History of GH and fat loss
Growth hormone (GH) is a very powerful fat mobilizer that has been studied by scientists since the 1920s when early animal experiments showed that treated animals from the pituitary were consistently slimmer than untreated control animals. But it wasn’t until 1945, when GH was first isolated from the pituitary, that researchers started to conclusively link the pituitary’s effects on fat mobilisation to this polypeptide.
Describe lipolysis.
The physiological process known as lipolysis breaks down stored triacylglycerol to produce fatty acids, which the body uses as an energy source. Triacylglycerol is hydrolyzed into fatty acids and glycerol and then released into the bloodstream for oxidation and ATP synthesis. Triacylglycerol is stored within the lipid droplets of adipocytes. Understanding the distinctions between mobilisation and oxidation will be crucial, but a thorough examination of lipolysis is outside the purview of this essay.
The relationship between GH and fasting and the stress hormone
By its very nature, GH is a stress hormone, and stressful activities like fasting and exercise increase endogenous production. But for the remainder of this post, we’ll concentrate more on how GH functions while people are fasting and how it relates to those who want to get the most out of the lipolytic potential of their exogenous GH stack designs. About six hours after eating, the fasting (postabsorptive) phase begins. During this time, the body’s main goals are to provide, convert, and preserve fuel substrates. Endogenous GH secretion is significantly increased at this time and may continue for 48–72 hours. In contrast to the frequency of the pulses and inter-pulse trough levels, the increase of released GH is directly correlated with pulse amplitude. While levels of catabolic hormones all rise during fasting, GH is the only anabolic hormone that increases.
Mechanisms of action – lipolysis mediated by GH
It’s crucial to comprehend the multiple metabolic changes brought on by the increased rates of GH production. Maintaining glucose homeostasis during a fast is the body’s first goal to supply enough glucose to the brain and other tissues (like red blood cells) that depend on it. To do this, the body changes its propensity for ingesting fuel from fat substrates to concurrently save vital glucose and protein reserves. Since there is no evidence of dietary glucose consumption, the mobilisation of glycogen will take place concurrently with this shift in muscle tissues and the liver’s preference for fat substrates as a source of energy. In the absence of dietary glucose, the liver also releases a significant quantity of glucose into the blood to assist maintain blood glucose levels. This is possible in large part because of the concurrent decline in blood insulin levels, which stop the released glucose from entering muscle and fat cells.
Additionally, the increased GH causes an insulin resistance condition that is essential for maintaining the body’s priceless glucose stores. By reducing glucose oxidation and, in turn, the demand for gluconeogenic precursors from muscle protein reserves, GH’s insulin-antagonistic actions effectively kill two birds with one stone. There are some theories on whether GH itself or the rise in FFAs is the main cause of this enhanced insulin resistance, but those ideas start to go into the realm of cellular transport and signalling pathways, so we’ll keep that topic for another time. To summarise, higher GH production during fasting inhibits glucose uptake in peripheral tissues by inhibiting GLUT-1, avoids glucose oxidation by increasing insulin resistance, and preserves amino storage both directly and indirectly.
Although it is commonly known that GH affects lipolysis, the precise processes by which it does so are still relatively unclear. As GH can decrease adipose tissue lipoprotein lipase (LPL), activate hormone-sensitive lipase (HSL), and counteract insulin’s antilipolytic actions, it has been hypothesised that this may have several aspects. Since HSL is directly engaged in the triacylglycerol hydrolyzation process, increased HSL expression in adipocytes boosts their lipolytic capacity. After activation, HSL moves to the intracellular fat droplet’s periphery where it hydrolyzes triacylglycerol into FFA and glycerol. Many people are also aware of it as the enzyme that controls the pace of lipolysis. It’s important to note, however, that not all research has consistently demonstrated that GH raises HSL mRNA levels in adipocytes.
