Life extension has been a goal of humans since long before Ponce de León’s search for the mythical fountain of youth. Since the early 1980s, a number of books advocating the use of vitamins, minerals, hormones, drugs, and other compounds to extend life have made the best-seller lists. Many—though not all—of the recommendations to slow down the aging process do make sense and appear to be scientifically sound. This chapter will focus on such recommendations.
First, some definitions: life expectancy refers to the average number of years of life a person in a given population is expected to live, while life span refers to the maximal age obtainable by a member of a species. Health spanrefers to the number of years of healthy life—our true goal. After all, why live longer if you are debilitated, live in a nursing home, and don’t recognize your children?
On the surface it appears that in the United States, impressive gains in extending life have been made since the beginning of the 20th century. In 1900 the average life expectancy was 45 years. Now it is 75.6 years for men and 80.8 years for women.1 However, if we examine what was really responsible for this increase in life expectancy, it is almost entirely due to decreased infant mortality. If infant mortality is taken out of the calculations, life expectancy really improved only a maximum of six years during this time. In adults reaching 50 years of age, life expectancy has increased a few years at best.
The primary strategy for increasing life expectancy involves reducing causes of premature death. Obesity, smoking, and alcohol abuse contribute greatly to premature death and in many cases are the underlying contributors to the majority of the top 10 causes of death. As detrimental as smoking is, obesity has become equal to or greater than smoking as the most important risk factor for premature death as well as shortened health span.2
Top 10 Causes of Death in 20091
NUMBER OF DEATHS
1. Heart disease
3. Chronic lung disease
6. Alzheimer’s disease
8. Influenza and pneumonia
9. Kidney failure
Longevity: Myths and Reality
Myths still circulate about certain groups of people (the Hunzas of Pakistan, Georgians in the Caucasus region of Europe, and inhabitants of Andean villages in Ecuador, for example) who are reported to live to an extremely old age, between 125 and 150 years. However, detailed scientific reports have refuted these claims.3–5
For example, one group of investigators studying the people of Vilcabamba, Ecuador, to determine whether the degree of bone loss that occurred during aging was different in that population compared with the U.S. population, made a revealing discovery.3 They did an initial survey and went back for a follow-up five years later, at which time a number of individuals reported being 10 years older than they had been during the first survey. From studying existing birth records it became obvious that there was considerable exaggeration of age. In this society as well as in the other societies associated with longevity, social standing increases with increasing age.
In the country of Georgia, in the Caucasus region of Europe, it has been demonstrated that the majority of reported centenarians (people older than 100 years) are actually in their 70s and 80s; they just look as if they are 140 years old as a result of their arduous existence.4
The current official world record of longevity is 122 years, reached by a Frenchwoman, Jeanne Louise Calment. Born on February 21, 1875, she lived through France’s Third and Fourth Republics, and into its Fifth. She was 14 when the Eiffel Tower was completed in 1889. She died on August 28, 1997. In her later years, she lived mostly off the income from her apartment, which she sold cheaply in 1966 to a lawyer, André-François Raffray. He had agreed to make monthly payments on the apartment in exchange for taking possession when she died, but he never got to move in. He died at the age of 77, a year before Jeanne Calment; his family was required to keep making the payments.
What Causes Aging?
Answers to the question “What causes aging?” are coming rapidly as a result of research in gerontology, the science of aging. There are many interesting theories of aging; however, only the most significant will be briefly discussed below. There are basically two types of aging theories: programmed theories and damage theories. Programmed theories believe there is some sort of genetic clock ticking away that determines when old age sets in, while damage theories believe aging is a result of cumulative damage to cells and genetic materials. Our opinion is that both are valid. Arguments like this seem to repeat themselves in science—a case in point is the nature of light, which functions as both a particle and a wave. Well, human aging is the result of both programmed cell life and cellular damage.
The Hayflick Limit
In 1912 in a laboratory at the Rockefeller Institute, Dr. Alexis Carrel, one of the foremost biologists of his time, began an experiment that would last for more than 34 years. Dr. Carrel set out to find out how long he could keep chicken fibroblasts dividing. Fibroblasts are connective tissue cells that manufacture collagen. Fed with a special broth containing an extract of chick embryo, the chicken fibroblasts grew quite well in flasks. They would divide and form new cells, with the excess cells being periodically discarded by the researchers. The tissue culture system kept dividing for 34 years, until two years after the death of Dr. Carrel, when his coworkers finally discarded the culture. Dr. Carrel’s work prompted the idea that cells are inherently immortal if given an ideal environment.6
This idea was not discarded until the early 1960s, when Dr. Leonard Hayflick observed that human fibroblasts in tissue culture wouldn’t divide more than about 50 times.7 Why the discrepancy? It appears Dr. Carrel had inadvertently added new “fresh” fibroblasts contained in the embryo broth used as nutrition for the tissue culture. New cells had repeatedly been added to the tissue cultures.
