Beriberi and its dietary management

Introduction (What is beriberi?)

According to Kennedy (2013), beriberi refers to a cluster of symptoms caused primarily by a nutritional deficit in Vitamin B1 (thiamine). Beriberi has conventionally been divided into three separate entities, relating to the body system mainly involved (peripheral nervous system or cardiovascular) or age of patient (infantile). Beriberi is one of several thiamine-deficiency related conditions which may occur concurrently, including Wernicke’s encephalopathy (when mainly affects the central nervous system), Korsakoff’s syndrome (when it reaches psychiatric aspects), and Wernicke-Korsakoff syndrome (with both neurologic and psychiatric symptoms).

Historically, Beriberi has been endemic in regions dependent on what is variously referred to as polished, white, or de-husked rice. This type of rice has its husk removed in order to extend its lifespan, but also has the unintended side-effect of removing the primary source of thiamine.

According to Sechi and Serra (2007), thiamine in the human body has a half-life of 18 days and is quickly exhausted, particularly when metabolic demands exceed intake. Thiamine is involved in a variety of glucose metabolism-related and neurological functions. After modification in the body to a diphosphate form, thiamine is involved in a vast array of functions:

  • Carbohydrate metabolism
  • Production of the neurotransmitters glutamic acid and gamma-Aminobutyric acid (GABA), through the citric acid cycle
  • Lipid metabolism, necessary for myelin production
  • Amino acid metabolism
  • Neuromodulation.

Neurons are very sensitive to ionic and metabolic changes produced in their immediate environment, which initially affect metabolism, electrical activity and performance, but then can lead to cell death.

History of beriberi

According to the Oxford English Dictionary (1937), the origin of the term ‘beriberi’ comes from a Sinhalese phrase meaning “weak, weak” or “I cannot, I cannot”, the word being duplicated for emphasis.

In 1630, a Dutch physician named Jacobus Bontius (Jacob de Bondt; 1591–1631) encountered the disease while working in Java. In the first known description of beriberi, he wrote: “A certain very troublesome affliction, which attacks men, is called by the inhabitants beriberi (which means sheep). I believe those, whom this same disease attacks, with their knees shaking and the legs raised up, walk like sheep. It is a kind of paralysis, or rather tremor: for it penetrates the motion and sensation of the hands and feet indeed sometimes of the whole body.” (Berg, Tymoczko and Stryer, 2002).

In the late 1800s, beriberi was studied by Takaki Kanehiro, a British-trained Japanese medical doctor of the Japanese Navy (Itokawa, 1976).  Beriberi was a serious problem in the Japanese navy: sailors fell ill an average of four times a year in the period 1878 to 1881, and 35% were cases of beriberi. In 1883, Kanehiro learned of a very high incidence of beriberi among cadets on a training mission from Japan to Hawaii, via New Zealand and South America. The voyage lasted more than 9 months and resulted in 169 cases of sickness and 25 deaths on a ship of 376 men. With the support of the Japanese Navy, he conducted an experiment in which another ship was deployed on the same route, except that its crew was fed a diet of meat, fish, barley, rice, and beans. At the end of the voyage, this crew had suffered only 14 cases of beriberi and no deaths. This convinced Kanehiro and the Japanese Navy that diet was the cause. In 1884, Kanehiro observed that beriberi was endemic among low-ranking crew who often were provided nothing but rice, but not among crews of Western navies and nor among Japanese officers who consumed a more varied diet.

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In 1897, Christiaan Eijkman, a Dutch physician and pathologist, demonstrated that beriberi is caused by poor diet, and discovered that feeding unpolished rice (instead of the polished variety) to chickens helped to prevent beriberi. The following year, Sir Frederick Hopkins postulated that some foods contained “accessory factors” – in addition to proteins, carbohydrates, fats, and salt – that were necessary for the functions of the human body. In 1901, Gerrit Grijns (May 28, 1865 – November 11, 1944), a Dutch physician and assistant to Christiaan Eijkman in the Netherlands, correctly interpreted the disease as a deficiency syndrome, (Grijns, 1901) and between 1910 and 1913, Edward Bright Vedder established that an extract of rice bran is a treatment for beriberi. Nonetheless, as late as 1911, the Encyclopaedia Britannica Eleventh Edition described it as “believed…to be caused by an infective agent of a parasitic nature” (Chisholm,1911). In 1929, Eijkman and Hopkins were awarded the Nobel Prize for Physiology or Medicine for their discoveries.

Causes of beriberi

Latham (1997) highlighted the primary cause of beriberi to be a diet low in Vitamin B-1. According to him, the disease is very rare in regions with access to vitamin-enriched foods. Other dynamics can contribute:

  • Alcohol abuse can make it difficult for your body to absorb and store Vitamin B-1.
  • Genetic beriberi is a rare condition that prevents the body from absorbing Vitamin B-1.
  • Pregnant women and anyone with hyperthyroidism (over-active thyroid gland) need extra vitamin B-1.
  • Prolonged diarrhoea can make it difficult for your body to absorb Vitamin B-1.
  • Some diseases (e.g., liver disease) impair your body’s ability to use Vitamin B-1.
  • Infants drinking breast milk or formula low in Vitamin B-1.
  • Kidney dialysis can increase your risk of beriberi.
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Classification of beriberi

Spinazzi, Angelini & Patrini (2010) classified beriberi into three major categories how they affect various individuals affected by it. They are

  • Dry beriberi specially affects peripheral nervous system
  • Wet beriberi specially affects the cardiovascular system and other bodily systems
  • Infantile beriberi affects also the children of malnourished mothers.

