Understanding the Past: What Was the Original Hypothesis of Beriberi?

January 2, 2026 •

3 min read

In the late 19th century, beriberi was a widespread and deadly scourge, particularly in Southeast Asia, and its cause was a medical mystery. This prevailing confusion shaped the early investigation into what was the original hypothesis of beriberi, leading researchers to incorrectly suspect an infectious agent rather than a dietary deficiency.

Quick Summary

Early theories for beriberi centered on a bacterial or infectious cause, which was the dominant medical thinking of the late 1800s. This initial hypothesis was challenged and eventually overturned by observations connecting diet, specifically polished rice, to the disease's development.

Key Points

Infectious Cause: The original hypothesis for beriberi was that it was caused by a bacterial or microbial infection, following the prevailing germ theory of the late 19th century.
Christiaan Eijkman's Role: Dutch physician Christiaan Eijkman conducted experiments on chickens in Java, observing that they developed a beriberi-like paralysis when fed polished white rice.
Initial Toxin Theory: Eijkman incorrectly theorized that polished rice contained a toxin and that a substance in the rice husk, the 'anti-beriberi factor,' neutralized it.
Grijns's Correction: Eijkman's successor, Gerrit Grijns, correctly reinterpreted the findings, proposing that beriberi was a deficiency disease caused by the lack of a vital nutrient.
The Vitamin Discovery: The beriberi research directly led to the discovery and eventual isolation of thiamine (vitamin B1), the substance missing from polished rice.
Dietary Link: Early observations from Japanese naval physician Takaki Kanehiro also pointed toward a dietary cause, noting beriberi's prevalence on rice-heavy diets and its decline with varied nutrition.
Accidental Nature: The pivotal observation that linked diet and beriberi was accidental, highlighting the importance of keen observation in scientific research.

The Dominant Infectious Theory of the Late 19th Century

During the late 1800s, influenced by germ theory, the scientific community largely believed that diseases like beriberi were caused by microorganisms. This led to investigations in the Dutch East Indies focusing on an infectious cause.

The Pekelharing and Winkler Mission: In 1886, a Dutch commission identified what they believed was a specific microbe responsible for beriberi.
Eijkman's Initial Role: Christiaan Eijkman, a bacteriologist, continued this search for a 'beriberi bacillus,' attempting to infect chickens with blood from patients, although these experiments were inconclusive.
Public Health Response: The focus on microbes led to public health measures like sanitation, which were ineffective against beriberi.

The Accidental Discovery That Changed Everything

Eijkman's breakthrough came from an accidental observation of his laboratory chickens developing a beriberi-like paralysis when fed polished white rice. The symptoms disappeared when their diet was switched back to unpolished rice.

The Dietary Change: A temporary change in the chickens' diet to leftover polished rice from the military hospital correlated with the onset of paralysis. Their recovery coincided with a return to unpolished rice.
Eijkman's New Hypothesis: Eijkman correctly linked the illness to the polished rice diet. However, he initially hypothesized that polished rice contained a toxin neutralized by a substance in the husk of unpolished rice, calling it the 'anti-beriberi factor'. While his mechanism was wrong, he established the link between diet and the disease.

From Toxin Theory to Deficiency Disease

Eijkman's work set the stage for understanding beriberi, but his successor, Gerrit Grijns, refined the hypothesis.

Grijns's Crucial Interpretation: In 1901, Grijns proposed that beriberi was caused by the absence of a vital nutrient in polished rice, not the presence of a toxin. This was a pivotal shift towards the concept of deficiency diseases.
The Isolation of Thiamine: This led to the search for the specific factor. Casimir Funk coined the term 'vitamine' in 1912 based on a concentrate from rice polishings. The substance was later isolated and identified as thiamine (vitamin B1) in 1926. Eijkman and Frederick Hopkins received the Nobel Prize in 1929 for their work on vitamins.

Comparison of Historical and Modern Beriberi Explanations


Aspect	Original Infectious Hypothesis (c. 1886)	Refined Deficiency Theory (c. 1901 onwards)
Cause	An unknown pathogenic bacterium or microbe.	Lack of a specific 'accessory factor' or nutrient (later identified as thiamine).
Mechanism	Contagion, or toxin produced by bacteria.	Inadequate dietary intake of a protective substance.
Source of Problem	Unsanitary conditions; blood or other bodily fluids.	Diet of heavily processed (polished) grains like white rice.
Evidence	Isolation of supposed 'micrococcus' from blood.	Eijkman's chicken experiments, observation of population dietary habits.
Cure	Ineffective sanitation efforts.	Providing unpolished rice or thiamine supplements.
Outcome	Initial research failures and misdirection.	Foundation of modern vitamin and nutritional science.

The Legacy of the Beriberi Discovery

The investigation into beriberi demonstrates the scientific process, where initial hypotheses are tested and refined. Eijkman's work, though based on an incorrect toxin theory, was crucial in linking diet to the disease. This research ultimately led to the discovery of vitamins, transforming nutritional science and public health. The story highlights the importance of observation and challenging established ideas. It shifted medical understanding from solely infectious models to recognizing the role of nutrition, saving countless lives through dietary interventions and food fortification. You can explore more about the Nobel Prize awarded for this discovery at the official Nobel Prize website, which details the contributions of Eijkman and Hopkins.

Conclusion

The original hypothesis of beriberi as an infectious disease, driven by the germ theory of the time, was ultimately disproven. The key turning point was the observation linking a diet of polished rice to the disease, leading to the groundbreaking discovery that beriberi is a deficiency disease caused by a lack of thiamine. This fundamental shift not only provided a cure for beriberi but also opened the door to the field of vitamin research and modern nutritional science.

Frequently Asked Questions

A Dutch medical commission led by Cornelius Pekelharing and Clemens Winkler initially proposed an infectious, bacterial cause for beriberi after observing patients in the Dutch East Indies in the 1880s.

Christiaan Eijkman challenged the original infectious hypothesis with his accidental discovery involving chickens. He noticed that chickens fed polished rice developed beriberi symptoms, while those fed unpolished rice did not.

Eijkman initially thought that polished rice contained a toxin and that the rice husk contained a substance that could neutralize this toxin. This was an incorrect but crucial stepping stone to the correct understanding.

Gerrit Grijns was Eijkman's successor who correctly reinterpreted the experimental findings. He proposed that beriberi was caused by a deficiency of a vital nutrient, not the presence of a toxin.

The term 'vitamine' was coined by biochemist Casimir Funk in 1912 after isolating a concentrated substance from rice polishings that cured beriberi symptoms in pigeons.

Beriberi is caused by a deficiency of thiamine, also known as vitamin B1. This vitamin is essential for nerve and heart function and for converting carbohydrates into energy.

Yes, Japanese naval physician Takaki Kanehiro observed in the 1880s that beriberi was more prevalent among sailors with rice-heavy diets and that introducing more varied foods reduced the disease.

The infectious hypothesis proved incorrect because direct attempts to transmit the disease failed, and a change in diet, rather than sanitation, proved to be the effective preventative measure.