Saturday, August 29, 2015

The Psychology of Physics

Physics—the study of the material world—was transformed in the late 1600s by the all-pervasive power of (Isaac) Newton's mechanics and then again in the late 1800s by (James Clerk) Maxwell's electromagnetic theories. These two British men established the Classical Theory in physics. Isaac Newton’s work was the culmination of centuries of philosophical debate about the nature of the world and the composition of material objects. The vindication of these philosophical thoughts came by Newton’s Classic Mechanics which pictured the universe as a perfect machine. Classical Mechanics uses common-sense notions of how matter and forces exist and interact. It assumes that matter and energy have definite measureable attributes such as where an object is in space and its speed. It also assumes that objects may be directly influenced only by their immediate surroundings, known as the principle of locality. The universe was seen as a tangible, orderly system that followed very exact and specific mechanical rules:
1. A body remains at rest or moves with constant velocity when an external force acts on it.
2. The rate of change of momentum of a body is proportional to the force on the body
3. When two bodies interact they exert on each other equal, but opposite forces.
Maxwell's electromagnetic theory, expanded this view of the world, and by consolidating a lot of independent research, established a classic view of electrodynamics. Primarily this theory explained how the related fields of electricity and magnetisms behave through waves. Although Maxwell’s electromagnetic theory was a stepping-stone for Einstein’s 1905 paper “On the Electrodynamics of Moving Bodies” (the first sentence starts by referencing Maxwell), at the time this theory was the ultimate expression of Classical Theory.
The beauty of Classical Theory was that it worked. Classical Mechanics had specific and definitive applications. We could predict the motion of objects in the world and the motion of celestial bodies in the Universe. All that we could observe was explainable. Best of all, Classic Mechanics is intuitive and all encompassing. For more than half a century Classical Theory reigned supreme to such a degree that physicist in the 1900s believed—as Philipp von Jolly counseled the 16-year-old Max Planck when he was admitted to the University of Munich—that the objectives of physics in explaining the material universe was more or less accomplished. The belief was that the main theories were in place and that all the great discoveries had been made, and only a few minor details needed filling in. Classical Theory was that good.
But Classical Theory was short on explaining constructs that we intuitively “knew.” What is “force” “body” and “interact” what is “attraction”, “gravity” and “energy”? These concepts have no explanation in physics. Our current knowledge is limited to defining how they behave, but we are unable to understand what these concepts are. The only place where these concepts have meaning is in our thinking because these concepts are intuitive. We know instinctively what a “body” is, or gravity or energy. These are constructs that we seem to accept readily as though we see the world through such constructs. Our perception—of seeing reality in chunks and simplified action—is so strong that we seem to preconceive the world, without questioning.
It was the work of Gestalt psychologists that brought such preconceptions to light. In 1912, Max Wertheimer published his paper on phi motion—which examined the impression of movement through flickering of lights—widely recognized as the start of Gestalt psychology. Together with Wolfgang Köhler and Kurt Koffka they helped establish theories of Gestalt psychology. The central theorem was that the whole is other than the sum of the parts and they argue that the whole exists independently from its parts. That is why we “see” a body, we see “interactions” and movement and “force” (push and pull). The fundamental principle of Gestalt perception is the law of prägnanz (German for pregnant but meaning pregnant with meaning as in brevity)—a shorthand and simplified version of reality. Gestalt psychology argue that we simplify the world in order to perceive it. We tend to organize our experience of the world in a manner that is regular, orderly, symmetrical, and simple. Gestalt psychologists have identified eight methods we use to simplify the world, primarily by grouping objects together. In an every changing world, having the ability to summarize and simplify the world means that we can perceive situations quicker, predict outcomes faster and thereby gaining time in order to be able to react earlier. We group things together and make them coherent. These are the tricks of magicians. Gestalt psychologists have defined such methods as laws and include the Laws of Proximity, Similarity, Closure, Symmetry, Common Fate, Continuity, Good Gestalt and, Past Experience.
1. Law of Proximity—When objects are close to each, sharing similar motion or sequence we see them as related. We see the behavior of one influencing the other so they share an affinity a similar fate.
2. Law of Similarity—Similar objects on the basis of function, behavior, shape, color, threat and other characteristics that we are sensitive to are seen as related.
3.Law of Closure—Our intent on making things whole extends to when objects have missing parts. This eliminates a lot of the variance so that despite the uniqueness of faces, for example, we see the face despite irregularities. If the law of closure did not exist we will have to interpret each face as a jumble of features.
4.Law of Symmetry—We balance objects in space. A symmetrical field of vision is easier to see because it simplifies the multiple objects into aa pattern, a perceptual algorithm. All we need to see is the symmetry, the uniform pattern rather than individual elements.
5. Law of Common Fate—We see the path that objects travel from and heading towards. We see objects that share similar paths of motion, or direction of motion as grouped together.
6. Law of Continuity—when an object is hidden from view we tend to still see it despite that the object might be behind another object, or when an object is partly hidden we assume that it is whole the the object in front is obscuring the backround object. We are less likely to see objects that change direction quickly or change shape quickly.
7. Law of Good Gestalt—We aim to eliminate variance, complexity and unfamiliarity which implies a global order to the world.
8. Law of Past Experience—history and temporal association implies that under some circumstances visual stimuli are categorized according to past experience. The experience of grouping two objects together in the past determines that we are likely to see them as grouped in the future.
These individual laws of grouping are not separate processes. They define a perceptual bias to group objects into a pattern. Each of these laws defines how we conceive of the world as a model with individual units sharing common attributes. We can say that the capacity to group things together exposes our perception as an algorithm, a formula. We do not perceive a visual reel of reality, a cinematographic version of reality in our heads—although we might conceive of our perception as such. In fact what these Gestalt laws tell us is that we see patterns in our experience of the world—we are not forming patterns, we are seeing patterns.
Algorithms, patterns, formulas or heuristics simplify the world into generalizable configurations.  This view of perception is supported by studies from preliterate societies and how they manage to count and subtract. Like a map that represents the geography of a place, preliterate societies have mathematical maps that help them to work out numerical outcomes. We simplify our experience with the physical world through formulas and algorithms. This is how our brain works.  In 2008, Michael Frank with the Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, and his colleagues reported how the Pirahã Amazonian tribe despite having no language to express numbers, not even one, are able to perform exact matches with large numbers of objects perfectly. Although they were inaccurate on matching tasks involving memory, because they did not have the benefit of language to retrieve information, their capacity to conceive of numbers was equal to other literate groups. They had a schematic way of conceptualizing numbers. We do this algorithmically, using perceptual formulas and patterns to conceive our material world.
Having such a translation of reality embedded within us, the question is whether we also preconceived classical physics. Whtether Classical Theory was indeed physics or a study of our own preconceived perceptual biases. We can see the similarity between the laws of Gestalt psychology and those of Classical Mechanics: 1. A body remains at rest or moves with constant velocity when an external force acts on it, 2. The rate of change of momentum of a body is proportional to the force on the body, 3. When two bodies interact they exert on each other equal, but opposite forces. All of these laws conform to the laws of Gestalt perception. Our perceptual biases are in tune with Newtonian physics. So is Classical Mechanics similarly a biased view of the world?
The fact that we have a mathematical formula—through Classic Mechanics—that predicts the speed, direction and change of objects is an indication of how we perceive objects in motion rather than an indication of the reality. Although our perception is necessarily based on a physical reality that we—like physicists—are trying to predict, our perception is not a reflection of reality but a translation. A translation based on prediction. Predicting reality is very different from “seeing” reality. Just because I can predict an outcome does not mean that, because of my accurate prediction, I understand the reality. Betting shops do this all the time. The problem is Quantum Mechanics. Here comes a theory that challenges what reality is, not as we perceive it to be (Classic Mechanics) but as it seems to be (Quantum Mechanics).
In physics, a quantum is the minimum amount of any physical entity involved in an interaction. Although many scientists have used the term before, it was Max Planck in 1900 that used "quanta" to mean "quanta of matter and electricity, gas, and heat.” Leading Albert Einstein to suggest in 1905 that radiation existed in spatially localized packets that he called "quanta of light". Einstein renamed Planck’s quanta packages as photons and used Planck’s quantum theory to describe the photoelectric effect, for which he would receive his Nobel Prize in 1921. The penultimate expression of quantum physics is Schrodinger’s cat paradox where quantum superposition—entanglement theory—dictates that a cat (in Schrodinger's example) has to be both simultaneously alive and dead at the same time. Although this IS weird—leading Einstein to talk about “spooky action at a distance” and Schrodinger himself to give up quantum physics to focus on philosophy and biology—this is a reality that must be necessarily uncomfortable because it disrupts our own perceptual framework of how the world behaves. Our psychology is insulted.
For the first time we are exploring the world as it truly is rather than how we think it should be. The Greek philosopher Heraclitus wrote around 500 BCE that we can never step in the same river twice. With this observation we have some semblance of what true reality looks like. A universe eternally in a state of flux, having multiple realities, depending on where I—the observer—am.
Did Classical Mechanics simply reflect a detailed exposition of Gestalt psychology? Quantum physics is saying yes. We do not know what reality is except what we are now learning through Quantum Mechanics. Classical Mechanics exposed the psychology of perception. Quantum physics will start to help us understand the weird and the wonderful—what we will come to know—reality.
References:
Franka, M. C., Everettb, D. L., Fedorenkoa, E., & Gibsona, E. (2008). Number as a cognitive technology: Evidence from Pirahã language and cognition. Cognition, 108, 819-824.
For an intriguing perceptive of how psychology was enfluence by physics--which was brought to my attention after this blog was published--please refer to this very readable paper, I have Dave Edwards to thank for this edification:
Wilcox, S., & Edwards, D. A. (1982). Some Gibsonian perspectives on the ways that psychologists use physics. Acta Psychologica, 52(1), 147-163.
© USA Copyrighted 2015 Mario D. Garrett

