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My eBooksDO you have any of genereaux's books on hand, by chance. Links would be greatly appreciated!
Is there any way to force the body to deplete vitamin A stores that doesn't involve following a low A diet ???
Your suspicion is right : I would like to give it a try but I am lazy to introduce (yet another) such a big shift in diet.
Has this been mentioned elsewhere or you say it by your own experience ? I mean in specific relation to depleting vitamin A.Water fasting :)
Has this been mentioned elsewhere or you say it by your own experience ? I mean in specific relation to depleting vitamin A.
I'm not really sure that is a safe option for me.
@Amazoniac I hear what you are saying, but think for a second about the hamsters and Grant himself. Your basic premise, and correct me if I am wrong, is that just getting rid of vitamin A could have consequences and it is not fixing an underlying issue. You have been mocking the "poison" part. Fair enough.
What about the hamsters? If it will take several generations to deplete hamsters of A, if Grant consuming little to no A for so long does not seem detrimental, then by reason, if there is a need for A, and there probably is, that need is much more contextual then anyone has assumed. Or the amount needed is much lower and the amount of liver we have all consumed is enough for a lifetime.
Basically, the point you are putting across is not playing out with regards to people's actual vitamin A needs.
Water fasting :)
That’s wonderful, I feel the same.
I took a couple months but I find the mental/cognitive changes probably the most impressive especially since they seem to be sticking. It’s been consistent for close to 6 months now. Waking up everyday feeling well is an indescribable feeling.
The first two studies showed fairly opposite effects. Causing the rats to become deficient showed that caused biochemical hyperthyroidism (I thought it was hard to make them deficient?). Whereas the human study on patients with cirrhosis showed giving them vitamin A increased their thyroid levels. Which is it???What I meant is that poison/"vitamin" A must be following metabolism, any changes will require you to adjust for more or less so that it matches your state, otherwise you have the unused poison that might build up or not enough to keep up with the rate of internal consumption.
I guess it depends on the infection, being more or less affected by the deprivation. It's also related to that shifting in inflammatory patterns by changes in "vitamin" A levels.
- Thyroid function and vitamin A deficiency
"Vitamin A has been shown to be necessary for the synthesis of a number of glycoproteins in the small intestine (19), in corneal (20) and tracheal (21) epithelium and a specific glycoprotein in serum (22)."
"There is little information available on the effects of vitamin A on thyroid function. Early work suggested that vitamin A deficiency increases the basal metabolic rate (7,8) and that vitamin A excess has the opposite effect (9). We have studied vitamin A deficient rats to further elucidate the effects of vitamin A on thyroid function."
"Many authors have reported the basal metabolic rate of vitamin A deficient animals to be higher than that of normal controls (7). In addition, there is an increased oxygen uptake in the diaphragms of vitamin A deficient animals compared to controls (13). Vitamin A in large doses has antithyroid effects in experimental animals. The increase in basal metabolic rate and the extent of weight loss produced by thyroid hormone are diminished by simultaneous administration of the vitamin. Thyroid size is also reduced (14). Massive doses of vitamin A have been given to several patients with hyperthyroidism with some lessening of symptoms (15). Vitamin A treatment decreases the severity of experimental thyroiditis in guinea pigs and rats (16)."
"Our data have shown that vitamin A deficiency produced biochemical hyperthyroidism and the previous reports of increased basal metabolic rate in vitamin A deficient animals suggest that this is a true thyrotoxicosis, rather than being due to peripheral organ resistance to thyroid hormone. The increase in hypothalamic TRH and pituitary TSH content, together with the failure of serum TSH to be suppressed and its retained responsiveness to TRH, are consistent with an abnormality in thyroid hormone feedback on the hypothalamic-pituitary axis. Vitamin A deficient rats appear to have central, but not peripheral, resistance to thyroid hormone similar to the situation in same cases recently reported in man (17,18). Whether vitamin A deficiency also has direct effects on the thyroid gland has not been elucidated by this study."
"In conclusion, we have shown that vitamin A deficiency in rats produces a biochemical hyperthyroidism . Our data are consistent with an abnormality in thyroid hormone feedback on the hypothalamic-pituitary axis. We could show no deficiency in anterior pituitary glycoprotein synthesis or release."
