Yet another study demonstrating that many mysterious, and sometimes severe\/fatal (e.g. ALS) muscle-related conditions may be not only bioenergetic in origin, but can trace their causes back to stressful childhood. The study below not only suggests that childhood stress can cause muscle dysfunction in adulthood by inhibiting oxidative phosphorylation (OXPHOS) and ATP synthesis, but that the effects was “dose-dependent”. Namely, each adverse even during childhood had an additional negative effect on ATP synthesis in adulthood, and thus muscle dysfunction severity. While the study does not speculate on mechanisms of action, my guess is that the lower OXPHOS\/ATP was driven by reduced thyroid function due to activation of the HPA axis due to the stressful event(s). Of course, HPA activation results in chronically elevated cortisol, and even mainstream medicine admits the latter has devastating effects on the musculoskeletal system. As such, muscle dysfunction in adulthood should be amenable to simple treatments with thyroid or anti-cortisol substances. If those are not accessible, something as simple as aspirin may be able to do the trick since aspirin is not only a metabolic booster, but its metabolite salicylic acid inhibits the enzyme 11b-HSD1, which is the rate-limiting step in cortisol synthesis. Pregnenolone, progesterone, DHEA and various quinones should also be therapeutic. Speaking of quinones, there have been a number of clinical trials with CoQ10 for muscle conditions, but the results have been inconsistent. Aside from the often-insufficient dosages, one of the reasons for the inconsistent results may be that benzoquinones such as CoQ10 are MAO-A inhibitors and that mechanism has a known anti-metabolic effects by decreasing the degradation of serotonin. Using naphthoquinone (e.g. vitamin K) or anthraquinone (e.g. emodin) derivatives may be a better approach as the former are selective inhibitors of MAO-B (which has already been demonstrated to have therapeutic effects in muscle conditions) while the latter are more or less neutral when it comes to neurotransmitters, but happen to inhibit 11b-HSD1 (e.g. emodin), just like salicylic acid. So, something as simple as aspirin + vitamin K may be sufficient to restore proper muscle function.<\/p>\n
https:\/\/doi.org\/10.1126\/sciadv.adj6411<\/a><\/p>\n “…Forty-five percent of the sample reported experiencing one or more adverse childhood events. After adjustment, each additional event was associated with \u22120.08 SD<\/strong><\/span> (95% confidence interval = \u22120.13, \u22120.02) lower ATPmax<\/sub><\/strong><\/span>. No association was observed with Max OXPHOS. Adverse childhood events are associated with lower ATP production in later life.”<\/p>\n Childhood trauma may stymie muscle function later<\/a><\/p><\/blockquote>\n