Monday, August 3, 2015

Ontological Question

Relationships have history. The relationship we have with our environment has a history, a memory. The relationship we have with others has a history, and the relationship we have with ourselves also has a history. Our history determines how we interact with all these facets of life.

As very complex beings we learn, and continue to learn throughout our life, how we interact with our environment in the most efficient way possible. Efficient might mean taking shortcuts however.

Our brain does most of this automatically. We are not aware, unless we need to address something unexpected or something of importance. Most of the time we interact with the world through shortcuts. If we are wiping our hands we pick up a towel and use it. We might not be aware of the towel unless it is different (bright pink with green dots.) Otherwise, the utility of the towel suffices. We do not need to go deeper than that. The brain is very efficient at parsing the reality that we need, and nothing more. This is efficient and sensible with wiping our hands, but limited when we try and understand our world.  Martin Heidegger the german philosopher in Being and Time (1927) called this form of shortcut "ready to hand." Such an awareness of an object that is limited to its utility. We forget the structure of an object and focus on its utility, it function gains prominence in our mind and all else is diminished. Taking this idea further, we can (and do) apply this utility to people around us. We forget the humanity behind a person and get angry when their utility is not realized (they wanted to do something other than fulfill our desires or needs.)  And we do this with our own behavior as well.  Most of the time we function as complex robots. We undertake repetitive task unconscious, as a matter of habit. Driving to work, driving back home, it is all done with minimal conscious thought. This is Pierre Bourdieu's concept of habitus, action that is relegated away from consciousness. And there other other facets of life where we hold a subconscious reality of networks.  Especially as we become older and have more experience living, we build these habitus events to such an extent that we live our lives in an unconscious trance, what Heidegger calls "the nothing". Older adults get very good at this until something unexpected happens. Then what we thought was a simple task like driving, becomes an extremely complex and confusing task.

The reduction of competence among frail older adults is a perfect example of examining how these concepts determine our lives without us being aware of them. The easiest way to perceive this relationship with the world is that these layers of habitus build up into a source of capital. Capital refers to an investment--that we or others make--that we have access to.  In most cases, capital resides independent of us.  Bourdieu (1977) identified and separated such accumulated experiences into four basic capitals: individual’s economic capital (material wealth), social capital (social networking our friends and contacts) and cultural capital (knowledge, skills, education, and advantages that a person has, which give them a higher status in society), later he included symbolic capital (honor, prestige or recognition). To this list we also included body capital (Antoninetti & Garrett 2012) which is the expectation, by you and others, that your body will function as expected within a familiar environment. And there are other types of capital. Civilization is an investment, a civic capital that we can access. Economist talk about "human" capital. The investment in yourself which is normally defined by formal educational. While biologists talk about biological capital (Kemp & Moore 1979). Geography has “place capital” (structures that enhance the utility of a place, eg roads, walkability, street lightning). The interaction between individuals and their environment takes place in a nebulous dimension. And you can further break the type of capital  into different dimensions. But the gist is that relationships have history and build habits.

All philosophers extoll us that despite these unconscious constraints, we are however free. We are free to decide and self-determination. From Martin Heidegger to Paul Sartre there is this belief that being human means that we have some control. But why would we suffer this "anguish" of existence when we can ignore it and live in an unconscious mode? Why is Dasein--being in the present-- so important for Heidegger? Being a contrary, why not live in "they-selves" if the "our-selves" is so painful? If I was designing a new way of existing, would I elect to be aware of "being" and why?


Further readings:
Antoninetti, M., & Garrett, M. (2012). Body capital and the geography of aging. Area, 44(3), 364-370.
Bourdieu, P. (2011). The forms of capital.(1986). Cultural theory: An anthology, 81-93.

© USA Copyrighted 2015 Mario D. Garrett

Sunday, May 17, 2015

Fluoride Levels and Falls Among Elderly


In May 2015, the U.S. Centers for Disease Control and Prevention (CDC) released its mortality report showing that the only increase in unintentional injury that lead to mortality was due to falls among older adults.  While all other causes of mortality remained fairly stable, between 2000 and 2013, death from falls in older adults nearly doubled, from 30 to 57 deaths per 100,000 older adults.  In any given year, one in three older adults will have a fall and 20-30% of these victims will suffer a moderate or severe injury. A quarter will die before the year is over. This is a public health tragedy.
Men are 40% more likely than women to die from a fall. While older Whites are 2.7 times more likely to die from falls as their Black counterparts.

