Low Toxin Diet Grant Genereux's Theory Of Vitamin A Toxicity

[Blossom]

Hi @Blossom can you define “eating like a king or queen” for those of us following the thread, but are unclear as to what that points to? Maybe examples? Thank you in advance

Certainly, here are two posts where Ella talks about eating like a king or queen. My takeaway is that living (and eating enough) in a plentiful food environment and consuming many foods rich in vitamin A daily almost guarantees one won't be deficient.

He may still have adequate stores in adipose tissue, liver and other organs to see him through for some time. Do we know what fat% he is?

If young white educated females (mean age 22.4) in the US consume > 70% the RDA, then we can expect a male in his 50s, who has been eating fortified foods,
downing supplements like lollies and dining on (as McDougall puts it) foods of kings and queens, to have plenty on board.

Be nice to see his hormone profile as his levels of A & D diminish.

@Kyle Bigman, with a diet rich in animal products these days, no one should be vitamin A deficient unless there are malabsorption issues, pancreatitis, celiac's etc.

Don't forget the animals we eat are already supplemented with vitamin A and then we go and supplement on top of this because we are convinced we are deficient??? I doubt there is a need for the majority of people eating the foods of kings and queens to supplement vitamin A .

We saw with the Kempnar's rice diet, those individuals did exceptionally well, reversing disease conditions, for years on a diet completely devoid of retinol. We are talking here of adult men and women, not children and prepubescent children or young teenagers.

When Vitamin A was my molecule of interest, I was interested in its deficiency in mothers and their children and the changes in the cornea at puberty and the teen years. Times of rapid growth, hormonal changes and stress. The influence of poor food choices restrictive diets and the absence of protective foods.

Wealthy adult men who had access to unlimited food choices and supplementation were never on my horizon - they were not part of my demographics. I am happy Grant has recovered his health but I still feel his problem is to do with testosterone and andropause. It is wrong for him to be scaremongering and cherry picking the literature.

He leaves out so much of the valuable research on Vitamin A and makes one wonder why he has not taken a more balance approach.

Andropause is a time in a man's life when hormonal changes have the greatest impact on health. Now if Grant had developed keratoconus, I would be more interested in his plight. If his symptoms had not reversed, I would be in more fear of Vitamin A toxicity, unlike KC , which is difficult to halt or reverse. I fear more a deficiency in childhood than an excess in adulthood, eating a robust and varied diet. Supplementation is not recommended unless there is justification.

KC occurs in menopausal women although rare, on the pill, HRT, pregnancy etc. but in males who tend to be more predisposed to KC than females before and after the teen years, rarer in andropause. It halts during the 3rd and 4th decade. I have yet to meet a male who developed KC during andropause and would be certainly interested in knowing.

Grant is an engineer and has little appreciation on the biphasic nature of substances. He has problems with the concept that a deficit and a toxic dose can cause the same symptoms. Unfortunately this is a mentality shared on this forum by some (not all) that a tiny bit of a substance, as is found in food, is not as powerful as a lot which is found in supplementing. Not so. A small dose can be even more powerful than a large dose. We have learnt much from the research on endocrine disrupting molecules - a small dose can have very profound effects.

The human body is not a black box in the way engineers view problems. We have not even begun to scratch the surface in understanding its complexity and sophistication. We think we know, but we know ***t compared to the intelligence that exists in each and every cell. Nutritional sciences is in its infancy and we should not be so gun-ho thinking science has it all worked out. Nature may have, but man has a long way to go.

The body is not derelict. It is constantly trying to correct and adapt even though we continue doing stupid things to it.
Hormones and Endocrine-Disrupting Chemicals: Low-Dose Effects and Nonmonotonic Dose Responses

 

[Peater Piper]

There's this part from 'Extinguishing the fires':

"To test this hypothesis, after having my eczema almost completely clear, I ate a single medium raw carrot. The next morning, I had a significant spot of inflamed skin show up on both hands. It was about the size of a mosquito bite. It was right in the cusp between the thumb and index finger, and very peculiarly it was perfectly symmetrical on both hands."
A single medium raw carrot can't worsen a supposed toxicity to that extent, especially after having restricted vitamin A for quite a while. This is a sign that he's conserving something else through vitamin A restriction, quieting what isn't working right.

That sounds more like some kind of allergy to me. Toxicity doesn't just happen that quickly with that small of a dose. I'm open to Vitamin A toxicity, we know it can happen, but to go to the extreme that it's always a poison seems dubious to me. Even the comparison to iron is lacking, because even Peat acknowledges some iron is necessary, and a person doesn't go from iron depleted to iron overloaded after a single steak, yet a person depleting vitamin A for years gets overwhelmed by a tiny amount of beta carotene? Again, sounds more like some kind of an allergy.

 

[Mito]

Grant seems to be doing well.

From everything he’s told us that does seem to be the case. However, you have to consider that diseases caused by vitamin deficiencies can take many years to develop because the body is extremely adaptable. Some possible concerns are his declining serum cholesterol levels which may not be bad in itself but could signal lower cholesterol synthesis in tissues where we want it to remain high like the brain, adrenal glands, etc. His platelet count is below the reference range which could have many causes including low cofactors like Vitamin K and calcium or other things like spleen issues. Also his pulse rate is pretty low (55-60) which could imply reduced thyroid function.

That said he did eliminate his skin problem with his therapeutic diet and each of the possible concerns I pointed out, Grant views as indicative of improving health.

 

[tankasnowgod]

That sounds more like some kind of allergy to me. Toxicity doesn't just happen that quickly with that small of a dose. I'm open to Vitamin A toxicity, we know it can happen, but to go to the extreme that it's always a poison seems dubious to me. Even the comparison to iron is lacking, because even Peat acknowledges some iron is necessary, and a person doesn't go from iron depleted to iron overloaded after a single steak, yet a person depleting vitamin A for years gets overwhelmed by a tiny amount of beta carotene? Again, sounds more like some kind of an allergy.

To be fair, it's not even truly a test of Vitamin A. It's a test of Beta Carotene. He may have exposed some extreme carotenemia reaction. I'd be interesting to see Grant test a food with natural retinol (eggs, unfortified dairy, or liver) and also a retinol supplement, like retinal palmitate.

 

[InChristAlone]

He would say when you avoid a toxin for so long then have a big exposure you could react really strongly, whereas when you are constantly consuming it you dont notice the cumulative effects. But I dont really agree with that. Take alcohol for instance, being able to handle it without even a buzz even though you haven't had any in years I would say is improved health rather than feeling drunk from just one drink. But maybe vitamin A and carotenes are different once you have suffered from a sensitivity. Kinda like my reaction to caffeine. I know I will never be able to drink coffee ever again with reckless abandon. It's like my brain has been trained to know it isn't good for me. I could try to retrain it, but after suffering from doom and panic I never want to go back. So maybe that is why I can understand Grant never wanting to test out retinol because his skin problem was so traumatic. So maybe it's the trauma for him.

 

[Amazoniac]

So you are in agreeance it's a good thing it depletes A? Problem is I get very little of it 6 months a yr. I was talking to a lady who said as soon as the UV drops, taking A gives her anxiety and insomnia immediately.

No (Wagner, 2018). You are for me what Kartoffel is for Trawis, therefore we can't break the pact in agreeing on something.
Perhaps we need to sacrifice it in the process of absorbing light and synthesizing antidote D. The body already uses A in other processes anyway, sunlight will only increase the needs.


I was trying to predict the course of these experiments to know for how long the forum will need to put up with this. I should note that I have contacted a clever shaman through a private session and the entity reported good results so far.

The thread will lessen the intensity when it reaches 92 pages. On page 78 you'll be able to locate the first give-up post. On page 105 there will be a regretful one swearing to no longer be adhering to fads and 1 month later you'll find the person who posted switching to a different toy/tool.


But seriously, I think it's important to know what you're getting yourselves into..

