I needed to disable self sign-ups because I’ve been getting too many spam-type accounts. Thanks.
Why I don’t think that this is a legit theory anymore
@tim-2 I need to have a closer look at the methods behind the experiment at Sheffield. Off the top of my head, I find it concerning that only 3/16 men developed signs of deficiency. I also find that their VA deficient diet is too complex for me to confidently say that it is indeed VA free. For instance, the men consumed large quantities of skimmed powdered milk. Are we confident those were free of RA? Grant has already mentioned that pasteurization and other dairy processing techniques convert retinol to RA, and furthermore, preserve it with casein. Thanks for the reference though, it's all very interesting and I need to have a much closer look at this.
@ggenereux2014 did you ever look at the this experiment by chance?
RE: Dark adaptation began to deteriorate slightly after 5 mo
Yes, I did read that study. I think there might be something else going here. They’ve assumed the poor dark adaptation to it to be a key indicator and negative consequence of VAD developing.
That’s a nice assumption, but it could also have been from the detox setback cycle so many people here have encountered. As we stop ingesting VA, the liver starts dumping more retinyl esters back into circulation. That extra toxicity load could be the real reason for developing night blindness. I did not notice the skimmed powdered milk; so yes, that could be a contributor too.
As I’ve mentioned before, my personal experience is that I’ve encountered three different cycles of “night blindness” ( not really being blind, just poor night vision). But, without including any VA / carotenoids in my diet the condition has always fully recovered. Usually taking about ~3 months. All three times also corresponded with having quite dry eyes.
You argument is not simple, but it oversimplifies some key factors and reduces VA toxicity into exactly two inputs:
- Consumption of Retinol
- Consumption of BC
I've already explained to you why VA toxicity requires inputs on the detox side of the equation as well as the toxin side. Furthermore, even with your overly simplified model, I remain unconvinced that Saladino increased his VA consumption. Apart from liver, carnivore diets are naturally low in VA, while vegan diets are very high. In the end, you have no idea how much liver he eats and how much BC he ate while vegan.
This is the first indication that plant defensive compounds are implicated in his skin problems and not Vitamin A.
No, it's an indication that you've completely ignored some basic facts about BC and VA metabolism and detox. VA esters can be stored in the liver immediately unlike BC. VA requires special minerals, fats, and proteins for detox. Vegan diets are liable to be devoid of many of these components.
Saladino finds that he reacts to some plant foods and not others, with no correlation between beta-carotene content and symptoms.
So did Saladino manage to induce eczema by reintroducing some plant foods? Saying that he "reacted" is not meaningful enough in this context. I was unable to confirm.
The most obvious conclusion is that Saladino's skin problems are the result of an immune response to particular plant compounds found in only certain plant foods, and is not the result of Vitamin A consumption in the form of either retinoids or carotenoids.
It is not the most obvious conclusion, it is wild speculation on your part. What is more likely, that a nebulous, yet to be identified, plant compound is responsible for eczema, or VA? Not only VA has been demonstrated to cause eczema in toxic doses, but there's a mountain of evidence for the other skin diseases it causes. Moreover, it's been shown that affected skin lesions have abnormal VA metabolism and are preferentially used to store ingested VA [1]
I'm a little preoccupied to comment on your views regarding the philosophy of science. All I can say is that I hope that you apply them consistently. Saladino and his acolytes always disparage "bad science", epidemiology, biased researchers when defending red meat, but apparently the science behind VA is now bulletproof? A super majority of scientists is insufficient to declare saturated fat as bad, but is sufficient to declare retinoids as essential. Funny how that works.
If Vitamin A is a toxin, I am yet to hear anyone provide a good reason for why so many animals would store such large amounts of it, risking death, when they don't regularly store large amounts of anything else that is toxic, unless it is something like venom that is well-contained and has obvious deployment mechanisms and purposes.
PS: Can you stop claiming honey is a source of BC without evidence?
Just sharing my experience and thought on coffee.
I think coffee might be beneficial in the early stages of this diet because of the palmitic acid content. That could theoretically bind with VA stored in the liver and help expel it.
