Sinatra‘s Notebook

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youngsinatra

youngsinatra

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I continue to eat 200-400g of lean beef each day. No temperature crash, no neuro symptoms, no high blood pressure. I am amazed.. I think nicotinic acid fixed my zinc issues.

Thanks for your recommendation to try niacin for my issues with zinc, copper etc. <3 @charlie

For context: (2 weeks ago I wrote this in another thread)
I have been slowly titrating up nicotinic acid (to raise NAD+) for a few weeks now and I am able to tolerate 200g of lean beef a day for nearly a week now, which I couldn’t tolerate at all before that for almost 2 years. Everytime I tried eating it, even just small amount and just once, it led to a huge crash and extreme neurological issues. (neuropathy, difficulty walking, dizziness, blurry vision, skin turned white, nails turned blue due to hypoxia etc.) Same thing happened with oysters or zinc supplements.

Btw, I frequently tested serum zinc and it always was high even after restricting zinc for years.
 

maillol

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Are you still having issues with B6? I used to get neuropathy even from 1mg, didn't matter if it was pyridoxine or p5p. I tried B2 as per the above pathway but it didn't help. B12 helped a bit but then stopped working. I seem to have fixed it by eating some oats and black-eyed beans, molybdenum was my theory because pyridoxal is an aldehyde. No neuropathy now since January.
 
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youngsinatra

youngsinatra

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Are you still having issues with B6? I used to get neuropathy even from 1mg, didn't matter if it was pyridoxine or p5p. I tried B2 as per the above pathway but it didn't help. B12 helped a bit but then stopped working. I seem to have fixed it by eating some oats and black-eyed beans, molybdenum was my theory because pyridoxal is an aldehyde. No neuropathy now since January.
I find high molybdenum foods (esp. organic cannellini beans) very beneficial for multiple things. They improve bile flow, sulfation, aldehyde oxidation and it’s seems like there is some involvement of molybdenum in the activation of riboflavin. (turning it into FMN/FAD)

B2 without a sufficiently high intake of dietary molybdenum causes a stagnant bile flow in my case, even in low doses. I wrote about this 1-2 pages ago in this thread.

I cannot tolerate molybdenum supplements somehow.
 
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youngsinatra

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@maillol
I do believe molybdenum is involved in riboflavin metabolism, even though the research on it isn’t that clear. (Dr. Gregory Russel Jones from www.B12oils.com thinks similarly about Moly)

It’s one of the few things that really elevate my heart rate and seems to increase neurotransmitters like dopamine/norepinephrine. I think it’s activating things in the methylation cycle.
 

charlie

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I continue to eat 200-400g of lean beef each day. No temperature crash, no neuro symptoms, no high blood pressure. I am amazed.. I think nicotinic acid fixed my zinc issues.

Thanks for your recommendation to try niacin for my issues with zinc, copper etc. <3 @charlie
Man that is incredible!!! Thank you so much for sharing. Nicotinic acid is truly amazing stuff. So grateful we are able to witness the truly remarkable healing powers of it.
 
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youngsinatra

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Very nice thread about molybdenum and it’s importance:
(with awesome studies from @Amazoniac)


@maillol also found this — I have noticed that many people have a build-up of PLP (active B6) on their blood test and AO (aldehyde oxidase - dependent on FAD and Mo) helps to turn P5P into the 4-PA that can be excreted into the urine.
IMG_7889.jpeg


Molybdenum is so underrated. I didn’t eat beans for a week or so and my slow motility, poor bile flow and fatigue came back. High dose B‘s didn’t help and even worsened the problem. Back on beans and loving it! 🔥

With the combo of niacin, B2 (R5P) and beans, I feel like either my methylation or copper metabolism is getting ramped up, as I had a adrenaline reaction that I usually never get, but it actually feels good (as I am typically prone-to-be-stuck-in low adrenaline) The first 2 days my heart rate was 80-100 bpm which is unusually fast.

GRJ recommends more potassium when Moly causes high methylation/adrenaline reactions.
 
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maillol

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Very nice thread about molybdenum and it’s importance:
(with awesome studies from @Amazoniac)


@maillol also found this — I have noticed that many people have a build-up of PLP (active B6) on their blood test and AO (aldehyde oxidase - dependent on FAD and Mo) helps to turn P5P into the 4-PA that can be excreted into the urine.
View attachment 62366

Molybdenum is so underrated. I didn’t eat beans for a week or so and my slow motility, poor bile flow and fatigue came back. High dose B‘s didn’t help and even worsened the problem. Back on beans and loving it! 🔥

With the combo of niacin, B2 (R5P) and beans, I feel like either my methylation or copper metabolism is getting ramped up, as I had a adrenaline reaction that I usually never get, but it actually feels good (as I am typically prone-to-be-stuck-in low adrenaline) The first 2 days my heart rate was 80-100 bpm which is unusually fast.

GRJ recommends more potassium when Moly causes high methylation/adrenaline reactions.

Good find.

Magnesium, B12 and riboflavin are often mentioned regarding B6 metabolism but very rarely molybdenum. Imagine if all the people out there with B6 toxicity just need to eat some oats or beans.
 
