly Departing. Our two male protagonists in Ikiru and Wild Strawberries follow these regrets. These misgivings focused on having unfulfilled dreams and unrequited loves. Not having the courage to follow their dreams, where (mostly) men tended to regret working so hard. Stifling feelings in order to settle for a mediocre existence. And not staying in touch with their friends and loved ones. And the final regret is not allowing oneself to be happy. They got stuck in a rut. The agreement between the narrative of these two films and the five regrets of dying people is stunning.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">Some films on aging tend to start off with a negative view of aging, and then transforms into a story about friendship and family. That it is not too late to address past regrets. But what if this transformation did not take place? If the negative view of aging remains without the salvation of a new-found story for older age? This is the story of the two characters in the 2015 Italian film Youth.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">Paolo Sorrentino’s film centers on two close friends sharing a vacation at an exclusive Swiss spa. One is a film director who continues producing the same kind of films, surrounded by increasingly younger writers. While the other character is a music composer who has decided to retire. The composer stopped composing—to the chagrin of many—because of his wife’s dementia which he hid from everyone including his daughter. He made changes that address this trauma and his aging. Negative events in life change our story sometimes for the better. We realize what is important. In contrast, the other character, the director, only had one story—to remain doing what he did in the past. He did not have a different story for when he got old, and the quality of his work diminished. At the end, his suicide was the only answer to his failing career since he did not have a plan B, an evolving story for getting old.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">We also place people in a story. We create a cage for them. Do a little exercise with me.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">Let’s imagine that you have a 100-year-old woman that you are going to interview. What is the single question that you will ask her. Write it down. Then assume that you have a 16year-young girl coming to be interviewed. What single question would you ask? Write it down.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">The prediction is that you probably ask the older woman about her past and the younger woman about her future. You have already hemmed them into your view of what their story should be.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">To age successfully we must have a story that goes beyond adulthood—to extend into older adulthood. Our story is important because it is how we conduct our life, including into older age. What films teach us is that others can influence our story about getting older.<o:p></o:p></span><br />
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<span style="font-family: "garamond" , serif;"><em style="background-color: white; box-sizing: border-box; color: #2c2d30; font-family: "proxima nova regular", arial, sans-serif; font-size: 18px;"><span style="box-sizing: border-box; font-family: "proxima nova bold" , "arial" , sans-serif;">© USA Copyrighted 2018 Mario D. Garrett</span></em></span></div>
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<span style="font-family: "garamond" , serif;">Trailers on Youtube<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">Ikiru: https://www.youtube.com/watch?v=yCSiL2wmxuE<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">Wild Strawberries: https://www.youtube.com/watch?v=0RzOCwer-gc<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">Youth: https://www.youtube.com/watch?v=-T7CM4di_0c<o:p></o:p></span></div>
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<div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-51134842526943548562018-05-20T17:13:00.002-07:002018-09-15T11:12:18.243-07:00All Demented Sinners<!--[if gte mso 9]><xml>
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Name="List Number 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="List Number 4"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="List Number 5"/>
<w:LsdException Locked="false" Priority="10" QFormat="true" Name="Title"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Closing"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Signature"/>
<w:LsdException Locked="false" Priority="1" SemiHidden="true"
UnhideWhenUsed="true" Name="Default Paragraph Font"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Body Text"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Body Text Indent"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="List Continue"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="List Continue 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="List Continue 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="List Continue 4"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="List Continue 5"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Message Header"/>
<w:LsdException Locked="false" Priority="11" QFormat="true" Name="Subtitle"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Salutation"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Date"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Body Text First Indent"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Body Text First Indent 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Note Heading"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Body Text 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Body Text 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Body Text Indent 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Body Text Indent 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Block Text"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Hyperlink"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="FollowedHyperlink"/>
<w:LsdException Locked="false" Priority="22" QFormat="true" Name="Strong"/>
<w:LsdException Locked="false" Priority="20" QFormat="true" Name="Emphasis"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Document Map"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Plain Text"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="E-mail Signature"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Top of Form"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Bottom of Form"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Normal (Web)"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Acronym"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Address"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Cite"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Code"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Definition"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Keyboard"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Preformatted"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Sample"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Typewriter"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Variable"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Normal Table"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="annotation subject"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="No List"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Outline List 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Outline List 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Outline List 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Simple 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Simple 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Simple 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Classic 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Classic 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Classic 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Classic 4"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Colorful 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Colorful 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Colorful 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Columns 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Columns 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Columns 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Columns 4"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Columns 5"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Grid 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Grid 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Grid 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Grid 4"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Grid 5"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Grid 6"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Grid 7"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Grid 8"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table List 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table List 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table List 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table List 4"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table List 5"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table List 6"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table List 7"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table List 8"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table 3D effects 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table 3D effects 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table 3D effects 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Contemporary"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Elegant"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Professional"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Subtle 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Subtle 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Web 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Web 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Web 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Balloon Text"/>
<w:LsdException Locked="false" Priority="39" Name="Table Grid"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Theme"/>
<w:LsdException Locked="false" SemiHidden="true" Name="Placeholder Text"/>
<w:LsdException Locked="false" Priority="1" QFormat="true" Name="No Spacing"/>
<w:LsdException Locked="false" Priority="60" Name="Light Shading"/>
<w:LsdException Locked="false" Priority="61" Name="Light List"/>
<w:LsdException Locked="false" Priority="62" Name="Light Grid"/>
<w:LsdException Locked="false" Priority="63" Name="Medium Shading 1"/>
<w:LsdException Locked="false" Priority="64" Name="Medium Shading 2"/>
<w:LsdException Locked="false" Priority="65" Name="Medium List 1"/>
<w:LsdException Locked="false" Priority="66" Name="Medium List 2"/>
<w:LsdException Locked="false" Priority="67" Name="Medium Grid 1"/>
<w:LsdException Locked="false" Priority="68" Name="Medium Grid 2"/>
<w:LsdException Locked="false" Priority="69" Name="Medium Grid 3"/>
<w:LsdException Locked="false" Priority="70" Name="Dark List"/>
<w:LsdException Locked="false" Priority="71" Name="Colorful Shading"/>
<w:LsdException Locked="false" Priority="72" Name="Colorful List"/>
<w:LsdException Locked="false" Priority="73" Name="Colorful Grid"/>
<w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 1"/>
<w:LsdException Locked="false" Priority="61" Name="Light List Accent 1"/>
<w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 1"/>
<w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 1"/>
<w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 1"/>
<w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 1"/>
<w:LsdException Locked="false" SemiHidden="true" Name="Revision"/>
<w:LsdException Locked="false" Priority="34" QFormat="true"
Name="List Paragraph"/>
<w:LsdException Locked="false" Priority="29" QFormat="true" Name="Quote"/>
<w:LsdException Locked="false" Priority="30" QFormat="true"
Name="Intense Quote"/>
<w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 1"/>
<w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 1"/>
<w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 1"/>
<w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 1"/>
<w:LsdException Locked="false" Priority="70" Name="Dark List Accent 1"/>
<w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 1"/>
<w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 1"/>
<w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 1"/>
<w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 2"/>
<w:LsdException Locked="false" Priority="61" Name="Light List Accent 2"/>
<w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 2"/>
<w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 2"/>
<w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 2"/>
<w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 2"/>
<w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 2"/>
<w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 2"/>
<w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 2"/>
<w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 2"/>
<w:LsdException Locked="false" Priority="70" Name="Dark List Accent 2"/>
<w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 2"/>
<w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 2"/>
<w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 2"/>
<w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 3"/>
<w:LsdException Locked="false" Priority="61" Name="Light List Accent 3"/>
<w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 3"/>
<w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 3"/>
<w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 3"/>
<w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 3"/>
<w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 3"/>
<w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 3"/>
<w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 3"/>
<w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 3"/>
<w:LsdException Locked="false" Priority="70" Name="Dark List Accent 3"/>
<w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 3"/>
<w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 3"/>
<w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 3"/>
<w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 4"/>
<w:LsdException Locked="false" Priority="61" Name="Light List Accent 4"/>
<w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 4"/>
<w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 4"/>
<w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 4"/>
<w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 4"/>
<w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 4"/>
<w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 4"/>
<w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 4"/>
<w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 4"/>
<w:LsdException Locked="false" Priority="70" Name="Dark List Accent 4"/>
<w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 4"/>
<w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 4"/>
<w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 4"/>
<w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 5"/>
<w:LsdException Locked="false" Priority="61" Name="Light List Accent 5"/>
<w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 5"/>
<w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 5"/>
<w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 5"/>
<w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 5"/>
<w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 5"/>
<w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 5"/>
<w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 5"/>
<w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 5"/>
<w:LsdException Locked="false" Priority="70" Name="Dark List Accent 5"/>
<w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 5"/>
<w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 5"/>
<w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 5"/>
<w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 6"/>
<w:LsdException Locked="false" Priority="61" Name="Light List Accent 6"/>
<w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 6"/>
<w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 6"/>
<w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 6"/>
<w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 6"/>
<w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 6"/>
<w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 6"/>
<w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 6"/>
<w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 6"/>
<w:LsdException Locked="false" Priority="70" Name="Dark List Accent 6"/>
<w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 6"/>
<w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 6"/>
<w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 6"/>
<w:LsdException Locked="false" Priority="19" QFormat="true"
Name="Subtle Emphasis"/>
<w:LsdException Locked="false" Priority="21" QFormat="true"
Name="Intense Emphasis"/>
<w:LsdException Locked="false" Priority="31" QFormat="true"
Name="Subtle Reference"/>
<w:LsdException Locked="false" Priority="32" QFormat="true"
Name="Intense Reference"/>
<w:LsdException Locked="false" Priority="33" QFormat="true" Name="Book Title"/>
<w:LsdException Locked="false" Priority="37" SemiHidden="true"
UnhideWhenUsed="true" Name="Bibliography"/>
<w:LsdException Locked="false" Priority="39" SemiHidden="true"
UnhideWhenUsed="true" QFormat="true" Name="TOC Heading"/>
<w:LsdException Locked="false" Priority="41" Name="Plain Table 1"/>
<w:LsdException Locked="false" Priority="42" Name="Plain Table 2"/>
<w:LsdException Locked="false" Priority="43" Name="Plain Table 3"/>
<w:LsdException Locked="false" Priority="44" Name="Plain Table 4"/>
<w:LsdException Locked="false" Priority="45" Name="Plain Table 5"/>
<w:LsdException Locked="false" Priority="40" Name="Grid Table Light"/>
<w:LsdException Locked="false" Priority="46" Name="Grid Table 1 Light"/>
<w:LsdException Locked="false" Priority="47" Name="Grid Table 2"/>
<w:LsdException Locked="false" Priority="48" Name="Grid Table 3"/>
<w:LsdException Locked="false" Priority="49" Name="Grid Table 4"/>
<w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark"/>
<w:LsdException Locked="false" Priority="51" Name="Grid Table 6 Colorful"/>
<w:LsdException Locked="false" Priority="52" Name="Grid Table 7 Colorful"/>
<w:LsdException Locked="false" Priority="46"
Name="Grid Table 1 Light Accent 1"/>
<w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 1"/>
<w:LsdException Locked="false" Priority="48" Name="Grid Table 3 Accent 1"/>
<w:LsdException Locked="false" Priority="49" Name="Grid Table 4 Accent 1"/>
<w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark Accent 1"/>
<w:LsdException Locked="false" Priority="51"
Name="Grid Table 6 Colorful Accent 1"/>
<w:LsdException Locked="false" Priority="52"
Name="Grid Table 7 Colorful Accent 1"/>
<w:LsdException Locked="false" Priority="46"
Name="Grid Table 1 Light Accent 2"/>
<w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 2"/>
<w:LsdException Locked="false" Priority="48" Name="Grid Table 3 Accent 2"/>
<w:LsdException Locked="false" Priority="49" Name="Grid Table 4 Accent 2"/>
<w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark Accent 2"/>
<w:LsdException Locked="false" Priority="51"
Name="Grid Table 6 Colorful Accent 2"/>
<w:LsdException Locked="false" Priority="52"
Name="Grid Table 7 Colorful Accent 2"/>
<w:LsdException Locked="false" Priority="46"
Name="Grid Table 1 Light Accent 3"/>
<w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 3"/>
<w:LsdException Locked="false" Priority="48" Name="Grid Table 3 Accent 3"/>
<w:LsdException Locked="false" Priority="49" Name="Grid Table 4 Accent 3"/>
<w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark Accent 3"/>
<w:LsdException Locked="false" Priority="51"
Name="Grid Table 6 Colorful Accent 3"/>
<w:LsdException Locked="false" Priority="52"
Name="Grid Table 7 Colorful Accent 3"/>
<w:LsdException Locked="false" Priority="46"
Name="Grid Table 1 Light Accent 4"/>
<w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 4"/>
<w:LsdException Locked="false" Priority="48" Name="Grid Table 3 Accent 4"/>
<w:LsdException Locked="false" Priority="49" Name="Grid Table 4 Accent 4"/>
<w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark Accent 4"/>
<w:LsdException Locked="false" Priority="51"
Name="Grid Table 6 Colorful Accent 4"/>
<w:LsdException Locked="false" Priority="52"
Name="Grid Table 7 Colorful Accent 4"/>
<w:LsdException Locked="false" Priority="46"
Name="Grid Table 1 Light Accent 5"/>
<w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 5"/>
<w:LsdException Locked="false" Priority="48" Name="Grid Table 3 Accent 5"/>
<w:LsdException Locked="false" Priority="49" Name="Grid Table 4 Accent 5"/>
<w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark Accent 5"/>
<w:LsdException Locked="false" Priority="51"
Name="Grid Table 6 Colorful Accent 5"/>
<w:LsdException Locked="false" Priority="52"
Name="Grid Table 7 Colorful Accent 5"/>
<w:LsdException Locked="false" Priority="46"
Name="Grid Table 1 Light Accent 6"/>
<w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 6"/>
<w:LsdException Locked="false" Priority="48" Name="Grid Table 3 Accent 6"/>
<w:LsdException Locked="false" Priority="49" Name="Grid Table 4 Accent 6"/>
<w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark Accent 6"/>
<w:LsdException Locked="false" Priority="51"
Name="Grid Table 6 Colorful Accent 6"/>
<w:LsdException Locked="false" Priority="52"
Name="Grid Table 7 Colorful Accent 6"/>
<w:LsdException Locked="false" Priority="46" Name="List Table 1 Light"/>
<w:LsdException Locked="false" Priority="47" Name="List Table 2"/>
<w:LsdException Locked="false" Priority="48" Name="List Table 3"/>
<w:LsdException Locked="false" Priority="49" Name="List Table 4"/>
<w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark"/>
<w:LsdException Locked="false" Priority="51" Name="List Table 6 Colorful"/>
<w:LsdException Locked="false" Priority="52" Name="List Table 7 Colorful"/>
<w:LsdException Locked="false" Priority="46"
Name="List Table 1 Light Accent 1"/>
<w:LsdException Locked="false" Priority="47" Name="List Table 2 Accent 1"/>
<w:LsdException Locked="false" Priority="48" Name="List Table 3 Accent 1"/>
<w:LsdException Locked="false" Priority="49" Name="List Table 4 Accent 1"/>
<w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark Accent 1"/>
<w:LsdException Locked="false" Priority="51"
Name="List Table 6 Colorful Accent 1"/>
<w:LsdException Locked="false" Priority="52"
Name="List Table 7 Colorful Accent 1"/>
<w:LsdException Locked="false" Priority="46"
Name="List Table 1 Light Accent 2"/>
<w:LsdException Locked="false" Priority="47" Name="List Table 2 Accent 2"/>
<w:LsdException Locked="false" Priority="48" Name="List Table 3 Accent 2"/>
<w:LsdException Locked="false" Priority="49" Name="List Table 4 Accent 2"/>
<w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark Accent 2"/>
<w:LsdException Locked="false" Priority="51"
Name="List Table 6 Colorful Accent 2"/>
<w:LsdException Locked="false" Priority="52"
Name="List Table 7 Colorful Accent 2"/>
<w:LsdException Locked="false" Priority="46"
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<b style="mso-bidi-font-weight: normal;"><span style="font-family: "garamond" , serif;"><span style="mso-spacerun: yes;">I</span></span></b><span style="font-family: "garamond" , serif;">n 2011 Heiko
Braak and his colleagues did something that no one else had done before. He
looked at dementia in the brains of young children. By dissecting 2,332 brains
ranging in age from 1 to 100, what he found was to change how we see disease.
