Dandruff or scalp irritation? Try BLOO.

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  • Low calcium and vitamin D levels linked to premature hair graying

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  • The anti-cortisol mechanism of trenbolone

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    alfredoolivasA
    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
  • What Does The Tour de France Do To The Human Body?

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    LukeL
    Damn, talks about broken collarbones and today Vingegaard crashes and likely breaks his.
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    TexugoDoMelT
    What I have to say about the studies on “essential fatty acid deficiency (EFAD)” is that they are all incomplete, and it is necessary to piece the studies together like a puzzle, in addition to seeking out others that may not specifically address EFAD. 1. The overwhelming number of symptoms attributed to EFAD actually stems from the high metabolic rate caused by TEWL, which activates thermogenesis. If you neutralize TEWL in an EFAD-affected animal by increasing the humidity in the laboratory, it grows and develops normally without any symptoms. In many studies on EFAD, researchers mention “spontaneous recovery”—usually in the summer, lasting for long periods—followed by a worsening of symptoms, which they attribute to the seasons and their fluctuations in humidity. [image: 1783716841140-c2beaeab-cd4b-4280-893f-15ed7932ef46-image.jpeg] 2- The body is a dissipative system; if you remove n-3/n-6, the body changes the way it handles various processes that previously relied on them. It is a mistake in these studies to remove n-6 while keeping the diet essentially the same. I’ll give an example using zinc, a deficiency of which causes similar skin symptoms: [image: 1783716910557-18db4162-345c-48b3-8870-f9e63651d26c-image.jpeg] This table shows an EFAD (HCO) diet and a non-EFAD (corn oil) diet, and both have versions supplemented with zinc (C-2 and D-2); the key point here is that the protein source is casein (this detail will be important later): [image: 1783716961668-e9846a0d-82e0-4480-8775-ccff5e0a2872-image.jpeg] Now, in this table, it's the same thing, but supplemented with egg albumin instead of casein: [image: 1783717008090-135a94d7-db40-4a08-b637-c8e7375a8dae-image.jpeg] It can be seen from these two tables that EFAD causes skin problems if: There is a zinc deficiency The proteins are casein-based, rather than egg albumin. I was curious as to why the type of protein would influence the symptoms, so I remembered this: [image: 1783717055701-1fcf7b00-75a5-49ff-b33f-950b0a9deb48-image.jpeg] Egg albumin is rich in sulfur-containing amino acids. [image: 1783778512118-7b99813c-70e6-4d66-8021-ea93b7d1b7e9-image.jpeg] I considered the possibility of contamination with PUFA, but they also use soy protein, which I think theoretically poses a greater risk: [image: 1783717093452-c1514880-eaeb-428f-ada3-bac7bcafde56-image.jpeg] Is it possible that, with enough zinc, they could live indefinitely on an EFAD diet? Who knows... Well, if the problem is humidity, people who live by the beach can easily follow a diet like this and reap the benefits of the EFAD (resistance to endotoxins, inflammation, autoimmune diseases, snake venom, etc.). And btw, it is possible for a human to live well in EFAD, without skin problems, in a city as well. [image: 1783718698155-ec41016c-25cb-4832-b2a5-490f5885f41b-image.jpeg] (not mine) Thanks to learnmyhelpless at X for reminding me of zinc and EFAD relationship haha
  • Dinkov Distilled: Metabolic Theory of Health

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    alfredoolivasA
    @springsnow check DMs
  • Tuinone – Liquid Product with Thymoquinone

