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RECIPE FOR LONGEVITY

by

Jean E. Pierog R.N.,M.S. , NC

PROBLEM STATEMENT

 

We all age. Aging is a universal state of being rather than a disease. Webster defines "age" as "the length of time during which a being or thing has existed" (Webster, 1989). Because of its ubiquitous nature, I believe that most people would be very interested in learning about a nutritional program which could extend their life expectancy to the maximum lifespan and, at the very least, improve the quality of their functional years. Therefore, the focus of this research is to determine which nutritional and lifestyle factors will proactively contribute to a disease-free, disability-free, long life.

A second purpose of my research is to separate fact from fad. The anti-aging movement is afoot, and one must wade through medical breakthroughs, cosmetic industry claims, fitness formulas and all the nutritional guru promises in order to weed out the longevity practices which have merit. Besides the famous search for the Fountain of Youth by Ponce de Leon, seemingly all humans before him have toyed with life extension. The Han Emperor in the first century B.C. sought the advise of a Chinese alchemist to transform mercury into gold and then eat from utensils made of gold to achieve immortality. Even today, people in Japanese bathhouses will pay a premium to sit in a solid gold tub, hopeful that it may cure an illness or prolong life (Longevity, 2/95). Therefore, in order to establish myself as a credible practitioner of nutrition know how, I want to dispel the myths and present the legitimate and reproducible nutritional and lifestyle factors which can potentially maximize a healthy, productive life.

LIFE EXPECTANCY AND LIFESPAN

Today there are more and more people living to be centenarians in the United States. In 1986 there was one centenarian per 10,000 elderly (defined as over 65 years of age) and by the year 2080 that number is expected to be 250 per 10,000 (Rybash, et. al., 1991). The 1990 census reported 35,800 Americans over 100 years old and 28,000 of them were women. In addition, it is predicted by the Census Bureau that the number of Americans over 100 years old will more than double to 80,000 by the year 2000 (Parachin, 1994). In fact, the most rapidly growing segment of the population is the 85 and older group. Between 1960 and 1980, that group increased by over 141% (Rybash, et. al., 1991).

Although there are more centenarians today than ever before, and thus our life expectancy is gaining tremendous grounds, our potential lifespan has not changed. Life expectancy is the age at which an individual born into a particular cohort is expected to die, as a child born in 1900 had an average life expectancy of 48 years. If born today, your life expectancy would be 75 years for a man and 80 years for a woman. In this past century alone, the average life expectancy in the United States has increased by almost 40 years which is a greater gain than made during all of human history (Rybash, et. al., 1991). The most important contributing factors to this increase in life expectancy were improvements in public health and the discovery and use of antibiotics (Langer, 1995).

But how long can human beings live? Lifespan or "the maximum age that could be attained if an individual were able to avoid or be successfully treated for all illnesses and accidents" is generally agreed to be 110-120 years (Rybash, et. al., 1991). Interestingly, our potential lifespan has not changed in over one hundred thousand years, so the amazing increase in life expectancy does not reflect any reduction of the basic aging process itself (Walford, 1986). In fact, in Genesis 6:3, it states, "man...also is flesh:yet his days shall be an hundred and twenty years".

Walford (1986) writes that two persons have lived to 113 and one to 119 years. However, Georgakas (1995) states that Delina Filkins, 113, of New York is thus far the best documented centenarian (May 4, 1815-December 4, 1928). Currently, there is a woman living in England who is counting the minutes since she turned a documented 120 years (TV News, 1995). Many have claimed lifespans greater than 113 years and some up to 170 years, but Georgakas’ (1995) research has not borne these claims out.

