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Dear Carnivore Dieters, A Muscle Meat Only Diet is Extremely Healing Because it is a Low "vitamin A" Diet. This is Why it Works so Well...
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Low Toxin Testimonials Low Vitamin A Diet Testimonials
- Thread starter Blossom
- Start date
AncestralJoy
Member
- Joined
- Nov 9, 2020
- Messages
- 157
Wowsers! Just when you think you've gotten to the bottom of the barrel of rabbit holes to explore... I heard mention of this from Matt stones blog like a year ago (have been peating for 18months or so and cannot say I'm getting much better) but never investigated it. I will be exploring this and experimenting for myself
thank you to everyone for sharing their experiences and to @Blossom and @charlie for gathering the stories of others into one thread
thank you to everyone for sharing their experiences and to @Blossom and @charlie for gathering the stories of others into one thread
B
Braveheart
Guest
Too bad this didn't get answered....am curious, would like to see some replies to this question....
OP
You’re welcome.
All this talk about vitamin a being toxic makes me worried to supplement vitamin a, I have a dry red rash on my face which I have had for years and have often thought about trying high doses of vitamin a to see if it can fix it because nothing else is working but seeing this makes me hesitant but I have taken 8000iu of vitamin a now and then I sometimes get incredibly itchy face and scalp and I tried vitamin a one time and the itching was gone within hours this has been repeated many times if vitamin a is toxic how comes its the only thing that stops the itching?
The need for vitamin D in vitamin A toxicity is well established. Garrett Smith's darling vitamin A researcher, Anthony Mawson (whom he often quotes and speaks very highly of, speaks for himself:
"The seasonality and other observations on the epidemiology of influenza A are attributed to population-wide states of impaired innate immunity due to reduced exposure to sunlight during the winter months and a resulting deficiency of vitamin D [33-35]. Cannell's theory postulates that influenza epidemics are the result of a dormant disease that becomes active in response to vitamin D deficiency. Although the vitamin D deficiency hypothesis accounts for many hitherto unexplained facts about the epidemiology of influenza, gaps remain in understanding the pathogenesis, symptoms, and course of influenza infections.
Several observations reviewed in this paper suggest that vitamins A and D have interactive roles in influenza and that retinoids (the collective term for vitamin A and its natural and synthetic congeners) have an independent role in influenza infection and pathogenesis. For instance, solar radiation has opposite effects on vitamins A and D, catabolizing vitamin A but increasing the concentration of vitamin D; the effects of the two vitamins are mutually inhibitory; retinoids regulate airway epithelial cell growth, differentiation, and gene expression; the symptoms of influenza are similar to those of retinoid toxicity; supplementary and/or pharmacological concentrations of retinoids induce influenza-like symptoms; viral activity is regulated in part by retinoids; and retinoids influence the mechanisms that both inhibit and contribute to influenza pathogenesis.
It is hypothesized that reduced sunlight exposure and/or preexisting vitamin D deficiency simultaneously increase the accumulation, expression and potential toxicity of endogenous retinoids (i.e., decrease the vitamin D-to-vitamin A ratio), which trigger viral activation or increase host susceptibility to novel strains of influenza virus. Furthermore, while normal physiological concentrations ofretinoid appear to work with vitamin D to inhibit influenza pathogenesis, higher background concentrations (very low vitamin D: A ratios) worsen it and may induce the severe or lethal complications of the disease. In short, the outcome of influenza infections may depend in part on the ratio or balance between background concentrations of vitamin A and vitamin D. The role of vitamin D and vitamin A in influenza could also, of course, extend to genetic differences in the metabolism and availability of these vitamins (c.f. [62])."
If that wasn't enough, here's another bit:
"
The fat-soluble vitamins A, D, E, and K normally work interactively together. For instance, earlier suggestions that the function of vitamin D requires vitamin A [92] now find support in the important observation that the RXR ligand 9-cis-retinoic acid (9-cis-RA), a hormonally active form of vitamin A, potentiates vitamin D-dependent gene expression and thus has a role in vitamin D signaling that was previously unknown. It was found that when 9-cis-RA acid was unavailable, vitamin D could only bind weakly to DNA and exerted only a small effect on gene expression; conversely, the presence of 9-cis-RA conferred significant agonistic activity to a vitamin D receptor ligand with very low agonistic activity and also increased the differentiation of colon cancer cells by vitamin D. Most remarkably, the addition of 9-cis-RA restored the functioning of a mutant (defective) vitamin D receptor present in a hereditary form of rickets that cannot normally be cured by vitamin D [93].