With vitamin A avoidance, in 6 months there might be slight but noticeable changes in vision, especially if you are under stress, harbor challenging infections, sun expose frenquently, are active, require extraordinary tissue regeneration, eat plenty of proteid (anabolic stimulus) and began the trial assuming that your reserves were high when in fact they were somewhat low (from malabsorption for example). But clearer effects might only appear after 1-2 years, for people that are efficient in conserving, it can take more. Who knows what is compromised along the way.


- The Experimental Induction of Vitamin A Deficiency in Humans (!)

"Arroyave (16) reported that protein-malnourished children showed no signs of vitamin A deficiency because of growth depression. As soon as they obtained protein and began to grow, the vitamin deficiency symptoms were precipitated. In animal experiments, Rechcigl et al. (17) observed a precise linear relationship between growth rate and vitamin A utilization."

"Vitamin A deficiency was induced in humans by several researchers with the important aim to determine the daily requirement of the vitamin for healthy adults. This proved to be unexpectedly difficult because of the large but variable reserves of the vitamin stored in the livers of healthy persons. Moore (18), by analysis of livers of accident victims in England, found a median value of liver reserves of 324 IU/g for a healthy British adult, with the enormous variability of 10 IU to 1500 IU/g liver."

"A curious seasonal oscillation was observed in dark adaptation, which deteriorated after 5 mo in the subjects fed the deficient diet (Fig. 5), coinciding with the winter months (November to February), and showed recovery during the following summer months. This seasonal effect, which was observed again during a second winter, could not have been caused by seasonal changes in carotene content of the diet because that was rigorously controlled. Furthermore, the deterioration was not accelerated when fruit and vegetables were completely eliminated from the depleted diet for four summer months. Hume and Krebs (27) suggested that the effect may have been due to changes in temperature (Fig. 5), although why cold should lower plasma vitamin A level remains unexplained."

"These seasonal changes are reminiscent of the observations of Bloch (4) referred to above, reporting that all children in the Children’s Home consuming the fat-free milk diet came down with xerophthalmia during March, April and May. Of course, these months differ from those in the Sheffield experiment. Perhaps xerophthalmia follows a seasonal decline of plasma vitamin A in winter by a few months."

"A case of self-induced vitamin A deficiency was reported in 1969 by Sharman (28).4 A 20-year old man, who had been suffering from epilepsy from age 12 became convinced from reading the literature, that vitamin A caused his epileptic fits. He deliberately eliminated all vitamin A and carotenoids from his diet. His blood retinol dropped to 130 IU/L (normal, about 2000 IU/L) and the blood carotenoid level became extremely low. Subsisting on this diet for 4 years resulted in corneal xerosis and severe retinal damage (29). He reported that his epilepsy was much ameliorated; he had suffered only one fit during that period. Upon repletion with vitamin A, he recovered his ocular health. No information is available regarding his epilepsy subsequently. In order to investigate further a possible connection between vitamin A and epilepsy, Sharman (30) then studied 8 epileptic patients given a vitamin A-depleted diet for 2 years. No cases of night blindness were observed. When their plasma retinol level had reached 230 IU/L, they were given a vitamin A supplement. Although the patients reported fewer fits during the depletion period, there was no increase in the fits during repletion. The author (30) called his experiment a 'dietary contretemps.'"​

- Effects of vitamin A depletion in young adults

"It is seen, therefore, that normal, well fed adults did not present any of the alleged signs of subclinical vitamin A deficiency even after seven and one-half months on a depletion diet. Either or both of two factors may be responsible for such a result. Either the demand for vitamin A by the organism is not great enough to cause sufficient depletion of normal hepatic stores in seven and one-half months to result in the occurrence of the reported early signs of vitamin A deficiency, or these signs are not solely a result of uncomplicated vitamin A deficiency."

"That an extensive degree of depletion of stores of vitamin A is a prerequisite for the development of the subclinical signs of deficiency is borne out by animal studies in which the occurrence of these signs has been correlated with liver stores, by the greater prevalence of subclinical signs in children than in adults and in males than in females and by the relatively low incidence of defects in populations on vitamin-meager diets. In rats it has been shown that a lag exists between the exhaustion of hepatic stores and the appearance of loss of weight and xerophthalmia.19 In children and males the amount of vitamin A storage is less than in adults and females—in children because they have had less opportunity to acquire stores; in males (if a sex difference is accepted) because they store less and lose it more readily than females, as was shown in rats.20 Steven's and Wald's investigation in Labrador 21 revealed only a small percentage of night blindness, although to judge from the habitual dietaries a much greater percentage would have been expected. Josephs'22 study of the vitamin A content of the blood and dark adaptation in various socioeconomic groups showed that only in severe and prolonged vitamin A deficiency were these measurements affected. The failure for as long as six months of controlled vitamin-low diets to result in any of the specific signs of deficiency23 is also indicative that the depletion period studied was not ample. It is interesting to note that a theoretic calculation based on the average vitamin A content of human liver24 and the assumption that the rate of use is approximately 2,000 U. S. P. units per day shows that it would take from one to two years for the liver to lose its entire vitamin A stores if no vitamin A were present in the diet." [Read the previous article for more information supporting this]

"The second explanation offered for the negative findings of this study is that these signs are neither sensitive nor specific for subclinical vitamin A deficiency. The contradictory evidence concerning their diagnostic value supports such a contention."

"In respect to dark adaptation it has been shown that there is an inconsistency in the response of normal subjects to vitamin-low diets in the various laboratories as well as in the response of deficient subjects to massive doses of vitamin A.25 The specificity [I managed once to get this word right on the first attempt] of night blindness as an indication of vitamin A deficiency has also been challenged by the curative effect of vitamin C and riboflavin in some cases.20 There are indications, too, that several of the other symptoms may be more sensitive than dark adaptation as indicators of subclinical vitamin A deficiency.27 This is quite conceivable, since animal experimentation reveals that the vitamin A content of the retina persists even in the absence of hepatic stores.28"

"Two additional alleged subclinical signs which have received a reasonable share of attention are the decreased vitamin A content of the blood and changes in the structure of the skin. The former has obtained support from the work of May,5 Lewis, Bodansky and Haig27c and Yarbrough and Dann.6 These investigators found the blood level the most sensitive indicator of vitamin A deficiency. On the other hand, Josephs22 and Nylund23d with human beings and Brenner, Brookes and Roberts1 with rats found that there is a wide range in the blood level of normal subjects and that only in prolonged and severe deficiency is the blood level valuable diagnostically. Changes in the skin, such as keratinization and resulting horny papules known as toadskin, have been reported by Lehman20 in children on relief and by Steffens, Bair and Sheard23c in an adult maintained on a vitamin-low diet for one hundred and eighty days. This condition has been described as occurring in scurvy, pellagra and other deficiency diseases,30 the more severely affected patients being from the Orient, where the diet is totally inadequate in all the dietary constituents.31 Since the deficiencies are multiple, the assumption that the lack of vitamin A alone is responsible for the cutaneous changes is not justified, even though massive doses of vitamin A have been effective in causing a cure, for in general other concentrates are also administered."

"Since Bitot spots, conjunctival foam and changes in vascularity and translucency of the conjunctiva and cornea may occur in persons without vitamin A deficiency as well as in those in all stages preceding severe vitamin A deficiency, these signs are suggestive but not positive indications of deficiency."

"Moore30e in summing up the allowable claims for vitamin A deficiency stated:

'If, therefore, the claim that phrynoderma (toadskin) is acceptable as a manifestation of vitamin A deficiency, it is difficult to understand how night blindness can be accepted as an early or invariable symptom of vitamin A deficiency. But is phrynoderma due to a deficiency of vitamin A? There are a number of observers who hold it is not so.'"​

"From these existing uncertainties it is evident that much work needs yet to be done on the metabolism of vitamin A to elucidate the confusing evidence."​

- Hepatic stores of retinol and retinyl esters in elderly people

"Serum concentrations of vitamin A [] do not necessarily represent body stores. Over 90% of the total body vitamin A is stored in the liver, 9% in other tissues and only 1% is in plasma [4]. Retinol stored in the liver is mostly esterified with long-chain fatty acids, the main ester being palmitate, and a much smaller quantity is stored as free (unesterified) retinol. The serum concentration is dependent on the concentration of retinol-binding protein which is synthesized in the liver and is affected by malnutrition, malabsorption and systemic illness (e.g. malignancy), many of the factors that might affect total stores of vitamin A [4]. In humans and baboons, depletion of hepatic vitamin A stores correlates poorly with serum levels [5, 6]."