Why, if life expectancy has increased so impressively, has not the human lifespan? Leonard Hayflick, professor of anatomy at the University of California, San Francisco, School of Medicine and a "dinosaur" specialist on aging, states that nature did not design us for great longevity. The goal is survival of the species which translates to getting offspring to sexual maturation and independence. Therefore, by age 30 we are coasting on our reserves (Longevity, 2/95). Hayflick states that our life expectancy would increase to about 91 (from 75) if cancer, heart disease and strokes were cured, but it would add no more than 3 years to our lifespan. Why? Because at around 100 years of age, all of our organs’ functional abilities have dramatically declined, so our only hope of an intervention is to first discover the cause of aging. Currently, our chances for living to our maximal lifespan, approximately 115 years, are 1 in 4 billion (Longevity, 2/95)!

PREDICTORS OF LONGEVITY

 

What will increase your odds of being the 1 in 4 billion who lives to actualize your lifespan potential? The Roman historian and philosopher, Lucius Auraeus Seneca (4 B.C.-A.D. 65), thought he knew: "It is not the rich and the great, not those who depend on medicine, who become old; but such as use much exercise, are exposed to fresh air, and whose food is plain and moderate, as farmers, gardeners, fishermen, laborers, soldiers; and such men as perhaps never employed their thoughts on the means which have been used to promote longevity. It is among these people, chiefly, that the most astonishing instances of it are observed. Sometimes in these situations, man still attains to the amazing age of 150 years, and upward" (Health Letter, 10/92).

Although Seneca’s belief of a 150 year old in Roman times was a definite exaggeration (life expectancy was 22 years!), his "formula" for the longest living persons was probably fairly accurate.

Several others have formulated profiles that constitute predictors of the longevous. Dr. G. M. Humphry, professor of surgery at Cambridge, examined 900 patients who were at least 90 years old and approximately 52 were centenarians. The 100 year olds consisted of 36 women and 16 men. The following data was compiled:

-The majority were light to moderate eaters and consumed very little meat.

-Most awakened early and enjoyed outdoor work.

-40 of the 52 drank alcohol.

-Few reported having had many illnesses.

-44 said they were excellent sleepers, most of them averaging over 8 hours a night.

-A large number stated they were from long lived families, but long lived was not well defined.

-12 were first born children

-Over 2/3 of the women had been married and raised large families.

-10 out of the 11 who were over 102 years old were female, the oldest

being 105 years.

(Source: Georgakas, 1995)

One of the most famous studies designed to isolate the best predictors of life expectancy was the Duke Longitudinal Study of Aging. Based on this study of 270 volunteer men and women between the ages of 60-94, Palmore (in Rybash, et. al., 1991), developed a mathematical model that helped predict direct and indirect variables that influence life expectancy. The strongest predictors of longevity were:

-Only the father’s age at death was significant in predicting a child’s

longevity.

-Intelligence predictors were significant.

-Three socioeconomic predictors, education, finances, and occupation

were positively correlated with longevity.

-The following activity factors were significant:

Locomotor activities (physical mobility)

Secondary activity (number of organizations the person was a member of, time spent reading, number of meetings attended, leisure activities)

Nongroup activity (daily hobbies)

-Three sexual relations indicators were significant, including the frequency

of intercourse per week, the past enjoyment of intercourse in younger years, and the current pleasure of intercourse.

-Tobacco use was a significant negative predictor.

-Work satisfaction, religious satisfaction, usefulness and happiness were

all positively correlated with a long life.

-Three health predictors were significantly linked to longevity:

Physical functions rating based on objective health indices, i.e. ECG, audiogram, physical exam, etc.

Self rating of the person’s own health status

Health Satisfaction Score based on agreement/disagreement with 6 statements

(Source: Palmore, 1982, in Rybash, et. al., 1991)

 

 

PHYSIOLOGICAL CHANGES AS WE AGE

 

The human body does talk back, especially as we age! Although many physiological changes occur gradually, they seem to be most noticeable to us at around age 50, primarily because of the hormonal changes. Fifty seems to most people to be the "beginning of the end". Some of the age accompanying changes include:

Hormonal: Sex hormones decline as does libido and the ability to reproduce by age 50. Men’s testosterone levels have been on the decline since age 30 and continue the downward trend until age 80-90. Impotence and libido decline are more common, often due to psychological factors, central nervous system changes, and decreased pelvic circulation due to atherosclerosis (Chase, 1995). Male menopause, however, is a discrete event.

