Six capsules of a beet compound a day for eight weeks: two of six blood markers moved, and nobody can yet say what that means

Betaine is a small molecule the body makes from choline and also takes in from food; beets, spinach, wheat bran and wheat germ are rich in it. As a supplement it has a following in gyms and, lately, among people interested in ageing. Much of the excitement rests on laboratory work: liver cells that grew more mitochondria when bathed in betaine, gut cells that made fewer damaging oxygen by-products, rats whose antioxidant enzymes went up. Whether any of this happens in a person who swallows capsules has barely been tested. Researchers at Poznań University of Life Sciences set out to look.

Their trial, published online in the European Journal of Nutrition on 7 October 2026, recruited women aged 18 to 45 in Poznań with a body mass index of 25 or more and a waist over 80 cm, who were not dieting and had not taken betaine in the previous three months. Fifty-three were randomly assigned to 3 g of betaine a day or to rice flour, as six identical white capsules, three in the morning and three in the evening, for eight weeks. Neither the women nor the researchers knew who had which until the study was over. Blood was drawn after an overnight fast at the start and the end. In it the team measured two mitochondrial enzymes inside white blood cells, citrate synthase and cytochrome c oxidase, and four markers of antioxidant defence in plasma.

Forty-two women finished and were analysed, 19 on betaine and 23 on placebo. The clearest result was catalase, an enzyme that breaks hydrogen peroxide down into water and oxygen. Its activity rose from 43.1 to 53.8 units per litre in the betaine group and slipped from 51.2 to 47.5 on placebo, a difference between the groups that was statistically solid. Citrate synthase, often read as a rough gauge of how much mitochondrial machinery a cell holds, went from 196 to 272 in the betaine group and from 248 to 222 on placebo. The gap between those two changes just passed the usual test, but the rise in the betaine group alone did not, and the women's values were scattered very widely. The other four measures, cytochrome c oxidase, superoxide dismutase, glutathione peroxidase and oxidised glutathione, did not differ between the groups.

So what does a woman taking betaine gain? On this evidence nobody knows, and the paper doesn't pretend otherwise. It didn't measure how well the mitochondria worked, how much oxidative damage was going on, or anything a person could feel. The cells studied were white blood cells, which may not behave like muscle or liver. The authors write that their findings cannot establish an increase in mitochondrial content, and that a rise in catalase doesn't show hydrogen peroxide was being cleared any faster. A few more things are worth keeping in mind. The catalase reading in the betaine group started lower than the placebo group's and ended close to where placebo began, a pattern that chance differences at the start can produce by themselves (that reading is ours, not the paper's). This was a secondary analysis of blood stored from a larger project, 11 of the 53 women dropped out, and six outcomes were tested with no correction described for testing several at once. The women's weight and body fat were measured at every visit, but this paper doesn't report how they changed. The work was paid for by Poland's National Science Centre and the authors declare no conflict of interest. It is a careful first look in people, and it found less than the cell studies had promised.