@LucH I take the position that JAMA frames the supposed salutary effect of omega-3s as solely based on how it is anti-inflammatory and supposedly beneficial from the standpoint that all inflammation is bad. But inflammation is part of the healing process. When there is trauma or infection, inflammation is needed to allow white blood cells inside tissues to effect repair. We see this when we get injured and we see this when there in infection. To simply say that omega-3s are good because it is anti-inflammatory is like saying all oxidative processes are bad because antioxidants are good, which isn't the case as the simplistic association is just misleading. I also don't take much stock in meta-analysis. It's like 10 dogs outnumbering humans in an election and dogs getting their candidate to win. If there are 10 flawed studies with conclusion A and only 2 good studies with a conclusion B, hands down conclusion A wins.

@AlphaCog simply its a mindset link text

@DavidPS Let's reveal what the linked article claims. "The following foods contain compounds that have been shown to increase aromatase activity, thereby increasing the production of estrogen." Beef Lamb Your argument is that beef and lamb will increase the synthesis of testosterone because of their cholesterol content, thereby increasing the amount of estrogen that will be synthesized. That's not the claim that the article makes. It claims that lamb and beef increase aromatase activity. That is a different claim than your claim that eating beef or lamb will increase the amount of estrogen synthesized. You could have a given level of aromatase activity but because there are more substrates for aromatase, you produce more estrogen. The article's claim is far more radical, though I think your claim and the article's claims are both wrong. For one, lamb and beef are high in SFA. Aromatase is most highly expressed in adipose tissue. High PUFA adipose tissue expresses more aromatase than does low PUFA adipose tissue. Insofar as lamb and beef resaturate adipose tissue, they should decrease aromatase expression. Testosterone is also a mild aromatase inhibitor, as is its metabolite DHT.

@Rah1woot @Rah1woot said in Since when decreasing brain blood flow is good?: If blood flow was truly reduced, it would not also increase oxygen consumption in the way that it does (so it goes). This is helpful, because when reading about oxygen deprivation, that's tied to pain and stress instead of vasoconstriction, though the two are similar.

@DavidPS I've thought along the same lines but struggled to fit those concepts coherently together. expression of Hmgcs2, the gene encoding rate-limiting enzyme of ketogenesis, decreases significantly in Leydig cells from aged mice. Additionally, the concentrations of ketone bodies β-hydroxybutyric acid and acetoacetic acid in young testes are substantially higher than that in serum, but significantly diminish in aged testes. Silencing of Hmgcs2 in young Leydig cells drives cell senescence and accelerated testicular aging. So what I'll do is shower you and the others with my open questions: First in line for me is the question: Why is (testicular) Hmgcs2 being downregulated in aging? Obviously feeding BHB as the end product of ketogenesis increased testosterone. Therefore the underlying mechanism can't be about sex hormone substrate availability (cholesterol). Rather, it's about a decline in ketogenesis, i.e. a tissue energy depletion: "suppression of ketogenesis impairs steroidogenic function of LCs" Is it locally or systemically/predominantly hepatically? --> The study tells us it's locally, because testicular tissue concentrations are higher than serum and "BHB andAcAc concentrations in serum were comparable between the young and the aged group (Fig. 2k, l)." "Remarkably, the concentration of ketone bodies in the testes were more than tenfold higher than that in serum (Fig. 2i–l), implying ketone bodies might have testis-specific functions" Is there a decline in peripheral fatty acid circulation as a reason for declining tissue ketogenesis? In contrast to ketone bodies, free fatty acids don't really cross the blood--brain-barrier. Do they significantly cross the blood-testis-barrier? If it's not about fatty acids as a ketogenesis substrate, is it about peripheral protein circulation levels? If it's about neither upstream substrates, is there perhaps a tissue-specific decrease of utilization to Acetyl-CoA? Is the HMGGCS2-decreasing cause founded in a lack of carnitine or a lack of CoA? Will supplementation of carnitine or stimulation of CoA then attain similar results to exogenously supplying BHB for that matter? --> The authors have followed this strain of thought and injected AAV vectors to deliver and overexpress the Hmgcs2 gene, demonstrating "that Hmgcs2 overexpression increased the levels of H3K9ac and FOXO3a in aged testicular tissue, similar to the levels in young testes" --> So it's not immediately about any substrate levels but HMGCS2 activity itself. Does this lead back to epigenetic downregulation of bodily functions, in this case HMGCS2, and the concepts of DNMTi and HDACi? --> Clearly there's a positive association between acetylation of H3K9 and HMGSC2 expression in rats in that HMGSC2 induced higher H3K9ac. Is this reciprocal, i.e. would H3K9ac also induce HMGCS2? Or does H3K9ac come about by increased concentrations of the products of HMGCS2, like BHB, and the cellular energy abundance provided by it? --> The authors followed this and found: "Consistent with in vitro results, Western blot analysis revealed that BHB increased the levels of H3K9ac and FOXO3a in aged testicular tissue, similar to the levels observed in young testes (Fig. 7d, e)." Is this then a course of gradual decline, wherein a decrease of testicular ketone energy in turn decreases its own synthesis? Just as the observation that more BHB increases its own synthesis? I.e. a positive / negative feedback loop? Would, therefore, a one time course of exogenous BHB or induced Hmgcs2 overexpression "reset" testicular ketogenesis back to a youthful level, wherefrom it may once again gradually decline? --> Well, the authors fed exogenous BHB in addition to the control diet to 18-months old rats for a duration of 2 months. Those were then 20-months old rats. Unfortunately, no subgroup to follow up on wrt to their physical activity and testicular findings has been kept and reported on beyond that. "Last, we validated the changes in FOXO3a-related inflammation genes through quantitative RT-PCR analysis, revealing that inflammation-related genes were significantly upregulated in aged mice, and Hmgcs2 overexpression reduced the expression of these genes (Supplementary Fig. 9b–e). Overall, these data suggest that enhancing ketogenesis is sufficient to alleviate LCs senescence and testicular aging in aged mice."