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    jamezb46J
    @alfredoolivas What is androstane?
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    LucHL
    Talk with AI (Claude) to try to understand Crumblecooking’s comment. Some info to move the Schmilblick forward (to move things along). Context: Weak ground: researchers focused on patients diagnosed with either ADRD or mild cognitive impairment (MCI). A widely used supplement marketed for joint pain relief may be linked to faster progression of Alzheimer's disease, according to new research from the University of Florida. Researchers found that glucosamine significantly increased the attachment of sugar molecules to proteins within cells. Mice receiving glucosamine also showed worsening deficits in social memory, which is the ability to recognize and remember other individuals. When scientists chemically reduced this sugar-tagging activity, memory performance improved. "In the United States, there are about 7 million people living with Alzheimer's and millions more with related dementias such as Lewy body or frontotemporal dementia," said senior author Ramon Sun, Ph.D., director of the Center for Advanced Spatial Biomolecule Research and associate director for innovation of UF's McKnight Brain Institute. "A lot of these people actively take an over-the-counter supplement that could be making their disease progression worse." Comment from the forumer Crumblecooking: Add linoleic acid to this—the prostaglandin E₂ precursor—and you then have a powerful yeast➝hyphal transducer—more commonly known as potato chips, bread, and granola bars. Comment from LucH (me) (not yet posted): I know we have here a weak ground: already inflamed cells behind BBB by ROS perturb the cohesion, weakening the balance behind BBB: There is inflammation (via ROS) and perturbation in the brain cells as far as the homeostatic balance is concerned: Detailed explanation: The blood-brain barrier (BBB) is composed primarily of cerebral microvascular endothelial cells and astrocytes linked by tight junctions (TJs) and adhesion molecules (AMs). This system maintains the homeostatic balance between the brain parenchyma and the extracellular fluid. => Not a proof, OK. But more and more studies take this direction... How to Help a Leaky BBB before it’s too late (usual process for ¾ people above 80ies) a) Which useful molecules can cross the BBB: Aspirin (mind the platelet impact) Caffeine (coffee and tea) EGCG (green tea) Resveratrol Taurine Vitamin E Vitamin C Etc. See detailed information on reference 2. b) How to Heal a Leaky Blood-Brain Barrier Which Supplements Repair the Blood-Brain Barrier? Several B vitamins support blood-brain barrier health: a vitamin B1 (thiamine) deficiency disrupts the blood-brain barrier, and supplementation can restore it. Vitamins B12, B5, and B9 (folate) can restore the integrity of the blood-brain barrier. (4) Magnesium, as a cofactor in over 300 biochemical processes, affects brain neurotransmitters, enzymes, and hormones. Magnesium L-threonate is often used for its potential brain benefits and may help manage certain brain disorders, such as depression, Alzheimer's disease, and age-related memory loss. To be continued on the reference 1. Sources and references Useful link: Alzheimer's Cognitive Decline and Inflammation (In French but with links in English) https://mirzoune-ciboulette.forumactif.org/t2067-declin-cognitif-dans-alzheimer-et-inflammation#29882 What can get through the BBB? https://my.clevelandclinic.org/health/body/24931-blood-brain-barrier-bbb The list of what can make it through your BBB is extremely lengthy, so here are some examples … Antocyanins can cross the BBB Phenolic compounds that cross the blood–brain barrier exert positive health effects as central nervous system antioxidants. 2021 Food & Function. Dafne Velásquez-Jiménez et al. What supplements repair the blood-brain barrier? https://thefnc.com/research/nutrients-to-help-repair-your-blood-brain-barrier/#:~:text=B vitamins.,restore blood-brain barrier integrity Glutamine et cancer Un lien intéressant : https://www.julienvenesson.fr/glutamine-cancer/ A natural compound, EGCG from green tea, also shows promise. It counteracts the action of glutamate dehydrogenase, which converts glutamate into α-ketoglutarate, leading to the death of cancer cells. https://www.julienvenesson.fr/la-quercetine-ameliore-les-effets-du-the-vert-sur-la-sante/ Glutamine is the preferred amino acid of cancer cells, required for their growth. But if you try to limit this intake, the cancer will destroy muscle tissue to obtain it. You can try to ration it, but never eliminate it. Therefore, you limit it, you don't eliminate it. NB: Whenever I suffer from a weak / a thin layer of stomach mucin, I associate ¼ tsp glutamine and ¼ tsp taurine powder (+ 1.5 g magnesium bisglycinate). Take one hour before bedtime. Always associate both to dampen the possible glutamate pathway. Question for AI (Claude) I don’t want a comment or an analyze of my answer but I’d like an explanation for Crumblecooking’s comment: “Add linoleic acid to this—the prostaglandin E₂ precursor—and you then have a powerful yeast➝hyphal transducer—more commonly known as potato chips, bread, and granola bars.” => What is the mechanism? Asparagine becoming nitrosamine? Short answer for IA (summarized because in French and 2 pages A4 long) No, not linked to nitrosamine. Vocabulary: the yeast→hyphal morphological transition. Hyphal: Adjective derived from “hypha”, describing anything related to this filamentous form. We have a morphological change from the yeast form (isolated round cell) to the invasive filamentous form. So, ultra-processed foods rich in omega-6 oils potentiate the pro-Alzheimer's effect of glucosamine via a dual mechanism: local inflammation (PGE₂) + fungal dysbiosis, promoting a compromised intestinal mucosa/BBB. The hyphal transition of Candida increases epithelial permeability, exacerbating precisely the leaky BBB problem you describe (LucH talking with Claude). LucH said: Okay, I get it. It's a stimulant on already fragile ground. IA says: Exactly. That's the most accurate wording. A stimulator—not a primary cause—on an already weakened foundation: • Compromised BBB • Chronic low-grade inflammation • Already disrupted O-GlcNAcylation Glucosamine + PGE₂ don't initiate the disease; they accelerate what's already underway. That's why the study refers to aggravated progression, not a trigger. This ties in with your notion of a weak ground from the introduction—the underlying condition precedes it, the stimulator amplifies it.
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    R
    @dapose It varies, I don't take daily anymore as my body doesnt need it that much. Before I took powder so not exact dosages but approximately 300mg with a meal that doesnt have calcium and away from coffee. Genuinely life changing for me personally.
  • Actionable Steps Website

