iAge

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 mechanics—where object were treated as physical representation but much smaller—to 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 appears—which he termed readiness potential. In effect, by monitoring the brain's EEG we can predict rudimentary activity before people become conscious of it—such 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 this—although for academics this is really important—is 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 life—those 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 body—such as the allostatic load and IL-6—is 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-genes—which establishes an optimum level of chemical balance in response to our environment. Richard Rorty in 1979 said this beautifully “So the paradoxical conclusion offered earlier—that had physiology been more obvious psychology would never have arisen—can 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 works—needing to create separateness and pushing us into an egocentric world view—corrupts 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.

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.

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.

_____________

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.

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.

Lifespan

Lifespan is described by The Oxford English dictionary as “The length of time for which a person or animal lives or a thing functions.” Pragmatically, lifespan is defined as the period that the longest living member of a species has lived. Sometimes lifespan—or Maximum Lifespan—is used to refer to the longest period of time that a member of a species can live to. Scientists have not yet determined what the maximum length of time a human can live up to. This is an active theoretical field, and is home to lively speculation among some gerontologists. When it comes to humans, the oldest person that has ever lived defines lifespan. Verified by the Guinness World Records and the Gerontology Research Group, Jeanne Louise Calment, a French woman from Arles, lived to 122 years and 164 days. This lifespan remains the definition of human lifespan since her death in 1997.
In this regard, lifespan is an outlier—an extreme case of longevity. It is different from longevity, mean life span, average life span, life expectancy, individual lifespan, average age of death, average life expectancy and median age of death.
After the second World War, Max Klieber, a Swiss agricultural chemist, predicted that mass determines metabolism, and metabolism determines longevity. Larger animals tend to live longer. This theory has been elaborated in 2000 when a study that looked at nearly 4,100 longevity records of the highest documented age for a variety of fish, reptile, amphibian, bird, and mammalian species that included humans. There were four primary findings. First, longevity is positively correlated with body size between orders (e.g. the smaller rodents are shorter lived than the larger cetaceans) though not necessarily within orders—a biological grouping. As an example, longevity is not correlated with body size among seals and walruses. Second, animals that fly (i.e. birds and bats), or armored (turtles; armadillos) or live underground (moles; mole rats) tend to live longer than is predicted from body size alone. Third, there is great variance within species, so that lifespans vary by a factor of over 50 in mammals, herps and fish; and by over 15-fold in birds. Body size, metabolic rate, brain size all positively correlated with life span. Fourth, primates are long-lived mammals, the great apes (i.e. gorillas; chimpanzees) are long lived primates, and humans are extraordinarily long-lived great apes; human longevity exceeds nearly all other species both relatively and absolutely.
There is something uniquely human about great longevity, although it is not an exclusive characteristic of humans.
There are still some species that we have not yet observed a lifespan for. There are other species for whom we have not been able to observe mortality and therefore we do not have a lifespan for. There is a small jellyfish called turritopsis nutricula, that seems to regenerate itself from an adult back to an adolescent. A constant process of metamorphosis. These are also species that exhibit minimal aging. Kleiber’s Law was complicated by the work of Caleb Finch from the University of Southern California who—while researching aging among animals—found insignificant aging among rougheye rockfish (who can live up to 205 years), sturgeon (150 years for females), giant tortoise (152 years), bivalves and possibly lobsters. These included no observable age-related increases in mortality rate or decreases in reproduction rate after maturity, and no observable age-related decline in physiological capacity or disease resistance. Finch coined the term "negligible senescence" to describe very slow aging.
There have been three primary approaches to the study of lifespan; Genetic, Biological, and demographic using life expectancy and age of death. However, a new twist to lifespan studies emerged in a 2012 study by Kyung-Jin Min from the Inha University, and his Korean colleagues. These authors reported that during Chosun Dynasty between 14th to early 20th centuries Korean eunuchs lived 14 to 19 years longer than other (intact) men. Researchers were able to identify 81 eunuchs, who were castrated as boys, and determined that they lived to an average age of 70, significantly longer than other men of similar social status. Three of the eunuchs lived to 100. This is a centenarian rate that's far higher than would be expected today (one in 25,000.) Historically, but as recent as the 19th century, eunuchs were common across the world. Castrati boys—castrated beforepuberty—were among the most prized singers especially in catholic churches in Italy—the Sistine Chapel retained the last of the castrati singers—and Opera houses in Vienna. Elsewhere eunuchs were hired staff in harems and imperial palaces in Africa, China, Korea, Japan, and the rest of Asia and the Middle East. As well as in Europe and Russia.
