I came across this post, credit to William Wallace, PhD which got me thinking about Thiamine one of the many supplements people take without testing and the lack of meaningful testing:
Every molecule of glucose you eat has to pass through one enzyme to become ATP. That enzyme is pyruvate dehydrogenase. Its cofactor is thiamine.
Glycolysis breaks glucose down to pyruvate. That happens in the cytoplasm and doesn’t require thiamine. But pyruvate can’t enter the mitochondria as acetyl-CoA without PDH converting it, and PDH can’t function without thiamine pyrophosphate in its active site. If thiamine is missing, pyruvate gets shunted to lactate instead. The citric acid cycle starves. ATP production drops. Lactate accumulates.
This isn’t just a textbook pathway. Hanninen et al. measured thiamine status in 100 hospitalized heart failure patients and 50 controls. 33% of heart failure patients were thiamine deficient vs 12% of controls. A well-established driver: loop diuretics increase renal thiamine clearance. Nearly every heart failure patient is on one. Thiamine is water-soluble with total body stores of only 25-30 mg. Without daily replenishment, stores can be depleted in as little as 2-3 weeks.
This creates a plausible vicious cycle. Heart failure patients are put on furosemide. Furosemide depletes thiamine. Thiamine deficiency impairs cardiac energy metabolism. Cardiac function worsens. The diuretic dose goes up. More thiamine is lost. Supplementation trials have shown mixed results on ejection fraction, but the metabolic logic is sound and the deficiency is measurable.
Beyond heart failure: diabetes is independently associated with low thiamine status. Alcohol impairs thiamine absorption and increases excretion. Bariatric surgery reduces absorptive surface. High carbohydrate intake increases thiamine demand because carbohydrate metabolism is the pathway most dependent on it.
Thiamine status is not part of standard blood panels. If you’re on a loop diuretic, managing blood sugar, or recovering from surgery, it’s worth asking about.
Hanninen et al., J Am
Coll Cardiol, 2006.
The above which led to the discussion and a specific lab testing, which I’ll link here rather than give an interpretation.
What are your thoughts on Thiamine, it’s rank in your health concerns and the relevance to the lab test mentioned?
I am prediabetic. I therefore pay attention to my vit. B1 intake. I supplement with a general B vitamin pill 4 times a week, where the various B vitamins are at 125% RDA. However, separately, I also supplement 2 days a week with benfotiamine 300mg.
Thiamine and benfotiamine: Focus on their therapeutic potential
“Benfotiamine is more bioavailable and has higher tissue penetration than thiamine. Studies have shown its antioxidant and anti-inflammatory potential in activated immune and glial cells. It also improves complications observed in type 2 diabetes and has beneficial effects in mouse models of neurodegenerative disease. Benfotiamine represents an off-the-shelf agent used to support nerve health, promote healthy aging and support glucose metabolism.”
Effects of thiamine and benfotiamine on intracellular glucose metabolism and relevance in the prevention of diabetic complications
Thiamine is definitely one of those nutrients that seems overlooked until a deficiency develops. The connection between thiamine, mitochondrial energy production, and heart function is biologically plausible, especially in people using loop diuretics or managing conditions like diabetes. I think targeted testing makes more sense for higher-risk groups than routine supplementation for everyone. The challenge is that standard blood work often misses functional deficiencies, so choosing the right test and interpreting results in context is important.
The argument about the water soluble B vitamins is that excess is easily excreted. We know that is not the case for B6 and there are questions asked about some of the vitamers of B3, but B1 probably is in that category.
I am a fan of testing to know levels, but the standard tests I do give B9 and B12, but none of the other 6 B vitamins.
I am a vegetarian/pescatarian and do not supplement with Thiamine and other Bs and prefer plant-based food sources for that.
These foods are especially important if you eat less meat:
• Leafy greens (spinach, collards, turnip greens) — Excellent for folate (B9). Cooked spinach provides 39% DV per ½ cup.
• Legumes (peas, beans, lentils) — Provide B1, B2, B6, B9, and small amounts of B12 (in peas). Half‑cup peas provide 35% DV B1 and 25% DV B9.
• Whole grains (brown rice, barley, millet) — Good sources of B1, B2, B3, B5, B6. Processing removes B vitamins.
• Tofu — Provides B1, B2, B6, B9, and fortified versions may include B12. One cup of firm tofu gives 36% DV B1.