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youngsinatra

youngsinatra

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- Role of Vitamin A Metabolism in IIH: Results from the Idiopathic Intracranial Hypertension Treatment Trial (Figure 1)

2-Figure1-1.png

- Molecular Cloning of Retinal Oxidase/Aldehyde Oxidase cDNAs from Rabbit and Mouse Livers and Functional Expression of Recombinant Mouse Retinal Oxidase cDNA inEscherichia coli - ScienceDirect

"Retinal oxidase (EC 1.2.3.11) is a molybdenum-containing flavoenzyme with high enzymatic activity as to retinoic acid synthesis."​

- The Impact of Single Nucleotide Polymorphisms on Human Aldehyde Oxidase

"Aldehyde oxidase (AO) is a complex molybdo-flavoprotein that belongs to the xanthine oxidase family. AO is active as a homodimer, and each 150-kDa monomer binds two distinct [2Fe2S] clusters, FAD, and the molybdenum cofactor. AO has an important role in the metabolism of drugs based on its broad substrate specificity oxidizing aromatic aza-heterocycles, for example, N1-methylnicotinamide and N-methylphthalazinium, or aldehydes, such as benzaldehyde, retinal, and vanillin."​

- https://febs.onlinelibrary.wiley.com/doi/abs/10.1016/0014-5793(93)80818-F

:hattip gbolduev

- Molybdenum Intake Influences Molybdenum Kinetics in Men

"The objectives of this study were to determine physiologic adaptations that occur when humans are exposed to a wide range of molybdenum intake levels and to identify the pathways that are influenced by dietary intake. Four males consumed each of 5 daily molybdenum intakes of 22, 72, 121, 467, and 1490 ug/d (0.23, 0.75, 1.3, 4.9, and 15.5 mmol/d) for 24 d each. During each treatment period, oral and intravenous doses of 100Mo and 97Mo were administered. Serial plasma, urine, and fecal samples were analyzed for labeled and unlabeled molybdenum. Compartmental modeling was used to determine rates of distribution and elimination at each dietary intake level."
"Three pathways were sensitive to daily molybdenum intake: absorption efficiency, tissue uptake, and urinary output. The same pathways were sensitive to intake in the previous kinetic study when subjects consumed a low molybdenum diet of 22 ug/d for 102 d followed by molybdenum repletion with 467 ug/d (11). The subjects in this study were healthy young men and the responses may be different in other age groups or in women."​
"Urinary output appears to be the key pathway for regulating the body's exposure to molybdenum. Transitioning from 22 ug/d to 72 ug/d resulted in a tripling of the fraction of plasma molybdenum excreted into urine. Further transitioning from 121 ug/d to 467 ug/d resulted in an additional doubling of fractional transfer of plasma molybdenum into urine. Fractional transfer of molybdenum from plasma into urine did not increase further at highest level, which may suggest that the capacity for urinary excretion was exceeded. The high intake combined with the lack of increase in fractional excretion led to a substantial retention in molybdenum at the highest intake level."​
"Fractional uptake of molybdenum from plasma into tissues was constant for intakes below 467 ug/d but decreased by ~72% when daily molybdenum intake increased to 1490 ug. The decrease at the highest level could suggest the capacity of the tissues to store molybdenum was exceeded."​
"Absorption of molybdenum from the intestine increased at higher molybdenum intakes, which led to a decreased fractional transfer of molybdenum from the GIT into feces. Absorption efficiency was 90% for the lower intake levels and 94% for the higher intake levels. Increased absorption with increased intake may be due to saturation of binding of molybdenum to other food components as luminal Mo content increases."​
"Comparison of parameter values for the first phase of this study and the depletion phase of the previous study (11) provides insight into the effect of adaptation on molybdenum kinetics. In the depletion study, tissue deposition of molybdenum occurred more rapidly than in this study. In addition, transfer of molybdenum into the GIT via bile occurred more slowly in the previous study. Differences may be explained by the different lengths of treatment periods between the 2 studies (24 d for this study vs. 102 d for the previous study). It is likely that the subjects undergoing the shorter treatment period did not fully adapt to the intake level. The adaptation would result in conservation of tissue molybdenum during low intake."​
"The bioavailability of food-bound molybdenum was found to be lower than that for purified molybdenum. On average, the bioavailability of the food-bound molybdenum was 83%, as determined from fitting data for molybdenum in the supplement form vs. the food-bound form." "Our previous kinetic analysis (11) found the bioavailability of food-bound molybdenum to be 76%, in good accord with these findings. Another study also showed that the food matrix can alter molybdenum bioavailability (20). In that study, foods were intrinsically labeled with molybdenum, and although the kale matrix did not inhibit the absorption of molybdenum, the soy matrix reduced molybdenum bioavailability by 37% compared with the purified dose."​


- Mechanistic insights into the treatment of iron-deficiency anemia and arthritis in humans with dietary molybdenum
- Liver xanthine dehydrogenase and iron mobilization
- Sulfite Alters the Mitochondrial Network in Molybdenum Cofactor Deficiency
- A mechanism of sulfite neurotoxicity: direct inhibition of glutamate dehydrogenase
- The peak height ratio of S-sulfonated transthyretin and other oxidized isoforms as a marker for molybdenum cofactor deficiency, measured by electrospray ionization mass spectrometry
- Hypohomocysteinaemia and highly increased proportion of S-sulfonated plasma transthyretin in molybdenum cofactor deficiency
- Ahomocysteinemia in molybdenum cofactor deficiency
- A Turkish case with molybdenum cofactor deficiency
- Short-term response to dietary therapy in molybdenum cofactor deficiency
 
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youngsinatra

youngsinatra

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Breakfast
75g rice (weighed uncooked), 120g white cannellini beans, 200g 95/5 ground beef, 5g olive oil, 240g green kiwi, salt.
IMG_7893.jpeg


I am getting leaner by the day. Abs are getting visible :)

PS try chewing your food 30 times before swallowing.
 
EMF Mitigation - Flush Niacin - Big 5 Minerals

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