Sinatra‘s Notebook

[FitnessMike]

Oops I ment high nickel and chromium levels in stainless steel specifically.


What do you mean specifically?

do you ever check your t3/ft3 levels, do you have preferred levels for both markers that you feel best on?

there is a lot of info on t4/ft4 levels that we should be aiming for but not much on total and ft3.

I know that pulse, temps, and symptoms are a priority but there must be healthy levels for the ft3/total t3.

 

[youngsinatra]

do you ever check your t3/ft3 levels, do you have preferred levels for both markers that you feel best on?

there is a lot of info on t4/ft4 levels that we should be aiming for but not much on total and ft3.

I know that pulse, temps, and symptoms are a priority but there must be healthy levels for the ft3/total t3.

Sorry for the late reply. I cannot order total T3 at my private laboratory, so consequently I always ordered free T3 and T4.

 

[youngsinatra]

Biotin even in minor amounts (like 250 mcg) cause severe digestive issues, even when I filter the solution through a paper filter. It also causes neuropathy, dizziness, dry mouth, brain fog and visual problems - primarily blurry vision. Around 100-200mg of B5 resolve that relatively quickly.

I seem to do well with the B's, but I need to avoid B6 and biotin.

I also want to re-test my serum B6 at the start of the new year, as I once had tested it 3x above reference range when I took a lil bit of P5P (10-20mg) for a month or two. I have texted with someone that also had high persistent serum zinc levels (which were driving his copper levels down) despite no zinc supplementation and an adapted low dietary zinc intake and he correlated the serum zinc perfectly with his high serum B6 levels. Will test both together next time.

Effect of iron, vitamin B-6 and picolinic acid on zinc absorption in the rat - PubMed

True daily zinc absorption was determined in rats fed a high iron diet (220 ppm Fe; 16.5 ppm Zn), and adequate iron diet (30 ppm Fe) and a high iron diet with varying levels of pyridoxine-HCl (2-40 ppm). Zinc absorption in rats fed the high iron diet was significantly less than in rats fed the...

pubmed.ncbi.nlm.nih.gov

Very interesting study, that seem to prove that high B6 levels drastically increase zinc absorption, retention and lowers it's excretion.

 

[youngsinatra]

 

[youngsinatra]

I will do a serum vitamin B6 blood test today.

I am pretty sure that it will come back elevated and that this may explain my mysterious high serum zinc and low copper. Spoke to a few people on facebook with the exact same problem.

Gonna update y‘all later.

 

[FitnessMike]

I will do a serum vitamin B6 blood test today.

I am pretty sure that it will come back elevated and that this may explain my mysterious high serum zinc and low copper. Spoke to a few people on facebook with the exact same problem.

Gonna update y‘all later.

what foods that you eat would potentially drive b6 high?

 

[youngsinatra]

what foods that you eat would potentially drive b6 high?

I think some distinct metabolic problem causes the accumulation of B6, rather than a excess intake, but B6 has a relatively long half life.. so maybe there is something to that.

I joined the FB group „Understanding B6 Toxicity“ with 7000 + members and it’s so interesting to see so many posting their skyhigh B6 labs, even without supplements or high dietary intakes.

Also search „B6 toxicity“ on reddit. Tons of posts. Very interesting.

 

[FitnessMike]

yes, vitamins are so tricky, mostly due to high doses in supplements.

Do you think a b-vitamins blood test is a reliable way to test their status? would be great if we could measure their status.

 

[youngsinatra]

yes, vitamins are so tricky, mostly due to high doses in supplements.

Do you think a b-vitamins blood test is a reliable way to test their status? would be great if we could measure their status.

Dr. Gregory Russel Jones spoke about functional B vitamin deficiencies and high serum values as indicators. He thinks that hypothyroidism / suboptimal thyroid function is a cause of that.

He recommends organic acid testing, but I don’t know how useful that is. It’s one snapshot in time, and quite expensive. (300$ I think)

 

[youngsinatra]

Other than expected labs came back, but best copper/zinc labs so far, ever!

