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- Oct 30, 2015
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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.
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.