- The interrelationship of thyroid hormones with vitamin A and zinc nutritional status in patients with chronic hepatic and gastrointestinal disorders
"There are a number of animal studies suggesting a linkage between vitamin A metabolism and thyroid function. Early work suggested that vitamin A deficiency increases the basal metabolic rate (3) and that vitamin A excess has the opposite effect (4). We showed that vitamin A deficiency in rats increases plasma T3, T4, and free thyronine indexes (5). Vitamin A excess decreases serum T3, T4, and free indices while markedly increasing the percentage of dialyzable thyroid hormones (6). In addition, vitamin A appears to decrease the tissue sensitivity to thyroid hormones (6)."- The Effect of Vitamin A Supplementation on Thyroid Function in Premenopausal Women
"In the 10 patients with vitamin A levels <30 mcg/dl and abnormal dark adaptation, therapy with vitamin A returned vitamin A levels and dark adaptation to normal. Vitamin A therapy increased total T3 and T4 and their free indices as well as free T3 levels by dialysis (Table 3). During treatment there was a concomitant increase in RBP (p < 0.05) without an alteration in prealbumin [transthyretin] levels."
"Normal subjects receiving vitamin A showed a significant decrease in T3, FT3I[ndex], T4, and FT4I after 1 wk of therapy, but after a further 2 wk, thyroid functions had returned to normal. There was no alteration in free thyroid hormone levels as measured by dialysis. During vitamin A therapy there was an increase in vitamin A levels but not in RBP or PA."
"As a group our patients demonstrated the features of the low T3 syndrome, i.e., low serum T3 and FT3I levels with normal T4 levels and slightly increased TSH levels. Among our alcoholic cirrhotics low basal T3 levels correlated with RBP and PA levels but not with vitamin A levels. During therapy with vitamin A, the rise in T3 and free T3 levels was accompanied by an increase in RBP, without a concomitant increase in PA. These data suggest that the stimulation of RBP release from the liver by supplemental vitamin A, in patients with marginal vitamin A status, is closely linked to an increase in circulating thyroid hormone. It should be stressed that in our patients factors influencing liver function other than vitamin A supplementation remained constant. Our hospitalized patients were not consuming alcohol and had been without alcohol for periods of 4 wk to 8 months. All were consuming balanced diets, and although liver function was moderately disturbed, it remained constant during the interval of study. Increases in circulating thyroid hormone levels in our patients could be linked to the vitamin A therapy itself. However, in view of the transient decrease in thyroid hormone levels seen among normal subjects receiving supplemental vitamin A, who did not significantly increase their serum RBP levels, it seems that the increase in circulating RBP concentrations was one factor leading to the improvement in thyroid function."
"The exact role of RBP in maintaining thyroid function is unclear. There would appear to be two sites where vitamin A-RBP metabolism may interact with thyroid metabolism. First, in the liver itself, vitamin A-RBP metabolism may be linked to T4 and to T3 conversion. We have previously shown that vitamin A palmitate can enhance conversion of T4 to T3 in the rat liver homogenates (22)."
"Second, RBP may alter circulating concentrations of thyroid hormones through its role as a carrier for thyroid hormones in the plasma (7, 8). Although the binding sites to PA for the vitamin A-RBP complex and for thyroid hormones are thought to be separate (7), a number of studies in animals have shown that alterations in vitamin A-RBP levels in the plasma lead to reciprocal alterations in thyroid function (5, 6, 23) and similarly alterations in thyroid function alter vitamin A-RBP levels (12)."
"Recently Jennings et al. (24) have shown that the rate limiting step in T4 to T3 conversion in the liver appears to be entry of the T4 into the liver rather than the enzymatic conversion of T4 to T3. It is possible that the PA-RBP-ROH-T4 complex plays a crucial role in making T4 available to tissues."
"Another potential role of vitamin A in the pathogenesis of the low T3 syndrome is suggested by our in vitro observation (J. E. Morley, R. M. Russell, A. Reed, E. A. Carney, and J. M. Hershman, unpublished observation) that the vitamin A ester, vitamin A palmitate, increases the percentage of dialyzable thyroid hormones. An increase in the dialysable fraction of thyroid hormones is well recognized as being present in a variety of chronic illness including cirrhosis (1, 2). Chopra et al. (25) have presented evidence that part of this increase is due to a circulating factor that inhibits thyroid hormone binding. In normal subjects retinol esters are present only in very small concentrations (1.6 ± 0.4 mcg/dl in our normals) whereas in cirrhotics there is an increase in retinol esters (12.5 ± 1.6 mcg/dl in our group). The increase in retinol esters in cirrhotics is probably a result of impaired hepatic uptake of dietary vitamin A and possibly an increased release of vitamin A as free esters. This increase in retinol esters in cirrhotics may be one of the circulating inhibitors responsible for the increase in the dialyzable fraction of thyroid hormones in cirrhotic patients."
