Growth hormone (somatotropin) is normally released in several discrete, pulsatile bursts from the somatotroph cells of the anterior pituitary gland. Its levels increase transiently during the day, with the largest amounts appearing after the initiation of deep sleep and after a meal high in protein. The release of growth hormone is regulated by the hypothalamus and its mediators, such as growth hormone inhibiting hormone (somatostatin), growth hormone releasing peptide (ghrelin) and insulin-like growth factor (IGF-1). Growth hormone is a peptide made of 191 amino acids with a half-life of only about 25 minutes in the blood (which is comparatively long-lasting to other peptide hormones) and it exerts its effects by binding to the extracellular domain of the GH receptor mainly in liver, fat and bone cells. Its actions involve multiple organs and systems affecting longitudinal growth as well as lipid, protein, and carbohydrate metabolism.

There are numerous documented beneficial effects of replacement therapy for people with growth hormone deficiency which would seem attractive to both athletes and body builders. Such benefits include increased lean mass and decreased fat mass (predominantly abdominal), and reduced cardiovascular risk factors. In recent research on growth hormone replacement therapy, a sample of subjects with growth hormone deficiency increased their lean body mass up to 14 lbs and decreased fat mass by 15 lbs in just 6 months. After 12 months, increases in bone mineral density were observed. Growth hormone replacement also improved cardiovascular function by increasing left ventricular mass and cardiac output. Finally, this therapeutic use of human growth hormone is currently being researched to improve the vascularization of the retina in diabetics with retinopathy to preserve or improve vision.

After puberty, growth hormone gradually declines, most likely due to an increased release of somatostatin (GH-inhibiting hormone). Frailty with age is associated, in part, with this progressive change in the growth hormone axis, characterized by deterioration of lean mass, subsequent increase in relative obesity, decrease in metabolic rate and consequential reduction in caloric intake and nutrients such as calcium and protein. The reduced nutrient intake further reduces lean mass and the viscous cycle continues. Because of these age-ameliorating properties, growth hormone is often discussed as the drug that can make time stand still by slowing the process of aging. The naïve hypothesis is that growth hormone replacement will attenuate somatopause (age-associated reductions in GH) and lead to restored lean mass, increased lipolysis and improved function.

Clinical trials designed to examine the effects on HGH administration in humans have not supported the above benefits. For example, in the elderly HGH trials reduced fat mass and increased lean mass but did not improve measures of function or quality of life. In fact, the treatment decreased survival rate and increased length of hospitalization in subjects taking HGH compared to those who received placebo. This is consistent with animal studies which demonstrate a shorter lifespan in animals which express higher levels of growth hormone. In fact, research seems to indicate that in mammals there is a U-shaped relationship between mortality and growth hormone secretion. In patients with dwarfism, growth hormone replacement has numerous benefits which may increase lifespan. It is important to note, however, that in these patients, growth hormone is being elevated to normal levels (i.e. GH-Replacement).

A higher than normal level of growth hormone is associated with numerous adverse physiological events, ranging from skeletal to cardiovascular and metabolic disorders. For example, high growth hormone levels lead to increased cartilage thickening which may cause joint injury. The altered articular tissue can lead to joint dysfunction and pain and has lead to such conditions as osteoarthritis and symptomatic carpal tunnel syndrome. Excessive growth hormone is also related to cardiovascular complications such as concentric hypertrophy of both heart ventricles. The increased muscularity of the heart makes it more difficult to perfuse with oxygen and more susceptible to a fatal cardiac arrhythmia. The enlarged left ventricle can also lead to hypertension and artery disease. Finally, since growth hormone counteracts the effects of insulin on glucose and lipid metabolism there is usually a compensatory increase in insulin secretion. This decreased insulin sensitivity and hyperinsulinemia can lead to Type II diabetes. Furthermore, high levels of insulin can increase blood pressure by increased renal reabsorption of sodium and is associated with elevated markers of vascular inflammation and oxidative stress. These markers are linked to a heightened risk of vascular disease and mortality.

Although researchers have not thoroughly analyzed the effects of HGH in bodybuilding, anecdotal inferences can be made regarding the effects injected HGH has had on muscle hypertrophy. HGH by itself has shown little benefit in individuals with normal levels, but when mixed with testosterone there seems to be a synergistic effect that leads to an increase in protein synthesis. This would be consistent with the natural occurrence of protein synthesis in the body. HGH increases insulin-like growth factor (IGF) and likely increases the impression upon muscle cell DNA. Likewise injected and steroidal testosterone has direct influence on muscle cell DNA which affects the affinity for cellular improvements. This may explain the amazing hypertrophy exemplified in today’s bodybuilding competitions.

Taking HGH to improve performance, appearance and or to slow aging is not wise. Although there may be some acute benefits upon administration of the drug, the negative consequences do not justify the benefits. Reviewing the research would help one to realize that our endocrine system is tightly balanced by multifaceted mechanisms between target organs and the hypothalamus of the brain. Altering the normal physiology of this system can have deleterious effects in the long run, such as increased pain, diminished cardiac function, altered metabolism and a shorter lifespan.