Somatopause – The Decline of Growth Hormone and IGF-1 Levels With Age
Many are familiar with menopause in females and andropause in males, but few are familiar with somatopause, a condition affecting both males and females. Somatopause is characterized by declining or deficient growth hormone (GH) and Insulin-like growth factor 1 (IGF-1) levels as you age.
Growth hormone levels peak in adolescence and somatopause usually begins between the ages of 25 and 50, with growth hormone levels decreasing by 14% every 10 years of adult life.  Some men may even experience a growth hormone level decline of 50% every 7 years. 
Such a rapid decline of growth hormone levels can quickly lead to clinical GH deficiency. Declining or deficient growth hormone and IGF-1 levels are accompanied with cognitive decline, increased fat mass and cardiovascular risk, as well as decreased muscle mass and aerobic capacity.
This article will discuss the cause(s) of, dangers of, and treatment options for somatopause.
If undetected or left untreated somatopause can significantly impact your mental health, cardiovascular system, body composition, and metabolism.
What Causes Somatopause
Somatopause can occur in otherwise healthy individuals as a result of the normal aging process. The liver converts growth hormone in to IGF-1, which plays a significant role in muscle, bone, and cartilage building as well as fat burning.  Furthermore, the neural control of somatotropic cells, growth hormone producing cells in the pituitary gland, decrease in activity and as a result IGF-1 levels further drop. 
Ghrelin, also known as the hunger hormone, stimulates growth hormone secretion in both humans and animals.  As we age ghrelin levels decrease which in-turn reduces GH and IGF-1 levels.  Declining or low testosterone, also known as andropause was proposed to cause somatopause.
A small study of seven older males and six healthy young males found that testosterone deficiency did not directly increase growth hormone pulse frequency or maximum GH levels.  Unfortunately, researchers and clinicians have not found a way to completely eliminate the development of somatopause but continue looking in to this condition as it poses health risks.
The Dangers of Somatopause
If undetected or left untreated somatopause can significantly impact your mental health, cardiovascular system, body composition, and metabolism. Somatopause may also influence mortality rates. IGF-1 locally synthesized in the brain protects against oxidative stress and excessive beta amyloid production as well as encourages neuron generation, blood flow, and the complex formation of brain synapses. 
A large body of research suggests that excessive beta amyloid production is a primary driver for the development of Alzheimer’s disease.  Those with low IGF-1 blood levels experience impaired motor function, fluid intelligence, processing speed, short term memory, and cognitive control.  Decreased quality of life accompanies an alarmingly rapid cognitive decline.
Researchers tie numerous physical issues to somatopause. Decreased GH secretion and circulating IGF-1 levels decreases lean mass, increases fat mass, and increases cardiovascular risk indicators like low-density lipoprotein (LDL/Bad Cholesterol). 
Those with low IGF-1 blood levels experience impaired motor function, fluid intelligence, processing speed, short term memory, and cognitive control.
Low growth hormone levels decrease bone turnover and formation in both young and old individuals.  This decreased bone mass and mineral density increases the risk for osteoporosis in elderly men and women as well as significantly increases the likelihood of falls and fractures. 
IGF-1 plays a critical role in muscle protein synthesis, shuttling amino acids to muscles, and rebuilding muscle tissue after serious damage or injury.  Somatopause not only slows or halts muscle growth it also encourages muscle-wasting through decreased repair rates. Growth hormone-deficient individuals release let free fatty acids and have higher triglyceride levels. 
This slows or completely stops fat-burning while simultaneously encourage fat storage. Somatopause may be an athlete’s worst nightmare with its propensity to decrease muscle and increase fat mass.
Those with low growth hormone and IGF-1 levels have higher concentrations of inflammatory cytokines and homocysteine, an effective indicator of cardiovascular risk.  Low levels decrease blood flow, increase likelihood of stroke, heart attack, high blood pressure, and coronary heart disease.  Growth hormone and IGF-1 play critical roles in heart and artery health. Adequate levels may significantly decrease your cardiovascular risk.
Although GH and IGF-1 deficiencies negatively affect quality of life and physical state, there’s a growing body of evidence suggesting this deficiency extends life expectancy in animal studies.  However, one 8-year study of 376 males aged 73-94 found that those in the lowest 20% of IGF-1 levels had a 180% higher chance of dying compared to those in the highest 20%. 
The mechanism by which growth hormone and IGF-1 extends life remains under-investigation but commonly ends in the quality of life (adding life to your years) versus duration of life (adding years to your life) debate. Unfortunately low GH and IGF-1 levels protect against some issues but exacerbates others.
Growth hormone replacement therapy can increase bone strength and mineral density, decrease inflammation, and protect against cardiovascular risk.
Treatment of Somatopause
DISCLAIMER: If you suspect symptoms of somatopause please consult your healthcare profession before beginning any treatment option.
The most obvious and straightforward treatment method for somatopause is Growth Hormone Replacement Therapy (GHRT) via the intramuscular injection of recombinant human growth hormone (rhGH).  Clinical evidence shows that GHRT improves memory, alertness, concentration, body composition, bone strength, as well as decreases fat mass, LDL cholesterol, and inflammation. 
Once study examining rhGH injection in older males found it modestly increased lean mass by 2kg and decreased fat mass by 2kg.  Another found six months of GHRT without lifestyle changes increased lean mass by 2.1kg and 4.3kg in females and males respectively while also decreasing visceral fat mass by 14-50% and increasing maximum oxygen consumption by 6.8%. 
