From Wikipedia, the free encyclopedia - View original article

Classification and external resources

A sufferer – turn of the 20th century in southeast Asia
eMedicineped/229 med/221
Jump to: navigation, search
Classification and external resources

A sufferer – turn of the 20th century in southeast Asia
eMedicineped/229 med/221

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 involved (nervous or cardiovascular) or age of patient (infantile). Beriberi is one of several thiamine-deficiency related conditions, which may occur concurrently, including Wernicke's encephalopathy, Korsakoff's syndrome, and Wernicke-Korsakoff syndrome.

Historically, Beriberi has been endemic in regions dependent on polished rice. This refers to the practice of de-husking rice in order to extend its lifespan, which has the unintended side-effect of removing the primary source of thiamine.[citation needed]


Thiamine 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:

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.[citation needed]

Signs and symptoms[edit]

Symptoms of beriberi include weight loss, emotional disturbances, impaired sensory perception, weakness and pain in the limbs, and periods of irregular heart rate. Edema (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.

Beriberi is divided into three historical classifications:

Dry beriberi[edit]

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

A selective impairment of the large proprioceptive sensory fibers 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.[4]

Wet beriberi[edit]

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 edematous. Wet beriberi is characterized by:

Infantile beriberi[edit]

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 dyspnea and cyanosis and soon dies of heart failure. The following symptoms may be described in infantile beriberi:


Inadequate nutrition[edit]

Beriberi caused by inadequate nutritional intake is rare today in developed countries[citation needed] because of quality of food and the fact that many foods are fortified with vitamins.[citation needed] There are no reliable statistics for beriberi in developed countries in the 19th century or earlier; neither are statistics available before the last century in countries in extreme poverty.[citation needed]

Beriberi is a recurrent nutritional disease in detention houses even in this century. In the Ivory Coast, among a group of prisoners with heavy punishment, 64% were affected. Before beginning treatment, prisoners exhibited symptoms of dry or wet beriberi: neurological signs (swarming: 41%) and cardiovascular signs (dyspnoea: 42%, thoracic pain: 35%). Half of the patients (51%) presented oedemas of the lower limbs. The rate of healing was about 97%.[6]

Wernicke's encephalopathy[edit]

Beriberi may also be caused by shortcomings other than inadequate intake: diseases of the digestive tract or operations, alcoholism, dialysis, genetic deficiencies, etc. The name that includes all these causes and all symptomatic presentations is Wernicke's disease or Wernicke's encephalopathy.

Wernicke´s disease is one of the most prevalent neurological or neuropsychiatric diseases.[7] In autopsy series, features of Wernicke lesions are observed in approximately 2% of general cases.[8] Medical record research shows that about 85% had not been diagnosed, although only 19% would be asymptomatic. In children, only 58% were diagnosed. In alcohol abusers, autopsy series showed neurological damages at rates of 12,5% or more. Mortality caused by Wernicke's disease reaches 17% of diseases, which means 3.4/1000 or about 25 million contemporaries.[9][10] The rate of sufferers may be even higher, considering that early stages may have dysfunctions prior to the production of observable lesions at necropsy. In addition, uncounted numbers of persons can experience fetal damage and subsequent diseases.



The origin of the term 'beriber' comes from a Sinhalese phrase meaning "weak, weak" or "I cannot, I cannot", the word being duplicated for emphasis.[11][12][13][14]

In 1630, a Dutch physician named Jacob de Bondt (Jacobus Bontius; 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."[15]


Beriberi was first described over 4,500 years ago, in the Chinese medical book Neichang.[16] In Asia, where polished white rice (milled rice that has had its husk, bran, and germ removed) was the common staple food of the middle class, beriberi resulting from lack of vitamin B1 was endemic.

In the late 1800s, beriberi was studied by Takaki Kanehiro, a British-trained Japanese medical doctor of the Japanese Navy.[17] 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.[17] 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.[17] 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.

In 1897, Dr. 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.[18][19] 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,[20] and between 1910 and 1913, Dr. Edward Bright Vedder established that an extract of rice bran is a treatment for beriberi.[citation needed]. In 1929, Eijkman and Hopkins were awarded the Nobel Prize for Physiology or Medicine for their discoveries.