"[Our] results suggest that depletion of hepatic stores of vitamin A involving both retinyl esters and also free retinol occurs in elderly patients stressed by chronic disease and malnutrition. Although it is likely that careful biochemical and anthropometric examination during life might well have found evidence of malnutrition as well as disease in group II, the cachexia and weight loss of group III is evidence for significant malnutrition, as well as chronic disease in this group at the time of death [12]. The low levels of total hepatic retinol in groups II and III was mostly due to lower stores of retinyl palmitate and the other retinyl esters, and to a lesser extent reduced stores of free (unesterified) retinol."

"Huque [13] assessed hepatic reserves of vitamin A at random post-mortem examinations performed in London on a wide cross-section of the population and ages. In that study [if anything?] there was a 'downward trend' from the fifth decade, and by the eighth decade 11.6% of subjects studied had low hepatic reserves (<40 mcg/g), although this was not statistically significant. Our study found no effect of age on vitamin A levels over the range 66-96 years, although it was not designed to be an unselected cross-section of the population. Two subjects in group III had very low total hepatic retinols, which at the time of death were just above the critical level of 40 mcg/g."

"Apparent biochemical deficiencies of many vitamins are quite common in the elderly, although functional changes are not always shown. The last DHSS report on nutrition and health in old age in the United Kingdom found in the general population 30% riboflavin deficient, 15% folate deficient, 11% pyridoxine deficient and overall 7% had significant malnutrition, but vitamin A was not studied [14]. Indeed the clinical importance of depleted stores of vitamin A is not well understood. Vitamin A is needed for normal visual dark adaptation but is also essential for growth, the maintenance of squamous epithelial cells (such as the skin and cornea), testicular function and normal response to infection [15]. Depletion studies on volunteers in Sheffield found nonspecific abnormalities in general health, which correlated poorly with serum levels or dark adaptation [16]. Epidemiological work has suggested a possible link between low serum concentrations of vitamin A and cancer risk, particularly of the oesophagus and lung [17]. More recently it has been shown that in apparently fit Australian pre-school children vitamin A supplementation can decrease the incidence of upper respiratory tract infection [18], while in populations known to suffer severe depletion supplementation reduces infant mortality [19]."​

- Vitamin A in dietary supplements and fortified foods: Too much of a good thing?

"Individuals, especially those taking more than one multivitamin per day, may be at an unappreciated greater risk for hypervitaminosis A given that the current daily value (DV) for vitamin A is 5,000 IU (1,500 mcg) because it is based on the higher 1968 and not the current RDAs (6,7)."

mcg/0.3 = IU

Current RDA - 900♂ or 700♀ μg RAE/day [3000♂ or 2300♀ IU/day]
Upper limit for Preformed Vitamin A - 3000 μg RAE/day [10000 IU/day]

--
I've wondered for a long time if Ramón's reaction to vitamin A wasn't a sign of mild toxicity and his body asking him to stop [sdob it, doooooooololololoont]:

Ray Peat Email Exchanges - Ray Peat Forum Wiki

"I found that a very small amount of either vitamin A or magnesium chloride could cause big headaches for two or three days. If I had put vitamin A anywhere on my face or arms, enough would touch my lips to cause the headache. It wasn't the vitamin A or magnesium itself that did it, but some very powerful allergen in the chemically manufactured products."

"I have had bad headaches when I used vitamin A orally, and even getting a little on my lips was enough to do it."​

--
- Human Vitamin A Deficiency
- Multiple functions of vitamin A (also by Jorge, author of the first link)
- Hypervitaminemia A in the recovery stage of various diseases
- The Effect of Restricted Intake of Carotene and Vitamin A on Psoriasis Vulgaris — A Preliminary Report
- High prevalence of vitamin A deficiency in Crohn's disease patients according to serum retinol levels and the relative dose-response test
- A study of the influence of dietary vitamin A on the level of liver and serum cholinesterase in rats
- Prognostic Importance of Vitamins A, E and Retinol-binding Protein 4 in Renal Cell Carcinoma Patients
- Role of vitamin A in liver fibrosis
- Vitamin A poisoning in adults
- Hypervitaminosis A: A liver lover's lament
- Interactions of Vitamin A and Iodine Deficiencies: Effects on the Pituitary-Thyroid Axis
- Anti-sunshine vitamin A (similar to the UV publication from a previous post)
- Hepatic Injury from Chronic Hypervitaminosis a Resulting in Portal Hypertension and Ascites
- Roles of Vitamin A Metabolism in the Development of Hepatic Insulin Resistance
- Assessing Vitamin A Status: Past, Present and Future

 

[Tarmander]

I think everyone can agree that the theory is limited and incomplete as an explanatory mechanism. It is also working for Grant and many others with regards to autoimmune.

As a side note, Grant consumed red beans for years, and they had beta carotene in them. I think this is a glaring hole in the theory. The guy has had exposure to vitamin A, he is not completely deficit.

 

[lollipop]

Certainly, here are two posts where Ella talks about eating like a king or queen. My takeaway is that living (and eating enough) in a plentiful food environment and consuming many foods rich in vitamin A daily almost guarantees one won't be deficient.

Thank you @Blossom Makes sense. I also appreciate @Ella ‘s understanding that body is intelligent and trying to adjust itself in light of the goofy things we do to it - lol. My overall take on vibrant health seems to again and again come back to homemade foods, homegrown if possible, mixed macros, variety of fresh food, and limiting PUFA oils.

Edit: waaaay more factors influencing health - just speaking about diet in above assessment.

 

[Blossom]

Thank you @Blossom Makes sense. I also appreciate @Ella ‘s understanding that body is intelligent and trying to adjust itself in light of the goofy things we do to it - lol. My overall take on vibrant health seems to again and again come back to homemade foods, homegrown if possible, mixed macros, variety of fresh food, and limiting PUFA oils.

Yes, I agree. I also appreciate Ella and Anazonic’s efforts to give us a balanced perspective on the topic. One thing I learned when researching crypto-xanthines that was brought up earlier in the thread is that they are found in blood. With this being the case I think even red meat would contain some of this substance. It seems like nearly all natural foods always have some type of A and our fortification and supplementation are probably the main reason some people are becoming imbalanced.

 

[Amazoniac]

Yes, I agree. I also appreciate Ella and Anazonic’s efforts to give us a balanced perspective on the topic. One thing I learned when researching crypto-xanthines that was brought up earlier in the thread is that they are found in blood. With this being the case I think even red meat would contain some of this substance. It seems like nearly all natural foods always have some type of A and our fortification and supplementation are probably the main reason some people are becoming imbalanced.

Many people dislike liver but eat it anyway..

Hypervitaminosis A: A liver lover's lament

"In addition to liver disease due to hepatitis and dietary protein deficiencies, other factors can also potentiate vitamin A toxicity. Disease states that favor hepatotoxicity include renal failure; in such patients, vitamin A toxicity can develop with supplements as low as 4,000 IU per day (38)."

"The historical cases of intoxication by excess polar bear liver in Arctic explorers (19) have more recent counterparts in accounts of chronic hypervitaminosis A induced by the long-term frequent ingestion of beef liver in adults (41). One case of cirrhosis was attributed to the regular consumption of 2 to 3 large portions (6 to 8 ounces per week) of beef liver for 8 to 9 years, providing an average daily intake of 30,000 to 40,000 IU vitamin A. A similar pathogenesis of cirrhosis was reported by Babb and Kieraldo (42). Thus, excess intake of liver appears to be a definite hazard in terms of developing the liver complications of hypervitaminosis A."

