The human aging process is extremely complex and appears to affect all bodily functions equally. The tremendous advances in molecular biology over the past decade have made it possible to begin to study the basic mechanisms of aging at the molecular level and relate those findings to specific age‐related diseases at the cellular, tissue, and organ level. It is likely that these advances will demonstrate that there are multiple mechanisms underlying the aging process at all levels and that multiple interventions will therefore be necessary to arrest, slow, or reverse the aging process. Factors already known to be intimately involved in aging include environmental, dietary, and genetic influences; each appears to be involved. Consequently, no single agent is likely to be found that will arrest or reverse all aging processes. Current research efforts focus mostly on modulation of single aging processes and on one or two major organ systems of the body. It is essential to distinguish intrinsic aging from age‐dependent abnormalities, eg, in the cumulative assault of sunlight on the skin. Sunscreens block the cutaneous absorption of ultraviolet (uv) light radiation (280–315 nm) and prevent sunburning, premature aging, and cancer of the skin. Photoaged skin, long believed to be irreversibly damaged, has now been shown to undergo significant repair when uv exposures are stopped. Aging is associated with progressive deterioration in CNS function. A number of factors besides genetic considerations contribute to those degenerative changes, including nutritional elements and environmental toxins. The blood brain barrier (BBB) is a major modulator of nutrient delivery to the CNS. Senescence is associated with significant changes in BBB function including a decrease in BBB choline transport and brain glucose influx. Studies have confirmed that enhancing the cholinergic system could lead to reversal of age‐related memory loss. Evidence indicating an activation of cholinergic mechanisms exists for pyrrolidinone derivatives, including piracetam, oxiracetam, aniracetam, pyroglutamic acid, tenilsetam, and pramiracetam, and for vinpocetine, naloxone, ebiratide, and phosphatidylserine. All these drugs prevent disruptions of several learning and memory paradigms. Cardiovascular disease remains the most common age‐related disease and is the most common cause of morbidity and mortality in old age. Risk factors more prevalent in the elderly than in the young adult, that initiate and aggravate cardiovascular disease include hypertension, personality traits, genetics, diet, smoking, obesity, and impaired glucose tolerance. Pharmacological agents such as lovastatin are used for the treatment of hypercholesterolemia, and antiatherosclerogenic diets low in saturated fat and cholesterol, rich in fiber, and with substitution of polyunsaturated fat and restricted calories tend to normalize serum lipids and to cause lesions to involute. One important feature of aging is the remodeling of the ventricle and blood vasculature. Various agents such as vasodilators, hydroalazine, and isosorbide dinitrate have been used. Other possibilities include α‐blockers and calcium antagonists. Normal aging is associated with a gradual decline in the immune response. A number of approaches have been devised to prevent the loss of immune responsiveness or to restore it once it is declining or has been lost. Recovery of T‐regulatory effects on B‐cell differentiation has been reported in elderly patients treated with IL‐1 or IL‐2. Levamisole, C
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S, and the sodium salt of diethyl dithiocarbamate (imuthiol) restore T‐cell function. Hypoxanthine derivatives such as isoprinosine and NPT 15392 induce T‐cell maturation directly and promote T‐cell function. Melatonin, the pineal neurohormone
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‐acetyl‐5‐methoxytryptamine, has been shown to antagonize the immunosuppressive effects of anxiety stress in mice. The 8‐substituted guanosines have been found to stimulate nonspecific, as well as some specific immune responses. The transmembrane signaling component of cellular activation has been an area of intense research interest. The interactions between nutrition and immunity have been the subject of much investigation. It is now recognized that even mild deficiencies involving protein–calorie malnutrition or single nutrients are associated with impaired immune responses. Large doses of “essential” nutrients (eg, zinc) may have a deleterious effect on the immune system. However, corrections of deficiencies of iron, zinc, and vitamins C, E, and B complex are associated with improved immune responses in the elderly.