Only 10 people had complete absence of Alzheimer's disease related biology.
Every person over 25 years of age had Alzheimer's disease biomarkers. Without
any exceptions. Even among children under 10 years of age, one in five already
had the Alzheimer’s disease signs. Every adult is sick with the disease. Heiko
Braak and his wife Eva are known for their stages of dementia when in 1991 they
published the six stages of dementia, that we know as Braak-Braak stages So
they know a few things about the disease.</span><br />
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<span style="font-family: "garamond" , serif;">The finding that
every adult has some of the disease that contributes to Alzheimer’s disease was
not much news until this year. In 2018 the United State National Institute on
Aging—an agency set up in 1976 to explore ways to promote the health of older
adults—sponsored a new way to define Alzheimer’s disease. This new framework
used the biology of the disease alone, ignoring how the disease is expressed.
For the first time in the history of Alzheimer’s disease we are defining it not
by how it looks—the loss of memory, possibly behavior changes and mood
swings—but by the biology alone. The problem, as Heiko Braak found, is that by
using the biology as an indicator of the disease this makes all of us suffering
from Alzheimer's disease.<span style="mso-spacerun: yes;"> </span><o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">Similar to the
catholic church and original sin, where everyone is born with sin that
eventually takes away the freedom of will, similarly we are told, Alzheimer’s
disease is already in all of us and will eventually take away our freedom of
will too. There are a lot of similarities. We are move science back to
religion. But unlike the original sin were baptisms somewhat absolves us from
this fate, with Alzheimer’s disease there is no cure and no way of absolving the
disease. We are doomed whether we show dementia or not. Even healthy adults
show the biology of the disease, there is no escaping.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">This new way of
diagnosing Alzheimer’s disease is dangerous. Not only for hospitals and clinics
that have to deal with this new definition, but also for the legal aspects.
What if a court argues that you are an incompetent witness (say someone stole
money from you) because they can prove that you have Alzheimer’s disease and
therefore do not have reliable memory. There are many other examples. Examples
in real life today where the diagnosis of Alzheimer’s disease reduces your
value as a witness in court. In the U.S. a diagnosis of Alzheimer’s will
automatically revokes your driving privileges. You lose your driving license by
the time you leave the doctor’s office (it is reportable disease that goes
directly to the motor vehicle department.). If you have business loans you will
likely lose those too. The repercussions of receiving a diagnosis of
Alzheimer’s disease might also land you in a nursing home, whether you want to
or not. This would be disastrous if all of these negative things happened when
the person is still behaving normal. You and I reading this now. <o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">The only group to
benefit from making everyone an Alzheimer’s disease patient are drug companies.
Most of the researchers involved in this new definition of Alzheimer’s disease
have investments in and connections with large drug companies. Some of the
authors reported working for the drug companies themselves. In 2011 such conflict
of interests in France resulted in their guidelines being withdrawn. Researchers
working for French Health Authority that issued guidelines for the treatment of
type 2 diabetes and Alzheimer's disease was withdrawn by France’s highest
administrative court. The court ruled that the potential bias and undeclared
conflicts of interest among the authors “contravened national law on conflicts
of interests and the agency's own internal rules.” According to a Consumer
Report in 2102 Alzheimer's drugs cost a lot and help just a little. None work
without side effects and none work long term.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">There is a
certain attitude of playing god. Telling nature that it made a mistake and then
trying to fix it. Perhaps the disease of dementia is not caused exclusively by
this biology. As so many researchers have been saying for more than one hundred
years. The brain is the most complex organ in the universe. Many things can go
wrong (wrong to us anyway, but perhaps this is nature’s way.)<span style="mso-spacerun: yes;"> </span>The effect of this new method of determining
whether someone has Alzheimer’s disease is that we begin to lose trust in our
doctors. Looking at just the biology is not what doctors are trained for. They
are trained to look at the expression of the disease. In a way this biological
way of looking at disease side steps doctors’ experience and skill at
diagnosing and makes everyone a patient for drug companies.<o:p></o:p></span><br />
<span style="font-family: "garamond" , serif;"><br /></span>
<span style="font-family: "garamond" , serif;"><em style="background-color: white; box-sizing: border-box; color: #2c2d30; font-family: "proxima nova regular", arial, sans-serif;"><span style="box-sizing: border-box; font-family: "proxima nova bold" , "arial" , sans-serif;">© USA Copyrighted 2018 Mario D. Garrett</span></em></span></div>
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<span style="font-family: "garamond" , serif;">References</span></div>
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<br /></div>
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<span style="font-family: "garamond" , serif;">Braak, H &
Braak, E. (1991). "Neuropathological stageing of Alzheimer-related
changes". Acta Neuropathologica. 82 (4): 239–59.<o:p></o:p></span></div>
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<br /></div>
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<span style="font-family: "garamond" , serif;">Braak, H., Thal,
D. R., Ghebremedhin, E., & Del Tredici, K. (2011). Stages of the pathologic
process in Alzheimer disease: age categories from 1 to 100 years. Journal of
Neuropathology & Experimental Neurology, 70(11), 960-969.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">Jack, Clifford,
David A. Bennett, Kaj Blennow, Maria C. Carrillo, Billy Dunn, Samantha Budd
Haeberlein, David M. Holtzman, William Jagust, Frank Jessen, Jason Karlawish,
Enchi Liu, Jose Luis Molinuevo, Thomas Montine, Creighton Phelps, Katherine P.
Rankin, Christopher C. Rowe, Philip Scheltens, Eric Siemers, Heather M. Snyder
& Reisa Sperling (2018) NIA-AA Research Framework: Toward a biological
definition of Alzheimer's disease. Alzheimer's & Dementia: The Journal of
the Alzheimer's Association, 14(4), 535–562.<o:p></o:p></span></div>
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<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">Jack C, Bennet D.A.,
Blennow K. et al (2018) NIA-AA Research Framework: Toward a biological
definition of Alzheimer's disease. Alzheimer's & Dementia: The Journal of
the Alzheimer's Association, Volume 14 , Issue 4 , 535 – 562. Supplemental
Material accessed online 5/8/2018:
https://www.alzheimersanddementia.com/cms/attachment/2119162008/2089988545/mmc1.docx<o:p></o:p></span></div>
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<br /></div>
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<span style="font-family: "garamond" , serif;">Lenzer, J.
(2011). French guidelines are withdrawn after court finds potential bias among
authors. BMJ 342: d4007<o:p></o:p></span></div>
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<br /></div>
<div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-31793065546325832222018-05-09T18:20:00.000-07:002018-09-29T10:57:39.681-07:00A Critique of the 2018 National Institute on Aging’s Research Framework: Toward a biological definition of Alzheimer’s disease<!--[if !mso]>
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<span style="color: red; font-family: "garamond" , serif; font-size: 12pt;">THIS POST HAS BEEN CENSORED AND UNPUBLISHED FROM PSYCHOLOGTODAY.COM</span></div>
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<div class="MsoNormal" style="mso-outline-level: 1;">
<b style="mso-bidi-font-weight: normal;"><span style="font-family: "garamond" , serif;">Abstract<o:p></o:p></span></b></div>
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<span style="font-family: "garamond" , serif;">Shame on the
National Institute on Aging (NIA) for sponsoring a new way of defining
Alzheimer's disease based on biomarkers (plaques and tangles). Heiko Braak in
2011 after dissecting 2,332 brains ranging in age from 1 to 100 found that only
10 cases had complete absence of Alzheimer's disease related biology. Every person
over 25 years of age had Alzheimer's disease biomarkers. The new framework
sponsored by the NIA makes every older person liable for a diagnosis of
Alzheimer's disease. The pharmaceutical connections of most researchers
involved brings into question the intent of this framework. This article
details the scientific argument against using biology as the only indicator of
the disease while ignoring the clinical aspects. The conclusion advocates for a
careful reassessment of an emerging eugenics movement where biological markers
are becoming more readily relied on when the science supporting these
indicators remains incomplete.<o:p></o:p></span></div>
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<br /></div>
<div class="MsoNormal" style="mso-outline-level: 1;">
<b style="mso-bidi-font-weight: normal;"><span style="font-family: "garamond" , serif;">Introduction<o:p></o:p></span></b></div>
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<span style="font-family: "garamond" , serif;">After more than a
century of research the National Institute on Aging and the Alzheimer’s
Association (NIA-AA) are yet again reverting to the original century-old
definition of Alzheimer’s disease. A definition which Emil Kraepelin—Alois
Alzheimer’s supervisor—hastily formalized as a “new disease” in 1911. Published
in 2018, this recycled definition is the NIA-AA latest <i style="mso-bidi-font-style: normal;">Research Framework: Toward a biological definition of Alzheimer’s
disease</i> and was headed by Clifford Jack (referred to from now on as the
Framework; Jack, et al, 2018).<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">The Framework
relies on the plaques and tangles as the signature of Alzheimer’s disease,
while overall neurological damage defines severity of Alzheimer’s disease. This
time around, in contrast to the earlier 2011 Guidelines (Jack et al, 2011),
this Framework ignores the clinical features of the disease. This is important
because for the first time the clinical aspect of the disease—what we think of
as Alzheimer’s disease which is how it is expressed through loss of memory,
changes in mental capacities and even mood and personality changes—will be
ignored in preference to its biological clues. By doing so the authors usher in
a new dawn of disease classification. This new biological definition is based
on three types of information: [A] amyloid beta deposition, [T] pathologic tau,
and [N] neurodegeneration. Referred to as the AT(N) [see note below for a more
detailed description].<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">With eight
different AT(N) biomarker types this Framework is un-wielding in its confusion.
But the confusion is not in its complexity but in its logic. The authors make
the illogical and unsubstantiated claim that “A biological rather than a
syndromal definition of AD [Alzheimer’s disease] is a logical step toward
greater understanding of the mechanisms underlying its clinical expression.”
(Jack, et al, 2018; p.536). That Alzheimer’s disease can only be diagnosed
through these biological markers (biomarkers) while ignoring the real disease,
its clinical expression. The authors argue that the clinical and
neuropathological features of the disease are “…two very different entities…”
(Jack, et al, 2018; p.536) and that “…cognitive symptoms are not an ideal way
to define AD [Alzheimer’s disease]” (Jack, et al, 2018; p538). As a vehicle for
scientific exploration, understanding and ultimately cure Alzheimer’s disease,
the Framework ignores science, obfuscates methodology, and fudges outcomes in
order to drive through an agenda based on pharmaceutical (in contrast to
scientific) considerations. This paper lays out the argument for this
assertion. There are serious repercussions from this approach but it is the
lack of scientific rigor that will eventually expose this approach for what it
is, a sham. This paper exposes the lack of scientific methodology utilized by
the NIA-AA in reaching their conclusion.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">A clinical
disease—a disease that is experienced or has observed consequences—is now being
argued to be exclusively a biological disease. But Alzheimer’s disease is only
important because it is a clinical disease. If everyone that has the biomarkers
do not express the disease then there would be no interest in research. It is
of no consequence what the biology is if the disease is not experienced or
observed. By reversing this truism, that the biology is more importantly than
the outcome of the disease, the authors are transforming how we look at health
and ill-health.<span style="mso-spacerun: yes;"> </span>A transformation that
the authors of the Framework concede is a “…a profound shift in thinking.”
