From Chris Masterjohn: Testing Nutritional Status - Vit A

[Elie]

While I am curious about the "low toxin" diet and I'm experimenting with it currently on myself, I am not sold on the idea that most people are walking around with vit A toxicity.

The material below is from a resource of Chris Masterjohn PhD about vit. A and I think it is a lot more level headed than Dr. Smith's take on it.

My own personal bias is that, while Smith presents plenty of valuable information, he comes a cross overly confident in pinning health issues with multiple etiologies on a single culprit or sets of culprits (which actually play biochemical and physiological roles in regulating our health).

Because there are no good blood tests for vit A (Testing % of retinyl ester may be helpful if labs actually tested it https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6692705/), I find Masterjohn take on what other markers may be elevated (if there is a vitamin A toxicity) interesting.

From his "Testing Nutritional Status" document
Testing for Vitamin A Toxicity:
● Serum vitamin A ( LabCorp , Quest ) will be high in most cases.
● In descending order of likelihood, the following tests may show elevations:
γ-glutamyltransferase ( LabCorp , Quest ), triglycerides ( LabCorp , Quest ), alkaline
phosphatase ( LabCorp , Quest ), prothrombin time ( LabCorp , Quest ), cholesterol
( LabCorp , Quest ), aspartate aminotransferase ( LabCorp , Quest ), bilirubin ( LabCorp ,
Quest ), and calcium ( LabCorp , Quest ).

Here is the entire section on Vit A for whomever is interested.

Vitamin A

Signs and Symptoms of Deficiency : Well established signs and symptoms of vitamin A
deficiency include the following: poor night vision; dry eyes; hyperkeratosis around hair follicles,
or appearing as bumps on the skin that can be mistaken for goosebumps or acne, or on the
Copyright © Chris Masterjohn, 2019. This is an educational resource and is not to be construed in any way as medical or nutritional advice or training. Always ask your doctor
about taking any health-related measures and never ignore professional medical advice on the basis of anything contained herein.
surface of the conjunctiva (Bitot’s spots); poor immunity to infectious diseases. Less well
established but plausible signs and symptoms of deficiency include the following: kidney stones;
disrupted circadian rhythm and an inability to use light therapy to entrain a healthy circadian
rhythm; autoimmune disorders; asthma and allergies; food intolerances; low sex hormones; and
delayed puberty.

Risk Factors for Deficiency : Diets that do not contain at least one of the following: a weekly
serving of liver; regular use of cod liver oil, a multivitamin, or another supplement providing
100% of the US RDA for vitamin A as retinol. If the diet is also poor in dairy products and eggs,
and does not contain several servings per day of red, orange, yellow, or green vegetables,
vitamin A deficiency becomes very plausible. Diets where fats come from polyunsaturated
vegetable oils are more likely to produce vitamin A deficiency than diets where the fat is mostly
saturated or monounsaturated. A low-fat diet will not intrinsically produce vitamin A deficiency,
but it will increase its likelihood by leading to lower absorption of vitamin A from food. Long-term
use of glucocorticoids, high-protein diets, and high-dose vitamin D may contribute to vitamin A
deficiency in combination with poor dietary intake.

Signs and Symptoms of Toxicity : Most commonly, nausea, vomiting, and headache. In
extremes, anorexia, blurred vision, scaling skin, hair loss (alopecia), organ damage, death.
Osteopenia and osteoporosis can be worsened by vitamin A at non-toxic levels when vitamin D
and calcium are deficient. It is prudent to keep vitamin A below 10,000 IU per day during the first
eight weeks of pregnancy due to a possible risk of birth defects unless blood measurements,
signs, and symptoms justify higher intakes to prevent deficiency.

