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

Amazoniac

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On phytanic acid (again) since it was mentioned recently.

It's a metabolite from the side chain of the chlorophyll molecule.

- Phytanic acid consumption and human health, risks, benefits and future trends: A review

upload_2019-12-13_13-39-7.png


upload_2019-12-13_13-39-15.png

It occurs in large amounts (relative to poisonoids) in some foods such as butter.

- Diet and Refsum's disease. The determination of phytanic acid and phytol in certain foods and the application of this knowledge to the choice of suitable convenience foods for patients with Refsum's disease

upload_2019-12-13_13-39-39.png

upload_2019-12-13_13-39-57.png

You must have noticed on the first images that it's metabolized in a similar way as poisonol, their structure has commonalities as well. This leads us to another publication shared by professor (from prophecy?) Garrett:

- Prevention of Vitamin A Teratogenesis by Phytol or Phytanic Acid Results from Reduced Metabolism of Retinol to the Teratogenic Metabolite, All-trans-retinoic Acid

upload_2019-12-13_13-41-28.png


Note:
"[..]ligand binding to the RXR is not a prerequisite for the formation of RAR-RXR heterodimers[.]"

Why he leaves these details out and continues to neglect RARs?

But in reading the publication, at first the antagonism makes sense, however (as usual) there's no further questioning. The doses of poisonoids used were pharmacological, if the competition was proportional, butter wouldn't be a source of these toxins and have a detectable impact. For some reason this is ignored when claiming that casein has hidden poisonoic acid, why the same protective principle wouldn't apply here since it could contain substantial amounts of these acids?

Those levels were evaluated after dosing, when the body is still metabolizing them, however their behavior after the digestive period passes matters.. and so do the affinities.

- Anti-Peat - Grant Genereux's Theory Of Vitamin A Toxicity

"As an important metabolite of chlorophyll, phytanic acid can be produced in ruminating animals by their rumen bacteria. Humans do not efficiently absorb chlorophyll and cannot metabolize it; thus, levels of phytanic acid in the human body are entirely dependent on meat and milk products ingested in the diet. Consequently, phytanic acid cannot be considered as an endogenous ligand in humans, but may potentially act as such in ruminants. Furthermore, its low levels in human questions the physiological relevance of its activities as a nutritional RXR ligand. Thus, in human plasma phytanic acid concentrations ranged around 1.6 μM, which was highly dependent on dietary habits of healthy volunteers, with the highest level (5.8 μM) found in meat eaters and the lowest in vegans (0.9 μM) (Al-Dirbashi et al., 2008; Allen et al., 2008). Phytanic acid levels ranged around 1 μM in mouse plasma, but were approximatively 10-100 times lower in different tissues (Wanders et al., 2011). Such quantities were increased to 10 μM levels under supplementation with high amounts of phytol, a phytanic acid precursor (Wanders et al., 2011). Importantly, disruption of phytanol-CoA hydroxylase, the first enzyme in the α-oxidation in Refsum disease, leads to high accumulations of phytanic acid, which may reach up to 1000 times the level of a healthy person (Verhoeven and Jakobs, 2001), with highest levels found in the liver, heart, adipose and peripheral nervous tissues, and much lower in the brain (Cumings, 1971). Despite the wide range of symptoms, including peripheral neuropathy, retinal degeneration and cerebellar ataxia (see (Verhoeven and Jakobs, 2001) and references therein), no abnormalities relevant to general or even exacerbated RXR signaling were reported like, for instance, decreased thyroid hormone T4 levels, elevated triglyceride levels or reduced food intake. This further questions the relevance of phytanic acid and potential phytanic acid metabolites as RXR ligands."

upload_2019-12-13_13-42-27.png

Check out the ranges for each. These numbers are consistent with what the charlatan had posted:
- Effect of dairy fat on plasma phytanic acid in healthy volunteers - a randomized controlled study (subjects tracked for butter and cheese consumption)

He's claiming that it's good because it stems from competition with 9-cis poisonoic acid, which is a metabolite that's not even considered the main ligand candidate anymore. And as they commented above, in extreme levels, issues don't suggest that it's from an interaction with RXR. The guy is spreading confusion on multiple layers.


