Vitamania excerpt: The discovery of beriberi.

It Took a Horrible Wasting Disease—and Lots and Lots of Chickens—for Scientists to Discover Vitamins

It Took a Horrible Wasting Disease—and Lots and Lots of Chickens—for Scientists to Discover Vitamins

Health and medicine explained.
March 6 2015 8:08 AM

The Man Who Discovered Thiamin

Today, we take vitamin B1 for granted. But it took a horrible, wasting disease—and lots and lots of chickens—for scientists to discover it.

A chicken who presumably consumes plenty of thiamin.

Photo courtesy feryswheel/Flickr

This essay is adapted from Vitamania: From Vitamania: Our Obsessive Quest for Nutritional Perfection by Catherine Price, published by Penguin Press.

In the mid-1800s, a strange sickness was devastating parts of Southeast Asia. Known as beriberi, it began with intense swelling of the legs and feet and a general sense of numbness, especially in the extremities. Victims developed a distinctive gait, lifting their knees high in the air and swinging their legs forward so that their drooping toes wouldn’t catch on the ground. Their urine became concentrated and their appetites waned, even as their bodies wasted away. Eventually, they lost their voices and died in suffocating convulsions. Its cause was a mystery; no one knew a prevention, let alone a cure.

Today, we know that beriberi is caused by a deficiency in a vitamin called thiamin, also known as B1, that’s found in foods including yeast, grains, nuts, and meat. Thanks to our awareness of vitamins and to thiamin’s abundance in our diets, beriberi is no longer a threat. But while few people suffer from beriberi today, there’s no denying its historical significance. By establishing one of the first links between a dietary deficit and a specific disease, beriberi played a crucial role in kick​starting the process of scientific inquiry that led to the discovery of vitamins—which in turn opened the door to a broader understanding of both deficiency diseases and human nutrition as a whole.


This path was not straight, however, and the existence of vitamins wasn’t easy to figure out. In fact, when the Dutch physician Christiaan Eijkman arrived on the Indonesian island of Java in 1886 to investigate the causes of beriberi, he wasn’t searching for a nutritional cause at all. Instead, inspired by the most exciting medical event of the century—the discovery that diseases like malaria and cholera were caused by germs—he was on the hunt for a beriberi-​causing bug.

The emergence of this “germ theory” of disease in the late 1800s was inarguably one of the greatest medical advances in history. But for nutritional science its impact was more complicated. Germ theory’s central tenet—that disease is caused by the presence of something—hid the idea that disease could also be caused by something that is lacking. Germ theory’s light was so bright, so illuminating, that it blinded scientists to the idea that disease could be caused by something that wasn’t there.


Working in a hospital in what’s now Jakarta, Eijkman procured a flock of chickens—a lucky choice, since chickens and pigeons are two of the only animals other than humans that frequently develop the disease—and began injecting them with blood samples from human beriberi patients to see if he could infect the birds.

After a couple of months, he saw symptoms in some of his injected chickens that looked like the nerve damage that occurred in people with beriberi. Then again, he saw the same symptoms in his control group. But Eijkman was not deterred—many pathogen-borne diseases are transmitted by air, and the two groups of chickens had shared cages. He got some new chickens and put them into private cages. The controls still developed nerve damage. Concluding that perhaps his whole laboratory had become infected, Eijkman procured yet another group of chickens and kept them in a totally separate location. Then things got really strange: Not only did none of the new chickens get sick, but the sick birds began to recover. By November 1889, all signs of the disease had disappeared.


This bizarre mass recovery was good for the chickens, but it was bad for Eijkman, who appeared to have lost his animal model. However, Eijkman did not give up. Instead, he tried to find a variable that could have accounted for the sudden change. One day, the laboratory keeper told him something intriguing: In the month before the birds developed nerve damage, the cook had been providing leftover white rice from the hospital’s kitchen as their feed.

At the time, white rice, otherwise known as polished rice, was something of a luxury—or at least not something you’d give to laboratory chickens that you wanted to infect with a deadly disease. That cook had been replaced, and his successor, Eijkman later related, “refused to allow military rice to be taken for civilian chickens.” So the birds had been switched back to their usual rations of brown, unpolished rice. Soon thereafter, the nerve damage disappeared.

Today, we know why the polished rice caused problems. Rice polishings—like the outer coatings of many whole grains—contain thiamin, among other vitamins and nutrients. The more thorough the milling process, the less thiamin that remains.

Unaware of this—and still grasping for a bacterial explanation—Eijkman happened to strike up a conversation about his beriberi investigations with a friend who was the medical director of all the prisons in Java. The friend realized that different prisons on the island fed inmates different types of rice, and that prisons varied in how many cases of beriberi they reported. He offered to gather this data to determine whether rice had anything to do with human beriberi—and, therefore, whether Eijkman’s chicken work was relevant to the human disease. Sure enough, when the final numbers were tallied, it turned out that while only 1 out of 10,000 prisoners developed beriberi in the prisons that served mostly brown rice, 1 out of 39 developed it in those that served white. Among long-​term white-​rice–​eating prisoners, the rate went up to 1 out of 4.


While it took years and many more experiments for scientists to accept beriberi as a deficiency disease, Eijkman received the 1929 Nobel Prize in Physiology or Medicine for his recognition of this “anti-​beriberi factor,” which by then was known as thiamin, and for developing research methods that influenced later nutritional scientists and advanced vitamins’ discovery. Today, beriberi has become so uncommon that most of us don’t even know its name.

From our vantage point, it’s tempting to scoff at how long it took for the idea of vitamins and nutritional deficiency diseases to be accepted. But like all scientists, these researchers were working with incomplete information, interpreting their results in the context of their time. The fact that they didn’t figure everything out immediately does not reflect a failing on their parts. That’s just how the scientific process works.

From Vitamania: Our Obsessive Quest for Nutritional Perfection by Catherine Price. Reprinted by arrangement with Penguin Press, a member of Penguin Group (USA) LLC, A Penguin Random House Company. Copyright Catherine Price, 2015.