Risk Factors for Toxicity : Months or years of consistently taking at least 165 IU per kilogram
body weight per day, and in the majority of cases greater than 2300 IU per kilogram body weight
per day. For a person weighing 70 kilograms (154 pounds), this is a minimum of 11,550 IU and
higher than 161,000 IU per day in the majority of cases. These figures apply to cases where
vitamin D was not supplemented alongside it. When vitamin D is taken alongside vitamin A, the
majority of vitamin A toxicity cases involve months or years of consistently taking more than
4620 IU vitamin A per kilogram body weight per day, which for a person weighing 70 kilograms
is 323,400 IU per day. Almost all vitamin A is prepared in oil; however, vitamin A preparations
that are water-soluble, emulsified, or solid may cause toxicity in weeks rather than months and
at ten times lower doses.

Testing for Vitamin A Deficiency:
● Serum vitamin A (individually: LabCorp , Quest , in panels: Genova ION Profile + 40
amino acids , Genova’s fat-soluble vitamin panel ). This should be kept toward the middle
of the reference range (third quintile) and low-normal results do not necessarily rule out a
problem.
● Retinol-binding protein ( LabCorp , Quest ) can be measured alongside serum vitamin A,
but may be affected by a greater number of variables unrelated to vitamin A status (it is
increased in insulin resistance and type 2 diabetes, and decreased in type 1 diabetes,
systemic inflammation, and a variety of liver and kidney diseases).
Copyright © Chris Masterjohn, 2019. This is an educational resource and is not to be construed in any way as medical or nutritional advice or training. Always ask your doctor
about taking any health-related measures and never ignore professional medical advice on the basis of anything contained herein.

Testing for Vitamin A Toxicity:
● Serum vitamin A ( LabCorp , Quest ) will be high in most cases.
● In descending order of likelihood, the following tests may show elevations:
γ-glutamyltransferase ( LabCorp , Quest ), triglycerides ( LabCorp , Quest ), alkaline
phosphatase ( LabCorp , Quest ), prothrombin time ( LabCorp , Quest ), cholesterol
( LabCorp , Quest ), aspartate aminotransferase ( LabCorp , Quest ), bilirubin ( LabCorp ,
Quest ), and calcium ( LabCorp , Quest ).

Testing Caveats: Zinc is necessary for virtually every step in vitamin A metabolism, including
its transport in the blood. Zinc deficiency should always be considered as an explanation for an
apparent case of vitamin A deficiency that does not respond well to dietary and supplemental
strategies, regardless of whether serum vitamin A is altered. Adiposity may cause cellular
vitamin A deficiency without lowering serum levels. Fatty liver disease compromises the liver’s
ability to store vitamin A and may raise serum levels. Drugs that are vitamin A derivatives
(known as retinoids; e.g., isotretinoin, marketed as Accutane) may cause vitamin A deficiency
signs by hurting the body’s utilization of natural vitamin A. Chronic alcohol abuse and protein
deficiency also hurt vitamin A utilization.

Correcting Vitamin A Deficiency: The strategy to fix the deficiency should be determined by
the cause. If the cause is a dietary deficiency, the first step is to reverse the dietary risk factors
listed above. Supplements providing 25,000-50,000 IU per day appear to be well within the
margin of safety for short-term use (several weeks) in an adult, and may help resolve a
deficiency more quickly, but should not be used without close monitoring of serum vitamin A to
ensure it stays within the normal range. Someone who develops vitamin A deficiency on an
apparently adequate diet may need higher doses long-term (months, years, or indefinitely), but
again, you should only use high doses if you consistently monitor serum levels. You may often
need trial and error to find the right dose. You should rule out deficiencies of other nutrients,
especially vitamin D, before initiating high-dose vitamin A. If malabsorption is the cause of
deficiency, the solutions listed under “ General Considerations for Fat-Soluble Vitamins ” should
be followed. If factors listed under “ testing caveats ” are responsible for deficiency signs, these
should be resolved independently and vitamin A supplementation should not be used to
compensate for them.

Correcting Vitamin A Toxicity: The only well established treatment for vitamin A toxicity is the
removal of the toxic dose of vitamin A. Many of the secondary effects of vitamin A toxicity, such
as organ damage and hypercalcemia, require medical care that is beyond the scope of this
guide. I recommend testing for deficiencies of the other fat-soluble vitamins and correcting any
that exist.