"Another unusual presentation of vitamin A intoxication, possibly reflecting enhanced susceptibility, was reported by Schurr et al. (46) in a 10-year-old boy who showed severe signs of vitamin A toxicity attributed to a 5-year-long daily intake of a single multivitamin preparation containing 5,000 IU vitamin A. An apparently prolonged half-life of serum vitamin A was consistent with a defective clearance mechanism."

"Contrasting with retinol, carotenoids (even when ingested chronically in large amounts) are not known to produce toxic manifestations (11,61)."

"Once hypervitaminosis A is established, no effective treatment is available, save for low vitamin A diets. Experimentally, pretreatment with spironolactone or anabolic steroids (e.g., norbolethone, ethylestrenol, oxandrolone) inhibits the bone resorption induced by vitamin A overdosage (62). No effective way is presently available to accelerate the mobilization of excess vitamin A stores from the liver, which is a slow process: a half-life of 58 days was found by Weber et al. (37) and a 50% decrease in 286 days was found by Smith and Goodman (52)."

"Contrary to popular belief, liver-rich regimens are relatively contraindicated in patients with liver disease. The liver lover (hepatologist or not) is at increased risk: the liver is a main site of vitamin storage in the body, and its exessive consumption is a main cause of dietary-induced vitamin A toxicity."​

So, yeah, stop overconsumption, switch to carotenes, trust cravings and boost metabolism because this will use up vitamin A (many strategies so far have this in common).

Some random comments:

For people who are eating a lot of carotenes yet still crave carrots, some time ago when I contacted Raj about choline, I sent him the link to white carrots, he seemed interested. It's an alternative.
Regarding pigmentation as a way to discourage predators, I wonder how Garrett would explain ancient fruit that its pulp has a deep color.

Ingesting vitamin E instead of applying it on the skin should be better.

It might be possible to judge your state by keeping a bottle of vitamin A around and smelling or tasting it: it shouldn't be objectionable. I don't know if this works for a functional deficiency.

 

[Blossom]

Many people dislike liver but eat it anyway..

"In addition to liver disease due to hepatitis and dietary protein deficiencies, other factors can also potentiate vitamin A toxicity. Disease states that favor hepatotoxicity include renal failure; in such patients, vitamin A toxicity can develop with supplements as low as 4,000 IU per day (38)."

"The historical cases of intoxication by excess polar bear liver in Arctic explorers (19) have more recent counterparts in accounts of chronic hypervitaminosis A induced by the long-term frequent ingestion of beef liver in adults (41). One case of cirrhosis was attributed to the regular consumption of 2 to 3 large portions (6 to 8 ounces per week) of beef liver for 8 to 9 years, providing an average daily intake of 30,000 to 40,000 IU vitamin A. A similar pathogenesis of cirrhosis was reported by Babb and Kieraldo (42). Thus, excess intake of liver appears to be a definite hazard in terms of developing the liver complications of hypervitaminosis A."

"Another unusual presentation of vitamin A intoxication, possibly reflecting enhanced susceptibility, was reported by Schurr et al. (46) in a 10-year-old boy who showed severe signs of vitamin A toxicity attributed to a 5-year-long daily intake of a single multivitamin preparation containing 5,000 IU vitamin A. An apparently prolonged half-life of serum vitamin A was consistent with a defective clearance mechanism."

"Contrasting with retinol, carotenoids (even when ingested chronically in large amounts) are not known to produce toxic manifestations (11,61)."

"Once hypervitaminosis A is established, no effective treatment is available, save for low vitamin A diets. Experimentally, pretreatment with spironolactone or anabolic steroids (e.g., norbolethone, ethylestrenol, oxandrolone) inhibits the bone resorption induced by vitamin A overdosage (62). No effective way is presently available to accelerate the mobilization of excess vitamin A stores from the liver, which is a slow process: a half-life of 58 days was found by Weber et al. (37) and a 50% decrease in 286 days was found by Smith and Goodman (52)."

"Contrary to popular belief, liver-rich regimens are relatively contraindicated in patients with liver disease. The liver lover (hepatologist or not) is at increased risk: the liver is a main site of vitamin storage in the body, and its exessive consumption is a main cause of dietary-induced vitamin A toxicity."​

So, yeah, stop overconsumption, switch to carotenes, trust cravings and boost metabolism because this will use up vitamin A (many strategies so far have this in common).

Some random comments:

For people who are eating a lot of carotenes yet still crave carrots, some time ago when I contacted Raj about choline, I sent him the link to white carrots, he seemed interested. It's an alternative.
Regarding pigmentation as a way to discourage predators, I wonder how Garrett would explain ancient fruit that its pulp has a deep color.

Ingesting vitamin E instead of applying it on the skin should be better.

It might be possible to judge your state by keeping a bottle of vitamin A around and smelling or tasting it: it shouldn't be objectionable. I don't know if this works for a functional deficiency.

Thanks Amazonic. I’m guilty of eating liver even when it seemed repulsive. I do still have a bottle of retinyl palimate so I will go take a whiff while thinking of you. <3

 

[Mito]

The guy has had exposure to vitamin A, he is not completely deficit.

True but he tested his serum Vitamin A earlier this year. The results were 0.1 µmoI/L or 2.87 mcg/dL which is a severe deficiency considering the normal reference range of 32.5-78.0 mcg/dL.

 

[somuch4food]

Garrett Smith is linking Omega 3s and 6s to the same receptor (RXR) as vitamin A and stipulates that they are also a cure to Xerophthalmia:
What if the so-called RXR (Vitamin A receptor) was improperly named?
Broken logic: xerophthalmia (dry eye) is said to be a Vitamin A deficiency, yet most who have it aren't Vitamin A deficient?

Anecdotally, I had an ADD episode following a week of indulging in walnuts and hummus made with canola oil. I'm also having a similar episode following ingestion of sweet potatoes. Can the RXR receptor cause focusing troubles and anxiety issues?

 

[somuch4food]

Theory about Nitric Oxide balancing Retinoic Acid activity in relation to ADHD and misbehavior:
https://www.hindawi.com/journals/isrn/2012/589792/

 

[MarcelZD]

Thanks Amazonic. I’m guilty of eating liver even when it seemed repulsive. I do still have a bottle of retinyl palimate so I will go take a whiff while thinking of you. <3

On paper liver always seemed like such an awesome food: high protein, lean, micronutrient-packed, extremely cheap. One would think it'd taste like a slice of heaven.

I've talked to several people who grew up eating beef liver and they still hate it. I personally don't think I'll ever eat one again.

 

[tankasnowgod]

On paper liver always seemed like such an awesome food: high protein, lean, micronutrient-packed, extremely cheap. One would think it'd taste like a slice of heaven.

I've talked to several people who grew up eating beef liver and they still hate it. I personally don't think I'll ever eat one again.

Funny, it's been love or hate for me. Calf liver was awesome.

Recently, it's been A LOT more hate, though. I think I will be waiting at least six months, and then, re-evaluate.

 

[Amazoniac]

As a coincidence the highlights are orange.

- Book Series: Vitamins And Hormones

It's a good book on nutrition and endocrimology written by a single author [!], unrelated to marital status; not that I have anything against marriages; not that disclosing these things makes any difference for you; not that I'm wasting our times then, it has a point, but not that it should distract you from the fact that the person is indeed knowledgeable; not that being ignorant is our problem; not that I'm in a position to judge what is a problematic or not; I mean, I respect everybody regardless if you're Dutch or not; by the way, I haven't chosen this specific nationality implying that the rest is inferior; just to clarify, I'm not using 'rest' with disdain, all life matters; not that I'm saying this so that I'm in good terms with everyone, I'm fine if I don't get along with some of you; not that I didn't want to be in good terms with those that I'm not right now; I just prefer things to be as clear as possible to avoid confusions or being interpreted the wrong way. Anyway..​

"Infants and persons suffering from various forms of gastroenteritis, both acute and chronic, have a much reduced ability to undertake the [carotene] conversion. In diabetes and in hypopboydism the conversion is almost completely blocked. Cretins, lacking a functional thyroid gland, are quite unable to convert carotene to vitamin A."

"Restoration to the normal state [after depletion] was best achieved by feeding rather than injecting supplies of vitamins."