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  • Feeling good on low protein

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    alfredoolivasA
    @sunsunsun Yeah, I personally haven't noticed a drop in strength though, despite losing 19lbs, but that is probably because I take tren. Though in all fairness, very little.
  • Advanced Glycation End-Products (AGEs) in Coffee

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    LucHL
    @AlphaZance said: Metabolic stress drives the formation of AGEs, but Ray Peat has not addressed existing AGEs in foods. yes, but you didn't find the right doc. The etymology of the word glycation doesn't only rely on sugar. You d' better take care of "lipid glycation" and not only from sugar sources. Request for IA: glycation doesn't only rely on sugar but much more on fat alteration. Google answer: You are on the right track! While sugar drives classic glycation, fat alteration (lipoxidation) is a massive, often underappreciated driver of Advanced Glycation End-products (AGEs). The Lipid-AGE ConnectionLipoxidation: When fats oxidize, they create reactive, unstable molecules (like dicarbonyls). These intermediate compounds then cross-link with proteins just as sugar molecules do, directly forming harmful AGEs.The Maillard Reaction: Heat processing (such as frying or grilling) animal foods high in both fat and protein yields the highest levels of dietary AGEs. The Interplay: Both pathways are deeply connected under "carbonyl stress". How to Manage Both Sugar and Fat Risks To minimize the buildup of AGEs and slow down cellular aging, you can focus on a few evidence-backed lifestyle and dietary strategies: Watch Your Cooking Methods: Avoid cooking foods—especially meats and fats—at high temperatures. Steaming, boiling, or poaching creates significantly fewer AGEs than frying, broiling, or grilling. Balance Dietary Fats: The type of fat you eat matters. Clinical trials suggest that increasing consumption of monounsaturated fats (MUFAs) and Omega-3 fatty acids can help control and beneficially affect your glycation markers. Maintain Stable Blood Sugar: Even though fat oxidation is crucial, reducing refined sugar and fructose intake lowers the available "fuel" for traditional sugar-protein glycation.Leverage Antioxidants: Oxidative stress is the catalyst for fat alteration. Consuming antioxidant-rich foods or using targeted anti-glycation interventions helps neutralize free radicals. Scientific Sources & Evidence To dive deeper into the science of how fats and sugars alter your cells and skin, review these authoritative resources: [1, 2] https://www.lifeextension.com/wellness/aging/glycation https://www.skinnutritioninstitute.com/blog/glycation-how-fat-ages-your-skin-and-destroys-collagen-clone Glycation & Oxidation: Explore the exact breakdown of how lipid damage forms AGEs through Advanced Glycation End-products (AGEs): an emerging ... - PMC. [1] https://pmc.ncbi.nlm.nih.gov/articles/PMC4648888/&ved=2ahUKEwjPyLaG4-iUAxXlkP0HHRf_BQEQy_kOegoIAggACAEIJxAC&opi=89978449&cd&psig=AOvVaw2nBJNpgaZPrk0yj1bOffN0&ust=1780497191863000 Lipoxidation Pathways: Read about how both carbohydrates and lipids drive carbonyl stress at Glycation, oxidation, and lipoxidation in the development of ... Ibidem Cellular & Skin Impact: Understand how these molecular processes affect your skin's health and elasticity in Sugar is altering your skin in ways no anti-ageing serum can ... Ibidem
  • BIOHACKING by Nathan Hatch, "F*** Portion Control"