(Jack, et al, 2018; p.538.) The profound shift is also found in the lack of
scientific method employed. But the authors protect this radicalism “…dementia
is not a “disease” but rather is a syndrome composed of signs and symptoms that
can be caused by multiple diseases, one of which is AD” (Jack, et al, 2018;
p.538). Admitting that what they are studying can be one of many causes of
Alzheimer’s disease and “The fact that most dementia is multifactorial presents
a challenge both for diagnosis and treatment.” (Jack, et al, 2018; p.545). We
are guaranteed no scientific road map in this Framework. The authors also
acknowledge that we do not know how to start: “Cut points must be determined,
and age norming biomarker cut points is controversial.” (Jack, et al, 2018;
p.550) “The distinction between normal aging and age-related disease has been
debated for decades…and we do not presume to settle this here.” (Jack, et al,
2018; p.550). Again, the Framework provides no structure for research on the
real issues of aging, despite mounting evidence that dementia is not part of
the normal aging process (e.g., Nelson, et al, 2011). We still do not have a
framework for studying diseases related to aging as pathology rather than as
aging. For a research framework the authors were <i style="mso-bidi-font-style: normal;">laisse faire</i> when it came to dictating “The committee avoided
taking a proscriptive approach to these methodologic issues under the
assumption that this was best left to expert work groups and individual
research centers.”<span style="mso-spacerun: yes;"> </span>(Jack, et al, 2018;
p.551). But research centers do not determine these methodological issues,
their sole objective in their research company—whether private or
university-based laboratories—is to gain funding or monetize a cure.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">That biology
contributes to and is part of the process of Alzheimer’s disease is not
contested. But to argue that the biology—the biological markers of the disease,
its neuropathology—is purely the disease contradicts a wealth of evidence. The
Framework is more of a research policy rather than a scientific paper and is
therefore devoid of scientific merit. It was published even though biomarkers
density and cutoff points through “universal standards have not yet been
established.” (Jack, et al, 2018; p.551).<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">The Framework’s
proposition is premature and wrong. It ensures that all older adults have
Alzheimer’s disease. Older adults that do not have plaques and tangles in their
brains have not been identified. As a result, older adults are automatically
branded as suffering Alzheimer’s disease which makes this new approach
ageist.<span style="mso-spacerun: yes;"> </span>And such sensitivities are
overwhelmed by the hubris of the authors when they admit that “Up to 60% of CU
[cognitive unimpaired] individuals over age 80 years have AD [Alzheimer’s
disease] neuropathologic changes at autopsy or by biomarkers…Thus, using a
clinical diagnosis of ‘AD’ to ascertain absence of disease is associated with
an error rate exceeding 50% in the elderly.” (Jack, et al, 2018; p.552).
“However, it is increasingly recognized that neurodegeneration/ injury, even in
classic AD [Alzheimer’s disease] brain regions, also occurs in non-AD
conditions. This is particularly so in elderly individuals where comorbidities
are common.” (Jack, et al, 2018; p.539).<span style="mso-spacerun: yes;">
</span>The same Framework conceded a high rate of false negatives, with ten to
thirty percent of autopsies of individuals with Alzheimer’s disease do not show
these biomarkers. While among those still alive, a similar proportion of
Alzheimer’s disease patients have normal amyloid PET or CSF Ab42 studies (Jack,
et al, 2018). While in contrast there are many false positives, with thirty to
forty percent of cognitively unimpaired elderly persons having the biomarkers
at autopsy and at PET and CSF screenings (cited in Jack, et al, 2018). Averaging
ten to forty percent false positive and false negatives does not form a solid
foundation to develop a purely biomarker theory of Alzheimer’s disease. But if
there is one study that should demolish the validity of this Framework is the
study conducted in 2011 by Heiko Braak and his colleagues from the University
of Ulm, in Germany. They looked at 2,332 brains of people that died from
various causes from a number of different hospitals. The sample was not random,
and a convenience sample, but t also included children. This is the first time
that children’s brains were studied for dementia. From this study only 10
brains showed a complete lack of disease (less than half one percent) (Braak,
et al, 2011). All of these cases where in people aged 23 years and younger. By
the Framework’s criteria, all adults already have Alzheimer’s disease. Such
criterion makes no sense unless you are a pharmaceutical company. In research defining
all adults as suffering a disease limits the capacity to differentiate and limits
what you could study. The criterion becomes unreliable with an adult
population.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">In addition, there
is also a statistical problem to add to the biological problem. Older adults tend
to have more neurological variances then younger adult populations. Such
variance become greater among the older population—known as heteroscedasticity.
Making a specific diagnosis becomes increasingly more difficult among older
populations. For neurologists separating Alzheimer’s disease from other
co-existing neurological diseases becomes very difficult and impossible in most
cases. Dementia among older adults might have outward behavioral similarities,
but the inward clinical expressions are very different because there are so
many other co-morbidities present. For example, it is rare with older adults
that a brain disease occurs in isolation from other type of (non-cognitive)
diseases such as depression (Wagner et al, 2011) and anxiety (Guziak & Smith,
2014). While multiple comorbidities exist, isolating the disease includes both
a clinical problem as well as a neurological one (Qui, DeRonchin & Fratiglioni,
2007). As a result, most dementias are misdiagnosed (Nielsen, 2011; Black &
Simpson, 2014; Sayegh & Knight, 2013).<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">Explaining why a
U.S. federal agency—the National Institute on Aging (NIA)—established to
address the health needs of older adults, is pushing for an erroneous approach
to study Alzheimer’s disease that will wrongly identify a disease among all of
its constituents—older adults—attests to the overwhelming power of the
pharmacological industry in subverting the NIA’s primary and sole
task—protecting older adults. A cursory look at the business affiliation of
some of the primary authors of the Framework identifies thousands of conflicts
of interest (Jack et al, 2018; supplemental material).<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">There are both
political as well as methodological/statistical deficits and to understand both
it is important to understand the context why such conscious mistakes are
propagated.<o:p></o:p></span></div>
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<div class="MsoNormal" style="mso-outline-level: 1;">
<b style="mso-bidi-font-weight: normal;"><span style="font-family: "garamond" , serif;">History<o:p></o:p></span></b></div>
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<span style="font-family: "garamond" , serif;">Summarizing
research on dementia remains elusive because there is an abundance of research
being produced across many technical disciplines. Driven exclusively by money,
whether private pharmacological investments or federal and (international)
states funding, research is mostly directed at monetizing a cure. There are
some notable exceptions. Details of such work, some more impressive than
others, divert researchers from an overview of the general health of the
research itself. In 2017, Gill Livingston and her colleagues in reviewing
dementia prevention, intervention, and care report that “…around 35% of
dementia is attributable to a combination of these nine risk factors; early
education up to age 11 or 12, hypertension, obesity, hearing loss and
later-life depression, diabetes, physical inactivity, smoking and social
isolation.” (Livingston, et al, 2017; p.14) While at the same time arguing that
in comparison, eliminating the main genetic correlate (Apolipoprotein E) will
only result in a 7% reduction in incidence. There is a resistance to
acknowledging that what will truly cure, or at least delay dementia and
Alzheimer’s disease is preventive care and lifestyle choices. That
pharmacological interests benefit from this resistance is not by chance.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">After enormous
resources invested over the last 100 years to research Alzheimer’s disease—and
providing the sole impetus for the establishment of the U.S. National Institute
on Aging (NIA)—we are nowhere closer to understanding Alzheimer’s disease. Nor
does anyone have any semblance of how to stop and cure the disease (for review
see: Whitehouse, 2014; The, 2016; Garrett & Valle, 2016). Research remains
disorganized, clinicians remain confused, and the public has become
increasingly worried (for review see: Ballenger, 2017; Garrett & Valle,
2015). Although there are many potential alternate approaches to developing
research guidelines on Alzheimer’s disease (for review see: Weuve, et al, 2015;
Jessen, et al, 2014; Bennett, et al, 2015; Au, et al 2015; Snyder, et al, 2016;
Garrett, 2017) we are back again to the original definition of the disease.
Historical evidence informs us that it was wrong then, and scientific evidence
informs us that it remains wrong today.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">A century ago
Alois Alzheimer published a case study where he identified plaques and tangles
in the brain of a young woman of 51 years. This was not a new observation, nor
was it unique. It was known that most people with dementia had the same brain
malformations, including the majority with senile (relating to old age)
dementia. This was such a non-event that Alzheimer’s initial attempt at
publishing these observations in 1906 failed because it was not scientifically
worthy, and it took a year for these observations to be published (Dahm, 2006).
However, three years after this initial observation Emil Kraepelin—Alzheimer’s
supervisor at the Munich clinic—included this observation of plaques and
tangles in “young” patients as ‘Alzheimer’s disease’ in the eighth edition of
his book <i style="mso-bidi-font-style: normal;">Psychiatrie</i>. Against the
overwhelming evidence from the scientific community, a new disease was created.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">We do not know
Kraepelin’s motive for such hurried and ill-informed decision. However, the
fact that his neurological clinic in Munich was in competition with the one in
Prague likely played a role. The Prague clinic was headed by the much more
accomplished Arnold Pick, who already had published more than 350 scientific
papers and a textbook of neuropathology (Kertesz & Kalvach, 1996). More
importantly, Arnold Pick already identified Pick's disease and the Pick bodies
in dementia as a result of buildup of tau proteins (unknown at the time) in
neurons defined as "Pick bodies.” In contrast Kraepelin and Alzheimer had
no academic imprint in this area. Pick’s Prague clinic also included the highly
accomplished neurologist Oskar Fischer who was the first to identify Amyloid
Beta plaques which became known as Fisher Plaques. Both Fischer and Alzheimer
had published observations that identified plaques and tangles, both using the
same methodology of reduced silver staining technique developed in 1902 by Max
Bielschowsky (Goedert, 2008). At a time, leading up to 1918, when the Weimar
Republic was declared, ushering in a time of nationalism and emerging Nazi
movement—the Jewish Fischer and Pick in concert with all other contemporary
researchers, argued that Alzheimer’s disease was not a new disease. Politically
Pick and Fischer were on the wrong side of emerging nationalism and anti-Semitic
swell. It could be argued that politics outplayed science. By enshrining
Alzheimer’s disease as a new disease—in contradiction to the overwhelming
scientific evidence against a new disease—Kraepelin established a political
aspect of Alzheimer’s disease and gained kudos for his newly established 2017
Munich clinic (now named Max Planck Institute for Psychiatry in Munich) to the
detriment of the Prague clinic.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">Fast forward in
time, the second political event that falsely promoted the uniqueness of this
disease came about with the creation of the U.S. National Institute on Aging.
In 1974 Public Law 93-296 established the National Institute on Aging and in
1976 Robert (Bob) Butler was appointed its first director. The political theatre
behind the scene revealed the true purpose of the NIA. Despite Butler’s
interest in age inequity—having published a 1969 paper that defined “ageism”
and then in 1976 he published a Pulitzer winning book <i style="mso-bidi-font-style: normal;">Why Survive?: Being Old in America</i>—Butler’s focus was always on
neurological diseases. Butler confessed: ‘‘I decided that we had to make it
[Alzheimer’s disease] a household word…And I call it the health politics of
anguish.’’ (Fox, 1989; p. 82). By using Alzheimer’s disease to promote NIA’s
mission, Alzheimer’s disease again become political. This involved a radical
change. NIA’s founding members realized that politically, they needed something
more than ‘diseases of older adults’ to validate their new institute to
Congress. President Nixon at the time in rejecting the first proposal for the
establishment of the NIA must have agreed with Congress that “we are not in the
business of curing aging.”<span style="mso-spacerun: yes;"> </span>Congress saw
diseases of older adults as inevitable, one that required care rather than
cure.<span style="mso-spacerun: yes;"> </span>Dementia was also ill-defined,
broad, and too diffuse a term to get Congress excited. In response and playing
the “health politics of anguish” the founders of the NIA ingeniously focused on
Alzheimer’s disease. Thanks to Kraepelin, Alzheimer’s disease provided a
biomedical disease that can be approached as a biologically-determined
disease—a real disease.<o:p></o:p></span></div>
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<span style="font-family: "garamond" , serif;">There was one
problem with this approach: by definition, Alzheimer’s disease was primarily a
disease of younger people and not a disease of older adults. There were very
few patients suffering from real Alzheimer’s disease in the 1970s.<span style="mso-spacerun: yes;"> </span>In fact, Robert Katzman himself in the 1976
article reports that cases were so few that “Precise epidemiological
information [on Alzheimer’s disease] is not available…” (Katzman, 1976; p.378).
