Are we Suppose to Live Longer?

The late Sherwin Nuland in his 1995 book How We Die described the process of extreme old-age death very eloquently: “Whether it is the anarchy of disordered biochemsitry or the direct result of its opposite-a carefully orchestrated genetic ride to death-we die of old age because we have been worn and torn and programmed to cave in. The very old do not succumb to disease-they implode their way into eternity.”

The most persuasive argument for the biology of death is the Hayflick Limit. In 1961, going against the thinking at the time, biologists Leonard Hayflick and Paul Moorhead noticed that their cell cultures were dying after replicating a certain number of times. At the time Alex Carrel—a Nobel prize winner in surgery—held the thinking at that time, that cells are naturally immortal. We do bad things to them to kill them. Taking a direct leaf from the biblical story of Adam and Eve, we are held responsible for our own mortality.

In contrast, Hayflick demonstrated that normal human fibroblasts cells divide about 70 times in 3% oxygen—which is the same as human internal conditions—before stopping replicating.  Refuting the idea that normal cells are immortal. The mechanism was not yet known at the time of this observation. But a Russian scientist Alexey Olovnikov hypothesized in 1971, and later confirmed in 1984 by  Nobel prize winners Elizabeth Blackburn and Carol Greider for the necessity of proteins called telomeres at the end of the DNA which get shorter with every division until they get too short to allow for more replication.

Although this is an eloquent theory, there is large variance in correlating telomere length with aging. The telomeres are not proportional to longevity. Nuno Gomez from the University of Texas Southwestern Medical Center and his colleagues, undertook the largest comparative study involving over 60 mammalian species, reported that telomere length inversely correlates with lifespan, while telomerase (an enzyme that promotes the growth of telomeres) correlates with size of the species.

Assuming human fibroblasts endure 70 divisions—as Hayflick says in his 1994 book How and Why We Age—there are more than enough cells for several lifetimes. Biologically it is feasible that individual cells in our body can maintain their level of division  and renewal for at least 150 years. And yet no one has lived beyond 122 years.

In addition, it seems that telomeres do not provide us with a complete picture.  The Italian biologist Giuseppina Tesco and her colleagues in 1998—refuting earlier studies—found that fibroblast taken from centenarians showed no difference in the number of replications compared to cells from younger donors.  It could be that within the body, cells can be replaced with new ones—rather than simply renewed.

Adult stem cells have been identified in many organs and tissues of older adults, including brain, bone marrow, peripheral blood, teeth, heart, gut, liver, blood vessels, skeletal muscle, skin, ovarian epithelium, and testis. They are thought to reside in a “stem cell niche" which is a specific area within each tissue. We all have these and yet some of us seem to use them up quickly, perhaps we started with fewer stem cells, or perhaps the environment that we live in degraded them faster.

Older people are more likely to have experienced more environmental stressors that damage stem cells, and utilized more of their stem cells. Once they run out or become disabled, stem cells cannot be replaced.

And then this might be the symphony that Sherwin Nuland talks about.  Because dying cells secrete chemicals that disrupt other cells in their immediate environment even a small percentage dying cells, can have a much broader domino effect on neighboring cells. There is a tipping point before an implosion into eternity.

 © USA Copyrighted 2014 Mario D. Garrett

How Old Are You?

Just under 11 years old should be the answer. Seriously. Biologically our body averages about 11 years old.

Jonas Frisen, a stem cell biologist at the Karolinska Institute in Stockholm developed a method for determining the age of each organ. Although some cells remain with us the duration of our life--neurons of the cerebral cortex, cells of your inner lens in our eyes, muscle cells of your heart—the rest of our body is in a constant frenzy of change and rejuvenation.

Even our brain changes and renews itself. Joseph Altman first discovered brain cell regeneration—or neurogenesis—in 1962. Recently Elizabeth Gould of Princeton Unviersity, reported that each day's memories might be recorded in the neurons generated that day. Our brain might be going through daily renewal and change. With white matter in the brain—the predominant matter—renewing itself faster then the grey matter—which just covers the surface of the cortex. While all these changes are going on in the brain everything else is changing and renewing itself.