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    J
    This guy is a born liar and a fraud. His 'expert' research is incredibly sloppy and cherry picked. He has a raging ego, extremely thin skin and a tedious need to be the singular guru on ALL life matters. I challenged him on his claims on his blog about how much vitamin C he takes. He claims he only uses natural, acerola-based vitamin C, and claims he typically takes 4 grams a day for a few days and then settles on 2-3 grams a day. I found the brand he takes, crunched the numbers and worked out that if he was telling the truth, he'd be spending up to $400 a MONTH on this one supplement. I pointed this out to him and he wrote back calling me a "dumbass" and saying "of course I don't spend that much money on Vitamin C". Which means he out-and-out lied. He's also now making vague claims in his updated book that he had leukemia in the past. Previously he only mentioned the thyroid cancer. But now, leukemia too, because his WBC was slightly off. He is desperate to convince people he was at death's door and single-handedly fixed his multiple life threatening diseases. He's a dishonest loser, who loves to throw in comments implying he's hot af. He isn't. He's vain, preachy and profoundly wide of Ray Peat's mark.
  • The significance of the dopamine receptor D2

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    MauritioM
    Combined inhibition of dopamine D1/D2 receptors induces cognitive and emotional dysfunction through oxidative stress and dopaminergic neuron damage Results: Low-dose co-DR1/2I significantly increased MAO-B and ROS levels (p < 0.01) and decreased SOD activity (p < 0.01) in the substantia nigra, striatum, and hippocampus. MAO-B activity positively correlated with ROS (r = 0.916, p < 0.001) and negatively correlated with SOD (r = −0.685, p < 0.001), whereas ROS negatively correlated with SOD (r = −0.661, p < 0.001) in co-DR1/2I-treated mice. The medium- and high-dose groups exhibited spatial memory impairment (longer escape latency, p < 0.05) in the water maze and more anxiety-like behavior (reduced central zone time, p < 0.01) in the open field test; however, no abnormalities in motor coordination were observed in the rotarod test (p > 0.05). Immunofluorescence and WB confirmed a reduction in the dopaminergic neuron count after co-DR1/2I.
  • Estradiol increases binding of DHT in prostate two fold in vivo

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    S
    @bio3nergetic said:What one most likely witnesses is big med making matters worse, but walking away silently pointing at made-up villains. >> Sounds like Finasteride and Dutasteride
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    jamezb46J
    @haidut If red blood cell deformability is among the sequelae that endurance exercise produces, I wonder if something like pentoxifylline might be useful. I understand that much of the damage that occurs to red blood cells in ultra-endurance exercise is secondary to the mechanical strain to which RBCs are subject due to being physically compressed at the soles of the feet with every step or else during their turbulent and high pressure flow through arteries of a person basically running for their lives, but I would like to know if using a stack like Pentoxifylline + Meldonium to cut down on the FAO, keeping carbohydrates going every 20 minutes or so, might compare.
  • Prolactin receptor antagonist may cure baldness and reverse hair graying

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    alfredoolivasA
    There are extracellular and nucleus prolactin receptors. Prolactin binds both and this drug, as it's an antibody, only binds to the extracellular receptors giving us an idea of what effects anatagonising the extracellular receptors does but does not tell us what the nuclear receptors do and therefore cannot show the full picture of what prolactin actually does. There exists many case reports of hair loss from dopamine agonists, so your suggestions may be harmful in this regard. Estrogen receptor alpha for example has different effects than estrogen receptor beta for hair growth is an example of the flaws behind what people infer from this study
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