By Dr Conor Kerley, PhD, cardiovascular and nutrition researcher.
One of these two nutrients was found because a laboratory assistant tried to save money on chicken feed.
In 1890 the chickens in Christiaan Eijkman's laboratory in Batavia got sick. Eijkman was a Dutch physician who had been sent to Java four years earlier to find the germ responsible for beriberi, a disease that ran through the barracks and the prisons and the hospitals of the Dutch East Indies, and the assumption of the age was that it had to be an infection which somebody with a microscope would eventually catch. He was looking for a bacterium and he never found one. What he found instead was that his birds had developed a nerve disease that looked uncomfortably like the thing he was supposed to be studying in people, and then, some months later, that the birds recovered on their own. Diseases do not generally do that, so he went and asked the man who fed them what had changed.
The answer was rice. To save money the attendant had been taking boiled polished rice from the military hospital kitchen and giving it to the chickens, and when that arrangement stopped and the birds went back to their ordinary feed, the illness went with it. The variable was not a germ but a grain with its husk taken off [1].
Eijkman never quite believed his own answer, and thought for years that polished rice carried a toxin the husk neutralised rather than that the husk carried something the body needed. The clean confirmation came from a colleague. Between May and September 1896 Adolphe Vorderman surveyed a hundred prisons across Java and Madura and sorted them by the rice they served: where the inmates ate mostly unpolished rice, beriberi turned up in fewer than one man in ten thousand, and where they ate polished white rice it was one in thirty-nine [2]. The substance itself was not crystallised out of the husk until 1926, and in 1929 Eijkman shared a Nobel Prize for having been the first person to demonstrate experimentally that a disease could be caused by something absent from food [3].
The something was thiamine, which we now call vitamin B1.
Why the heart noticed
The part of that history I keep returning to is that beriberi does not present one way. It has a nerve form, which is what Eijkman saw in his birds, and it has a cardiac form, in which a severe shortage of the vitamin produces failing hearts in the young and otherwise well, and does so quickly.
That falls out of what thiamine does. Its active form is a required cofactor for three enzymes, two of which sit at the entrance to and inside the citric acid cycle, which is how your cells fully burn glucose into ATP, the currency every cell spends to do anything at all. Take thiamine away and the cycle cannot run to completion, so the fuel arrives and the machinery that unpacks it stalls. Every tissue depends on that, but heart muscle contracts continuously from before you are born until the day you die and leans harder on oxidative energy than almost anything else you own, with no reserve to coast on and no shift it can skip. When the supply chain breaks, the tissue with the highest standing demand is the one that shows it first, which is why a deficiency of something in a rice husk announces itself as a heart problem.
Thiamine contributes to the normal function of the heart [4]. Read with the biochemistry underneath it, that is not a soft sentence but a description of a requirement, and there are not many nutrients you can draw a line that direct between a molecule and an organ for.
Chromium
Chromium is where the writing gets shorter, and I would rather say so than pad it out. It is a trace mineral, needed in micrograms rather than milligrams, and it sits on the glucose side of the formula: chromium contributes to the maintenance of normal blood glucose levels [5].
The study everyone starts with is Richard Anderson and colleagues, published in Diabetes in 1997 [6]. It ran in Beijing, in a hundred and eighty people over four months, comparing chromium picolinate against a dummy pill. What they measured was HbA1c, the three-month average of blood sugar, reported as a percentage, which is the measure that counts in this field and the one the berberine trials use too. After four months the placebo group sat at 8.5%, and the chromium groups came in lower, with glucose and insulin measures moving the same way. On a measure where a single point is a substantial move rather than noise, that is the part that made people look twice.
I will not tell you the mechanism, because I would be improvising. The thiamine story above is unusual in how completely it closes, with the enzymes and the cycle and the organ and the history all locking together, and chromium does not close like that in anything I have on my desk.
Eijkman spent a decade hunting a germ that was not there while the answer sat in a bag of rice in the hospital kitchen. The husk had it, the polishing took it off, and the heart was the first place anyone noticed.
References
- Eijkman C. Antineuritic vitamin and beriberi. Nobel Lecture, 1929. NobelPrize.org.
- Vandenbroucke JP. Adolphe Vorderman's 1897 study on beriberi: an example of scrupulous efforts to avoid bias. Journal of the Royal Society of Medicine. 2013;106(4):142–146. PMID 23481433.
- The Nobel Prize in Physiology or Medicine 1929, awarded jointly to Christiaan Eijkman and Sir Frederick Gowland Hopkins. NobelPrize.org.
- EFSA NDA Panel. Scientific Opinion on the substantiation of health claims related to thiamine (claim ID 20, the normal function of the heart). EFSA Journal. 2009;7(9):1222.
- Commission Regulation (EU) No 432/2012 of 16 May 2012 establishing a list of permitted health claims made on foods. Official Journal of the European Union. L 136, 25.5.2012:1–40.
- Anderson RA, Cheng N, Bryden NA, et al. Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with type 2 diabetes. Diabetes. 1997;46(11):1786–1791. PMID 9356027.
Last reviewed: 10 September 2026. This article is educational and is not medical advice.
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