An American woman’s reproductive capability comes to completion at the average age of 52. Menopause signals low estrogen levels, hot flashes, weight gain, decreased vaginal secretions and libido, as well as an increase in risk of heart disease and osteoporosis.

Immune: The thymus gland begins to deteriorate after the teenage years and is virtually gone by old age. This gland is responsible for the body’s defense system via T-lymphocyte education; as it shrinks the T cells decline in number and effectiveness.

B lymphocytes also decline and lose their ability to release antibodies and form clones. Additionally, the antibodies that do form are directed against the body’s own tissues, increasing the risk of autoimmune illnesses.

Skeletal: American women begin to lose bone mass at a rate of 1% a year after age 35. This rate of loss intensifies as menopause occurs, making women more susceptible to osteoporosis than men. Men start losing bone mass at about age 55 and usually lose 10-15% by the time they reach 70 (Mayo Health Letter, 6/91). In addition, there is degeneration and calcification on the articulating surfaces of our joints. Structural changes in collagen lead to increasing stiffness of the joints, ligaments and tendons.

Respiratory: Aerobic capacity diminishes and the ability of muscles to utilize oxygen declines about 1% a year, primarily as a result of sedentary living. The airways and support tissue harden, bronchi degenerate and the intercostal cartilage’s mobility and elasticity are reduced. These changes lead to a reduced vital capacity, reduced oxygen diffusing capacity, chest wall rigidity and a decrease in functional reserve capacity (Rybash,. et. al., 1991).

Muscular: Fat increases and muscle mass, including both the number and size of muscle fibers, decreases starting at age 30, becoming visibly obvious at age 50. We burn calories at a slower rate as a result of muscle mass decline. Strength declines and maximum grip strength slips to 75 lbs. from 100 lbs. by the mid 50’s. There is evidence that, at least in men, a natural reduced production of human growth hormone levels accelerates muscle loss (Harvard Health Letter, June, 1992). Range of motion and reduced speed of movement occurs. Body shapes shift, posture changes and height shrinks. The gait is affected by changes in the center of gravity, stride length and speed and the width of the stance (Rybash, et. al., 1991).

Cardiovascular: By age 50, there are elastic changes in the aorta and heart, so the heart muscle enlarges in order to pump blood through this less pliable network of arteries. Heart valves degenerate and calcify. The heart muscle itself is more irritable and its contractions are weaker. Heart muscle oxygen uptake is decreased, fibrosis occurs and there is an increase in vagal control. These changes contribute to blood pressure elevation, a decrease in maximum heart rate, a decrease in maximum coronary flow, and a diminished cardiac reserve (Rybash, et. al., 1991). Total blood cholesterol and low density lipid protein cholesterol increase.

Skin: Wrinkling increases from the loss of collagen and overgrowth of elastin (protein). Sun is a major culprit in skin damage. Hair begins to gray in people of European descent by age 50; usually a decade latter in African-Americans. Balding occurs in 50% of men and is evident by age 50 (Chase, 1995).

Mental, Vision, Hearing: Short term memory declines but long term memory remains intact. Also unaffected by time are cognition and character (personality). By age 70, nerve impulses travel 10-15% more slowly and our ability to react is slower (Mayo Health Letter, 6/91). Eyes are showing age related changes by age 40 when farsightedness sets in as the eye’s lens loses its elasticity and ability to accommodate nearby objects. Pupils are less responsive to light and dark, therefore poor night vision and more sensitivity to glare occur. Hearing loss, although a gradual, lifelong process, becomes more perceptible in the 50’s since high frequency sounds are more difficult to detect (Chase, 1995).

