https://bioenergetic.forum/post/60591

IL-6 isn't an "inflammatory protein". It is a transient signalling molecule of immune involvement..it raises when you go for a walk and eat a carb heavy meal, so is walking and eating inflammatory too? You can't look at cytokines in isolation..cytokines are not inflammation..they are the response to something like PAMP's e.g PRR's,TLR2/4, Dectin-1, CARD9, DAMP's e.g TLR-9, TNF-a, IL-β, hypoxia e.g chronic HIF-1a signalling , mitochondrial ineffiency e.g reduced PGC-1a, reduced OXPHOS that immune function has decided it doesn't have the energy or resources to resolve, so the threat assessment never reaches the resolution phase e.g IL-10, Tregs, M1-M2, SPM's like it would with food poisoning, wound healing, bacterial infections that induce aggressive acute immune function like c.difficile infections and waterborne illness Inflammation is the dysregulated response of immune function to a perceived threat that it does not have the facility to, or has not received the gating to resolve, so it just manages the situation. That "management" is the inflammation as it wastes NAD, forces longer windows of aerobic glycolysis, induces more hypoxia. Not cytokines .which means all these studies are particularly nonsense. Furthemore there isn't anything in cacao xanthines or polyphenols or any other polyphenol for that matter that can resolve inflammation. The keyword is resolve..it can transiently inhibit NF-kB through IKK, and it can push Nrf2(this would probably just result in even more redox stress though without resolution), but neither of these things equal resolution..without the signalling cacscade i mentioned earlier, there is no getting out of "inflammaging" or chronic inflammation and because inflammaging is largely driven by hypoxia through things like uncoupling of eNOS, BH4, mitochondrial inefficiency etc this is something you cannot reverse beyond a certain point or age..inflammaging to use the cringe term, is inevitable and you might as well just call it aging.

@DavidPS The criteria was to be 20 years old, and have information about the participants's atherosclerotic cardiovascular disease, dietary niacin intake or covariates. "Our research focuses on participants aged 20 years and older who completed an interview. Data analysis was conducted from July to September 2024. We excluded pregnant women or individuals with missing data on atherosclerotic cardiovascular disease, dietary niacin intake, or covariates. " Perhaps covariates includes obesity, but I don't know.

Context Indoor air contains 100 times more microplastics than previously estimated, according to this study. Every day, an adult inhales 68,000 microplastic particles, and a child nearly 47,000. This is one hundred times more than previously thought, according to the study from the University of Toulouse published in the journal PLOS ONE. https://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0328011 2025 Researchers analyzed the air in homes, offices and cars and found extremely high concentrations of PM10 particles, which come from textiles, furniture, cables and carpets. NB: MPP and NPP: micro-plastic and micro-plastic particles Useful link (in French, translator needed) https://www.julienvenesson.fr/microplastiques-nanoplastiques-effets-sante/#:~:text=Effets sur le système respiratoire,et peuvent même les détruire. How to protect the brain: Optimize protection against neuroglia and inflammation Let’s say we’re going to try to protect both against stroke and Alzheimer's, although I am aware that this requires "scientific confirmation". “Amyloid plaques and tau protein deposits in the brain are considered the main biological features of Alzheimer's disease. Recently, myelin sheath degeneration has emerged as a new hypothesis and target in the etiology of Alzheimer's disease. A decrease in myelination and oligodendrocyte function precedes the pathological accumulation of amyloid and tau proteins.” (Graciani et al., 2023, Desai et al., 2009, Desai et al., 2010). Put differently, there is inflammation, with accumulation of a tau protein, degeneration of the myelin sheaths (which protect the nerves) and therefore poor conduction of nerve impulses. So, if we accept this hypothesis, we should try to calm things down (excitoxicity and neuro-inflammation via TNF-alpha, but not only that). Indeed, nothing is settled down, established in advance, or rigid if you prefer. Since nothing is set in stone, we're relying on probability: by addressing inflammation and protecting our communication channels, we aim to give the brain the tools to resist longer. It's not a guaranteed miracle cure, but a common-sense strategy to minimize damage. Electrical glitch or chemical short circuit? That's the big debate: which comes first? In the brain, everything operates in a loop: a malfunctioning ion channel (electrical) alters the release of neurotransmitters (chemical), and inflammation (chemical) then modifies the sensitivity of receptors (electrical). It's a vicious cycle. Protecting the Brain: Optimizing Protection against Neuroglia and Inflammation Since there is disruption in cellular communication, resulting in inflammation and impaired elimination of toxins and dysfunctional debris, I’ll suggest some approaches. Their relevance will vary depending on the individual's condition. Think of this as a toolbox. Here, I’ll simply mention a few molecules / clues from my own research. More details can be found at the link below. There’re probably other ones, like emoxypine succinate, although I’ve never heard of it before coming to this forum (not available in my country; unknown to VIDAL). Healthy membranes to facilitate blood circulation. Baby aspirin (325 mg) in case of insufficient fluidity. Anti-inflammatory and pro-metabolic. Mind side effects on platelet renewal. UCDA: Details on how Ursodiol acid protects the brain (with a physician prescription). Suggested optimization for these nutrients: resveratrol, Theracurmin, EGCG (green tea). B1, B9, B12, DHA and iodine. Betaine HCl if lazy digestion after the evening meal (with meat). Taurine *** and magnesium Physical activity Open to suggestions More details on this link if you want to go deeper with one molecule (in French) https://mirzoune-ciboulette.forumactif.org/t2161-le-cerveau-contamine-par-le-plastique-comment-s-en-proteger#30544 More info on taurine (in French) https://mirzoune-ciboulette.forumactif.org/t1866-infos-sante-divers-sce-2#29009 https://mirzoune-ciboulette.forumactif.org/t1840-quest-ce-qui-rend-la-taurine-si-importante#25227 (an article that explains the ins and outs of this amino acid).

