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Beri-Beri - A serious illness
Beriberi disease has been known for over 4500 years, in ancient China as well as in biblical times and in ancient Rome and Greece. The ancient Egyptians reported people with paralyzed and rotting muscles, the Japanese feared the plague, which transformed people into living skeletons. In China, Beri-Beri destroyed cardiac functions, in short: the disease led to a cruel death in countless people.
Beriberi is a classic avitaminosis, more precisely a vitamin B1 deficiency. The disease occurs primarily with husked rice as the main diet, but also among alcoholics. The scientific history of the disease shows that it could not just be a vitamin deficiency.
Stumble like a sheep
The Dutchman Jacob de Bondt described a disease common in Indonesia in 1630: According to this, those affected had a walk “like sheep”, ie shaky and with trembling knees. Therefore, the locals called the plague Beriberi - that is, sheep.
It was a collective term for a variety of symptoms: some suffered from emaciated limbs, others had swollen legs, yet others suffered from diarrhea or constipation; Sick people lay paralyzed on earth, and many died within a few days.
Japan's fight against the plague
In the 19th century, the previously strictly isolated island kingdom opened up to exchange with Europe. German-speaking and Japanese physicians tried different methods to treat beriberi. However, since neither knew anything about the cause of the disease, the western doctors were just as unsuccessful as their Japanese colleagues.
At that time, most doctors assumed that Beri-Beri was a virus or a bacterium. The Japanese Kanehiro Takaki, however, doubted this after examining sick soldiers from the Japanese Navy. As with scurvy, which has been known as a malnutrition condition since the 18th century, he suspected improper nutrition as a suspect.
As in many Asian countries, the normal diet of ordinary people in Japan at that time consisted of husked rice. Takaki now had the crew of one ship continue to eat hulled rice, and that of the second ship received additional meat, vegetables, barley and fish. After nine months at sea, 161 of 376 sailors suffered from Beriberi on the first ship, 25 died of it, and only 14 fell ill on the second ship.
Takaki had shown that the disease was related to the diet of hulled rice. But this discovery remained controversial. But Takaki prevailed and the Japanese army introduced his diet to the Navy. In six years, Beriberi's illnesses in marines dropped from 40% to zero. In 1890, the Japanese government passed a law that required Takaki's mix to be used to supply soldiers.
Leftovers and sick chickens
It took 200 years for a Dutch doctor to systematically examine the disease. Christiaan Eijkman (1858-1930) came to Indonesia in 1886 and suspected a bacterium as the causative agent. He examined patients at the military hospital in Batavia and observed chickens in the yard of the hospital. The chickens also contracted the condition after eating husked rice from kitchen scraps.
Eijkman rejected his bacterial theory and thought the disease was related to rice. He made a study in which he had the chickens alternately peeled and unshelled rice and found that he could trigger the disease in the animals with peeled rice and heal again with unshelled rice. His assistant Gerrit Grijns also recognized that meat and peas also defeated the disease.
The hypothesis was now that white rice was missing a substance that the nervous system needed existentially, but which was present in the bowl of the rice.
Umetaro Suzuki (1874-1943) discovered the “anti-Beriberi factor” in the rice bowl in 1910. He called him oryzanine. Casimir Funk in London, independent of Suzuki, isolated an alleged “anti-Beriberi factor” in 1911, which was actually ineffective. However, his research led to the term “vital amine” for substances present in the body that prevented diseases. The term vitamins was derived from this.
Robert Williams synthesized vitamin B1 (thiamine) in 1936, which B.C.P. Jansen and W. Donath had previously isolated from rice grains. Beriberi is considered a vitamin B1 deficiency.
What do we need thiamine for?
Vitamin B1 is necessary for the body to convert carbohydrates and sugar. Vitamin B1 supports the supply of energy to the body.
Eijkmann rejects the Nobel Prize
In 1929, Eijkmann received the Nobel Prize in Medicine for his discoveries on the cause of Beriberi, more precisely “for his discovery of the antineuritic vitamin”. There was a scandal: Eijkmann did not accept the price. He said he did not believe in vitamin B1 deficiency as the cause of beriberi and never would have said so. Rather, beriberi is tied to the cooked rice diet and would not occur with any other diet.
Old traditions confirmed his skepticism. The Chinese Chao Yünan catch had already been in the 7th century CE. Beriberi was described so precisely that there was no doubt that the disease was the same - and at that time there had been no husked rice.
Japanese professors supported Eijkmann's doubts: Shibayama and Miyamoto reported numerous miners on the Sunda island of Banka, many of whom contracted Beri-Beri even though they had only eaten unpeeled rice. There would even be mines where workers would eat unpeeled rice and still have beriberi more often than miners who would eat peeled rice.
The thesis that the suffering is not related to husked rice also confirms the spread in other Asian countries. In India, for example, people ate a lot more parboiled rice, which hardly spread in China and Japan. Despite an equally high proportion of rice in the diet, however, fewer Indians fell ill with the disease. Conversely, from the 1920s onwards, when rice was exported from Japan to Burma, Thailand and the Philippines, Beriberi also raged in these countries.