Falls are the most common cause of traumatic brain injuries (TBI).5
Half of all fatality because of falls  are due to TBI.7

The most common injuries when older fall are fractures to spine, hip, forearm, leg, ankle, pelvis, upper arm, and hand.  Of these, the most serious is hip fracture. In a large number of cases leading to death. In contradiction, although falls remains on the increase from 1996 to 2010, hip fracture rates declined significantly for men and women (13). Over 95% of hip fractures are caused by falls. It is not known what factors are contributing to this trend. This seemingly contradictory evidence

A woman's bone density declines by about 30% between the ages of 50 and 80 increasing 5 years after menopause. Although bone density is not the only factor in hip fracture risk. Over 90% of hip fractures occur upon falling. Although many elderly people suffer spontaneous hip fractures because of advanced osteoporosis, the immediate cause is a fall. But this information is not validated. If a fall was instigated by a spontaneous hip fracture, the older adult is more likely to find an "excuse" for the fall rather than accept (and understand the mechanics) or a spontaneous fracture. There are distinct breaks if it is due to a fall or due to a spontaneous hip fracture.


Falls can be complex, and the literature has numerous causal pathways--from increased medication, older and frailer adults, better reporting, better health surveillance,  heavier older adults--all of which are valid. But there is one cause that is not mentioned.

Most researchers assume that an older adult fall and then break their hip. Or if they fall, they try and find behavioral reasons for the fall.  However it is also likely that there is a spontaneous hip fracture which causes the older adult to fall. There is a spontaneous hip fracture and then the person falls. Such fracture can easily be determined. As yet CDC has not undertaken this study. It would be relatively easy to review the X-rays from those that died. This study would not even need an Institutional Review Board. But until that study is done we can only conjecture the cause of these hip fractures.

It could be that there is an environmental cause to the increase in fractures related to state policies that the Federal agency supports: fluoridation of our water. There is overwhelming evidence that fluoridation in our water is toxic. Although the topical application of fluoride on teeth has been found to be beneficial, the ingestion of fluoride continues to receive negative outcomes. The argument that it improves dental health becomes less realistic when more than a quarter of adults over the age of 60 have dentures. The fact that this policy of water fluoridation ignored older adult health is already established. What is being established now is that it is harmful to older adults.

One of the reasons why falls are on the increase is because the bones of older adults in the U.S. are being made brittle because of fluoridation of water and that these spontaneous fractures are causing some or most of the falls. Multiple studies support this assertion: Fluoride therapy may be implicated in the pathogenesis of hip fractures which may occur in treated patients despite a rapid, marked increase in bone mass. (6)  Fluoride appears to be a key factor in the pathogenesis of stress fractures (7) [T]he six hip fractures occurring in patients receiving fluoride during 72.3 patient years of treatment is 10 times higher than would be expected in normal women of the same age (8) Thirteen cases of spontaneous fissure or fracture of the lower limbs observed in 8 patients under treatment with sodium fluoride are reported (9). (Fluoridation)...to worsen a patient’s clinical state (1) Increasing the dose of fluoride increases the risk of nonvertebral fractures  (2) 1 year of fluoride administration seemed to reduce bone strength by 17-30% (3) patients treated with sodium fluoride,...All fractures were spontaneous in onset... three times that in untreated osteoporosis. (4) Fluoride treatment was “associated with a significant three-fold increase in the incidence of nonvertebral fractures (5) fluoride-induced microfractures (10)
sustained spontaneous bilateral hip fractures during treatment with fluoride, calcium, and vitamin D for osteoporosis (11) Three or four of the fractures in the fluoride group appeared to be spontaneous hip fractures...the fluoride treatment here was probably partly responsible for the fractures in our cases. (12)
CDC needs to review the X-rays of all older adults that die due to falls. Ascertain the level of spontaneous hip fractures. Examine the correlation with fluoridation in the public water system. Measure the accumulation of fluoride in older adults. Engage in a systematic review of fluoridation on older adult comprehensive health including skeletal, digestive system and neurological.

  • There is no correlation among countries that fluoridate their water and hip fractures. 
    In 2002 in an international comparative study John Kanis from the WHO Collaborating Center for Metabolic Bone Diseases, University of Sheffield Medical School, Sheffield, United Kingdom and his colleagues reported some dramatic variance in hip fracture incidence from different regions of the world. Lifetime risk at the age of 50 years varied from 1% in women from Turkey to 28.5% in women from Sweden. The risk for women was correlated with that for men. Countries were categorized by 10-year probabilities comprising very high risk (Norway, Iceland, Sweden, Denmark, and the United States), high risk (Taiwan, Germany, Switzerland, Finland, Greece, Canada, The Netherlands, Hungary, Singapore, Italy, United Kingdom, Kuwait, Australia, and Portugal), medium risk (Hong Kong, France, Japan, Spain, Argentina, and China), and low risk (Turkey, Korea, Venezuela, and Chile). Only 6 OECD countries have more than 50% of their populations drinking fluoridated water: Australia (80%), Chile (70%), the Irish Republic (73%), Israel (70%), New Zealand (61%), and the United States (64%).

1. Gutteridge DH, et al. (2002). A randomized trial of sodium fluoride (60 mg) +/- estrogen in postmenopausal osteoporotic vertebral fractures: increased vertebral fractures and peripheral bone loss with sodium fluoride; concurrent estrogen prevents peripheral loss, but not vertebral fractures. Osteoporosis International 13:158-70.

2. Haguenauer D, et al. (2000). Fluoride for the treatment of postmenopausal osteoporotic fractures: a meta-analysis. Osteoporosis International 11:727-38.

3 Sogaard CH, et al. (1994). Marked decrease in trabecular bone quality after five years of sodium fluoride therapy–assessed by biomechanical testing of iliac crest bone biopsies in osteoporotic patients. Bone 15: 393-99.

4. Schnitzler CM, et al. (1990). Bone fragility of the peripheral skeleton during fluoride therapy for osteoporosis. Clinical Orthopedics (261):268-75.

5. Riggs BL, et al. (1990). Effect of Fluoride treatment on the Fracture Rates in Postmenopausal Women with Osteoporosis. New England Journal of Medicine 322:802-809.

6. Bayley TA, et al. (1990). Fluoride-induced fractures: relation to osteogenic effect. Journal of Bone and Mineral Research 5(Suppl 1):S217-22.

7. Orcel P, et al. (1990). Stress fractures of the lower limbs in osteoporotic patients treated with fluoride. Journal of Bone and Mineral Research 5(Suppl 1): S191-4.

8. Hedlund LR, Gallagher JC. (1989). Increased incidence of hip fracture in osteoporotic women treated with sodium fluoride. Journal of Bone and Mineral Research 2:223-5.

9. Orcel P, et al. (1987). [Spontaneous fissures and fractures of the legs in patients with osteoporosis treated with sodium fluoride]. Presse Med 16:571-5.


10. Dambacher MA, et al. (1986). Long-term fluoride therapy of postmenopausal osteoporosis. Bone 7: 199-205.

11. Gerster JC, et al. (1983). Bilateral fractures of femoral neck in patients with moderate renal failure receiving fluoride for spinal osteoporosis. British Medical Journal (Clin Res Ed). 287(6394):723-5.


12.  Inkovaara J, et al. (1975). Phophylactic fluoride treatment and aged bones. British Medical Journal 3: 73-74.

13. Stevens JA, Rudd RA. The impact of decreasing U.S. hip fracture rates on future hip fracture estimates. Osteoporosis International 2013. DOI 10.1007/s00198-013-2375-9.

Monday, May 4, 2015

Geography of Aging and the Illusion of Self

I think of myself as an entity, as "me."  Separate and distinct from "them" and the outside world. This "me" allows my mind to cleverly edit, interpret and re-interpret the world as though I am consistently at the center of everything that I interact with.  My mind also draws a linear story-line from my childhood directly to my older-adulthood.  I do not have to think about it because my mind automatically narrates a story for me that is complete where I am at the center and the rest is on the periphery. A story of "me" and "them", a logical relationship. I have an explanation for everything even though most events in my life are outside of my control.  This gives me the impression that I am "me", separate, distinct and unique, and then there is a "them" an outside. I have conscious will and participate in the world as a free unique and independent agent.