"The zinc-deficient cirrhotics had markedly depressed T3 and FT3I levels but in the six patients treated with zinc we could not demonstrate a significant increase in T3 levels. Zinc deficiency in rats is associated with a decrease in T3 levels greater than that seen with comparable caloric restriction (26). Zinc is necessary for RBP release from the liver in rats (14) and, as such, the alterations in thyroid function seen in the patients with zinc deficiency may be secondary to deranged RBP metabolism. In our patients treated with zinc, however, RBP levels did not rise."
"Increased prolactin levels are well recognized as being present in cirrhosis (27, 28). There was no correlation of prolactin levels with vitamin A or RBP levels, but the patients with low zinc levels had high prolactin values. Renal failure is also associated with low zinc levels (29) and increased prolactin levels (30). Zinc and a number of other heavy metals have been shown to suppress prolactin release from isolated pituitaries in vitro (31). There is a possible role of zinc deficiency in the pathogenesis of the prolactin increases seen in cirrhosis and renal failure. However, the failure of prolactin levels to decrease during zinc therapy mitigates against this possibility."
"In conclusion, our data suggest that disturbances of vitamin A-RBP metabolism may play a role in the pathogenesis of the low T3 syndrome seen in patients with chronic gastrointestinal disorders. The association of deranged thyroid function with zinc deficiency may be secondary to zinc-induced disturbances in RBP. Further studies are necessary to elucidate the basic interrelationship of vitamin A-RBP with thyroid function as the associations reported could reflect tertiary metabolic consequences of the complicated set of events after vitamin A therapy and this may not be due to a causal relationship."
Liver hits can manifest on skin quite fast:
- I Need To Get The Yellow Fever Vaccine. Any Advice ?
Digestive transit time can change how much propoison you adsorb:
- Carotene Absorption, Dietary Fat, And Meal Interactions
I'm without audio, but it seems to be those trials (Alpha-Tocopherol/Beta-Carotene trial, etc) that they have stuffed people with antioxidants. You must be familiar with them.
If depleting yourself of poison and staying that way was an easy fix, people would be doing it for a long time, there have been phases in which it was demonized before. Doesn't seem like a sustainable option for the long-term, but I'm aware that people are improving, so I would just pay attention to when it starts plateauing and avoid being uncneiancauerely restrictive; gradual normalization is better than purging anyway. But I don't think my words make much difference at this point, this topic is going in circles.
- Eclampsia in the Real Organism: A Paradigm of General Distress Applicable in Infants, Adults, Etc.
"B vitamin deficiencies alone are enough to cause the liver's underactivity, and to cause estrogen dominance, and a simple vitamin A deficiency causes an inability to use protein efficiently or to make progesterone, and in itself mimics some of the effects of estrogen."
- The problem of Alzheimer's disease as a clue to immortality Part 2
"In a variety of cell types, vitamin A functions as an estrogen antagonist, inhibiting cell division and promoting or maintaining the functioning state. It promotes protein synthesis, regulates lysosomes, and protects against lipid peroxidation. Just as stress and estrogen-toxicity resemble aging, so does a vitamin A deficiency. While its known functions are varied, I think the largest use of vitamin A is for the production of pregnenolone, progesterone, and the other youth-associated steroids. One of vitamin E's important functions is protecting vitamin A from destructive oxidation. Although little attention has been given to the effects of unsaturated fats on vitamin A, their destruction of vitamin E will necessarily lead to the destruction of vitamin A. The increased lipid peroxidation of old age represents a vicious circle, in which the loss of the antioxidants and vitamin A leads to their further destruction.
To produce pregnenolone, thyroid, vitamin A, and cholesterol have to be delivered to the mitochondria in the right proportion and sufficient quantity. Normally, stress is balanced by increased synthesis of pregnenolone, which improves the ability to cope with stress. Lipid peroxidation, resulting from the accumulation of unsaturated fatty acids, iron, and energy deficiency, damages the mitochondrias' ability to produce pregnenolone. When pregnenolone is inadequate, cortisol is over-produced. When progesterone is deficient, estrogen's effect is largely unopposed. When both thyroid and progesterone are deficient, even fat cells synthesize estrogen."
