Low Toxin Studies The acute and chronic toxic effects of vitamin A, 2006

mosaic01

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Abstract: The acute and chronic effects of vitamin A toxicity are well documented in the literature. Emerging evidence suggests that subtoxicity without clinical signs of toxicity may be a growing concern, because intake from preformed sources of vitamin A often exceeds the recommended dietary allowances (RDA) for adults, especially in developed countries. Osteoporosis and hip fracture are associated with preformed vitamin A intakes that are only twice the current RDA. Assessing vitamin A status in persons with subtoxicity or toxicity is complicated because serum retinol concentrations are nonsensitive indicators in this range of liver vitamin A reserves. The metabolism in well-nourished persons of preformed vitamin A, provided by either liver or supplements, has been studied by several research groups. To control vitamin A deficiency, large therapeutic doses are administered in developing countries to women and children, who often are undernourished. Nevertheless, little attention has been given to the short-term kinetics (ie, after absorption but before storage) of a large dose of vitamin A or to the short- and long-term effects of such a dose given to lactating women on serum and breast-milk concentrations of retinol and its metabolites. Moreover, appropriate dosing regimens have not been systematically evaluated to ascertain the quantitative improvement in vitamin A status of the women and children who receive these supplements. The known acute and chronic effects of vitamin A toxicity have been reported previously. However, further research is needed to ascertain the areas of the world in which subclinical toxicity exists and to evaluate its effects on overall health and well-being.

Full text: https://www.sciencedirect.com/science/article/pii/S0002916523292710

"Indeed, observational studies suggest that more than 75% of people may be routinely ingesting more than the recommended dietary allowance (RDA) for vitamin A, much of it as preformed vitamin A (16). Until recently, little research investigated hypervitaminosis A in these situations."
 
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Peater

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Very interesting...after 18 years does the research suggest even more is required?
 

Bogdar

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"Interestingly, whereas alcohol consumption was shown to decrease hepatic retinoid levels, these levels are actually increased in extra-hepatic tissues, leading to the concept that alcohol stimulates the mobilization of hepatic retinoid stores to extra-hepatic tissues. To summarize the multiple studies which have investigated this phenomenon, there is evidence to suggest the chronic alcohol consumption increases tissues retinoid levels in specific brain regions, the colon, esophagus, kidney, lung, testes and trachea [18,19,20,21,22,27,40]. It is important to note that although all of the studies mentioned above were focused on the effects of chronic alcohol consumption, it is also known that acute ethanol exposure can affect tissue retinoid levels. Similar to the effects of chronic alcohol consumption, acute alcohol exposure has been shown to precipitate a decline in hepatic retinoid content, with a concomitant increase in extra-hepatic tissue retinoid levels (specifically serum, adipose, and kidney) [27,41,42]."
 

Peater

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"Interestingly, whereas alcohol consumption was shown to decrease hepatic retinoid levels, these levels are actually increased in extra-hepatic tissues, leading to the concept that alcohol stimulates the mobilization of hepatic retinoid stores to extra-hepatic tissues. To summarize the multiple studies which have investigated this phenomenon, there is evidence to suggest the chronic alcohol consumption increases tissues retinoid levels in specific brain regions, the colon, esophagus, kidney, lung, testes and trachea [18,19,20,21,22,27,40]. It is important to note that although all of the studies mentioned above were focused on the effects of chronic alcohol consumption, it is also known that acute ethanol exposure can affect tissue retinoid levels. Similar to the effects of chronic alcohol consumption, acute alcohol exposure has been shown to precipitate a decline in hepatic retinoid content, with a concomitant increase in extra-hepatic tissue retinoid levels (specifically serum, adipose, and kidney) [27,41,42]."
Good spot, this seems important! The question is: Is it better locked in the liver or released into the tissues? Maybe it's helping the body use/process it appropriately.

The study seems to agree with the official stance even while concurring that alcoholics are deficient in all sorts of nutrients.

It has long been recognized that alcoholics are generally malnourished and can suffer from vitamin A deficiency (VAD) [6,7]. A common consequence of alcoholism is loss of night vision (nyctalopia), a condition that is associated with VAD
 
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mosaic01

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Yeah alcohol just washes retinol out of the liver and puts it into tissues and organs, not something good.

Small amounts of pure alcohol like vodka could be therapeutic, I don't know.
 

tallglass13

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How did they determine Hepatic Vitamin a status, I did not see that. Biopsy? I did like this finding though.
Conflicting results have been published on the effect of vitamin A supplementation to rats chronically consuming alcohol, with one group reporting an enhancement of liver injury (increased lipid accumulation and increased indicators of steatohepatitis) [32,33],
 
EMF Mitigation - Flush Niacin - Big 5 Minerals

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