I eat all of the above foods so I shouldn’t be deficient I think. My B12 was measured last year and it was 1400, much higher than needed - at that time I supplemented B12 following an advice that all vegetarians should supplement it. IMO variety of plant-based diet is important. It should replace (hopefully) supplementing. I cook every day and eat close to 30 different veggies per day, many of which are raw. Do you think I could still be deficient?
A total of 17,310 Chinese adults were included. During a median 9.0 (interquartile range, 4.1–10.0) years of follow-up, 1324 (13.1%) death cases were observed. Overall, there was a J-shaped relationship of dietary thiamine intake with all-cause mortality. Compared with thiamine intake in quartile 2 to 3 (0.74–1.10 mg/day), the adjusted hazards ratio and 95% confidence interval (HR [95% CI]) for quartile 1 (<0.74 mg/day) and quartile 4 (≥1.10 mg/day) were 1.19 (1.00, 1.42) and 1.60 (1.33, 1.93), respectively. Similar results were found in the propensity score analysis. Moreover, the harmful effect of higher dietary thiamine intake (quartile 4 vs. quartile 2–3) on mortality was greater in non-smokers than in smokers (P for interaction <0.05).
Conclusions:
There was a J-shaped relationship of dietary thiamine intake with all-cause mortality in general Chinese adults, with a minimal risk at 0.74 to 1.10 mg/day. Our findings highlight the importance of maintaining appropriate dietary thiamine intake to promote population health.
I would still be careful with the B12. It won’t last a long time if you have stopped supplementing. B12 lies at the core of gene expression (along with B9).
I don’t know a lot about fish and B vitamins, however.
I don’t want to overdo B1 supplemenntation. Twice a week benfo is just making sure I top off and prevent any deficiency at a cellular level (given that my glucose handling, as a prediabetic, is suboptimal). Benfo metabolites can accumulate with steady high dose supplementation (thiamine diphosphate), I prefer not to.
Thiamine deficiency - symptomatic - is quite rare. Thiamine is added to all processed wheat products in the US and I think most processed rice. I thought it was all processed carbs but might be fair to say most.
It is not added to alcohol so we see it quite rarely in alcoholics. Sugar given in IVF to a drunk can precipitate acute issues causing encephalopathy. Which is why everyone is given thiamine when they have a history of alcohol abuse.
I’m guessing the pyruvate builds up in neurons without the thiamine to take care of it.
I’ve had ER docs tell me that thiamine induced encephalopathy doesn’t happen anymore.
Bariatric patients can get thiamine deficiency and I’ve seen the encephalopathy. They are typically given 50mg daily (rda is 1-2 mg) but get deficient if they don’t take and throw up a lot - ie take is very little calories.
There is an ongoing clinical trial in MCI with benfotiamine. Promising results from phase 2 trial with slowing of progression in MCI. Quite significant really - like 50%.
I haven’t found any data regarding problems with too much benfotiamine but I’m not saying it couldn’t be a problem. I take 300 mg a day. In the MCI trial, the dose was 600 mg a day. The intent was to drive levels high to force it across the BBB. Studies have been done up to 1200 mg per day.
My birth grandmother passed away in 1949 at age 39 from heart failure and the family lore is of the opinion that it was due to beriberi. A second cousin I met as an adult who was 10 years old at the time said she wasn’t allowed to eat with them because grandma was struggling to feed her family after being left alone to provide for 10 children. This cousin said the only food in the house was white rice. My mom was the last child born and was 2 months old when grandma died. It does seem to be a plausible cause of her death since fortification wasn’t robust across the US at that time. I’ve often wondered how much or little this may have impacted my mom since she was certainly malnourished for the first couple of months of her life. The lady I knew as grandma, who took my mom in and raised her, said she only weighed 8 pounds at 2 months old and the only food in the house when she was made aware of the situation was a little spoiled milk. I’m thankful my mom survived but it’s crazy to think this was possible in the US a mere 77 years ago.
Thank you for sharing that story of pain and courage. My grandparents had similar experiences.
In many ways, conditions have improved less for US children than many might believe. Given footnotes on methodology and assumptions, a best-case comparison in childhood food insecurity comparing 1945 to 2024 places the former at 24-28% of the childhood population and the latter at 14-17%. The current situation – which in my opinion should be unacceptable in the wealthiest nation – is almost entirely due to the extreme and still growing disparities in opportunity, income, and wealth.
I have not tested my thiamin BUT I did add benfotiamin to my stack to improve my glucose metabolism and the glucometer says it works well. I see the difference with and without it. I will stay on it but I do think I will add thiamin to my blood testing at least once a year. It was a GAMECHANGER for my glucose metabolism.