@sabupa I believe it's too much sunlight without or with minimal protection, He lives in Costa Rica.
Daytime exposure should not be super high.

@Mulloch94

It's my bad I didn't watch your YouTube links and I apologize. I thought the term sugar fasting referred to fasting from sugar, and didn't watch the videos thinking it still is about sugar bad.

So yes, it's good there are such videos popping up. I hope they snowball and would lead to the eventual widescale debunking of the sugar is bad lie, which is so entrenched.

Thanks for sharing!

@Korven

So far I have used 3 AI- Gemini, Deepseek, and Delphi.

I don't claim they are representative of AI in its full potential whether it be good or bad. But I want to use it to the fullest extent to bridge my own admittedly imperfections as a regular human with a regular IQ, whatever that is.

Though my preference is that I don't use AI to do things I can do well over the years, which are cognitive skills I have learned, if not mastered in varying degrees, to make me highly functional unaided by automation such as AI. Which is to say I won't let it compose phrases, paragraphs, essays, poems, articles, books, letters, and poems, and scripts for me. Nor keep me from mentally find my way through calculations, approximations, using rules of thumbs when needed. True enough, I use Waze for directions when driving, but don't use it in my own locality as I want to keep the ability to find my way through the city the way taxicab drivers have that honed as disuse equates to misuse and that would be s detriment to my brain and it's neurons.

But when it comes to health as centered especially on bioenergetics, and as much as I've learned a great extent from Ray Peat, I haven't fully tapped into his knowledge of metabolic principles particularly in the way all his research, sorting wheat from chaff, narratives from truths, and all condensed into his writings and interviews. The body of knowledge we would find in his writing, as we know it forms our understanding of bioenergetics, which is the umbrella of knowledge involving notable great minds such as Szent Gyogi, Otto, Ling et al.

Which is why in my interaction with Delphi's AI that tried to capture Ray Peat's essence based on all his writings and interviews and whatever that can be gleaned from his life's works, I have found myself asking many questions of clarification and guidance that helps me fill many gaps of information I have that without it would be something I feel would longer on to my death unquestioned with problems in my health unresolved and uncorrected, and me unhealed. I think that using Delphi's implementation of emulating a clone of ideas and mindset, I have in the past few days found some stirrings of hope that my healing journey can resume and also end in short time with success.

What is Delphi AI is answered in this article that has a video clip of an interview by Maria Bartiromo of the founder of Delphi Lara Lajevardian from last year:

https://www.foxbusiness.com/media/maria-bartiromo-interviews-lifelike-artificial-intelligence-clone

And here is a series of questions that I have asked the AI and the answers I had gotten, which I find extremely helpful:

https://delphi.ai/ray-peat/talk/conversation/shared/69881fbc-cf44-49df-b31c-281571391e30

I hope you can give it a try for your own use. I think you will be pleasantly surprised at what it can do.

@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.

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Useful info for other readers to optimize weight (prevention)
Sweeteners and their impact on the microbiota + possible weight gain
Dr Philippe Veroli – SCE 10/23
Poison for your "good" gut bacteria
Most sweeteners pass through the digestive tract undigested and therefore arrive unaltered in contact with the intestinal flora, on which they have a direct impact.
The population of beneficial bacteria decreased, while that of eleven opportunistic bacterial genera increased. In addition, Butyrivibrio bacteria, associated with blood sugar control, were less abundant! ( 8 )
Artificial Sweeteners Help You… Gain Weight
Studies show that consumers of so-called diet drinks also have an increased risk of obesity (9). In fact, their risk of premature death is similar to those who consume sugary drinks (10)! A recent American study (11) even showed that the combined consumption of a sweetener (sucralose) and sucrose significantly disrupts carbohydrate metabolism and causes a chronic increase in blood glucose and insulin levels, which is not the case with the consumption of sucralose or sucrose alone. However, diet products are always consumed with other sources of sugar (bread, fries, pastries), which explains why products containing sweeteners can contribute to excess weight gain. This disruption is very rapid, as it was observed after consuming the sweetener only seven times over a two-week period. Furthermore, the absence of calories prevents satiety and increases sugar cravings. There is therefore no reason to consume light industrial products, neither for body weight management nor for general health.
(…)
Sweeteners manipulate the brain
Normally, the brain's reward system is activated when it receives sugar. With sweeteners, this system is disrupted: the brain no longer receives its usual dose of sugar, and the craving for sugar is increased, leading to snacking, preferably on fatty and sweet foods, to compensate for the disappointment registered by the neurons. We have seen that aspartame consumption leads to the formation of phenylalanine, aspartic acid, and methanol. These substances enter the brain and can inhibit the synthesis and release of several neurotransmitters (dopamine, norepinephrine, and serotonin), which normally regulate brain neurological activity (16). Furthermore, aspartame alters the expression of genes regulating the excitation-inhibition balance in the amygdala, a brain region that regulates anxiety and fear.
Excerpt from this article:

Prise de poids, diabète : les substituts du sucre sont-ils tous cancérigènes ? (Weight gain, diabetes: are all sugar substitutes carcinogenic?)
Dr Philippe Veroli – SCE 10/23
https://mirzoune-ciboulette.forumactif.org/t1998-microbiote-info-diverse#29338
Sources & References
8. Dorin Harpaz D, Yeo LP, Cecchini F, et al. Measuring Artificial Sweeteners Toxicity Using a Bioluminescent Bacterial Panel. Molecules 2018, 23(10), 2454. doi.org/10.3390/molecules23102454
9. Fowler SP et coll. Fueling the obesity epidemic? Artificially sweetened beverage use and long-term weight gain. Obesity 2008; 16: 1894-900.
10. Mullee A et coll. Association between soft drink consumption and mortality in 10 European countries. JAMA Intern. Med. 2019; e192478.
11. Dalenberg JR et coll. Short-term consumption of sucralose with, but not without, carbohydrate impairs neural and metabolic sensitivity to sugar in humans. Cell Metab. 2020; 31: 493-502.
16. Choudhary AK, Lee YY. Neurophysiological symptoms and aspartame: What is the connection?. Nutritional neuroscience, 2018, vol. 21, no 5, p. 306-316.

@CrumblingCookie Thank you so much.

I have found a lab that can test all pathogens you mentioned. Any other pathogens I should test? Aspergillus and Saccharomyces maybe? I suspect the pathogen in my gut might be producing ethanol

@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.

@tubert makes sense! thx

@ThinPicking Thanks for the info. Please don't trouble yourself too much.

Still think it's a troll account. Taking isotretinoin proactively because testosterone could give him acne... not even 14 year old me could have come up with that.

@alfredoolivas

Have you used Deus Medical before? Seeing lots of Mixed reviews.

He's the guy that gave that famous talk at the ancestral health symposium about CO2. Pretty great. It's funny because that meet-up is like mostly low carbers, and here this guy is just casually destructing the whole process of fat metabolism and why it sucks lmao. https://www.youtube.com/watch?v=nGv4JZB2yws&t

@wester130 cabergoline is the cheapest, best value and most effective ergot derivative for lowering prolactin and cortisol - it is one of the main drugs used to treat cushings syndrome.

@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."