 

[cs3000]

Other than expected labs came back, but best copper/zinc labs so far, ever!

nice, what are you attributing that to?

 

[youngsinatra]

nice, what are you attributing that to?

T4/T3 + B vitamins + lots of coconut water (1L/day)

B1, B2, B5, folate, B12.

 

[FitnessMike]

T4/T3 + B vitamins + lots of coconut water (1L/day)

B1, B2, B5, folate, B12.

but you dont have much supplement b vitamins these days right? its from beef right?

 

[youngsinatra]

but you dont have much supplement b vitamins these days right? its from beef right?

I do supplement, but low doses. I take some regularly but not every day. Like 10mg B1, 25 mg B2, 50 mg B5, 400 mcg folate, 0.5 mg B12.

I don’t eat red meat, so no beef :)

 

[FitnessMike]

I do supplement, but low doses. I take some regularly but not every day. Like 10mg B1, 25 mg B2, 50 mg B5, 400 mcg folate, 0.5 mg B12.

I don’t eat red meat, so no beef :)

ok fam, i too take low Bs now and feel better, food is deprived i guess

 

[FitnessMike]

How much protein do you feel best on?

 

[youngsinatra]

How much protein do you feel best on?

40g each meal. So 160g a day roughly.

 

[youngsinatra]

Riboflavin:

• Essential to the production of energy from food in the form of ATP (adenosine triphosphate)
• Active form is FAD (flavin adenine dinucleotide) and FMN (flavin mononucleotide, also calledriboflavin 5’-phosphate) which are cofactors for oxidation-reduction reactions in energy production
• FAD assists methylation reactions throughout body
• Coenzymes derived from riboflavin are called flavins
• Enzymes that use a flavin coenzymes are called flavoproteins
• Flavins metabolize drugs and toxins
• Hypothyroidism reduces the conversion of riboflavin into FMN and FAD to levels seen in clinical riboflavin deficiency, also known as a deficiency caused by low intake
• Low B2 can impair methylation reactions in the brain, which may present clinically as depression and low detoxification capacity
• Activates glutathione reductase, which regenerates the antioxidant glutathione
• Plays a key role in iron utilization
• Aids in mobilization of ferritin from tissues; helpful for anemia
• FAD is a cofactor for methylenetetrahydrofolate reductase (MTHFR) so for people who arehomozygous for 677C→T MTHFR gene, riboflavin will lower their homocysteine
• Recycles folate into a usable methyl-donor form (converts 5,10-methylene TH4-folate to 5-methylTH4-folate)
• People with 677C→T MTHFR gene tend to respond well to B2 therapy to lower blood pressure
• Cofactor to xanthine oxidase, which synthesizes uric acid and aids in purine catabolism
• FMN is a cofactor to pyridoxal 5’-phosphate oxidase, which converts vitamin B6 into its active form
• FAD is a cofactor that converts P-5-P into pyridoxic acid that can be excreted in the urine (low activity of this enzyme causes B6 build-up)
• Cofactor in the conversion of retinol (vitamin A) to retinoic acid (retinal dehydrogenase)
• Cofactor to kynurenine mono-oxygenase, which converts tryptophan into niacin containing enzymes NAD and NADP
• Cofactor to NAD(P):quinine oxidoreductase which aids in detoxification and chemoprevention
• Cofactor to protoporphyrinogen oxidase which synthesizes hemoglobin
• Cofactor to dihydrolipoyl dehydrogenase which aids energy metabolism
• Cofactor to fatty acyl-CoA-dehygrogenase which aids in fatty acid oxidation
• Cofactor to succinate dehydrogenase which is used in the Krebs cycle for energy production
• Cofactor to NADH dehydrogenase (also called ubiquinone oxidoreductase) which functions inmitochondrial respiration
• Cofactor to sphinganine oxidase which synthesizes sphingosine (component of nerve tissue)
• Cofactor to monoamine oxidase which aids in metabolism of several neurotransmitters such asserotonin, melatonin, epinephrine and norepinephrine
• Role in mitochondrial energy metabolism may explain its efficacy in migraine prophylaxis
• Role in glutathione reductase implicates riboflavin deficiency in cataract formation
• Minimizes pain associated with inflammation
• Augments the antinociceptive (painkiller) effects of morphine

