Dr. Chris Masterjohn talks about What to Do About Why You Should Manage Your Thiamin Status and How to Do It

Why You Should Manage Your Thiamin Status and How to Do It

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Dr. Chris Masterjohn talks about What to Do About Why You Should Manage Your Thiamin Status and How to Do It

Thiamin, or vitamin B1, is central to both energy metabolism and antioxidant defense. While its deficiency causes many problems, out of all the B vitamins its deficiency is most neurological in nature, because energy metabolism of the brain becomes severely compromised, and because neurotransmitters derived from protein cannot be produced. In its most severe form, beriberi, it can cause loss of muscle control, twitching, muscles freezing into awkward positions, and seizures.

Carbohydrates require twice as much thiamin as fat. This means, on the one hand, that high-carbohydrate diets increase the need for thiamin, and on the other hand, that people who are deficient in thiamin may have neurological symptoms that resolve when they go on a low-carbohydrate, high-fat diet.

Thiamin is widely distributed in foods. Historically, diets high in refined grain produced beriberi, but now refined grains are enriched in thiamin, so its deficiency is rarely caused by diet. However, certain foods such as raw fish and moths that are eaten in some cultures contain thiamin antagonists, gastrointestinal microbes can degrade thiamin, and there are various environmental causes of thiamin deficiency, such the algae that grow in dead zones. As such, environmental exposure to thiamin antagonists may be a more common cause of thiamin deficiency than poor dietary intake.

Still, some foods are much higher in thiamin than most others, with whole grains, legumes, yeast, and red meat being among the best sources.


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Ways You Can Use the Podcast Notes

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Thiamin Status Show Notes

00:58 Cliff Notes

12:58 Thiamin is centrally involved in energy metabolism and is required to metabolize fat, protein, and especially carbohydrate.

13:57 Thiamin is critical to the pentose phosphate pathway, which supports antioxidant status, detoxification, the recycling of vitamin K and folate, and the synthesis of fatty acids, cholesterol, neurotransmitters, and nucleotides.

15:04 Clinical thiamin deficiency syndromes: beriberi, Wernicke’s encephalopathy, and Korsakoff’s psychosis.

17:55 Signs and symptoms of moderate thiamin deficiency: poor glucose tolerance, poor antioxidant status, poor vitamin K or folate status, feeling better on a low-carb diet.

18:34 Dietary causes of thiamin deficiency; food sources of thiamin are meat, legumes, whole grains, and enriched, fortified grains.

21:49 Other causes of thiamin deficiency: persistent vomiting, alcoholism, GI diseases that cause malabsorption, liver diseases, HIV/AIDS, and diabetes.

24:31 Thiamin antagonists can occur in raw fish and shellfish, seasonally in ferns, and in the larvae of the African silkworm Anaphe venata.

27:14 Sulfite destroys thiamin in vitro; the metabolism of sulfur amino acids, found primarily in animal protein, generates sulfite; molybdenum is required to detoxify sulfite.

29:23 Thiamin-destroying bacteria and fungi have been found in the human gut; infections and indoor toxic molds may cause thiamin antagonism.

30:30 Markers of thiamin status: whole blood thiamin pyrophosphate, erythrocyte transketolase activity.

34:32 Thiamin’s role in energy metabolism: pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, and branched-chain alpha-keto acid dehydrogenase.

37:27 Other functional markers of thiamin deficiency: elevated alpha-ketoglutarate, alanine, lactate, and possibly pyruvate on the Genova ION Profile with 40 amino acids or some other combination of plasma amino acids and urine organic acids.

40:55 Keep in mind that all of the thiamin-dependent enzymes in energy metabolism also require lipoic acid.

41:55 How to address thiamin deficiency: fix the dietary pattern, consider supplementation (thiamin hydrochloride, benfotiamine, or thiamin pyrophosphate), and address any relevant medical conditions.

Lab Tests Related to Thiamin Status

Whole blood thiamin pyrophosphate (LabCorp) and erythrocyte transketolase activity (available from HDRI as “ETKA” on their requisition form) are low in thiamin deficiency.

On the Genova ION Profile + 40 amino acids or an equivalent combination of plasma amino acids and urine organic acids, alanine, alpha-ketoglutarate, lactate, and possibly pyruvate are elevated in thiamin deficiency.

Links and Research Related to Thiamin

Institute of Medicine (US) Panel on Micronutrients. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. 2001.

The “Thiamin” chapter of Ross, Modern Nutrition in Health and Disease. 2012.

McCarrison. Studies in Deficiency Disease. 1921.