"Microscopically, A-deficiency is associated with keratinising squamous metaplasia of mucous epithelia—that is, mucous membranes change from a single layer of mucin secreting and ciliated epithelium to multiple layers of epithelial cells, with overlying keratin, resembling those of the skin. The increase in thickness of the necks of the underlying mucous glands plugs their orifices and seals off their secretion. Obstruction of pancreatic ducts by keratotic plugs blocks the release of pancreatic enzymes into the small intestine. At the subcellular level, there is disruption of lysosomal and other cellular membranes both in deficiency and in excess of vitamin A, and it is probable that an optimal amount of vitamin A for the species is essential for the integrity of pericellular and intracellular membranes. (Fell, 1964.)"

"It is important to remember too, that serum levels of vitamin A may not correlate with liver levels, either in the normal or the undernourished subject. It is possible to have large stores of the vitamin, with little in the circulation, or to have a normal serum level in association with a depleted liver."

"The importance of vitamin A metabolism in the adrenal gland has long been recognised. Numerous experiments have shown that A-deficiency reduces resistance to stress, lowers insulin tolerance, and impairs glucogenesis. By histological techniques, the vitamin can be demonstrated in high concentration in the cells of the zona fasciculata, suggesting its importance for glucocorticoid synthesis. Adrenal sections often show masses of 'lipochrome' pigment in the cells of the zona reticularis. This is a carotenoid pigment and may represent a store of vitamin A precursor. The pigment is seldom, if ever, seen in the medulla, and its presence in the cortex lends support to the view that it participates in steroid synthesis."

"A needed for glucocorticoid synthesis in all probability exceeds that for mineralocorticoid synthesis by a factor of 30 to 300 times. This may be the reason why aldosterone synthesis is not affected until the very latest stages of vitamin A depletion."

"There has been a suggestion that aldosterone synthesis may even rise in A deficiency, with resulting increased plasma sodium content and decreased plasma potassium. If this is so, then the compensatory hypertrophy in the zona glomerulosa may represent an attempt to restore glucose homeostasis, with plasma sodium changes arising as an unwanted side effect of raised aldosterone synthesis."

"In A-deficient animals there is hypoplasia of the adrenals and marked diminution of the total quantity of progesterone elaborated by the glands. The pregnenolone to progesterone conversion requires two enzymes, ß-hydroxysteroid dehydrogenase (E.C. 1.1.1.51) and isomerase (E.C. 5.3.3.1). Grangaud, Nicol and Delaunay (1958), in a series of experiments carried out both in vivo and in vitro have shown that vitamin A aldehyde (retinal) activates these enzymes. Vitamin A acid (retinoic acid) and vitamin A alcohol (retinol) are equally effective in accelerating the enzyme activity. The actual concentration of a vitamin is an important factor in steroid hormone synthesis. In this particular reaction, however, Grangaud et al.9 found that the concentration might vary within fairly wide limits, in marked contrast to the narrow limits essential in sex hormone synthesis (vide infra). This observation implies that an optimal concentration for oestrogen or androgen synthesis might be quite ineffective for progesterone synthesis."

"ß-hydroxysteroid dehydrogenase is present in almost all the steroid producing glands of vertebrates and is apparently the rate limiting enzyme in steroid synthesis. Therefore vitamin A has a key role to play in hormonal production."

"In very mild A depletion, only the deoxycorticosterone to corticosterone step appears to be inhibited. Several authors have shown that in the severely depleted rat, many steps in steroid synthesis are inhibited, including mevalonic acid to cholesterol, cholesterol to progesterone, cholesterol to deoxycorticosterone and deoxycorticosterone to corticosterone. At this late stage, which can be detected by the inability of ACTH injections to restore glucogenesis, it is possible that the A deficiency has caused irreversible degeneration of adrenocortical cells, and in fact this can be confirmed by histological examination. Severe A-deficiency can be considered to be a chemical adrenalectomy as far as glucocorticoid synthesis is concerned."

"One of the major effects of A deficiency is the reduced rate of glycogen synthesis in the liver; this is the only effect of A-deficiency which can be restored to normal by cortisone. Glycogenesis stops early in the A-deficient animal, at the same time as weight gain ceases. No enzymatic defect in the liver has been found to account for this. The enzyme systems for the synthesis of glucose from triose are unaffected, and there is no lack of high energy phosphate."

"One of the more interesting effects of cortisone in the normal animal is a fall in liver vitamin A reserves, and a rise in the level of circulating vitamin A esters."

"High protein diets which induce rapid growth call for increased amounts of vitamin A, as do diets deficient in vitamin A, which protects the vitamin A in food from destructive oxidation. It is possible that male animals have greater need for the vitamin, because they become more quickly depleted than do females, and are less rapidly restored to normal by correction of the deficiency."

"The synthesis of testicular hormones is impaired in A-deficiency, and this is followed by atrophic changes in the male accessory organs (prostate and seminal vesicles)."

"Advanced A-deficiency in the male rat is equivalent virtually to a chemical castration, and is associated with degenerative changes in the germinal epithelium of the testis and the production of abnormal spermatozoa. The response of the accessory organs to injections of testosterone remains normal, indicating that the deficiency interferes with the synthesis or release of androgens, and not with the state of receptivity of the target cells."

"The mode of action of vitamin A in maintaining the integrity of mucous membranes is not yet known, but it is suggested that its action in inhibiting the conversion of cysteine to cystine and the oxidation of sulphydryl groups prevents the excessive keratinization which results from cross linking of newly formed disulphide bonds. The importance of vitamin A in steroid production is likely to become more apparent in the future as more support is gained for the idea that steroid sulphates are not merely waste products of steroid metabolism, but important intermediary metabolites. It may be that the role of vitamin A in sulphur metabolism is its most important aspect."

"The effect of excessive doses of vitamin A is even more damaging than deficiency, and may involve necrosis and sloughing of the entire male germinal epithelium. Present evidence suggests that its toxic effect is exerted on lysosomal membranes, with the uncontrolled release of proteolytic and lipolytic enzymes into the tissues. The glucocorticoids tend to counteract this effect of vitamin A and to stabilise both lysosomal and mitochondrial membranes. It is likely that both hormones and vitamin A are required in strictly balanced ratio for membrane integrity in living cells."​

- Vitamin A reserves of the human liver in health and disease

Spoiler: Liver reserves obtained at autopsies

Blue Units * 0.6 = IU
If I'm not wrong, this unit is characterized by the intensity of the color that appears when this compound reacts with vitamin A.


"[..]the experimental rat lives a life of complete ease in a room kept at constant temperature, and is thus protected both from fatigue and from the sudden climate changes, which so often mark the initial point of illness in the human. If the enormous apparent superfluity of vitamin A capable of accumulation in the liver serves any immediate purpose, as opposed to representing provision for the distant future, it is conceivable that a level of " optimal " as opposed to " minimal " vitamin action may exist. In this case an increased store of vitamin A might be a deciding factor in assisting the animal to withstand the strains of ordinary life."

- The vitamin A reserve of the adult human being in health and disease (same author, worth reading)

Thanks Amazonic. I’m guilty of eating liver even when it seemed repulsive. I do still have a bottle of retinyl palimate so I will go take a whiff while thinking of you. <3

It can be easier when it's an unconscious decision. You can familiarize with the smell every day, and when you need it, you'll remember it.

Dreamlands, Netherlands.

 

[MarcelZD]

Funny, it's been love or hate for me. Calf liver was awesome.

Recently, it's been A LOT more hate, though. I think I will be waiting at least six months, and then, re-evaluate.

Perhaps a taste for liver really does depend on your body's VA status. As has been mentioned, Grant speculates that we 'inherit' some of our mother's VA through breast milk and maybe in the womb, which would explain why many people can barely even stand the smell of liver. I would say though that the vast majority of modern Westerners do not like liver at all unless it is very processed like in patés in such.

 

[InChristAlone]

No (Wagner, 2018). You are for me what Kartoffel is for Trawis, therefore we can't break the pact in agreeing on something.
Perhaps we need to sacrifice it in the process of absorbing light and synthesizing antidote D. The body already uses A in other processes anyway, sunlight will only increase the needs.


