Vitamin B1 and insulin: the forgotten vitamin of glucose metabolism

Let's start with insulin

You eat, your digestion releases glucose among other things, and that glucose enters your bloodstream. Your pancreas detects this rise and secretes insulin, which then sends a message to various tissues: 'Energy is available.' In muscle and adipose tissue, insulin promotes the movement of transporters called GLUT4 toward the cell membrane, allowing glucose to enter the cell more easily.

But here is something fundamental: the story of glucose does not end at the cell's door. On the contrary, it almost begins there.

Imagine your cell as a factory

Insulin helps bring raw material into the factory — that raw material is, notably, glucose. But now this raw material must be processed, and to do so the cell has an entire chain of biochemical reactions at its disposal. Glucose is converted, among other things, into pyruvate.

And that pyruvate arrives at an absolutely critical crossroads: it can be used to fuel the mitochondria and contribute to energy production. But to cross that step efficiently, a critically important enzyme must be working — pyruvate dehydrogenase. And can you guess what this enzyme needs? Vitamin B1 — more precisely, it uses an active form of vitamin B1 called thiamine pyrophosphate (or thiamine diphosphate) as a cofactor. In other words, B1 helps the cell convert the product of glucose into fuel that the mitochondria can actually use.

And this is where the mitochondria come into play

You know I often talk about mitochondria. Why? Because they are, in a sense, the power plants of our cells. When metabolism is functioning properly, some of the carbon derived from glucose can enter the Krebs cycle and then feed the mitochondrial respiratory chain. And at the end of that chain, we produce ATP.

ATP is our cellular energy currency. Your brain needs it, your muscles need it, your heart needs it, your liver needs it — virtually every cell in your body needs it. Vitamin B1 therefore acts right at the heart of the transition from nutrient to cellular energy.

But B1 is involved at several points

And that is what makes this vitamin particularly interesting: it is not only required by pyruvate dehydrogenase. It also plays a role in the functioning of α-ketoglutarate dehydrogenase, an enzyme of the Krebs cycle, and is involved in another extremely important enzyme, transketolase.

Transketolase belongs to what is known as the pentose phosphate pathway. I will spare you the biochemistry lecture: simply remember that this pathway is involved, among other things, in managing glucose intermediates and in producing molecules important for the cell's antioxidant defenses, notably via NADPH. B1 therefore sits at a true crossroads: glucose → energy → mitochondria → cellular redox balance.

So what does this have to do with insulin resistance?

This is where we need to be precise. Vitamin B1 is not insulin, it does not replace insulin, and we do not currently have sufficient evidence to say: 'Take vitamin B1 and you will reverse your insulin resistance.' That would be scientifically false.

That said, B1 is necessary for normal glucose metabolism. This means that a cell lacking thiamine has poorer conditions for using energy substrates normally. Experimental studies do indeed show that thiamine deficiency disrupts glucose utilization and can also alter insulin secretion.

And here is something even more interesting

When we look at people with diabetes, we find a rather striking association. A systematic review and meta-analysis published in the journal Metabolism compared various thiamine markers in people with and without diabetes: overall, people with diabetes had lower concentrations of several circulating forms of thiamine. And the association appeared particularly strong in people who also had albuminuria — that is, kidney damage associated with diabetes.

But be careful: association does not mean causality. We cannot simply say 'they are lacking B1, therefore they developed diabetes.' It can also work the other way around: diabetes can alter the metabolism and elimination of thiamine, needs may differ, kidney function may play a role. Several mechanisms are probably at work simultaneously.

So does giving vitamin B1 improve blood sugar levels?

We have some interesting results. In a small double-blind randomized trial, people with hyperglycemia received 300 mg of thiamine per day for six weeks: blood glucose measured two hours after a glucose load decreased with thiamine. That is interesting.

But only twelve people completed the study. And above all, the study did not demonstrate any significant improvement in insulin levels or HOMA-IR with thiamine. It is therefore a signal — not sufficient evidence to recommend high doses of B1 as a treatment for prediabetes or diabetes.

And what is benfotiamine?

You may come across this name in dietary supplements. Benfotiamine is a thiamine derivative that has been extensively studied in the context of diabetes, notably because of interest in the possibility of increasing transketolase activity and redirecting certain glucose intermediates away from pathways that may contribute to the complications of hyperglycemia. This is biologically very interesting. But here again, an interesting biological mechanism does not automatically mean a demonstrated clinical benefit.

And as it happens, we now have a 2026 study

This is important, because I want to talk to you about the most recent data, not simply revisit old studies that tell us what we would like to hear. The BOND study, published in January 2026, followed people with type 2 diabetes and diabetic polyneuropathy for one year. Participants received either benfotiamine 300 mg twice daily or a placebo, and the researchers examined an extensive range of neurological parameters.

Benfotiamine did indeed raise the concentrations of various thiamine markers, but it did not produce any significant improvement in the primary neurological outcomes studied compared to placebo. And I find this study particularly interesting, because it reminds us of something fundamental in medicine: raising the level of a molecule in the blood does not necessarily mean improving a disease.

So why continue to take an interest in vitamin B1?

Because its physiological role is barely in doubt at all. We need thiamine to metabolise carbohydrates properly: it is an essential vitamin, and our body cannot produce enough of it on its own — so we must obtain it from our diet. And unlike a fat-soluble vitamin that can be stored in large amounts for a very long time, our thiamine reserves are relatively limited.

Who is particularly at risk of a B1 deficiency?

Certain situations should raise a flag: a very unbalanced or restrictive diet, chronic heavy alcohol consumption, certain digestive diseases with malabsorption, prolonged vomiting, certain bariatric surgeries, certain states of malnutrition, and probably certain situations of increased metabolic demand. Modern data show that thiamine deficiency still exists and may be underdiagnosed, including in developed countries.

And where do we find vitamin B1?

It is found notably in whole grains, legumes, seeds, nuts, pork, and various fortified foods. And this is once again a good example of something I often explain: our metabolism does not only need calories — it needs micronutrients to convert those calories into something usable. You can have an enormous amount of fuel; if certain essential engine parts are missing, the engine does not run normally.

Should you therefore take B1 if you are insulin resistant?

Not systematically, and that is probably the most important conclusion of this article. Today, the data do not justify considering thiamine as a stand-alone treatment for insulin resistance. If you are insulin-resistant, the interventions we need most remain physical activity, maintaining or increasing muscle mass, reducing sedentary behaviour, appropriate nutrition, sleep quality, reducing excess visceral fat when it is present, and, when necessary, appropriate medical treatments. Vitamin B1 replaces none of that.

But it teaches us something essential about metabolism

We tend to think: sugar → insulin → diabetes. The reality is infinitely more interesting. To have good metabolic health, glucose must enter cells properly, we must be sensitive to insulin, we must have sufficient muscle mass, but we must also be capable of efficiently converting nutrients inside the cells. And for that, we need enzymes, functional mitochondria, and micronutrients that serve as cofactors. Vitamin B1 is one of those fundamental cofactors.

I am Dr Florian Vallecillo. And if I were to leave you with one idea today, it would be this: to understand metabolism, do not look only at how much glucose is circulating in your blood or how much insulin your pancreas is producing. Ask yourself this too: what are your cells actually capable of doing with that energy?

It is precisely there that micronutrients such as vitamin B1 take on their full importance. Insulin helps glucose enter the cell; vitamin B1 helps the cell convert that fuel into energy. And that distinction, in my view, allows us to understand much more clearly what metabolic health truly is.