A brochure of a certain “Dr. Belkin”, “How to give dinner to an enemy or the healing power of a night hunger,” has recently come into the hands. (Google: “… Belkin Greg – immunologist, allergist, candidate of medical sciences …”). The brochure, among others, points out such dangers of late dinner as the suppression of the production of growth hormone and insulin resistance (there are no references to research, as always).
If this is true, then eating at night can really provoke fat accumulation. I think a possible mechanism is this: growth hormone (somatotropin) stimulates protein synthesis. Protein synthesis is a very energy intensive process. Therefore, if it goes slower, then the energy is spent less. So it can form its surplus, which is deposited in the form of fat.
The mechanisms of the effect of insulin resistance on obesity are more complicated; they appear, apparently, again through the inhibition of protein synthesis. First, because Insulin is also a stimulator of protein synthesis, the loss of sensitivity to it will slow down anabolism. Secondly, insulin resistance, due to the increased amount of glucose and blood in the blood, leads to a decrease in the secretion of somatotropin.
And what have the late dinner? If we assume that abundant food intake at night can lead to the fact that, due to low activity of muscles and brain during sleep, the concentration of glucose and fats in the blood for a long time increases, then this can actually inhibit the synthesis of somatotropin and provoke insulin resistance.
Another possible effect of late dinner on weight gain is through a violation of the quality of sleep and / or circadian rhythms. Assuming this possibility, the connection will be obvious: a violation of the quality of sleep and a disturbance of the circadian rhythms really provoke obesity, including and due to the development of insulin resistance and inhibition of somatotropin secretion. This topic has been studied quite well.
Unfortunately, it was not possible to find direct indications whether late mealtime (and not just its composition and total caloric content) affect somatotropin secretion or insulin resistance. Hypothetically, such a connection could be. For example, it is known that one of the somatotropin secretion stimulants is ghrelin hormone (also known as “hunger hormone”). Produced by the stomach when it is empty. Therefore, it can be assumed that, due to the fullness of the stomach with a rich dinner, the level of ghrelin decreases, this can actually adversely affect the secretion of growth hormone. But these are just my assumptions, I repeat that I don’t have specific information about this.
About sleep disorders … here, too, is not so simple. Indeed, some studies have shown such a correlation, but I did not find a description of the mechanisms. Therefore, it is necessary to guess that in this correlation is the cause, and what is the effect. After all, a rich late dinner, and sleep disturbance can be a consequence of, for example, psycho-emotional overload during the day.
I did not find evidence that supposedly “at night the body sleeps and digests food badly”. Specially re-read the physiology of digestion in several textbooks. (If someone has information on this, please reset the link).
Production of growth hormone (GH) is reported to be controlled by insulin (3). Excess insulin can indirectly affect the hypothalamus by affecting GH-releasing hormones and regulating somatostatin secretion or directly, at the level of the pituitary gland. Recently, an animal model has shown that one of the main goals of hyperinsulinemia is the regulation of GH secretion. The decrease in secretion / synthesis of GH is associated with an increase in the levels of secreted insulin, both as a result of a high-fat diet and in mice with genetically suppressed leptin secretion (1, 2). The effect of insulin on GH, however, is not accompanied by any effect on the expression of GH-releasing hormone and somatostatin in the hypothalamus of obese mice, confirming a direct effect on the pituitary level (1). Pituitary gland tissue is sensitive to insulin: insulin receptors are found similarly to insulin-sensitive tissues, such as adipose, liver, and skeletal muscle. Moreover, there is evidence that pituitary cells retain insulin sensitivity, while cells of other peripheral tissues increase resistance to chronic hyperinsulinemia in the state of obesity (1, 3).
In humans, a decrease in GH secretion in people with obesity is associated with metabolic disorders (4, 5). Elevated insulin levels as a component of metabolic syndrome may be the main cause of obesity-induced decrease in GH secretion (6, 7). Impaired GH production in people with obesity is manifested by the suppression of spontaneous secretion along with a decrease in the sensitivity of the pituitary to somatotropin in response to all known pharmacological stimuli. In particular, substances known to stimulate GH production: hormone releasing hormones, ghrelin / GH secretagogues ( GHS ) and arginine ( 8-11 ). However, the mechanism of insulin-induced suppression of the synthesis of GR is incomprehensible.
