R.A.S HEMAT, MB;BCh, FRCSI, DUL.

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Somatopause is the decline in growth hormone (GH) level that occurs gradually from young adulthood throughout life, and it occurs in both sexes at roughly the same rate. This decline in GH leads to a decline in IGF-1, the hormone-like substance that is made in the liver in response to GH. The decline in IGF-1 also parallels the decline of all the attributes related to testosterone. Reduction of GH (and IGF-1) leads to increase in body fat, waistline, waist to hip ratio (an indicator for risk of heart attack), LDL cholesterol, average days of illness, and hospitalisation rate. Testosterone levels decline gradually in men, starting from age 30, and this decline continues throughout life. In both sexes, along with this decline in testosterone, comes a decrease in libido, lean body mass, strength, energy, mood, sexual performance and mental acuity. Lifestyle modification, sound nutritional practice, and careful monitoring are essential to achieve the maximum benefit from hormone modulation. Men and women, GH reduces body fat by 14%. Men on both GH and testosterone would decrease body fat by 17-18%. GH reduces LDL (bad cholesterol). GH reduces total cholesterol, and the ratio of total cholesterol to HDL (coronary risk ratio) also declines, indicating less risk for heart attack. Testosterone in men lowers triglycerides and raises HDL cholesterol, both of which reduce risk for heart attack. These effects of testosterone in relation to cholesterol vary in women. Growth hormone makes sleep better and awaken refreshed with more energy and improved aerobic capacity. Average bone density increases over the course of a year. The skin becomes thicker and smoother with fewer wrinkles. Spider veins also tend to decrease as a virtue of thickening of the skin. The cholesterol profile usually improves as LDL cholesterol generally is reduced with the use of GH. Finally, there is an enhanced feeling of well being, often described as mood elevation. The goal for laboratory measuring is to see the testosterone level rise to the upper normal for men.

Adiposity is associated with a reduction in the frequency of GH secretory bursts and a significant shortening of the circulatory half-life of GH, both of which reduce integrated daily plasma GH concentrations. Because both ageing and obesity are associated with elevation of plasma insulin levels, one possible mechanism for the above effects is an increase in insulin action on hypothalamic and pituitary IGF-I receptors, resulting in enhanced feedback inhibition of GH, and hence IGF-I, secretion. Ageing is associated with increased insulin resistance and a rise in fasting glucose levels, whereas GH deficiency is typically accompanied by enhanced insulin sensitivity and episodes of fasting hypoglycaemia. Over the adult lifespan total body fat increases by approximately18% in men and 12% in women, in part due to decreased physical activity. This accumulation is greater in the abdominal-visceral than the subcutaneous fat compartment.

Rates of skeletal depletion vary widely among individuals so that some people do not become significantly oesteopenic with advancing age. Bone mineral loss is a predictable accompaniment of ageing in both women and men. Peak skeletal mass in women is achieved at about age 35, after which bone mass falls at a rate of 0.5-1%/year until the menopause, subsequent to which the rate of loss accelerates to 2-3%/year for the next 5-10 years and continues at a slower rate thereafter. Peak bone mass in men is about 25% higher than in women and occurs at about age 35-40, after which there is a continued steady age-related loss of skeletal mass of about 0.3% per year.

The characteristic syndrome adult GH deficiency (GHD) consisting of decreased mood and well-being, with alteration in body composition and substrate metabolism.

There is a potential role of GH in the progression of congestive heart failure. Endothelial dysfunction is a prominent feature of CHF. GH plays a role in vascular reactivity. A 3 month treatment with GH corrects endothelial dysfunction and improves non-endothelium-dependent vasodilation in patients with CHF. Growth hormone (GH) administration to patients with chronic heart failure (CHF) corrects their vascular dysfunction.

Inflammation plays an important role in atherosclerosis, and inflammatory markers are predictive of cardiovascular events. Long-term growth hormone replacement in men reduces levels of inflammatory cardiovascular risk markers, decrease central fat, and increases lipoprotein(a) and glucose levels without affecting lipid levels.

GH administration increases energy expenditure, independent of changes in lean body mass, in healthy, obese, and GH-deficient subjects.

Low thyroid levels cause decreased body temperature, increased cholesterol, and increased body fat. Low thyroid levels can contribute to a subjective feeling of sluggishness and low energy as well as depression.
Insulin and cortisol are the two hormones that promote aging and promote degenerative disease.

Testosterone supplementation (T) in men improves strength and increases de novo protein synthesis as well as muscle mass. T has also been shown to decrease body fat and particularly visceral body fat, increase libido in normal men and increase libido and sexual performance in hypogonadal men. Mood is also improved with T in both hypogonadal and older community dwelling men. Higher endogenous testosterone has been correlated in many studies with a reduction in a number of cardiovascular risk factors, among them lower - blood pressure, total cholesterol (TC), LDL-cholesterol (LDL), triglycerides (TG), visceral body fat, waist-hip ratio (WHR), serum insulin, fasting and post-prandial glucose, higher HDL-cholesterol (HDL) and greater insulin sensitivity.

July, 2003

Articles by R.A.S Hemat

Note: The information in this article has been excerpted from the following books: urotext-ebook simplifying urology, Principles of modern urology, Principles of orthomolecularism, Andropathy by Dr. R.A.S HEMAT. Permission is granted to copy and redistribute this document electronically as long as it is unmodified. This article may not be sold in any medium, including electronic, CD-ROM, or database, or published in print, without the explicit, written permission of Dr. R. A. S. Hemat.

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Dr. R.A.S HEMAT declares no conflicts of interest or financial interests in any product or service mentioned in this article, including grants, employment, stock holdings, gifts, or honoraria.