thirties5txt

Peters (1936) described the biochemical investigations that lead to an
understanding of the requirement for vitamin B1 (thiamine) in respiring
tissues. Pigeons were used as the experimental animal, and behavioral
effects of both acute and chronic lack of vitamin B1 described. The
major acute symptom was opistotonus, a spastic state with the head
arched back; sometimes emprostotonsus was observed, with the bird
falling forward in cartwheel convulsions. Preliminary to these states,
birds became unresponsive to visual stimuli or hypersensitive to noise or
strong light. Opistotonus occurs also in cases of human beri-beri.

Increased lactic acid was found in the brains of birds sacrificed for
chemical analysis; the increase was greatest in the optic lobes and lower
parts of the brain. Symptoms of vitamin B1 deficiency could not be
produced by injections of lactic acid, thus were not due to its toxic
effects. Chronic deficiency of vitamin B1 led to foci of hemorrhage or
congestion in pons, medulla, cerebellum, and optic lobes.

In vitro studies of fresh brain tissues revealed a decreased uptake of
oxygen and decreased production of adenosine triphosphate (ATP),
which could be restored by adding vitamin B1. Further study revealed
that pyruvic acid was removed by addition of vitamin B1 and metabolized
in a pathway other than that producing lactic acid. Disruption of
metabolism caused by lack of vitamin B1 could be compared to that
produced by potassium cyanide (KCN) and narcotics. The investigations
of Peters predate the full elucidation of the citric acid cycle by Krebs in
1937.