Higdon, Linus Pauling Micronutrient Information Center. Thiamin. 2013.

Alaei Shahmiri. High-dose thiamine supplementation improves glucose tolerance in hyperglycemic individuals: a randomized, double-blind cross-over trial. 2013.

Hoyt. Optic neuropathy in ketogenic diet. 1979.

Balk. Wild birds of declining European species are dying from a thiamine deficiency syndrome. 2009.

Evans. Thiaminases and their effects on animals. 1975.

Kreinbring. Structure of a eukaryotic thiaminase I. 2014.

Ayoade. Seasonal ataxia: A case report of a disappearing disease. 2014.

Riley. Increasing thiamine concentrations in lake trout eggs from Lakes Huron and Michigan coincide with low alewife abundance. 2011.

Lepak. Clupeid response to stressors: the influence of environmental factors on thiaminase expression. 2013.

Zhu. Pharmacokinetics of the transdermal delivery of benfotiamine. 2016.

Park. Comparative Pharmacokinetic Analysis of Thiamine and Its Phosphorylated Metabolites Administered as Multivitamin Preparations. 2016.

Jayaprakash. Wernicke's Encephalopathy – ‘Pushing the Envelope' of Patient's Profile: A Case Report. 2016.

Thomson. The evolution and treatment of Korsakoff's syndrome: out of sight, out of mind? 2012.

Nishimoto. High-dose Parenteral Thiamine in Treatment of Wernicke's Encephalopathy: Case Series and Review of the Literature. 2017.

Other Posts About Thiamin

Masterclass With Masterjohn: Pyruvate Dehydrogenase: Why Carbs Leave Your Thiamin Working Overtime

Masterclass With Masterjohn: Thiamin, Carbs, Ketogenic Diets, and Microbes

Masterclass With Masterjohn: Pyruvate Dehydrogenase: The Pentose Phosphate Pathway: The Many Essential Roles of Glucose

Masterclass With Masterjohn: How to Interpret Urinary Tests of TCA Cycle Intermediates

Search the site for thiamin for even more results.

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Testing Nutritional Status: The Ultimate Cheat Sheet

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6 Comments

  1. Maybe the wrong thread but it’s the closest one I could find…

    Many neurologists are recommending 400 mg of B2 along with magnesium for neurological conditions. Dr. Weil recommends something like 40 or 50 mg and the RDA says something like 1.5 mg per day. If one subscribes to your philosophy of getting B vitamins (and especially B vitamins) from a whole food source, is there any other way that you could recommend upping the B2 intake, i.e. any other food source you could recommend with high bioavailabilty? Or do you think this situation is similar to the CoQ10 story that you so eloquently tell… where most of it in endogenously produced. Would love any thoughts.

    P.S. You’re beyond amazing!

  2. C. Weber in his book “Potassium Nutrition” (2011) stresses a relationship between potassium status and thiamine: specifically he stresses that someone with a (chronic?) potassium deficiency will develop heart disease in the presence of adequate thiamine. (I’m not sure, but it seems that he also believes that too much thiamine (as in the case of mega-dosing B-1, typically of most vitamin B supplement) in the case of deficient potassium is problematic, although I can’t find his references for that at the moment).
    He also stresses that if someone has what he calls “wet” heart disease associated with the thiamine deficiency (beri-beri), that potassium supplementation will “dangerously aggravate” the condition. He claims that this “wet” heart disease due to vitamin B-1 deficiency is impossible if potassium is deficient.
    Given the above, it would seem very important, esp. if one has a diagnosed heart condition, but perhaps even if not, to determine both potassium and thiamine status, and even more so if one is considering supplementing either of the above.
    Would you please comment on your understanding of this matter, esp. in light of the potentially vast under-diagnosis of vitamin B-1 deficiencies? Does Weber have it right (or have I misunderstood him)?
    Thank you!

  3. Is there enough thiamine in red meat for people who only eat meat as their diet? Curious why the “carnivore” group doesn’t report symptoms of this deficiency. Does it just take time for the deficiency to appear? (like B12 in vegans).

  4. Hey Chris,

    Great info, as always!

    Please consider doing a podcast on A66G, G1958A, MAOA, MAOB, BCO1, PEMT, and FADS1. Thank you!

  5. As always, fascinating stuff!
    Any idea of what is the prevalence of thiamin deficiency in the US and the world?
    Are there stats on how many people get the emergency transfusions of thiamin?

    In the end, how worried or not should we be?

    1. since i used to drink alcohol, now have insulin reistance and have a family history of parkinson’s i’m personally very concerned about my levels.

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