My personal experience with coffee:
Before starting my diet:
Seriously addicted, an absolute must have in the AM and during the mornings.
~ Year Four:
Could take it or leave it kind of thing, stopped drinking it (cold turkey, just one day of very mild withdrawal symptoms)
Year Five:
Started back on the sauce, but for no good reason really. I just liked the digestive kick-start it provided first thing in the AM. But, I was down to just one cup per day.
Year Six:
Started to really have a negative response to coffee. Didn't like it much anymore, and it was definitely causing me to pee way too often. So, I had become much more sensitive to it. I stopped cold-turkey again, negligible withdrawal symptoms.
Year Seven:
Off the coffee; don't think I'll ever start it again.
"Beta - carotene content in the samples had the highest value of 0.43±0.10mg/100g in Raw tomatoes and the least value of 1.78×E-7 mg/100g in Honey samples"
This is just the first hit from a Google search. It's a tiny amount in the honey they measured, but I've seen at least one other paper that showed variable amounts of beta-carotene for honey derived from different plants. Regardless, Saladino is probably getting way more beta-carotene from animal fat than from honey, so for this particular argument it doesn't really matter what the content is in honey.
Yes, Saladino got eczema from reintroducing some plant foods and not others. I didn't specify that because I thought it was clear enough what I was referring to.
Have you not heard about lectins and other phytochemicals being correlated with various immune reactions in people? It's not a nebulous idea. It's the most likely reason the carnivore diet is so successful for so many immune disorders, it helps heal the gut lining and removes plant compounds from the diet that the immune system has developed an overly dramatic response to. This benefit is seen in people who eat lots of liver, which is probably the most bioavailable source of Vitamin A there is.
Vegan diet containing carotenoids but no retinoids = eczema
Carnivore diet containing both carotenoids and retinoids = no eczema
Carnivore diet containing both carotenoids and retinoids + one plant food that may or may not contain carotenoids = eczema
You really don't follow the logic on that?
Don't confuse the science for the messaging that comes after the science. Saturated fat may have been vilified for a long time, but that position wasn't born out by the science. I don't dismiss the fact that the benefits of Vitamin A are probably being blown way out of proportion, and that we most likely need very little of it, but a little is more than none, and the body is apparently very good at storing fat soluble molecules for long periods of time, so we would potentially expect some people to be able to go for years without needing to ingest significant amounts of Vitamin A.
We and other animals store mercury when we ingest so much that we cannot eliminate it, or when our ability to eliminate it is compromised. When we aren't exposed to excessive mercury, we don't wind up storing it (to my knowledge). Vitamin A, on the other hand, is actively taken up, stored, and regularly transported around the body in the blood using Retinol Binding Protein. We have all these specific mechanisms for Vitamin A regulation and metabolism around the body. How do you not see the difference?
You are arguing that, because there is evidence of hypervitaminosis A in humans and animals, then Vitamin A is simply a toxin. So anything that can accumulate to excess amounts is a toxin? Water is nothing but a toxin? Oxygen is nothing but a toxin?
To summarize my point again, it is quite clear that we are susceptible to accumulating Vitamin A in toxic amounts, but it also quite clear that we and other animals evolved to actively take up, distribute, metabolize, and eliminate Vitamin A based on the various quantities ingested at different times. Even going by the RDA's, which are probably far too high, mammalian liver stores more of the daily value of Vitamin A than any other substance...why the hell would the liver intentionally store Vitamin A, including beta-carotene that is actively converted to retinoids, when the liver otherwise tries to dump all the other crap from plants that our body doesn't use as quickly as possible? The obvious and most parsimonious answer is that we use Vitamin A for physiological processes. What is the alternative? I haven't heard one that makes more sense from you, Grant, or anyone else.
Re: honey
Yes, I know of that paper. That amount is absolutely tiny and we have no reliable numbers for other types of honey. I think it's far more likely that honey is a meaningful source of BC - especially the pale bee honey that's available to most of us. Could you cite some papers regarding the contents of BC in animal fats? As far as I'm aware, animal fats may only contain retinol esters. Even here, it really depends on the animal fat. I know tallow has essentially none, while there's some controversy surrounding lard.