- Neurological, Psychiatric, and Biochemical Aspects of Thiamine Deficiency in Children and Adults

"Peroxisomes play an important role in the catabolism of hydrogen peroxide, as well as in the shortening of very long fatty acids (which cannot undergo a direct mitochondrial β-oxidation catabolism) and α-oxidation (49). In the latter process, the TPP-dependent enzyme 2-hydroxyacyl-CoA lyase 1 (HACL1) catalyzes the cleavage of 3-methyl-branched and straight chain 2-hydroxy long-chain fatty acids (50). Phytanic acid (a 3-methyl-substituted, 20-carbon branched-chain fatty acid), unlike most fatty acids, is unable to undergo β-oxidation because of an existing methyl group in the 3-position (51). As such, it is broken down by HACL1 by an initial α-oxidation (52, 53). This branched-chain fatty acid is obtained through the diet, specifically from dairy products and red meat. The disruption of phytanic acid catabolism, due to inadequate levels of TPP, leads to triglyceride accumulation, which may cause deleterious effects such as cerebellar ataxia, peripheral polyneuropathy, vision and hearing loss, anosmia, and, in some instances, cardiac dysfunction and epiphyseal dysplasia (54). The symptoms caused by thiamine deficiency are shared by Refsum’s disease, which is caused by pathogenic mutations in HACL1 (55). Some of the symptoms are also observed in the autosomal recessive systemic disorder Zellweger syndrome and other peroxisomal-related diseases including the neonatal adrenoleukodystrophy. Zellweger syndrome is caused by pathogenic mutations in the pexin genes, which encode for proteins essential for the assembly of functional peroxisomes. It is characterized by deficits in the peroxisomal fatty acid oxidation pathway causing severe neurological and liver dysfunction as well as craniofacial abnormalities."​
 
Last edited:

InChristAlone

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On phytanic acid (again) since it was mentioned recently.

It's a metabolite from the side chain of the chlorophyll molecule.

- Phytanic acid consumption and human health, risks, benefits and future trends: A review


It occurs in large amounts (relative to poisonoids) in some foods such as butter.

- Diet and Refsum's disease. The determination of phytanic acid and phytol in certain foods and the application of this knowledge to the choice of suitable convenience foods for patients with Refsum's disease


You must have noticed on the first images that it's metabolized in a similar way as poisonol, their structure has commonalities as well. This leads us to another publication shared by professor (from prophecy?) Garrett:

- Prevention of Vitamin A Teratogenesis by Phytol or Phytanic Acid Results from Reduced Metabolism of Retinol to the Teratogenic Metabolite, All-trans-retinoic Acid

View attachment 15922

Note:
"[..]ligand binding to the RXR is not a prerequisite for the formation of RAR-RXR heterodimers[.]"

Why he leaves these details out and continues to neglect RARs?

But in reading the publication, at first the antagonism makes sense, however (as usual) there's no further questioning. The doses of poisonoids used were pharmacological, if the competition was proportional, butter wouldn't be a source of these toxins and have a detectable impact. For some reason this is ignored when claiming that casein has hidden poisonoic acid, why the same protective principle wouldn't apply here since it could contain substantial amounts of these acids?

Those levels were evaluated after dosing, when the body is still metabolizing them, however their behavior after the digestive period passes matters.. and so do the affinities.