The youngest part of our body is our intestines that are only 2-3 days old, while our taste buds replenish themselves every ten days. Then within weeks, our skin and lungs completely replenish themselves (2-4 weeks). Every few months our liver is replaced (5 months) and nails (6-10 months). The every four months, after travelling over 300 miles and going through the heart 170,000 times, 60 times per hour our red blood cells are given respite and are renewed.

Our annual makeover includes new hair (for those that have hair, every 3-6 years) new bones (every 10 years) and lastly, most of our heart (every 20 years).

So the question is why do we look so old if we are only 11 years old?

This is the central question in gerontology. As we renew each organ in our body—and we chronologically age—the rate of change decreases and we get more errors in new cells. There are many possible reasons for this, and all could apply. It could be that our genetic material gathers faulty changes and its information becomes gradually degraded. Like a cassette tape that is repeatedly copy.

It could also be because the cells themselves becomes less efficient at cleaning after themselves leaving behind them a lot of cellular trash. It could be that our stem cells—that exist even in older adults—eventually become less efficient with age as they are bombarded with toxins, harmful rays and temperature changes. Sometimes when we damage an organ—for example damaging our lungs by smoking—the scaring tissue cannot be renewed and replaced. We in effect stop our body from staying young.

This is why looking younger also means that you are younger and live longer. In the Danish Twin study Axel Skytthe and his colleagues reported that among monozygotic twins who share the same genes—the twin that looked younger is more likely to live longer. But there are no short cuts. Undergoing plastic surgery does not result in longer life because there is also the Hayflick Limit…each of our 30 trillion cells in our body has a time bomb. At some point the cells reach their own individual lifespan and stop reproducing.  

 © USA Copyrighted 2014 Mario D. Garrett

A Heart to Heart Talk

In 2002 Paul Pearsall from the University of Hawaii and his colleagues from the University of Arizona looked at the unique memory experiences being reported by heart transplant patients over a ten-year period. After interviewing 150 patients he reports nine cases were recipients of a new heart took on characteristics and desires/fears of their heart donors. These included changes in preferences for food, music, art, sexual, recreational, and career, as well as specific memories only privy to the donors.

Weird stuff.  Explaining such outcomes is difficult if you want to stay in the realm of science.

In Chinese Traditional Medicine it is believed your heart stores your memory. Reigniting painful memories of secondary school pedagogy when we were told to learn “by heart.”  So where is memory?

We are learning about the language of how the environment communicates. And such knowledge is adding to our knowledge of how we see our internal body communicating.  

An example of what this language might look like can be found in the plant kingdom. In short distance communication, Nigel Raine from the University of London and his colleagues observed how ants provide a useful service for the acacia plants by guarding the plant they live on. Tomatoes and tobacco plants have similar symbiotic arrangements. Wouter Van Hoven from Pretoria University reports that acacias also produce leaf tannin in quantities lethal to the antelope and thereby killing the antelopes while at the same time emitting ethylene into the air which can travel up to 50 yards warning other acacias to step up their own production of leaf tannin within just five to ten minutes. Willows have been found to have a similar strategy when they are being eaten by caterpillars. These are complex communication strategies.

Jim Westwood, a plant scientist at Virginia Tech showed how a parasitic weed known as dodder/strangleweed, uses its RNA—its genetic material--to communicate with their host plants that they are nurturing from, in order for the host plant to lower its defenses.

Back to our bodies, the Danish biologist Bente Klarlund Pedersen is looking at a handful of myokines—a protein he identified and named—and their role in helping skeletal muscle retain memory. He acknowledges there are several hundred other secreted proteins giving internal body communication a complex language.

There is also evidence that midkine--another protein--is exchanged between the lungs and kidneys so that they “know” each other’s status. However, little is known about how the information is transferred from one organ to the other. Paul Pearsall’s findings should make us think about how our bodies stay in balance and how memory is not solely the prerogative of the brain. When this balance is disrupted, what messages is the dying organ sending out? What is our body communicating at the end of life?