Nutrition Related Changes: (from Harvard Health Letter , 10/92;Rosenberg, et. al., 1989).

-Taste and smell: Taste buds and papilla decrease on the tongue. There is a decrease in taste and olfactory nerve endings. These may lead to a decrease in the palatability of foods, a loss of the ability to detect salt and sweet and therefore a lower food intake.

-Saliva: Saliva production decreases and may possibly lead to poorer carbohydrate breakdown.

-Esophageal function and swallowing is subject to disordered contractions. The muscular alimentary organs (esophagus, stomach, small intestine and colon) lose much tone with age. Therefore, food is channeled to the stomach at a slower rate and the stomach takes longer to process it.

-Gastric function: Our production of hydrochloric acid (HCL), intrinsic factor and pepsin declines in 20% of the population over age 60. This atrophic gastritis causes rapid emptying of liquids, an increase in the pH of the small bowel and bowel bacterial overgrowth. The results of these changes are that there is a decrease in the bioavailability of minerals (calcium), proteins and vitamins (vitamin D), a decreased absorption of vitamin B12 and folate, and an increase in bacterial folate synthesis to counteract malabsorption.

-Liver: The liver shrinks in size and blood flow and its ability to metabolize drugs is reduced. This may cause a decrease in albumin synthesis and drug doses may need to be adjusted. The gallbladder becomes sluggish in its release of bile into the small intestine, increasing the likelihood of gallstones.

In addition, the pancreas secretes slightly lower bicarbonate and enzymes and the intestines change very little. The intestinal microflora does have bacterial overgrowth if atrophic gastritis is present.

THEORIES OF AGING

 

If you want to become one of the wealthiest and most popular person in the world, discover the secret of aging. No one has the answer, but there are several theories. The theories fall into two classes of aging mechanisms, random damage or wear-and-tear versus genetically programmed obsolescence. Random damage aging is that which occurs in a sporadic fashion such as damage caused by environmental toxins, X-rays, free radicals, ultra-violet light, etc. Our bodies have repair mechanisms, but these decline with age or are otherwise imperfect. The planned obsolescence concept of aging involves aging clocks which produce a programmed sequence of changes and shutdowns to various body systems, resulting in physiological deterioration as time goes by. Examples of these aging clocks are menopause and male pattern baldness (Pearson & Shaw, 1982).

Although there are two camps on aging, neither one in and of itself is adequate to explain the aging process. In fact, most biological theories of aging include both wear-and-tear as well as genetic mechanisms as contributory to the aging process. The following are the most popular theories operating today, and fall under three broad categories: Cellular, Physiological and Macrobiological (Rybash, et. al., 1991).

CELLULAR THEORIES

 

These are theories that propose aging may be a result of malfunctions or processes that occur within the cells of the body.

Hayflick’s Limit: Prior to Leonard Hayflick’s pioneering research, scientists thought that human cells could live and proliferate forever if given the right nutrients and environment. In the early 1960’s, Hayflick examined the development of fibroblasts, connective tissue cells, in laboratory bottles. He found that they divided only 50 times; as the cells approached their 50th doubling, cell multiplication began to take longer. After about 50 population doublings the cells lived for a few days but finally died of a variety of causes. Hayflick had demonstrated that cells from a specific species can divide only a limited number of times, known as Hayflick’s limit (Moore, 1992). In addition, he showed that cells from older people divided fewer times and cells from embryos doubled the most. However, the cells of even very elderly do divide, implying that we rarely live to the end of our potential lifespan. Hayflick’s landmark experiment has been validated and reproduced many times.

Interestingly, some cells are immortal, including primitive bacterial cells, human germ cells (those that become the egg and sperm cells), and cancer cells. In fact, HeLa is the code name for some legendary cervical cancer cells which have been alive since 1952 and have undergone many more replications than human cells. When these were fused with normal mortal human cells, the immortal cancer cells became mortal (Moore, 1992). Hayflick, therefore, believes that the aging process is a direct function of the cellular machinery and the loss of the ability to divide is 1 of 200 different changes that occur in the aging cell.