Beriberi due to mold?
Eijkmann made another important argument: healthy soldiers died in 48 hours after eating rice. But that could not be due to malnutrition. In fact, diseases due to a lack of certain vitamins and minerals are long-term in nature. A rapid course of symptoms until death after a meal and within a few hours is rather typical of poisoning.
Eijkmann therefore suspected a neurotoxin as the cause of Beriberi. For example, mold poisons that form on the rice could be considered. At the time, however, this thesis found little support because medicine assumed that cooking destroys such poisons.
In 1969, the Japanese scientist Kenji Uraguchia reinforced Eijkmann's assumption: he discovered Penicillium citreoviride, a mold that grows on rice. This produces the nerve poison citreoviridine. It attacks nerve cells in the brain and spine and stops the energy supply to the tissue. That would also explain the extreme weakness of the Beriberi patients.
The mold develops the poison more intensely at low temperatures and high humidity, which are typical for northern Japan. Rice from this region was exported to many areas where Beriberi was rampant.
The various symptoms of the disease can be explained by the different doses of poisons that this mold produces, depending on the respective climate.
Mold or thiamine deficiency?
Nevertheless, a mold and a lack of vitamin B1 are not mutually exclusive. An intake of vitamin B1 helps against beriberi. Just as various vitamins play a crucial role in the immune system, vitamin B1 could be the body's antidote to the poison citreoviridine.
This would also explain why beriberi occurs less often when peeled rice is consumed, but does not disappear completely: thiamine would be a natural protection of the rice plant against mold, which can contain an infestation, but not completely prevent it.
In any case, beriberi is extremely rare in countries where people get enough vitamins, for example from bread or breakfast made from cereal products. The disease also mainly occurs today in people who suffer from alcohol abuse, which makes it difficult for the body to absorb and store thiamine.
The dry form of the disease is shown by various nerve disorders such as a lack of reaction to pain, double vision, disorientation, delusions and loss of memories. Confused thinking and fantasies that replace lost memories are typical.
The main symptom of a wet Beri-Beri is edema, especially in the legs, but also on the anus, face or trunk. Shortness of breath, shortness of breath and an accelerated pulse are also typical, as well as extensive neck veins with a visible pulse. The heart appears enlarged.
A patient with a wet beriberi is in mortal danger, even if he looks as if he is doing well. He can die from acute circulatory failure.
Causes of beriberi
No matter whether it is caused by a mold or not, the main reason that the disease breaks out is a lack of vitamin B1. Thiamine is naturally found in fresh fruit, milk, green vegetables, meat and whole grain bread. A diet based primarily on peeled rice does not provide the body with vitamin B1.
Genetic causes are unlikely. Suffering occurs in people who have no family history of the disease. However, the disease can occur in people who cannot naturally absorb vitamin B1. The disease actually runs differently here, and the question is whether it is the syndrome examined in Japan and Indonesia: People who have genetic problems ingesting vitamin B1 develop deficiency symptoms over the years and do not die within fewer days at Beriberi.
Infants can suffer from vitamin B1 deficiency if the mother stores too little of it in their body and the milk source that babies have is the mother's milk. Chronic diarrhea can also lead to thiamine deficiency.
When to the doctor?
In the event of a possible Beri-Beri disease, you should definitely see a doctor, simply because the symptoms are non-specific in both the dry and the wet form of the disease. Nerve disorders and heart rhythm problems can have a variety of causes.
A doctor can also fix other problems associated with thiamine deficiency. You should suspect Beri-Beri of the following risks if you show the corresponding symptoms: With a one-sided diet with peeled rice, with repeated diets that were associated with insufficient vitamin supply, with severe alcohol abuse.
Simply taking vitamin B1 supplements without medical advice is not recommended. If you don't have a thiamine deficiency, you can take too much vitamin B1. However, overdoses increase blood sugar and can damage the heart and liver.
Treating or preventing the disease still means providing the patient with vitamin B1. For example, the amount of rice in the diet needs to be reduced, and if people eat a lot of rice, they should resort to unpeeled and / or parboiled travel. Even a broken out Beri-Beri doesn't have to be a fatal disease today.
A fish and rice diet should at least be supplemented with other foods. Mussels, shrimp and the raw meat of animals contain thiaminase, an enzyme that breaks down vitamin B1. If you already suffer from a lack of vitamin B1, you should temporarily do without fish.
In northern Japan, when the disease was rampant, people's diet consisted primarily of rice and fish. The fish would have also caused a thiamine deficiency. (Dr. Utz Anhalt, Somayeh Ranjbar)
Author and source information
This text corresponds to the specifications of the medical literature, medical guidelines and current studies and has been checked by medical doctors.
Dr. phil. Utz Anhalt, Barbara Schindewolf-Lensch
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ICD codes for this disease: E51ICD codes are internationally valid encodings for medical diagnoses. You can find yourself e.g. in doctor's letters or on disability certificates.