@yerrag Wow. Those are some additional challenges. Coincidentally, my brother just survived a 4 day hospital stay for congestive heart failure. I think your perspective of leaning on Peat and alternative counterculture, as a defense against status quo medical pathology, is the general perspective of most of us. But, just as you say, it's challenging, and can be daunting, because we are limited. I hope more alternative and naturopathic doctors adopt bioenergetic and similar principles to help those like us to bridge the gap, so we don't have to play doctor. There does seem to be a trend of some going that way. My thought is that it really won't be at its best until it's local, so we can have real-doctor support.

This is the fatty acid composition of the three fats. Margarine actually only has slightly higher PUFA content than olive oil and less MUFA than it. So overall margarine contains less unsaturated fats than olive oil does. One reason olive oil performs so well despite its high UFA content, might be its polyphenol content, containing oleocanthal, hydroxytyrosol or even small amounts of policosanol. I've talked about their pro-metabolic, testosterone enhancing effects here: https://bioenergetic.forum/topic/3624/olive-leaf-extract-increases-t3-t4-lowers-tsh?_=1748111089619 [image: 1748110991784-1000015133.png]

Canadian rancher Maggie is laughing at this study [image: 479882288_122215646534203038_8548433945113970019_n.jpg?_nc_cat=110&ccb=1-7&_nc_sid=aa7b47&_nc_eui2=AeEONy5dG5Kx5-34XHtxhRQBt5ClT8lPVV63kKVPyU9VXjMr1mkTi5uagTB2CxAehkeMCdDBREO5RBO6pNTE93Mh&_nc_ohc=46Rx1dxfwK4Q7kNvwHmX991&_nc_oc=AdmQT2HphoIoZDS5BY83m388IDQ46DPQi6doYYGDnPlUdOM_9e35SSXFjPrvkAF8swp6HaOwxtxUB8czLyOGK_S4&_nc_zt=23&_nc_ht=scontent.faep14-2.fna&_nc_gid=WOU-dhxC1Pp9RB-E-Ol0oA&oh=00_AfLaHX6bWJHfDaQa_ouMnc4b-wYLn9Thp0GkPwaUIA7U-Q&oe=68368F06]

Maybe something to do with tonicity, vascular tone and everything thereafter. Onset in reverse, I wonder what causes that. https://pmc.ncbi.nlm.nih.gov/articles/PMC11293686/ (Only a sample.) If "the next pandemic" had an energy mandate as or opposed to a vaccine mandate. I wonder what would happen.

the study in women athletes had them taking ridiculously high doses, something like 1g a day of TTFD iirc. it is dopamingeric, the first time i took a 25mg alinamin f tablet i got pronounced euphoria. it’s popular in japan.

@haidut I remember the announcement and recruiting for this study in 2020 iirc. Then everything vanished and reportedly the project's budget was cut and the study shelved. WTF was going on there. How did they finish it anyway? Who allowed them to now release their results? Too many polito-economic-corruptory questions.

@haidut Wow no surprise the SSRIS are really from the bad guys. Do you have a recommendations for what a person with PSSD should do? (Post ssri sexual dysfunction) Would love to hear your thoughts……. Thanks