On the other hand, the evidence suggests that in the event of major perturbations in either vitamin A or D, due to dietary or other factors, there is an inverse, mutually inhibitory relationship between them in that vitamins A and D counterbalance their potentially toxic individual effects [94]. For instance, while vitamin A can reduce the toxicity of vitamin D (e.g., [92, 95]), vitamin D can also interact inversely with vitamin A and reduce the toxicity of vitamin A. Although little is known about the effect of reduced sunlight exposure and/or deficient vitamin D levels on vitamin A metabolism, even small to moderate doses of vitamin D in chickens reduce liver vitamin A stores and lower the level of vitamin A in blood [96]. Exposure of chickens to UV light (which produces vitamin D) likewise reduces liver stores and blood levels of retinol [97]. In humans, concomitant supplementation with vitamin D greatly increases the dose of vitamin A required to cause toxicity; for instance, Myhre et al. [98] found that the median dose for inducing vitamin A toxicity was >2,300 IU/kg of body weight per day higher when vitamin D was added to the diet. For a hypothetical 75 kg person representing the median, vitamin D supplementation would have allowed an additional 175,000 IU vitamin A/day before toxicity symptoms were likely to be reported. In the Nurses' Health Study, a positive association was found between retinol intake and fracture risk in that vitamin D intake increased as retinol intake increased, but at a lower rate. In a multivariate analysis controlling for many factors, vitamin D was found to be protective against retinol-associated risks of fracture [99].
The potential toxicity of high intakes of vitamin A may thus depend in part on the amount of vitamin D consumed. On the other hand, vitamin D deficiency would be expected to increase the potential toxicity of vitamin A. Indeed, consumption of preformed retinol, even in the usual amounts consumed in the United States in the forms of multivitamins, may cause osteoporotic bone changes in adults with low vitamin D concentrations [76]. Scandinavian countries, which have the highest fracture rates in Europe and even worldwide [100], have higher average intakes of vitamin A and are also at far higher latitudes (60 degrees), where vitamin D "winters" (periods of time in which vitamin D cannot be produced by the action of sunlight on the skin) are longer and vitamin D is less available from the sun, even in the months when sunlight is present.
With regard to the impact of vitamin A on vitamin D, in humans the amount of vitamin A in a single serving of liver inhibits the rise in serum calcium induced by vitamin D [101]. Retinoic acid can antagonize the action of vitamin D and its active metabolite 1,25-dihydroxycholecalciferol in rats [102]. A high intake of retinol also completely abolished the protective effect of vitamin D on distal colorectal adenoma, women in the highest quintile of vitamin D intake ingested about 10,000 IU/day of retinol, and there was a strong correlation overall between dietary intakes of vitamins A and D [103].
Sunlight in the ultraviolet (UV-B) spectrum converts a cholesterol precursor, 7-dehydrocholesterol, into the activated form of vitamin D (calcitriol). Thirty minutes of whole-body exposure of pale skin to sunlight with clothing or sunscreen can result in the synthesis of from 10,000 to 20,000 IU of vitamin D. Further radiation converts excess vitamin D in the skin into inactive metabolites. Melanin pigment also accumulates in skin, thereby decreasing the production of vitamin D [104]. On this basis it has been suggested that, in order to maintain serum levels of 25(OH)D at the optimal range of 50 ng/mL during a vitamin D "winter", 4,000 IU vitamin D should be consumed per day [105]."
this bit is interesting:
"High temperatures increased liver vitamin A utilization; moreover, identical twin calves exposed to solar radiation for 38 days lost more hepatic vitamin A than their cotwins in the shade [106]. Thus, rising temperatures and greater sunlight in the summer months could catabolize tissue concentrations of vitamin A to such a degree that it would prevent influenza viruses from making use of it to replicate. "
"The seasonality and other observations on the epidemiology of influenza A are attributed to population-wide states of impaired innate immunity due to reduced exposure to sunlight during the winter months and a resulting deficiency of vitamin D [33-35]. Cannell's theory postulates that influenza epidemics are the result of a dormant disease that becomes active in response to vitamin D deficiency. Although the vitamin D deficiency hypothesis accounts for many hitherto unexplained facts about the epidemiology of influenza, gaps remain in understanding the pathogenesis, symptoms, and course of influenza infections.
