luckycel
Iron
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Introduction
The relationship between free fatty acids (FFAs) and growth hormone (GH) inhibition is very well established. FFAs are one of the strongest physiological brakes on GH secretion, acting both at the pituitary and indirectly through hypothalamic pathways to suppress GH pulse amplitude and frequency. When FFAs are elevated, as commonly occurs in obesity, sedentary lifestyles, insulin resistance, high-fat feeding, chronic stress, and even prolonged fasting, the result is a marked reduction in GH release.This relationship has been demonstrated repeatedly in metabolic and endocrine research. Any intervention that raises circulating FFAs reliably suppresses GH secretion, and interventions that lower FFAs reliably enhance it. GH inhibition has been observed when FFAs are increased through lipid heparin infusion, high lipolytic states, obesity, insulin resistance, high fat feeding, prolonged fasting, and other metabolic conditions that elevate circulating fatty acids. The consistency of these findings shows that FFAs act as a primary metabolic signal that downregulates GH output.
In(The Effect of Free Fatty Acids on Growth Hormone(GH)-Releasing Hormone-Mediated GH Secretion in Man), they injected six normal young men with saline(normal FFAs) and a lipid-heparin solution, which significantly increased FFAs. It was shown that elevated FFAs reduced GNRH-stimulated GH secretion 3.4-fold; in other words, the group with elevated FFAs showed a 70% reduction in peak GH(~20 ng/mL absolute GH suppression):
In another study(Free Fatty Acids Block Growth Hormone (GH) Releasing Hormone-Stimulated GH Secretion in Man Directly at the Pituitary), researchers again elevated FFAs by infusing subjects with a lipid–heparin solution (250 mL of 10% Intralipid + 2500 U heparin). Ten normal men were tested twice, once under normal FFA conditions and once after lipid-heparin elevation of FFAs. The lipid–heparin infusion increased circulating FFAs from 0.41 ± 0.03 to 3.12 ± 0.40 mmol/L, producing a substantial rise similar to other FFA-elevation protocols.
GH secretion following GHRH stimulation was significantly impaired. Although GH levels were lower at all time points, the suppression reached statistical significance at 45, 60, and 90 minutes, confirming that elevated FFAs blunt the GH response over the full GH secretory window. Importantly, individual data revealed an all-or-none suppression pattern: 5 subjects showed complete abolition of GH response, while 5 exhibited normal responses, demonstrating that sufficiently elevated FFAs can entirely shut down GHRH-stimulated GH secretion.
To further examine timing, a more aggressive lipid-heparin infusion protocol was used (−90 to 0 min plus an extra heparin pulse). This produced a dramatic spike in FFAs from 1.06 ± 0.19 to 11.61 ± 0.83 mmol/L, and under these conditions, the GH peak of 15.8 ± 3.5 ng/mL was almost eliminated, falling to 0.9 ± 0.2 ng/mL. As the authors report:
These in vivo findings were then corroborated with in vitro experiments using cultured rat anterior pituitary cells. Both caprylic and oleic acid directly suppressed basal GH release as well as GH release stimulated by GHRH or forskolin, while leaving prolactin secretion unaffected, demonstrating that FFAs have a direct, pituitary-level inhibitory action independent of hypothalamic influence.
The authors explicitly conclude:
Now, all of the studies I’ve shown so far have been about increasing FFAs, not decreasing them, but there’s also a ton of evidence showing that suppression of FFAs, even in people with already normal FFAs, does increase GH:
In(Effect of acipimox, a lipid lowering drug, on growth hormone (GH) response to GH-releasing hormone in normal subjects), 11 normal male volunteers were tested with or without acipimox, a drug that blocks lipolysis and lowers FFAs. Subjects received a placebo or 500 mg acipimox, then were given growth hormone-releasing hormone (GHRH). The GH response to GHRH was significantly higher in those pretreated with acipimox than in those given a placebo, and in the placebo group, FFA levels rose progressively while GH response declined. This indicates that preventing FFA rise enhances GH release in normal men.
Another study(Effect of nicotinic acid administration on plasma HGH, FFA and glucose in obese subjects and in hypopituitary patients) reported that administration of nicotinic acid in obese as well as normal subjects caused an acute reduction of plasma FFAs followed by a progressive rise in plasma human growth hormone (HGH). This rise in GH occurred as FFAs dropped, supporting the inverse relationship between FFAs and GH.
Collectively, the evidence shows that suppressing FFAs removes a major inhibitory influence on the GH axis, allowing the body to restore stronger, more physiologic GH pulses. Understanding how to modulate FFAs, through either natural or pharmacological means, provides a powerful framework for enhancing endogenous GH production.
So, how do you suppress FFAs?
If your goal is to naturally support growth hormone (GH) secretion by lowering FFAs, focusing on lifestyle factors is a good place to start. Improving insulin sensitivity, engaging in regular exercise, eating carbohydrate-rich meals to trigger insulin-mediated suppression of lipolysis, and generally maintaining a healthy metabolic profile can all help lower free fatty acids (FFAs) and remove their inhibitory effect on GH. However, if you want a more direct and reliable way to suppress FFAs, pharmacologic agents such as niacin or acipimox are the most effective. While many people are skeptical of niacin because it is an over-the-counter vitamin, acipimox is actually a derivative of niacin and works on the same principle. Most discussions on niacin and GH recommend the immediate-release (flush) form, but this only increases GH for about three hours before levels drop, which is too short-lived to provide any noticeable effect. There haven’t been direct studies on sustained-release (SR) niacin and GH, but SR niacin suppresses FFAs just as effectively, and since lowering FFAs disinhibits GH secretion, it’s reasonable to hypothesize that SR niacin could provide a more prolonged enhancement of GH pulses.
Of course, this should all be taken with a grain of salt; there is no evidence that niacin will increase bone mass or height. Still, it is a cheap and reasonably effective supplement for disinhibition of GH release, and if one is trying to naturally maximize GH for bone growth and height, taking around 2 grams before bed could theoretically provide the strongest effect while sleeping.