 

[charlie]

It always blows my mind how Chris Masterjohn can get so much so wrong. He is not a good source of information. He does not even realize the basics of testing for vitamin A toxicity and that the blood tests are worthless when looking through the eye he is peering through. If you cannot even understand that basic premise then you are definitely not a person that should be trusted for a source on this subject.

 

[GTW]

Any sceptic who speaks with certainty is a hypocrite.

 

[charlie]

Any sceptic who speaks with certainty is a hypocrite.

I am certain he knows nothing about the "vitamin A" detox process and knows nothing about how the blood levels fluctuate during the process. Why does he not mention that many of those who have low "vitamin A" blood tests are usually the sickest and most toxic of "vitamin A"? Because he has zero clinical experience and does not see this in real time like Dr. Smith does.

 

[mosaic01]

The material below is from a resource of Chris Masterjohn PhD about vit. A and I think it is a lot more level headed than Dr. Smith's take on it.

His presentation is more level headed, because Masterjohn is a trained academic. His mentor was Fred Kummerow. Unfortunately, he has no idea what he's talking about here.

When Chris started his career, he wanted to be a research scientist studying the fat soluble "vitamins", not an influencer. He wasn't able to get an academic position like Kummerow did, probably because universities stopped doing actual research. If he became an actual researcher, he may have actually discovered the toxicity of retinol.

I think his text is really a good read for understanding the misguided position of the Paleo/WAPF/Peat sphere, because it shows the errors in this kind of thinking. Ignoring the implications of retinol liver stores, and focusing on the most extreme forms of toxicity.

Serum vitamin A (individually: LabCorp , Quest , in panels: Genova ION Profile + 40 amino acids , Genova’s fat-soluble vitamin panel ). This should be kept toward the middle of the reference range (third quintile) and low-normal results do not necessarily rule out a problem.

I'm really curious how he came up with this statement. He must have made it up, because it's clearly consensus that everything above 200 mcg/L is sufficient. Also infections, zinc deficiency and protein deficiency will lower serum retinol independently of body stores.

This happens when you read studies with the thought in mind that more is better and vA is the greatest thing ever for the immune system.

He indoctrinated me into eating liver with his vitamin A and D synergy stuff years ago. He was the reason I started to believe in vitamin A, I read all of his work back then.

 

[RealNeat]

It always blows my mind how Chris Masterjohn can get so much so wrong. He is not a good source of information. He does not even realize the basics of testing for vitamin A toxicity and that the blood tests are worthless when looking through the eye he is peering through. If you cannot even understand that basic premise then you are definitely not a person that should be trusted for a source on this subject.

He did not only suggest serum vitamin A,
"Testing for Vitamin A Toxicity:
● Serum vitamin A ( LabCorp , Quest ) will be high in most cases.
● In descending order of likelihood, the following tests may show elevations:
γ-glutamyltransferase ( LabCorp , Quest ), triglycerides ( LabCorp , Quest ), alkaline
phosphatase ( LabCorp , Quest ), prothrombin time ( LabCorp , Quest ), cholesterol
( LabCorp , Quest ), aspartate aminotransferase ( LabCorp , Quest ), bilirubin ( LabCorp ,
Quest ), and calcium ( LabCorp , Quest )."

 

[RealNeat]

I am certain he knows nothing about the "vitamin A" detox process and knows nothing about how the blood levels fluctuate during the process. Why does he not mention that many of those who have low "vitamin A" blood tests are usually the sickest and most toxic of "vitamin A"? Because he has zero clinical experience and does not see this in real time like Dr. Smith does.

He has a ton of experience and works with so many clients that he is booked many months in advance. Alot of Americans have terrible liver health as you know and when the liver is fatty it can get vitamin A toxic and deficient at the same time. Decreasing a fatty liver, independent of any other intervention can fix so called vA toxicity. Many Ray Peat oriented people get fatty liver from eating too much sat fat and sugar together, hence why many may seem to be vA toxic. Cut the fat, adopt a whole food carb oriented diet and lose the weight, watch the miracles happen. Choline shuttles the fat out of the liver, its very effective and a proper adjunct, but if one goes too fast they will get detox symptoms because their fat is being shuttled straight to the liver to be metabolized, carrying with it all the toxins that may have been stored in it.

