In the 1870s, an epidemic struck Indonesia. The disease was familiar to people in east Asia; Indonesians knew it as beriberi, from the word “beri” which means “weak,” and it had been an occasional problem in the region for thousands of years. But suddenly it became one of the most common diseases in east Asia. It started with the weakness and fatigue that gave the disease its name, but patients also grew restless and irritable. Their stomachs hurt, and they didn’t want to eat. Then their limbs began to tingle and burn, or sometimes went numb. For many patients, the ordeal ended in heart failure. During autopsies, doctors noticed degeneration of the nerves and the muscle of the heart. And in some Indonesian towns, as many as half the infants in the community died this way, along with frightening numbers of adults.
Indonesia was a Dutch colony at the time, and the beriberi epidemic worried colonial officials so much that the Dutch Army set up a research institute in Batavia, on the island of Java, to find out what was causing the epidemic and how to fight it. And in 1886, they sent a young Dutch Army surgeon named Christiaan Eijkman. Eijkman, born on August 11, 1858, had joined the Army on the promise that they would pay his way to medical school in return for a few years’ service as an Army doctor in the East Indies (the Dutch colonies which included Java), but debilitating malaria symptoms had forced his return to Europe after the first two years. When he returned to Java in 1886, Eijkman was fresh from two years of study under bacteriologist Robert Koch, who had discovered the bacterium that causes tuberculosis. Eijkman had been fascinated by the idea of finding the microbes that caused human illness, and it was that prospect that drew him back to Java, despite his lingering malaria and the painfully recent loss of his wife earlier that year. (Batavia turned out to be a positive move for Eijkman, who remarried in 1888, around the same time he became director of the research institute there.)
Eijkman thought he was on the right track when he arrived in Batavia. His predecessors at the research institute had found microbes in the bodies of dead beriberi victims, which they and Eijkman thought might be the culprit behind the epidemic. Monkeys and rabbits injected with the microbes didn’t seem to get sick, but Eijkman thought the disease might just take a long to incubate in mammals — so rather than keep waiting, he bought a bunch of chickens. He injected some of them with the microbes, leaving the others as a control group, but within a month, all of his chickens were sick (in chickens, beriberi shows up as leg paralysis). The infected chickens must have passed the disease to the control chickens, Eijkman reasoned, and it had spread through his flocks like wildfire. So he did what any rational person would do — he bought a bunch more chickens.
He kept the new chickens more isolated, but they still got sick — and then they all got well again, for no apparent reason. Fortunately for a lot of future beriberi patients, Eijkman had enough sense to talk to the guy who fed his chickens. It turned out that around the time the first batch started getting sick, he’d been feeding them cooked white rice (which had been polished to remove the brown husk from the grains) left over from the nearby hospital. Shortly before the second batch of birds mysteriously recovered, the supply of hostpital leftovers had run out, and Eijkman’s chickens went back to a diet of uncooked brown rice. Eijkman put two and two together and realized that the only solution was to do more science.
He split them into four groups for a five-week experiment, and the results pointed a finger firmly at white rice. In one group, a sick chicken and two healthy chickens ate brown rice for five weeks, and by the end of the experiment, all three chickens were fine. Another pair of healthy chickens at brown rice for five weeks and stayed healthy; two more healthy chickens, injected with the bacteria from the dead beriberi patients, also stayed healthy on a diet of brown rice. But four healthy chickens who ate white rice for five weeks all got sick; when Eijkman switched their diet to brown rice, they got better. Repeating the experiment with a fresh batch of chickens produced the same result. (In the midst of all this, Eijkman’s son Peter was born; as you might predict from his childhood, Peter also grew up to be a doctor.)
Still hoping to pin the epidemic on a pathogen, Eijkman speculated that perhaps the rice had grown some sort of microbe in storage, or else cooking fueled the growth or virulence of a microbe no one had seen yet. More trials ruled out both of those possibilities, though; cooking the rice wasn’t the problem. Cooked brown rice was perfectly safe. And in fact, polished rice served up with a side order of the recently-removed husks was also perfectly safe. Eijkman revised his hypothesis: clearly the rice grains’ husks contained an “anti-beriberi factor” that protected against whatever dangerous toxin or pathogen lurked in the grain itself. That helped explain the epidemic; polished white rice had become very popular in much of east Asia after the introduction of steam-driven machinery for polishing the grains, because people liked its taste better. In societies where many people at mostly rice, the result was disastrous.
By 1895, with the epidemic still raging, he realized it was time to see how all this played out in human patients, so he did another round of experiments, this time of the “wildly unethical by modern standards” variety. Specifically, he tested the effects of diet on inmates in Java’s prisons. As expected, prisoners who ate mostly polished white rice were more likely to develop beriberi.
But it was Eijkman’s successor, Gerrit Grins, who realized the problem wasn’t anything in the rice grains — it was simply that the body needed something that was in the husks, and without it, things started breaking down. That was a pretty novel idea in European circles at the time; people knew that it was important to get more or less the right balance of carbohydrates, fats, proteins, and salts, but no one had realized yet that other chemicals (which we now call vitamins) also played an important role in keeping the body healthy and functional. On the other hand, around the time Eijkman was on his way back to Java in 1886, a Japanese naval doctor named Takaki Kanehiro realized that sailors who got barley, vegetables, fish, and meat were less likely to suffer from beriberi — or kakke, as it was known in Japan — than those who ate mostly rice. He proved his point, and the Japanese Navy issued regulations for proper diets at sea — and the Emperor of Japan made Takaki a baron. Takaki didn’t share Eijkman’s 1929 Nobel Prize in Medicine, however, and neither did Grinjs nor the team that finally isolated the compound itself, now called thiamine or Vitamin B1, in 1926.
It turns out that the body needs to take in a certain amount of Vitamin B every day in order to help convert carbohydrates, fates, and proteins into glucose and to maintain the health of the skin, liver, and nervous system. Beans, brown rice, chickpeas, lentils, peas, and pork are all good sources of Vitamin B, and since the 1940s, regulations in many countries require products like white rice and white flour to be enriched with Vitamin B.