Signs and symptoms of beriberi

Symptoms of beriberi include weight loss, emotional disturbances, impaired sensory perception, weakness and pain in the limbs, and periods of irregular heart rate. Oedema (swelling of bodily tissues) is common. It may increase the amount of lactic acid and pyruvic acid within the blood. In advanced cases, the disease may cause high output cardiac failure and death. Symptoms may occur concurrently with those of Wernicke’s encephalopathy, a primarily neurological thiamine-deficiency related condition.

Katsura & Oiso (1976) stated the signs and symptoms of beriberi based on their various classes.

Dry beriberi

Dry beriberi causes wasting and partial paralysis resulting from damaged peripheral nerves. It is also referred to as endemic neuritis. It is characterized by:

  • Difficulty in walking
  • Tingling or loss of sensation (numbness) in hands and feet
  • Loss of tendon reflexes
  • Loss of muscle function or paralysis of the lower legs
  • Mental confusion/speech difficulties
  • Pain
  • Involuntary eye movements (nystagmus)
  • Vomiting.

A selective impairment of the large proprioceptive sensory fibres without motor impairment can occur and present as a prominent sensory ataxia, which is a loss of balance and coordination due to loss of the proprioceptive inputs from the periphery and loss of position sense.

 Wet beriberi

Wet beriberi affects the heart and circulatory system. It is sometimes fatal, as it causes a combination of heart failure and weakening of the capillary walls, which causes the peripheral tissues to become oedematous. Wet beriberi is characterized by:

  • Increased heart rate
  • Vasodilatation leading to decreased systemic vascular resistance, and high output cardiac failure
  • Elevated jugular venous pressure
  • Dyspnoea (shortness of breath) on exertion
  • Paroxysmal nocturnal dyspnoea
  • Peripheral oedema (swelling of lower legs)

 Infantile beriberi

Infantile beriberi usually occurs between two and six months of age in children whose mothers have inadequate thiamine intake. In the acute form, the baby develops dyspnoea and cyanosis and soon dies of heart failure. The following symptoms may be described in infantile beriberi:

  • Hoarseness, where the child makes moves to mourn but emits no sound or just faint moans, caused by nerve paralysis
  • Weight loss, becoming thinner and then marasmic as the disease progresses
  • Vomiting
  • Diarrhoea
  • Occasionally convulsions were observed in the terminal stages
  • Pale skin
  • Oedema
  • Ill temper
  • Alterations of the cardiovascular system, especially tachycardia (rapid heart rate).
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Dietary management of beriberi

A balanced diet containing all essential nutrients will prevent a thiamine deficiency and the development of beriberi. People who consume large quantities of junk food need to take vitamin supplements and should improve their diets.  The best food sources of thiamine are lean pork, beef, liver, brewer’s yeast, peas and beans, whole or enriched grains, and breads. The more refined the food, the lower the thiamine. Some food products are enriched with thiamine, along with riboflavin, niacin, and iron, to prevent dietary deficiency. During the milling process, rice is polished and all the vitamins in the exterior coating of bran are lost. Boiling the rice before husking preserves the vitamins by distributing them throughout the kernel. Food enrichment programs have eliminated beriberi in Japan and the Philippines. Like all B vitamins, thiamine is water soluble, which means it is easily dissolved in water and thus not stored in the body, thus requiring sustained intake. It will leach out during cooking in water and is destroyed by high heat and overcooking.

Conclusion

Based on the sign and symptoms which highlighted how beriberi affects different individual, it is undoubtedly a very discomforting circumstance that required a rapt attention. Beriberi can be managed my eating a balanced diet to prevent a thiamine deficiency and the development of beriberi.

References

Berg, J.; Tymoczko, J. & Stryer, L. (2002). “The Disruption of Pyruvate Metabolism Is the Cause of Beriberi and Poisoning by Mercury and Arsenic”. Biochemistry (5th ed.)

Chisholm, H, ed. (1911). “Beri-beri”. Encyclopædia Britannica 3 (11th ed.). Cambridge University Press. pp. 774–775.

Grijns, G. (1901). “Over polyneuritis gallinarum”. Geneeskundig Tijdschrift voor Nederlandsch-Indie 43: 3–110.

Itokawa, Y. (1976). “Kanehiro Takaki (1849–1920): A Biographical Sketch”. Journal of Nutrition 106 (5): 581–8.

Katsura, E. & Oiso, T. (1976). “Chapter 9. Beriberi”. World Health Organization Monograph Series No. 62: Nutrition in Preventive Medicine (Geneva: World Health Organization).

Kennedy, R. (2013). Doctors’ Medical Library – Beriberi (Thiamine Deficiency)(B1 Deficiency) retrieved from http://www.medical-library.net/content/view/826/41/

Latham, C. (1997). “Chapter 16. Beriberi and thiamine deficiency”. Human nutrition in the developing world (Food and Nutrition Series – No. 29). Rome: Food and Agriculture Organization of the United Nations (FAO)

Oxford English Dictionary (1937): “Beri-beri… a Cingalese word, f. beri weakness, the reduplication being intensive …”, page 203

Sechi, G. & Serra, A. (2007). “Wernicke’s encephalopathy: new clinical settings and recent advances in diagnosis and management”. Lancet neurology 6 (5): 442–55

Spinazzi,  M.; Angelini, C. & Patrini, C. (2010). “Subacute sensory ataxia and optic neuropathy with thiamine deficiency”. Nature Reviews Neurology 6 (5): 288–93.