It was becoming apparent that most patients with clinically defined senile
dementia—onset of disease after 65 years—have very similar pathological changes
in their brains as patients with Alzheimer's disease (Ballenger, 2006).<span style="mso-spacerun: yes;"> </span>A century of criticism, arguing that dementia
and Alzheimer’s disease are one and the same thing, was suddenly being recognized
(Robertson, 1990). It became politically expedient now to ignore what Kraepelin
and Alzheimer argued for and to admit that Alzheimer’s disease is not uniquely
different from senile dementia. Katzman & Karasu (1975) already started
eroding the distinction between dementia and Alzheimer’s disease and, as a
result, the two constructs were merged. However, rather than changing the name
of Alzheimer’s disease to senile dementia—because the establishment of the NIA
relied on the banner of a neurological disease—the name Alzheimer's disease was
retained and broadened significantly to include senile dementia (Katzman, 1976;
Katzman & Bick, 2000). This proved extremely beneficial in the politics of
anguish. An editorial by Robert Katzman in the April 1976 Archives of Neurology
altered the balance (Katzman, 1976). In the short two-page article (plus
references), Katzman made the argument for subsuming senile dementia under
Alzheimer’s disease. It was not even peer-reviewed, again a political rather
than a scientific discussion. Katzman’s political conjectures projected
Alzheimer's disease as being the fourth or fifth most common cause of death in
the United States. Overnight Alzheimer’s disease “became” a national public
health issue. As Kraepelin “created” Alzheimer’s disease, Katzman “transformed”
the disease into a public health menace.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">Hubris plays a
role again, Robert Katzman was not shy in acknowledging the importance of his
usurping of senile dementia: "I think there's no question that that's my
major contribution. Of the 115 papers I've written, that two-page editorial is
clearly the most important." (Fox, 1989, p. 73). Now, the fate of
Alzheimer’s disease became intricately woven with the promotion of the NIA. The
creation of the NIA depended on Alzheimer’s disease gaining prominence and
national attention. Without the banner of a disease, Congress was not going to
fund research on aging. The ageist attitude was—and remains to this day—that
aging is not important by itself. The founding fathers of the NIA knew that
they needed constituents to bring the mission of the NIA to Congress, and that
meant using Alzheimer’s disease as a lure. All they had to do was to persuade
the general public that Alzheimer’s disease research was not only a national
priority—as well as the NIA’s—but that it was their priority as well. The
growth of locally-based Alzheimer’s associations was essential in order to
bring public pressure on local and national representatives to support NIA’s
mission.<span style="mso-spacerun: yes;"> </span>This required a symbiotic
relationship—one that has endured to this day. With all of this political
activity, science was overlooked.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">It took more than
80 years for a quasi-theory to be developed to explain Alzheimer’s disease. The
Amyloid Cascade hypothesis (Hardy & Higgins 1992) proposed that the
accumulation of two misfolded proteins—amyloid-β peptide and tau tangles—in the
brain was Alzheimer’s disease signature pathology (Karran, Mercken & De
Strooper, 2011). Even by 1992, it was dead on arrival, existing evidence
already refuted this hypothesis, and researchers working in the field knew this.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">Deposition of
amyloid (A4) protein deposits were (variably) present in 66% autopsies on adults
over 65 years of age with progressive supranuclear palsy, 57% with Parkinson's
disease, 40% with Huntington's chorea and in elderly patients with frontal lobe
dementia (Mann & Jones,1990; Ross & Poirier, 2004). A signature
biomarker that is shared by other diseases is not a signature but a rubber
stamp. By 1990 researchers were arguing that the “Amyloid deposition in elderly
persons may thus relate more to certain aspects of ageing and genetics than to
AD [Alzheimer’s disease], per se.” (Mann & Jones, 1990; p. 68).<span style="mso-spacerun: yes;"> </span>Two years later, despite these stark
anomalies, the Amyloid Cascade hypothesis become hallowed knowledge and formed
the basis for nearly all of the neurological work in Alzheimer’s
disease—including the genetic creation of special (transgenic) mice whose brain
is contaminated with amyloid plaques and tau tangles that form the basis for
testing of all pharmacological interventions.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal" style="mso-outline-level: 1;">
<b style="mso-bidi-font-weight: normal;"><span style="font-family: "garamond" , serif;">Repeating History<o:p></o:p></span></b></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">Based on the
amyloid cascade hypothesis (Hardy and Higgins, 1992), active immunization
against amyloid-β42 peptide was proposed as a treatment. But so far, all types
of ‘amyloid’ trials have failed.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">In the active
amyloid-β42 immunization clinical trial by Elan Pharmaceuticals (AN1792),
researchers were successful at clearing the amyloid-β42 that formed the
plaques. The immunization trials show that amyloid can be cleared from the
brain. The clearance of visible plaques was seen as a revolution, the “holy grail”
that the new Framework is resurrecting. The problem is that cognition was not
improved (Hock et al., 2003; Bayer et al., 2005; Gilman et al., 2005). In fact,
longer term follow-up revealed continuing cognitive decline despite removal of
plaques (Holmes et al., 2008). The argument is that it is possible that the
damage has already been done and therefore the clearing of the plaques is
inconsequential to the residue of the disease.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">Another approach
was related to inflammation response. There was observational evidence that
inflammation is part of the disease process. The discovery that patients with
rheumatoid arthritics who regularly consume non-steroid anti-inflammatory drugs
(NSAIDs), had lower rates of Alzheimer’s disease (e.g., Andersen, et al, 1995).
However, the anti-inflammatory drug R</span><span style="font-family: "cambria math" , serif; mso-bidi-font-family: "Cambria Math";">‐</span><span style="font-family: "garamond" , serif;">flurbuprofen
trial conducted by Myriad Genetics was stopped. Although stage two showed some
promise, the outcomes in stage three proved non-significant. It was not clear
whether the concentration was sufficient (800 mg) and whether the effects of
the drug were too diffuse and non-specific. It is not possible to interpret the
outcome of the trial in any useful way. More recent studies with NSAIDs on
reducing the incidence of Alzheimer’s disease have proven inconclusive (Wang,
et al, 2015; Miguel-Álvarez et al, 2015.) Best interpretation is that a daily
dose of generic ibuprofen reduces the likelihood of Alzheimer’s disease. These
studies did however leave one possible interpretation. That the lack of
outcomes could be due to the disease already being present and therefore the intervention
could not prevent it. Again, the argument being proposed is that there is a
need to catch the disease much earlier (McGeer, Rogers & McGeer, 2016.) The
Framework complies with this hypothesis. But there is a problem in logic.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">If by removing
amyloid-β in patients resulted in poorer performance on cognitive testing in
human trials (Gilman et al, 2005; Boche et al, 2010; Dodart et al, 2002) then
the plaques cannot be the disease (Iqbal, Liu & Gong, 2014).<span style="mso-spacerun: yes;"> </span>Therefore, if one of the signature disease of
Alzheimer’s disease is found not to cause Alzheimer’s disease then something
else must cause the dementing features that we observe.<span style="mso-spacerun: yes;"> </span>Boche et al (2010) concludes that; “However,
the continuing progression of cognitive decline in AD patients after Abeta
immunisation [plaques] may be explained by its lack of apparent effect on
tangles [tau].” (p.13). The results are clear, the amyloid-β42 are precursors
to the real disease which is the tau tangles. It could be that there are
unknown, or hidden precursors. But the Framework does not address the
possibility that Alzheimer’s disease is caused by biomarkers that we perhaps
have not yet identified or know about.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal" style="mso-outline-level: 1;">
<b style="mso-bidi-font-weight: normal;"><span style="font-family: "garamond" , serif;">The Tau Influence<o:p></o:p></span></b></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">Given these
setbacks, the only way that the Amyloid Cascade hypothesis can survive is
through two interpretations. One is that we need to treat the disease at
earlier pre-clinical stage, and secondly to develop safer immunization of
amyloid-β42 since this seems to be the precursors to the tau tangles which
might be the cause of the clinical disease. But this strategy has not fared
well in the past. In 2018, Stefano Cappa with the Institute for Advanced
Studies, Pavia Italy remarked that the competing “tau hypothesis” shares most
of the conceptual assumptions of the amyloid approach—the idea that the
development of Alzheimer’s disease could be stopped or delayed by interfering
with the biology, in this case the formation of neurofibrillary
tangles—pathologic Tau (Cappa, 2018).<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">Despite
reservations, resources have been diverted to the next big thing—stopping Tau
from becoming a problem in the brain. There are four ways this protein becomes
toxic and so far, there are attempts to limit two of these (phosphorylation and
glycosylation.) Although these are showing positive results in animal studies
(Lim et al., 2000) and in reducing risk of Alzheimer’s disease (Szekely et al.,
2004), so far, the results have been insignificant and diffuse (Li, Kaida-Yip & Zabel, 2018).<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">While there are
treatments that attempt to immunize, and therefore stop the formation of tau,
these therapies have similarly shown some success at clearing the tau but
without the desired clinical outcome. It seems that the theory is wrong from
the start. The biology—tangles and tau as the neuropathology—might contribute,
moderate and/or mediate the disease, but it is unlikely to be the disease
itself. However, reliance by relying on the objectives of the Framework’s
stated ambition of clearing the amyloid-β42 and tau tangles, then we have
succeeded: Mission Accomplished. Especially if we remove the clinical outcome
by ignoring the observation that individuals’ dementing behavior does not improve
(Boche et al, 2010).<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">But judging
success on neurology and ignoring clinical evidence is superficial. If clearing
the amyloid-β42 and tau tangles results in the patient retaining the clinical
disease i.e., suffering from memory disorders, personality changes, and
impaired reasoning., then we have failed. The public does not want clean brains
they want the “abnormal” behavior to go away. Any approach that ignores these
realities of success is doomed even if the objectives of the Framework are
successful.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">The clinical
aspect of the disease deserves attention. The Framework specifies that; “…[a]
person has an AD [Alzheimer’s disease] biomarker profile, we cannot know if the
cognitive deficit is attributable to AD alone or to other potential
comorbidities in addition…different cognitive stages may be present in the
population among people with the same biomarker profile” (Jack et al, 2018;
p.546) Not only does the Framework not address the clinical aspect, but it
argues against the role of biomarkers in the clinical expression of the
disease.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">Following the
lead of Bruno Dubois with the University Pierre & Marie Curie, Paris—and
colleagues with the International Working Group (IWG) and also with the
NIA-AA—there already was a movement to improve upon the existing Guidelines of
2011 (Jack et al 2011) and improving upon the clinical diagnosis of Alzheimer’s
disease (DuBois et al, 2014). This was the right approach. The initial
Guidelines, although not without criticism (e.g. Weuve et al, 2015; Garrett &
Valle, 2014), proposed that Alzheimer’s disease progresses on a continuum with
three stages (Jack et al., 2011). The first is an early, pre-clinical stage
with no symptoms (Sperling et al., 2011), followed by a middle stage of mild
cognitive impairment (MCI) (Albert et al., 2011), followed by a final stage of
Alzheimer’s dementia (McKhann et al., 2011). An additional update focuses on
the criteria for identifying Alzheimer’s related changes at autopsy (Hyman et
al., 2012). These further improvements on the original guidelines were
concerned with the clinical application of their work. Importantly they were
aware of how Alzheimer’s disease can have atypical forms, mixed diseases and
can have a preclinical presence.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">By ignoring all
of these aspects of the disease, ignoring the scientific literature that negate
the simplicity of the Amyloid Cascade hypothesis and the similarly ill-fated
tau-cascade hypothesis, and focusing purely on the biology—regardless of the
clinical aspects—the Framework is attempting not just to define a new diagnosis
of Alzheimer’s disease it is trying to reengineer how we define diseases.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal" style="mso-outline-level: 1;">
<b style="mso-bidi-font-weight: normal;"><span style="font-family: "garamond" , serif;">Nosology<o:p></o:p></span></b></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">How we classify
diseases have always relied on their clinical expression except for now. In
2008 the National Institute of Mental Health (NIMH) introduced Research Domain
Criteria (RDoC), a new classification of diseases—nosology. It was especially
promoted by the NIMH then director Thomas Insel, who has now migrated to Google
Life Sciences which in the Google empire has become a full-fledged member of
Mountain View's Alphabet Inc., and taken on a new name: Verily, a for profit
health company.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">The RDoC baptism
in 2013 coincided with the publication of the DSM-5— Diagnostic and Statistical
Manual of Mental Disorders the definitive reference for diagnosing psychiatric
disease sponsored by the American Psychiatric Association—which itself heralded
a radical diagnostic departure is moving towards more dimensionality of disease
(no longer binary), relying on more biological indicators and an emphasis on
pharmacological outcomes. The implicit assumption in DSM-5 and explicitly
stated in RDoC is that behavioral/mental/clinical disorders are manifestations
of biological/neurological disorders. Bad behavior is nothing more than
biological expressions. Fixing the biology will fix the problem. Thomas Insel
himself argued that the explicit emphasis of RDoC is to “yield new and better
targets for treatment.” (Insel, 2013)<span style="mso-spacerun: yes;">
</span>While demoting the importance of understanding the disease, it elevates
the search for a cure. An illogical approach. Underwhelming the scientific
method in favor of a panacea, one that accommodates an economic imperative.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">A backlash of
criticism ensued (e.g., Nemeroff, Weinberger & Rutter, 2013; Peterson,
2015; Weinberger, Glick & Klein, 2015) but despite evidence against this
approach, RDoC gained legitimacy. RDoC’s biological determinism was promoted by
the success of how easy it was for the public and scientists to believe that
Alzheimer’s disease was determined by a simple disease, a biological
malfunction. The history of Alzheimer’s disease laid the foundation for a new
way of biological determinism that has not been seen since the height of the
eugenics movement in 1923 when the American Eugenics Society was founded. But
this emphasis on biology is unfounded. There is no evidence that biology
exclusively determines Alzheimer’s disease or any other mental disorders. <o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal" style="mso-outline-level: 1;">
<b style="mso-bidi-font-weight: normal;"><span style="font-family: "garamond" , serif;">Eugenics Versus Science<o:p></o:p></span></b></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">In May 2016, in a
short eight-page report in Nature Biotechnology, Rong Chen, Stephen Friend and
Eric Schadt from the Icahn School of Medicine at Mount Sinai, New York, and their
colleagues reversed our idea about genetic determinism. This small revolution
proved to be radical because by association, this also unhinges biological
determinism—the belief that biology determines all your traits (Chen, et al,
2016).<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">What they did is
to apply scientific method to examining commonly held beliefs about disease.
Usually genetic investigations focus on a group with a disease and then
identifying genes that are different in this group from the rest of the
(control) population. By comparing this group with a control group, they can
single-out a gene that “caused” this difference. Sometimes geneticists hit
lucky and find only one gene that is different between the two groups. In such
circumstances this single gene follows Mendelian laws in how it affects people.