But this belief is a mirage, an illusion of the mind. The idea that we are separate from others is not the complete picture, and this knowledge is just now starting to be exposed. To re-envisioning who we are we have to understand how the "me" came about. This is a radical idea. Such radical ideas have happened before in our collective history and they have changed how we think about who we are.

There have been a number of radical thinkers who transformed how we think of ourselves.  The first such radical thinker moved us away from mythology, and the notion that everything that happens is because "god wants it to happen." Thales of Miletus was a 6th century BC  philosopher who suggested that we should observe physical events without assigning the cause to "god." He admonished philosophers to try and understand what they observe as separate from god. This was the birth of science. As a result we began to understand that there is a causal pattern to the world. That there is a logical sequence that does not require the intervention of busy gods. The development of science took us into an amazing logical world that was hidden to us before. We came to see the world in more detail. As a finely tuned mechanical watch. This assurance of solidity was however shattered in the early 1900s on two fronts. The first to dispel the solidity of how we see our world was Sigmund Freud. Freud developed the concept of an unconscious mind that hid psychological energies from us such as the Oedipus complex, libido and death drive among others. Freud's main contribution was the acceptance that we do not know "us", that we have a reality that is hidden from us.  What Freud did for psychology, Albert Einstein did for our concept of outside reality. Einstein, a theoretical physicist, developed a general theory of relativity which together with quantum mechanics and the law of the photoelectric effect evolved into quantum theory. Einstein transformed Newtonian mechanicswhere object were treated as physical representation but much smallerto one where at great microscopic details these realities changed into energy and shivering mass. He conceived of the world as composed of waves of energy,  a vibrating nexus of excited mass. These ideas later flourished into an idea of reality as a probability of energy waves. Completely transforming how we look at the universe we believed to be solid.

These ideas came from a culmination of prior small developments that helped Thales, Freud and Einstein make a conceptual leap. We are now ready for another leap. Another way of looking at ourselves...again.

It started when scientists started finding that conscious thought is a product of an unconscious process. We are "aware" because there is an earlier process that we are not aware of that wants us to be aware. The late Benjamin Libet from UCSF was a pioneer in showing that a conscious decision can be monitored neurologically sometimes as much as ten seconds before the activity appearswhich he termed readiness potential. In effect, by monitoring the brain's EEG we can predict rudimentary activity before people become conscious of itsuch as moving your index finger. More recently, Itzak Fried from UCLA recorded single neurons and found that the readiness potential isn't a diffuse state of readiness, but is a very specific set of instructions. Our consciousness was an after thought to a specific decision that has already been taken.  This resulted in what Daniel Wegner called in his 2002 book "The Illusion of Conscious Will." It is an illusion that we cannot dispel, despite knowing that it is an illusion, because it is how we think. We think that we have conscious will.

If there is no conscious will, then it brings into question the validity of the division of self/mind and brain/body that René Descartes defined in the 1600s. This Cartesian Dualism has constrained our thinking for more than four centuries. This belief is that there is a separation of the mind from the body and that the self is not defined by the mind but something higher. But this is proving to be wrong. But more important than thisalthough for academics this is really importantis that if our consciousness is part of a pre-determined process, then what other realities are there that we are not aware of? If there is no such thing as a self/mind and brain/body division, then what is there?  I think of "me" as the product of a coherent sequential story that lead me here as a sentient being in a determined place, undertaking a conscious activity. I feel responsible for where I am and what I am doing. Which is why nationalism is so strong even though where we are born is a random event. Most people take ownership of their situation.

Because our brain is so vast in its complexity it is able to create a representation of the world. It uses this model to predict. That is how we survive and flourish. Prediction is also the basis for all scientific theory. My brain builds a virtual reality and interacts within this model. Very much like a computer game where I "am" the avatar. And very much like the avatar, my mind makes me unique, distinct and sequential being with a history that I own. Our reality is a creative process. We create this reality. We negotiate with our body and our mind about how to tell this story of reality. On one side is the concept of "me" and on the other the story of "others." The reality is that there is a place where there is no distinction. Our body holds that special place. It is both part of the environment and part "me". The illusion is the "me."  This is especially true of routines of everyday lifethose activities and customary habits that are expected and anticipated. Routines are patterns of behavior that we build over time and internalized. We are unaware of these habits of behaving. And it is not just that we are unconscious of them but that our body has adapted without making us aware, and we know about these changes because we can measure them.

Stress chemicals in the bodysuch as the allostatic load and IL-6is higher in people that live in communities with greater densities of poor older adults and in racially segregated communities. This relationship was found to be independent of important individual level risk factors (e.g. smoking or obesity). A stressful environment—such a poor neighborhood—results in negative changes in the chemical composition in our bodies. These chemical states initiate other changes. Changing chemical composition in our bodies have lasting effects because they switch the expression of some genes. These epi-genes can be switched on and off, establishing a consistent optimum level of chemical balance within the body. Environmental factors such as mercury in water, second-hand smoke, diet including foliate, pharmaceuticals, pesticides, air pollutants, industrial chemicals, heavy metals, hormones in water, nutrition, and behavior have been shown to affect epi-genetics.  Furthermore, epi-genetic changes are associated with specific outcomes such as cancer, diabetes, obesity, infertility, respiratory diseases, allergies, and neurodegenerative disorders such as Parkinson’s and Alzheimer’s diseases. Our body changes our epi-geneswhich establishes an optimum level of chemical balance in response to our environment. Richard Rorty in 1979 said this beautifully “So the paradoxical conclusion offered earlierthat had physiology been more obvious psychology would never have arisencan be reaffirmed. Indeed, we can strengthen it and say that if the body had been easier to understand, nobody would have thought that we had a mind.” (p 239).

Who we are is not who we think we are. Thales, Freud and Einstein have shown us how our perception is incomplete. The next frontier is the idea of self. Our body has a memory that we are unaware of. There is a reality in our body that reflects the geography of our communities, including people that we interact with on a consistent basis. This is necessarily unconscious since the body is complex. Our consciousness is an afterthought of decisions already taken in order to provide the illusion of active participants, an avatar. It provides us with the illusion of "me". But it is an illusion.  The reality is that there is no "me" but a place of interaction. A place where the illusion of a unique "me" interacts with the outside world, the geography the community and significant others.Who I am is not who I think I am. And we feel this reality sometimes as a spiritual existence. Something that extends human identity beyond the self. Learning compassion, empathy and love is when we truly become one with this reality. Try and translate love without referring to a world where their is a union of beings, of community of geographies. All religions start from this understanding, but the way that our mind worksneeding to create separateness and pushing us into an egocentric world viewcorrupts this initial insight and re-interprets it as "them" and "us." But what we are learning is that there is a union of those around us and the geography that we live in. Our identify of self is an afterthought.

The body and the mind  have already determined its strategy for existence. And if I accept that there is not just a "me" but also a "we" inside my body then I can understand how my environment, my community, family and friends can determine my behavior and outcomes, as much as I think I do myself. My interaction with the world leaves evidence in my genes just as I leave traces in my world.

