Doctor Garrett Smith, ND, a naturopath, recently purported to analyze my health, making inferences from blog posts, pictures, and comments I’ve made on the internet, concluding that I am suffering from vitamin A toxicity.
Smith runs a “comprehensive Poison/’Vitamin A’ Detox program” and lists an invitation to contact his office to work with him as part of this program at the end of his article.
Smith follows Grant Genereux in believing that vitamin A is a toxin and not a vitamin at all.
Here I would like to respond to Smith’s analysis of my health.
The Nature and Extent of My Health Problems
First, for clarity, a few points about my health. The problems I am currently suffering from are, on a scale of 0-10, at about 0.5-1. The main problems are twitching, paresthesia, and a gait abnormality that started almost two years ago when I took terbinafine for a fungal infection. The night I started terbinafine, the twitching was at a 7-8 out of 10. After several days of experimenting with electrolytes, I got it down to a 1-2 out of 10. After developing strategies around acid-base balance, I got it down to a 0.5 out of 10, where it gave way to a subtle paresthesia in my cheeks, which very slowly has lessened in intensity and frequency to the point where it is now subtle and infrequent. The gait abnormality got progressively worse while on terbinafine, slowly reaching a 3 out of 10, and went away when I got off it. It recurred twice in the last year, and in both cases I suspected that B vitamin deficiencies were at the root of it, and I made it almost completely disappear within days by altering my B vitamin intake.
At the time I also was living in a moldy apartment and had very high levels of barium in my urine, which I traced to makeup I used to shoot my videos and paint dust from a chipping windowsill. I had also been under psychological stress from quitting my job and starting a business with no clear business plan, and had been putting my body through a lot of physical stress with CrossFit and Olympic lifting. All of these could have been contributors.
My Suspicions About Their Causes
Among all the potential hypotheses, I find it very interesting that terbinafine works by inhibiting the synthesis of ergosterol in fungal cell walls, and is 60% active against human cholesterol synthesis. My cholesterol, even on a diet very rich in saturated fat and cholesterol, never rises above 160. This year it has ranged between 142 and 157. Over 15 years ago I was a vegan, and my cholesterol was 106. I developed severe psychiatric problems that completely disappeared on a diet rich in organ meats. The parallel between the cholesterol-reducing activities of veganism and terbinafine, my always-low cholesterol levels, and the known association between very low cholesterol and neurological problems, makes me want to find a common explanation for these events.
My suspicion is that I have a rare, late-onset, moderate-severity genetic defect in synthesizing something that is not found in plants, rich in organ meats, and not found in any supplements I was taking as a vegan. So far my attempts to find a genetic defect in cholesterol synthesis have not been borne out, so my next suspicions are in candidates that would indirectly compromise my synthesis of cholesterol (for example, a problem synthesizing acetyl CoA, which is needed for cholesterol synthesis).
Although my symptoms in their current state are not debilitating and are barely even a nuisance, I am currently working with a neurologist to identify the exact nature of the issue and plan to work next with a geneticist who can help me investigate my hypotheses about my genetics. Of course I am open to discovering completely non-genetic causes for this and I will follow the data where it leads me.
Can Dr. Smith Diagnose Me Using Blog Posts?
Dr. Smith does not have access to any of my lab work or imaging, did not ask me any questions about my data or my case history, did not ask me any questions to clarify anything I’ve said, and did not contact me to tell me about his analysis. I do not believe it is possible for him to make reasonable conclusions without access to my data. Below, I will provide what I consider data that refutes his hypothesis.
Do I Have Vitamin A Toxicity?
The probability of vitamin A toxicity can be assessed using both blood work and data about vitamin A intake.
A meta-analysis of 259 case reports found that the following serum markers were most commonly elevated: retinol in 89% of cases, γ-glutamyltranspeptidase in 83%, lipids in 80%, triglycerides in 75%, alkaline phosphatase in 67%, prothrombin time in 53%, cholesterol in 50%, aspartate aminotransferase in 49%, bilirubin in 48%, and calcium in 46%.
I had my serum retinol checked prior to going on terbinafine precisely because I had a fungal infection and a history of health problems that seem to resolve when my vitamin A intake is high, and because vitamin A deficiency can cause vulnerability to fungal infections. My serum retinol was 45 in a range of 38-98, which is only 12% of the way into the normal range. The bottom of the range is approximately 1.4 mcmol/L or 39.5 mcg/dL, which is the level that rules out 95% of visual defects due to vitamin A deficiency. This is the marker that is most commonly elevated above the top of the reference range in vitamin A toxicity, but was near the bottom of the reference range, only slightly above the level that guarantees freedom from an important clinical sign of deficiency.