Maximum Lipolysis rate
Is there a real (or hypothetical) cap on the rate at which lipolysis will occur as we strive to build a stack that optimises its potential? We truly do have a solution, at least in terms of the maximum pace at which GH delivered intravenously may induce lipolysis. This dosage, which corresponds to an average peak GH concentration of 32.4mcg/litre, was discovered to be about 3mcgs/kg. The dosage was not dependent on gender or age and is about like 1.2 to 1.5 IUs for a 100 kg lean guy. Any dosage over this does not truly have a bigger effect on lipolysis. Unexpectedly, this also represents the maximum amount of endogenous, spontaneously occurring secretory bursts. This is thought to be a restriction or bottleneck brought on at least in part by the extra-renal clearance rates in combination with the levels of circulating GHBP.
Pharmaceutical Biochemistry and Biodynamics
Pharmacokinetics describes how a chemical is absorbed, distributed, and excreted through the body, whereas pharmacodynamics describes the effects a substance has on the body. To effectively use GH’s lipolytic capabilities, ensure that GH is administered optimally, and avoid protocol designs that are improperly set, it is crucial to comprehend both as they relate to GH. It would be in our best interests to try not to squander GH because it may be expensive to acquire.
The pharmacokinetics of GH are significantly influenced by the routes of administration. Endogenous GH is released in a pulsatile manner, as was previously stated, and is promptly removed from serum by the body’s intrinsic negative regulatory feedback. One would need to utilise intravenous delivery once every 2-3 hours, which is how often it takes for the ultra-short feedback (GHRH suppressing its secretion) to clear, to imitate this secretory activity most accurately. But I don’t recommend or promote this unless it’s done so under medical supervision, therefore this article will instead concentrate on the two most common ways to administer GH: subcutaneous and intramuscular.
Combinatory Synergies
We would do well to select substances that have the potential to have cumulative or synergistic effects upon one another when constructing a fat loss stack that enhances lipolytic potential. We already covered a few of the many methods by which GH exerts its lipolytic effects. The beta-adrenergic receptors are involved in one of its important routes. Therefore, it makes sense that if we can improve the beta-sensitivity pathways and/or expression, we would be able to further enhance the lipolytic response to our stack. Androgen receptors, which are found in adipose tissues, allow androgens to directly cause powerful lipolytic actions. Androgens have also been proven to stimulate beta-adrenergic receptor expression, which is interesting in and of itself because it is a distinct mechanism that GH employs. This might be a powerful synergy in our stack design techniques because I’ve already highlighted how increasing the number of linked receptors in adipocytes could boost sensitivity and eventually lipolytic capacity.
Applications in real life and a sample stack design
Now that the background information has been cleared up, how would one go about creating a stack and delivering hormones?
I believe it is obvious that while taking a GH dose, one will want to be fasting. Although, unlike endogenous GH, the lipolytic effects of rHGH are not completely muted in the presence of meals, breaking this rule would be a grave mistake.
A single 2IU GH injection would be produced by following the fasting rules and using a dosage that is intended to provide the greatest lipolytic effect. Since we would likely already be fasting, performing this as soon as we wake up in the morning would be ideal for us. This would be a suitable strategy to employ for the injection because subcutaneous injections have a longer clearance period, especially if you want to stay fast for many hours after the injection. I would also think about engaging in organised activity (either in the form of LISS or weight training) during this starving window for a potential added influence on fat mobilisation rates.
If one could eat all their meals quickly and go into the evening in a semi-fasted condition, they could very likely give themselves a second 2IU injection of GH before going to bed by following the same instructions. There is even evidence, as was mentioned previously in the article’s body, that subcutaneous dose in the evening increases bioavailability. Therefore, if forced to pick between AM and PM, I would suggest taking the medication at this time. If not, provided they follow the right fasting parameters, employing a 2IU injection method both in the AM and PM can potentially optimise one’s lipolytic capacity over 24 hours.
Combining this GH dose regimen with an androgen stack can increase fat loss potential overall. For this reason, as well as to reduce the chance of lean tissue atrophy during prolonged periods of intake deficits, one should think about supraphysiological AAS. Varying androgen types may result in a somewhat different rate of fat loss; however, this is outside the purview of this page. Here, even a straightforward testosterone based AAS stack design would be ideal. Based on their synergistic effects with androgens and GH described in the article, adding both exogenous thyroid and clenbuterol to the stack will further increase the total lipolytic capacity. Due to their unique characteristics, T4 and clenbuterol can both be taken once a day. I advise folks who use T3 to take at least two dosages every day, spaced 12 hours apart.