Hayflick found that if he froze cells in culture after 20 divisions, they would “remember” that they had 30 doublings left when they were thawed and refed. Fifty cell divisions or doublings are called the Hayflick limit. As fibroblasts approach 50 divisions, they begin looking old. They become larger and accumulate an increased amount of lipofuscin, the yellow-brown pigment responsible for age spots—those brownish spots that appear on the skin as the result of cellular debris and lipofuscin clumping together.
The Telomere-Shortening Theory
Based on the Hayflick limit, experts on aging theorized there is a genetic clock ticking away within each cell that determines when old age sets in. The latest, and most likely, programmed theory of aging is the telomere shortening theory. Telomeres are the endcap segments of DNA (our genetic material). The concept that shortening of the telomere with each cellular replication leads to aging was first proposed by a Russian scientist, Alexaie Olovnikov, in 1971, and also by James Watson (the codiscoverer of the structure of DNA) in 1972. But it wasn’t until 1990 that the telomere theory of aging really began to be accepted.8 New evidence supports the notion that telomeres are, in fact, the “clocks of aging.”
Each time a cell replicates, a small piece of DNA is taken off the end of each chromosome. At conception, telomeres are about 10,000 base pairs long. By birth they will have already been shortened by 5,000 base pairs. Compared with the rest of the chromosome, the telomere is small. An average chromosome is 130 million base pairs long, or about 25,000 times as long as the telomere at birth. Every time a body cell replicates, the telomere gets shorter. The shorter the telomere gets, the more it affects gene expression. The result is cellular aging.
In addition to serving as a clock for aging, the telomere is also involved in protecting the end of the chromosome from damage, allowing for complete replication of the chromosome, controlling gene expression, and aiding in the organization of the chromosome. The telomere determines not only the aging of the cell but our risk for cancer, Alzheimer’s disease, and other degenerative diseases.9
Perhaps the greatest support for the telomere theory of aging is Hutchinson-Gilford syndrome. You most likely have never heard of this condition, but you are likely to have heard of its common name, progeria. This syndrome was first described in 1886. Children with progeria are extraordinarily rare, 1 in 8 million births, but if you have ever seen one, you will never forget it. The child typically shows symptoms of aging during the first year of life and generally dies of “old age” by the age of 13. Another rare syndrome known as Werner’s syndrome is less severe—typically symptoms begin to manifest themselves in the early 20s and death usually occurs by age 50.
Much has been learned from children with progeria. If progeria is a reflection of accelerated aging—and few would argue that it isn’t—it may hold the key to understanding how to truly extend life expectancy and even life span. Researchers have been working intensively to find the mechanism responsible for the accelerated aging of progeria. The answer appears to be telomere shortening. Compared with normal children, at birth children with progeria have telomeres like those of a 90-year-old. In Werner’s syndrome, telomeres are of normal length at birth but appear to shorten faster than normal.
The key to extending maximal human life span will ultimately involve preserving or restoring telomere length (as well as decreasing chromosomal damage, cellular oxidation, and many other factors). Several measures have already been shown to achieve this goal. Simply adopting a comprehensive dietary and lifestyle change consistent with good health has been shown to preserve telomere length.10 Physical exercise has been shown to be associated with preserving telomere length.11 And meditation has also been shown to preserve telomere length by reducing the negative effects of stress.12 Higher vitamin D levels are associated with longer telomeres (as discussed in more detail below).13 Last, strategies that reduce inflammation are very important in reducing the rate pf telomere shortening.14 Levels of inflammatory markers in the blood correlate with telomere shortening. For more information on natural ways to reduce these inflammatory markers, see the chapter “Silent Inflammation.”
The Free Radical Theory
The best damage theory is the free radical theory of aging. This theory contends that damage caused by free radicals contributes to aging and age-associated disease.15,16 Free radicals are defined as highly reactive molecules that can bind to and destroy cellular compounds. Free radicals may be derived from our environment (sunlight, X-rays, radiation, chemicals) or from ingested foods or drinks, or they may be produced within our bodies during chemical reactions. The majority of free radicals present within the body are actually produced within the body. However, exposure to environmental and dietary free radicals greatly increases the free radical load of the body. In addition to aging, free radicals have been linked to virtually every disease associated with aging, including atherosclerosis, cancer, Alzheimer’s disease, cataracts, osteoarthritis, and immune deficiency.