- Anti-Peat - Grant Genereux's Theory Of Vitamin A Toxicity

"As an important metabolite of chlorophyll, phytanic acid can be produced in ruminating animals by their rumen bacteria. Humans do not efficiently absorb chlorophyll and cannot metabolize it; thus, levels of phytanic acid in the human body are entirely dependent on meat and milk products ingested in the diet. Consequently, phytanic acid cannot be considered as an endogenous ligand in humans, but may potentially act as such in ruminants. Furthermore, its low levels in human questions the physiological relevance of its activities as a nutritional RXR ligand. Thus, in human plasma phytanic acid concentrations ranged around 1.6 μM, which was highly dependent on dietary habits of healthy volunteers, with the highest level (5.8 μM) found in meat eaters and the lowest in vegans (0.9 μM) (Al-Dirbashi et al., 2008; Allen et al., 2008). Phytanic acid levels ranged around 1 μM in mouse plasma, but were approximatively 10-100 times lower in different tissues (Wanders et al., 2011). Such quantities were increased to 10 μM levels under supplementation with high amounts of phytol, a phytanic acid precursor (Wanders et al., 2011). Importantly, disruption of phytanol-CoA hydroxylase, the first enzyme in the α-oxidation in Refsum disease, leads to high accumulations of phytanic acid, which may reach up to 1000 times the level of a healthy person (Verhoeven and Jakobs, 2001), with highest levels found in the liver, heart, adipose and peripheral nervous tissues, and much lower in the brain (Cumings, 1971). Despite the wide range of symptoms, including peripheral neuropathy, retinal degeneration and cerebellar ataxia (see (Verhoeven and Jakobs, 2001) and references therein), no abnormalities relevant to general or even exacerbated RXR signaling were reported like, for instance, decreased thyroid hormone T4 levels, elevated triglyceride levels or reduced food intake. This further questions the relevance of phytanic acid and potential phytanic acid metabolites as RXR ligands."


Check out the ranges for each. These numbers are consistent with what the charlatan had posted:
- Effect of dairy fat on plasma phytanic acid in healthy volunteers - a randomized controlled study (subjects tracked for butter and cheese consumption)

He's claiming that it's good because it stems from competition with 9-cis poisonoic acid, which is a metabolite that's not even considered the main ligand candidate anymore. And as they commented above, in extreme levels, issues don't suggest that it's from an interaction with RXR. The guy is spreading confusion on multiple layers.


- Neurological, Psychiatric, and Biochemical Aspects of Thiamine Deficiency in Children and Adults

"Peroxisomes play an important role in the catabolism of hydrogen peroxide, as well as in the shortening of very long fatty acids (which cannot undergo a direct mitochondrial β-oxidation catabolism) and α-oxidation (49). In the latter process, the TPP-dependent enzyme 2-hydroxyacyl-CoA lyase 1 (HACL1) catalyzes the cleavage of 3-methyl-branched and straight chain 2-hydroxy long-chain fatty acids (50). Phytanic acid (a 3-methyl-substituted, 20-carbon branched-chain fatty acid), unlike most fatty acids, is unable to undergo β-oxidation because of an existing methyl group in the 3-position (51). As such, it is broken down by HACL1 by an initial α-oxidation (52, 53). This branched-chain fatty acid is obtained through the diet, specifically from dairy products and red meat. The disruption of phytanic acid catabolism, due to inadequate levels of TPP, leads to triglyceride accumulation, which may cause deleterious effects such as cerebellar ataxia, peripheral polyneuropathy, vision and hearing loss, anosmia, and, in some instances, cardiac dysfunction and epiphyseal dysplasia (54). The symptoms caused by thiamine deficiency are shared by Refsum’s disease, which is caused by pathogenic mutations in HACL1 (55). Some of the symptoms are also observed in the autosomal recessive systemic disorder Zellweger syndrome and other peroxisomal-related diseases including the neonatal adrenoleukodystrophy. Zellweger syndrome is caused by pathogenic mutations in the pexin genes, which encode for proteins essential for the assembly of functional peroxisomes. It is characterized by deficits in the peroxisomal fatty acid oxidation pathway causing severe neurological and liver dysfunction as well as craniofacial abnormalities."​
Interesting, I guess we can just forget about phytanic acid then.
 

