The Hormonal Seesaw

There are two categories of hormones, as determinant forces of metabolism, that which the body always strives to keep in balance.

Anabolic Hormones

They stimulate “build-up”, which means the synthesis of complex molecules from simpler ones. In other words, taking simple molecules and making them something bigger and storing them. These biochemical reactions require energy. Lipogenesis (generating fat) is an anabolic process with insulin being the driving force behind it. Insulin, growth hormone, testosterone, and estrogen are anabolic. Insulin is the most powerful one, which stand for storing sugar (glycogen) and fat (adipocyte) for the times when we are not eating.

Catabolic Hormones

They stimulate the breakdown of complex molecules into simpler ones. These biochemical reactions release energy. Adrenaline, cortisol, and glucagon are catabolic hormones. In the state of fasting, when insulin is low, glucagon, which strongly opposes the action of insulin, is high. Glucagon tells the liver to break down the fatty acids (lipolysis) for the process of gluconeogenesis, (generating sugar) which means creating new glucose the body needs when glycogen is depleted.

If insulin is higher than glucagon, then anabolic pathways are predominant, which means creating and storing fat. Conversely, if the glucagon is higher than insulin, the catabolic pathways are predominant, resulting in the breaking down of stored fatty acids into an energy source. Sugar and carbohydrates increase insulin and reduce glucagon. Fat decreases insulin but it will increase glucagon.

The body always strives to keep a balance between anabolic and catabolic hormones. If anyone any one of the anabolic or catabolic hormones decreases or increases, an imbalance occurs and consequently the body moves and adjusts to regain the balance. There are always some minor imbalances in our hormonal see-saw but if there is too much hormone weight on one side for the long term, it leads to multiple diseases.

Excess consumption of sugar and carbohydrate causes a hormonal imbalance because it sends too much (anabolic) insulin into the bloodstream. Subsequently, to regain balance, the body must reduce other anabolic hormones such as growth hormone. That is why, when the insulin is high, the level of human growth hormone is very low. On the contrary, in the state of fasting, in the absence of insulin, the human growth hormone and sex hormone are high. Why are people becoming increasingly less sexually active? Because, as a result of excess consumption of carbohydrates and subsequent high-level insulin, the sex hormone is diminishing.

Adults with growth hormone deficiency are associated with abdominal obesity and insulin resistance. Chronic low levels of human growth hormone, as a result of excess insulin, express themselves in the form of different diseases such as weakening the immune system and atherosclerosis, among others. [1] All tissues require constant rebuilding, a process which requires growth hormones. With a low level of growth hormone, the arteries fail to repair themselves, which leads to heart disease.

When the insulin is constantly high, the body counteracts this imbalance by decreasing other anabolic hormones such as growth hormone, while increasing catabolic hormones such as thyroid T3 and T4. Too-high levels of T3 and T4 lead to goiter, an abnormal enlargement of your thyroid gland.

IGF-1 (an insulin-like growth factor) is a growth factor that plays a major role in tumor proliferation. [2] This is due to the level of insulin, as there is a direct relationship between the high level of insulin and IGF-1. [3] To counteract the imbalance caused by a high level of insulin, the body increases the (catabolic) thyroid hormone T3. When T3 is high, the IGF-1 also increases [4], which promotes the formation of cancer. The conclusion is the lower insulin the lower IGF-1, which in turn reduces the risk of tumor progression. [5]

Glucagon and Autophagy

Autophagy is an evolutionarily conserved process of great significance by which the cells remove and recycle old organelles, damaged cell membranes, protein debris, oxidized particles, and pathogens. This process takes place in the state of fasting when the body realizes the necessity of saving energy by eliminating and recycling the long-lived proteins. In other words, you drastically clean up the junk out of your body.

Two potent inducers of autophagy are amino acid deprivation and the hormone glucagon. When amino acids are depleted (through fasting), the glucagon plays its catabolic effect on old organelles by breaking them down into their building blocks, namely amino acids, to be utilized for new protein synthesis and energy supply. What promotes glucagon? Fasting. Remember, when insulin is high, glucagon is low. When insulin is low, glucagon is high.

So, fast to stimulates glucagon, and thus activates the process of autophagy.

The beauty of fasting and having a subsequent low level of insulin is that two things happen simultaneously:

1. It activates autophagy, by stimulating the glucagon.

2. It creates new parts, by stimulating the human growth hormone.

This is what you can call rejuvenating. It’s free. You can do it today. At home. Just stop eating all the time.

This paragraph is scientific. – You can skip it.

Glucagon and Ketogenesis

Insulin inhibits lipolysis and ketogenesis. Glucagon does the opposite, inhibiting lipogenesis but stimulating lipolysis and ketogenesis. In the state of fasting, the liver switches from carbohydrate utilization and fatty acid synthesis (lipogenesis) to fatty acid oxidation and ketogenesis. [6] Glucagon is the primary hormone involved in the induction of fatty acid oxidation and ketogenesis in the liver. The initiating event of ketogenesis is a change in the ratio of insulin to glucagon. When insulin is low, glucagon gains dominance, triggering lipolysis and simultaneously inhibiting lipogenesis.

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Scientific References

[1] Kim SH, Park MJ. Ann Pediatr Endocrinol Metab. 2017 Sep;22(3):145-152. doi: 10.6065/apem.2017.22.3.145. Epub 2017 Sep 28. Review. PMID: 29025199

[2] IGF System in Cancer, Weroha SJ, Haluska P. Endocrinol Metab Clin North Am. 2012 Jun;41(2):335-50, vi. doi: 10.1016/j.ecl.2012.04.014. Review. PMID: 22682634

[3] The relative roles of growth hormone and IGF-1 in controlling insulin sensitivity, Clemmons DR. J Clin Invest. 2004 Jan;113(1):25-7. PMID: 14702105

[4] Research Article Serum Resistin and Insulin-Like Growth Factor-1 Levels in Patients with Hypothyroidism and Hyperthyroidism. Serum IGF-1 levels decrease in hypothyroid status. Ceren Eke Koyuncu,1 Sembol Turkmen Yildirmak,1 Mustafa Temizel,2 Tevfik Ozpacaci,3 Pinar Gune1,4 Mustafa Cakmak,5 and Yilksel Gillen Ozbanazil Received 20 July 2012; Revised 28 December 2012; Accepted 20 January 2013, Academic Editor: Jack R. Wall

[5] Department of Biochemistry, Pt. B.D. Sharma, University of Health Sciences, P.G.I.M.S, Rohtak, (Haryana), India. Ghalaut VS, Yadav S, Ghalaut PS, Yadav A, Sachdeva A, Yadav R, Sharma TK, Shankar V. Clin Lab. 2012;58(3-4):227-31. PMID: 22582495.

[6] McGarry JD, Foster DW, Regulation of hepatic fatty acid oxidation and ketone body production, Ann. Rev. Biochem, 1980, 49: 395-420. Laffel L, Ketone bodies: a review of physiology, pathophysiology and application of monitoring to diabetes, Diabetes/Metabolism Research and Reviews, 2015, 15: 412–426. Mitchell GA et al., Medical aspects of ketone body metabolism. Clin Invest Med, 1995, 18: 193-216.