In the 18th century there was a Christian sect called the Skoptzy, also known as the White Doves, whose male members—in order to attain their ideal of sanctity—subjected themselves to castration. They believed that the Messiah would not come until the Skoptsy numbered 144,000 (Rev. 14:1,4). Further East, in China, eunuchs played a more central role in government. Although in this context, castration was mostly apunishment, some subjected themselves to the procedure in order to gain employment. At the same time, during the Ottoman period, especially from the 16th century on, black eunuchs from Ethiopia or Sudan were in charge of the harem in the Ottoman court. Many of these boys were castrated at a monastery in Upper Egypt by Coptic priests. The practice was pervasive and endemic.
But the first time that eunuchs featured in longevity debates was with the observation by Serge Abrahamovitch Voronoff in the early 1900s. And it was not a positive observation. Voronoff—a French surgeon of Russian descent—worked at a hospital in Cairo from 1896 to 1910 where he had the opportunity to observe eunuchs. He noted their obesity, lack of body hair, and broad pelvises, as well as their flaccid muscles, lethargic movements, memory problems, and lowered intelligence. He concluded that the absence of testicles was responsible for aging and that their presence should prompt bone, muscle, nerve, and psychological development. He saw aging as the result of the lack of substance from the testicles and ovaries. This is all before we knew abouthormones. Voronoff gained fame for his technique of grafting monkey testicle tissue on to the scrotum of men to increase the lifespan. Voronoff and his predecessor and mentor Charles-Édouard Brown-Séquard—although ridiculed at the time—developed the field of endocrinology, the study of hormones. Voronoff observations was that castration had retarding effects. In 1999 Jean Wilson and Claus Roehrborn investigated the long-term effects of castration and concluded enlargement of the pituitary gland and decreased bone mineral density. There were also some reported growth of breasts in the Ottoman court eunuchs, which is also evident in photographs of Skoptzy men and Chinese eunuchs. Shrinkage of the prostate was common among eunuchs. However the authors could not resolve whether lifespan differed in their study. Such a study was done earlier in 1969, by James Hamilton and Gordon Mestler from the Department of Anatomy, State University of New York College of Medicine. In the turn of the 1900 it was common practice to castrate cognitively challenged children, a practice encouraged by the strong eugenics movement at that time. The study looked at mortality of patients in a mental institution with a population of 735 intact White males, 883 intact White females, and 297 White eunuchs. They reported that survival was significantly better in eunuchs than in intact males and females. This survival advantage started at age 25 years and continued throughout their life. The life expectancy for eunuchs was 69.3 years compared to 55.7 years in intact males. Males castrated at 8-14 years of age—before sexual maturation—were longer lived than males castrated at 20-39 years of age—after sexual maturation. Castration reduced the age of death by 0.28 years for every year of castration from age 39 and younger.
There are many changes that happen as a result of castration. The world was very different 600 years or even 100 years ago. In most cases it was a very violent world where men suffered early mortality through wars, famine, and petty violence. Eunuchs, because of their demeanor might have escaped that onslaught of violence. They might also have had more nurturing qualities that extended to looking after themselves better. We will never know.
What we observe in science tells us a very different story. Pragmatically we know that sex, and the activity surrounding sex, increases longevity. Howard Friedman in the Longevity Project longitudinal study provided our first glimpse into female orgasms and longevity. The study which was begun in 1921 by Lewis Terman of Stanford University, California looked at 1548 children with high intelligence born around 1910. Now in their nineties, the study morphed into a gerontological study. One of the interesting and pertinent findings was that women who had a higher frequency of orgasm tended to live longer than their less fulfilled sisters. No data on men was collected from this study. But a separate study in in the town of Caerphilly in south Wales, England, provided evidence for males as well. George Davey Smith from Department of Social Medicine, University of Bristol,, England, and his colleagues interviewed nearly 1,000 men about their sexual frequency, then followed up on their death records ten years later. The results determined that men who had two or more orgasms a week had died at a rate half that of the men who had orgasms less than once a month. And importantly there was a dose effect, where the more times these men had orgasms the longer they lived. These observations have been replicated in Sweden and in the USA for both male and female.

The most conclusive evidence on what promotes lifespan however comes from the masters of longevity themselves—centenarians. In the Blue Zones the cluster of centenarians teach us about the pragmatisms of living longer and sexual activity is a significant part of their life.

© USA Copyrighted 2015 Mario D. Garrett