Human growth hormone & obesity

We have previously explained that Obesity Syndrome is a medical condition characterised by the following:

• Hyposomatotropism (Human Growth Hormone deficiency)
• Hyperinsulinemia (over-reactive insulin)

Human Growth Hormone (hGH) deficiency is known to cause the following:

• Increase in body fat (especially around the abdomen)
• Decrease of lean muscle
• Decrease of strength and stamina
• Reduction of capacity to exercise
• Decrease in bone density
• Changes in blood cholesterol concentrations (increase in LDL and decrease in HDL)
• Increased risk of developing mild diabetes (non-insulin resistant)
• Excessive tiredness
• Anxiety and depression
• Feelings of social isolation
• Increased sensitivity to cold or heat

This sounds remarkably like Metabolic Syndrome which is defined as a cluster of symptoms including:

• Excess body fat (especially abdominal)
• Insulin resistance
• High blood pressure
• High cholesterol (especially LDL)

The difference is that one is symptomatic and the other is causative. In plain language, this means that Metabolic Syndrome is a name given to a set of symptoms, whereas Hyposomatotropism (hGH) deficiency) can actually cause all of these symptoms.

hGH (somatotropin) is produced in the pituitary gland which itself controls many of the body’s vital processes. Its production peaks around the age of 20 years, declines steadily over the next 20-30 years ending up at naturally lower levels towards the end of a person’s life.

hGH plays several roles in the body throughout our life including growth during childhood and adolescence, building lean muscle mass, mobilising fat for energy needs and maintaining bone mineral density. hGH is sometimes referred to as the anti-aging hormone for this reason. Underlying levels of hGH are a reliable indicator of biological age and overall health.

Fat cells respond to hGH directly via a cellular receptor. hGH breaks down triglycerides within the fat cells which in turn releases fat. hGH also suppresses the fat cells’ ability to accumulate more fat.

Peak secretion of hGH occurs mostly during deep sleep (Delta or Slow-Wave sleep) and is directly and significantly suppressed by high insulin levels. hGH is secreted in a circadian (24 hour) pattern and studies have proven that going to sleep later than your usual bedtime will severely reduce the amount of hGH produced.

Studies show that abnormally low levels of hGH can be caused by hyperactive insulin production and that the metabolic effects of hGH are directly and inversely affected by insulin. It has long been recognised that obesity is characterised by abnormally low levels of hGH which in turn makes it more difficult to lose weight thus creating a vicious cycle.

Put simply, when insulin levels rise abnormally, hGH production is suppressed resulting in several adverse health effects including faster fat storage and reduced release of fat from the fat cells, in other words Obesity Syndrome.

It is this over-reactivity of insulin which is of interest to me as I believe it signals the beginning of Obesity Syndrome, although science still appears unable to shed any light on what causes it in the first place.

References

Barreto-Filho JAS et al, Familial isolated growth hormone deficiency is associated with increased systolic blood pressure, central obesity, and dyslipidemia, Endocrinology Division of the Federal University of Sergipe, 49060-100 Aracaju, Brazil, Journal of Clinical Endocrinology & Metabolism, May 2002; 87(5):2018-2023

Bowen R, Austgen L, Rouge M, Pathophysiology of the Endocrine System, Department of Biomedical Sciences, Colorado State University, 2006

Buijs MM et al, Blunted lipolytic response to fasting in abdominally obese women: evidence for involvement of hyposomatotropism, Department of General Internal Medicine, Leiden University Medical Center, Leiden, Netherlands, Published in American Journal of Clinical Nutrition, Mar 2003; 77(3):544-550

Carrel AL, Allen DB, Effects of growth hormone on body composition and bone metabolism. Department of Pediatrics, University of Wisconsin Medical School, USA, published in Endocrine, Apr 2000; 12(2):163-172.

De Marinis L et al, Growth hormone secretion and leptin in morbid obesity before and after biliopancreatic diversion: relationships with insulin and body composition. Institute of Endocrinology, Catholic University School of Medicine, Rome, Italy. Published in Journal of Clinical Endocrinology & Metabolism, Jan 2004; 89(1):174-180

Hussain MN, Sirek A, Cukerman E, Sirek OV, Insulin dependence of the actions of growth hormone and somatostatin on splanchnic biogenic amines of the dog, Published in Hormone & Metabolic Research, Jul 1986; 18(7):436-440

Mendelson WB et al, Suppression of sleep-related prolactin secretion and enhancement of sleep-related growth hormone secretion, Published in The Journal of Clinical Investigation, Sep 1975; 56(3): 690–697

Shadid S, Jensen MD, Effects of growth hormone administration in human obesity, Endocrine Research Unit, Mayo Clinic, Rochester, MN 55905, USA, Obesity Research, Feb 2003; 11(2):170-175

Takahashi Y, Kipnis DM, Daughaday WH, Growth hormone secretion during sleep, Washington University School of Medicine, Department of Medicine, Metabolism Division, St. Louis, Missouri, Published in The Journal of Clinical Investigation, Sep 1968; 47(9): 2079–2090