Telomeres appear to be especially susceptible to oxidative damage, so telomere shortening may actually fit very nicely as the underlying result of cumulative free radical damage.
Cigarette smoking is a good example of how to increase free radical load. Many of the deleterious health effects of smoking are related to the inhalation of extremely high levels of free radicals. Other external sources of free radicals include radiation; air pollutants; pesticides; anesthetics; aromatic hydrocarbons (petroleum-based products); fried, barbecued, and charbroiled foods; alcohol; coffee; and solvents such as formaldehyde, toluene, and benzene, found in cleaning fluids, paints, gasoline and furniture polish. Obviously, reduced exposure to these sources of free radicals is recommended in a life extension program.
Most free radicals in the body are toxic oxygen-containing molecules. It is ironic that the oxygen molecule is the major source of free radical damage in our bodies. Oxygen sustains our lives in one sense, yet in another it is responsible for much of the destruction and aging of the cells of our bodies. Similar to the way oxygen reacts with iron to form rust, oxygen, in its toxic state, is able to oxidize molecules in our bodies. As you probably already know, compounds that prevent this type of damage are referred to as antioxidants.
In addition to damaging cell membranes and proteins, free radical damage extends to our DNA. The genetic material is responsible for transmitting the characteristics of one generation of cells to another. Damage to the DNA structure results in mutations (expression of different genetic material), or the cells simply die or are destroyed. DNA is constantly bombarded by free radicals and other compounds that can cause damage. Fortunately, the body has enzymes that (mostly) repair damaged DNA. The differences in life spans among mammals are largely a result of an animal’s or human’s ability to repair damaged DNA. For example, the maximal life span of a human (about 120 years) is more than twice as long as that of a chimpanzee (about 50 years) because our DNA repair is much more effective.17
Research has shown that old cells are not able to repair DNA as rapidly as young cells. It appears that nature has set the rate of DNA repair at less than the rate of damage, so that animals can accumulate mutations and evolve. If repair were perfect, there would be no evolutionary processes.
Glycosylation and Aging
Another damage theory that deserves mentioning is the glycosylation theory. In a nutshell, this theory involves the continued attachment of blood sugar (glucose) molecules to cellular proteins until finally the protein ceases to function properly. For example, cholesterol-carrying proteins that have been glycosylated do not bind to receptors on liver cells that halt the manufacture of cholesterol. As a result, too much cholesterol is manufactured. Excessive glycosylation and the formation of what are referred to as advanced glycation end products (AGEs) have many adverse effects: inactivation of enzymes, damaging structural and regulatory proteins, impaired immune function, and increased likelihood of autoimmune diseases. Like free radical damage, AGEs are associated with many chronic degenerative diseases.18Diets that promote glycosylation and poor glucose control are also linked to telomere shortening.
Obviously we want to avoid excessive glycosylation. This can be done by keeping blood sugar levels under control by consuming a low-glycemic diet (and, if needed, using special nutritional factors such as PolyGlycopleX, alpha-lipoic acid, and others). For more information, see the chapter “Diabetes.”
Extending Life Span
Can life span be increased and the aging process slowed? The answer is definitely yes. However, we want to discourage readers from seeking a single “magic bullet” to halt the aging process. Instead we want you to realize that the best steps that can be taken to slow down the aging process and reduce your risk of the major causes of premature death is to adopt the guidelines described in Section II, “The Four Cornerstones of Good Health”:
• A positive mental attitude
• A health-promoting lifestyle
• A health-promoting diet
• Supplementary measures
Severe restriction of calories is a consistent and reproducible way of dramatically increasing life span in laboratory rats, mice, and primates.19 However, it is not known if caloric restriction has the same value for humans. From population data accumulated by insurance companies and others, the following conclusion can be made: individuals who are either overweight or severely underweight (the latter condition is typically due to severe disease, such as end-stage cancer) have the shortest life span, while those individuals whose weight is just below the average weight for height have the longest life span.
As stated in the chapter “The Healing Power Within,” the better shape you are in physically, the greater your odds of enjoying a healthier and longer life. Most studies have showed that individuals who are not physically fit have an eightfold greater risk of having a heart attack or stroke than do physically fit individuals. Researchers have estimated that for every hour of exercise, there is a two-hour increase in longevity. That is quite a return on an investment.
