primarily concerned w ith the dam age th a t occurs inside the cells over time. Program m ed theories center around the idea th a t aging results in large part from a sort of genetic clock th a t decides w h e n cells can no longer operate and reproduce at a rate sufficient enough to m ain ta in optim al health. These distinctions are no t necessarily m utually exclusive, bu t they do serve as a useful guide for discussing current thinking on h o w and w hy we age the w ay we do.
DAMAGE THEORIES
While the em phasis and nam es m ay vary (e.g., free radical theory, cross-linking theory, radiation theory, DNA repair theory, oxidative stress theory, im m u n e theory, m em b ran e theory, w aste accum ula
tion theory, calorie restriction theory, etc.), free radicals lie at the h eart of m ost dam age theories of aging.
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118 Gary Null's Ultimate Anti-Aging Program
First identified m ore th a n forty years ago by G erschm an, and cham pioned as the key to aging ever since by biochemist D enham H arm an of the University of Nebraska, free radicals are molecules w ith unpaired electrons in their outer shell. Such molecules can w reak havoc on norm al cells by atte m p tin g to steal an electron from a n o th e r molecule in order to restore their balance. In doing so they can initiate a destructive cycle th a t may m ultiply and quickly spread, destroying healthy cells in the process. This m ore or less infectious p attern can continue indefinitely.
Free radicals are powerful oxidizing agents th a t cannot be avoided altogether in th a t a majority naturally result from m any norm al reactions in the body involving cellular respiration. While it is required for life and responsible for as m u ch as 95 percent of our m olecular energy, oxygen itself is in fact the m ost prevalent free radical found in the body. Unfortunately, w h e n not kept in check by an adequate supply of antioxidants, w hich attack th em directly and prevent new ones from forming, free radicals can lead to all kinds of degenerative problems such as atherosclerosis, cancer, Alzheimer's disease, cataracts, osteoarthritis, neurological disorders, and im m u n e deficiency.
The free radicals m ost critical to the aging process include su p er
oxide anion, hydrogyn radical, singlet oxygen, hydrogen peroxide, and hypochlorous acid. At the molecular level, they can wage an assault on several fronts, such as dam aging im m u n e cells (white blood cells), lysomes (digestive enzym es), and u n sa tu ra te d fatty acids (lipid peroxidation), destroying DNA and causing DNA m u ta tions, h ard e n in g cell and nuclear m em branes, breaking off cell m e m b ran e proteins, etc.
The specific site of free radicals is a key factor in determ ining their degree of danger. Most can be found in the m itochondria, w here they cause the least harm . The m itochondria are the cells' chief engines and are su rrounded by the cell m em branes. These m em branes, also a com m on location for free radicals, are particu larly vulnerable because they are composed of u n sa tu ra te d fatty acids. An interesting aspect is the w aste products free radicals leave behind in the w ake of their dam age to cell m em branes. M any cells, particularly heart and nerve cells, accum ulate lipofuscin, a yellow pigm ent, increasingly as they age. Lipofuscin, often referred to as age spots, comes from oxidized fat moleculcs. Some suggest that
eventually the buildup of this molecular trash becomes a b u rd e n th a t dam ages the cell itself and causes it to stop functioning p ro p erly.
Free radicals perhaps do their greatest dam age th ro u g h a process of fusing DNA and protein molecules, referred to as cross-linking.
Unlike the other contents of cells, the body cannot produce n e w strands of DNA. The best it can do is repair them , bu t not always.
In addition to dam aging DNA, cross-linking results in the body's essential proteins becom ing stiff an d therefore unable to function correctly. This process is responsible for m an y of th e sym ptom s m ost often associated w ith aging— cataracts, wrinkles, brittle bones, k id ney failure, h ardening of the arteries, and im m u n e deficiency. Cross- linking is particularly prevalent in diabetics, as glucose fuels the process, and helps explain w h y diabetes is a disease recognized for its severe p rem atu re aging effects.
In order to com bat the dangers of free radicals it is im p o rtan t to identify w here they come from. As previously stated, many, if not the majority, of free radicals occur naturally in th e body. They are produced as a by-product of norm al cellular activity, as well as in response to b oth psychological an d physical stress, an exam ple being excessive exercise. However, free radicals can increasingly be found in our environm ent in the form of toxic w aste, chemicals, pesticides, sunlight, radiation, and cigarette smoke, as well as d i
etary sources such as coffee, alcohol, fried and barbecued foods, etc.
The trick to keeping free radicals u n d e r control is to avoid external sources w h ere possible, and to m ak e certain th a t the body is well supplied w ith antioxidants to w ard off those w e cannot.
M ost people are familiar w ith at least some of th e benefits a ttrib uted to such popular antioxidants as vitam in C, vitam in E, and beta- carotene. The first line of defense against a n excess buildup of oxy
gen at the m olecular level consists of three protective enzymes n a t u rally found in the body: superoxide dism utase (SOD), catalase, and glutathione peroxidase.
Free radicals are defeated essentially by being trapped, or iso
lated, and not allowed to seek out electrons from neighboring cells.
Free radicals can th e n be m etabolized and tu rn ed into harm less paired oxygen molecules or simply water. Dietary sources of antio x i
dan ts (nonenzym atic com pounds) can produce similar effects.
While dietary antioxidants such as vitam in C are useful in the
120 Gary N ull's U ltim ate A nti-A ging P ro g ram
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fight against free radicals, this is not the only place they are needed in the body. The m ore antioxidants involved in this fight, the less are available overall. If n eith er the protective enzymes nor dietary sources of antioxidants can stem the rising tide of free radicals, the cells a tte m p t to destroy th e m themselves. This burn s up vital energy the cells require for m ore im p o rtan t activities.
While free radicals destroy h ealthy cells, those cells th at are not being destroyed are expending m ore and m ore resources both in a tte m p ts to keep the free radical o n slaught at bay and to clean up and repair the dam age th a t already has been done. Eventually so m e
thing is going to give. And th a t som ething increasingly moves from the m olecular level outw ard, taking the form of heart disease, c a n cer, diabetes, arthritis, senile dem entia, Alzheimer's disease, a w e a k ened im m u n e system, and n u m ero u s o th e r ills.
Key to u n d e rsta n d in g w h y free radicals are central to dam age theories of aging concerns th e issue of m ain tain in g oxygen balance w ith in the body. Techniques designed to successfully m ain ta in this delicate balance are at the heart of m ost n a tu ra l anti-aging protocols today.