Recent research is now looking at the tip of the chromosome called the telomere as the structure that may be the timekeeper of the cell. Whenever a cell divides, the telomeres are shaved down slightly. On average, the length of the telomeres of a 70 year old are much shorter than those of a child. It has been proposed that once the telomeres fall below a certain length, death will follow. Interestingly, immortal cancer cells produce an enzyme called telomerase which is normally quiescent in human cells but becomes activated in cancer cells and rebuilds the telomeres (Angier, 1992)!

Free Radical Theory: Dr. Denham Harman is the father of this theory which he proposed in the late 1950’s, and believes it to be a major cause not only of aging, but of other diseases such as cancer and cardiovascular disease. Free radicals are chemical components of cell metabolism which are missing one or two electrons from their outer shells, causing them to react with the electrons of other more stable molecules. As a result, the free radicals are involved in a chemical reaction that transforms both the fee radical as well as the otherwise stable molecule (Moore, 1992). Some free radicals are essential for normal metabolic reactions, but the body provides enzymes such as superoxide dismutase (SOD) and glutathione peroxidase to control these free radicals. The uncontrolled free radicals (those not controlled by enzymes and free radical scavengers such as vitamins C and E), can cause changes which include: 1) accumulative, damaging oxidative alteration in collagen, elastin, DNA and RNA; 2) breakdown of the large carbohydrate molecule that makes up mucous; 3) accumulation of age pigments via oxidative linkage involving lipids and proteins; 4) lipid membrane peroxidation; and 5) narrowing of small arteries and capillaries secondary to toxic peroxidation products of serum, blood vessel wall irritants and the suppression of the synthesis of prostacyclin (blood thinner) (Pearson & Shaw, 1982).

Cells themselves are packed with antioxidants such as vitamin E, vitamin C, vitamin A, beta carotene, SOD and glutathione peroxidase. This discovery of cellular antioxidants gave fuel to the free radical theory, and many proponents have suggested antioxidants as the "cure" to aging or at least preventing degenerative diseases. Dr. Harmon, in the 1960’s, actually fed lab rodents large amounts of antioxidants, but the mortality curve was not enhanced, although fewer premature deaths occurred (Moore, 1992). To date, after four decades of research, there is no proof that antioxidants can delay the aging process.

Mutation Theory: Aging, according to this theory, is caused by mutations in the DNA of the cells in the vital organs of the body. As the cells continue to divide, the mutations are passed on to new cells. As these mutated cells increase, the function of the vital organ is impeded, and disease and aging ensue. The causes of such genetic damage could be due to extrinsic factors such as environmental toxins, contaminants in the food, ultraviolet radiation exposure, etc. Intrinsic factors include errors in DNA replication or a breakdown in the DNA-RNA communication system (Rybash, et. al., 1991).

Genetic Switching Theory: According to this theory, certain genes will switch off and thereby cause aging. Since the genes are off, the DNA cannot be produced and the cell ages, then dies, and eventually the organ loses its function. Each of the body’s cells is genetically programmed with a biological aging clock (Rybash, et. al., 1991).

With respect to the genetic theory, there is evidence that some people may have senescence genes. Werner’s Syndrome affects about 1 in a million babies and there are currently 200 persons in the United States with this illness. Its hallmarks are early signs of advanced age when the person is only 20. By 40, they are near death if not already dead. Persons with Werner’s are susceptible to cancer, heart disease and osteoporosis...diseases of the elderly. Their cells only divide 10 or 20 times as opposed to the usual 50. Apparently 40-50 genes of these people are working overtime and some of these genes are unique to Werner’s victims. Apparently scientists in Japan have tracked the senescence genes to human chromosome # 1 (Newsweek, 1990).