Maintaining muscle mass must be a major goal in any life extension plan. Muscle mass increases in childhood and peaks during the late teens through the mid- to late 20s. After that there starts a decline in muscle mass that is rather slow but unfortunately very consistent. From 25 to 50 the decline in muscle mass is roughly 10%. In our 50s the rate of decline accelerates slightly, but the real decline usually begins at 60. By the time people reach the age of 80 their muscle mass is a little more than half of what it was in their 20s.
Sarcopenia is the term for degenerative loss of skeletal muscle mass and strength as we age. Sarcopenia is to our muscle mass what osteoporosis is to our bones. The degree of sarcopenia as we age is a predictor of mortality and disability.20 It is linked not just to a significantly shorter life expectancy but also to decreased vitality, poor balance, slower gait speed, more falls, and increased fractures. In the prevention of osteoporosis, we want to build bone while we are young to help us preserve it longer through the aging process; the same is true for muscle tissue. And just as it is important to engage in dietary, lifestyle, and exercise strategies to fight osteoporosis in our later years, we must do the same to fight sarcopenia. You must build muscle to maintain your health.21
Interestingly, the same dietary factors linked to accelerated aging are linked to sarcopenia, while the dietary practices associated with good health are associated with protection against sarcopenia. While diet is unquestionably critical, for most people perhaps the most important step to preventing sarcopenia is to engage in a regular strength training program—that is, to lift weights or perform resistance exercises.22The benefits of strength training are vast, particularly for women and for people over 50. In addition to helping burn more fat, a larger muscle mass is associated with a healthier heart, improved joint function, relief from arthritis pain, better antioxidant protection, better blood sugar control, and higher self-esteem. While many women do not strength-train because they fear gaining weight, just the opposite occurs: building muscle mass actually helps to more effectively burn calories.
Dietary protein is also essential in supporting muscle growth and fighting sarcopenia, especially when combined with exercise.22 The best choice for protein supplementation is whey. Whey protein has the highest biological value of all proteins. Biological value is used to rate protein based on how much of the protein consumed is actually absorbed, retained, and used in the body. One of the reasons the biological value of whey protein is so high is that it has the highest concentrations of glutamine and branched-chain amino acids found in nature. These amino acids are critical to cellular health, muscle growth, and protein synthesis. Whey protein is also high in cysteine, which promotes the synthesis of glutathione—which, as we discuss in the chapter “Detoxification and Internal Cleansing,” plays a major role in helping us get rid of toxins.
Although the most popular use of whey protein is by bodybuilders and athletes looking to increase their protein intake, whey protein is also used to support recovery from surgery, to prevent the wasting syndrome seen with AIDS, and to offset some of the negative effects of radiation therapy and chemotherapy. This increased efficiency of protein use is particularly important in battling sarcopenia. Whey protein supplementation has also been demonstrated in clinical trials to produce greater strength and muscle mass gains in elderly subjects involved in a weight training program, compared with a placebo as well as other types of protein.23
The typical recommendation to boost protein levels is 25 to 50 g per day, though for severe sarcopenia the dosage recommendation is 1 g/kg.
A Comprehensive Nutritional Approach to Preventing Sarcopenia
• Reduce the amount of saturated fat, trans-fatty acids, cholesterol, and total fat in the diet by eating only lean sources of protein and more plant foods.
• Increase intake of omega-3 oils by eating flaxseed oil, walnuts, and cold-water fish such as salmon. Eat at least two, but no more than three, servings of fish per week.
• Increase the intake of monounsaturated fats and the amino acid arginine by eating regular but moderate amounts of nuts and seeds, such as almonds, Brazil nuts, coconut, hazelnuts, macadamia nuts, pecans, pine nuts, pistachios, and sesame and sunflower seeds, and by using a monounsaturated oil, such as olive, macadamia, or canola oil, for cooking purposes.
• Eat five or more servings per day of a combination of vegetables and fruits, especially green, orange, and yellow vegetables, dark-colored berries, and citrus fruits.
• Limit the intake of refined carbohydrates. Sugar and other refined carbohydrates lead to the development of insulin resistance, which in turn is associated with increased silent inflammation, a major contributor to sarcopenia.
• Utilize the benefits of whey protein by taking 25 to 50 g whey protein per day.
