@haidut thank you

Just my simplified take on arthritis, as more and more I am swayed to think that there is only arthritis, and that arthritis is caused by low metabolism, and very much so because CO2 deficiency from low mitochondrial metabolism makes the ecf acidic, enough so that some salts, urate salts being one, precipitate, and cause the formation of crystals that cause wear and tear on our joints. I profess ignorance though, on the matter of the different forms of arthritis, as when I attempt to understand the different forms of arthritis, the explanations given in the literature always lead to draw blanks, which makes me either an embecile thet fails to comprehend or simply that the literature is just playing on words and terms that give different names to a banana. The added complexity is a ploy to distract from the one true cause of arthritis, if I may dare say so. Which is why Ray points to hypothyroid as the cause of arthritis, which I first thought of as a rather simplistic explanation. But if I can relate to cause and effect, and dig deeper into it, it is not as complicated as it appears to be. The key is acid base balance. As simple as that. When we have an abundance of CO2 because our body makes a lot of it at our disposal, we have the best pH buffer available for our lungs and kidneys to manage acid base balance. When alkaline, it can turn into an acid called carbonic acid, and when acidic, CO2 can turn into bicarbonate. This is based on Le Chatelier's principle, where the direction of a reaction is in the direction of the stress that it relieves. What better way to provide a surfeit of CO2 in our body than to be producing energy using mitochondrial oxidation. Vitamin B1 is a crucial link in a chain of nutrients and substances and processes that enable mitochondrial oxidation. Simply being deficient in one link makes rhe chain broken, and a broken chain only leads to low metabolism, and the resulting imbalance in pH, usually acidic, will just cause the formation of salt crystals that irritate and inflame and destroy tissues. I know enough how to monitor my acid base balance, so I know what remedial actions to take to keep my acid base balance from being chronically in an imbalanced state. Many bad things happen in a chronic state of acid base imbalance. I have high uric acid, yet I don't have any arthritis, much less gout. Only because my optimal acid base balance keeps uric acid crystals from forming. I don't have tachycardia (high heart rate) because my heart muscle pumps well and isn't strained because the muscle contracts and relaxes effortlessly because of good acid base balance. I don't fear cancer because I believe that an acidic ecf is what causes regulatory and harmless and commensal microbes to turn into virulent parasites that cause cancer to develop. Yes, vitamin B1 is important, but such studies are subordinate to putting all the pieces of rhe puzzle together to form a whole picture. This is where we need work on, as without this perspective one can end up taking one supplement after another and not progressing from his poor state of health.

But then there is the fact that it is literally the most unpleasant food ever concoted by man.

Brown Rice Inhibits Development of Nonalcoholic Fatty Liver Disease in Obese Zucker (fa/fa) Rats by Increasing Lipid Oxidation Via Activation of Retinoic Acid Synthesis Abstract Background White rice and its unrefined form, brown rice, contain numerous compounds that are beneficial to human health. However, the starch content of rice can contribute to obesity, a main risk factor for nonalcoholic fatty liver disease (NAFLD). Objectives We investigated the effect of rice consumption on NAFLD and its underlying molecular mechanism. Methods We randomly divided 7-week-old male obese Zucker (fa/fa) rats, an animal model of NAFLD, into 3 groups (n = 10 each) fed 1 of 3 diets for 10 weeks: a control diet (Cont; AIN-93G diet; 53% cornstarch), a white rice diet (WR; AIN-93G diet with cornstarch replaced with white rice powder), or a brown rice diet (BR; AIN-93G diet with cornstarch replaced with brown rice powder). Liver fat accumulation and gene expression related to lipid and vitamin A metabolisms, including retinoic acid (RA) signaling, were analyzed. Results Hepatic lipid values were significantly decreased in the BR group compared with the Cont group, by 0.4-fold (P < 0.05). The expression of genes related to hepatic fatty acid oxidation, such as carnitine palmitoyltransferase 2, was approximately 2.1-fold higher in the BR group than the Cont group (P < 0.05). The expression of peroxisomal acyl-coenzyme A oxidase 1 and acyl-CoA dehydrogenase medium chain was also significantly increased, by 1.6-fold, in the BR group compared with the Cont group (P < 0.05). The expression of VLDL-secretion-related genes, such as microsomal triglyceride transfer protein, was also significantly higher in the BR group (2.4-fold; P < 0.05). Furthermore, aldehyde dehydrogenase 1 family member A1, an RA synthase gene, was 2-fold higher in the BR group than the Cont group (P < 0.05). Conclusions Brown rice prevented development of NAFLD in obese Zucker (fa/fa) rats. The beneficial effects of pregelatinized rice on NAFLD could be manifested as increased fatty acid oxidation and VLDL secretion, which are regulated by RA signaling. https://www.sciencedirect.com/science/article/pii/S002231662200339X