Amazoniac

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Interesting, I guess we can just forget about phytanic acid then.
Model, I wouldn't dismiss it, there are more sources as well (from the second link):

upload_2019-12-14_7-28-1.png

upload_2019-12-14_7-28-6.png

It could work under some conditions (for example, a transient mitigation of poisonemia when a lot of liver is consumed in comparison to purified poisonyl palmitate), but he's distorting it all. The rationelle is apsurq: at the same time that he claims poison/"vitamin" A to be a dispensible toxin because there are alternative ligands that can substitute for poisonoids and fulfill all of the functions through activation of a single class of receptors (?), he's there suggesting that the very same ligands that can do such thing are protective when they compete with poisonoids and bind in their place, yet if this is successful, you end up with a substance that has poisonoid-like activity: why is not toxic and how is it protective? It's either admitting that poison A is required or that the alternative ligands cannot replace it since they don't trigger the same events; and he obviously did not have range of activation in mind because he suggested that the alternative worked better than a poisonol metabolite (9-cis poisonoic acid).

I forgot to comment that the doses used in the third publication above lead to spillover of poisonoids in circulation, which is when the antagonism gains relevance. Some of you already consider poisonyl acetate problematic, what about plain poisonol administered in high doses in the experiment (50 mg/kg; mice)? Still, the effect of phytanic acid on poisonol metabolism when the followed for a longer period wasn't as counteractive as he makes it sound.

upload_2019-12-14_7-28-15.png

And how can we extrapolate this to butter consumption?
 
Last edited:

LLight

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The rationelle is apsurq: at the same time that he claims poison/"vitamin" A to be a dispensible toxin because there are alternative ligands that can substitute for poisonoids and fulfill all of the functions through activation of a single class of receptors (?), he's there suggesting that the very same ligands that can do such thing are protective when they compete with poisonoids and bind in their place, yet if this is successful, you end up with a substance that has poisonoid-like activity: why is not toxic and how is it protective?

Maybe retinoids have cytotoxic properties that are not related to their activities with respect to the receptor.
 

Amazoniac

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Maybe retinoids have cytotoxic properties that are not related to their activities with respect to the receptor.
Inappropriate gene transcription is a major concern when they go awry (hence the attention to congenital malformation), so if you have a substance that can be an agonist to the same extent (if not better) as he suggests, you'd be left in trouble. Phytanic acid didn't affect poisonol to the extent that it affected downstream metabolites, but alleviated issues: it's another hint that the transcription aspect is involved. Since it had an impact on the equivalent of 250,000 mcg of poisonol, according to his logic, 100 mcg from butter is nothing for it to oppose, yet if this occurred, what's there to make the alternative activators work?
 
Last edited:

postman

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On phytanic acid (again) since it was mentioned recently.

It's a metabolite from the side chain of the chlorophyll molecule.

- Phytanic acid consumption and human health, risks, benefits and future trends: A review


It occurs in large amounts (relative to poisonoids) in some foods such as butter.

- Diet and Refsum's disease. The determination of phytanic acid and phytol in certain foods and the application of this knowledge to the choice of suitable convenience foods for patients with Refsum's disease


You must have noticed on the first images that it's metabolized in a similar way as poisonol, their structure has commonalities as well. This leads us to another publication shared by professor (from prophecy?) Garrett:

- Prevention of Vitamin A Teratogenesis by Phytol or Phytanic Acid Results from Reduced Metabolism of Retinol to the Teratogenic Metabolite, All-trans-retinoic Acid

View attachment 15922

Note:
"[..]ligand binding to the RXR is not a prerequisite for the formation of RAR-RXR heterodimers[.]"

Why he leaves these details out and continues to neglect RARs?

But in reading the publication, at first the antagonism makes sense, however (as usual) there's no further questioning. The doses of poisonoids used were pharmacological, if the competition was proportional, butter wouldn't be a source of these toxins and have a detectable impact. For some reason this is ignored when claiming that casein has hidden poisonoic acid, why the same protective principle wouldn't apply here since it could contain substantial amounts of these acids?