I was trying to predict the course of these experiments to know for how long the forum will need to put up with this. I should note that I have contacted a clever shaman through a private session and the entity reported good results so far.

The thread will lessen the intensity when it reaches 92 pages. On page 78 you'll be able to locate the first give-up post. On page 105 there will be a regretful one swearing to no longer be adhering to fads and 1 month later you'll find the person who posted switching to a different toy/tool.


But seriously, I think it's important to know what you're getting yourselves into..

With vitamin A avoidance, in 6 months there might be slight but noticeable changes in vision, especially if you are under stress, harbor challenging infections, sun expose frenquently, are active, require extraordinary tissue regeneration, eat plenty of proteid (anabolic stimulus) and began the trial assuming that your reserves were high when in fact they were somewhat low (from malabsorption for example). But clearer effects might only appear after 1-2 years, for people that are efficient in conserving, it can take more. Who knows what is compromised along the way.


- The Experimental Induction of Vitamin A Deficiency in Humans (!)

"Arroyave (16) reported that protein-malnourished children showed no signs of vitamin A deficiency because of growth depression. As soon as they obtained protein and began to grow, the vitamin deficiency symptoms were precipitated. In animal experiments, Rechcigl et al. (17) observed a precise linear relationship between growth rate and vitamin A utilization."

"Vitamin A deficiency was induced in humans by several researchers with the important aim to determine the daily requirement of the vitamin for healthy adults. This proved to be unexpectedly difficult because of the large but variable reserves of the vitamin stored in the livers of healthy persons. Moore (18), by analysis of livers of accident victims in England, found a median value of liver reserves of 324 IU/g for a healthy British adult, with the enormous variability of 10 IU to 1500 IU/g liver."

"A curious seasonal oscillation was observed in dark adaptation, which deteriorated after 5 mo in the subjects fed the deficient diet (Fig. 5), coinciding with the winter months (November to February), and showed recovery during the following summer months. This seasonal effect, which was observed again during a second winter, could not have been caused by seasonal changes in carotene content of the diet because that was rigorously controlled. Furthermore, the deterioration was not accelerated when fruit and vegetables were completely eliminated from the depleted diet for four summer months. Hume and Krebs (27) suggested that the effect may have been due to changes in temperature (Fig. 5), although why cold should lower plasma vitamin A level remains unexplained."

"These seasonal changes are reminiscent of the observations of Bloch (4) referred to above, reporting that all children in the Children’s Home consuming the fat-free milk diet came down with xerophthalmia during March, April and May. Of course, these months differ from those in the Sheffield experiment. Perhaps xerophthalmia follows a seasonal decline of plasma vitamin A in winter by a few months."

"A case of self-induced vitamin A deficiency was reported in 1969 by Sharman (28).4 A 20-year old man, who had been suffering from epilepsy from age 12 became convinced from reading the literature, that vitamin A caused his epileptic fits. He deliberately eliminated all vitamin A and carotenoids from his diet. His blood retinol dropped to 130 IU/L (normal, about 2000 IU/L) and the blood carotenoid level became extremely low. Subsisting on this diet for 4 years resulted in corneal xerosis and severe retinal damage (29). He reported that his epilepsy was much ameliorated; he had suffered only one fit during that period. Upon repletion with vitamin A, he recovered his ocular health. No information is available regarding his epilepsy subsequently. In order to investigate further a possible connection between vitamin A and epilepsy, Sharman (30) then studied 8 epileptic patients given a vitamin A-depleted diet for 2 years. No cases of night blindness were observed. When their plasma retinol level had reached 230 IU/L, they were given a vitamin A supplement. Although the patients reported fewer fits during the depletion period, there was no increase in the fits during repletion. The author (30) called his experiment a 'dietary contretemps.'"​

- Effects of vitamin A depletion in young adults

"It is seen, therefore, that normal, well fed adults did not present any of the alleged signs of subclinical vitamin A deficiency even after seven and one-half months on a depletion diet. Either or both of two factors may be responsible for such a result. Either the demand for vitamin A by the organism is not great enough to cause sufficient depletion of normal hepatic stores in seven and one-half months to result in the occurrence of the reported early signs of vitamin A deficiency, or these signs are not solely a result of uncomplicated vitamin A deficiency."

"That an extensive degree of depletion of stores of vitamin A is a prerequisite for the development of the subclinical signs of deficiency is borne out by animal studies in which the occurrence of these signs has been correlated with liver stores, by the greater prevalence of subclinical signs in children than in adults and in males than in females and by the relatively low incidence of defects in populations on vitamin-meager diets. In rats it has been shown that a lag exists between the exhaustion of hepatic stores and the appearance of loss of weight and xerophthalmia.19 In children and males the amount of vitamin A storage is less than in adults and females—in children because they have had less opportunity to acquire stores; in males (if a sex difference is accepted) because they store less and lose it more readily than females, as was shown in rats.20 Steven's and Wald's investigation in Labrador 21 revealed only a small percentage of night blindness, although to judge from the habitual dietaries a much greater percentage would have been expected. Josephs'22 study of the vitamin A content of the blood and dark adaptation in various socioeconomic groups showed that only in severe and prolonged vitamin A deficiency were these measurements affected. The failure for as long as six months of controlled vitamin-low diets to result in any of the specific signs of deficiency23 is also indicative that the depletion period studied was not ample. It is interesting to note that a theoretic calculation based on the average vitamin A content of human liver24 and the assumption that the rate of use is approximately 2,000 U. S. P. units per day shows that it would take from one to two years for the liver to lose its entire vitamin A stores if no vitamin A were present in the diet." [Read the previous article for more information supporting this]

"The second explanation offered for the negative findings of this study is that these signs are neither sensitive nor specific for subclinical vitamin A deficiency. The contradictory evidence concerning their diagnostic value supports such a contention."

"In respect to dark adaptation it has been shown that there is an inconsistency in the response of normal subjects to vitamin-low diets in the various laboratories as well as in the response of deficient subjects to massive doses of vitamin A.25 The specificity [I managed once to get this word right on the first attempt] of night blindness as an indication of vitamin A deficiency has also been challenged by the curative effect of vitamin C and riboflavin in some cases.20 There are indications, too, that several of the other symptoms may be more sensitive than dark adaptation as indicators of subclinical vitamin A deficiency.27 This is quite conceivable, since animal experimentation reveals that the vitamin A content of the retina persists even in the absence of hepatic stores.28"

"Two additional alleged subclinical signs which have received a reasonable share of attention are the decreased vitamin A content of the blood and changes in the structure of the skin. The former has obtained support from the work of May,5 Lewis, Bodansky and Haig27c and Yarbrough and Dann.6 These investigators found the blood level the most sensitive indicator of vitamin A deficiency. On the other hand, Josephs22 and Nylund23d with human beings and Brenner, Brookes and Roberts1 with rats found that there is a wide range in the blood level of normal subjects and that only in prolonged and severe deficiency is the blood level valuable diagnostically. Changes in the skin, such as keratinization and resulting horny papules known as toadskin, have been reported by Lehman20 in children on relief and by Steffens, Bair and Sheard23c in an adult maintained on a vitamin-low diet for one hundred and eighty days. This condition has been described as occurring in scurvy, pellagra and other deficiency diseases,30 the more severely affected patients being from the Orient, where the diet is totally inadequate in all the dietary constituents.31 Since the deficiencies are multiple, the assumption that the lack of vitamin A alone is responsible for the cutaneous changes is not justified, even though massive doses of vitamin A have been effective in causing a cure, for in general other concentrates are also administered."

"Since Bitot spots, conjunctival foam and changes in vascularity and translucency of the conjunctiva and cornea may occur in persons without vitamin A deficiency as well as in those in all stages preceding severe vitamin A deficiency, these signs are suggestive but not positive indications of deficiency."

