@mexican_coke_fan the information is contradictory

@calvinklein21101 said in Vitamin A may prevent/treat motor neuron diseases, including the lethal ALS:

something going wrong in their metabolism

I read Poisoning for Profits and my first inclination wasn't to start rattling on about my liver while chomping rice and beans all day. Something about it seems to ring with them.

Have you also tried bromantane? I wonder how it compares to amantadine.

@Serotoninskeptic

The values above need to be revised. The doses of calcium needed in practice to complex with oxalate are higher than expected, and how calcium interacts with phosphate is relevant:

"The degree of interference reported here (~166 mg phosphorus for every 500 mg ingested calcium—0.4 mmol phosphorus for every mmol calcium) is substantially less than might have been predicted from simple stoichiometry. A 1:1 molar ratio for CaHPO4 would predict binding of 388 mg phosphorus by 500 mg calcium and, for Ca3(PO4)2 at a Ca:P molar ratio of 1.5:1.0, 258 mg phosphorus would be bound per 500 mg calcium. A molar ratio of 1:1 seems more likely at digestate pH values below 7.0. Even at the upper end of the confidence interval for the regression model—210 mg (6.8 mmol)—binding would still be substantially less than the lowest stoichiometric prediction. This discrepancy may be partly due to rapid absorption of phosphorus in the duodenum well before calcium and phosphorus complexes can form in the chyme. In any event it undoubtedly reflects the complexity and multiplicity of the interactions within the digestive residue."

(10.1080/07315724.2002.10719216)

Compare them:

Predicted: Ca 1:1 P Practical: Ca 2.5:1 P

For oxalate:

Predicted: Ca 1:1 Oxa Practical: Ca ?:1 Oxa

If we treat the interaction with oxalate as that with phosphorus (2.5:1) and adjust for mass (2.5:2), we would need 125 mg of calcium for every 100 mg of soluble oxalate.

One problem is guessing how much is soluble from the total oxalate content of a food. Based on the last two 'Cooked' columns (⇈), it's all over the place.

Another problem is the additional confounders. Member 'blabla' posted this elsewhere:

cab6428c-10ca-4047-a0e4-08d21350c5b1-image.png
⠀(10.1097/01.asn.0000127864.26968.7f)

Up to 800 mg: dietary calcium alone More than 800 mg: dietary calcium and supplements (400 mg and 1000 mg)

Only the supplements were dosed with the labeled oxalate, suggesting that indirect interference is possible, but notice the degree of variations at low intakes. If you must supplement, it's preferable to dose in the same meal:

edacf8d3-917e-41a6-b44f-6a24525a3abb-image.png
⠀(10.4065/79.1.91)

But when the diet contains enough calcium (1000 mg), adding more seems unnecessary because a further reduction is minimal.

did anyone buy it from ebay?

@thyroidchor27

P5P can help to reduce homocysteine.

@mikeyd

So if you can’t tolerate wheat and have SIBO, what foods would you recommend? I too, have issues with many fruits. I try to peel the skin off of most fruits before I eat them. I think this helps but I still feel inflamed. I skin dates, peaches etc. I can’t eat apples or pears at all. Please help, like you I’ve had it probably for 10 years but only heard of term SIBO this year.

Elevated fructose in the brain is a sequester to protect it because of AD. Much like the protein plaques, which have been erroneously blamed as a result of AD.

The rationale was: carbon dioxide goes through cells' lipids and releases a proton inside once hydrated. Then, let's find another compound that's also not barred by lipids and releases even more protons. This led to 2,6-DHBA.

It overlooks that the very property that makes the selected compound a greater acidifier is also what makes it extraordinarily prone to deprotonate prematurely. The ability to pass through lipids is likely to be compromised with the early proton release. If it could be injected into the tumor, it would still be uncertain if it could be taken up by target cells.

Healthy Cancerous Extracellular pH 7.4 ↓6.5 Intracellular pH 7.1 ↑7.5

For direct internal acidification, it would be more fitting to seek weak rather than strong acids, those that can take advantage of the bump in transitioning from the extracellular to intracellular compartment (6.5↗7.5) to deprotonate the molecule where intended.

Relevant for many and thank you as always.

This info will be passed on.

Also, if b.i. progesterone actually maintained or reduced the size of a meningioma.

Hello, Jorge (or your bot).

That these vitamins increase the risk of cancer complications is not a reason to avoid supplementation, but to be more cautious with them.