While these findings are positive the study did not explicitly discuss short and long-term side effects. Growth hormone replacement therapy can increase bone strength and mineral density, decrease inflammation, and protect against cardiovascular risk.
Unfortunately growth hormone replacement therapy isn’t cheap; running somewhere in the neighborhood of $12,000 to $15,000 per year, including lab screenings.  Furthermore, unlike Testosterone Replacement Therapy (TRT), growth hormone replacement therapy is almost never covered by insurance if it’s used to treat an age-related decline in growth hormone blood levels.
Injection of rhGH also poses a number of serious risks and side effects. Increasing IGF-1 levels may expedite cancer cell reproduction and increase insulin resistance.  If you’re pre-diabetic or have a family history of diabetes then GHRT may cause full-blown diabetes. Other side effects include fluid retention, joint pain, and tingling. 
Physicians have been using growth hormone replacement therapy for decades as a viable option for GH-deficient individuals. Patients are strongly encouraged to perform extensive research before making this life-altering decision as treatment for the remainder of your life is usually required.
If you also have low testosterone levels then some physicians may decide to prescribe both growth hormone and testosterone replacement therapy (TRT). Although the combination of these therapies has extremely limited research, one study found that combining both increased 1-repetition maximum strength and aerobic capacity via increased maximum oxygen consumption compared to GHRT-only or TRT-only groups. 
While this may sound like the perfect combination for rebuilding muscle, strength, and cardiovascular capacity, patients and physicians should exercise caution. There is very little research examining the short and long-term side effects of combining these two therapies. One could imagine an exponentially higher likelihood of harsh side effects and health complications as both significantly affect body chemistry and metabolic processes.
The least expensive option for slowing somatopause is proper diet, sleep, and exercise. Sleep and exercise are the two primary drivers for growth hormone secretion in normal, healthy individuals.  Combining GH injection with exercise may increase maximum oxygen consumption beyond exercise alone. 
Before considering growth hormone replacement therapy it’s paramount you’ve dialed-in all other GH-influencing aspects of your life. You should have 7-8+ hours of uninterrupted sleep per night, be exercising regularly by incorporating both resistance and cardiovascular training, as well as eating a protein and essential fatty acid-rich diet. Optimizing these three variables will ensure natural GH production stays as high as possible.
1) Anawalt, Bradley D., and Geroge R. Merriam. “NEUROENDOCRINE AGING IN MEN: Andropause and Somatopause.” ScienceDirect. Endocrinology and Metabolism Clinics of North America, Sept. 2001. Web.
2) Rothenberg, Ron. “Growth Hormone Replacement for Normal Aging.” American Academy of Anti-Aging Medicine. N.p., 2005. Web.
3) Toogood, A. A., P. A. O’Neill, and S. M. Shalet. “Beyond the Somatopause: Growth Hormone Deficiency in Adults over the Age of 60 Years.” National Center for Biotechnology Information. J Clin Endocrinol Metab, Feb. 1996. Web.
4) Giustina A, Veldhuis JD. Pathophysiology of the neuroregulation of growth hormone secretion in experimental animals and the human. Endocr Rev 1998; 19 (6): 717-797.
5) Giordano, R., et al. “Somatopause Reflects Age-related Changes in the Neural Control of GH/IGF-I Axis.” National Center for Biotechnology Information. J Endocrinol Invest, 2005. Web.
6) Ariyasu, H., et al. “Efficacy of Ghrelin As a Therapeutic Approach for Age-related Physiological Changes.” National Center for Biotechnology Information. Endocrinology, July 2008. Web.
7) Toshinai, K., and M. Nakazato. “[Hormone Replacement Up-to-date. Ghrelin, Growth Hormone and Somatopause].” National Center for Biotechnology Information. Clin Calcium, Sept. 2007. Web.
8) Orrego, J. J., et al. “Physiological Testosterone Replenishment in Healthy Elderly Men Does Not Normalize Pituitary Growth Hormone Output: Evidence Against the Connection…” National Center for Biotechnology Information. J Clin Endocrinol Metab, July 2004. Web.
9) Sattler, Fred R. “Growth Hormone in the Aging Male.” Best practice & research. Clinical endocrinology & metabolism 27.4 (2013): 541–555. PMC. Web.
10) Murphy, M. Paul, and Harry LeVine. “Alzheimer’s Disease and the Β-Amyloid Peptide.” Journal of Alzheimer’s disease : JAD 19.1 (2010): 311. PMC. Web.
11) Savine, R., and P. H. Sönksen. “Is the Somatopause an Indication for Growth Hormone Replacement?” National Center for Biotechnology Information. J Endocrinol Invest., 1999. Web.
12) Lombardi, G., et al. “Somatopause: Dismetabolic and Bone Effects.” National Center for Biotechnology Information. J Endocrinol Invest, 2005. Web.
13) Liao, Ruo-xi et al. “Management of Osteoporosis with Calcitriol in Elderly Chinese Patients: A Systematic Review.” Clinical Interventions in Aging 9 (2014): 515–526. PMC. Web.
14) Giordano, R., et al. “Growth Hormone Treatment in Human Ageing: Benefits and Risks.” National Center for Biotechnology Information. Hormones (Athens), June 2008. Web.
15) Martin, F. C., A. L. Yeo, and P. H. Sonksen. “Growth Hormone Secretion in the Elderly: Ageing and the Somatopause.” National Center for Biotechnology Information. Baillieres Clin Endocrinol Metab, July 1997. Web.