The symbiotic relationship exposes humans to a greater sense of belonging within their geography since we carry our geography within us in our bodies. If we are going to understand how extreme-longevity occurs we need to understand this construct much better than we do today. And perhaps our understanding of why happy people, people that volunteer, people that are religious, people that are in love, live longer should not be seen as a strategy but as an expression of people that are in touch with this reality of who they truly are...a union of their geography and their community.

© USA Copyrighted 2015 Mario D. Garrett

Further Reading:

Libet, B. (1985). "Unconscious Cerebral Initiative and the Role of Conscious Will in Voluntary Action". The Behavioral and Brain Sciences 8: 529–566. doi:10.1017/s0140525x00044903.

Wegner, D. M. (2002). The illusion of conscious will. MIT press.

Garrett M. D. (2014) Geograph of Elderly. Oxford Bibliography.
Online: http://www.oxfordbibliographies.com/view/document/obo-9780199874002/obo-9780199874002-0062.xml


Tuesday, April 28, 2015

Humans are Cleverly Stupid Beings

Quick note to put things in perspective:  If the whole of the electromagnetic spectrum were positioned on a tape measure and it was stretched to 2,000 miles, the amount of visible light that humans see is less than one inch.  So, on a logarithmic scale of frequency, visible light is 2.3% of the whole electromagnetic spectrum, while on a linear scale it is 0.0035%. The human eye see less than 100th% of the universe.The perception of loudness relates roughly to the sound power to an exponent of 1/3. For example, if you increase the sound power by a factor of ten, listeners will report that the loudness has increased by a factor of about two (101/3 ≈ 2). This is a major problem for eliminating undesirable environmental sounds, for instance, the beefed-up stereo in the next door apartment. Suppose you diligently cover 99% of your wall with a perfect soundproof material, missing only 1% of the surface area due to doors, corners, vents, etc. Even though the sound power has been reduced to only 1% of its former value, the perceived loudness has only dropped to about 0.011/3 ≈ 0.2, or 20%.

The range of human hearing is generally considered to be 20 Hz to 20 kHz, but it is far more sensitive to sounds between 1 kHz and 4 kHz. For example, listeners can detect sounds as low as 0 dB SPL at 3 kHz, but require 40 dB SPL at 100 hertz (an amplitude increase of 100). Listeners can tell that two tones are different if their frequencies differ by more than about 0.3% at 3 kHz. This increases to 3% at 100 hertz. For comparison, adjacent keys on a piano differ by about 6% in frequency.

Friday, April 24, 2015

Ménage à Trois: Sex, Dementia and the Law

There are events in life that are more colorful than the black and white reality of our moral principles. The monochrome reality of our moral world is sometimes outshone by the Technicolor nature of reality. People that are suffering from dementia expose some of these layers of moral predicaments.

The recent case of a husband assumed to have continued to have sex with his wife when she was in a nursing home brought to light the spectrum of colors of this issue. This is the story of Donna Lou Young andHenry V. Rayhons in Duncan, Iowa. A week after her death at the age of nearly 79 Henry was charged with raping Donna at a nursing home where she was staying. As with rape charges there are tests and exposure of behavior that was intended to remain behind closed doors in the bedroom. Henry was eventually found not to be guilty, but the emotional damage diminished his dignity, his humanity as a husband. This case raises questions about who you are when you are diagnosed with dementia, and more importantly, what the law allows you to do, or allow others to do with you.

That same week there was the case of a lord of the House of Commons with enough evidence of child abuse but was not brought to court because he had dementia. Greville Janner, now Lord Janner, was a very active pedophile alleged with 22 sex offenses of indecent assaults and buggery during 1969 and 1988, involving nine children in state-run children’s homes. Despite remaining an active member of the House of Lords still attending meetings, the director of public prosecutions, Alison Saunders—similar to the U.S.  city/district attorney—found it “against the interest of the country” to prosecute a likely pedophile because he was suffering from dementia.

Dementia can shield as well as expose you to the imperfections of the law. But sometimes the problem is not the person that is suffering from the disease, but their loved ones. Sex in nursing homes brings about that added dimension of ageism. The monochromatic belief is that older adults should not be having sex, especially those with dementia. But this attitude denies people's history, experience, expression and dignity.

The case at Windmill Manor in Itoralville, Iowa, where two patients with dementia become emotionally and physically involved, to the ostensible benefit to both, resulted in the couple becoming separated and the managers at the nursing home losing their job. In contrast, when there is an acceptance that dementia is a disease that erodes your memory and who you are, there is acceptance of such physical foibles. Supreme Court Justice Sandra Day O'Connor acceptance of her husband’s affair with a female resident at the same nursing home is a Technicolor reality. A situation that has been immortalized in Alice Munro's 1999 short story "The Bear Came Over The Mountain." Sometimes there is an appreciation that sex might be one form of communication remaining among many dead forms of expression. If you we appreciate and understand this, how far will we go to satisfy the needs of a demented patient? Sex and religion head butt often, but when it is your loved one would you support their needs.? The Australian case of a daughter of a dementia nursing home resident who procures a sex worker for her father with the blessing of the nursing home staff might seem liberal, but what if the nursing home was one of many run by religious organizations?

These are not easy moral decisions. And there are more Technicolor layers that await to become exposed. The LGBT older adults who have to go back in the closet when they enter an assisted living facility or a nursing home. Or the ostensibly heterosexual resident who suddenly (to the caregivers) develops an interest in same-sex residents. What if the other person was not a resident but a caregiver?  And not ignoring the sexual abuse of residents with dementia by their caregivers. 

The law has always meddled with sex, and it has always been on the wrong side of history. Sex with dementia would prove a tricky moral and legal issue. In a nationally representative study of more than 3000 U.S. older adults with dementia reported that 59% of the men and 51% of the women were sexually active when they had a partner. Overall, whether they had a partner or not, 46% of the men and 18% of the women with dementia were sexually active. The certainty is that the Technicolor of the reality of sex among those diagnosed with dementia will continue to confound us and to make us relinquish our monochromatic morals for a less rigid one with many hues.

© USA Copyrighted 2015 Mario D. Garrett

References
Lindau, S. T., Dale, W., Feldmeth, G., Gavrilova, N., Langa, K. M., Makelarski, J. A., & Wroblewski, K. (2018). Sexuality and Cognitive Status: A US Nationally Representative Study of Home‐Dwelling Older Adults. Journal of the American Geriatrics Society, 66(10), 1902-1910.

Friday, March 27, 2015

Life Expectancy

Life expectancy is akin to the median rather than an average age of death. The median is a statistic, that defines when  half a given population is expected to die before that age, and the other half will survive beyond that period. In physics it is close to the half-life of elements. This statistic is not an average (mean), it is a-mid point. Most confuse life expectancy with the average age of death. But it is best described as a mid-point. Gerontologists use life expectancy to define aging of populations. But there are nuances—both statistical and biological—that heed caution about interpreting historical life expectancy data. The problem is that life expectancy is equated with lifespan, and the two are not related.
In 2002, Jim Oeppen and James Vaupel from the Max Planck Institute for Demographic Research showed that life expectancy in some of the world’s developed countries (and Chile) has been increasing steadily by about 2.5 years per decade since the mid-19th century. Although they leave out contradictory evidence from across the world, including a large country like Russia—this argument that life expectancy is constantly improving also ignores latest life expectancy figures from the USA. For Blacks/African Americans in the United States life expectancy is declining.  Despite these realities, there is no denying that long-term stable decline in mortality suggests a continued rise in life expectancy. The dispute is not with life expectancy but with lifespan.