- Fats, functions and malfunctions.
"Transthyretin, which carries both vitamin A and thyroid hormones, is sharply decreased by stress, and should probably be regularly measured as part of the thyroid examination."
I think I stopped it in October or November of last year. I definitely think it’s low A.Blossom, I was just reading in another thread that you also were taking 10,000 iu of Vitamin D daily for about the same time period. Do you still take the Vitamin D? Do you think it has had any impact on your new feelings of well being, or do you only credit low Vitamin A?
I looked back in my notes and on 10/23/18 I recorded that I had stopped D a couple days prior not feeling like I needed it anymore.I think I stopped it in October or November of last year. I definitely think it’s low A.
If you use Cronometer maybe you can create two tables with two average meals; one with your summer 2009 diet and one with the 2012-13 diet. It would be interesting to see which other things are different besides the A and carotenes.I originally didn't bother to read this topic, because the title alone of vitamin A being toxic sounded so insane. I've avoided this topic for months. I clicked on it anyway 3 days ago. I have read almost the entire thread now and Grants book ETFOH, I also listened to the podcast of Matt Stone 180degreehealth on Vitamin A.
There might be something to this Theory of Vitamin A being toxic, when I look at my own health journey over the years:
When I first discovered Raypeat.com (summer 2009) I just cut out all PUFA's and didn't bother with anything else. My diet from 2009-2012 was mainly white rice, potatoes, beef, chicken-breast, dark chocolate, and liquids were coffee, coke, and milk. Milk is not fortified with vitamin A and D in the Netherlands so milk is quite low in vitamin A (30 IU per quart I think). This diet overall was very low in vitamin A. Interestingly, I was at my most healthy at this period. I had zero health issues and felt great.
When I started to research Ray Peat more intensely at the end of 2012- begin 2013, I began to eat "strictly Peat". So lots of cheese (cheese has added beta carotene here), orange juice, carrot salad, some eggs, liver, leafy greens and also taking stuff like Estroban. Coincidentally, I developed some health problems over the years. I began having asthma and develop eczema on my arms and legs. I have been experiencing asthma and eczema for a few years now. It's never gotten better despite Peating for years, Strange huh?
Yeah sounds like you are making the connection. Eczema on a high vitamin A diet is the first sign your liver is starting to become overburdened by it. I know Grant didn't feel the need to use sunlight, but I think it could help speed up the process since UV destroys A in the skin.I originally didn't bother to read this topic, because the title alone of vitamin A being toxic sounded so insane. I've avoided this topic for months. I clicked on it anyway 3 days ago. I have read almost the entire thread now and Grants book ETFOH, I also listened to the podcast of Matt Stone 180degreehealth on Vitamin A.
There might be something to this Theory of Vitamin A being toxic, when I look at my own health journey over the years:
When I first discovered Raypeat.com (summer 2009) I just cut out all PUFA's and didn't bother with anything else. My diet from 2009-2012 was mainly white rice, potatoes, beef, chicken-breast, dark chocolate, and liquids were coffee, coke, and milk. Milk is not fortified with vitamin A and D in the Netherlands so milk is quite low in vitamin A (30 IU per quart I think). This diet overall was very low in vitamin A. Interestingly, I was at my most healthy at this period. I had zero health issues and felt great.
When I started to research Ray Peat more intensely at the end of 2012- begin 2013, I began to eat "strictly Peat". So lots of cheese (cheese has added beta carotene here), orange juice, carrot salad, some eggs, liver, leafy greens and also taking stuff like Estroban. Coincidentally, I developed some health problems over the years. I began having asthma and develop eczema on my arms and legs. I have been experiencing asthma and eczema for a few years now. It's never gotten better despite Peating for years, Strange huh?
I don't use cronometer. But here two different average day of eating. One in the period 2009-2012, and the other 2013-2019:@Vinero or if you can make a detailed list of both average meals I'll put it myself in the cronometer. I'm being too curious.
I think that was my first mistake.nutrisorb-A
It looks like this summer will be 5 years for Grant according to ETFOH.I think Grant is closed to 3.5-4 yrs on zero vitamin A. I am only close to 4 months, but now getting significant improvements in eyesight, I have Presbyopia in my left that is now healing.
There is another member attempting the zero vitamin A diet for mice:
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Feel free to check out my youtube channel documenting the health of two 8 week old female mice on a zero vitamin A diet.
Yi at LDT
Qny feedback, comments or suggestions are welcome
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