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May 03, 2022 6 min read
The socioeconomic impact of the pandemic increased the need for a solution that allows safe facilitation of restrictive health measures. Most of the urgent efforts are directed toward creating a proper vaccine or efficient medical treatment for the virus.
However, preventive measures based on understanding the epidemiology of the disease can also be of utmost importance in reducing its spread.
In this article, I’ll examine the possible role of growth hormone deficiency and/or resistance in the high-risk groups of patients for COVID-19 disease and potentially other colds/viruses. This is based on the updated epidemiological data of the pandemic and the known levels of growth hormone in different risk groups of patients as well as the effect of growth hormone on the immune system.
There is probably a lacking variable in the elderly that makes them more vulnerable to the severity of disease. Growth hormone level decline in the serum as men age.
Starting at about 30 years old, there is a progressive decline of growth hormone secretion by approximately 15% for every decade of adult life after that. Integrated measurements of daily growth hormone secretion demonstrate that secretion peaks at puberty at about 150 microgram/kg/day and then decreases to approximately 25 microgram/kg/day by age 55(1).
Interestingly, infants (less than 12 months old) exhibit a more severe form of the disease than other pediatric age groups. Growth hormone levels are high in the mid-term fetus and at birth and then decline sharply in the first few weeks and more slowly over the next few months, reaching prepubertal levels by around 6 months old(2).
The observational characteristics between aging and adult growth hormone deficiency syndrome combined with this decrease in growth hormone/Insulin-like growth factor-I with aging have raised the question of whether aging is a growth hormone deficient state(3).
It is worth noting that the reported curve of COVID-19 mortality, matches well the pattern of decline of growth hormone level throughout the life of human subjects.
It seems that there is a relative protective factor in the female gender. It has long been known that growth hormone secretion is greater in women than in men despite similar reference ranges of serum insulin-like growth factor in adult men and women. It has also been reported that sex steroids influence not only growth hormone secretion but also the local synthesis of insulin-like growth factor-I in target tissues and the expression of the growth hormone receptor in various other tissues(4).
As men grow older, testosterone levels decline gradually with free testosterone concentrations falling by about 50% between ages 25 and 75 years.
The gradual decline of testosterone with aging is parallel to the age-related fall in growth hormone secretion levels, resulting in lower circulating levels of insulin-like growth factor-I.
Testosterone exerts a stimulatory effect on growth hormone secretion at the pituitary level, which is called a “push effect.” On the other hand, estrogen increases growth hormone secretion only through its inhibitory effect on insulin-like growth factor-I production in the liver with resultant feedback stimulation of growth hormone release from the pituitary: “a pull effect”(5).
Spontaneous and stimulated growth hormone secretion is higher in young women than in postmenopausal women or young men. The difference was found to be strongly correlated with estrogen concentrations(6).
Growth hormone secretion declines more rapidly with increasing age in men than in women between the third and fifth decades. Although spontaneous growth hormone secretion falls progressively with advancing years, an abrupt reduction over the menopausal years does not occur, and most of the change is explained by age-associated increases in the body or abdominal fat(7).
There is strong evidence that growth hormone negatively regulates many pro-inflammatory cytokines such as CRP (c-reactive protein), IL-6 (Interluekin-6), and TNF-α (tumor necrosis factor alpha)
Serum levels of CRP, IL-6, and TNF-α are increased in adults with growth hormone deficiency and fall in response to growth hormone replacement(8).
Monocyte production of IL-6 and TNF-α is increased in patients with growth hormone deficiency and reduced by growth hormone treatment(9). These data indicate that growth hormone directly or indirectly reduces inflammation by modulating serum levels of cytokines and markers of inflammation.
Meanwhile, there is evidence that estrogen inhibits signaling of several members of the cytokine receptor family, including prolactin, IL-6, and leptin(10).
Thus, deficiency in both growth hormone and estrogen is associated with increased serum concentrations of CRP, IL-6, and TNF-α. In addition and support of the above data; findings from a recent study suggest that there might be an association between low IGF1 (and possibly GH) and
poor outcome in patients with Covid-19(11).
Research indicates that endocrine and neuroendocrine systems greatly influence the immune system(12).
Growth hormone has an important role in the development of the immune system and may enhance the growth of the thymus gland which is responsible for the production of immune cells called T cells, the mediator of cell-mediated immunity(13).