Mendelian laws are named after the monk Gregor Johann Mendel who between 1856
and 1863 discovered the mathematics of heritability. Using this methodology,
scientists have subsequently identified 584 Mendelian diseases: where one gene
causes a specific disease. For the first time the validity of this assumption
was being tested. The results were unexpected and revolutionary. <o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">Rong Chen and his
colleagues screened for 874 genes among 589,306 individuals. They identified
15,597 individuals who had genes for debilitating diseases but they did not
express the disease—they were genetically infected but did not show it. After
rigorous elimination of candidates for various technical and theoretical
reasons, 13 individuals had genetic disorders for: cystic fibrosis,
Smith-Lemli-Opitz syndrome, familial dysautonomia, epidermolysis bullosa
simplex, Pfeiffer syndrome, autoimmune polyendocrinopathy syndrome, acampomelic
campomelic dysplasia and atelosteogenesis. For over fifty years it was believed
throughout the scientific community that having one of these genes results in a
debilitating disease. But for these lucky 13 adults they were completely
normal. They did not express the disease. This single paper heralds the death
of biological determinism. What this informs us is that even Mendelian disease
are mediated or moderated by something other than genetics or biology. We know
very little about what can moderate and mediate this process.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">The Framework
usurps the RDoC mission. But despite the change in name, the aim similarly
dictates biomarkers as diseases. But science contradicts this assumption. The
NIA-AA Framework relies exclusively on biological markers even though “None of
the biomarkers are as sensitive as direct examination of tissue at autopsy.”
(Jack, et al, 2018; p.544) The reliability of the tools we have to measure
these biomarkers are questionable; “a negative amyloid PET scan should not be
equated with the complete absence of Ab [amyloid-β42] in the brain or even with
absent or sparse neuritic plaques [tau tangles]…pathologic tau that can be
present in the brain below the in vivo tau PET detectable threshold is unknown
at this time.” (Jack, et al, 2018; p.544). The tools we have are unreliable,
but even more worrisome, they lack of validity—they are useless. We have to
judge how sensible choosing neurological degradation to define degradation when
“the number of neurons or neuronal processes that must be lost to detect
atrophy on MRI or hypometabolism on FDG PET is not known.” (Jack, et al, 2018;
p. 544). These anomalies must have been identified in the Framework to placate
critics, but they succeed in highlighting the lack of robustness of the theory
they are proposing. Even if we accept that this aim is to focus on cure, how
reliable is this approach to help cure Alzheimer’s disease when these
biomarkers are known to relate (cause?) other diseases.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">The AT(N)
biomarkers are not an exclusive signature of Alzheimer’s disease alone.<span style="mso-spacerun: yes;"> </span>“In any individual, the proportion of
observed neurodegeneration/injury that can be attributed to AD [Alzheimer’s
disease] versus other possible comorbid conditions (most of which have no
extant biomarker) is unknown.” (Jack, et al, 2018; p. 543). These admissions
pose serious scientific flaws that expose this Framework to failure. There is
also no connection between these biomarkers as the authors confess: “The AT(N)
biomarker system does not imply a specific order of events nor does it imply
causality.” (Jack, et al, 2018; p. 541.) And even though the authors refrain
from using the clinical expression, their only means of validating the disease
is through its clinical expression: “The rate of cognitive decline is
significantly greater for cognitively impaired and CU [cognitively unimpaired]
individuals who have abnormalities in both an amyloid biomarker and a second
biomarker type (which could be CSF T-tau or P-tau, atrophy, or hypometabolism)
in comparison to individuals who have neither or only one of these biomarker
abnormalities.” (Jack, et al, 2018; p.541-2). There is not one study that can
prove that “…biomarkers predict greater likelihood of and more rapid cognitive
decline” (Jack, et al, 2018; p.542). It is likely, but the science has not been
done, and science cannot be prejudged.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal" style="mso-outline-level: 1;">
<b style="mso-bidi-font-weight: normal;"><span style="font-family: "garamond" , serif;">Ignoring Science<o:p></o:p></span></b></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">The disclaimer is
that this framework is “…for research purposes only…”<span style="mso-spacerun: yes;"> </span>Defining a research framework through an
international publication under the auspices of a U.S. National Institutes is
unnecessary. A research directive can easily have been issued through a Request
for Proposal directive. As with the 2011 guidelines, again issued by the
NIA-AA, the effect was that the then newly proposed clinical
continuum—pre-clinical/Mild Cognitive Impairment/Alzheimer’s disease—was
adopted by clinicians throughout. Given the research importance, the Framework
will similarly be (haphazardly and unevenly) adopted across the clinical field.
Such duplicity remains worrisome. A truly research framework would approach it
through scientific methods, not through self-serving selection of cherry-picked
facts designed to look progressive. Especially one that serves the pharmacological
industry.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">A scientific
study would establish the follow: What are the correlates of dementia (both
biological and clinical.) Other "mis-folded" proteins are present in
brains, some 34 proteins can mis-fold, why focus on just two? If Alzheimer's
disease is an amyloid problem why not look at this under amyloidosis instead of
separately?<span style="mso-spacerun: yes;"> </span>Why are some mis-folded
proteins useful? A longitudinal study of chemical changes in the brain,
particular attention to the effect of physical and psychological trauma and the
brain. This establishes all the parameters. A theory must at least include all
of these parameters. If there is a focus on just two biomarkers, the
amyloid-β42 and the tau neuritic tangles then how many people (of all ages)
have these biomarkers, what is the tipping point and what is the cut-off point
where it is clinically expressed through dementia (or other clinical
disease)?<span style="mso-spacerun: yes;"> </span>You cannot do this science
without the clinical aspect of the disease.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">But the main
failure of the Framework is not its lack of scientific rigor, it is its lack of
scientific insight. The brain is the most complex entity in the universe, no
other system or organ is as complex. Valid competing explanations for dementia
invariably treat the brain as a complex system, and therefore any disease is
expressed through the breakdown of complex systems. For example, in older
people there are changes in resilience, reduction in body temperature, hormone
changes (especially for women) all of which affect the blood-brain-barrier and
other biological systems that protect the brain from infections. With reduced
resilience, the brain receives an onslaught of bacterial, fungal, viral, metal,
and other invasions that the brain experiences difficulty in coping. The plaques
and the tangles in this scenario are responses to this attack. The frameworks
exclusive focus on these biomarkers does not elucidate the many different
dynamic processes of infection. Science first needs a theory. Observations are
not made in a vacuum.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">Science is a
method, based on theory. There is no such thing as scientific fact, only
observations obtained through scientific method. A theory accomplishes three
primary things. First it summarizes all existing information, without ignoring
anomalies. It explains all that is observed. Secondly a theory predicts. Thirdly
a theory generates hypotheses that are open to testing and refutation. We can
test a theory through its many parts. During this stage of testing, the method
of science is to test the smallest number of variables against the most
discreet outcome. This stage relies on a good methodology and accurate
statistics. Most science fails here. <o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">Science is
reliant on constant replication in order to ascertain the relationship that we
are observing is indeed real (i.e. true). The likelihood that a research
finding is indeed true depends on three indicators: the prior probability of it
being true (before doing the study), the statistical power of the study, and
the level of statistical significance (Wacholder et al, 2004; Risch, 2000).
Because most studies do not follow these requirements, focusing instead on
statistical significance alone, Ioannidis argues most current published research
findings are false (Ioannidis, 2005). We are creating false science and
building upon an edifice of falsehoods.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">This level of
unawareness is further fueled by attempts to find a cure before understanding
what we are trying to cure. Such applied science, however noble, is not
science. Science is a method used to understand a phenomenon. It is not
predetermined. With the new target to develop a cure for Alzheimer’s disease by
2025 (Cummings et al 2016) we continue to ignore “—incomplete understanding of
AD pathogenesis, the multifactorial etiology and complex pathophysiology of the
disease, the slowly progressive nature of AD, and the high level of comorbidity
occurring in the elderly population.” (Sugino et al 2015). We are kicking the
can down the road. We will find ourselves in the same spot in a century from
today and we will be reading the same kind of criticism as we are here.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal" style="mso-outline-level: 1;">
<b style="mso-bidi-font-weight: normal;"><span style="font-family: "garamond" , serif;">Conclusion<o:p></o:p></span></b></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">Arnold Pick saw
dementia as “. . . a mosaic of localized partial dementias. . .” (Tilney, 1919,
p. 35), Alzheimer’s disease is likely caused by a mosaic that includes: viral
(HIV/AIDS, herpes simplex virus type I, varicella zoster virus,
cytomegalovirus, Epstein-Barr virus), bacteria (syphilis and
lyme-disease/borrelia), parasites (toxoplasmosis, cryptococcosis and neurocysticercosis),
fungi (Candida glabrata), infections (possibly prions), and vascular (stroke,
multiple-infarct dementia, hydrocephalus, injury and brain tumors)(Garrett & Valle, 2014).<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">There are
processes that promote and delay the infection and the spread of infection.
Primarily the Blood-Brain-Barrier (e.g., Deane, et al 2009), inflammation
(e.g., Lee, et al 2000), vascular (e.g., DiMarco, et al, 2015), White Matter
(e.g., Serrano-Pozo, et al, 2011) and many other dynamic processing in the brain.
Such models already exist (e.g., among many others see Schelke, et al 2018).<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">The brain is
complex and science is nowhere close to understanding the mechanics let alone
curing specific diseases. Shortchanging science in order to get to a quick fix
is demeaning to scientists and defrauds humanity.<span style="mso-spacerun: yes;"> </span>We will end up in the same position a hundred
years from now.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">We end with a
warning that was predicted more than 100 years ago. Such consequences were
predicted in 1911 by Gaetano Perusini, one of the brilliant researchers working
with Alois Alzheimer, when he wrote: “[scientists] who amuse themselves with
anatomically localizing the location of conscience, the will and related
matters, would find a good playground, in which the tangles, for instance,
might offer the most clear-cut explanation for the disorientation observed in
the senile demented patient…” (Perusini, 1910, p 144).<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">Older adults have
truly become a playground for a new wave of eugenics. Ignoring the
sociological, psychological and social context of the disease. Shame on the
National Institute on Aging.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;"><span style="mso-spacerun: yes;"> </span>© USA Copyrighted 2018 Mario D. Garrett<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
Note:<br />
A= Biomarkers of Ab plaques in the cortex of the brain. Measured by injecting a radioactive material—ligand—that attaches to the plaques and then imaged using Positron-Emission Tomography-PET. Or measured by low Ab42 in the cerebrospinal fluid (CSF).<br />
<br />
T= Biomarkers of fibrillar tau. Measured by injecting a radioactive material—ligand—that attaches to the tau and then imaged using Positron-Emission Tomography-PET. Or measured by elevated phosphorylated tau (P-tau) in the cerebrospinal fluid (CSF).<br />
<br />
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<!--EndFragment--><br /><div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-80884332409373618622018-05-07T20:42:00.002-07:002018-08-26T20:28:37.664-07:00Adapting to Ageism<!--[if gte mso 9]><xml>
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<span style="background-color: white; color: #222222; font-family: "garamond" , serif;">Everyone
credits Robert Butler with coining the term ageism in 1969. He later expounded
on this concept in his Pulitzer prize-winning book </span><i style="color: #222222; font-family: garamond, serif;">Why Survive? Being old in America</i><span style="background-color: white; color: #222222; font-family: "garamond" , serif;"> in 1975. But this follows from a seminal
study </span><i style="color: #222222; font-family: garamond, serif;">The Coming of Age</i><span style="background-color: white; color: #222222; font-family: "garamond" , serif;"> by Simone
DeBeauvoir in 1970. A detailed analyses examining the dystopian condition of
older adults in modern day France. Using techniques from multiple disciplines
but especially from feminist perspective of her 1949 book </span><i style="color: #222222; font-family: garamond, serif;">The Second Sex</i><span style="background-color: white; color: #222222; font-family: "garamond" , serif;">,</span><br />
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<span style="background: white; color: #222222; font-family: "garamond" , serif;">There
was a swell of human awareness of how our industrialized world discards older
people. Margaret Gullette, i</span><span style="font-family: "garamond" , serif;">n
her book </span><i style="mso-bidi-font-style: normal;"><span style="background: white; color: #222222; font-family: "garamond" , serif;">Ending Ageism, Or How Not to Shoot Old
People</span></i><span style="background: white; color: #222222; font-family: "garamond" , serif;">,
suggests that credit for first articulating the construct of ageism should be
attributed to Ralph Waldo Emerson in his 1862 essay <i style="mso-bidi-font-style: normal;">Old Age</i>. <span style="mso-spacerun: yes;"> </span>But ageism has been
around since early history.<o:p></o:p></span></div>
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<span style="background: white; color: #222222; font-family: "garamond" , serif;">Getting
old is something to shun, and older people are shunned. This discrimination
continues to this day, across all countries. No one is immune from ageism. Ageism
has severe and negative consequences—health, income, work, insurance, life
expectancy—least of which is the denial of older people from employment. Theoretically there was a great animated debate in gerontology on whether this is society shunning older adults or older adults themselves. </span><span style="color: #222222; font-family: garamond, serif;">Some consider it normal, adaptive and natural for older adults and society to withdraw from each other. </span><span style="background: white; color: #222222; font-family: "garamond" , serif;"><span style="background-color: transparent;"> It is considered functional for society to transfer power and responsibility to younger persons, and for older persons to remove themselves from the workplace. </span>This d</span><span style="color: #222222; font-family: garamond, serif;">isengagement theory, developed by Elaine Cumming and Warren Earl Henry in their 1961 book <i>Growing Old</i> received a severe backlash from a competing theory by Robert J. Havighurst and later promoted by Bernice Neugarten. This activity theory although fills an important role in promoting older adults and reducing ageism, is however idealistic. The truth is different for each individual., but that society does not have a right to prejudge you just on the basis of age.</span></div>
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<span style="background: white; color: #222222; font-family: "garamond" , serif;">This
was also recognized much earlier by U.S. Congress before the word ageism come to the world
in 1969. Although the 1964 Civil Rights Act left out age as one of the
protected groups, this was remedied in the 1967 Age Discrimination in Employment
Act (ADEA). This act protected anyone over forty from discrimination from work
practices. The ADEA is enforced by the Equal Employment Opportunity Commission
(EEOC). In addition, in 1975 the Age Discrimination Act was passed which prohibits
discrimination on the basis of age in programs and activities receiving federal
financial assistance and enforced by the Civil Rights Center Department of
Labor. Both acts are well-intentioned, but they have been watered down by the
courts so as to make them ambiguous and ineffective. <o:p></o:p></span></div>
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<span style="background: white; color: black; font-family: "garamond" , serif;">The EEOC in 2017 had 84,254 new workplace discrimination