One suggestion was to offer B-vitamins in separate products, something like:

Mitochondrial function and toxicity: role of the B vitamin family on mitochondrial energy metabolism Mitochondrial function and toxicity: role of B vitamins on the one-carbon transfer pathways

But it's challenging to have a clear separation of vitamins because of interrelationships. Pyridoxin was excluded from their 'energy metabolism' group, but it's directly involved in glycogen use and the transaminases to prepare amino acids for oxidation. Biotin was included, but associated with anabolic functions, and one of the catabolic pathways would be dependent on the vilified (adenosyl)cobalamin. If all came down to an energy problem, the nucleotides of the energy-releasing coenzymes involve folate in their syntheses.

Cancer Cells Tune the Signaling Pathways to Empower de Novo Synthesis of Nucleotides

0fa521f5-78b7-4401-88c7-079d8641aa8d-image.png

Growth-promoting substances don't just fuel cancer, they're also needed for cell and tissue regeneration.

Supplementation is discouraged for folate, cobalamin, and choline (or betaine). We know that the message is reaching a community that doesn't consume a lot of leaves (foliage→folate), nor legumes. The availability of folate in oranges is arguably lower than expected.

Properties of Food Folates Determined by Stability and Susceptibility to Intestinal Pteroylpolyglutamate Hydrolase Action

Tipping the reliance in favor of folate-cobalamin over choline might yield extra glycine, that can be formed for every folate cycled. The simultaneous restriction of these vitamins, along with a predisposition to their insufficiency, malabsorption syndromes, and the adoption of a diet low in methionine doesn't seem promising.

Do we have indications that the population is adequate in the anabolic vitamins and can afford a restriction? Because the typical consumption and positive reactions to supplementation suggest otherwise.

Not only a deficiency of any vitamin tends to predispose to cancer, but cancer is not the only disease to worry about. Cardiovascular problems and infections are major threats.

Digestion weakens in advanced age and disease, making it helpful to have available these vitamins in purified form. The issue here is that you're leaving for other vendors to do the dirty job of guaranteeing adequacy in a considerable number of people that would benefit from the carcinogenic nutrients.

Thank you for sharing this interesting new angle. It fits very well with the recent interest in the connection between antibiotics and AD. In the last three years, several large studies looking at the efficacy of antibiotics have been started, and they should probably yield some very interesting results. In the end, it all comes down to your gut and endotoxins.

@haidut said in Pregnenolone (P5) may treat for COVID-19, by increasing dopamine:

Given that the mechanism of action reported by the study (dopamine enhancement) is so generic, the findings of the study possibly apply to other respiratory viral infections (URTI) too

Dopamine was quite important in renal function the last time I checked, renal function quite important to the RRAS, the RRAS quite important to the "spike protein" (an ACE2 inhibitor, allegedly).

It's highly likely to me that it does apply to other URTI. In which case I wonder why we're using the word "covid". Other means to walk believing masses back are available.

@stag

I wonder if their theories can be shown on blood tests.
Although I know how Dr. Peat feels about free T4 and free T3 labs, an rT3 might be good to track in such cases.

My rT3 indeed does go down when I increase my T3 while taking T4/T3.

Thank you for sharing this - I will look into their therapies further.

@haidut Your work is much appreciated! What do you think of using ALCAR (Acetyl-L-carnitine) to raise dopamine? From personal experience it seems to be able to do this on an empty stomach.
Here is one study -that begs the question what kind of electrical sim were they using?:

Effect of acetyl-L-carnitine on the dopaminergic system in aging brain

*Abstract

We studied the effect of acetyl-L-carnitine (ALCAR) on dopamine release and the effect of long-term acetyl-L-carnitine treatment on age-related changes in striatal dopamine receptors and brain amino acid levels. In striatal tissue that had been incubated with [3H]dopamine, acetyl-L-carnitine increased the release of [3H]dopamine evoked by electrical stimulation. In striatal tissue from aged mice administered acetyl-L-carnitine for 3 months, the release of [3H]dopamine evoked by electrical stimulation was higher than that of its aged control; the release after a second stimulation was similar in the two groups. There was a significant decline in the number of D1 striatal dopamine receptors with age. The Bmax was 51% lower in 1.5-year-old mice than in 4-month-old animals. Administration of acetyl-L-carnitine for 3 months diminished the reduction in the binding of [3H]SCH-23390. [3H]Spiperone binding to D2 receptors was not decreased with age and was not affected by acetyl-L-carnitine treatment. Age-related decreases in levels of several amino acids were observed in several brain regions. Acetyl-L-carnitine lessened the reduction in the level of taurine only in the striatum. The findings confirm the multiple effects of acetyl-L-carnitine in brain, and suggest that its administration can have a positive effect on age-related changes in the dopaminergic system.*

interesting

do you agree with this tier list?

https://bioenergetic.forum/topic/2838/protein-tier-list