Diminished secretion of growth hormone is responsible in part for the decrease of lean body mass, the expansion of adipose-tissue mass, and the thinning of the skin that occur in old age.

No abstract

Body composition changes progressively in mid and late adulthood. Lean body mass in men over 50 years old contracts at an average rate of-0.6% per year. Body weight tends to remain stable because of a reciprocal expansion of adipose mass. The shrinkage of the lean body mass reflects the atrophy of skeletal muscles, skin and visceral organs. Because growth hormone causes expansion of the lean body mass and contraction of the adipose mass, and because growth hormone secretion tends to diminish in late adulthood, it has been postulated that geriatric hyposomatotropism is a contributory cause to the body composition changes described above. The authors have tested this hypothesis by recruiting 45 independent men over 61 years old with plasma somatomedin C level below 0.35 U/ml, indicating little or no detectable growth hormone secretion. The 21-month protocol was as follows: baseline period 0–6 months, experimental period 6–18 months and post-experimental period 18–21 months. During the experimental period, 26 men (group I) received approximately 0.03 mg/kg of biosynthetic human growth hormone (hGH) subcutaneously 3 times a week, while 19 men (group II) received no treatment. Plasma somatomedin C was measured monthly. The following outcome variables were measured at 0,6, 12 and 18 months: lean body mass, adipose mass, skin thickness (dermis plus epidermis), sizes of the liver, spleen and kidneys, the cross sectional areas often muscle groups, and bone density at 9 skeletal sites. Lean body mass and adipose mass were also measured at 21 months. In group I, hGH treatment raised the plasma somatomedin C level and maintained it in the range 0.5–1.5 U/ml. Significant changes occurred in the following outcome variables, expressed as percent change at 18 months over baseline: lean body mass +6%, adipose mass -15%, skin thickness +4%, liver volume +8%, spleen volume + 23%, sum of ten muscle areas +11 %. Three months after hGH treatment stopped, about one half of the hGH-induced increment in lean body mass had disappeared and about one third of the hGH-induced decrement in adipose mass had reappeared. During hGH treatment, 9 subjects developed carpal tunnel syndrome and 4 subjects developed gynecomastia. The adverse side effects disappeared spontaneously within 3 months after cessation of hormone treatment. In group II, the somatomedin C level remained below 0.35 U/ml. At the 18-month time point, there was a significant decline in lean body mass to 96% of initial baseline and in skin thickness to 94% of initial baseline. These observations are consistent with the hypothesis that diminished growth hormone secretion in the later years of adulthood is a contributory cause to the body composition changes which occur with advancing age.

Aging is characterized by a progressive decline of cellular functions. The aging liver appears to preserve its function relatively well. Aging is associated in human liver with morphological changes such as decrease in size attributable to decreased hepatic blood flow. Ultrastructural analysis of the human liver has revealed that the integrity of mitochondria and enzymatic activity remain mostly unchanged with aging. Reactive oxygen species (ROS) are involved in the aging process and result mainly from nonenzymatic processes in the liver. Endogenous free radicals are generated within mitochondria and suspected to cause severe injury to mitochondrial DNA. This damaged DNA accumulates with aging. In addition, polyunsaturated fatty acids, highly sensitive to ROS, decrease in liver mitochondria from human centenarians, a feature acquired during evolution as a protective mechanism to favor longevity. Diet is considered the main environmental factor having effect on lifespan. It has a major impact on aging liver, the central metabolic organ of the body. The ubiquitin proteolytic pathway in the liver serves to destroy many proteins, among them p21 which is encoded by abundant mRNA in senescent cells, can inhibit cell proliferation and favors DNA repair. Drug therapy in the elderly may be complicated by several factors such as decline in body weight, renal function, liver mass and hepatic blood flow, making adverse drug reactions more frequent. Hepatic drug metabolism is mainly mediated by the cytochrome P₄₅₀ system and drug interactions in the elderly are likely related to the progressive decline of this system after the fifth decade of life and another decrease in individuals aged >70. Antihypertensive therapy in the elderly depends upon either hepatic or renal function and should be adjusted accordingly. Finally, telomerases are the biological clocks of replicative lifespan. Shortening of telomeric ends of chromosomes correlates with aging and decline in the replicative potential of the cell: replicative senescence. Telomere DNA of human somatic cells shortens during each cell division thus leading to a finite proliferation. Transfection of the telomerase reverse transcriptase gene results in elongation of telomeres and extension of lifespan. This also applies to humans. Replicative senescence in human cells evolved as a mechanism to protect them from continuous divisions leading to multiple mutations. Longer-lived species such as humans had to develop replicative senescence to ensure that they would have the increased protection that their longevity necessitates.

These observations show that when elderly men with low circulating IGF-I concentrations are treated continuously with hGH, elevation of plasma IGF-I above 1.0 units/ml is associated with a substantial frequency of carpal tunnel syndrome or gynaecomastia. It may be that the effects of the hormone in expanding lean body mass and reducing adipose mass can be achieved, and the side-effects avoided, by maintaining the mean IGF-I level in the range 0.5-1.0 units/ml.

No abstract

Serum cholesterol was measured in 129 men (average age 70.6; range 41-96) of a Veterans Administration Nursing Home, and was correlated with other items in an extensive clinical data base. Serum cholesterol was less than 150 mg/dl in 13% of the subjects, and was less than 160 mg/dl in 18%. Cholesterol greater than 280 mg/dl occurred in 8%. Serum cholesterol varied directly (p less than 0.02) with: body weight, serum albumin, serum total protein, serum sodium, ability to walk, and ability to feed oneself; and indirectly (p less than 0.02) with death rate, degree of functional dependence, and serum SGOT and LDH. Nursing home men with cholesterol less than 150 mg/dl had a death rate of 63% during the 14 months after the cholesterol analysis, compared to a death rate of 9% in men with cholesterol greater than 150 mg/dl (p less than 0.05). Death rate during the year after the analysis was 52% if cholesterol was below 160 mg/dl, compared to 7% if it was above this threshold (p less than 0.05).

One million individuals in the United States alone are estimated to be current or past users of anabolic-androgenic steroids. In the United States fifty-percent of anabolic-androgenic steroid users administer their compounds intramuscularly, and twenty-five percent of adolescent anabolic-androgenic steroid users share needles, placing these young adults at risk for infections related to injection. To examine the medical literature for reports of infections attributable to anabolic-androgenic steroids, we conducted a MEDLINE (1966-1998) and AIDSLINE (1980-1998) world literature review to examine all references that attributed infections to anabolic-androgenic steroid injection. Infections associated with anabolic-androgenic steroid injection include three cases of HIV, one case of hepatitis B, one case of hepatitis C, eight abscesses, and a case of fungal endophthalmitis. No cross-sectional or prospective studies exist that document the risk of infections related to anabolic-androgenic steroid injection. These serious infectious complications of anabolic-androgenic steroid injection may be avoided with education and prevention techniques. Infections occurring in anabolic-androgenic steroid users are not as common as in intravenous drug users.