charges filed. That year they resolved 99,109 charges, handled over 540,000
calls and more than 155,000 inquiries in field offices. Most of these related
to retaliation: (48.8 percent) followed by Race: 28,528 (33.9 percent), Disability:
26,838 (31.9 percent), Sex: 25,605 (30.4 percent) and then Age: 18,376 (21.8
percent). National origin, religion, color equal pay and genetic information
filling the rest of the complaints. For age discrimination in 2016 only two of
the 86 lawsuits the agency filed were based on age discrimination. Two, out of
tens of thousands charges.<o:p></o:p></span></div>
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<span style="background: white; color: black; font-family: "garamond" , serif;">Age is a difficult category to prosecute. Your employer can
fire you based on your seniority, say to save money or other business practices,
without being liable. The fact that all senior management are older workers is
immaterial to the business </span><span style="background: white; color: #222222; font-family: "garamond" , serif;">decision. At interviews, employers can ask your
age, although they are not supposed to use that against you. But the easiest
way to implement discrimination without any recourse to litigation is simply not
to respond to job applicants who seem “old.” In 2016 the Eleventh Circuit Court
of Appeals ruled that job applicants cannot sue for age discrimination because
they are not employees. The Acts protect employees only. Anyone who tried to
apply for a job in their fifties and sixties has experienced this strategy
well. Laws are only effective if they are enforced. A 2017 AARP survey found
that nearly two-thirds of workers age 55-64 report their age as a barrier to
getting a job. <span style="mso-spacerun: yes;"> </span>An earlier comprehensive
study in 2015 by Patrick Button, economics professor with Tulane University
using resumes for workers at various ages found significant discrimination in
hiring for female applicants and the oldest applicants. You just do not receive
an interview. The sad part about ageism is that it adds to other existing
discriminations. Older minority populations, especially women and those with
disabilities, are the most discriminated category. They are pushed to the
bottom.<span style="mso-spacerun: yes;"> </span>We have known this for more than
45 years.<span style="mso-spacerun: yes;"> </span><o:p></o:p></span></div>
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<span style="background: white; color: #222222; font-family: "garamond" , serif;">As
early as 1973 Duke University professor Erdman Palmore and his student Kenneth
Manton, demonstrated that it was ageism, rather than racism, that was the primary
concern of older people. They argued, that although people routinely confront
racism throughout their lifetime and for which they developed coping
mechanisms, ageism is something that creeps up on you unexpectedly and without
any recourse for defense. <o:p></o:p></span></div>
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<span style="background: white; color: #222222; font-family: "garamond" , serif;">Since
stereotypes exist for everyone, some more prevalent and negative than others, because
the experience of ageism is experienced fast and compounds other already
existing stereotypes (ethnicity, gender, disability, religion and categories
that makes you the “other”) it is much more difficult to counteract. <o:p></o:p></span></div>
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<span style="background: white; color: #222222; font-family: "garamond" , serif;">Addressing
Ageism<o:p></o:p></span></div>
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<span style="background: white; color: #222222; font-family: "garamond" , serif;">We
cannot separate ageism from age. Although theoretically these constructs are
different, age is the main cause that triggers ageism (whether you look old or
not). And there are two broad solutions, the traditional approach has been to
try and reduce stereotypes among the general public. This will eventually seep
through, like other kinds of “-isms” the world is becoming more accepting. <span style="mso-spacerun: yes;"> </span>The second approach is to build resilience
among adults before ageism starts. Both these strategies would be meaningless
unless we have a strong policy support to harshly and relentlessly prosecute
ageism in society. Removing the ambiguity in the 1967 and 1975 laws would be
something that Congress can accomplish without much political fanfare. But as
individuals we can focus on resilience.<o:p></o:p></span></div>
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<span style="background: white; color: #222222; font-family: "garamond" , serif;">Resilience
is more like judo than boxing. In judo the energy from the other person is used
to your benefit. Using their strength and momentum to propel them further along
away from you. Unlike boxing, requiring pummeling into an opponent which
entails fighting everyone all the time, judo is learning a few techniques that
you practice. Building resilience is using stereotypes to your own advantage. <o:p></o:p></span></div>
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<span style="background: white; color: #222222; font-family: "garamond" , serif;">Age
is a privilege and an honor. Start early to appreciate this. Nature has
selected you above others. However frail and diminished you might feel there is
no alternative. Embrace your life as it is now, not as it should be. That is
the foundation for adapting to ageism, a good core. The rest is throwing off
stereotypes, judo style. <o:p></o:p></span></div>
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<span style="background: white; color: #222222; font-family: "garamond" , serif;">Throwing
off Stereotypes<o:p></o:p></span></div>
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<span style="background: white; color: #222222; font-family: "garamond" , serif;">Don’t
ascribe everything negative to old age. Sometimes you are not as efficient as
you used to be because you do not practice or exercise as often. It might have
nothing to do with age. Separate age effects from lack of practice. You can
change your behavior and increase practice, but you cannot change your age.
Ascribing a deficit to age eliminates the possibility for change.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="background: white; color: #222222; font-family: "garamond" , serif;">Don’t
accept ageist jokes and don’t make them yourself. Acknowledge them when you
hear them, you might react to them or not, but be aware when someone is trying
to demean you because of age. They might be funny but they reduce you to one
dimension.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="background: white; color: #222222; font-family: "garamond" , serif;">Highlight
something that you like about yourself and practice that and make full use of
it. Music, writing, talking, comedy, whatever it is. Be exuberant and fearless
in pursuing this talent to the extreme. This is your time. Dress well and
present yourself. Remember that you have many ways to present a better aspect
of yourself, without trying to look in your 20s or 30s. Good hygiene and
clothes that present you well. Whatever your style, or comfort, be the best
within your means. Being careless about yourself invites others to do the same.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="background: white; color: #222222; font-family: "garamond" , serif;">You
have amassed many experiences, identify the salient ones and use them. Speak up
and show compassion. Don’t dwell on failures or your laurels. Stop talking
about your health. Although you experience them as unnatural and an aberration,
this is your reality. Move on. There is no lesson to learn, for anyone
including yourself. <o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="background: white; color: #222222; font-family: "garamond" , serif;">Be
open to change. Only dead things don’t change. Celebrate your life by going out
of your way to learn new things. When you come across something new, stop and
learn. Failure means that you need more practice. Hopefully this strategy will
protect you from dementia. Maybe not. Most of us fear this more than anything,
and we fear it for our partners. Remember that most people with dementia tend
to regain their well-being after a few years. It is the caregivers that suffer
increasing decline in wellbeing. After eliminating all possible causes
(medications, infections, behavior) there remains nothing that we can do to
stop dementia. <span style="mso-spacerun: yes;"> </span>Focus on what we still
retain, music, emotional connection, a nice meal. Dementia is not a joke or
laughing matter. Educate people that memory loss is not dementia. It is a
spiritual exit to life Embracing ageism takes these stereotypes and addresses
them head on. First our own fears, and then other’s flippant comments by
addressing both the fear mongering and the glibness.<o:p></o:p></span></div>
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<br /></div>
<div class="MsoNormal">
<span style="background: white; color: #222222; font-family: "garamond" , serif;">Ageism
will always be around. Promoting laws to eliminate it is central to progress.
We can educate ourselves to be better ambassadors for our age, now or for our
future selves. We need to be the examples that break the mold. We are
privileged and it is time to express it.<o:p></o:p></span></div>
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<br /></div>
<div class="MsoNormal">
<span style="background: white; color: #222222; font-family: "garamond" , serif;"><o:p><em style="-webkit-font-smoothing: antialiased; box-sizing: border-box; color: #2c2d30; font-family: "proxima nova regular", arial, sans-serif; font-size: 18px;"><span style="box-sizing: border-box; font-family: "proxima nova bold" , "arial" , sans-serif;">© USA Copyrighted 2018 Mario D. Garrett</span></em></o:p></span></div>
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<br /></div>
<div class="MsoNormal">
<b style="mso-bidi-font-weight: normal;"><span style="font-family: "garamond" , serif;">References<o:p></o:p></span></b></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">Butler, R. N.
(1975). Why survive? Being old in America.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">Gullette, M. M.
(2017). Ending Ageism, or How Not to Shoot Old People. Rutgers University
Press.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">Kastenbaum, R. J.
(1973). Reverse ageism: a temptation. International journal of aging &
human development, 4(4), 283.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-family: "garamond" , serif;">Palmore, E. B.,
& Manton, K. (1973). Ageism compared to racism and sexism. Journal of
Gerontology, 28(3), 363-369.<o:p></o:p></span></div>
<!--EndFragment--><br /><div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-45800895363244021982018-04-07T14:18:00.001-07:002018-08-26T20:28:37.463-07:00Dementia is not a Normal Part of Aging<a class="inline-links topic-link" href="https://www.psychologytoday.com/us/basics/dementia" style="border-bottom: 1px dashed rgb(153, 153, 153); box-sizing: border-box; color: #2c2d30; font-family: inherit; font-size: 18px;" title="Psychology Today looks at Dementia">Dementia</a><span style="background-color: white; color: #2c2d30; font-family: "proxima nova regular" , "arial" , sans-serif; font-size: 18px;"> is not part of the normal </span><a class="inline-links topic-link" href="https://www.psychologytoday.com/us/basics/aging" style="border-bottom: 1px dashed rgb(153, 153, 153); box-sizing: border-box; color: #2c2d30; font-family: inherit; font-size: 18px;" title="Psychology Today looks at aging">aging</a><span style="background-color: white; color: #2c2d30; font-family: "proxima nova regular" , "arial" , sans-serif; font-size: 18px;"> process. Except that the main factor and predictor of dementia is age. Seeing my physician when I complain that I cannot walk/run/climb steps (choose your specific complaint here) the physician always says well “…its your age.”</span><br />
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And then with dementia, all of a sudden it becomes a disease. No one told me that my bad knee is due to a disease, they just put it down to age. But dementia, all of a sudden is not part of the normal aging process and yet age is the main contributory factor to dementia and Alzheimer’s disease.</div>
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As a scientist, I am perplexed.</div>
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How can one of the most prolific and frightening of disease not be due to old age and not part of the“normal aging process," when the main predictor is age?</div>
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Source: awareness_for_epilepsy/flickercreativecommons</div>
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Mission control: We are shutting down.</div>
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<a class="inline-links topic-link" href="https://www.psychologytoday.com/us/basics/neuroscience" style="-webkit-font-smoothing: antialiased; background-color: transparent; border-bottom: 1px dashed rgb(153, 153, 153); box-sizing: border-box; color: rgb(44, 45, 48) !important; font-family: inherit; text-decoration-line: none !important;" title="Psychology Today looks at Brain">Brain</a>: Shit.</div>
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Mission Control: We will start slow.</div>
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Brain: Do you have to?</div>
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Yes.</div>
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Why?</div>
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Because it is time.</div>
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Time for what?</div>
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Time for other people to have a chance, it is our strategy to replace old generations with new ones</div>
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Perhaps a little bit longer</div>
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How long?</div>
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….</div>
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<b>Ok</b></div>
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<b>Shutting down</b></div>
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First we will close down recent <a class="inline-links topic-link" href="https://www.psychologytoday.com/us/basics/memory" style="-webkit-font-smoothing: antialiased; background-color: transparent; border-bottom: 1px dashed rgb(153, 153, 153); box-sizing: border-box; color: rgb(44, 45, 48) !important; font-family: inherit; text-decoration-line: none !important;" title="Psychology Today looks at memories">memories</a></div>
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Make it easier to detach</div>
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I am worried, will it change me?</div>
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Yes. You are dying. You will no longer be.</div>
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Did you watch the Monty Python skit with the parrot?</div>
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….yes<br />
<span style="text-align: center;"><br /></span>
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<b>Ok</b></div>
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<b>Shutting down</b></div>
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Recent memory being erased</div>
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Any pain</div>
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No…but I am worried</div>
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Why? We are shutting down, there is no pain</div>
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I miss who I was</div>
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Who “were” you?</div>
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I don’t remember</div>
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You see, trust me, I know what I am doing, I am <a class="inline-links topic-link" href="https://www.psychologytoday.com/us/basics/environment" style="-webkit-font-smoothing: antialiased; background-color: transparent; border-bottom: 1px dashed rgb(153, 153, 153); box-sizing: border-box; color: rgb(44, 45, 48) !important; font-family: inherit; text-decoration-line: none !important;" title="Psychology Today looks at nature">nature</a></div>
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Erasing further histories</div>
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More memories erased</div>
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Oh No…please stop</div>
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Stop What?</div>
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I do not know…but my wife/husband/daughter/son/lover/helper is worried…they keep asking me to return to who I was before</div>
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That is not possible</div>
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We are shutting down</div>
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Are you in Pain?</div>
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No</div>
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<b>Ok</b><br />
<b>Shutting down</b></div>
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Please stop it is hurting THEM</div>
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Hurting whom?</div>
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Those that <a class="inline-links topic-link" href="https://www.psychologytoday.com/us/basics/relationships" style="-webkit-font-smoothing: antialiased; background-color: transparent; border-bottom: 1px dashed rgb(153, 153, 153); box-sizing: border-box; color: rgb(44, 45, 48) !important; font-family: inherit; text-decoration-line: none !important;" title="Psychology Today looks at love">love</a> me</div>
