Vitamin A Is A Powerful Anti-obesity Agent By Lowering Cortisol

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Thanks for this. Hard to gleen anything from such studies as there can be a lot of uncontrolled factors. For one thing, they mentioned that the people tended to get their vitamin A from supplements if they were in the higher groups and suggested that they would also be getting other micronutrients from such supplements, so it's difficult to know which micronutrients are responsible for any perceived improvement in health. But, the higher levels didn't seem to hurt them either. I'm not sure what to make of it. I guess the only thing I can do is try increasing it myself and see if I notice improvements.
There are so many variables…

“For example, too much vitamin D can deplete your vitamin A levels. It's also been postulated that vitamin A toxicity could sometimes be caused by a vitamin D deficiency. Vitamin A toxicity has been associated with birth defects, liver issues, vomiting, and lowered bone density.”

 
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Here is a little side note….

“Can I take vitamin A supplement while using retinol?


Retinoids: These medications are a synthetic form of vitamin A and are sometimes prescribed in high doses. People who take retinoids should not take additional vitamin A supplements. In addition, these drugs can cause severe birth defects.”
 

mosaic01

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Thanks for this. Hard to gleen anything from such studies as there can be a lot of uncontrolled factors. For one thing, they mentioned that the people tended to get their vitamin A from supplements if they were in the higher groups and suggested that they would also be getting other micronutrients from such supplements, so it's difficult to know which micronutrients are responsible for any perceived improvement in health. But, the higher levels didn't seem to hurt them either. I'm not sure what to make of it. I guess the only thing I can do is try increasing it myself and see if I notice improvements.

I just realized that the technique they used to create the association is bogus.

They included everyone <50, then <40 and so on. But this isn't legitimate. To compare the groups, he would have needed to only include those between 50 and 40, then 40 and 30, and so on. Otherwise those in the lowest symptom group will always skew the results in favor of a higher average of retinol intake, because they are included in the other groups as well. It creates the illusion of a linear association.

It's all just a game of numbers based on a survey, and a survey is impossible to really give you an objective idea of how much vitamin A someone consumes.
 

charlie

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revenant

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What about studies like this one?


"Administration of vitamin A at birth increased weaning weight and enhanced marbling fat development. Thus, vitamin A administration provides a practical method for increasing marbling and early growth of beef cattle."
 

Jamsey

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The study above about “vitamin a increasing fat cells” not only has nothing to do with obesity, but also is testing ethanol and vitamin a coadministration, and admits that the dose of vitamin a used has no effect on the liver when administered alone.


From the study quoted above,



“The latter was most dramatically documented in another study in which rats were given a combination of vitamin A supplementation and ethanol up to 9 months (49). There was striking hepatic inflam- mation and necrosis, accompanied by a rise in serum enzymes (glutamic dehydrogenase, AST). As expected, vitamin A supplementation resulted in an increased number of fat-storing cells … In the rat, vitamin A in amounts used in the previous studies (47, 49) was not shown by itself to produce fibrosis nor does ethanol treatment per se result in such an effect in rodents. It has been postulated before that toxicity of excess vitamin A may result from the overflowof vitamin A from its form associated with the retinol-binding pro- tein to an esterified form which circulates with the lipoproteins (51,52).However, it is apparent that retinol itself is not directly responsible for the enhanced toxicity after chronic ethanol consumption, since levels of vita- min A in the liver were in fact much lower than in the controls. Since retinol can be further metabolized by liver microsomes, particularly when the latter system is “induced” by chronic ethanol consumption (44, 45, 53, 54),one can postulate that some of these metabolites produced in increased amounts (possibly by some specific forms of cytochrome P-450)might also participate in the enhanced toxicity, but at the present time direct experi- mental evidence to support such a hypothesis is lacking.”

From the cited study (49):

Rats were fed up to 9 months diets supplemented with vitamin A in an amount that, by itself, had no apparent adverse effect on the liver. When associated with chronic ethanol administration, vitamin A supplementation strikingly exacerbated ethanol-induced abnormalities: fat accumulation was increased and numerous giant mitochondria were observed.”
 
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