Those levels were evaluated after dosing, when the body is still metabolizing them, however their behavior after the digestive period passes matters.. and so do the affinities.

- Anti-Peat - Grant Genereux's Theory Of Vitamin A Toxicity

"As an important metabolite of chlorophyll, phytanic acid can be produced in ruminating animals by their rumen bacteria. Humans do not efficiently absorb chlorophyll and cannot metabolize it; thus, levels of phytanic acid in the human body are entirely dependent on meat and milk products ingested in the diet. Consequently, phytanic acid cannot be considered as an endogenous ligand in humans, but may potentially act as such in ruminants. Furthermore, its low levels in human questions the physiological relevance of its activities as a nutritional RXR ligand. Thus, in human plasma phytanic acid concentrations ranged around 1.6 μM, which was highly dependent on dietary habits of healthy volunteers, with the highest level (5.8 μM) found in meat eaters and the lowest in vegans (0.9 μM) (Al-Dirbashi et al., 2008; Allen et al., 2008). Phytanic acid levels ranged around 1 μM in mouse plasma, but were approximatively 10-100 times lower in different tissues (Wanders et al., 2011). Such quantities were increased to 10 μM levels under supplementation with high amounts of phytol, a phytanic acid precursor (Wanders et al., 2011). Importantly, disruption of phytanol-CoA hydroxylase, the first enzyme in the α-oxidation in Refsum disease, leads to high accumulations of phytanic acid, which may reach up to 1000 times the level of a healthy person (Verhoeven and Jakobs, 2001), with highest levels found in the liver, heart, adipose and peripheral nervous tissues, and much lower in the brain (Cumings, 1971). Despite the wide range of symptoms, including peripheral neuropathy, retinal degeneration and cerebellar ataxia (see (Verhoeven and Jakobs, 2001) and references therein), no abnormalities relevant to general or even exacerbated RXR signaling were reported like, for instance, decreased thyroid hormone T4 levels, elevated triglyceride levels or reduced food intake. This further questions the relevance of phytanic acid and potential phytanic acid metabolites as RXR ligands."


Check out the ranges for each. These numbers are consistent with what the charlatan had posted:
- Effect of dairy fat on plasma phytanic acid in healthy volunteers - a randomized controlled study (subjects tracked for butter and cheese consumption)

He's claiming that it's good because it stems from competition with 9-cis poisonoic acid, which is a metabolite that's not even considered the main ligand candidate anymore. And as they commented above, in extreme levels, issues don't suggest that it's from an interaction with RXR. The guy is spreading confusion on multiple layers.


- Neurological, Psychiatric, and Biochemical Aspects of Thiamine Deficiency in Children and Adults