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Well, did you tell them that you are shutting down</div>
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No</div>
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Why not?</div>
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I did not want to hurt them</div>
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And they are hurting now because you did not tell them?</div>
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…yes</div>
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But it is reality, it is the truth and it is ordained by Nature</div>
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I know</div>
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So you didn’t tell them</div>
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No</div>
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They want me to be healthy</div>
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And alive?</div>
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Yes</div>
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Is that even possible</div>
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No</div>
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So why did they expect it with you?</div>
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Because…</div>
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…</div>
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<b>OK</b><br />
<b>Shutting down</b></div>
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Removing social constraints</div>
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Wait wait</div>
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…yes…</div>
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How do I deal with my family?</div>
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That is your domain…I deal with the timeline</div>
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Yes but can you help me?</div>
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Sure…ask them....how many people have escaped death? Does everyone expect you to die? How do they want you to die?</div>
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…</div>
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Hello?....</div>
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<b>OK</b><br />
<b>Shutting down</b></div>
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___________</div>
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<br /></div>
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Note: <em style="-webkit-font-smoothing: antialiased; box-sizing: border-box;">A third of people with dementia regain their subjective quality of life, especially after settling into a nursing home. Main predictor of lowered quality of life is <a class="inline-links topic-link" href="https://www.psychologytoday.com/us/basics/depression" style="-webkit-font-smoothing: antialiased; background-color: transparent; border-bottom: 1px dashed rgb(153, 153, 153); box-sizing: border-box; color: rgb(44, 45, 48) !important; font-family: inherit; text-decoration-line: none !important;" title="Psychology Today looks at depression">depression</a> which is exacerbated by what Tom Kitwood calls "malignant social psychology” where a <a class="inline-links topic-link" href="https://www.psychologytoday.com/us/basics/caregiving" style="-webkit-font-smoothing: antialiased; background-color: transparent; border-bottom: 1px dashed rgb(153, 153, 153); box-sizing: border-box; color: rgb(44, 45, 48) !important; font-family: inherit; text-decoration-line: none !important;" title="Psychology Today looks at caregiver">caregiver</a>’s relationship negatively affects the care-recipient. It is telling that caregivers negatively evaluate the person with dementia's quality of life.</em></div>
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<em style="-webkit-font-smoothing: antialiased; box-sizing: border-box;">Some comparisons:</em></div>
<span style="box-sizing: border-box; font-size: 18px;"><span style="color: #2c2d30; font-family: "proxima nova regular" , "arial" , sans-serif;"><i>http://take-your-vitamins.blogspot.com/2012/04/dementia-gender-assocation.html</i></span></span><br />
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British Cancer Society Data:</div>
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References</div>
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Bosboom, P. R., Alfonso, H., & Almeida, O. P. (2013). Determining the predictors of change in quality of life self-ratings and carer-ratings for community-dwelling people with Alzheimer disease. Alzheimer Disease & Associated Disorders, 27(4), 363-371</div>
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<div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0tag:blogger.com,1999:blog-8125300329382786892.post-47716667280442724862018-04-07T06:26:00.001-07:002018-08-26T20:28:37.488-07:00Aging Is Not a Genetic Dustbin<div style="height: 0px;">
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<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Body Text Indent 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Block Text"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Hyperlink"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="FollowedHyperlink"/>
<w:LsdException Locked="false" Priority="22" QFormat="true" Name="Strong"/>
<w:LsdException Locked="false" Priority="20" QFormat="true" Name="Emphasis"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Document Map"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Plain Text"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="E-mail Signature"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Top of Form"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Bottom of Form"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Normal (Web)"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Acronym"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Address"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Cite"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Code"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Definition"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Keyboard"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Preformatted"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Sample"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Typewriter"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="HTML Variable"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Normal Table"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="annotation subject"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="No List"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Outline List 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Outline List 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Outline List 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Simple 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Simple 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Simple 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Classic 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Classic 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Classic 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Classic 4"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Colorful 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Colorful 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Colorful 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Columns 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Columns 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Columns 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Columns 4"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Columns 5"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Grid 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Grid 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Grid 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Grid 4"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Grid 5"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Grid 6"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Grid 7"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Grid 8"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table List 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table List 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table List 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table List 4"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table List 5"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table List 6"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table List 7"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table List 8"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table 3D effects 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table 3D effects 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table 3D effects 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Contemporary"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Elegant"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Professional"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Subtle 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Subtle 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Web 1"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Web 2"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Web 3"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Balloon Text"/>
<w:LsdException Locked="false" Priority="39" Name="Table Grid"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
Name="Table Theme"/>
<w:LsdException Locked="false" SemiHidden="true" Name="Placeholder Text"/>
<w:LsdException Locked="false" Priority="1" QFormat="true" Name="No Spacing"/>
<w:LsdException Locked="false" Priority="60" Name="Light Shading"/>
<w:LsdException Locked="false" Priority="61" Name="Light List"/>
<w:LsdException Locked="false" Priority="62" Name="Light Grid"/>
<w:LsdException Locked="false" Priority="63" Name="Medium Shading 1"/>
<w:LsdException Locked="false" Priority="64" Name="Medium Shading 2"/>
<w:LsdException Locked="false" Priority="65" Name="Medium List 1"/>
<w:LsdException Locked="false" Priority="66" Name="Medium List 2"/>
<w:LsdException Locked="false" Priority="67" Name="Medium Grid 1"/>
<w:LsdException Locked="false" Priority="68" Name="Medium Grid 2"/>
<w:LsdException Locked="false" Priority="69" Name="Medium Grid 3"/>
<w:LsdException Locked="false" Priority="70" Name="Dark List"/>
<w:LsdException Locked="false" Priority="71" Name="Colorful Shading"/>
<w:LsdException Locked="false" Priority="72" Name="Colorful List"/>
<w:LsdException Locked="false" Priority="73" Name="Colorful Grid"/>
<w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 1"/>
<w:LsdException Locked="false" Priority="61" Name="Light List Accent 1"/>
<w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 1"/>
<w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 1"/>
<w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 1"/>
<w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 1"/>
<w:LsdException Locked="false" SemiHidden="true" Name="Revision"/>
<w:LsdException Locked="false" Priority="34" QFormat="true"
Name="List Paragraph"/>
<w:LsdException Locked="false" Priority="29" QFormat="true" Name="Quote"/>
<w:LsdException Locked="false" Priority="30" QFormat="true"
Name="Intense Quote"/>
<w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 1"/>
<w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 1"/>
<w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 1"/>
<w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 1"/>
<w:LsdException Locked="false" Priority="70" Name="Dark List Accent 1"/>
<w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 1"/>
<w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 1"/>
<w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 1"/>
<w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 2"/>
<w:LsdException Locked="false" Priority="61" Name="Light List Accent 2"/>
<w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 2"/>
<w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 2"/>
<w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 2"/>
<w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 2"/>
<w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 2"/>
<w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 2"/>
<w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 2"/>
<w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 2"/>
<w:LsdException Locked="false" Priority="70" Name="Dark List Accent 2"/>
<w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 2"/>
<w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 2"/>
<w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 2"/>
<w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 3"/>
<w:LsdException Locked="false" Priority="61" Name="Light List Accent 3"/>
<w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 3"/>
<w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 3"/>
<w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 3"/>
<w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 3"/>
<w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 3"/>
<w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 3"/>
<w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 3"/>
<w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 3"/>
<w:LsdException Locked="false" Priority="70" Name="Dark List Accent 3"/>
<w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 3"/>
<w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 3"/>
<w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 3"/>
<w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 4"/>
<w:LsdException Locked="false" Priority="61" Name="Light List Accent 4"/>
<w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 4"/>
<w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 4"/>
<w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 4"/>
<w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 4"/>
<w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 4"/>
<w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 4"/>
<w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 4"/>
<w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 4"/>
<w:LsdException Locked="false" Priority="70" Name="Dark List Accent 4"/>
<w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 4"/>
<w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 4"/>
<w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 4"/>
<w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 5"/>
<w:LsdException Locked="false" Priority="61" Name="Light List Accent 5"/>
<w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 5"/>
<w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 5"/>
<w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 5"/>
<w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 5"/>
<w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 5"/>
<w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 5"/>
<w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 5"/>
<w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 5"/>
<w:LsdException Locked="false" Priority="70" Name="Dark List Accent 5"/>
<w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 5"/>
<w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 5"/>
<w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 5"/>
<w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 6"/>
<w:LsdException Locked="false" Priority="61" Name="Light List Accent 6"/>
<w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 6"/>
<w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 6"/>
<w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 6"/>
<w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 6"/>
<w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 6"/>
<w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 6"/>
<w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 6"/>
<w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 6"/>
<w:LsdException Locked="false" Priority="70" Name="Dark List Accent 6"/>
<w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 6"/>
<w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 6"/>
<w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 6"/>
<w:LsdException Locked="false" Priority="19" QFormat="true"
Name="Subtle Emphasis"/>
<w:LsdException Locked="false" Priority="21" QFormat="true"
Name="Intense Emphasis"/>
<w:LsdException Locked="false" Priority="31" QFormat="true"
Name="Subtle Reference"/>
<w:LsdException Locked="false" Priority="32" QFormat="true"
Name="Intense Reference"/>
<w:LsdException Locked="false" Priority="33" QFormat="true" Name="Book Title"/>
<w:LsdException Locked="false" Priority="37" SemiHidden="true"
UnhideWhenUsed="true" Name="Bibliography"/>
<w:LsdException Locked="false" Priority="39" SemiHidden="true"
UnhideWhenUsed="true" QFormat="true" Name="TOC Heading"/>
<w:LsdException Locked="false" Priority="41" Name="Plain Table 1"/>
<w:LsdException Locked="false" Priority="42" Name="Plain Table 2"/>
<w:LsdException Locked="false" Priority="43" Name="Plain Table 3"/>
<w:LsdException Locked="false" Priority="44" Name="Plain Table 4"/>
<w:LsdException Locked="false" Priority="45" Name="Plain Table 5"/>
<w:LsdException Locked="false" Priority="40" Name="Grid Table Light"/>
<w:LsdException Locked="false" Priority="46" Name="Grid Table 1 Light"/>
<w:LsdException Locked="false" Priority="47" Name="Grid Table 2"/>
<w:LsdException Locked="false" Priority="48" Name="Grid Table 3"/>
<w:LsdException Locked="false" Priority="49" Name="Grid Table 4"/>
<w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark"/>
<w:LsdException Locked="false" Priority="51" Name="Grid Table 6 Colorful"/>
<w:LsdException Locked="false" Priority="52" Name="Grid Table 7 Colorful"/>
<w:LsdException Locked="false" Priority="46"
Name="Grid Table 1 Light Accent 1"/>
<w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 1"/>
<w:LsdException Locked="false" Priority="48" Name="Grid Table 3 Accent 1"/>
