@yerrag That should reduce LPS in the long term, so i think it's unlikely to be the mechanism

ETIFOXINE Has anybody tried it? It seems to be a GABAergic that strongly increases (neuro-)steroids. Here you can see that it strongly increases Pregnenolone, Progesterone and the infamous 5aDHP in the brain, especially in higher doses. It also seems to increase andogens T + DHT in lower doses while it suppresses them in higher doses. [image: 1784979396693-bd4c3d95-fe6e-4e8a-b8ed-0e539a733f0f-image.jpeg] https://www.pismin.com/10.1016/j.psyneuen.2017.05.022 Different study similar findings: "Exposure of frog hypothalamic explants to graded concentrations of etifoxine produced a dose-dependent increase in the biosynthesis of 17-hydroxypregnenolone, dehydroepiandrosterone, progesterone and tetrahydroprogesterone, ..." https://pubmed.ncbi.nlm.nih.gov/25785994/ Etifoxine reverses weight gain on a HFD https://pubmed.ncbi.nlm.nih.gov/32679124/ Etifoxine restores mitochondrial oxidative phosphorylation (in vitro) https://pmc.ncbi.nlm.nih.gov/articles/PMC8657969/ It seems to increase GABA-A receptors or at least amplify its function. https://pubmed.ncbi.nlm.nih.gov/10854897/

@haidut I am wondering if it is really inflammation that is causing mitochondrial dysfunction and not the other way around. I have a large store of bacteria that I keep having to kill and each time there is a kill plenty of endotoxins are released and they are a major source of inflammation. And it suppresses mitochondrial activity to the point that even the conversion of cholesterol to pregnenolone and downstream prosuction of hormones and steroids are very much affected. To such effect that taking hormones like thyroid and pregnenolone and progesterone can hardly make a dent. I had to inhibit the nfkb inflammatory response using turmeric and black pepper in order to see my cholesterol level go down and my hormonal production go up. But it is hard to keep endotoxins low when there is a large colony of pathogenic microbes and in my case it is feom periodontal infection having translocated to my vascular and lymphatic system where it get more embedded over time especially as it gets protected by biofilms. One way I see out of this conundrum of killing pathogens by relying on our endogenous ROS from our own innate immune system and from use of pharma antibiotics or herbal antibacterials,, which all end up producing endotoxins; is to engage antibacterial peptides such as LL-37 in neutrophils and macrophages - to kill pathogens with the benefit of not leaving behind endotoxins that both inflame and cause oxidative stress. More sunshine to produce high levels of Vitamin D (50-80 ng/dl) together with plenty of butyric acid in the gut gives the body a high endogenous supply of LL-37 to achieve effective antimicrobial activity without endotoxic side effects.

L-form, aka protoplast or spheroplast, yeasts and fungi are likely the much more widespread and pressing issues next to biofilms. IMO of a more widespread importance than the specialty case of additional biliary survival as per this thread's original topic. Such L-form variants (predominated by filamentous Aspergillus, plus Candida parapsilosis and others) were found in autistic children, and often their mothers yet not in healthy controls. Acquisition of the L-forms especially during gestation and infancy is suspected to confer a particular kind of life-long immunological blindness to these. Dysbiotic microbiota in autistic children and their mothers: persistence of fungal and bacterial wall-deficient L-form variants in blood, 2019 An according collection of case studies, albeit with a strong conflict of interests (authors are heavily involved in Mosaic Diagnostics, formerly Great Plains Laboratory, with their urine organic acid tests): Case Study: Rapid Complete Recovery From An Autism Spectrum Disorder After Treatment of Aspergillus With The Antifungal Drugs Itraconazole And Sporanox, 2020 The seemingly most powerful antifungal combination discovered so far which targets the fungal membranes and therefore equally well any L-form persister fungi variants is Itraconazole or Posaconazole + a HIV protease inhibitor like Atazavir (+Ritonavir as a systemic inhibitor of degradation via Cyp3A4 to boost ATV's impact. RTV can be very cheap; thus no biggie): Enhanced antifungal activity of posaconazole against Candida auris by HIV protease inhibitors, atazanavir and saquinavir, 2024 There are a few more studies published on combinations like this without the particular use of spheroplasts but on "normal" fungi, too. Such combos also overcome aquired resistancies by upregulated efflux pumps (CDR1/2) and the filaments and biofilm abilities. @sunsunsun

@Lejeboca said: Nah, the Picard guy is anti-high-metabolic, judging by his papers (See my post https://bioenergetic.forum/post/65534 .) Glad he does not reference Ray or other metabolism giants to support his work. Isn't the title of that implying a lack of substrate for a healthy response to the load though. Picard will have to walk past a statue of Ray, Georgi and Danny on his way in to Starfleet Academy.

So then, Mitolipin to the rescue

Looks like Picard's work supports the "rate of living theory". For example, in his Cellular allostatic load is linked to increased energy expenditure and accelerated biological aging hypermetabolism, defined as "increased energy expenditure", it is concluded that "a robust and specific temporal association be­tween hypermetabolism and premature cell death, aligning with pro­spective observations in the human literature where hypermetabolism increases mortality risk. Finally, our experimental modulation of OxPhos and total J_ATP suggest that total energy expenditure, rather than flux through mitochondrial OxPhos, may have a particularly influential ef­fect on cellular aging". Hmm... but the references that they use could be mined further for some gems.

Okay the speculation of trenbolone being 8x as anabolic as testosterone (that I may of said?), may be true. According to the “Anabolics 11th Edition”, trenbolone is 5x as anabolic as nandrolone acetate. Therefore, using Vigorous’ “dubious maths” it is 6x as anabolic as testosterone. Given that in humans, it was given at 75mg hex ester every 2 weeks, it’s totally plausible. 225mg every week of T for a burn patient doesn’t seem crazy. Nandrolone decanoate is given at 100mg a week. That’s 125mg T a week in terms of matching anabolism So for those reading, tren is approximately 6-8x as anabolic as testosterone https://youtu.be/OeRFm_9uRk0?si=NVbrAiiAchxIUS_1