Have you not heard about lectins and other phytochemicals being correlated with various immune reactions in people?
Absolutely not with eczema. Google is also drawing a blank. So if it's just your speculation, let's remind ourselves that VA is a *proven* cause of eczema. While lectins and other phyotchemicals, as bad as they may be, aren't known to be related to the disorder in any way whatsoever.
This benefit is seen in people who eat lots of liver, which is probably the most bioavailable source of Vitamin A there is.
The benefit is seen until they saturate their liver and adipose with VA. After that, they end up croaking. Lots of fellows on this forum readily confirm that.
You really don't follow the logic on that?
There is no logic to follow here. Your statements again completely ignore detox mechanisms. They don't even discuss the quantities of VA in each form. I still have no idea why you're so confident that Saladino increased his VA intake when he stopped being vegan. In all the studies I've seen, the total amount of VA matters much more than the form of VA (synthetic, retinol, BC).
Vitamin A, on the other hand, is actively taken up, stored, and regularly transported around the body in the blood using Retinol Binding Protein. We have all these specific mechanisms for Vitamin A regulation and metabolism around the body. How do you not see the difference?
The body does these things not because it wants to, but because the alternative is even worse. Retinol in the wild is dissolved in highly valuable fatty acids that our body needs. BC is present in almost all fructose rich fruit - another incredibly important source of calories and nutrients. We can't afford to simply not digest any foods that contain retinol. There's no magic button in the intestine to eject all the retinol & BC and there was never an evolutionary need to create one.
Water is nothing but a toxin? Oxygen is nothing but a toxin?
Notice the really good evidence proving that oxygen and water is essential. In comparison, the evidence in favor of VA is a house of cards. Whether it's with the early experiments, or the general vagueness behind the biological functions that demand this vitamin, anytime one starts poking, serious flaws become readily apparent.
Quote from tim on October 29, 2021, 9:43 amI've posted this before but it was a long time ago. The whole of this article is an important read for anyone doubting the essentiality of vitamin A.
The Experimental Induction of Vitamin A Deficiency in Humans
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.
........
The Sheffield Experiment
A most extensive and elaborate human experiment was carried out by Hume and Krebs (27) at the height of the Second World War in Sheffield, England from 1942 to 1944, at the request of the Ministry of Food, to provide information on the human requirement of vitamin A or carotene “more accurate than was then available.” As subjects, 20 men and 3 women were recruited, aged between 19 and 34 y. They were conscientious objectors to military service and, therefore, highly motivated to cooperate as experimental subjects. Sixteen subjects received a vitamin A and carotene-deficient diet, analyzed for adequacy in nitrogen, fat, carbohydrate, calcium, phosphate, iron, thiamin, riboflavin, nicotinic acid and ascorbic acid. Vitamin D was given as a supplement. Analyses of 12 different foods and of quantities of each food consumed in 2 sample weeks were carried out in five laboratories specializing in vitamins and nutrition (Universities of Cambridge, Oxford, Liverpool, Reading and Sheffield). In particular, total carotenoids and α- and β-carotene and vitamin A were determined in the deficient diet. Unavoidable total carotene was found to be ∼70 iu/d consumed. Even this was suppressed during 4 mo in 1943, when all fruits and vegetables were withheld. The deficient diet was tested in rats to ensure that it was biologically deficient in vitamin A activity. Plasma concentrations of carotene and vitamin A were measured simultaneously in two laboratories and checked against each other.
As controls, 2 subjects received the deficient diet with 2500 iu vitamin A/d (as esters) in oil; 5 subjects received 5000 iu of β-carotene, either as pure carotene in oil, or in previously analyzed carrots or spinach per day.