© USA Copyrighted 2014 Mario D. Garrett

Our Own Virtual Reality Box

We live in our very complex mind. Our brain works by modeling the external world in order to be able to organize and predict behavior. This is how we survive. Our brain is designed as a virtual reality box—VRbox—where we can test it by interacting with reality. Our VRbox is a powerful tool that allows us to behave within an external environment that is otherwise utterly incomprehensibly in its complexity. And we interact by taking shortcuts based on this simplified model of reality.

Even though our brain is a most complex structure, reality is infinitely more complex. Each one of us having a slightly different model to play with and with over 7,251,078,000 such unique VRboxes there are bound to be some that have an aberrant representation of the world.

Our model of reality is necessarily distorted—since it is a representation, a model. We have common shared moral principals. But in some people their VRbox allows them to rationalize heinous crimes. This is the case of Jimmy Saville and his predatory sexual crimes against over 450 mainly children victims. What he was doing was right by himself. We all do the right thing, we just need to understand what “right” means in our VRbox.

In one interview in The Guardian, Wednesday 9 July 2014,  David Hare characterized Saville as “in a lurid and sweaty argument with his maker, trying to pile up credit points to balance the final ledger against what he knows full well to be his sins.” Saville’s VRbox allowed him to rationalize his behavior on a simple scale balancing his impressive philanthropic work with his heinous crimes.

There is not one representation, one individual VRbox that represent reality. Similar to language, although we might speak with different accents and have a different vocabulary, we all hold certain common rules. Our VRbox loves rules which is why we are so good at developing rules in science, philosophy and behavior—this is known as nomothetic. But we are also aware that we need to test our VRbox against reality to identify our uniqueness—this is known as idiographic. Our VRbox performs both these activities at the same time and there is no distinction. The dichotomy is false.

We start developing these rules very early on in life at the same time that we start defining our uniqueness. Piaget and Kohlberg showed how the brain needs to develop before we can form moral principles. In older age our cognitive capacity s fully formed and our testing of reality is at an apex. Hume’s “is” vs. “ought” dichotomy are tools we use to gauge how accurate our representation is.  By adulthood the rules inside our VRBox become stronger then reality. We become more reliant on our VRBox “ought” rather than the “is”. This is our model of the world and our sense of self. We get so good at this that we do this automatically all the time. The brain models, thinking is a process of getting there.

© USA Copyrighted 2014 Mario D. Garrett

Financial Elder Abuse by Banks, Casinos and Lawyers

We think we know a lot about who perpetrates elder financial abuse. They are usually men, relatives, if not sons, of the victim. They tend to have some alcohol/drug abuse issues, have unreliable work history, and are dependent on the victim for their livelihood.  They are young poor lost male adults. 

This is the type of perpetrator that we prosecute. But this is not the only type of perpetrator that abuses older adults. There are more serious financial elder abuse crimes that remain invisible…or they are made invisible because they are just “too big too fail”: Casinos, banks, lawyers. These businesses are so elusive that, so far, there has not been one prosecution of financial elder abuse against any of them.

In 2011, in the most recent federal review of elder abuse by the Government Accountability Office, the report completely ignored abuse by casinos, banks and by lawyers. Health and Human Services and the Justice Department devoted a total of $11.9 million in grants for elder justice activities in fiscal year 2009. This is in addition to funds donated by charitable organizations such as the California Endowment to research elder abuse. However there is very little progress in terms of slowing down or preventing elder abuse. Which is not surprising since none of these efforts are aimed at prevention.  Prevention is difficult when the perpetrator is random, but the context changes if these abuses are institutional.

What is required is a national policy with a long-term strategy. Although the Older Americans Act of 1965--fifty year ago—has called attention to the importance of federal leadership in the elder justice area, no national policy priorities currently exist, which results in district attorney reacting to petty crime rather than institutionalized financial elder abuse.