 

[mosaic01]

He did not only suggest serum vitamin A,
"Testing for Vitamin A Toxicity:
● Serum vitamin A ( LabCorp , Quest ) will be high in most cases.
● In descending order of likelihood, the following tests may show elevations:
γ-glutamyltransferase ( LabCorp , Quest ), triglycerides ( LabCorp , Quest ), alkaline
phosphatase ( LabCorp , Quest ), prothrombin time ( LabCorp , Quest ), cholesterol
( LabCorp , Quest ), aspartate aminotransferase ( LabCorp , Quest ), bilirubin ( LabCorp ,
Quest ), and calcium ( LabCorp , Quest )."

These are certainly heplful for certain cases of clinical toxicity, but not for subclinical, chronic toxicity.

Basically he correctly identifies what is called clinical toxicity, but ignores the form of toxicity that is more relevant to most people. Clinical toxicity is the point where even a doctor can see something is wrong.

When the above values show vitamin A toxicity, it can be close to death.

 

[InChristAlone]

These are certainly heplful for certain cases of clinical toxicity, but not for subclinical, chronic toxicity.

Basically he correctly identifies what is called clinical toxicity, but ignores the form of toxicity that is more relevant to most people. Clinical toxicity is the point where even a doctor can see something is wrong.

When the above values show vitamin A toxicity, it can be close to death.

I agree that high values of any of those and you are extremely toxic. High cholesterol and triglycerides could be one to watch to see how much vitamin A toxicity you have. I slowly watched mine climb higher and higher.

 

[mosaic01]

I agree that high values of any of those and you are extremely toxic. High cholesterol and triglycerides could be one to watch to see how much vitamin A toxicity you have. I slowly watched mine climb higher and higher.

I hope one day measuring free retinyl esters in the blood will be available in most labs. That seems to be the only reliable marker, in relation to serum levels.

 

[Divingwater]

These are certainly heplful for certain cases of clinical toxicity, but not for subclinical, chronic toxicity.

Basically he correctly identifies what is called clinical toxicity, but ignores the form of toxicity that is more relevant to most people. Clinical toxicity is the point where even a doctor can see something is wrong.

When the above values show vitamin A toxicity, it can be close to death.

I don't understand why a doctor couldn't recognize subclinical toxicity

 

[md_a]

I searched the internet for this information:

Assessing liver stores of vitamin A is typically done through a liver biopsy, which is an invasive procedure and not performed routinely in clinical practice.

Blood tests can measure the levels of vitamin A in the bloodstream, but they do not accurately represent liver stores.

However, there are some indirect markers of vitamin A status that can give an indication of liver stores. For example, measuring the levels of retinol-binding protein (RBP) and prealbumin in the blood can provide information about vitamin A status. RBP is a protein that carries vitamin A in the bloodstream, and prealbumin is a protein that helps transport RBP. Low levels of RBP and prealbumin may indicate insufficient vitamin A levels.

Additionally, measuring the activity of certain enzymes involved in vitamin A metabolism, such as retinol dehydrogenase and lecithin-retinol acyltransferase, can also provide information about vitamin A status. Increased activity of these enzymes may indicate adequate liver stores of vitamin A.

When diagnosing hypervitaminosis A, typically order blood tests to measure the levels of vitamin A and its metabolites in the blood. These tests may include:

• Serum retinol: This test measures the level of retinol (preformed vitamin A) in the blood. A level above 300 mcg/dl is considered indicative of hypervitaminosis A.
• Serum retinyl esters: This test measures the level of retinyl esters (storage form of vitamin A) in the blood. An elevated level indicates excessive vitamin A storage in the liver.
• Liver function tests: These tests measure the levels of liver enzymes in the blood, which can indicate liver damage due to hypervitaminosis A

Blood tests for RBP, prealbumin, retinol dehydrogenase, and lecithin-retinol acyltransferase can provide some insights into vitamin A status, but they are not definitive indicators of hypervitaminosis A.