Glutathione- and Sulfur-Containing Amino Acids
Whey protein is also a rich source of the sulfur-containing amino acids methionine and cysteine, which are important components of a life extension plan. Typically, as people age the content of these amino acids in the body decreases.24 Since research has shown that supplementing the diets of mice and guinea pigs with cysteine increases life span considerably, it has been suggested that maintaining optimal levels of methionine and cysteine may promote longevity in humans.
The mechanism may be because methionine and cysteine levels are a major determinant in the concentration of sulfur-containing compounds, such as glutathione, within cells. Glutathione assumes a critical role in the body’s defense against a variety of injurious compounds, combining directly with these toxic substances to aid in their elimination. When increased levels of toxic compounds or free radicals are present, the body needs higher levels of glutathione, and hence methionine and cysteine. Good dietary sources are whey protein, fish, eggs, brewer’s yeast, garlic, onions, and nuts.
The free radical theory of aging really lends itself to nutritional intervention by antioxidant compounds, which act as free radical “scavengers.” The body has several enzymes that prevent the damage induced by specific types of free radicals. For example, superoxide dismutase prevents the damage caused by the toxic oxygen molecule known as superoxide. Catalase and glutathione peroxidase are two other antioxidant enzymes found in the human body.
The level of antioxidant enzymes and the level of dietary antioxidants determine the life span of mammals. Human beings live longer than chimpanzees, cats, dogs, and many other mammals because we have a greater quantity of antioxidants within our cells.25,26 Some strains of mice live longer than other strains because they have higher levels of antioxidant enzymes. Presumably, the reason some people outlive others is that they have higher levels of antioxidants in their cells. This line of thinking is largely why many cutting-edge physicians recommend increasing the level of antioxidant mechanisms within cells.
A significant number of studies have clearly demonstrated that diets rich in antioxidants can definitely increase life expectancy. In addition, diets rich in antioxidants reduce the risk for cancer, heart disease, and many other diseases linked to premature death.
Dietary antioxidants of extreme significance in life extension include vitamins C and E, selenium, beta-carotene, flavonoids, and sulfur-containing amino acids. Not surprisingly, these same nutrients are also of great significance in cancer prevention, as aging and cancer share many mechanisms.
An important class of dietary antioxidants for longevity is the carotenes, the most widespread group of naturally occurring plant pigments. For many people (physicians included) the term carotene is synonymous with provitamin A, but only 30 to 50 of the more than 400 carotenoids that have been identified are believed to have vitamin A activity.
Considerable evidence now demonstrates that carotenes do much more than just serve as a precursor to vitamin A. For example, carotenes have potent antioxidant effects. Although research has primarily focused on beta-carotene, other carotenes such as lycopene, lutein, and astaxanthin are more potent in their antioxidant activity and are deposited in tissues to a greater degree. It should also be kept in mind that while research tends to focus on beta-carotene intake, eating a diet rich in beta-carotene means that you are also getting many other carotenes.
Concentration of Carotenoids and Maximum Life-span Potential
The Influence of Carotene Content on Life Span Potential
It appears that tissue carotenoid content is one of the most significant factors in determining life span in mammals, including humans.26 Since tissue carotenoids appear to be the most significant factor in determining a species’ maximal life span potential, it only seems logical that individuals with the optimal level of carotenoids in their tissues would be the ones that would live the longest.
Consumption of foods rich in carotenes (green leafy vegetables, pumpkin, sweet potatoes, carrots, etc.) and supplementation with palm oil carotene complex, carotene complexes from algae (as opposed to isolated, synthetic beta-carotene), lycopene, lutein, or astaxanthin are the best methods of increasing tissue carotenoid levels. High carotene intake may also offer significant benefit to the immune system—the thymus gland is largely composed of epithelial cells, and carotenes concentrated in those cells are able to significantly reduce the shrinkage the thymus gland undergoes during normal aging and stress. In addition, studies have shown that thymus-gland-mediated immune functions could be improved with carotene supplementation (see the chapter “Immune System Support”).
Another group of plant pigments with remarkable protection against free radical damage is the flavonoids. These compounds are largely responsible for the colors of fruits and flowers. However, these compounds serve other functions in plant metabolism besides contributing to the plants’ aesthetic quality. In plants, flavonoids serve as protectors against environmental stress. In humans, flavonoids appear to function as biological response modifiers. That is, they modify the body’s reaction to other compounds, such as allergens, viruses, and carcinogens, as evidenced by flavonoids’ anti-inflammatory, anti-allergenic, antiviral, and anticancer properties. Flavonoid molecules are also quite unusual in their antioxidant and free radical scavenging activity, in that they are active against a wide variety of oxidants and free radicals.
