4 replies to this topic

[CuriousMonkey]

Hello,

 

I am trying to find any previous posts that focused on the topic of determining what is optimal nutrient status in the body. For example, I've found studies that found Vitamin C levels in the blood higher than the standard reference range were associated with the lowest risk of all-cause mortality. This points to higher levels of vitamin c itself or as an indicator of something else is of benefit. I've looked on the forum and have not found any discussions that focus on this specific topic. If they exist, I appreciate links to them. If they don't I'd welcome input (with scientific references) as to what is the optimal status in the body for all vitamins, minerals, fatty acids, and amino acids, if known.

 

Thank you. 

[mikeinnaples]

That is impossible to answer without completely knowing and understanding your genetics, epigenetics, and activity. For example, a double MTHFR mutation as compared to someone without it would drastically change not only the amount but the form of nutrient you should shoot for.

[aza]

maybe not, but its still an interesting question i think would be interesting to discuss. For example, i've been looking into retinol lately, found a few interesting papers. Although they all unfortunately use 25,000 iu without other dosages, way above the recommended upper limit. It would be nice to see the effect of lower dosages. Also i admit i dont have the full links to many of the studies and necessarily understand everything about them, i know very little about cytokines and cancer ect. To save time and space, im going to primarily post the results, i focused on the rt's

 

Plasma retinol and total carotenes and fracture risk after long-term supplementation with high doses of retinol    http://www.nutrition...0452-8/abstract

Over a median follow-up of 7.8 y, 123 participants with plasma samples reported an incident fracture. Although plasma retinol concentrations were markedly higher than those reported in observational studies, no association was observed between plasma retinol and risk for any fracture (hazard ratio  , 0.86 μmol/L; 95% confidence interval [CI], 0.65–1.14) or osteoporotic fracture (HR, 0.97 μmol/L; 95% CI, 0.66–1.43). A lower risk for any fracture was suggested with increasing plasma total carotenes (HR, 0.85 μmol/L; 95% CI, 0.71–1.01).

 

The effect of vitamin A supplementation on thyroid function in premenopausal women. https://www.ncbi.nlm...pubmed/23378454

Baseline concentrations of thyroid hormones, RBP and TTR were not significantly different between groups. Vitamin A caused a significant reduction in serum TSH concentrations in obese (p = 0.004) and nonobese (p = 0.001) groups. Serum T3 concentrations also increased in both obese and nonobese vitamin A-treated groups (p < 0.001). Serum T4 decreased in all 3 groups after treatment. The results showed a significant reduction in serum RBP in the obese group after vitamin A supplementation (p = 0.007), but no significant change was seen in serum TTR.

 

Serum TSH concentrations in vitamin A-treated subjects were significantly reduced; therefore, vitamin A supplementation might reduce the risk of subclinical hypothyroidism in premenopausal women.

 

Vitamin A supplementation and serum Th1- and Th2-associated cytokine response in women. https://www.ncbi.nlm...pubmed/24024773

Vitamin A treatment significantly reduced serum concentrations of IL-1β in obese vitamin A-treated subjects (from 3.58 ± 0.36 to 2.45 ± 0.23 pg/ml, p < 0.006). Serum concentrations of IL-4 and IL-13 were also reduced in obese and nonobese vitamin A-treated subjects (p < 0.05). A significant reduction in IL-1β/IL-4 ratio in the obese vitamin A-treated group was also observed (p = 0.03).

 

Decline in serum concentrations of IL-1β and IL-1β/IL-4 ratio in obese women suggests that vitamin A is capable of regulating the immune system and possibly reducing the risk of autoimmune disease in this group. Further studies are needed to explore the possible underlying mechanisms.

 

This next study is a weird one with a whopping dosage.

Safety and efficacy of dose-intensive oral vitamin A in subjects with sun-damaged skin. https://www.ncbi.nlm...pubmed/15041701

The vitamin A doses of 50000 and 75000 IU/day for 1 year proved safe and equally more efficacious than the 25000 IU/day dose and can be recommended for future skin cancer chemoprevention studies.

