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Theories of Aging

some cancers.5

However, not all researchers agree that free radicals and other oxidants are the primary cause of aging. When I spoke with Dr. Dean, he told me that “The free radical theory is important, and the consumption of a broad range of antioxidants is certainly beneficial. However, in clinical [animal] studies in which antioxidants have been used, no increase in maximum lifespan has been achieved. I believe that the real key is to consider the hypothalamic theory, and to use various nutrients (and in some cases pharmaceutical drugs) that will restore hypothalamic sensitivity.”

BUILT-IN BREAKDOWN THEORIES
The following theories center around the notion that aging is a direct consequence of our genetic programming: the reason we get old and gray is automatically built into our DNA.

HYPOTHALAMIC THEORY OF AGING
The hypothalamic theory of aging holds that the major degenerative diseases are caused by the failure of developmental programs that facilitate the changes between growth stages. These programs, such as hormonally orchestrated changes, are called upon in the “normal” course of aging. Although diseases caused by the failure to accommodate developmental changes are not genetically programmed, they occur in a predictable pattern.

Developmental programs govern our ability, as we age, to adjust and balance when moving from one stage of growth and development to the next. One such succession of programs would be the sexual changes that occur from puberty through to maturity (from menarche through to menopause in women). These programs fail, not in their developmental tasks, but by interfering with the body’s ability to return to homeostasis. Homeostasis is the process whereby we control many regulatory mechanisms of our bodies – body temperature, blood sugar levels, cholesterol levels – allowing them to remain within certain limits. Homeostasis enables the body to respond to both internal and external stresses, and yet maintain all of these various physiological and biochemical parameters within tolerable ranges.

An example of the conflict between developmental and homeostasis mechanisms involves the hormone testosterone. In a young child, the production of a small amount of testosterone does not invoke homeostasis and prevent the emergence of puberty. If testosterone’s stimulatory powers were adequate to suppress hormones that cause production of the amount of testosterone needed to ensure puberty, then testosterone levels would never rise. The same would be true for the effects of the female sex hormones, estrogen and progesterone. In the developmental “jump” from one early stage to the next, homeostasis is more readily achieved. Later in life, the jump is not so smooth and hormonal homeostasis is never completely reachieved. The imbalance that results then leads to prostate problems and – something from which men may not currently be able to escape – prostate cancer.

Viewed in terms of the brain’s regulator of these mechanisms, the hypothalamus, the answer is to help restore the loss of sensitivity that results from failure to reestablish homeostasis. A fundamental approach to retarding the aging process and reversing many age-related diseases would use resensitizers that act to restore the brain’s regulatory (hypothalamic) sensitivity. These include the phospholipid phosphatidylserine, the trace mineral vanadyl sulfate, among other substances. Also able to help restore hypothalamic sensitivity is the antidiabetic drug biguanide Metformin® (a glucophage) that increases insulin sensitivity.

DISPOSABLE SOMA THEORY OF AGING
All body cells are somatic cells except for gametes (sex cells). Somatic cells require fewer resources for maintenance than more precious molecular structures such as those that comprise the DNA of gametes. Evolution has given maximum protection to gametes so that the organism remains in sound condition long enough to pass its genetic material onto future generations. After the ability to procreate ends, there is simply no biological reason to keep the body around. From the perspective of evolution, it’s not how long the individual organism survives that counts; it’s about preserving the gene pool.8 Hence, after reaching sexual maturity, we age and die. Our prehistoric ancestors probably didn’t live much beyond 20, on average. The disposable soma theory is static in that it does not readily suggest any solutions to aging but instead represents traditional acceptance to the inevitability of death.

IMMUNOLOGICAL THEORY OF AGING
The immune system appears to be involved in many age-related diseases, many of which are responsive to therapies involving improvement in the immune functions, especially in the elderly. Many studies have shown the immune system peaks at puberty and then gradually declines with age. As the quality and quantity of immune T cells starts to drop, so does the ability to respond to disease. Evidence points to the thymus, which shrinks with age, as key to understanding immune aging.9 It’s decline is generally associated with an increase in susceptibility to infections and a greater incidence of autoimmune diseases in the elderly.

Because of this, certain antibodies become less effective as one ages, and fewer new diseases can be combated effectively by the body. This causes cellular stress and eventual death. An immune-enhancement program would include various nutrients such as the amino acid arginine, choline, and Vitamin B5, DHEA, progesterone, thyroid, and others.

GENETIC THEORY OF AGING
When experiments had been conducted on the number of times that a human cell can divide outside of the body, the limit appears to be less than 100 times. This suggests that cell division is genetically programmed, and indeed as the body ages, cell division is limited even more. It is thought that when cell division ends, so does life.

TELOMERE THEORY OF AGING
Every time a healthy cell divides, the ends of its chromosomes grow shorter. These chromosomal endcaps, calledtelomeres, protect the genetic material and put a limit on the number of times a somatic cell can divide. Recently, it has been shown that shorter telomeres are capable of significantly fewer doublings than those with longer telomeres. Thus telomere length may be a biomarker of cell aging and when telomeres get too short, cell replication slows, and then ends. The organism dies.

An enzyme called telomerase, has been found to protect telomeres from the shortening process caused by repeated cell divisions. It is thought that the reason that telomeres grow shorter with somatic cell divisions is to reduce the risk of cancer, runaway, out-of-control cells that keep multiplying without limit which can be a great danger to the body. Many researchers believe, however, that this safety feature built into the way our cells divide is also one of the factors responsible for aging and death.10

CHOOSING PROTECTIVE STRATEGIES
While there are diehard adherents for each of the theories of aging summarized in this article, I think that most researchers would agree that many factors contribute to the aging process. This is why it makes good holistic sense to choose a variety of longevity strategies, including an immune enhancement program, an antioxidant regimen, mitochondrial protection supplements, and more. If you’re covered on as many fronts as possible, you stand a better chance of being around as more longevity breakthroughs come along.

References

  1. Holmes GE, Bernstein C, Bernstein H. Oxidative and other DNA damages as the basis of aging: a review.Mutat Res 1992 Sep;275(3-6):305-15.
  2. Beckman K, Ames B. The free radical theory of aging matures. Physiol Rev 1998 April(2):547-81.
  3. Ozawa T. Mitochondrial DNA mutations associated with aging and degenerative diseases. Exp Gerontol1995 May-Aug;30(3-4):269-90.
  4. Linnane AW, Marzuki S, Ozawa T, Tanaka M. Mitochondrial DNA mutations as an important contributor to ageing and degenerative diseases. Lancet 1989 Mar 25;1(8639):642-5.
  5. Ward J. Free radicals, antioxidants and preventive geriatrics. Aust Fam Physician 1994 Jul;23(7):1297-301,1305.
  6. Lee C-K, Klopp RG, Weindruch R, Prolla TA. Gene expression profile of aging and its retardation by caloric restriction. Science 1999;285:1390-3.
  7. Waldholz M. New gene-scanning techniques reveal biochemical clues to aging process. Wall Street Journal, August 27, 1999,p. B6.
  8. Kirkwood TB. The nature and causes of aging. Ciba Found Symp 1988;134:193-207.
  9. Makinodan T, Hirayama R. Age-related changes in immunologic and hormonal activities. IARC Sci Publ1985;(58):55-70.
  10. Mehle C, Ljungberg B, Roos G. Telomere shortening in renal cell carcinoma. Cancer Res 1994 Jan 1;54(1):236-41.

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