Older adult abuse victims tend to be vulnerable. There are many meanings to this, and it usually stands as a euphemism—a nice way of say that the victim is demented or cognitively impaired.  But some older adults are still vulnerable without being demented.

A case in point. An 86 years old woman who in the height of bank bankruptcies in 2010 went to take her money out of a local branch—the bank subsequently went belly up—and transfer the money to another bank. The bank manager told her that this was not possible because of financial elder abuse laws, and the banks have to be careful about such large transfer by older adults. She was eventually allowed to transfer $10,000, once a week; this is financial elderly abuse 

When casinos ply older customers with alcohol, giving them access to medication that impair judgment, and then making loans available so that the incapacitated customer can still play (and lose millions of dollars); this is elderly abuse.

When a lawyer changes the last testament and will of an older demented client so that the lawyer becomes the primary or sole beneficiary of their estate; this is financial elder abuse. These are all documented cases yet there is no known case where these have been prosecuted under elder abuse laws.

Why are we going for the low hanging fruits? District Attorneys need to fill in the vacuum left by the lack of national policy priorities. We need to go for perpetrators that are quietly doing more financial harm to older adults which we can prevent. We need leadership in developing a long-term policy before we are drowned in the deluge of elder abuse cases.

© USA Copyrighted 2014 Mario D. Garrett

No Pissing Joke

The 2003 Sleep in America Poll by the National Sleep Foundation—the latest data we have for older adults—reports that two out of three people (65%) ages of 55 and 84 reported having to wake up during the night to go to the bathroom to urinate at least a few nights per week. This condition is called nocturia and is often normal part of getting older. It can also be an indication of other medical conditions including infection, a tumor of the bladder or prostate, a condition called bladder prolapse, or disorders affecting sphincter control. It is also common in people with heart failure, liver failure, poorly controlled diabetes and some medications which are also associated with nocturia. But usually, as we get older, the chemical regulation in our body changes making us less able to retain fluid, and therefore producing more urine. That and the fact that our bladder shrinks as we age creates the need to empty during the night.

This is of course preferable to incontinence.

Urinary incontinence drastically reduces your quality of life and is likely to contribute to an earlier nursing home placement. Unfortunately, urinary incontinence—where urine escapes unexpectedly—is a common problem among older women and men.

Older women are twice more likely to experience urinary incontinence than older men and the reasons are different for men and women. Pregnancy and childbirth, menopause, and the anatomical structure urinary tract account for this difference. Whereas both women and men can become incontinent from injury to nerves, birth defects, stroke, multiple sclerosis, and other physical problems.

Although it is more common the older a person becomes, urine incontinence is not inevitable with age, it is a medical problem.  There are behavioral and physical exercises that can help including medications, biofeedback, stimulation of nerves to the bladder (neuromodulation) vaginal mechanic devices (pessary) and finally surgery (including catheters), are all options for specific type of incontinence.

For men other then the obvious differences—pregnancy and childbirth (including heavy triathlon exercise for some women), menopause, and anatomical differences—urinary incontinence can be caused by nerve damage and/or by prostate problems. The prostate gland, which sits behind the pipe (urethra) that releases urine, commonly becomes enlarged with age. As the prostate enlarges, it may squeeze the urethra restricting the flow. Up to 90 percent in men in their seventies and eighties have some restricting flow problems.

In addition, one of the causes of urinary incontinence is poorly prescribed medications. Four main types of medication can cause urine incontinence. These are medications prescribed for high blood pressure, depression and for sleeping problems. The complication is that these might be the same medications that are used to address urine incontinence in the first place. Unless you face up to it, urine incontinence only gets worse. There are multiple avenues to explore in treatment, but the only first step is to discuss this with your primary care provider. The solution might be found after exploring many avenues but keeping it a secret is not an option.

© USA Copyrighted 2014 Mario D. Garrett

Is Dementia caused by Aluminum through Fluoridation?