"Moore30e in summing up the allowable claims for vitamin A deficiency stated:

'If, therefore, the claim that phrynoderma (toadskin) is acceptable as a manifestation of vitamin A deficiency, it is difficult to understand how night blindness can be accepted as an early or invariable symptom of vitamin A deficiency. But is phrynoderma due to a deficiency of vitamin A? There are a number of observers who hold it is not so.'"​

"From these existing uncertainties it is evident that much work needs yet to be done on the metabolism of vitamin A to elucidate the confusing evidence."​

- Hepatic stores of retinol and retinyl esters in elderly people

"Serum concentrations of vitamin A [] do not necessarily represent body stores. Over 90% of the total body vitamin A is stored in the liver, 9% in other tissues and only 1% is in plasma [4]. Retinol stored in the liver is mostly esterified with long-chain fatty acids, the main ester being palmitate, and a much smaller quantity is stored as free (unesterified) retinol. The serum concentration is dependent on the concentration of retinol-binding protein which is synthesized in the liver and is affected by malnutrition, malabsorption and systemic illness (e.g. malignancy), many of the factors that might affect total stores of vitamin A [4]. In humans and baboons, depletion of hepatic vitamin A stores correlates poorly with serum levels [5, 6]."

"[Our] results suggest that depletion of hepatic stores of vitamin A involving both retinyl esters and also free retinol occurs in elderly patients stressed by chronic disease and malnutrition. Although it is likely that careful biochemical and anthropometric examination during life might well have found evidence of malnutrition as well as disease in group II, the cachexia and weight loss of group III is evidence for significant malnutrition, as well as chronic disease in this group at the time of death [12]. The low levels of total hepatic retinol in groups II and III was mostly due to lower stores of retinyl palmitate and the other retinyl esters, and to a lesser extent reduced stores of free (unesterified) retinol."

"Huque [13] assessed hepatic reserves of vitamin A at random post-mortem examinations performed in London on a wide cross-section of the population and ages. In that study [if anything?] there was a 'downward trend' from the fifth decade, and by the eighth decade 11.6% of subjects studied had low hepatic reserves (<40 mcg/g), although this was not statistically significant. Our study found no effect of age on vitamin A levels over the range 66-96 years, although it was not designed to be an unselected cross-section of the population. Two subjects in group III had very low total hepatic retinols, which at the time of death were just above the critical level of 40 mcg/g."

"Apparent biochemical deficiencies of many vitamins are quite common in the elderly, although functional changes are not always shown. The last DHSS report on nutrition and health in old age in the United Kingdom found in the general population 30% riboflavin deficient, 15% folate deficient, 11% pyridoxine deficient and overall 7% had significant malnutrition, but vitamin A was not studied [14]. Indeed the clinical importance of depleted stores of vitamin A is not well understood. Vitamin A is needed for normal visual dark adaptation but is also essential for growth, the maintenance of squamous epithelial cells (such as the skin and cornea), testicular function and normal response to infection [15]. Depletion studies on volunteers in Sheffield found nonspecific abnormalities in general health, which correlated poorly with serum levels or dark adaptation [16]. Epidemiological work has suggested a possible link between low serum concentrations of vitamin A and cancer risk, particularly of the oesophagus and lung [17]. More recently it has been shown that in apparently fit Australian pre-school children vitamin A supplementation can decrease the incidence of upper respiratory tract infection [18], while in populations known to suffer severe depletion supplementation reduces infant mortality [19]."​

- Vitamin A in dietary supplements and fortified foods: Too much of a good thing?

"Individuals, especially those taking more than one multivitamin per day, may be at an unappreciated greater risk for hypervitaminosis A given that the current daily value (DV) for vitamin A is 5,000 IU (1,500 mcg) because it is based on the higher 1968 and not the current RDAs (6,7)."

mcg/0.3 = IU
View attachment 11289​

Current RDA - 900♂ or 700♀ μg RAE/day [3000♂ or 2300♀ IU/day]
Upper limit for Preformed Vitamin A - 3000 μg RAE/day [10000 IU/day]

--
I've wondered for a long time if Ramón's reaction to vitamin A wasn't a sign of mild toxicity and his body asking him to stop [sdob it, doooooooololololoont]:

Ray Peat Email Exchanges - Ray Peat Forum Wiki

"I found that a very small amount of either vitamin A or magnesium chloride could cause big headaches for two or three days. If I had put vitamin A anywhere on my face or arms, enough would touch my lips to cause the headache. It wasn't the vitamin A or magnesium itself that did it, but some very powerful allergen in the chemically manufactured products."

"I have had bad headaches when I used vitamin A orally, and even getting a little on my lips was enough to do it."​

--
- Human Vitamin A Deficiency
- Multiple functions of vitamin A (also by Jorge, author of the first link)
- Hypervitaminemia A in the recovery stage of various diseases
- The Effect of Restricted Intake of Carotene and Vitamin A on Psoriasis Vulgaris — A Preliminary Report
- High prevalence of vitamin A deficiency in Crohn's disease patients according to serum retinol levels and the relative dose-response test
- A study of the influence of dietary vitamin A on the level of liver and serum cholinesterase in rats
- Prognostic Importance of Vitamins A, E and Retinol-binding Protein 4 in Renal Cell Carcinoma Patients
- Role of vitamin A in liver fibrosis
- Vitamin A poisoning in adults
- Hypervitaminosis A: A liver lover's lament
- Interactions of Vitamin A and Iodine Deficiencies: Effects on the Pituitary-Thyroid Axis
- Anti-sunshine vitamin A (similar to the UV publication from a previous post)
- Hepatic Injury from Chronic Hypervitaminosis a Resulting in Portal Hypertension and Ascites
- Roles of Vitamin A Metabolism in the Development of Hepatic Insulin Resistance
- Assessing Vitamin A Status: Past, Present and Future

I don't know why you keep giving me so much to break apart and analyze, I have a lot of time. And my hobby is researching. I like to pick things apart.

That first link is great. It is no surprise they got better with cod liver oil as Dr. Smith thinks maybe the vitamin A receptor was improperly named, as DHA also binds to it. What if the so-called RXR (Vitamin A receptor) was improperly named?

And that DHA is essential for proper eye development. Oh but this is the Ray Peat forum and we don't believe in the essentiality of DHA

Maybe both ligands attach to the receptor to perform the job. And as we know if the diet is deficient in A then likely there isnt much butter which seems to protect against vitamin A toxicity. I will keep consuming butter

About the discrepancy in seasons. That is also no surprise. Metabolism goes very low by the end of winter after so much cold and darkness and chicken skin becomes an issue regardless of how much A is in the diet. Like I have said in the past my son gets the bumps and his diet is not A deficient, then they disappear in May with increased sunlight exposure with also no changes in diet. But that goes against that paper claiming vitamin A deficiency is the cause of chicken skin. If UV is anti-A then he should have gotten it more in the summer. Things just don't add up. Also these researchers dont understand that when the diet is deficient it will start dumping stores of it and symptoms can flare.

When Chris Masterjohn said he became deficient in a matter of a week on vacation and then taking a large dose stopped his allergy symptoms was not because he needed so much A it was because his body was fianlly dumping all this retinol he was consuming and thus an increase in yucky symptoms. When he took the large dose the detox stopped and he was fine again. (No one becomes deficient in a fat soluble vitamin in a week)

 

[InChristAlone]

As a coincidence the highlights are orange.

- Book Series: Vitamins And Hormones

It's a good book on nutrition and endocrimology written by a single author [!], unrelated to marital status; not that I have anything against marriages; not that disclosing these things makes any difference for you; not that I'm wasting our times then, it has a point, but not that it should distract you from the fact that the person is indeed knowledgeable; not that being ignorant is our problem; not that I'm in a position to judge what is a problematic or not; I mean, I respect everybody regardless if you're Dutch or not; by the way, I haven't chosen this specific nationality implying that the rest is inferior; just to clarify, I'm not using 'rest' with disdain, all life matters; not that I'm saying this so that I'm in good terms with everyone, I'm fine if I don't get along with some of you; not that I didn't want to be in good terms with those that I'm not right now; I just prefer things to be as clear as possible to avoid confusions or being interpreted the wrong way. Anyway..​

"Infants and persons suffering from various forms of gastroenteritis, both acute and chronic, have a much reduced ability to undertake the [carotene] conversion. In diabetes and in hypopboydism the conversion is almost completely blocked. Cretins, lacking a functional thyroid gland, are quite unable to convert carotene to vitamin A."