Luke Pamer/https://unsplash.com/
Source: Luke Pamer/https://unsplash.com/
Although life expectancy in some selected countries is increasing—and it has been for some years after the second world war—this does not mean that such increases are linear or that the end point has moved—lifespan has remained static. Even though there will be more centenarians both in terms of numbers—prevalence, because we have a larger population—but also in terms of percentage—incidence, because of improved public health—centenarians are exceptional beings. The reality is that human biology will preclude survival to age 100 for most people. Even for those that live to 100, the likelihood that they survive to become supercentenarians (110 years old) is 1 in 6 million.  As Fanny Janssen and his colleagues in the Netherlands reported, at some point there will be a wall.  A wall that is both biological and psychological.                          
Studies that show continuing increases in life expectancy cannot be used to argue that there is no lifespan, or that the lifespan can be increased. Life expectancy is an aggregate statistic. In the case where life-expectancy increases and the maximum number of years that you can live remains the same, means that more people reach the end, but they still reach an end. Although life-expectancy algorithm is different from median, and can reflect outliers, changes in life expectancy just tells us that more people are living longer but not to what age. In reality life-expectancy is still an estimate based on earlier survival probabilities. This is the reason it is used in gerontology because it provides an indication of the average person and ignores those exceptional people that live up to and beyond 100 years of age—1 per 25,000—and those who die in infancy—6.15 per 1,000. Especially in the past when there was a high rate of child mortality and very low rate of centenarians, life expectancy was a good estimate. Nowadays it is not. A more appropriate statistics is the modal age of death--the most common age at which people die. What we find is that through time, life expectancy and modal age are converging.
That is just what Juliana da Silva Antero-Jacquemi from the Institute of Biomedical  and Epidemiology Research in  Sport, France, and her colleagues used. They analyzed 19,012 Olympian competitors and 1,205 supercentenarians—who lived up to 110 years—that died between 1900 and 2013. Although most Olympians had longer life expectancy than most general population, they did not live as long as supercentenarians. However, what they identified is that there was a common death trend between Olympians and centenarians—indicating a similar mortality pressures over both populations that increase with age. The authors argue that mortality trend is better explained by a biological “barrier” model—that there is a static lifespan.
The issue of whether there are limits to life expectancy—a lifespan—received theoretical backing from demographers who argue that fundamental limits to life expectancy are likely. And that this is similarly to be determined, in part, if not on the whole, by our genes which drives an intense search for longevity genes in both animal models and humans. Human family studies have indicated that a modest amount of the overall variation in adult lifespan (approximately 20–30%) is accounted for by genetic factors. Genetic influences on lifespan are minimal prior to age 60 but increase thereafter. Although these studies look at monozygotic twins—identical twins—there might be other confounding factors.
There is a problem with estimating age at very old age. In 1986, given continued reports of claims of extreme age, Norris and Ross McWhirter, the editors of the Guinness Book of World Records, noted the need to validate such assertions when they repeatedly stated that there is no single subject is more obscured by obfuscation than the extremes of human longevity. And the inaccuracy increases with the older the person is reported to be. Stephen Coles reports how the U.S. Census Bureau dropped its estimate of centenarians from 2,700 in 1990 to 1,400 centenarians in 2000 after checking the dates of birth with the claimed ages at the Social Security Administration. However, even this conservative number was found to be inflated as there were only 139 persons aged 110 or older. And then, even this number is likely to be exaggerated since the true number, based on physician uncertainty about their age, is more likely to be between 75 and 100 persons.
One of the classic example of such uncertainty occurred in the 1973 issue of National Geographic when Alexander Leaf gave a detailed account of his journeys to regions of purported long-living people: the Hunzas in Pakistan, the Abkhazians in the Soviet Union, and Ecuadorians in Vilcabamba. According to this article, there were ten times more centenarians in these countries than in most Western countries despite poor sanitation, prevalence of infectious diseases, high infant mortality, illiteracy, and a lack of modern medical care. Unfortunately in 2009, a fantastic age claim by Sakhan Dosova of Kazakhstan, age “130 years” was supported in an issue of Scientific American, despite the lack of early-life documentation.
These inaccuracies in reporting extreme long age have received a lot of attention from demographers. Eventually a resurgence of longevity myths in the 1970s were finally debunked which lead to Alexander Leaf himself acknowledging that people lied to him in order for them to improve their social status and to promote local tourism. More recently demographers have become increasingly concerned with the accuracy of unprecedented growth of extreme longevity in developed countries. As a consequence more careful checks are being implemented which has resulted in a systematic refutation of numerous cases of extreme age since they appeared to be undocumented or exaggerated. One such example was when in 1999, Sardinian data was presented showing extreme male longevity. This pushed demographers to assess the validity of the data and lead to the development of a robust methodology for asserting the true age of participants.
Life expectancy vs. Lifespan
One of the most persuasive arguments that lifespan is separate from life expectancy is that even if we eliminate most diseases associated with age, we will still die.  Of course, we can only do this statistically.  Kenneth Manton and his colleagues from Duke University eliminated one disease at a time in their statistical modeling. What they found is that if we eliminate all of age-related diseases we expect to see those over 87 years of age to live an addition 5.7 years for males (estimated for 1987) and 6.5 years for females. This is about the same improvement in life expectancy at 65 in the last 100 years in the USA (5.7 years.) If you are 65 years old today, you have a 50/50 chance of living an additional 5.7 years than if you were living in the 1900s. In the last hundred years, the great improvement in life expectancy is not amongst older adults, but among newborns and infants and have very little to do with clinical care at later ages. Statistically, as we have shown before, if we live longer than the life expectancy, the statistic of life expectancy at birth will not change, and life expectancy at other ages will only improve slightly.
Most older adults suffer from not just one, but multiple, health conditions. So if we conjecture that we can cure one disease, say cancer, we will still be faced—sooner rather than later—with another disabling disease that might kill us slower. Douglas Manuel with the Institute for Clinical Evaluative Sciences, Toronto, Canada, and his colleagues calculated what happens when they eliminated specific killer diseases from their data. They 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. On the other hand, eliminating musculoskeletal conditions, would result in a year of good health for women and under half a year for men. And that is what we are finding across the world.  Even if we eliminated all diseases we might improve the life expectancy but not lifespan. Life expectancy and lifespan, despite their close association are separate statistical and theoretical constructs.
© USA Copyrighted 2015 Mario D. Garrett
_____________
Note: Life expectancy is a statistical formula to enumerate the average life left. Although it is different from median, the two are in reality very similar and produce very similar results. It is much easier to see life expectancy as a median, a mid-point because it illustrates how we can have an increase in life-expectancy and yet our maximum life that we can attain remains static.