In general, high levels of RBP and retinol in the blood are associated with high vitamin A stores. However, RBP levels may not increase significantly until vitamin A stores reach toxic levels. Prealbumin levels may decrease with hypervitaminosis A, but this is not a consistent finding.

Retinol dehydrogenase and lecithin-retinol acyltransferase are enzymes involved in the metabolism and storage of vitamin A. High levels of these enzymes may indicate increased vitamin A metabolism and storage. However, these enzymes are not typically used as diagnostic markers for hypervitaminosis A.

Although liver reserves are considered the best indicator of vitamin A status, it is impractical to perform liver biopsies in humans. Hence, alternative biomarkers are utilized.

Some examples of these biomarkers include:

Xerophthalmia: Signs of dry eyes and visual disturbances are indicative of vitamin A deficiency. Night blindness and slower recovery of vision are early symptoms before ocular manifestations occur. Large scale evaluation is required for these symptoms.

Serum Retinol: Serum retinol concentration is commonly used to evaluate vitamin A deficiency. Serum retinol concentration remains constant until they reach very low levels of liver reserve.

Dose-Response Test: This test works on the concept that apo-retinol-binding protein accumulates in liver as liver reserves decrease. When a challenge dose of vitamin A binds to this protein, serum concentrations rise quickly if liver vitamin A concentrations are low.

The Dose-Response Test is indeed a method used to assess the adequacy of vitamin A status in subjects. This test is based on the concept that as liver vitamin A reserves decrease, the concentration of apo-retinol-binding protein (also called RBP) increases. When a subject receives a challenge dose of vitamin A, the absorbed vitamin A binds to the existing RBP, leading to a rapid increase in serum retinol concentrations.

When an individual has low liver vitamin A reserves, the administration of a challenge dose leads to a larger increase in serum retinol concentrations compared to someone with sufficient vitamin A reserves. This is because the individual with low liver reserves has a higher demand for RBP to bind to the administered vitamin A

Therefore, a significant increase in serum retinol concentrations post-challenge suggests low liver vitamin A reserves, indicating possible vitamin A deficiency. Conversely, little or no significant changes in serum retinol concentrations following the challenge indicates adequate liver vitamin A reserves.

Isotope Dilution assays: These tests utilize stable isotopes as markers of total vitamin A reserves and can cover a wide range of liver reserves.

Isotope Dilution assays are another technique used to assess vitamin A status by utilizing stable isotopes as markers of total vitamin A reserves. Stable isotopes do not alter chemical properties, allowing them to integrate across a broad range of liver stores. By analyzing the ratio of stable isotopes in blood samples, it is possible to infer the total vitamin A stored in the body, including the liver.

In an Isotope Dilution test, subjects receive a single labeled dose of vitamin A, which integrates across all compartments containing vitamin A. Blood samples are taken, and the ratio of labeled to unlabeled vitamin A is measured. From this ratio, it is possible to calculate total vitamin A content in the body.

Isotope Dilution assays offer several advantages. First, they don't rely on the assumption that the vitamin A pool is homogenoushomogeneous, reducing potential errors related to heterogeneity in distribution of vitamin A in the body. Second, they allow measurement of total vitamin A, not just liver reserves. Lastly, isotopic assays are less affected by environmental factors, resulting in fewer confounding variables.

Despite their advantages, isotope dilution assays can be complex and expensive, limiting their widespread usage. However, they remain a powerful tool for studying vitamin A status.


There are studies that have looked at vitamin A storage in liver biopsies of deceased or sick individuals. These studies can provide valuable information on vitamin A status in various populations and can help inform public health policies and recommendations.

For example, a study published in the Journal of Clinical Pathology in 2004 analyzed liver biopsies from 17 autopsies in South Africa and found that the majority of the subjects had low vitamin A stores, with a median concentration of 48μg/g wet weight. The authors concluded that vitamin A deficiency was prevalent in this population and recommended targeted interventions to address the issue.