The best way to ensure an adequate intake of flavonoids is to eat a varied diet rich in colorful fruits and vegetables. The richest dietary sources of flavonoids include citrus fruits, berries, onions, parsley, legumes, green tea, and red wine. As far as flavonoid supplements go, the best choices are flavonoid-rich extracts, particularly procyanidolic oligomers (PCOs) such as grape seed and pine bark.27,28 Green tea and Ginkgo biloba extracts also offer significant benefits in promoting longevity.
While there is significant overlap among these flavonoid-rich extracts, Ginkgo biloba deserves some special mention. In herbal medicine, for centuries it was believed that plants were signed by the Creator with some visible or other clue that would indicate their therapeutic use. This concept is commonly referred to as the “doctrine of signatures.” Ginkgo’s signature is its long life and resistance to the environment. Ginkgo biloba is the world’s oldest living tree species. The sole surviving species of the family Ginkgoaceae, the ginkgo tree can be traced back more than 200 million years to the fossils of the Permian period and for this reason is often referred to as a “living fossil.”
Once common in North America and Europe, the ginkgo was almost destroyed during the Ice Age in all regions of the world except China, where it is has long been cultivated as a sacred tree. The ginkgo tree was brought to America in 1784 to the garden of William Hamilton near Philadelphia. The ginkgo is now planted throughout much of the United States as an ornamental tree, as it will grow where other trees quickly die. Ginkgo is the tree most resistant to insects, disease, and pollution. As a result, it is frequently planted along streets in cities.
Although the notion of a doctrine of signatures is fanciful, the bottom line is that Ginkgo biloba extract can be very useful in increasing the quality of life in the elderly. Many symptoms common in the elderly are a result of insufficient blood and oxygen supply. Ginkgo biloba extract has demonstrated beneficial effects in improving blood and oxygen supply to the brain and as a result may help improve a number of common symptoms of aging, including short-term memory loss, dizziness, headache, ringing in the ears, hearing loss, and depression.29,30
Resveratrol is a plant compound similar to flavonoids. It is found in low levels in the skin of red grapes, red wine, cocoa powder, baking chocolate, dark chocolate, peanuts, and the skin of mulberries. Red wine is perhaps the most widely recognized source of resveratrol; however, red wine contains only 1 mg per glass. Most resveratrol supplements use Japanese knotweed (Polygonum cuspidatum) as the source. Resveratrol occurs naturally in two forms: cis-resveratrol and trans-resveratrol. Trans-resveratrol is much more bioactive and clinically beneficial than cis-resveratrol.
Resveratrol has received a lot of attention as a longevity aid, but the scientific basis for this relies on test tube and animal studies—there are only a few published human studies at this time, and many questions remain to be answered.31,32 We do know that resveratrol activates an enzyme, sirtuin 1, that plays an important role in the regulation of cellular life span; it also promotes improved insulin sensitivity. The effects of resveratrol in animal studies are very similar to the benefits noted with calorie restriction, but are obtained without actually reducing calorie intake. Its longevity-promoting effects have been demonstrated in yeast, fish, and mice but have not yet been properly assessed in humans. At this time we prefer to recommend less expensive and more substantiated measures, such as ensuring optimal vitamin D levels (discussed below).
The list of the benefits of vitamin D supplementation is growing at a rapid pace. Perhaps the greatest benefit may be in extending life. An analysis of studies of vitamin D supplementation showed that participants who took vitamin D supplements had a 7% lower risk of death compared with those who did not.33 Of course, this result is not surprising. It is now known that virtually every cell in our body has receptors for vitamin D. It has been shown to protect against certain cancers (particularly breast and prostate), autoimmune diseases such as multiple sclerosis and type 1 diabetes, and heart disease.34
A 2007 study added another major benefit for vitamin D and also provides an explanation for its longevity-promoting effects: vitamin D may slow aging by increasing the length of telomeres.35 In the study, scientists examined the effects of vitamin D on the length of telomeres in white blood cells of 2,160 women ages 18 to 79. The higher the vitamin D levels, the longer the telomere length. In terms of the effect on aging, there was a five-year difference in telomere length in those with the highest levels of vitamin D compared with those with the lowest levels. Obesity, smoking, and lack of physical activity can shorten the telomere length, but the researchers found that increasing vitamin D levels overcame these effects. What this five-year difference means is that a 70-year-old woman with higher vitamin D levels would have a biological age of 65.