© USA Copyrighted 2015 Mario D. Garrett
Further Readings
Carnes BA Olshansky SJ and Hayflick  L. “Can Human Biology Allow Most of Us to Become Centenarians?” Gerontol A Biol Sci Med Sci. 68 (2): 136-142.(2013).
Coles, L. Stephen. "Aging: The reality demography of human supercentenarians." The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 59, no. 6: B579-B586. (2004).
Deiana, L., L. Ferrucci, G. M. Pes, C. Carru, G. Delitala, A. Ganau, S. Mariotti et al. "AKEntAnnos. The Sardinia Study of Extreme Longevity." Aging (Milan, Italy)11, no. 3: 142-149. (1999).
Gavrilov, Leonid Anatolʹevich and Gavrilova Natalʹia Sergeevna. "The biology of life span: a quantitative approach." http://www.popline.org/node/315135(link is external) (1991). (Accessed September 2014)
Hadhazey A. “Can someone live to be a supercentenarian? A woman in central Asia claims to have just celebrated her 130th birthday, a new record for keeping the grim reaper at bay.” Scientific American. (2009).
Hayflick, Leonard, and Paul S. Moorhead. "The serial cultivation of human diploid cell strains." Experimental cell research 25.3: 585-621. (1961).
Hayflick, Leonard. "How and why we age." Experimental gerontology 33.7: 639-653. (1998).
Hjelmborg, Jacob vB, et al. "Genetic influence on human lifespan and longevity." Humangenetics 119.3: 312-321. (2006).
Janssen, Fanny, et al. "Stagnation in mortality decline among elders in the Netherlands." The Gerontologist 43.5: 722-734. (2003).
Kannisto V. Development of Oldest-Old Mortality 1950-1990: evidence from 28 developed countries. Odense, Denmark: Odense University Press. (1994).
Leaf A. “Every day is a gift when you are over 100.” National Geographic. 99. (1973).
Leaf A. “Getting Old.” Scientific American 29–36 (1973).
Leaf A. “Long-lived populations: extreme old age.” Journal of the American GeriatricsSociety. 30(8):485–487. (1982).
Manton, Kenneth G. "Past and future life expectancy increases at later ages: Their implications for the linkage of chronic morbidity, disability, and mortality." Journal of Gerontology 41, no. 5: 672-681 (1986).
Manton, Kenneth G., and Tolley Dennis H. "Rectangularization of the survival curve implications of an ill-posed question." Journal of Aging and Health 3.2: 172-193 (1991).
Manuel, Douglas G., Mark Leung, Kathy Nguyen, Peter Tanuseputro, and Helen Johansen. "Burden of cardiovascular disease in Canada." Canadian Journal of Cardiology 19.9: 997-1004. (2003).
McMichael, Anthony J., Martin McKee, Vladimir Shkolnikov, and Tapani Valkonen. "Mortality trends and setbacks: global convergence or divergence?." The Lancet 363, no. 9415: 1155-1159. (2004).
Notzon, Francis C., Yuri M. Komarov, Sergei P. Ermakov, Christopher T. Sempos, James S. Marks, and Elena V. Sempos. "Causes of declining life expectancy in Russia." Jama 279, no. 10: 793-800. (1998).
Olshansky JS, Antonucci T, Berkman L, Binstock RH, Boersch-Supan A, Cacioppo JT, Carnes BA, Carstensen LL, Fried LP, Goldman DP, Jackson J, Kohli M, Rother J, Zheng Y & Rowe J. 2012. “Differences In Life Expectancy Due To Race And Educational Differences Are Widening, And Many May Not Catch Up.” Health Affairs, August (2012).
Oeppen Jim &  Vaupel James W. “Broken Limits to Life Expectancy.” Science 10 May: Vol. 296 no. 5570 pp. 1029-1031 . (2002).
Palmore, Erdman B. "Longevity in Abkhazia: a reevaluation." The Gerontologist 24, no. 1: 95-96. (1984).
Poulain M, Pes G, Salaris L. “A Population Where Men Live As Long As Women: Villagrande Strisaili, Sardinia.” Journal of Aging Research. Volume (2011).
Schoenhofen, Emily A., Diego F. Wyszynski, Stacy Andersen, JaeMi Pennington, Robert Young, Dellara F. Terry, and Thomas T. Perls. "Characteristics of 32 supercentenarians." Journal of the American Geriatrics Society 54, no. 8: 1237-1240 (2006).
Wilmoth JR “The earliest centenarians a statistical analysis.” In: Jeane B, Vaupel J eds. Exceptional Longevity from prehistory to the present. Odense Denmark: Odense University Press, 1996
Young, Robert D., Bertrand Desjardins, Kirsten McLaughlin, Michel Poulain, and Thomas T. Perls. "Typologies of extreme longevity myths." Current gerontology and geriatrics research 2010 (2011).