Books: 1. Luque R. M., Kineman R. D. (2006) Impact of obesity on the growth hormone axis. Evidence for a direct inhibitory effect of hyperinsulinemia on pituitary function. Endocrinology 147, 2754–2763. [PubMed]
2. Buettner R., Newgard C. B., Rhodes C. J., O’Doherty R. M. (2000) Correction of diet-induced hyperglycemia, hyperinsulinemia, and skeletal muscle insulin resistance by moderate hyperleptinemia. Am. J. Physiol. Endocrinol Metab. 278, E563–E569. [PubMed]
3. Brothers K. J., Wu S., DiVall S. A., Messmer M. R., Kahn C. R., Miller R. S., Radovick S., Wondisford F. E., Wolfe A. (2010) Rescue of obesity-induced infertility in female mice due to a pituitary-specific knockout of the insulin receptor. Cell Metab. 12, 295–305. [PMC free article] [PubMed]
4. Pataky Z., Bobbioni-Harsch E., Golay A. (2010) Obesity. A complex growing challenge. Exp. Clin. Endocrinol. Diabetes 118, 427–433. [PubMed]
5. De Marinis L., Bianchi A., Mancini A., Gentilella R., Perrelli M., Giampietro A., Porcelli T., Tilaro L., Fusco A., Valle D., Tacchino R. M. (2004) Growth hormone secretion and leptin in morbid obesity before and after biliopancreatic diversion. Relationships with insulin and body composition. J. Clin. Endocrinol. Metab. 89, 174–180. [PubMed]
6. Lanzi R., Luzi L., Caumo A., Andreotti A. C., Manzoni M. F., Malighetti M. E., Sereni L. P., Pontiroli A. E. (1999) Elevated insulin levels contribute to the reduced growth hormone (GH) response to GH-releasing hormone in obese subjects. Metabolism 48, 1152–1156. [PubMed]
7. Lanzi R., Manzoni M. F., Andreotti A. C., Malighetti M. E., Bianchi E., Sereni L. P., Caumo A., Luzi L., Pontiroli A. E. (1997) Evidence for an inhibitory effect of physiological levels of insulin on the growth hormone (GH) response to GH-releasing hormone in healthy subjects. J. Clin. Endocrinol. Metab. 82, 2239–2243. [PubMed]
8. Scacchi M., Orsini F., Cattaneo A., Grasso A., Filippini B., Pecori Giraldi F., Fatti L. M., Moro M., Cavagnini F. (2010) The diagnosis of GH deficiency in obese patients. A reappraisal with GHRH plus arginine testing after pharmacological blockade of lipolysis. Eur. J. Endocrinol. 163, 201–206. [PubMed]
9. Pijl H., Langendonk J. G., Burggraaf J., Frölich M., Cohen A. F., Veldhuis J. D., Meinders A. E. (2001) Altered neuroregulation of GH secretion in viscerally obese premenopausal women. J. Clin. Endocrinol. Metab. 86, 5509–5515. [PubMed]
10. Procopio M., Maccario M., Grottoli S., Oleandri S. E., Boffano G. M., Camanni F., Ghigo E. (1995) Short-term fasting in obesity fails to restore the blunted GH responsiveness to GH-releasing hormone alone or combined with arginine. Clin Endocrinol. (Oxf.) 43, 665–669. [PubMed]
11. Maccario M., Procopio M., Grottoli S., Oleandri S. E., Razzore P., Camanni F., Ghigo E. (1995) In obesity the somatotrope response to either growth hormone-releasing hormone or arginine is inhibited by somatostatin or pirenzepine but not by glucose. J. Clin. Endocrinol. Metab. 80, 3774–3778. [PubMed]
Last news about anabolics
Sleep, circadian regulation of insulin secretion and growth hormone
Effect of sleep / circadian regulation on GH secretion
The effect of sleep on GH is much greater than the effect of the circadian rhythm. Thus, peak levels of increase in GH are observed at the beginning of the onset of sleep, regardless of the time of its onset (Honda et al., 1969; Born et al., 1988; Pietrowsky et al., 1994; Weibel et al., 1997). After a person’s sleep is disturbed, when it resumes, the increase in GH occurs much later (Beck et al., 1975). During sleep, there are several bursts of GH secretion (Takahashi et al., 1968; Van Cauter et al., 1992). For example, Van Cauter and colleagues (1992) reported on a 2-hour rhythm of excretion of GH during sleep. Cyclic increases in GH levels are associated with periods of “slow” sleep, however, not all researchers agree with these data (Sassin et al., 1969b; Jarrett et al., 1990; Gronfier et al., 1996). Moreover,Holl et al (1991), when measuring GH levels every 30s during sleep, noted that GH levels are highest with slower sleep compared with stage 1, 2 and fast eye movement sleep. Levels of GH are not reduced in all people lacking slow sleep, while stimulation of slow sleep with hydroxybutyrate did not lead to an increase in GH secretion (Sassin et al., 1969a; Van Cauter et al., 1997). Sleep deprivation also did not affect the secretion of GH during a night’s sleep (Honda et al., 1969).
Fig. Effect of sleep / circadian regulation on GH secretion. The rectangle allocates the time of night sleep from 24 to 8 hours. The solid blue line shows the fluctuation of GH levels during the day. The dotted line shows the endogenous circadian system (Morris et al, 2012).
Effect of GH on sleep
Ambiguous results were obtained regarding the effect of GH on human sleep. Some researchers report that intravenous administration of GH reduces the duration of slow sleep and increases fast sleep, while others do not observe the effect on sleep patterns (Mendelson et al., 1980b; Kern et al., 1993).
Effect of sleep / circadian rhythm on insulin and regulation of glucose
Researchers have identified a circadian rhythm of regulation of glucose and insulin levels (Morgan et al., 1998; Shea et al., 2005). The peak of secretion is observed in the late night or early biological morning. Scheer and colleagues (2009), reported peaks of elevated glucose levels within the circadian rhythm, are observed during the biological night, but not insulin levels.
Glucose levels and insulin secretion are increased during night and day sleep with constant administration of glucose (Frank et al., 1995). This is probably due to the fact that usually brain activity during sleep is less (Boyle et al., 1994). Also, an increase in glucose during sleep under conditions of continuous intravenous administration may cause less absorption of glucose to the muscles and is caused by the counterinsulin-like effect of growth hormone secretion (Moller et al., 1990; Van Cauter, 2005). In the second half of sleep, in the case of continuous administration of glucose, the secretion of glucose and insulin is reduced, which is apparently due to increased glucose utilization during fast sleep and wakefulness (Boyle et al., 1994; Van Cauter, 2005).
Morris CJ, Aeschbach D, and Frank AJL Scheer. Circadian System, Sleep and Endocrinology Mol Cell Endocrinol. 2012 February 5; 349 (1): 91-104. doi: 10.1016 / j.mce.2011.09.003.