DIET OF POLISHED RICE, ASSOCIATED WITH AFFLUENCE, CAN CAUSE BERIBERI

from ResearchGate's "Thiamine: The Spark of Life."

It is now well known that thiamin deficiency is the major cause of beriberi, a disease that had affected humans for centuries.  The name “Kakke” was the term used for the disease in Japan and this word can be found in documents as early as 808 (Inouye K, Katsura E. 1965).  Until the 17^th century, the majority of the population in Japan took unpolished rice as the staple food.  Polished rice was associated with relative affluence since it looked better on the table when served.  Epidemics of beriberi have been known to occur in association with increased affluence simply because it was expensive to take the rice to the mill.  When white rice was served to friends, it became a signature of the newly acquired affluence.  As the ingestion of well-milled white rice became nationwide, so the incidence of the disease increased.  This is because the B group vitamins are in the discarded husks.  The first national statistics on mortality appeared in 1899 and showed a death rate of 20 per 100,000.  This dropped to 0.5 in 1959 after its nutritional association was discovered.  Of considerable interest to us today, for reasons that will appear later in the chapter, the peak incidence of the disease occurred in August and September every year.  Factory workers would take their lunch between factory buildings.  If the sun came round so that it shone into the corridor, some workers would get the first symptoms of the disease.  It was evident that the sun’s rays would stress them sufficiently to initiate these symptoms.  It was therefore hardly surprising that the etiology in the early 1900s before its nutritional association became common knowledge, was considered to be from infection.  

The discovery of the relationship of thiamine with malnutrition came in the late decades of the 19^th century, but it was many years before scientific knowledge caught up.  A Japanese naval surgeon by the name of Takaki studied in England from 1875 to 1880.  He noted that beriberi was less common in the British Royal Navy than in navy personnel in Japan where the diet on ships was very different.  In 1882, a Japanese naval vessel sailed on a 272-day voyage.  On its return, 61% of the crew had succumbed to beriberi.  Two years later, another ship completed the same voyage but was provided with an ample supply of dried milk and meat, giving a carbon to nitrogen ration of 16:1.  Only 14 crew members had developed beriberi.  Takaki concluded that a lack of nitrogenous food was the cause of the disease, a notable contribution before vitamins were known.  

In 1890, Eijkman found that polished rice, given to pigeons, caused polyneuritis and the histopathology was similar to that seen in humans in beriberi.  Funk and Cooper isolated an “anti-beriberi factor” from rice polishing in 1910 and this was crystallized in 1926 and called Vitamine (Jansen BCT, Donath W F. 1926).  It was not until 1936 that thiamin was synthesized (Williams R R, 1938) leading to an explosion of basic science and clinical experimentation.  The work of Sir Rudolph Peters (Peter R A, 1936) exposed the vitally important association of thiamin with what was later to become the science of oxidative metabolism. 

Dr. Derrick Lonsdale, founder of Hormones Matter and author of Thiamine Deficiency Disease, Dysautonomia, and High-Calorie Malnutrition (2017), says that Thiamine is the therapeutic remedy to beriberi like symptoms that emanate from a thiamine deficiency.  The preferred form of Thiamine is not necessarily the water-soluble, B1, but instead the fat-soluble B1, Allithiamine is preferred because it gets into the tissue and not just circulate in your blood.    

This explains our condition:

Because mild to moderate TD [Thiamine Deficiency] results in pseudo hypoxia in the limbic system and brainstem, emotional and stress reflexes of the autonomic nervous system are stimulated and exaggerated, producing symptoms often diagnosed as psychosomatic disease.

If the biochemical lesion is recognized at this stage, the symptoms are easily reversible. If not, and the malnutrition continues, neurodegeneration follows and results in a variety of chronic brain diseases. 

What then is the remedy to Thiamine Deficiency?  Thiamine, of course.  But you want the fat-soluble Thiamine, B1, called Allithiamine, for this gets into the relevant brain, muscle, and nerve tissue.