Beriberi

Beriberi – First in a series on nutritional deficiency diseases.  A little history, a little medicine, and some disease names you have heard of but may not know much about.

Dry Beriberi

This discussion of beriberi is the first in what I hope to be an interesting historical and clinical discussion of the major nutrient deficiencies.  One of the cool things about these disorders is their names.  Beriberi (vitamin B1 or niacin), scurvy (Vitamin C), rickets (vitamin D), pellagra (vitamin b2 or niacin) and pernicious anemia (vitamin B12) are a few of the names that make learning about these disorders a bit more fun.

Beriberi was long known to be endemic in Asia, and in sailors who had long trips at sea.  It’s not clear where the name beriberi came from, but in 1884 a Japanese physician Takaki Kanehiro who had trained in England noted that beriberi was very common in low ranking sailors who ate just rice on long voyages, but not noted in officers and western sailors who had a more western style diet.  In one of the early medical case control experiments Kanehiro duplicated a training mission on which half of the cadets had developed beriberi, with the variable being a diet supplemented by milk, bread, meat and vegetables.  In the study the rate of beriberi was reduced from nearly 50% to <10%, and deaths from about 8% to zero from beriberi.  This demonstrated that the disease was a nutritional deficiency.  This was duplicated in animal studies shortly thereafter.

Beriberi and Likely Rickets Also

From here it was a matter of about 20 years before vitamin B1, or thiamine was demonstrated to be the deficient dietary vitamin in beriberi.  Thiamine is found in many foods commonly consumed in a western diet, especially unrefined grains, fresh foods, fresh meat, legumes, meats and milk.  For this reason beriberi is rare in most developed countries.  In addition many foods are fortified with thiamine.  Today beriberi is seen primarily in areas of famine and in chronic alcoholics.  Alcohol may inhibit thiamine absorption and metabolism.  In emergency rooms today part of the standard cocktail of medications given to any suspected alcoholic is parenteral thiamine, to prevent the precipitation of Wernicke-Korsakoff syndrome. In Wernicke’s encephalopathy is manifest by confusion, nystagmus, anisocoria, and progression to coma and death in severe cases if untreated.  Korsakoff’s psychosis presents as amnesia, confabulation and hallucinations.  These occur together as a type of beriberi in alcoholics given IV glucose without thiamine available to allow normal metabolism to take place.

An interesting aside is that arsenic poisoning can interrupt glucose metabolism in a way very similar to thiamine deficiency, leading to a arsenic induced syndrome very similar to beriberi.

Beriberi is classically described as wet beriberi or dry beriberi.  Wet beriberi presents as congestive heart failure with a preponderance of edema.  The findings tend to be severe edema, wasting, shortness of breath, and rapid heart rate.  Dry beriberi is a type of peripheral neuropathy which leads to wasting, numbness and tingling or pain of the extremities, trouble walking, confusion, nystagmus and sometimes vomiting.

Children in developing countries can develop beriberi that can be rapidly fatal.

Thankfully most of the developed world followed the lead of the US after 1940 in fortification of food supplies by adding thiamine to flour to make fortified bread and cereals, essentially eliminating beriberi as a regularly occurring disease.