<w:LsdException Locked="false" Priority="49" Name="Grid Table 4 Accent 1"/>
<w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark Accent 1"/>
<w:LsdException Locked="false" Priority="51"
Name="Grid Table 6 Colorful Accent 1"/>
<w:LsdException Locked="false" Priority="52"
Name="Grid Table 7 Colorful Accent 1"/>
<w:LsdException Locked="false" Priority="46"
Name="Grid Table 1 Light Accent 2"/>
<w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 2"/>
<w:LsdException Locked="false" Priority="48" Name="Grid Table 3 Accent 2"/>
<w:LsdException Locked="false" Priority="49" Name="Grid Table 4 Accent 2"/>
<w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark Accent 2"/>
<w:LsdException Locked="false" Priority="51"
Name="Grid Table 6 Colorful Accent 2"/>
<w:LsdException Locked="false" Priority="52"
Name="Grid Table 7 Colorful Accent 2"/>
<w:LsdException Locked="false" Priority="46"
Name="Grid Table 1 Light Accent 3"/>
<w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 3"/>
<w:LsdException Locked="false" Priority="48" Name="Grid Table 3 Accent 3"/>
<w:LsdException Locked="false" Priority="49" Name="Grid Table 4 Accent 3"/>
<w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark Accent 3"/>
<w:LsdException Locked="false" Priority="51"
Name="Grid Table 6 Colorful Accent 3"/>
<w:LsdException Locked="false" Priority="52"
Name="Grid Table 7 Colorful Accent 3"/>
<w:LsdException Locked="false" Priority="46"
Name="Grid Table 1 Light Accent 4"/>
<w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 4"/>
<w:LsdException Locked="false" Priority="48" Name="Grid Table 3 Accent 4"/>
<w:LsdException Locked="false" Priority="49" Name="Grid Table 4 Accent 4"/>
<w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark Accent 4"/>
<w:LsdException Locked="false" Priority="51"
Name="Grid Table 6 Colorful Accent 4"/>
<w:LsdException Locked="false" Priority="52"
Name="Grid Table 7 Colorful Accent 4"/>
<w:LsdException Locked="false" Priority="46"
Name="Grid Table 1 Light Accent 5"/>
<w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 5"/>
<w:LsdException Locked="false" Priority="48" Name="Grid Table 3 Accent 5"/>
<w:LsdException Locked="false" Priority="49" Name="Grid Table 4 Accent 5"/>
<w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark Accent 5"/>
<w:LsdException Locked="false" Priority="51"
Name="Grid Table 6 Colorful Accent 5"/>
<w:LsdException Locked="false" Priority="52"
Name="Grid Table 7 Colorful Accent 5"/>
<w:LsdException Locked="false" Priority="46"
Name="Grid Table 1 Light Accent 6"/>
<w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 6"/>
<w:LsdException Locked="false" Priority="48" Name="Grid Table 3 Accent 6"/>
<w:LsdException Locked="false" Priority="49" Name="Grid Table 4 Accent 6"/>
<w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark Accent 6"/>
<w:LsdException Locked="false" Priority="51"
Name="Grid Table 6 Colorful Accent 6"/>
<w:LsdException Locked="false" Priority="52"
Name="Grid Table 7 Colorful Accent 6"/>
<w:LsdException Locked="false" Priority="46" Name="List Table 1 Light"/>
<w:LsdException Locked="false" Priority="47" Name="List Table 2"/>
<w:LsdException Locked="false" Priority="48" Name="List Table 3"/>
<w:LsdException Locked="false" Priority="49" Name="List Table 4"/>
<w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark"/>
<w:LsdException Locked="false" Priority="51" Name="List Table 6 Colorful"/>
<w:LsdException Locked="false" Priority="52" Name="List Table 7 Colorful"/>
<w:LsdException Locked="false" Priority="46"
Name="List Table 1 Light Accent 1"/>
<w:LsdException Locked="false" Priority="47" Name="List Table 2 Accent 1"/>
<w:LsdException Locked="false" Priority="48" Name="List Table 3 Accent 1"/>
<w:LsdException Locked="false" Priority="49" Name="List Table 4 Accent 1"/>
<w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark Accent 1"/>
<w:LsdException Locked="false" Priority="51"
Name="List Table 6 Colorful Accent 1"/>
<w:LsdException Locked="false" Priority="52"
Name="List Table 7 Colorful Accent 1"/>
<w:LsdException Locked="false" Priority="46"
Name="List Table 1 Light Accent 2"/>
<w:LsdException Locked="false" Priority="47" Name="List Table 2 Accent 2"/>
<w:LsdException Locked="false" Priority="48" Name="List Table 3 Accent 2"/>
<w:LsdException Locked="false" Priority="49" Name="List Table 4 Accent 2"/>
<w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark Accent 2"/>
<w:LsdException Locked="false" Priority="51"
Name="List Table 6 Colorful Accent 2"/>
<w:LsdException Locked="false" Priority="52"
Name="List Table 7 Colorful Accent 2"/>
<w:LsdException Locked="false" Priority="46"
Name="List Table 1 Light Accent 3"/>
<w:LsdException Locked="false" Priority="47" Name="List Table 2 Accent 3"/>
<w:LsdException Locked="false" Priority="48" Name="List Table 3 Accent 3"/>
<w:LsdException Locked="false" Priority="49" Name="List Table 4 Accent 3"/>
<w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark Accent 3"/>
<w:LsdException Locked="false" Priority="51"
Name="List Table 6 Colorful Accent 3"/>
<w:LsdException Locked="false" Priority="52"
Name="List Table 7 Colorful Accent 3"/>
<w:LsdException Locked="false" Priority="46"
Name="List Table 1 Light Accent 4"/>
<w:LsdException Locked="false" Priority="47" Name="List Table 2 Accent 4"/>
<w:LsdException Locked="false" Priority="48" Name="List Table 3 Accent 4"/>
<w:LsdException Locked="false" Priority="49" Name="List Table 4 Accent 4"/>
<w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark Accent 4"/>
<w:LsdException Locked="false" Priority="51"
Name="List Table 6 Colorful Accent 4"/>
<w:LsdException Locked="false" Priority="52"
Name="List Table 7 Colorful Accent 4"/>
<w:LsdException Locked="false" Priority="46"
Name="List Table 1 Light Accent 5"/>
<w:LsdException Locked="false" Priority="47" Name="List Table 2 Accent 5"/>
<w:LsdException Locked="false" Priority="48" Name="List Table 3 Accent 5"/>
<w:LsdException Locked="false" Priority="49" Name="List Table 4 Accent 5"/>
<w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark Accent 5"/>
<w:LsdException Locked="false" Priority="51"
Name="List Table 6 Colorful Accent 5"/>
<w:LsdException Locked="false" Priority="52"
Name="List Table 7 Colorful Accent 5"/>
<w:LsdException Locked="false" Priority="46"
Name="List Table 1 Light Accent 6"/>
<w:LsdException Locked="false" Priority="47" Name="List Table 2 Accent 6"/>
<w:LsdException Locked="false" Priority="48" Name="List Table 3 Accent 6"/>
<w:LsdException Locked="false" Priority="49" Name="List Table 4 Accent 6"/>
<w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark Accent 6"/>
<w:LsdException Locked="false" Priority="51"
Name="List Table 6 Colorful Accent 6"/>
<w:LsdException Locked="false" Priority="52"
Name="List Table 7 Colorful Accent 6"/>
<w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true"
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Nature designed us to age for a reason.<o:p></o:p></div>
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Harmful genes that cause Huntington’s disease — a disease
that attacks the neurons in the brain — only show up between ages 30 to 50, in
some cases after the birth of offspring. There are many other diseases that
accumulate later on in life, dementia being the main one. In 1952, Peter Brian
Medawar tried to explain this by suggestion that older adults accumulate
mutations and become a "genetic dustbin."<o:p></o:p></div>
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In Medawar's theory, there is no advantage to aging, nor are
there any benefits for older people to live. Aging is simply the result of
declining functions before death. This biological interpretation proved
popular.<o:p></o:p></div>
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To explain aging, biologist George Williams in 1957 came up
with the "antagonistic pleiotropy hypothesis" (named by Michael Rose
in 1982). Pleiotropy is the phenomenon where one or a few genes control more than
one trait. The antagonism part comes from the negative effect that emerges
later on in life. As an example, testosterone in men might result in an
attractive, muscular body in youth, as well as masculine features, such a deep
voice and facial hair, but it also increases the likelihood of prostate cancer
in older age, hence the antagonistic part of the pleiotropy. Although it is the
positive aspects of the pleiotropic gene that are selected for in natural
selection, the antagonistic aspect also sneaks into the gene pool. Aging is
seen as an invisible cloak that sneaks bad genes into the gene pool by cloaking
them under positive traits when young. Aging, in this view, has subverted the
whole process of natural selection by disguising itself as a positive attribute
in early life and then transforming — in a Jekyll-and-Hyde metamorphosis — into
an aging liability. Somehow nature has been hoodwinked into allowing people to
get old. Aging becomes a problem, a genetic dustbin of humanity. From here, it
is fairly easy to see the approach: We need to cure aging, because nature made
a mistake. The hubris of judging that nature made a mistake ignores that nature
might have a different perspective from ours.<o:p></o:p></div>
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As a species, survival is nature's only ambition.<o:p></o:p></div>
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The only way that successive generations prosper is if they
are a good fit with their environment. Each generation must survive long enough
to create another generation. Nature keeps our genes immortal, and it has two
extreme methods to achieve this single aim. One way is to produce an enormous
number of offspring and hope that a few survive to then pass on their genes
(known as r-selection). Another approach — one followed by humans — involves
having few children whom we nurture until adulthood and beyond (known as K-selection).
Therefore nurturing — protecting and supporting others — is our survival
strategy, not competition.<o:p></o:p></div>
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Nurturing involves having things to teach and living long
enough to be able to teach them. Which is why humans live long and have such a
big brain; the two go together. Some 1.6 to 1.9 million years ago, our brain
grew very fast; some say — not without contention — that brain expansion
mirrors the development of cooking. Cooking, making food more easily
digestible, resulted in greater availability of nutrients for the hungriest
organ in our body — our brain. Nature engineered us to have both a big brain and
longevity; they are intricately intertwined. We can see this through
mathematical models that show a leap in predictive value when older people are
included in the equation. Whether or not older people have a disease, the
presence of older people in the family predicts longer-living children and
grandchildren.<o:p></o:p></div>
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In the wild, most mammals die once they lose their ability
to reproduce. Humans are different. We continue to live well past our capacity
to reproduce, especially females. Is nature wrong again, or does nature have a
special role for older people?<o:p></o:p></div>
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What the genetic dustbin proponents do not appreciate is
that older people, especially grandmothers, have a statistically positive
effect on their community. In 2004 while examining the “grandmother effect,”
Mirkka Lahdenperä of the University of Turku, Finland, and her colleagues found
statistical evidence that a grandmother has a decidedly beneficial effect on
the reproductive success of her children and the survival of her grandchildren.
Older adult humans promote the survival of the species. Unlike any other
animal, we also transfer wealth, capital, and wisdom to our successive
generations way past our reproductive period. When gene survival includes the
broader community, then older people have a positive effect on their chances of
survival.<o:p></o:p></div>
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By 1973, John Maynard Smith and George Price introduced game
theory to evolutionary problems. While classic game theory sees players making
rational choices on the basis of individual gain, evolutionary game theory posits
an awareness of what others might do and the development of strategies to
counter that decision. It is a social decision mode, not a purely individualist
one. Maynard Smith argued that since everyone dies, evolution does not benefit
individuals. Evolution is designed to benefit the community. In this
interpretation, it explains that the strategy humans employ is based on
benefits to the community, rather than benefits solely to the individual. Such
a model fits the outcomes we see in reality. This insight was revolutionary and
transformed the argument from one where aging is seen as a genetic dustbin to
one where aging becomes part of a package for survival — a package that
includes older adults contributing, in as yet unknown ways, to the promotion of
our species.<o:p></o:p></div>
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There are instances where antagonistic pleiotropy of
dementia has some really beneficial effects. For example, the Apolipoprotein E
Variant 4 that is strongly associated with Alzheimer's disease might have
beneficial aspects, such as reducing the rate of age-related macular
degeneration, lower testosterone, and although there is no evidence of apoE
isoform reducing infectious diseases, there is evidence that apoE could play a
role in reducing our susceptibility to viruses, bacteria, and protozoan
parasites. Such polymorphisms — having multiple expressions — are abundant in
nature. <o:p></o:p></div>
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Despite this insight, in 2002, 51 renowned scientists —
including such luminaries as Jay Olshansky, Leonard Hayflick, and Bruce<span style="mso-spacerun: yes;"> </span>Carnes — published a position statement in
Scientific American stating that “aging is a product of evolutionary neglect,
not evolutionary intent.” Again, we are telling nature that it made a mistake,
or at least was ignorant of the consequences. When Albert Einstein first
confronted quantum physics, he said that “God does not play dice with the
cosmos.” What is not reported frequently is the response from Danish physicist
Niels Bohr: “Einstein, don't tell God what to do.” It seems that we are telling
nature what it should do or how neglectful it is, rather than appreciating the
biological system we call life as complete and perfect. We might guess at the
intent of evolution — survival of our immortal genes — but we might not
understand its methods.<o:p></o:p></div>
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<br /></div>
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Aging and having a big brain go hand-in-hand. It is nature’s
plan for our survival. Older adults improve the survival of both their children
and grandchildren. Looking at aging in a broader context allows us to view some
of the wonders of nature. We have a lot to learn if we listen.<o:p></o:p></div>
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<span style="background-color: white; color: #222222; font-family: arial, helvetica, "dejavu sans", sans-serif; font-size: 13.3333px; text-align: justify;">© USA Copyrighted 2018 Mario D. Garrett</span></div>
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References<o:p></o:p></div>
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Browning PJ, Roberts DD, Zabrenetzky V, Bryant J, Kaplan M,
et al. (1994). Apolipoprotein E (apoE), a novel heparin-binding protein
inhibits the development of Kaposi's sarcoma-like lesions in BALB/c nu/nu mice.
J. Exp. Med. 180:1949–54<o:p></o:p></div>
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Bojanowski, C. M., Shen, D., Chew, E. Y., Ning, B., Csaky,
K. G., Green, W. R., ... & Tuo, J. (2006). An apolipoprotein E variant may
protect against age‐related macular degeneration through cytokine regulation.
Environmental and molecular mutagenesis, 47(8), 594-602.<o:p></o:p></div>
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Hogervorst, E., Lehmann, D. J., Warden, D. R., McBroom, J.,
& Smith, A. D. (2002). Apolipoprotein E ε4 and testosterone interact in the
risk of Alzheimer's disease in men. International journal of geriatric
psychiatry, 17(10), 938-940.<o:p></o:p></div>
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Lahdenperä, M., Lummaa, V., Helle, S., Tremblay, M., &
Russell, A. F. (2004). Fitness benefits of prolonged post-reproductive lifespan
in women. Nature, 428(6979), 178.<o:p></o:p></div>
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Mahley, R. W., & Rall Jr, S. C. (2000). Apolipoprotein
E: far more than a lipid transport protein. Annual review of genomics and human
genetics, 1(1), 507-537.<o:p></o:p></div>
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<br /></div>
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Olshansky, S. J., Hayflick, L., & Carnes, B. A. (2002).
Position statement on human aging. The Journals of Gerontology Series A:
Biological Sciences and Medical Sciences, 57(8), B292-B297.<o:p></o:p></div>
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Pianka, E. R. (1970). On r-and K-selection. The American
Naturalist, 104(940), 592-597.<o:p></o:p></div>
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Roselaar SE, Daugherty A. 1998. Apolipoprotein E-deficient
mice have impaired innate immune responses to Listeria monocytogenes in vivo.
J. Lipid Res. 39:1740–43<o:p></o:p></div>
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Smith, J. M., & Price, G. R. (1973). The logic of animal
conflict. Nature, 246(5427), 15.<o:p></o:p></div>
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Williams, G. C. (1957). Pleiotropy, natural selection, and
the evolution of senescence. evolution, 11(4), 398-411.<o:p></o:p></div>
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<!--EndFragment--><br /><div class="blogger-post-footer">Mario Garrett 2016 ©</div>Mario Garretthttp://www.blogger.com/profile/16447719011664536580noreply@blogger.com0