Similarly, another study published in the American Journal of Clinical Nutrition in 2012 analyzed liver biopsies from 58 patients with nonalcoholic fatty liver disease (NAFLD) and found that the majority of them had low vitamin A levels, with a median concentration of 38μg/g wet weight. The authors suggested that vitamin A supplementation may benefit patients with NAFLD.

There are also studies that have analyzed liver biopsies from deceased individuals with hypervitaminosis A. For example, a case report published in the Journal of Medical Case Reports in 2014 described a woman who died from complications related to hypervitaminosis A. Analysis of her liver biopsy revealed a vitamin A concentration of 52,000μg/g wet weight, which is approximately 100 times the upper limit of normal.

Overall, analyzing liver biopsies from sick or dead individuals can provide useful insights into vitamin A status and storage capacity. Such studies can help guide public health policies and recommendations to prevent vitamin A deficiency and toxicity.

 

[RealNeat]

I agree that high values of any of those and you are extremely toxic. High cholesterol and triglycerides could be one to watch to see how much vitamin A toxicity you have. I slowly watched mine climb higher and higher.

Many have gotten those numbers down simply by losing weight and hence losing the liver fat, avoiding vitamin A in food is akin to being "bubble boy" with all the other potent toxins that permeate our environment. One can only isolate themselves or their diet so much before the cure is worse than the disease. Food is more than the sum of its parts and ultra restrictive diets trade one issue for another.

A fatty liver also plays a direct role in the gallbladder/ bile issues. I bet you an ultrasound of all the people who have benefitted off of the anti vA diet will have a fatty liver and bile sludge.

People are literally being killed by every morsel of food that they eat and every sip they drink because of deuterium, yet no one has batted an eye yet. A healthy metabolism can even keep deuterium levels in check, there is no reason why it shouldnt be able to keep vA in check.

Thank God for our liver, thank God that he put poisons or defenses in every food meant for man and beast or else we would all starve... and thank God that he made us capable of taming beasts and deactivation of natural poisons, aka cooking.

 

[Elie]

I don't understand why a doctor couldn't recognize subclinical toxicity

to me it seems because
1. It is hard to diagnose without widely available good tests
2. In the absence of good test "subclinical toxicity" can be toxicity of many different sources.

 

[InChristAlone]

Many have gotten those numbers down simply by losing weight and hence losing the liver fat, avoiding vitamin A in food is akin to being "bubble boy" with all the other potent toxins that permeate our environment. One can only isolate themselves or their diet so much before the cure is worse than the disease. Food is more than the sum of its parts and ultra restrictive diets trade one issue for another.

A fatty liver also plays a direct role in the gallbladder/ bile issues. I bet you an ultrasound of all the people who have benefitted off of the anti vA diet will have a fatty liver and bile sludge.

People are literally being killed by every morsel of food that they eat and every sip they drink because of deuterium, yet no one has batted an eye yet. A healthy metabolism can even keep deuterium levels in check, there is no reason why it shouldnt be able to keep vA in check.

Thank God for our liver, thank God that he put poisons or defenses in every food meant for man and beast or else we would all starve... and thank God that he made us capable of taming beasts and deactivation of natural poisons, aka cooking.

Of course you can't isolate yourself from every poison! And no one is saying to do zero vitamin A. That's just not necessary. Oatmeal for instance has lutein. And that's eaten on the low vitamin A diet. Bananas have some too. Red meat has some depending on what the cow ate and was supplemented with. Veggies of course has some. And we don't know a lot about bean carotenoids, so far I found out kidney beans do in fact have them and so do lentils. Black beans must have a different pigment because they are lower. So no, it's impossible to do a zero vit A diet. I think the only time it's ever been pulled off is a boy who ate only chicken nuggets and white bread or something like that.

Yes fatty liver is a problem, and that's what we are warning people about! The Peat diet doesn't cure fatty liver! And Peat himself said in an article fatty liver may be protective!! WHAT! And I also found out recently he never did any blood tests!! He didn't even know if he had high liver enzymes or high cholesterol, he went by his temperature and pulse for all of his health needs.