Many authors[who?] agree that patients rarely present with thiamine deficiency alone, and therefore that the disease process in beriberi is multifactorial.[citation needed]

Beriberi is managed with thiamine supplementation. This can be done intravenously or orally.[citation needed] Supplementation can be monitored using blood tests. Patients' health can be improved within an hour of starting treatment, and rapid and dramatic recovery can occur within hours of administration. In emergency situations where concentrated thiamine supplements are unavailable, feeding the patient with a thiamine-rich diet (e.g. whole grain brown bread) will lead to recovery, though at a much slower rate.[citation needed]

See also[edit]


  1. ^ a b c d Sechi, G; Serra, A (2007 May). "Wernicke's encephalopathy: new clinical settings and recent advances in diagnosis and management". Lancet neurology 6 (5): 442–55. doi:10.1016/S1474-4422(07)70104-7. PMID 17434099. 
  2. ^ Hirsch, JA; Parrott, J (2012 Mar 6). "New considerations on the neuromodulatory role of thiamine". Pharmacology 89 (1-2): 111–6. doi:10.1159/000336339. PMID 22398704. 
  3. ^ a b c d e f Katsura, E.; Oiso, T. (1976). "Chapter 9. Beriberi". In Beaton, G.H.; Bengoa, J.M. World Health Organization Monograph Series No. 62: Nutrition in Preventive Medicine (Geneva: World Health Organization). 
  4. ^ Spinazzi, Marco; Angelini, Corrado; Patrini, Cesare (2010). "Subacute sensory ataxia and optic neuropathy with thiamine deficiency". Nature Reviews Neurology 6 (5): 288–93. doi:10.1038/nrneurol.2010.16. PMID 20308997. 
  5. ^ a b c d e f Latham, Michael 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). ISSN 1014-3181. 
  6. ^ Bull Soc Pathol Exot. 2011 Dec;104(5):347-51. doi: 10.1007/s13149-011-0136-6. Epub 2011 Feb 18.
  7. ^ Cernicchiaro, Luis (2007), Enfermedad de Wernicke (o Encefalopatía de Wernicke) [Wernicke´s Disease (or Wernicke´s Encephalopathy)] (in Spanish) 
  8. ^ Salen, Philip N (1 March 2013). Kulkarni, Rick, ed. "Wernicke Encephalopathy". Medscape. 
  9. ^ Harper, CG; Giles, M; Finlay-Jones, R (1986 Apr). "Clinical signs in the Wernicke-Korsakoff complex: a retrospective analysis of 131 cases diagnosed at necropsy". J Neurol Neurosurg Psychiatry 49 (4): 341–5. PMID 3701343. 
  10. ^ Harper, C (1979 Mar). "Wernicke's encephalopathy: a more common disease than realised. A neuropathological study of 51 cases". J Neurol Neurosurg Psychiatry 42 (3): 226–31. PMID 438830. 
  11. ^ Oxford English Dictionary: "Beri-beri... a Cingalese word, f. beri weakness, the reduplication being intensive ...", page 203, 1937
  12. ^ A Sinhalese-English Dictionary, Rev. Charles Carter: "බැරි බැරි.රෝගය, a. the diseaseberi beri, a form of neuritis accompanied by dropsy &c..." , page 448, 1924
  13. ^ Beriberi, Information about Beriberi
  14. ^ "Beriberi". Online Etymology Dictionary. Retrieved 8 July 2013. 
  15. ^ Berg, Jeremy M; Tymoczko, John L; Stryer, Lubert (2002). "The Disruption of Pyruvate Metabolism Is the Cause of Beriberi and Poisoning by Mercury and Arsenic". Biochemistry (5th ed.). ISBN 978-0-7167-3051-4. 
  16. ^ Kiela, Pawel R (2010). "Unraveling the pathophysiology of alcohol-induced thiamin deficiency". American Journal of Physiology - Renal Physiology 299 (1): F26–27. doi:10.​1152/​ajprenal.​00266.​2010. 
  17. ^ a b c Itokawa, Yoshinori (1976). "Kanehiro Takaki (1849–1920): A Biographical Sketch". Journal of Nutrition 106 (5): 581–8. PMID 772183. 
  18. ^ Challem, Jack (1997). "The Past, Present and Future of Vitamins". Archived from the original on 8 June 2010. [unreliable medical source?]
  19. ^ Christiaan Eijkman, Beriberi and Vitamin B1,, Nobel Media AB, retrieved 8 July 2013 
  20. ^ Grijns, G. (1901). "Over polyneuritis gallinarum". Geneeskundig Tijdschrift voor Nederlandsch-Indie 43: 3–110. 


External links[edit]