Growth hormone is also produced by lymphoid organs, such as the thymus, the spleen, and immune cells. Clinical studies have also suggested a significant role of growth hormone in immune regulation, and the growth hormone receptor is expressed on different subpopulations of lymphocytes(14).
Growth hormone stimulates T and B cell proliferation and immunoglobulin formation. Having an immune-regulatory effect in addition to their
anabolic effects, growth hormone and insulin-like growth factor 1 (IGF-1), may act to protect the host from lethal bacterial infection as well.
In summary, the severity of the disease of COVID-19 seems to be matched with a relative deficiency and/or resistance of growth hormone in some groups of patients.
There definitely is a need for further studying the role of growth hormone in the unique epidemiological pattern of COVID-19 and other viruses so that it can help in the early detection and management of the high-risk groups. It would be interesting to know the role of growth hormone in preventing other viruses, bacterial infections, and/or colds.
If you're looking to improve your body's chances at fighting off pathogens of all types, the best thing you can do is make sure you get plenty of sleep, stay hydrated, exercise daily, eat lots nutrient-dense food.
You can also add a supplement like The Immune Stack to ensure your body has all it needs to perform its best no matter what you may come in contact with on a day-to-day basis.
References:
1. Hersch, E.C. and G.R. Merriam, Growth hormone (GH)-releasing hormone and GH secretagogues in normal aging: Fountain of Youth or Pool of Tantalus? Clin Interv Aging, 2008. 3(1): p. 121-9.
2. Leger, J., et al., Growth factors and intrauterine growth retardation. II. Serum growth hormone, insulin-like growth factor (IGF) I, and IGF-binding protein 3 levels in children with intrauterine growth retardation compared with normal control subjects: prospective study from birth to two years of age. Study Group of IUGR. Pediatr Res, 1996. 40(1): p. 101-7.
3. Sherlock, M. and A.A. Toogood, Aging and the growth hormone/insulin like growth factor-I axis. Pituitary, 2007. 10(2): p. 189-203.
4. Johansson, A.G., Gender difference in growth hormone response in adults. J Endocrinol Invest, 1999. 22(5 Suppl): p. 58-60.
5. Hamdy, M.H.E.a.A., A Suggested Role of Human Growth Hormone in Control of the COVID-19 Pandemic. Frontier Endocrinology, 2020.
6. van den Berg, G., et al., An amplitude-specific divergence in the pulsatile mode of growth hormone (GH) secretion underlies the gender difference in mean GH concentrations in men and premenopausal women. J Clin Endocrinol Metab, 1996. 81(7): p. 2460-7.
7. Clasey, J.L., et al., Abdominal visceral fat and fasting insulin are important predictors of 24-hour GH release independent of age, gender, and other physiological factors. J Clin Endocrinol Metab, 2001. 86(8): p. 3845-52.
8. Sesmilo, G., et al., Effects of growth hormone administration on inflammatory and other cardiovascular risk markers in men with growth hormone deficiency. A randomized, controlled clinical trial. Ann Intern Med, 2000. 133(2): p. 111-22.
9. Serri, O., et al., Alterations of monocyte function in patients with growth hormone (GH) deficiency: effect of substitutive GH therapy. J Clin Endocrinol Metab, 1999. 84(1): p. 58-63.
10. Leung, K.C., et al., Estrogen inhibits GH signaling by suppressing GH-induced JAK2 phosphorylation, an effect mediated by SOCS-2. Proc Natl Acad Sci U S A, 2003. 100(3): p. 1016-21.
11. Ilias, I., et al., Covid-19 and Growth Hormone/Insulin-Like Growth Factor 1: Study in Critically and Non-Critically Ill Patients. Front Endocrinol (Lausanne), 2021. 12: p. 644055.
12. Tang, M.W., et al., Insight into the Endocrine System and the Immune System: A Review of the Inflammatory Role of Prolactin in Rheumatoid Arthritis and Psoriatic Arthritis. Front Immunol, 2017. 8: p. 720.
13. Napolitano, L.A., et al., Growth hormone enhances thymic function in HIV-1-infected adults. J Clin Invest, 2008. 118(3): p. 1085-98.
14. Hattori, N., et al., GH, GH receptor, GH secretagogue receptor, and ghrelin expression in human T cells, B cells, and neutrophils. J Clin Endocrinol Metab, 2001. 86(9): p. 4284-91.