That’s not a subtle effect — that’s a quarter of your growth factor capacity eliminated by poor sleep habits. Research from the University of Chicago demonstrated that restricting sleep to 4 hours per night for just one week reduced IGF-1 levels by a staggering 24%. Growth hormone is released in pulsatile fashion during deep sleep, with the largest spike occurring in the first 90 minutes after falling asleep. You can have solid testosterone levels and still underperform if your IGF-1 is in the gutter. Over a decade of coaching clients on hormone optimization, I’ve found that most people obsess over their testosterone numbers while completely ignoring IGF-1. Some clients with modest testosterone increases report dramatic subjective improvements. This IGF-1 reduction is one reason some natty plus practitioners combine enclomiphene with MK-677, a growth hormone secretagogue that raises IGF-1.
When all three are optimized—along with insulin sensitivity, training, and recovery—the results are dramatic and sustainable. But without proper androgen signaling and estrogen control, IGF-1 alone often produces a soft, underpowered physiquerather than dense, strong muscle. ASTB was designed to optimize the entire anabolic environment, not just inflate testosterone numbers. Estrogen is not the enemy—but excess estrogen is anabolic poison.
It plays a critical role in growth and development, particularly during childhood and adolescence. The relationship between IGF-1 and testosterone is complex and not a direct cause-and-effect. This would suggest greater nerve CV is a possibility with higher IGF-1 levels, and this has been demonstrated in an earlier study by examining IGF-1 knockout mice (Gao et al., 1999). At the spinal level, motor neurons express IGF-1 receptors and are protected from glutamate toxicity with IGF-1 treatment in motor neurons from E15 rat embryos (Vincent et al., 2004), although the timing of the treatment is important to recovery (Vincent et al., 2004). In a rat facial nerve avulsion model, IGF-1Ea- and MGF-preserves 37% and 88% more motor neurons when treated a week before injury compared to the untreated nerve avulsion group, respectively (Aperghis et al., 2004).
In recent years, IGF-1 has become the new buzzword in the muscle-building world. There are no supplements that consistently and reliably increase IGF-1 to a clinically significant degree without potential risks. Are there any supplements that directly increase IGF-1 safely and effectively? Intermittent fasting can impact IGF-1 levels, typically by causing a temporary decrease during the fasting period.
The best way to measure your IGF-1 levels is through a blood test. It is almost never the first or even second line of treatment for low testosterone. Are there specific medical conditions where IGF-1 supplementation might be considered to indirectly help with low testosterone? Moreover, there are potential side effects that need careful consideration.
Anabolic effects of AR and testosterone upregulation after RE occur through a combination of both genomic i.e., transcriptional capacity, and non-genomic i.e., translational efficiency, pathways (Kraemer et al., 2020). With aging, there is a linear decline in bioavailable circulating testosterone in both men and women (Kraemer et al., 1998; Hakkinen et al., 2000), with these reductions leading to osteoporosis in both sexes (Mohamad et al., 2016). Finally, it is important when overviewing the role of testosterone in controlling muscle mass, to consider older adults. Moreover, females do not have Leydig cells; the cells which are likely the source of the acute RE-induced increase in testosterone in men (Kvorning et al., 2007).

Gender : Female