The primary role of the adrenal hormone dehydroepiandrosterone (DHEA) is as a precursor for all other steroid hormones in the human body, including sex hormones and corticosteroids. Because DHEA levels tend to decline with aging, it has been postulated that raising DHEA through supplementation may offer some protection against the effects of aging. In fact, the benefits of DHEA supplementation may extend well beyond an antiaging effect. Over the last decade a number of studies have demonstrated that declining levels of DHEA are linked to such conditions as diabetes, obesity, elevated cholesterol levels, heart disease, arthritis, and autoimmune diseases. In addition, DHEA shows promise in enhancing memory and improving mental function in the elderly as well as increasing muscle strength and lean body mass, improving immune function, and enhancing quality of life in aging men and women.36–38It also has been shown to improve insulin sensitivity. In a two-year study, 57 men and 68 women ages 65 to 75 were randomly assigned to take 50 mg DHEA or a placebo once per day. Year one was a randomized, double-blind trial. Year two was an open-label continuation. DHEA replacement improved insulin sensitivity, reduced plasma triglycerides, and lowered inflammatory markers (cytokines IL6 and TNFα).39
Although DHEA may prove useful in maintaining vim and vigor, we think it is not likely to significantly increase a person’s life span. While some strains of rats live longer when taking DHEA, others do not. But probably the biggest argument against DHEA as something that will dramatically extend a healthy person’s life is the observation that DHEA levels are normal in children with progeria. Surely if DHEA were a significant factor in aging, levels would be low in such children.
Nonetheless, although DHEA probably will not extend a person’s life span, it will often improve the health span. Our opinion is that DHEA offers significant benefits when used appropriately. One of the concerns that we have with DHEA is that it is not like vitamin C or many other nutrients that have virtually no toxicity. DHEA is a hormone, and there is relatively little information on its long-term safety. It is safe if used appropriately, but it is a big gamble if abused.
For men ages 40 to 50, we recommend DHEA for reduced libido, fatigue, diabetes, and extended high levels of stress. We suggest basing the dosage on blood levels of DHEA and testosterone; typically, the dosage will range from 15 to 25 mg per day. For women who have not yet passed through menopause, we do not recommend DHEA unless there is confirmation that their DHEA levels are in fact low. The reason is that as many women approach menopause there is actually a rise in DHEA levels. Taking extra DHEA may lead to acne and increased facial hair. After menopause we recommend using DHEA with caution and in low dosages ranging from 5 to 15 mg unless the woman has an autoimmune disease or diabetes. For men over 50, again we recommend using blood or saliva measurements to determine the dosage. For men desiring to increase their libido, improve their sense of well-being, and feel younger, our goal has been to raise their testosterone and DHEA levels to those of men in their early 20s. Typically, we have found the dosage required to achieve this goal is between 25 and 50 mg. As men and women reach their 70s, they may require higher levels, but until more is known about DHEA we would rather err on the side of being conservative.
Melatonin (not to be confused with melanin, the compound responsible for producing skin pigment) is a hormone manufactured from serotonin and secreted by the pineal gland. The pineal gland, a small pea-sized gland at the base of the brain, has been a source of curiosity since antiquity. The ancient Greeks considered the pineal gland the seat of the soul, a concept that was extended by the philosopher Descartes. In the 17th and 18th centuries physicians associated “madness” with the pineal gland. Physicians in the early 1900s believed the pineal gland was somehow involved with the endocrine system. The identification of melatonin in 1958 provided the first solid scientific evidence of an essential role for the pineal gland. It is now thought that the sole function of the pineal gland is to manufacture and secrete melatonin.
Melatonin is critically involved in the synchronization of hormone secretion. The natural biorhythm of hormone secretion is referred to as the circadian rhythm. The human body is governed by an internal clock that signals the secretion of various hormones at different times to regulate body functions. Melatonin plays a key role as the biological timekeeper of hormone secretion. Melatonin also helps control periods of sleepiness and wakefulness. Release of melatonin is stimulated by darkness and suppressed by light.