"Restoration to the normal state [after depletion] was best achieved by feeding rather than injecting supplies of vitamins."

"Microscopically, A-deficiency is associated with keratinising squamous metaplasia of mucous epithelia—that is, mucous membranes change from a single layer of mucin secreting and ciliated epithelium to multiple layers of epithelial cells, with overlying keratin, resembling those of the skin. The increase in thickness of the necks of the underlying mucous glands plugs their orifices and seals off their secretion. Obstruction of pancreatic ducts by keratotic plugs blocks the release of pancreatic enzymes into the small intestine. At the subcellular level, there is disruption of lysosomal and other cellular membranes both in deficiency and in excess of vitamin A, and it is probable that an optimal amount of vitamin A for the species is essential for the integrity of pericellular and intracellular membranes. (Fell, 1964.)"

"It is important to remember too, that serum levels of vitamin A may not correlate with liver levels, either in the normal or the undernourished subject. It is possible to have large stores of the vitamin, with little in the circulation, or to have a normal serum level in association with a depleted liver."

"The importance of vitamin A metabolism in the adrenal gland has long been recognised. Numerous experiments have shown that A-deficiency reduces resistance to stress, lowers insulin tolerance, and impairs glucogenesis. By histological techniques, the vitamin can be demonstrated in high concentration in the cells of the zona fasciculata, suggesting its importance for glucocorticoid synthesis. Adrenal sections often show masses of 'lipochrome' pigment in the cells of the zona reticularis. This is a carotenoid pigment and may represent a store of vitamin A precursor. The pigment is seldom, if ever, seen in the medulla, and its presence in the cortex lends support to the view that it participates in steroid synthesis."

"A needed for glucocorticoid synthesis in all probability exceeds that for mineralocorticoid synthesis by a factor of 30 to 300 times. This may be the reason why aldosterone synthesis is not affected until the very latest stages of vitamin A depletion."

"There has been a suggestion that aldosterone synthesis may even rise in A deficiency, with resulting increased plasma sodium content and decreased plasma potassium. If this is so, then the compensatory hypertrophy in the zona glomerulosa may represent an attempt to restore glucose homeostasis, with plasma sodium changes arising as an unwanted side effect of raised aldosterone synthesis."

"In A-deficient animals there is hypoplasia of the adrenals and marked diminution of the total quantity of progesterone elaborated by the glands. The pregnenolone to progesterone conversion requires two enzymes, ß-hydroxysteroid dehydrogenase (E.C. 1.1.1.51) and isomerase (E.C. 5.3.3.1). Grangaud, Nicol and Delaunay (1958), in a series of experiments carried out both in vivo and in vitro have shown that vitamin A aldehyde (retinal) activates these enzymes. Vitamin A acid (retinoic acid) and vitamin A alcohol (retinol) are equally effective in accelerating the enzyme activity. The actual concentration of a vitamin is an important factor in steroid hormone synthesis. In this particular reaction, however, Grangaud et al.9 found that the concentration might vary within fairly wide limits, in marked contrast to the narrow limits essential in sex hormone synthesis (vide infra). This observation implies that an optimal concentration for oestrogen or androgen synthesis might be quite ineffective for progesterone synthesis."

"ß-hydroxysteroid dehydrogenase is present in almost all the steroid producing glands of vertebrates and is apparently the rate limiting enzyme in steroid synthesis. Therefore vitamin A has a key role to play in hormonal production."

"In very mild A depletion, only the deoxycorticosterone to corticosterone step appears to be inhibited. Several authors have shown that in the severely depleted rat, many steps in steroid synthesis are inhibited, including mevalonic acid to cholesterol, cholesterol to progesterone, cholesterol to deoxycorticosterone and deoxycorticosterone to corticosterone. At this late stage, which can be detected by the inability of ACTH injections to restore glucogenesis, it is possible that the A deficiency has caused irreversible degeneration of adrenocortical cells, and in fact this can be confirmed by histological examination. Severe A-deficiency can be considered to be a chemical adrenalectomy as far as glucocorticoid synthesis is concerned."

"One of the major effects of A deficiency is the reduced rate of glycogen synthesis in the liver; this is the only effect of A-deficiency which can be restored to normal by cortisone. Glycogenesis stops early in the A-deficient animal, at the same time as weight gain ceases. No enzymatic defect in the liver has been found to account for this. The enzyme systems for the synthesis of glucose from triose are unaffected, and there is no lack of high energy phosphate."

"One of the more interesting effects of cortisone in the normal animal is a fall in liver vitamin A reserves, and a rise in the level of circulating vitamin A esters."

"High protein diets which induce rapid growth call for increased amounts of vitamin A, as do diets deficient in vitamin A, which protects the vitamin A in food from destructive oxidation. It is possible that male animals have greater need for the vitamin, because they become more quickly depleted than do females, and are less rapidly restored to normal by correction of the deficiency."

"The synthesis of testicular hormones is impaired in A-deficiency, and this is followed by atrophic changes in the male accessory organs (prostate and seminal vesicles)."

"Advanced A-deficiency in the male rat is equivalent virtually to a chemical castration, and is associated with degenerative changes in the germinal epithelium of the testis and the production of abnormal spermatozoa. The response of the accessory organs to injections of testosterone remains normal, indicating that the deficiency interferes with the synthesis or release of androgens, and not with the state of receptivity of the target cells."

"The mode of action of vitamin A in maintaining the integrity of mucous membranes is not yet known, but it is suggested that its action in inhibiting the conversion of cysteine to cystine and the oxidation of sulphydryl groups prevents the excessive keratinization which results from cross linking of newly formed disulphide bonds. The importance of vitamin A in steroid production is likely to become more apparent in the future as more support is gained for the idea that steroid sulphates are not merely waste products of steroid metabolism, but important intermediary metabolites. It may be that the role of vitamin A in sulphur metabolism is its most important aspect."

"The effect of excessive doses of vitamin A is even more damaging than deficiency, and may involve necrosis and sloughing of the entire male germinal epithelium. Present evidence suggests that its toxic effect is exerted on lysosomal membranes, with the uncontrolled release of proteolytic and lipolytic enzymes into the tissues. The glucocorticoids tend to counteract this effect of vitamin A and to stabilise both lysosomal and mitochondrial membranes. It is likely that both hormones and vitamin A are required in strictly balanced ratio for membrane integrity in living cells."​

- Vitamin A reserves of the human liver in health and disease

Spoiler: Liver reserves obtained at autopsies

View attachment 11293
Blue Units * 0.6 = IU
If I'm not wrong, this unit is characterized by the intensity of the color that appears when this compound reacts with vitamin A.


"[..]the experimental rat lives a life of complete ease in a room kept at constant temperature, and is thus protected both from fatigue and from the sudden climate changes, which so often mark the initial point of illness in the human. If the enormous apparent superfluity of vitamin A capable of accumulation in the liver serves any immediate purpose, as opposed to representing provision for the distant future, it is conceivable that a level of " optimal " as opposed to " minimal " vitamin action may exist. In this case an increased store of vitamin A might be a deciding factor in assisting the animal to withstand the strains of ordinary life."

- The vitamin A reserve of the adult human being in health and disease (same author, worth reading)


It can be easier when it's an unconscious decision, so you can familiarize with the smell every day, and when you need it, you'll remember it.

Dreamlands, Netherlands.

Interesting very interesting.
Most Peat fans are getting absurd amounts of retinol and yet many need to supplement progesterone (also thyroid). Could it be that the reason the adrenal glands have dimished synthesis of progesterone because it doesnt need to deal with all that extra retinol .

About insulin.... What do we make of that user who got type 1 diabetes after 5 months on the Ray Peat diet? In her 50's!!!
She said she had taken a vitamin A supplement.

Higher reserves of A in a number of disease states. Very interesting.