Genetics of Longevity

    The most persuasive argument for the genetic influence on lifespan is the different lifespan of species. The best explanation we have of this absolute and static lifespan is the concept of the Hayflick Limit—a genetic program that kills cells.  In 1961—going against the thinking at the time—biologists Leonard Hayflick and Paul Moorhead noticed that their cell cultures were dying after replicating (mitosis) a certain number of times.  But during this period Alex Carrel—a Nobel Prize winner in surgery—held the thinking that cells are naturally immortal. We do bad things to them to 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 percent oxygen—which is the same as human internal conditions—before stopping replicating. This stopping of replication has become the Hayflick Limit.  Refuting the idea that normal cells are immortal and establishing a biological basis for lifespan—the Hayflick Limit has established itself as the primary theory of what determines human lifespan.
            The mechanism was not yet known at the time of this observation. But in 1971, a Russian scientist Alexey Olovnikov, hypothesized the involvement of the end caps of the DNA that controlled this Hayflick Limit. Elizabeth Blackburn and Carol Greider—who won the Nobel Prize in Biology for their studies—later confirmed this in 1984. They found evidence of proteins called telomeres at the end of the DNA which get shorter with every division (mitosis) until they get too short to allow for more replication.  This telomeric theory identifies the mechanism of how the Hayflick Limit exists.
            Although this is an eloquent theory, there is large variance in correlating telomere length with aging and with lifespan. Firstly, telomeres are not proportional to longevity. There are three main arguments against using telomeres as the sole explanation of lifespan. Nuno Gomez from the University of Texas Southwestern Medical Center and his colleagues, undertook the largest comparative study involving over 60 mammalian species, and they reported that telomere length inversely correlates with lifespan. They also found that while telomerase—an enzyme that promotes the re-growth of telomeres—correlates with size of the species. The larger the species, the more telomerase, and therefore there is more maintenance of telomeres.  In addition, it seems that telomeres do not provide a complete understanding of lifespan. The second argument against the telomeric theory of lifespan comes from 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 quicker, perhaps we started with fewer stem cells, or perhaps theenvironment that we live in degraded them faster. Older adults are more likely to have used up their supply of stem cell or experienced more stressors that damaged their stem cells.  Once stem cells run out or become disabled, they cannot be replaced by the body. So there is also a limit for the utility of our endowed stem cells. The third argument comes from Leonard Hayflick himself, who observed that assuming human fibroblasts endure 70 divisions, there are more than enough cells for several lifetimes.  So although the Hayflick Limit predicts that there has to be a lifespan—an upper limit to longevity—the evidence suggests that that limit could not have yet been achieved.
Aside from the genetic explanations of lifespan there is also the observable reality of demography—the study of changes and patterns in population. An earlier theoretical observation made by a British actuary Benjamin Gompertz was published in 1825. He observed a law of geometric progression in death rates as we grow older. The insight was a mathematical formulae which has the probability of dying doubling about every 7 or 8 years following puberty. This is known as the Gompertz curve and is constant in all observations of human (and most other species) mortality. The only modification to this curve is that it is shifting to the right allowing later—delayed—death mortality. This has been predicted through the rectangularization of this curve. While the decline at the end of life has been termed as the entropy in the life table. This theory argues that the Gompertz curve will be pushed up but that the lifespan will remain virtually unchanged, making a rectangular path. Under such a scenario, most people will live up to a maximum lifespan and then die. Until then, the life expectancy will increase but the age of death will remain virtually static and always below 122.           
Some geneticists argue that we have not achieved the theoretical lifespan.  As a consequence these scientists claim that we can increase the lifespan.  There are many studies in this area but three act as seminal archetypes of the type of work being conducted.
The first type is a classic experiment by Michael Rose who began manipulating the life spans of fruit flies by allowing them to reproduce only at late ages. This forced researchers to pay attention to the survival and reproductive vigor of the flies through their middle age. The subsequent progeny of flies evolved longer life spans and greater reproduction over the next dozen generations.
The second type of experiment uses examples from nature, which they then emulated in the laboratory and involved growth hormones.  At U.C San Francisco Cynthia Kenyon chemically knocked out certain genes in flatworms, the gene daf-2 which partially disables receptors that are sensitive to two hormones – insulin and a growth hormone called IGF-1. This mutation—which was original seen in nature and then replicated in the laboratory—nearly doubled the flatworms’ lifespan. These long-lived worms looked and acted younger than their control group, implying that extending the lifespan also extends healthy life.
Then there is the genetic observation with mice, in particular the work done by Richard Miller, and his infamous mouse called Yoda (who is now deceased.) Like other dwarf mice, Yoda had a natural genetic mutation that obstructs the production of growth and thyroid hormones. Dwarf mice tend to grow to only about a third the size of normal mice, which helps them live about 40 percent longer. There are three types of mice that share this longevity characteristic. The Snell and Ames dwarf mice have been bred to inherit mutations in Pit-1 and Prop1 genes, respectively, which disrupt the embryonic development of the pituitary gland. While the Laron dwarf mouse has a targeted gene deletion of either the growth hormone receptor (GHR-KO) or the growth hormone binding protein (GHBP-KO). So even though this mouse produces growth hormone, it is still growth-restricted because it is unable to respond to the hormone. The common denominator in all these mice is that they have stunted growth which correlates with increased lifespan.
Increasing the lifespan in all cases of genetic studies—manipulation or observation—is related to stunted growth or late life progeny. It has been argued that this delayed growth stamps an expiration date onto our genes.  If we are stunted in growth or our parents delayed producing us, then our body seems to know that it needs to live longer in order to pass on its genes.  There are two complementary theories that explain these observations.
The theory of Antagonistic Pleiotropy argues that some genes have contradictory effects at different age. Genes which might enhance your reproductive success—genes that increase testosterone in men, resulting in more muscle mass and masculine secondary sexual characteristics—may at the same time have detrimental effects on survival later in life—in testosterone example elevated risk of cancer. Natural selection tends to favor these kinds of genes because they maximize fitness, as higher mortality in the post-reproduction stage will have little impact on fitness compared to increased number of offspring. The second theory is the Disposable Soma Theory. This theory states that—given that there are finite resources to maintain and repair cells and organs, the body does a balancing act—the body protects itself just long enough so that we are able to pass on our genes. A similar argument is made by Leonard Hayflick to distinguish age related changes from lifespan who argues that longevity—whish is distinct  from age changes—is indirectly determined by the genome.
            Another area of research that compliments the genetic work on life span is the burgeoning research on Caloric Restriction (CR). Initially discovered in 1935 in mice, CR has been shown to increase the lifespan in yeast, insect, and in non-human primates.  In humans CR is still undergoing testing, although initial results suggest prolongation of life as well as prevention of age-related are likely outcomes. The mechanism seems to emulate the genetic work of life prolongation, in that the CR elicits a hormesis event—a low level stressor that stimulates positive response where epigenetic switches are triggered.
            As with all genetic work there are many confounders. From the genotype to the phenotype and then there is the environment. Even if we accept that stunted growth might improve lifespan, other factors might negate such gains.  And that is the case with a southern Ecuador group where more than 250 individuals are thought to have Laron syndrome—IGF-1 deficiency in primary growth hormone—which is caused by a mutation in the growth hormone receptor gene with affected individuals growing to less than 4 feet tall. Although Laron patients appear to be protected against developing cancer. However, this apparent protection does not translate to a longer lifespan due to trauma and alcoholism. There is a schism between lifespan and theoretical lifespan…human behavior.
© USA Copyrighted 2015 Mario D. Garrett
Further Readings
Aguiar-Oliveira M.H., et al. “Longevity in untreated congenital growth hormone deficiency due to a homozygous mutation in the GHRH receptor gene.” J Clin Endocrinol Metab.;95(2):714–21. (2010).
Bartke A &  Brown-Borg H. “Life extension in the dwarf mouse.” Curr Top Dev Biol.  63:189–225.(2004).
Calabrese, Vittorio, Carolin Cornelius, Salvatore Cuzzocrea, Ivo Iavicoli, Enrico Rizzarelli, and Edward J. Calabrese. "Hormesis, cellular stress response and vitagenes as critical determinants in aging and longevity." Molecular aspects of medicine 32, no. 4 .279-304. (2011).
de Cabo, Rafael, Didac Carmona-Gutierrez, Michel Bernier, Michael N. Hall, and Frank Madeo. "The Search for Antiaging Interventions: From Elixirs to Fasting Regimens." Cell 157, no. 7: 1515-1526. (2014).
Finch, Caleb E. "Variations in senescence and longevity include the possibility of negligible senescence." The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 53.4: B235-B239. (1998).
Finch, Caleb E., and Malcolm C. Pike. "Maximum life span predictions from the Gompertz mortality model." The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 51.3: B183-B194. (1996).
Fotios, D and Kirkwood TBL. "Modelling the disposable soma theory of ageing." Mechanisms of ageing and development. 126.1: 99-103. (2005).
Gomes, Nuno, et al. "Comparative biology of mammalian telomeres: hypotheses on ancestral states and the roles of telomeres in longevity determination." Aging cell. 10.5: 761-768. (2011).
Greider, Carol W., and Elizabeth H. Blackburn. "Identification of a specific telomere terminal transferase activity in Tetrahymena extracts." Cell. 43.2: 405-413. (1985).
Hayflick, Leonard and Moorhead Paul S. "The serial cultivation of human diploid cell strains." Experimental cell research. 25.3: 585-621. (1961).
Hayflick, Leonard. "How and why we age." Experimental gerontology 33.7: 639-653. (1998).
Kenyon C. Could a hormone point the way to life extension?. elife. 2012;1:e00286. doi: 10.7554/eLife.00286. Epub .  Oct 15. (2012)
Kenyon C. The first long-lived mutants: Discovery of the insulin/IGF-1 pathway for aging. Philos Trans R Soc Lond B Biol Sci. 366, 9-16 (2011).
Kenyon, Cynthia, et al. "A C. elegans mutant that lives twice as long as wild type." Nature 366.6454: 461-464.(1993)
Keyfitz, N. 1977. Applied Mathematical Demography. 1st ed. New York: John Wiley.
Laron, Z., Kopchick, J. (Eds.), Laron Syndrome - From Man to Mouse. Lessons from Clinical and Experimental Experience. Springer. (2011).
Manton, Kenneth G. "Past and future life expectancy increases at later ages: Their implications for the linkage of chronic morbidity, disability, and mortality." Journal of Gerontology 41, no. 5: 672-681. (1986).
Manton, Kenneth G., and H. Dennis Tolley. "Rectangularization of the survival curve implications of an ill-posed question." Journal of Aging and Health 3.2: 172-193. (1991).
Miller, Richard A. "Genes against aging." The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 67.5: 495-502. (2012).
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