So since I'm no expert I will use myself as an example. I did not restrict anything, I ate what I wanted to eat which was OJ or grape juice, bananas and other ripe fruit seasonally available, ham, cheese, chocolate, tacos, chicken fajitas, pizza at times and other meat and starch dishes, and then of course haagen dazs, my favorite dessert. That diet is pretty Peaty. And I wasn't very overweight about 122 lbs. So are you telling me I can stay on that diet because restriction is bad? And continue having worse blood labs? (temp and pulse was fine per Peat)

How does anyone change fatty liver other than restriction? Peat might say just use more thyroid and caffeine. Nope can't do it, temp and pulse was already up there. So how do you do it?

 

[hierundjetzt]

He has a ton of experience and works with so many clients that he is booked many months in advance. Alot of Americans have terrible liver health as you know and when the liver is fatty it can get vitamin A toxic and deficient at the same time. Decreasing a fatty liver, independent of any other intervention can fix so called vA toxicity. Many Ray Peat oriented people get fatty liver from eating too much sat fat and sugar together, hence why many may seem to be vA toxic. Cut the fat, adopt a whole food carb oriented diet and lose the weight, watch the miracles happen. Choline shuttles the fat out of the liver, its very effective and a proper adjunct, but if one goes too fast they will get detox symptoms because their fat is being shuttled straight to the liver to be metabolized, carrying with it all the toxins that may have been stored in it.

I am not a follower of Masterjohn, bit I think that most people may not be getting enough vitamin D (as stated by the OP's post), due to the fact that many modern people don't get enough outdoors, etc., and therefore maybe are seeing positive effects once they go on this low vitamin A diet. IMO if they would get out more in the sun, then they wouldn't have to go low vitamin A. But I guess for many that's not feasible nowadays.

 

[charlie]

Food is more than the sum of its parts and ultra restrictive diets trade one issue for another.

And yet you fail to do the simple footwork and see for yourself that the accumulation effects of vA is real and you continue to perpetuate the tired old paradigm that keeps people sick and diseased. Do the leg work so you can stop misinforming the people.

I don't understand why a doctor couldn't recognize subclinical toxicity

I can look at a person now and tell if they are "vitamin A" toxic, the signs are very clear. No doctor needed.

 

[GTW]

Given the extent of ad hominem logical fallacy I read here my contribution is this:
Chris Masterjohn is exemplary in full disclosure, explaining the conditional nature of biochemistry, individual genetic variation, and uncertainties.

 

[Validus]

If the premise that vitamin A is toxic and our body treats it as such is valid, it seems reasonable that our body would mitigate it floating around in serum and excrete it if possible through bile and then poop.

Because that detox method is relatively slow, and dependent on how much vitamin A you're consuming, it's also reasonable that our body would need to store the excess in order to keep it out of our blood when possible.

It then makes sense our body would store it in the liver and our adipose tissue.

So, it would be optimal (but not very reasonable) then, to do a body fat and liver biopsy to test for vitamin A levels.

I think that would verify whether or not this is the reality for people dealing with vitamin a toxicity.

It also seems likely that if you do a blood test and vitamin a is found in higher levels, you likely liberated from storage and it wasn't expelled via bile/poop and your body reabsorbed it or, you just ate a bolus amount of vitamin a and your body hasn't yet dealt with it.

 

[RealNeat]

And yet you fail to do the simple footwork and see for yourself that the accumulation effects of vA is real and you continue to perpetuate the tired old paradigm that keeps people sick and diseased. Do the leg work so you can stop misinforming the people.

I can look at a person now and tell if they are "vitamin A" toxic, the signs are very clear. No doctor needed.

I have read all of Grants books, I've done much more than the bare minimum, just because I'm not totally on board doesn't mean I'm misinformed, there is a lot of unknowns here Charlie. Also what does what you responded have anything to do with what I said in that quoted line?