In gerontology there are many divisive issues. Surprisingly, fluoridation is one of them. When more than a quarter of older adults do not have their teeth—in some parts of the country like the fluoridated states of Kentucky and West Virginia four out of ten older adults do not have their own teeth—but they are still made to drink water that has been fluoridated, there is a clear disregard for older adult health.

There are many reasons for fluoridation. However, scientific studies are inconclusive, of poor quality, and in all cases disregard older adults—especially those without teeth. In addition, there is the evangelical fervor from both sides of the argument—public health versus personal choice—which muddy an already complex scientific issue.

The link between fluoridation and ill health is not a direct one but involves the uptake of a known nerve toxin aluminum. Correlational studies linking aluminum with Alzheimer’s disease have been published since 1965. Half a century ago injecting aluminum in rat brains, three independent studies produced the tangle-like structures that characterize Alzheimer’s disease. Subsequently, numerous international studies have found more Alzheimer’s disease in areas with high aluminum levels in drinking water.

In 2011, the Japanese researchers Masahiro Kawahara and Midori Kato-Negishi made a forceful argument between aluminum and Alzheimer's disease. After decades of attempts to discredit this link, the authors point to strong evidence of aluminum as a culprit in forming the amyloid plaques in the brain. This and other studies continue to support the clinical studies done in rats that identify aluminum as toxic for the brain. The only problem was that aluminum does not naturally enter the brain.

There is a barrier between the body and the brain that stops metals reaching the brain. In 2013 Akinrinade and his colleagues from Bingham University in Nigeria, showed that the relationship between fluoride and aluminum is important in escaping into this barrier.  Fluoride combines with aluminum to form aluminum fluoride, which is then absorbed by the body where it eventually combines with oxygen to form aluminum oxide or alumina. Alumina is the compound of aluminum that is found in the brains of Alzheimer's disease. Fluorine attaches to aluminum and influences its absorption. Li Fucheng and his colleagues from Beijing, China, described high incidences of osteoporosis, osteomalacia, spontaneous bone fractures and dementia in villages in Guizhou Province, China where they were eating maize which had been baked in fires of coal mixed with kaoline. Kaoline contains aluminum and fluorides. These diseases are very similar to those occurring in European dialysis patients, unwittingly treated with water and gels containing aluminum.

The implications of this fluoride-aluminum relationship to Alzheimer’s disease are not linear. The solubility of aluminum and probably the ease with which it is absorbed varies markedly with the high acidity and alkalinity of water. In general, however, aluminum is most soluble in acidic water, especially if it contains fluorides.

The public health argument for fluoridation has never been made for older adults. Such institutional ageism is bad science and much worse this is bad public health. 

© USA Copyrighted 2014 Mario D. Garrett

Fluoridation and Dementia

Since 1962, on the recommendation of the United States Public Health Service, fluoride is used in the public drinking water supplied to about 2 out of 3 Americans. The decision to add fluoride to drinking water is made locally. The types of fluoride include fluorosilicic acid, sodium fluorosilicate, and sodium fluoride.

Studies have consistently shown positive outcomes for fluoridation in the health of teeth of children, adults and older adults—although these studies have been contested. The bigger contention is whether we need to indiscriminately fluoridate our teeth by ingestion of fluoride through our water supply without being able to control the level of exposure, the varying sensitivity of the recipient, and its accumulation in the body.

Fluoride is also ingested from fruit juices, sodas, popular breakfast cereals, lettuce and raisins and anything grown with pesticides since fluoridation is an effective killer of pests.

However beneficial the fluoridation is to the health of teeth it does not tell us the whole story, especially on the overall health of older adults. Since 25 percent of adults 60 years old and older no longer have their natural teeth, the arguments for the benefit of fluoridation is somewhat toothless.

Sodium fluoride is a bone anabolic drug. Healthy adult kidneys excrete 50 to 60% of the fluoride ingested each day. The rest accumulates in the body, largely in bones and pineal gland. The fluoride concentration in bone steadily increases over a lifetime and we are more likely to see large concentrations in older adults.  But the growth in bone quantity might be detrimental.