 

[youngsinatra]

 

[FitnessMike]

Riboflavin:

• Essential to the production of energy from food in the form of ATP (adenosine triphosphate)
• Active form is FAD (flavin adenine dinucleotide) and FMN (flavin mononucleotide, also calledriboflavin 5’-phosphate) which are cofactors for oxidation-reduction reactions in energy production
• FAD assists methylation reactions throughout body
• Coenzymes derived from riboflavin are called flavins
• Enzymes that use a flavin coenzymes are called flavoproteins
• Flavins metabolize drugs and toxins
• Hypothyroidism reduces the conversion of riboflavin into FMN and FAD to levels seen in clinical riboflavin deficiency, also known as a deficiency caused by low intake
• Low B2 can impair methylation reactions in the brain, which may present clinically as depression and low detoxification capacity
• Activates glutathione reductase, which regenerates the antioxidant glutathione
• Plays a key role in iron utilization
• Aids in mobilization of ferritin from tissues; helpful for anemia
• FAD is a cofactor for methylenetetrahydrofolate reductase (MTHFR) so for people who arehomozygous for 677C→T MTHFR gene, riboflavin will lower their homocysteine
• Recycles folate into a usable methyl-donor form (converts 5,10-methylene TH4-folate to 5-methylTH4-folate)
• People with 677C→T MTHFR gene tend to respond well to B2 therapy to lower blood pressure
• Cofactor to xanthine oxidase, which synthesizes uric acid and aids in purine catabolism
• FMN is a cofactor to pyridoxal 5’-phosphate oxidase, which converts vitamin B6 into its active form
• FAD is a cofactor that converts P-5-P into pyridoxic acid that can be excreted in the urine (low activity of this enzyme causes B6 build-up)
• Cofactor in the conversion of retinol (vitamin A) to retinoic acid (retinal dehydrogenase)
• Cofactor to kynurenine mono-oxygenase, which converts tryptophan into niacin containing enzymes NAD and NADP
• Cofactor to NAD(P):quinine oxidoreductase which aids in detoxification and chemoprevention
• Cofactor to protoporphyrinogen oxidase which synthesizes hemoglobin
• Cofactor to dihydrolipoyl dehydrogenase which aids energy metabolism
• Cofactor to fatty acyl-CoA-dehygrogenase which aids in fatty acid oxidation
• Cofactor to succinate dehydrogenase which is used in the Krebs cycle for energy production
• Cofactor to NADH dehydrogenase (also called ubiquinone oxidoreductase) which functions inmitochondrial respiration
• Cofactor to sphinganine oxidase which synthesizes sphingosine (component of nerve tissue)
• Cofactor to monoamine oxidase which aids in metabolism of several neurotransmitters such asserotonin, melatonin, epinephrine and norepinephrine
• Role in mitochondrial energy metabolism may explain its efficacy in migraine prophylaxis
• Role in glutathione reductase implicates riboflavin deficiency in cataract formation
• Minimizes pain associated with inflammation
• Augments the antinociceptive (painkiller) effects of morphine

Have you seen any tangible effect from hopping on b2?

I remember @haidut said this in one of his old threads.

The FAD/FADH ratio is intimately connected to the NAD/NADH one. Of the 32 molecules of ATP produced from one glucose, about 80% are from the various mechanisms that use NAD as a cofactor while the remaining 20% are from the FAD/FADH reactions. So, riboflavin is also very important for metabolism and perhaps more responsive to supplementation as it is easier to get deficient in it.