"Peroxisomes play an important role in the catabolism of hydrogen peroxide, as well as in the shortening of very long fatty acids (which cannot undergo a direct mitochondrial β-oxidation catabolism) and α-oxidation (49). In the latter process, the TPP-dependent enzyme 2-hydroxyacyl-CoA lyase 1 (HACL1) catalyzes the cleavage of 3-methyl-branched and straight chain 2-hydroxy long-chain fatty acids (50). Phytanic acid (a 3-methyl-substituted, 20-carbon branched-chain fatty acid), unlike most fatty acids, is unable to undergo β-oxidation because of an existing methyl group in the 3-position (51). As such, it is broken down by HACL1 by an initial α-oxidation (52, 53). This branched-chain fatty acid is obtained through the diet, specifically from dairy products and red meat. The disruption of phytanic acid catabolism, due to inadequate levels of TPP, leads to triglyceride accumulation, which may cause deleterious effects such as cerebellar ataxia, peripheral polyneuropathy, vision and hearing loss, anosmia, and, in some instances, cardiac dysfunction and epiphyseal dysplasia (54). The symptoms caused by thiamine deficiency are shared by Refsum’s disease, which is caused by pathogenic mutations in HACL1 (55). Some of the symptoms are also observed in the autosomal recessive systemic disorder Zellweger syndrome and other peroxisomal-related diseases including the neonatal adrenoleukodystrophy. Zellweger syndrome is caused by pathogenic mutations in the pexin genes, which encode for proteins essential for the assembly of functional peroxisomes. It is characterized by deficits in the peroxisomal fatty acid oxidation pathway causing severe neurological and liver dysfunction as well as craniofacial abnormalities."​
I think the reason he recommends butter is because he likes butter. He said something about never wanting to go on a super restrictive diet again and that's why his food list is higher in VA than Grants. I think there is confirmation bias, he tries to find reasons as to why the foods he wants to eat are ok in a low VA context. It seems to me that the best way to consume dairy without getting a lot of VA is to eat the lowest fat and "unenriched" dairy product you can find, as both retinol and retinoic acid is fat soluble. There might be some retinoic acid in the casein but unless you're adding like pure casein powder to your food I don't think it's a major source. To me there is a clear difference on how I feel on 0.1% fat milk and 0.5% fat milk.
 

Momentum

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I'm concerned about retinol, vitamin A, et al. Sorry to be a newbie, but due to the below I'm concerned.

Pretty sure I have IIH (idiopathic intracranial pressure). Awaiting a doctor's appointment to confirm. In the meantime I was researching the "best type of MRI to diagnose" and came across the following information (which as someone who took 8 years worth of tetracycline in high school and college, then a round of Accutane at 25 this is rather concerning.)
Regarding IIH found in:
".....and patients with a variety of endocrine conditions.4,8 It is associated with the use of several medications, most notably vitamin A derivatives and tetracycline antibiotics.9,10" http://www.ajnr.org/content/38/3/471

"Retinol-binding protein and retinol analysis in cerebrospinal fluid and serum of patients with and without idiopathic intracranial hypertension.
Abstract
BACKGROUND:
Several studies have implicated vitamin A-related compounds in the pathogenesis of idiopathic intracranial hypertension (IIH). The goal of this study was to compare cerebrospinal fluid (CSF) and serum concentrations of retinol and retinol-binding protein (RBP) in subjects with and without IIH.

RESULTS:
The retinol/RBP ratio was greater in CSF than in serum, especially in subjects with IIH.

CONCLUSIONS:
The finding of increased levels of unbound retinol in the CSF of subjects with IIH provides further evidence that vitamin A may be involved in the pathogenesis of IIH. Comparative statistical analyses revealed multivariate relationships that demonstrate the need to further investigate correlations between vitamin A and RBP levels in CSF and serum. https://www.ncbi.nlm.nih.gov/pubmed/18090557?dopt=Abstract

So, how is this reversed? Should a person with this issue take vitamin A, what form? What else may help? Thanks!
 

Ihor

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Does anyone ever heart information which departments such as beef or other animals liver store more ratinol and which less? I probably want to try a small amount of liver again for a long time, for nutritional substances, but a large dose of vitamin A alarms me, and if there is such a part, then the whole liver on the counter I just asked the butcher to cut it off for me.
 

tallglass13

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What are your sources of Poison A? If I were to increase my Poison A, I would make sure it was a food high in glucaric acid. Glucaric acid helps to detox retinoic acid according to Dr Garret. Apples might be the best food to add to your diet, since they are very high in glucaric acid and have a small amount of Poison A. 100 IU per apple according to this site: Apples
Hey Vinero, I like that website, but they have beef as having 85 IU of Poison A. I think white canned tuna had less 75 iu according to that website. Any thoughts?
 

postman

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Hey Vinero, I like that website, but they have beef as having 85 IU of Poison A. I think white canned tuna had less 75 iu according to that website. Any thoughts?
Most databases and studies I have seen say it has somewhere between 20-30 IU per 100g. Keep in mind that pretty much all livestock is supplemented with vitamins.
 