Christa Danielson and her colleagues compared the incidence of hip fractures in patients 65 years of age or older in three communities where two were without water fluoridated--to 1 ppm. Surprisingly, they found a small but significant increase in the risk of hip fracture in both men and women exposed to fluoridation. Other studies have found similar results. Suggesting that low levels of fluoride may increase the risk of hip fracture in the elderly and there seems to be a dose relationship with the higher the concentration of fluoride the higher the risk of hip fractures. It seems that fluoride may increase bone quantity—osteofluorosis, osteosclerosis—but it might also decrease bone quality and bone strength.

Just as troubling for older adults, is the evidence that Patočka Strunecká and her colleagues from  Charles University in the Czech Republic exposed. They found that long-term action of aluminofluoride complexes may represent a serious and powerful risk factor for the development of Alzheimer’s disease. In another study, rats fed for one year with 1-5 ppm fluoride in their water—the same level used in fluoridation programs—using either sodium fluoride or aluminum fluoride, resulted in the formation of beta-amyloid deposits—associated with Alzheimer’s disease.

Since the  US Environmental Protection Agency lists fluoride as having “substantial evidence of developmental neurotoxicity”  we expect to see other negative outcomes of fluoridation. Fluoridation is one area that demand better clinical trials with older adults. Perhaps by eliminating fluoridation we can put some teeth into laws protecting the health of older adults.

 © USA Copyrighted 2014 Mario D. Garrett

Traveling with Dementia

Most people have become accustomed to the rhythm of airport security checks— lap top out, jacket off, shoes off, belt and any metals onto the tray, and then waiting patiently for instructions. These routines become second nature, except when some cognitive impairment like dementia starts eroding this familiarity. Traveling alone is a necessity for most people but we need to rethink how viable this is with early stage dementia.

People with dementia might not feel comfortable taking their jacket off or their shoes. Such (familiar) behaviors in unfamiliar surroundings are likely to agitate the older adult. And a security checkpoint is not the most accommodating venue to address anxiety and agitation. These scenarios will become more frequent with an increasing prevalence of dementia and other cognitive disorders. And it is not just at the security gate.

On Friday, May 3rd 2013, an 83-year-old Victoria Kong walked past the assistance agent waiting to meet her at the gate as she deplaned from her flight from Barbados to Washington D.C. She was found the following Monday in wooded area about 200 yards from the airport perimeter. She died of hyperthermia. Victoria King suffered from dementia and wondered out of the airport oblivious to the pickup arrangements made for her by her relatives. Most airlines do not have an escort policy/program in place for adults, traveling alone with cognitive impairment. Airlines only have escort policies/programs in place for minor children traveling alone.

In addition, most airlines do not include dementia as needing medical clearance, and although there are some provisions offered by airports and some airlines—in most cases dictated by law—these provisions are insufficient given the type of problems likely to be experienced by persons suffering from dementia. The increasing prevalence of dementia in the population and the lack of training of security personnel and flight attendants make this a recipe for more common friction.

Although in the early stages of dementia older adults might behave normal, this sense of normalcy might evaporate in an unfamiliar environment, or confusing situations as air travel has increasingly become. New faces, new environments, a change in daily routine, not to mention a time zone change, can prove to be a challenge for the dementia traveller.

You might get escort passes to help the person on board and then someone at the other end to escort the person out of the airport, but the flight itself might prove disorientating. Flight attendants should not be dealing with—at best—agitated passengers.

If we are to address this growing friction, education needs to come from both ends. Caregivers and family members need to understand the limitations of their loved one and that unfamiliar and stressful situations compound cognitive unease. Air travel is a stressful event at the best of times. On the other side, security personnel and air flight attendants need to learn to identify and defuse agitation because  of dementia.  Although it might be difficult to distinguish anxiety and agitation because of dementia from other types of erratic behavior  (alcohol, drugs or stress), the only way to reduce these misunderstandings is by not putting the older adult with dementia in that position in the first place. 

 © USA Copyrighted 2014 Mario D. Garrett