Cross Link Theory: Cross linking is "the progressive formation of chemical bonds as bridges between large molecules such as proteins and nucleic acids" (Pearson & Shaw, 1982). Some controlled cross links are essential for life, but undesirable cross linking damage such as skin wrinkles and hardened arteries are not desirable. As one grows older, the body becomes stiff, less agile, and less elastic due to cross linking at the molecular level. This is due to collagen being "welded" together by cross- links. Causes of this cross link process include acetaldehyde (found in smog, cigarette smoke and alcohol when converted by the liver), free radicals and sun exposure. In addition, glucose may be a cause of cross linking, making proteins in and between our cells stick together. Cross linking is implicated in the natural process of aging such as the development of cataracts, lung damage and declining kidney function. In fact, diabetics do age quicker in all these areas and live about 1/3 shorter lives. Of interest is a new drug, aminoguanidine, which seems to act like flypaper and the proteins stick to it instead of to one another. The drug is currently under clinical investigation for diabetics, but is a very promising agent for prevention of cross linking (Newsweek, 1990). The body’s own cross link scavengers are the macrophages.

 

PHYSIOLOGIC THEORIES

 

These theories focus on the breakdown of physiological control mechanisms.

Autoimmune Theory: The immune system is at its peak in adolescence and gradually declines with age. As the immune system ages, along with the organism, it is less and less able to distinguish between foreign invading proteins and the body’s own normal, healthy cells. Why the body attacks itself is not clear; it may be due to the presence of a "death agent", accumulated cellular errors or other unknown factors (Georgakas, 1995). Evidence and support for this theory stems from the fact that many autoimmune diseases such as rheumatoid arthritis and adult onset diabetes occur as one grows older. It has also been shown that AIDS progresses more rapidly in adults over 40 years old.

Hormonal Theory: The glands of the endocrine system secrete hormones that travel throughout the body. The hormonal changes are controlled by the brain, particularly the pituitary gland and the hypothalamus. As we age, our endocrine system declines, though this is not well understood. Denckla (1974) states that the hypothalamus occasionally stimulates the pituitary gland to release antithyroid or "blocking" hormones that move in the blood cells throughout the body. These blocking hormones which are released after puberty, keep the body from uptaking thyroxine, the hormone that is requisite for normal cellular metabolism. The imbalances generated by the lack of thyroxine produce mutations, free radicals, toxins and autoimmunity which all contribute to aging (Rybash, et, al., 1991).

MACROBIOLOGICAL THEORY

This theory is concerned with a more general perspective of aging rather than the micro views above.

Homeostatic Imbalance Theory: This theory speaks to the body’s internal balance or homeostasis mechanisms. One’s internal environment is tightly controlled by the internal organs and feedback mechanisms of the neuroendocrine system. As children and young adults we have 4-10 times the functional capacity necessary to sustain life. These reserves enable us to restore homeostasis to the body during times of stress. There is a linear decline of these reserves beginning at age 30. Therefore, as the reserves decline, so does the body’s ability to maintain homeostasis and we die. After age 30, a person’s mortality rate doubles every eight years, probably due to the decline in organ function (Rybash, et. al., 1991).

Since there is no satisfactory explanation for aging, the treatment for aging must address symptoms rather that causes. However, if the causes could be determined, aging would be reduced to the category of a disease, and treatment would be aimed at eliminating the cause. Examining the above theories has implications for the Nutrition Consultant. If research on diet, supplements or lifestyle factors could be shown to reduce free radicals, prolong cell life, interfere with crosslinking, enhance immune function or stimulate the endocrine system, we could suggest a program that would hedge one’s bets against the disabilities of aging. In Part Two, a variety of longevity nutrition approaches are explored.

Copyright 1999 by Healthlinks.Net. All Rights Reserved, no portion of this article may be copied, reproduced or distributed without the written permission of the author and healthlinks.Net Ltd.


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