My recent data indicate that my triglycerides (88 in a range of <150), alkaline phosphatase (84 in a range of 40-115), bilirubin (0.8 in a range of 0.2-1.2), cholesterol (142 in a range of <200), aspartate aminotransferase (25 in a range of 10-40) and calcium (9.4 in a range of 8.6-10.3) are all in range.
I don’t have a prothrombin time measurement, but this is elevated when blood clotting becomes defective, and I have no indication of excess bleeding.
I don’t have γ-glutamyltranspeptidase, but since it’s not a specific marker of vitamin A toxicity, it’s unlikely that the absence of one marker would reveal a problem contradicted by seven other markers.
Vitamin A Intake
According to the above-cited meta-analysis, the main risk factor for vitamin A toxicity arise 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.
I do eat animal products that are rich in vitamin A, but I rarely exceed one or two servings of liver per week. At the time of the fungal infection that preceded the onset of my symptoms, I was eating some liver but was not supplementing with vitamin A. When I went on the terbinafine, I tried some B vitamins that made the fungal infection much worse, so I became paranoid of taking any supplements.
There’s no way that during this time I was exceeding an average of 10,000 IU of vitamin A per day.
The terbinafine helped roll back the fungal infection, but it lingered. After I was off the terbinafine and most of the neurological problems had subsided, I tried experimenting with ways to clear up the fungal infection for good. I found that supplementing with 10,000 IU of vitamin A per day, a half a shot of vodka per day (which I suspect enhances the conversion of retinol to retinoic acid by increasing expression of alcohol and aldehyde dehydrogenases), and regular use of a mixed UVA/UVB tanning bed did the trick and completely cleared up my skin.
Currently, I do eat meat, eggs, and either take some liver capsules or eat ground beef mixed with liver, but my liver consumption does not exceed an average of 4-8 ounces per week, capsules and food combined. I don’t take vitamin A on top of this unless I feel like I might be getting sick.
My lab data, vitamin A intake, and case history all contradict the idea that I have vitamin A toxicity, or that vitamin A toxicity caused any of my neurological issues.
I’m certainly open to changing my mind, but I’m more interested in following what the data best indicate rather than falling into a “pro-” or “anti-” vitamin A school of thought.
My Alcohol Use
Smith opens by suggesting I drink alcohol in a way that negatively impacts my health:
In this article, I will lay out the science that shows that Chris has a severe and worsening chronic Vitamin A toxicity problem, severe B-vitamin (particularly thiamine) deficiency problems, and that both of those issues are being exacerbated by continued alcohol consumption.
I'm not going to re-post any of the post's associated pictures, as I think the words above are enough. I did note that in two of the three associated pictures he posted he was holding a beer, and in this post he talks about four drinks in one night while the picture is of yet another beer.
While it’s true that I occasionally will drink four drinks in one night, I keep myself to an average of four drinks per week. If I have four drinks one night, I’ll abstain for a week.
People who drink occasionally or an average of up to two drinks per day have the lowest total mortality. Those who drink an average of two drinks per day have the lowest risk of developing type 2 diabetes. Those who drink an average of one or two drinks a day have the lowest risk of colorectal cancer. Those who drink an average of one drink per day have the lowest risk of stroke. Those who drink an average of between ¼ a drink per day and two drinks per day have the lowest risk of cardiovascular disease.
I don’t think we can assume that these associations represent causal relationships. However, I find it plausible that low doses of ethanol have a hormetic effect, which means it is bad in high doses but a little bit can be good for you. From my personal experimentation, I believe I do best when I have an average of a half a drink per day, which is 3-4 drinks per week.
It’s clear that ethanol is a toxin, that it can destroy the liver at high enough doses, and that alcoholics suffer from all kinds of health problems. Ethanol interferes with vitamin A’s function, and inhibits the absorption, activation, and/or storage of not just thiamin, as Smith notes, but of virtually every B vitamin. However, it’s entirely possible that small amounts of ethanol are beneficial. For example, one of the reasons ethanol hurts vitamin A function is that ethanol is metabolized by some of the same enzymes that activate vitamin A, which means that ethanol competes with vitamin A for use of those enzymes and inhibits its activation. But ethanol also causes us to make more of these enzymes so that we can metabolize it. It’s quite possible that small intermittent doses of ethanol could enhance vitamin A activation by increasing the activity of the enzymes that activate it.