The first observed change was a rapid drop in the plasma level of carotene after 3 mo from 1500 iu to 120–400 iu/L. Vitamin A began a slow decline after 8 mo but decreased to ≤300 iu/L in only 2 of the 17 subjects by 1 y and one other after 1.5 y. Dark adaptation began to deteriorate slightly after 5 mo, with an increase in the transition time from cone to rod vision (Fig. 4), although a substantial impairment in dark adaptation occurred in only three subjects, preceded by the drop in plasma vitamin A level to 300 iu/L in 1–1.5 y. The three other subjects of the six remaining after 1.5 y showed no ill effects except a slight decline in plasma vitamin A.
Audiometry tests showed a loss of hearing in three of the deprived subjects and an improvement after dosing with the vitamin. They also exhibited slight hyperkeratosis of hair follicles. Hematologic tests could not confirm the steep decline of blood platelets reported by Wagner (26).
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.
Therapeutic tests were undertaken in the Sheffield study with the three subjects who showed the significant impairment in dark adaptation. One subject was given vitamin A orally as esters in oil (1300 iu/d) and showed the first improvement in dark adaptation in 2 wk. Two subjects were dosed with 2500 iu of β-carotene in oil. One recovered normal vision within 3 wk; complete recovery took 5.5 mo for the other. Subjects consuming cooked vegetables were found to excrete 59–76% of the food's carotene in their feces. The investigators found that, among the control volunteers who ate the depleted diet together with different amounts of carotene supplements, the dose of 5000 iu/d taken from various sources over 14–17 mo was just sufficient to maintain health and vision, although blood levels of vitamin A were somewhat lower than normal.
In their final summary, Hume and Krebs (27) recommended 2500 iu/d of vitamin A as the daily requirement. They considered this to be “an estimate … to cover individual variations and to leave a margin of safety.” For carotene, taking account of individual variation, Hume and Krebs proposed 3000 iu daily as a “minimum effective dose.” However, if supplied in cooked vegetables, because of losses in feces, they recommended 7500 iu/d “as being a figure roughly representative of the different sources of carotene in the diet.”
Tim, thanks for the information. Interestingly, some of them, but not all, developed vision problems. This is consistent with the experience of people on this forum: while many people can eat zero vitamin A, others have problems. I've read studies, and I'm inclined to believe that VA damage to the eyes is indeed the cause. Specifically by 13-cis RA
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC4533586/
Although I think there are other factors here besides detoxification.
I have always been interested in these seasonal fluctuations of diseases. Reading Hirsch's book, I found that this is typical for many diseases. For example, beriberi, whose peak incidence has always been during the monsoon rainy season.
Well, you've swallowed the "Vitamin A is a toxin" pill and there's clearly nothing anybody is going to present that will satisfy your requirements for evidence to the contrary, so I'm going to stop wasting my time on that subject.
I've been buying a lot of tallow (bison, beef, lamb, all "grass-finished") over the past year. The lamb tallow has always been a slight off-white. The beef tallow was pretty similar, maybe slightly more yellow. The first batch of bison tallow I bought in the winter was a similar off-white. Then the next batch I got in the summer was bright yellow, as was the next one, and the next one. I obviously didn't test these for carotene content, but I think it's a pretty safe assumption that the bison tallow turned yellow from higher beta-carotene content from fresh, live forage in the summer rather than bison eating hay in the winter.
I've raised and butchered young and old chickens, and the older they are the more yellow their fat is. Some of the older laying hens were disgustingly yellow, which is undoubtedly beta-carotene accumulation because chickens are not herbivores and suck at converting all the beta-carotene in the commercial feed to retinoids. Same reason so many commercial eggs have bright yellow yolks - the hen's rations are loaded with beta-carotene.
Saladino's case is a classic elimination diet scenario, as are so many others like Mikhaila Peterson and Amber O'hearn who have shared their results from a carnivore diet. Reduce diet to meat and organs, symptoms go away, then reintroduce a single plant food (could be as innocuous as lettuce) and the immune response flares. Go back to meat and organs, symptoms disappear again. The increase in plant consumption, especially plants that haven't been prepared through traditional cooking methods, has increased far more dramatically in recent decades than consumption of animal sources of Vitamin A. Way more likely that a diversity of plant compounds are responsible for an uptick in immune problems and skin conditions than just Vitamin A, although I'm sure the extra beta-carotene is not benefiting hardly anyone.