Several observations reviewed in this paper suggest that vitamins A and D have interactive roles in influenza and that retinoids (the collective term for vitamin A and its natural and synthetic congeners) have an independent role in influenza infection and pathogenesis. For instance, solar radiation has opposite effects on vitamins A and D, catabolizing vitamin A but increasing the concentration of vitamin D; the effects of the two vitamins are mutually inhibitory; retinoids regulate airway epithelial cell growth, differentiation, and gene expression; the symptoms of influenza are similar to those of retinoid toxicity; supplementary and/or pharmacological concentrations of retinoids induce influenza-like symptoms; viral activity is regulated in part by retinoids; and retinoids influence the mechanisms that both inhibit and contribute to influenza pathogenesis.
It is hypothesized that reduced sunlight exposure and/or preexisting vitamin D deficiency simultaneously increase the accumulation, expression and potential toxicity of endogenous retinoids (i.e., decrease the vitamin D-to-vitamin A ratio), which trigger viral activation or increase host susceptibility to novel strains of influenza virus. Furthermore, while normal physiological concentrations ofretinoid appear to work with vitamin D to inhibit influenza pathogenesis, higher background concentrations (very low vitamin D: A ratios) worsen it and may induce the severe or lethal complications of the disease. In short, the outcome of influenza infections may depend in part on the ratio or balance between background concentrations of vitamin A and vitamin D. The role of vitamin D and vitamin A in influenza could also, of course, extend to genetic differences in the metabolism and availability of these vitamins (c.f. [62])."
If that wasn't enough, here's another bit:
"
The fat-soluble vitamins A, D, E, and K normally work interactively together. For instance, earlier suggestions that the function of vitamin D requires vitamin A [92] now find support in the important observation that the RXR ligand 9-cis-retinoic acid (9-cis-RA), a hormonally active form of vitamin A, potentiates vitamin D-dependent gene expression and thus has a role in vitamin D signaling that was previously unknown. It was found that when 9-cis-RA acid was unavailable, vitamin D could only bind weakly to DNA and exerted only a small effect on gene expression; conversely, the presence of 9-cis-RA conferred significant agonistic activity to a vitamin D receptor ligand with very low agonistic activity and also increased the differentiation of colon cancer cells by vitamin D. Most remarkably, the addition of 9-cis-RA restored the functioning of a mutant (defective) vitamin D receptor present in a hereditary form of rickets that cannot normally be cured by vitamin D [93].
On the other hand, the evidence suggests that in the event of major perturbations in either vitamin A or D, due to dietary or other factors, there is an inverse, mutually inhibitory relationship between them in that vitamins A and D counterbalance their potentially toxic individual effects [94]. For instance, while vitamin A can reduce the toxicity of vitamin D (e.g., [92, 95]), vitamin D can also interact inversely with vitamin A and reduce the toxicity of vitamin A. Although little is known about the effect of reduced sunlight exposure and/or deficient vitamin D levels on vitamin A metabolism, even small to moderate doses of vitamin D in chickens reduce liver vitamin A stores and lower the level of vitamin A in blood [96]. Exposure of chickens to UV light (which produces vitamin D) likewise reduces liver stores and blood levels of retinol [97]. In humans, concomitant supplementation with vitamin D greatly increases the dose of vitamin A required to cause toxicity; for instance, Myhre et al. [98] found that the median dose for inducing vitamin A toxicity was >2,300 IU/kg of body weight per day higher when vitamin D was added to the diet. For a hypothetical 75 kg person representing the median, vitamin D supplementation would have allowed an additional 175,000 IU vitamin A/day before toxicity symptoms were likely to be reported. In the Nurses' Health Study, a positive association was found between retinol intake and fracture risk in that vitamin D intake increased as retinol intake increased, but at a lower rate. In a multivariate analysis controlling for many factors, vitamin D was found to be protective against retinol-associated risks of fracture [99].
The potential toxicity of high intakes of vitamin A may thus depend in part on the amount of vitamin D consumed. On the other hand, vitamin D deficiency would be expected to increase the potential toxicity of vitamin A. Indeed, consumption of preformed retinol, even in the usual amounts consumed in the United States in the forms of multivitamins, may cause osteoporotic bone changes in adults with low vitamin D concentrations [76]. Scandinavian countries, which have the highest fracture rates in Europe and even worldwide [100], have higher average intakes of vitamin A and are also at far higher latitudes (60 degrees), where vitamin D "winters" (periods of time in which vitamin D cannot be produced by the action of sunlight on the skin) are longer and vitamin D is less available from the sun, even in the months when sunlight is present.