Regardless, I don’t think it makes sense to generalize from the harms of alcohol abuse to light drinking.
Do I Believe Food Can Cause Vitamin A Toxicity?
Smith goes on to suggest that I don’t believe that vitamin A from food can be toxic:
Chris Masterjohn is well-known in nutritional circles as being a superfan of the Weston A. Price Foundation's (WAPF) general dietary guidelines of consuming MASSIVE amounts of Vitamin A from foods (liver, eggs, dairy, cod liver oil, squashes, etc.) and incorrectly believing that food-based Vitamin A is somehow magickally, completely, and utterly non-toxic. How wrong they are, and their followers (who often become my clients trying to fix the damage) and their children pay the price for it.
Actually, my guide to managing nutritional status has a section on vitamin A toxicity, I have videos on my site about how to know if you have vitamin A toxicity and what to do about it, and the vitamin A lesson of Vitamins and Minerals 101 also has a section on vitamin A toxicity. I do not say anywhere that food vitamin A is exempt, and I routinely recommend a default of limiting liver to no more than eight ounces per week, partly on the basis of avoiding too much vitamin A.
Smith cites articles I wrote for the Weston A. Price Foundation as early as 2004, and of course my views have evolved since then. However, even at that time, Sally Fallon came to me of the persuasion that food vitamin A was not a problem while synthetic vitamin A was, and when she asked me to write articles on the topic, I did enormous amounts of research and wrote articles that nowhere supported that distinction. I instead argued what I saw in the literature, that vitamin D strongly protects against vitamin A toxicity, and that balance between nutrients was at least as important as the absolute amounts of the nutrients.
Can You Become Deficient in Vitamin A in One Month?
Smith goes on to argue that my belief one can become vitamin A deficient in a month is impossible:
Who can forget the article & video he did about how he somehow got ‘Vitamin A deficient' in less than one month, which is IMPOSSIBLE for anyone to do! How do I know this? First, with his assumed/implied Vitamin A-heavy diet, he is nowhere near deficient in Vitamin A. Vitamin A is fat-soluble, which means it is stored in the liver and all over the body. Medscape says: ‘An adult liver can store up to a year's reserve of vitamin A.' He absolutely did not ‘get deficient' in one month of eating a ‘low-Vitamin A' diet, certainly not when he regularly eats as many Vitamin A foods as he does! What likely happened is that his body started DETOXING/DUMPING that poison, causing him detoxification symptoms, because it FINALLY had the opportunity to do so!
The fact that the liver can hold a year’s worth of vitamin A does not mean that everyone’s liver at every moment is holding that much.
In fact, the RDA for vitamin A is explicitly based on providing enough vitamin A for liver stores to last for only four months, and the amount of vitamin A stored in the livers of Americans and Canadians varies 140-fold.
People with clinical vitamin A deficiency typically have liver stores of 10 micrograms per gram (mcg/g) or less, while 20 mcg/g provides a margin of safety.
More recent research suggests that the biochemical signs of vitamin A deficiency stop around 28.6 mcg/g, which is almost 50% higher than what the RDA shoots for, suggesting that the optimal intake of vitamin A might be closer to 5000 IU per day.
Current research also suggests the risk of hypervitaminosis occurs at liver stores that are ten times this, while outright toxicity occurs at liver stores that are 100 times this.
The window between the liver stores associated with freedom from deficiency and the liver stores associated with hypervitaminosis and toxicity is very large. While someone who gets the RDA for vitamin A should have a four-month reserve before hitting clinical deficiency signs or symptoms, people who currently have these signs and symptoms do not have any reserve at all. They are already in the range of liver stores (10 mcg/g or less) associated with clinical deficiency.
I have no idea what my liver stores are. Further, I do not know what my rate of vitamin A utilization is. The RDA assumes that you eliminate 0.05% of your liver stores per day, but for all I know I use up vitamin A at a faster rate. If that’s true, I would have deficient liver stores even getting more than the RDA, and I could easily slip into the range of clinical deficiency within a month.
Is My Fructose Malabsorption Caused by Vitamin A?
Smith cites something I apparently wrote that he doesn’t link to about “not being able to absorb fructose well.” I searched my site and can’t figure out where that quote is coming from. If it is a direct quote from me, I was simplifying.