Vinero

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Yes, Beef has some vitamin A in it. That's why I also eat a lot of turkey. Turkey is even lower in vitamin A according tot that website. I probably eat about 50% beef and 50% turkey for my protein. Also, beef is higher in zinc which could help the detox pathways.
 

tallglass13

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Most databases and studies I have seen say it has somewhere between 20-30 IU per 100g. Keep in mind that pretty much all livestock is supplemented with vitamins.
thanks. So, what does everyone think would be even lower VA diet , besides beef and rice. I think Beans and rice, and tilapia and rice, and then scallops and rice. I have been eating peanuts and raisins also.
 

postman

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thanks. So, what does everyone think would be even lower VA diet , besides beef and rice. I think Beans and rice, and tilapia and rice, and then scallops and rice. I have been eating peanuts and raisins also.
For protein, egg whites is probably the only protein food source that has zero VA. In increasing order, beans, then wild ruminants (like moose or venison for example), then beef, then chicken and turkey. I don't know about fish, all databases seem to have different opinions on those. For starches, white rice, white bread, white potatoes, white corn. There are plenty of others but they are quite fatty with PUFA. White fruits like lychee have zero VA, peeled pears and apples are also very low. For the raisins, make sure they're the dark ones and not the sultanas if you want to minimize VA.
 

tallglass13

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For protein, egg whites is probably the only protein food source that has zero VA. In increasing order, beans, then wild ruminants (like moose or venison for example), then beef, then chicken and turkey. I don't know about fish, all databases seem to have different opinions on those. For starches, white rice, white bread, white potatoes, white corn. There are plenty of others but they are quite fatty with PUFA. White fruits like lychee have zero VA, peeled pears and apples are also very low. For the raisins, make sure they're the dark ones and not the sultanas if you want to minimize VA.
Great! thanks for that
 

Gone Peating

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I'm concerned about retinol, vitamin A, et al. Sorry to be a newbie, but due to the below I'm concerned.

Pretty sure I have IIH (idiopathic intracranial pressure). Awaiting a doctor's appointment to confirm. In the meantime I was researching the "best type of MRI to diagnose" and came across the following information (which as someone who took 8 years worth of tetracycline in high school and college, then a round of Accutane at 25 this is rather concerning.)
Regarding IIH found in:
".....and patients with a variety of endocrine conditions.4,8 It is associated with the use of several medications, most notably vitamin A derivatives and tetracycline antibiotics.9,10" http://www.ajnr.org/content/38/3/471

"Retinol-binding protein and retinol analysis in cerebrospinal fluid and serum of patients with and without idiopathic intracranial hypertension.
Abstract
BACKGROUND:
Several studies have implicated vitamin A-related compounds in the pathogenesis of idiopathic intracranial hypertension (IIH). The goal of this study was to compare cerebrospinal fluid (CSF) and serum concentrations of retinol and retinol-binding protein (RBP) in subjects with and without IIH.

RESULTS:
The retinol/RBP ratio was greater in CSF than in serum, especially in subjects with IIH.

CONCLUSIONS:
The finding of increased levels of unbound retinol in the CSF of subjects with IIH provides further evidence that vitamin A may be involved in the pathogenesis of IIH. Comparative statistical analyses revealed multivariate relationships that demonstrate the need to further investigate correlations between vitamin A and RBP levels in CSF and serum. https://www.ncbi.nlm.nih.gov/pubmed/18090557?dopt=Abstract

So, how is this reversed? Should a person with this issue take vitamin A, what form? What else may help? Thanks!

I’m not sure. But it seems like if the issue is that the ratio of retinol to RBP is too high then one should consume less vitamin A until the issue is resolved.
 

thomas200

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I'm 1 year and 2 months almost on the diet, 18 y/o. First 7 months low A, last 6.5 months zero A. Incredible results so far, I will stop being so strict on myself Jan. 31st 2020
 

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