Thanks for the heads up on IL-11. It seems that it not only extends lifespan by almost 25% but it also extends healthspan. There are anumber of ways to increase lifespan by 10% but 25% is much less common.
807c445b-cc68-44cf-9bc6-3ccd7974578b-image.png

IL-11 inhibition is similar in effect to rapamycin (Sirolimus).

Inhibition of IL-11 signalling extends mammalian healthspan and lifespan

Makes sense when B1 is needed for mitochondrial respiration, but not the only one needed.

@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.

Interesting. Several years ago my gut was absolutely nuked by max dose clindamycin after a nasty infection that almost caused me to lose the use of an eye. The result was weeks of c difficile -like symptoms. The only thing that fixed it was boulardii.

Haidut on rpf: https://raypeatforum.com/community/threads/high-metabolism-quickly-destroys-chelates-endocrine-disruptors-like-bpa.25937/

Now this new study below shows that chemicals like BPA are highly vulnerable to reactive oxygen species (ROS). The authors used a type of "photodynamic therapy" to generate ROS and destroy more than 99% of the BPA in the sample after just 2 hours of exposure. Unfortunately, the mechanism they used would be toxic in people as they used titanium dioxide and UV light as catalysts for ROS generation. Fortunately, there are safer methods that have been shown to work in humans. For example, simply having higher metabolism means generating more ROS. As such, thyroid, progesterone and avoidance of PUFA may be able to achieve the same but likely over longer periods of time. This matches well with Peat's response when asked about endocrine disruptors - i.e. he said simply keeping metabolism high is probably the best protection. However, at some point of tissue saturation with the disruptors, another approach may be needed. Perhaps the safest approach to implement this in humans is with methylene blue (MB) and red light. Either one of these on its own has been shown to increase ROS generation. In the case of MB, this effect starts at tissue concentrations of about 1 uM/L, which for most people can be achieved with doses of 3mg-5mg.

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

Peatbot: Paying attention to the calcium to phosphorus ratio is important because it has significant implications for your overall health, particularly in terms of bone health, metabolic function, and the prevention of certain chronic conditions. Here are some key reasons:

Bone Health: Calcium and phosphorus are critical components of bone. An imbalance, particularly an excess of phosphorus relative to calcium, can lead to the mobilization of calcium from bones, weakening them and increasing the risk of fractures and osteoporosis.

Metabolic Function: Phosphorus is involved in energy metabolism, particularly in the formation of ATP (adenosine triphosphate), which cells use for energy. However, excessive phosphorus can disrupt this balance and lead to metabolic inefficiencies.

Parathyroid Hormone Regulation: High phosphorus levels can trigger the release of parathyroid hormone (PTH), which works to balance calcium and phosphorus levels in the blood. Chronic elevation of PTH can lead to bone resorption, where calcium is taken from the bones to balance the high phosphorus levels, leading to weakened bones.

Inflammation and Degeneration: An excess of phosphorus can contribute to inflammation and tissue degeneration. It can lead to the formation of calcium phosphate crystals in soft tissues, which are associated with chronic inflammation and degenerative diseases.

Calcium Deposition: High phosphorus levels can cause calcium to be deposited in soft tissues, such as arteries, rather than in bones. This can contribute to conditions like arteriosclerosis and other cardiovascular diseases.

Nutrient Interactions: The balance of calcium and phosphorus affects the absorption and utilization of other minerals, such as magnesium and sodium. An imbalance can disrupt these interactions and lead to deficiencies or excesses that affect overall health.

In summary, maintaining a proper calcium to phosphorus ratio is crucial for ensuring that calcium is used effectively in the body, supporting bone health, preventing chronic diseases, and maintaining overall metabolic balance.

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 👏 👍 😊