Smith suggests my issue with fructose is because of vitamin A toxicity:
Note the part about “not being able to metabolize fructose well.” Research has shown in rats that Vitamin A toxicity slows down a key enzyme directly involved in FRUCTOSE metabolism: Early effects of hypervitaminosis A on gluconeogenic activity and amino acid metabolizing enzymes of rat liver.
This study has nothing to do with my issue.
I have testing showing that I don’t absorb fructose well in my intestines. I don’t have any data suggesting that I have trouble allowing it to enter the glycolytic pathway.
Smith cites a study where 70,000 IU was given daily to rats weighing 70-90 grams, which is the bodyweight-adjusted equivalent of me consuming the absurd amount of 58,210,988 IU per day, something I’ve never even remotely approached.
The activity of phosphofructokinase-1 and pyruvate kinase were decreased. Phosphofructokinase-1 is an important enyzme that allows glucose to be used for energy. Fructose skips this enzyme when it enters glycolysis. Pyruvate kinase is important for the final burning of glucose and fructose for energy. There is nothing specifically impacting fructose about this effect.
And, again, my problem is intestinal fructose absorption, which does not necessarily have anything at all to do with glycolysis.
Do I Have Skeletal Deformations?
Smith suggests that my gait abnormality — which quickly disappeared in response to B vitamins the second and third time it happened, and which was never provoked by a change in vitamin A intake — is from vitamin A toxicity.
In support, he cites a study in cats where toxic levels of vitamin A caused extensive bone spurs in the cervical spine and an abnormal hindquarter gait. He also cites a study in pigs, where joint deformities are the cause of the gait abnormality.
To my knowledge, I do not have bone spurs in my cervical spine or joint deformities causing a gait issue.
Did Terbinafine Damage My Liver?
Terbinafine is an anti-fungal medication that has a known reputation for being very hepatotoxic (toxic to the liver). The liver happens to be the main location of both Vitamin A storage and detoxification. Damage that, damage everything.”
Here is my article about other antifungal medications that are known to inhibit the breakdown/detoxification of Vitamin A, eventually leading to chronic Vitamin A toxicity.
While terbinafine can damage the liver, I had my “liver enzymes” tested while I was on it. ALT and AST were both 22, which is right in the middle of the range. Right up until this summer, at my most recent test, my “liver enyzmes” have remained middle of the range.
I agree with Smith that liver damage will make vitamin A more toxic, because it can cause fibrosis, which requires vitamin A-storing cells to convert to cells that lay down scar tissue, causing the liver to lose its vitamin A-storing capacity. It’s unlikely I had this level of liver damage if my liver enzymes never budged.
Can We Make Inferences About Vitamin A From Accutane?
Smith goes on to equate Accutane with vitamin A, in order to invoke an Accutane/terbinafine drug interaction:
13-cis retinoic is also sold to people in pharmaceutical pill form. It's called isotretinoin, or more familiarly, ACCUTANE. There is NO difference between the 13-cis retinoic acid that you take in an ACCUTANE pill and the 13-cis retinoic acid that your body turns carotenoids and retinoids into in your body. If you choose to argue, please take that to the chemists and biochemists who know much more about these things than internet armchair “Appeal to Nature” fallacy warriors, OK? They will tell you that there is NO difference. They cannot tell the difference between “natural” 13-cis retinoic acid and “synthetic” 13-cis retinoic acid in any bodily fluid. Therefore, they are the SAME.
While some vitamin A is converted to 13-cis retinoic acid in the body, most of it is converted to all-trans retinoic acid. There are very good reasons to consider Accutane and vitamin A antagonists.
13-cis-retinoic acid interacts with the genome in a completely different and far less regulated way than all-trans retinoic acid. In a mouse model of emphysema, vitamin A is protective while 13-cis-retinoic acid is not. 13-cis-retinoic acid accumulates in the eyes of rats and interferes with vitamin A recycling; in fact, rats taking it took fifty times longer to recover from exposure to intense light than rats that did not take it. This is a sign of functional vitamin A deficiency.
This antagonism is also supported in human case reports. Accutane caused night blindness in a child with cystic fibrosis, and vitamin A supplementation resolved it. Two patients developed depression on Accutane; going off the drug and supplementing with 10-12,000 IU of vitamin A for seven to ten days resolved it, and they were able to go back on the drug without it recurring.
It is not an “armchair ‘Appeal to Nature’ fallacy to distinguish between Accutane and vitamin A. It is simply a requirement of scientific precision and logic to make this distinction.