With regard to the impact of vitamin A on vitamin D, in humans the amount of vitamin A in a single serving of liver inhibits the rise in serum calcium induced by vitamin D [101]. Retinoic acid can antagonize the action of vitamin D and its active metabolite 1,25-dihydroxycholecalciferol in rats [102]. A high intake of retinol also completely abolished the protective effect of vitamin D on distal colorectal adenoma, women in the highest quintile of vitamin D intake ingested about 10,000 IU/day of retinol, and there was a strong correlation overall between dietary intakes of vitamins A and D [103].
Sunlight in the ultraviolet (UV-B) spectrum converts a cholesterol precursor, 7-dehydrocholesterol, into the activated form of vitamin D (calcitriol). Thirty minutes of whole-body exposure of pale skin to sunlight with clothing or sunscreen can result in the synthesis of from 10,000 to 20,000 IU of vitamin D. Further radiation converts excess vitamin D in the skin into inactive metabolites. Melanin pigment also accumulates in skin, thereby decreasing the production of vitamin D [104]. On this basis it has been suggested that, in order to maintain serum levels of 25(OH)D at the optimal range of 50 ng/mL during a vitamin D "winter", 4,000 IU vitamin D should be consumed per day [105]."
this bit is interesting:
"High temperatures increased liver vitamin A utilization; moreover, identical twin calves exposed to solar radiation for 38 days lost more hepatic vitamin A than their cotwins in the shade [106]. Thus, rising temperatures and greater sunlight in the summer months could catabolize tissue concentrations of vitamin A to such a degree that it would prevent influenza viruses from making use of it to replicate. "
Adding A makes it go into storage instead of circulating. Thus temporarily reducing symptoms, but increasing toxic storage
lilsticky
Member
- Joined
- Nov 27, 2019
- Messages
- 291
excuse me but aren't you supposed to take/eat Vitamin A with Zinc? this might be why somebody mentioned eating a lot of legumes and recovering
What do you mean. No A in legumes or at least very low
aniciete
Member
Could that be why eating a piece of liver helps for a couple days and then rebounds with even worse flaky/skin issues?
Yeah, that's the assumed mechanism. It might also be why some feel better from A toxicty when taking E as it, in addition to being an anti-oxidant, (peat mentions it mainly being needful in the precense of pufa) seems to redirect A into the liver temporarily thus decreasing the circulating A
aniciete
Member
Thanks, I actually noticed the same thing when experimenting with E too
thats interesting! I had that effect initially but at my highest A it backfired giving me breathing problems.
nerfherder
Member
Oh wow that's amazing, Blossom. That is a huge change.
OP
Thanks! Unfortunately it started slowly creeping up again when I added back eggs and dairy after covid hit. I’ve been back on low ‘a’ strictly since March 7 after weaning down slowly at the first of the year and it once again came down quickly. It was 107/68 today.
nerfherder
Member
It's great that you can see the effect of reversing some of the diet changes then go back to 107/68. It is very encouraging for me, too!
frannybananny
Member
- Joined
- Apr 26, 2018
- Messages
- 704
Blossom, I am very confused by this post. What are you attributing all this stuff to? Drinking hot water? It is not clear.
Hi Blossom,
Wow, I am totally absorbed by the discussion here. I kept seeing this thread, and tonight I finally took the time to read more only to find that the one problem I have is the same problem he had.....ECZEMA! I have posted many times in various threads on eczema helps. I am now beginning to have some hope that trying a low-A diet for a few weeks just might be for me, to test Grant Genereux's hypothesis!
Your point above is very well put. We have not changed, but our food has! Tell me, do you still keep to a low-A diet? Do you have to supplement with calcium to compensate for removal of dairy? I'll keep reading through here to pick up what I can, but I was so excited to think this might be an easier fix than I had ever thought- and my current eczema flare-up has been off and on for the past 1-1/2 years now!
Thank you for posting your experiences- yours and others' are so encouraging to someone who has struggled with no answers to my skin problem.
I'd also like to know, and how are people covering their calcium needs? Supplements? Most abundant available calcium is from dairy, right?
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