 

We have had a long-term interest in vitamin A as a skin cancer chemopreventive agent and have completed Phase I, II, and III clinical trials with varying vitamin A doses (1 , 5) . In our Phase III trial, we documented a 32% risk reduction for squamous cell skin cancers associated with a mean 3.5-year vitamin A intervention at 25,000 IU/day in 2,297 participants with evidence of multiple AKs on the face and/or forearms (1) . Because there was virtually no vitamin A-related toxicity at the 25,000 IU/day dose level, we initiated the present study to evaluate the safety of 2- and 3-fold increases in vitamin A doses for a period of 1 year. As documented in this manuscript, vitamin A doses could be increased safely to 50,000 and 75,000 IU/day for the 1-year period with no evidence of differences in the rate of vitamin A-related toxicities in comparison with either placebo or 25,000 IU/day.

We previously published that long-term vitamin A dosing at 25,000 IU/day can raise cholesterol slightly and that this could increase coronary artery disease risk

 

Vitamin A supplementation reduces IL-17 and RORc gene expression in atherosclerotic patients. https://www.ncbi.nlm...pubmed/24845870

In atherosclerotic patients, vitamin A supplementation resulted in significant decrease in IL-17 gene expression by 0.63-fold in fresh cell, 0.82-fold in PHA-activated cells and 0.65-fold in ox-LDL-activated cells (P < 0.05 for all). RORc gene expression in fresh cells as well as ox-LDL-activated cells decreased significantly after vitamin A supplementation in atherosclerotic patients (P = 0.0001 for both). In PHA-activated cells, vitamin A supplementation significantly decreased RORc gene in both atherosclerotic patients and healthy subjects by 0.87-fold and 0.72, respectively, while in placebo group, the RORc gene expression significantly increased by 1.17-fold (P < 0.05 for all). Findings of this study suggest that vitamin A supplementation may be an effective approach to slow progression of atherosclerosis.

 

Vitamin A status is associated with T-cell responses in Bangladeshi men. https://www.ncbi.nlm...pubmed/19747427

Recommendations for vitamin A intake are based on maintaining liver stores of > or = 0.070 micromol/g, which is sufficient to maintain normal vision. We propose that higher levels may be required to maintain normal immune function.

 

Total T-cells, the naive T-cells:memory T-cells ratio and mitogen-induced lymphocyte proliferation were positively and significantly correlated with vitamin A stores (P < 0.05). Mitogen-stimulated IL-2, IL-4 and TNFalpha increased significantly (P < 0.05) in the vitamin A but not placebo group after supplementation, while IL-10 production was significantly and negatively correlated with vitamin A stores (P < 0.05). Segmented linear regression analysis revealed that naive T-cell counts and T-cell blastogenesis were positively associated with vitamin A stores above but not below 0.070 mumol/g liver. These data show that increasing vitamin A stores above the level that maintains normal vision enhances some measures of T-cell-mediated immunity, suggesting a difference in requirements for maintaining vision and immune function.

 

Then theres the supposed vitamin a/d ratio, which we dont really have enough information to go on. I have heard a 4/1 A/D ratio based on chickens and supplementation studies in kids. "In their first supplementation study, Linday et al'" used a total of 4,500 to 5,000 IU of vitamin A and 600 to 700 IU of vitamin D per day, yielding vitamin A/D ratios of 7.1 to 7.5. In their subsequent supplementation studies, these researchers used a basic dose of 3,500 to 3,750 IU of vitamin A and 600 to 700 IU of vitamin D

per day, yielding ratios of 5.4 to 5.8."

However, that doesn't count additional vitamin D from sunlight.

I have heard 2.5/1, probably based on guessing the amount of additional vitamin d from sunlight.

 

Frankly i think the optimal dose is possibly around 1/1 to 1.5/1 A/D.

If i assume the optimal vitamin d level is about 40ng/ml 

And use this https://www.vitamind...end-5000-iuday/

Then my body needs roughly 6000iu vitamin D a day.

Which then means that my optimal dose of retinol is potentially around 6000-9000iu.