He goes on to cite a drugbank.ca entry stating that terbinafine and isotretinoin (Accutane) can interact to produce “myopathy, rhabdomyolysis, and myoglobinuria.”
I don’t believe I have ever had myoglobinuria, as this would discolor my urine and I would see it. My neurologist has ordered blood tests that would reveal a myopathy and they are pending. In a case report of a terbinafine-isotretinoin interaction involved leukopenia, thrombocytopenia, and an EMG characteristic of myopathy. I don’t have leukopenia or thrombocytopenia, and my EMG was completely normal.
It’s an incredible stretch to generalize from isotretinoin (Accutane) to vitamin A from liver or butternut squash, and there’s nothing about my case that stands out as remarkably similar to isotretinoin-terbinafine interactions.
Is My Eczema Caused by Vitamin A Toxicity?
I agree with Smith that skin problems can be a sign of vitamin A toxicity. However, my eczema seems like it probably has a fungal basis, my vitamin A was at very low levels when the fungal infection was at its worst, and adding vitamin A was one of the most important things I did to clear my skin up in the post-terbinafine phase.
Did Tanning Deplete my Thiamin?
Smith then argues that tanning may have precipitated my gait abnormality by destroying thiamin.
Well, I have no disagreement here, but I don’t see why Smith is so focused on thiamin. UV light destroys many nutrients, including vitamin A, and including riboflavin, folate, and B12. It also causes DNA damage that increases the turnover of niacin.
One of my key hypotheses when the gait abnormality crept up this last time was that tanning was destroying B vitamins. So I started supplementing with all the B vitamins, including 100 mg/d of thiamin, and boom. Gone. While it sometimes seems there are traces remaining, by the time I went into the neurologist, she could not observe the gait abnormality when she asked me to walk.
Do I Have a Financial Interest Blinding Me to Vitamin A Toxicity?
Smith suggests my financial interest is blinding me to my vitamin A toxicity:
It should also be known that on his website he promotes discounts–and thus likely has financial arrangements with–at least two companies that sell organ meats in various forms. Why is this important? The old saying, ‘It is difficult to get a man to understand something, when his salary depends upon his not understanding it!' applies here.
Most of my revenue comes from sales of my cheat sheet, memberships in my Masterpass, and consultations. It’s true that I earn commissions from two companies that sell organ meats, but this is an exceedingly small proportion of my revenue. Year to date that has generated $2,720.76, which is a very small part of what I need to pay for my business expenses. Further, I actually give away these commissions to my members! This removes the incentive to sell a specific product and creates an incentive to deliver great content and deals to my members.
Sure, I make some money here, but not enough to blind me to vitamin A toxicity as the root cause of a neurological problem. I’d gladly give up $3K for the sake of my neurological health.
I find it deeply ironic that Smith draws attention to my finances and then concludes with this:
If you like what you see, know that I take private clients from around the world for “Nutritional Restoration” based on testing, not guessing. I also have a private network at https://nutrition-restored.mn.co where my “Vitamin A, Aldehydes, and Glyphosate Detox” Program can be purchased for the do-it-yourself-ers.
Interested in my comprehensive Poison/”Vitamin A” Detox program? Contact Us
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Smith and I both need to make money, but my revenue is not directly tied to my position on vitamin A in the way it would be if I were selling programs specifically about vitamin A or consultations specifically about correcting vitamin A-related problems.
I have no doubt that Smith offers these programs because he genuinely believes in their efficacy, but with financial interests that are directly rooted in vitamin A-related programs and guides, and an analysis of my health problem that literally leads directly into a sales pitch for his program, I don’t think it is fair to suggest that my own views are being shaped by my financial interests.
Looking for the Root Cause
Smith quotes me as saying, “The last bout of twitching is highly effectively managed with strategies targeting acid-base balance and glutamate (currently emphasizing beta-alanine and B6).”
Then he retorts:
“Managing” symptoms is not what I do. I am after the ROOT CAUSE.
Me too! That’s why I’m investigating what this actually is.
Which is more likely to turn up the root cause?
Seeing a neurologist with expertise in distinguishing between different neuromuscular disorders that may present similarly but have different root causes?
Or just assuming that all health problems of any sort are driven by vitamin A toxicity?
I’m inclined to think precisely identifying what is going on, and then doing additional work to investigate all the possible root causes, is the approach that will lead me to the root cause.
Smith is willing to jump to a conclusion of vitamin A toxicity without having access to my data or needing to discuss my case with me at all. I can’t imagine that’s an effective way to get to the root cause of anyone’s case.