Quote from Rudi on October 29, 2021, 4:43 pmRe: honey
Yes, I know of that paper. That amount is absolutely tiny and we have no reliable numbers for other types of honey. I think it's far more likely that honey is a meaningful source of BC - especially the pale bee honey that's available to most of us. Could you cite some papers regarding the contents of BC in animal fats? As far as I'm aware, animal fats may only contain retinol esters. Even here, it really depends on the animal fat. I know tallow has essentially none, while there's some controversy surrounding lard.
Have you not heard about lectins and other phytochemicals being correlated with various immune reactions in people?
Absolutely not with eczema. Google is also drawing a blank. So if it's just your speculation, let's remind ourselves that VA is a *proven* cause of eczema. While lectins and other phyotchemicals, as bad as they may be, aren't known to be related to the disorder in any way whatsoever.
This benefit is seen in people who eat lots of liver, which is probably the most bioavailable source of Vitamin A there is.
The benefit is seen until they saturate their liver and adipose with VA. After that, they end up croaking. Lots of fellows on this forum readily confirm that.
You really don't follow the logic on that?
There is no logic to follow here. Your statements again completely ignore detox mechanisms. They don't even discuss the quantities of VA in each form. I still have no idea why you're so confident that Saladino increased his VA intake when he stopped being vegan. In all the studies I've seen, the total amount of VA matters much more than the form of VA (synthetic, retinol, BC).
Vitamin A, on the other hand, is actively taken up, stored, and regularly transported around the body in the blood using Retinol Binding Protein. We have all these specific mechanisms for Vitamin A regulation and metabolism around the body. How do you not see the difference?
The body does these things not because it wants to, but because the alternative is even worse. Retinol in the wild is dissolved in highly valuable fatty acids that our body needs. BC is present in almost all fructose rich fruit - another incredibly important source of calories and nutrients. We can't afford to simply not digest any foods that contain retinol. There's no magic button in the intestine to eject all the retinol & BC and there was never an evolutionary need to create one.
Water is nothing but a toxin? Oxygen is nothing but a toxin?
Notice the really good evidence proving that oxygen and water is essential. In comparison, the evidence in favor of VA is a house of cards. Whether it's with the early experiments, or the general vagueness behind the biological functions that demand this vitamin, anytime one starts poking, serious flaws become readily apparent.
I've already posted this in another thread:
https://en.m.wikipedia.org/wiki/Carotene
"The typical yellow-coloured fat of humans and chickens is a result of fat storage of carotenes from their diets."
I think the same goes for other animals.
Personally, I easily admit that lectins, or oxalates or something else can cause diseases. To say that VA is always to blame means to be a big reductionist, imho.
Quote from Rudi on October 29, 2021, 2:11 pm@tim-2 I need to have a closer look at the methods behind the experiment at Sheffield. Off the top of my head, I find it concerning that only 3/16 men developed signs of deficiency. I also find that their VA deficient diet is too complex for me to confidently say that it is indeed VA free. For instance, the men consumed large quantities of skimmed powdered milk. Are we confident those were free of RA? Grant has already mentioned that pasteurization and other dairy processing techniques convert retinol to RA, and furthermore, preserve it with casein. Thanks for the reference though, it's all very interesting and I need to have a much closer look at this.
@ggenereux2014 did you ever look at the this experiment by chance?
It can take many years to develop signs of deficiency. I think if someone starts a low vitamin A diet with Hypervitaminosis A and they genetically tend to conserve vitamin A it could take a decade to start to develop xeropthalmia. There was a young boy in Australia who would have had little vitamin A to start with but it took many years to begin to develop xeropthalmia after he began a fussy low vitamin A diet.
Heat may oxidize retinol to retinoic acid however the amount of retinol lost during pasteurization isn't high as far as I know. Regardless, retinoic acid doesn't protect against VAD because it can't convert to retinaldehyde which is necessary for vision.