In addition to its role in synchronizing hormone secretion, melatonin has shown antioxidant and longevity-promoting effects in animal studies.40 For example, studies of rats showed that melatonin supplementation led to longer lives (31 months vs. 25 months). However, the clinical significance of melatonin’s antioxidant effects has not been fully determined in humans. What is known is that melatonin is very important in initiating a good night’s sleep, and this alone may have profound effects on life expectancy.40
Inadequate or poor-quality sleep accelerates the aging process, especially in the brain.41 With age, the percentage of deep slow-wave sleep has been shown to decrease, and interrupted sleep is extremely common. Poor sleep quality at any age triggers the stress response and leads to an increase in inflammation, but it is especially a problem as we get older. A number of lifestyle interventions, such as taking short daytime naps, maintaining a routine, and using bright light therapy in the morning, as well as supplemental interventions, have been found to increase deep slow-wave sleep, improve sleep quality, and prolong overall sleep time.42,43 For more information, see the chapter “Insomnia.”
• If infant mortality is taken out of the calculations, life expectancy really improved a maximum of only six years during the past century, while the burden of degenerative disease has skyrocketed out of proportion to the increase in longevity.
• Based on confirmed records, the oldest person lived to an age of 122 years 164 days.
• Increasing life expectancy involves reducing causes of premature death.
• The real goal is improving health span, not just life span.
• The latest, and most likely, programmed theory of aging is the telomere shortening theory.
• Telomeres, the end cap of our DNA molecules, are the “clocks of aging.”
• Free radical damage causes, and antioxidant nutrients prevent, cellular aging.
• Individuals who are either overweight or severely underweight have the shortest life span, while those individuals whose weight is just below the average weight for height have the longest life span.
• Researchers have estimated that for every hour of exercise, there is a two-hour increase in longevity.
• Maintaining muscle mass must be a major goal in any life extension plan.
• The level of antioxidant enzymes and the level of dietary antioxidants determine the life span of mammals.
• Ginkgo biloba extract has demonstrated beneficial effects in improving many symptoms associated with aging.
• Resveratrol has received a lot of attention as a longevity aid, but its scientific basis relies on test tube and animal studies—there are only a few published human studies at this time, and many questions remain to be answered.
• Vitamin D may slow aging by increasing the length of telomeres.
• Obesity, smoking, and lack of physical activity can shorten telomere length, but researchers have found that increasing vitamin D levels overcame these effects.
• Because DHEA levels tend to decline with aging, it has been postulated that raising DHEA through supplementation may offer some protection against the effects of aging
• Melatonin is not likely to extend life in humans based solely on its antioxidant effects; its benefits may be related to improved sleep quality.
The best way to ensure a long, healthy, high-quality life is to adopt the guidelines described in Section II, “The Four Cornerstones of Good Health,” and address any issue associated with premature death (smoking, obesity, alcohol abuse, etc.) as well as any health conditions that could prove fatal, such as atherosclerosis, diabetes, and cancer.
Specific recommendations and dosages of supplements for slowing the aging process are given below. While trying to lengthen your life span is important, we want to encourage you to focus on improving the quality of your life as well.
Follow the dietary guidelines in the chapter “A Health-Promoting Diet.” In particular, a high intake of colorful vegetables and fruits is essential to a life extension program because of the vitamins, minerals, carotenes, flavonoids, and dietary fiber found in these foods. It is also especially important to follow the dietary recommendations for reducing the risk of heart disease (atherosclerosis), such as increasing the intake of dietary fiber (especially soluble fiber, found in legumes, flaxseed, oat bran, pectin, etc.), olive oil, and fish, while reducing the consumption of saturated fats, cholesterol, sugar, and animal proteins.
• A high-potency multiple vitamin and mineral formula as described in the chapter “Supplementary Measures”
Key individual nutrients:
Vitamin C: 500 to 1,000 mg per day
Selenium: 100 to 200 mcg per day
Vitamin E (mixed tocopherols): 100 to 200 IU per day
Vitamin D3: 2,000 to 4,000 IU per day (ideally, measure blood levels and adjust dosage accordingly)
Fish oil: 1,000 mg EPA + DHA per day
• One of the following:
Grape seed extract (> 95% procyanidolic oligomers): 150 to 300 mg per day
Pine bark extract (> 95% procyanidolic oligomers): 150 to 300 mg per day
Green tea extract (> 80% polyphenol content): 300 to 500 mg per day
Ginkgo biloba extract (24% ginkgo flavonglycosides): 240 to 320 mg per day
Some other flavonoid-rich extract with a similar flavonoid content, super greens formula, or other plant-based antioxidant that can provide an oxygen radical absorption capacity (ORAC) of 3,000 to 6,000 units or higher per day
DHEA: as above
Melatonin: 3 mg at bedtime