Skin is a visible organ which suffers cross-linking damage. However, unlike other tissues, skin is exposed to considerable ultraviolet light (UV) energy from sunlight. Ultraviolet light is a major cause of skin cross-linking. This type of damage can be prevented or retarded by staying out of sunlight or using sun-block preparations containing esters of PABA (p-amino-
benzoic acid, a B vitamin). PABA and its esters absorb this UV energy, keeping it from injuring other skin cell components. Beta carotene (the yellow coloring matter in carrot juice, a nontoxic pro-vitamin A, converted to vitamin A on demand in the body) is also an effective protector of skin against UV damage. In fact, beta carotene is available as a prescription
drug in this country for people who are especially sensitive to
sunlight (photosensitive).
What do you do if you want a suntan but don’t want UV damage to your skin? One solution is to take canthaxanthin, available in Canada as a prescription drug, Orobronze®. It is a red pigment found in certain edible mush- rooms, shellfish, and in flamingo feathers. Canthaxanthin is a carotenoid like beta carotene and is without harmful (toxic) effects. (Acute overdose results in gastrointestinal discomfort.
Chronic overdose colors one orange or red, but this fades to a tan within one to three weeks.) It is used in some foods as a red coloring agent. Canthaxanthin, taken over a period of time, will yield a beautiful bronze color to the skin that looks like a suntan. In fact, it is being sold in Canadian drugstores now for just this purpose. Not only does it give a “tan” with-
out UV, the canthaxanthin even provides protection to the skin against UV damage. Using about 60 milligrams a day of the Canadian Orobronze® produces splendid results. Although not yet approved for this use by the FDA (though it is approved as a food coloring agent), this approach to a “sun” tan is much safer than the use of either the real sun or a UV-
A tanning booth. Since the FDA can do nothing to stop people from suntanning themselves in a conventional manner (causing unquestionable cross-linking skin damage as well as being the principal source of human skin cancer), their delay in the approval of canthaxanthin for this purpose can only injure the health of more Americans. Laws such as the FDA Kefauver Amendment of 1962 must be reexamined, because while politically popular, the cost to good health is far greater than the benefits. This law attempted to eliminate all hazards of drug use by requiring greatly increased safety testing as well as proof of efficacy. The result has been far fewer drugs introduced in the American marketplace.
The nucleic acids DNA and RNA, which are the master and working copies of your blueprints respectively, are also subject to cross-linking. In older animals, cross-linked DNA is less easily degraded by heat—it becomes more stable. However, this increased stability in DNA molecules may interfere
with decoding the genetic information and transcribing it to RNA, leading to errors or even failure of the cell to reproduce.
There are several methods which control the rate of cross-linking. In rats in which the pituitary has been removed from the brain, cross-links are greatly reduced. Limiting food intake in rats (which is capable of extending their life span) also resulted in a far lower rate of cross-linking. These methods may work because they slow down a biological death clock (programmed death) in the pituitary, a hypothesis formulated by Dr. W. Donner Denckla. The dietary restriction may slow the death clock by withholding nutrients necessary to run it. Removal of the pituitary would eliminate a death clock located there. These methods are, as yet, impractical as means of life extension in humans. A point made by Dr. Denckla, however, shows how it may be possible to accelerate what seems like “far out” research into practical use; if an inhibitor can be found to block the releasing factor of this postulated “death hormone,” the pituitary gland need not be removed.
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