That said, I figure the smartest thing to do is to take around 3000iu retinol from food, and let beta carotene's do the rest if needed. (although i take 6000iu myself.)

I dont trust carotene's to do the whole job due to poor conversion to retinol and this study here.  http://www.jbc.org/c...nt/287/19/15886 Naturally Occurring Eccentric Cleavage Products of Provitamin A β-Carotene Function as Antagonists of Retinoic Acid Receptors

Conclusion: β-Apocarotenoids function as naturally occurring retinoid receptor antagonists.

Significance: The antagonism of retinoid signaling by these metabolites may explain the negative health effects of large doses of β-carotene.

 

 

 

Edited by aza, 20 January 2017 - 11:04 AM.

[aza]

regarding retinol, i tried to figure out how much hunter gatherers would have eaten, but i made A LOT of assumptions and there is a lot of variance depending on the group. As a result, its more of a guesstimate then cold hard fact. Anyway, as far as i can a likely range of preformed vitamin A is 2000-7000iu a day which i think sounds reasonable. Also, check this out for vitamin E, http://suppversity.b...rmine-your.html

Edited by aza, 25 January 2017 - 06:10 AM.

[aza]

Unfortunately i have no references for that, as i said before its a rough guesstimate. It may turn out to be not that accurate, but in general it seems to be pretty reasonable as it is below the 10,000iu upper limit. Just don't take it as fact, or automatically assume the higher end is better then the lower range. I really do wish there were some clinical trials that used lower levels of vitamin A to determine the best dietary amount, but until then all we can do is speculate. Unless of course someone is aware of such a study.

 

Also, i just came across this study on choline. Looks like the need for it is highly variable from very low amounts to above the ai, although i would really like to see a study on how much is needed in the context of a diet high in betaine and folate (not folic acid).

Sex and menopausal status influence human dietary requirements for the nutrient choline  https://www.ncbi.nlm...les/PMC2435503/

"Twenty of the 26 men who completed the protocol developed organ dysfunction associated with choline deficiency. Of these 20 subjects, 6 manifested signs of choline depletion in response to the baseline diet (550 mg choline). One such subject who rapidly became depleted became replete on a diet containing 825 mg choline · 70 kg⁻¹ · d⁻¹. Specific repletion data are missing for the remaining 5 rapid depleters because they presented with greatly elevated laboratory values that met our stopping criteria. Thus, per protocol design, they were immediately switched to a diet providing 550 mg choline · 70 kg⁻¹ · d⁻¹ or an ad libitum diet, and their markers of deficiency returned to baseline values. Of the remaining 14 male subjects who developed organ dysfunction in response to a low-choline diet, 6 subjects became replete (organ function returned to normal) during the 25%-choline diet (137.5 mg · 70 kg⁻¹ · d⁻¹), 2 subjects became replete during the 50%-choline diet (275 mg · 70 kg⁻¹ · d⁻¹), and 3 subjects required 75% of the choline AI (412.5 · 70 kg⁻¹ · d⁻¹) to reverse signs of deficiency (Figure 2). Choline concentrations in one additional subject, who developed fatty liver when choline deficient, did not return to baseline after completion of the 550 mg choline · 70 kg⁻¹ · d⁻¹ choline-repletion diet. This subject then consumed an ad libitum diet for 2 wk, which was successful in fully reversing signs of deficiency."

 

"We observed no effect of folic acid supplementation on susceptibility or on mode of presentation. Previously published studies suggesting that folic acid supplementation might decrease requirements for choline used diets much higher in choline (150−300 mg choline/d) than ours (< 50 mg/d) (20, 21). Perhaps the effects of folate become apparent only when marginally adequate amounts of choline are supplied and not when diets are almost devoid of choline."

 

"Of the 57 subjects fed the low-choline or baseline diets, the current AI for choline was sufficient to prevent or reverse organ dysfunction associated with choline deficiency in 46 individuals (81%); the remainder needed 825 mg choline · 70kg⁻¹ · d⁻¹ or the amount of choline in an ad libitum diet (>550 mg · 70 kg⁻¹ · d⁻¹ (53)."