@CrumblingCookie I've done it today again and half an hour later noticed a face lift effect also my mood seems to be better. I kept forgetting about it but I'll try to do it more often.

@Korven said in Colostrum suppresses serotonergic signalling in (overtraining) rats: wonder if just popping a cyproheptadine can do this well

Comment “Results show that epigallocatechin gallate (EGCG), the main polyphenol in green tea, can neutralize the carbonyl-amino cross-linking reaction and inhibit LF formation, but the underlying mechanism is unknown." LF = lipofuscin. Article https://bioenergetic.forum/topic/9017/neuro-degeneration-a-multi-factorial-approach => I’d like to develop this approach. Not only from one side: multi-factorial. When talking about neuro-degeneration we should take the whole context into consideration to avoid plaque. After having read an article on the lack of B12 when bringing the RDA for aged people (> 40 yrs.) (1), I decided to write an article to show / to tell how I manage to optimize. Afterwards I submitted my plan to AI and ask it for comments. =>The prevention of neurodegenerative and vascular disorders rests on two pillars: metabolic flexibility and membrane integrity. See my "Metabolic Safety" Protocol if you want to go deeper.

@LucH - Excellent idea.

This thread from the former RPF has some interesting links related to choline. https://lowtoxinforum.com/threads/choline-an-essential-nutrient-for-public-health-that-were-not-getting-enough-of-in-our-diet.47355/

@LucH -Thanks for your cautionary words.

you need thiamine for oxidative metabolism not just t3, thiamine deficiency and hypothyroidism have identical symptoms, t3 uses thiamine alot faster so these studies may just be inducing beriberi

@CrumblingCookie - I do not know; but here is my guess. The first and last authors both work at "Laboratory of Extracellular Matrix Regeneration, Institute of Translational Medicine, Department of Health Sciences and Technology". Longevity is not within the Institute's purview. They reported the increase in longevity with the additional glycine but they did not expand on their findings. Similarly, at the bottom of page 4 of the PDF there is a section entitled "Synergistic longevity by combining α-ketoglutarate and 3 Gly : 1 Pro : 1 Hyp". Synergistic longevity may be outside the Institute's purview.

Apigenin inhibits xanthine oxidase so it can raise atp and lower uric acid.

Elderberry extract increases testosterone and steroidogenic enzymes strongly. It lowers aromatase and 5areductase, which is unfortunate. To me it doesn't feel like it lowers DHT at all. Quite the opposite. So I'm wondering if the increase in androgen receptors and steroidogenic enzymes is enough to compensate . And, 5aR isn't the only pathway towards DHT, and the backdoor pathway wasn't tested so maybe it has to do with that . https://pubmed.ncbi.nlm.nih.gov/39683564/

Also by the same group: Identifying obesity and dementia risk: body adiposity and neural connectivity in cognitively normal, mid-life adults (2025) Obesity is a risk factor for dementia, creating a chronic inflammatory state that results in white matter (WM) injury. Edge density imaging (EDI) is a novel technique that has demonstrated reliability in quantifying WM changes. Thirty obese and 20 non-obese cognitively normal adults underwent structural and diffusion-weighted magnetic resonance imaging. Visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) were quantified via VOXel Analysis Suite by separating signal intensities of adipose and non-adipose tissue. Scans were processed by a pipeline (MaPPeRTrac) to generate EDI. Among obese participants, there was a negative association between the VAT/SAT ratio and EDI, which was not seen among non-obese participants. Additionally, males had decreased EDI compared to females. The results of this study suggest that obesity, through WM damage, may confer increased risk of dementia, with sex as a potential differential factor. EDI demonstrates promise in delineating the neuropathology of obesity and dementia.

@yeyo12 My interpretation of the results were that caffeine co-administration with oxandrolone increased the absorption of the latter via inhibition of PGP.

@LucH You get enough cysteine from protein foods. Cysteine supplementation reverses methionine restriction effects on rat adiposity: significance of stearoyl-coenzyme A desaturase https://pubmed.ncbi.nlm.nih.gov/20871132/ Glutathione (GSH) drives cancer metastasis by promoting cell survival under hypoxia https://haidut.me/?p=2816 https://doi.org/10.1158/2159-8290.CD-24-1556