@haidut I had also read your previous post on that 300mg-biotin-per-day study and can attest by my own experience that there really are things opening up at thrice daily doses of about 100mg B7. Practically, however, I ran into a few issues. What are your opinions on these? Biotin: I don't understand how study participants could cope for so long with such high doses, since B7 competes with B5 for uptake? Especially with regard to restoration of myelin sheaths, cell membranes and endogenous fatty acid synthesis they are both interdependent. I kept running into deficiency of one or the other and had to alternate both at least once every few days. I felt that at such high doses, purity and fillers really become a significant issue. I've tried different brands because of this and they ranged from awful (with excessively much MCC) to something-is-still-off. Pharmaceutical quality in general is only >97.5% purity which by itself I consistently find totally inadequate in many cases. Perhaps related to 2). My GI system and BMs became unbearably upset by high biotin doses. I suspect biotin exhibits inhibiting effects on aminooxidases similar to thiamin (thiamin metabolites) through displacement of enzymatic flavoproteins? I'm convinced much of the beneficial effects in Antonio Costantini's high-dose-thiamin therapy stems from MAO inhibition in the ganglions. Riboflavin: Are such high bolus doses really sensible in people who are unaffected by that recognized genetic riboflavin transporter defect? .1) I have noticed much better effects and tolerability from single digit mg doses continually (3-4x) throughout the day instead of higher doses twice or once daily. .2) Someone on the forums reported to have had his actual serum/blood FAD and FMN levels tested with different amounts of B2 and that their ratio and the absolute value of FAD totally plumetted from high doses of B2, whereas FAD and also his symptoms improved with low doses. Side note: I have used B2 in amounts up to 2grs for clostridioides prophylaxis because of the studies on its redox effects and the aerobic-anaerobic gradient of the intestinal lining and its microbes. While such amounts are probably really not harmful, they made for purging and very awful BMs. Hope you are doing well! And thanks for all the work!

@haidut thank you

Makes sense to me, but surely not alone HaidutBot. It's almost old hat now, people referring to the gut as a 'second brain'. And sure enough, I could send myself to a psychologically uncomfortable place simply by eating orange peel (for example). And allegedly there's another stop on the axis. @ThinPicking said in Are Polls a Good Idea?: https://www.mdpi.com/1424-8220/22/23/9115 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7075501/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10002343/ https://www.ahajournals.org/doi/10.1161/STROKEAHA.123.040499 https://www.sciencedirect.com/science/article/abs/pii/S0306987719307145 https://www.sciencedirect.com/science/article/pii/S1568163721002865 https://www.frontiersin.org/articles/10.3389/fpsyg.2014.00278/full

@Jakeandpace Yes I do now. It definitely makes a difference. I'm just concerned to suggest it to someone else with masses in his colon that shouldn't start bleeding. I read in previous studies that aspirin does not cause bleeding but for me this definitely was the case. This family member is really in a bad state so I'm not sure if it's even worth it anymore.

@Mauritio Appreciate it. That was the conclusion I had arrived to as well but I have heard some people do t3 only. If you don't mind sharing what dose t3/t4 did you find works for you?

@haidut

For me salt drives my thirst.

Inhibition of gut-derived serotonin synthesis: a potential bone anabolic treatment Abstract Osteoporosis is a low bone mass disease most often caused by an increase in bone resorption not compensated by a similar hike in bone formation1. Since gut–derived serotonin (GDS) inhibits bone formation2, we asked whether hampering its biosynthesis could treat osteoporosis through an anabolic mechanism. To that end we synthesized and used LP533401, a small molecule inhibitor of Tph1, the initial enzyme in GDS biosynthesis. Oral administration once daily for up to 6 weeks of this small molecule prevents the development of and fully rescues, in a dose–dependent manner, osteoporosis in ovariectomized rodents because of an isolated increase in bone formation. These results provide a proof of principle that inhibiting GDS biosynthesis could become a novel anabolic treatment for osteoporosis. Or for the non-pharmaceutical approach: Peatbot: To lower gut serotonin, you can consider the following strategies based on the provided context: Avoid Foods Containing Fermentable Fibers and Starches: These include grains, beans, and other seeds that resist quick digestion and can promote intestinal irritation, leading to increased serotonin production. Consume Fibrous Foods with Antibacterial Properties: Foods such as bamboo shoots and raw carrots contain antibacterial chemicals that help reduce endotoxin and serotonin levels in the gut. Use Activated Charcoal: Activated charcoal can absorb many toxins, including bacterial endotoxin, which is likely to reduce serotonin absorption from the intestine. However, it should be used intermittently as it can also bind or destroy vitamins. Consider Theanine Supplementation: Theanine, an amino acid found in tea, has been reported to decrease the amount of serotonin in the brain by decreasing its synthesis and increasing its degradation. Supplement with Progesterone, Thyroid, and Niacinamide: These substances can help reduce serotonin formation and/or accelerate its elimination. Niacinamide, in particular, seems to increase serotonin uptake. Address Hypothyroidism: Since hypothyroidism is a common cause of increased serotonin, supplementing thyroid hormone until symptoms are resolved can help normalize serotonin levels. By implementing these strategies, you may be able to lower gut serotonin and mitigate its associated effects.

Though this study used supplementing it still jibes with what we've heard previously, that unsaturated fats don't provide the same satiety as most of the saturated ones. If your food isn't making you "feel full" then you might simply eat more of it. On another related note, who else here has read that a spoonful of beef tallow 10 or 20 minutes before a meal would result in quicker satiety and eating less? Interesting study btw, will pass it on, thank you for linking.