In 1933,
Maurice Tainter, a clinical pharmacologist from Stanford University, found that the ingestion of
2-4-Dinitrophenol (DNP) resulted in huge weight loss. Shortly thereafter, it was promoted as a
weight reduction
medication and subsequently added in over-the-counter drugs and offered to the public
with no need of a prescription.
The study of its pharmacologic
characteristics indicated that it contained the ability to fuel metabolism to incredibly high
levels without triggering major harm to vital organs and capacities. It was indicated to bring
about weight reduction by href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3550200/">uncoupling oxidative
phosphorylation, resulting in both increased fat metabolism and metabolic
rate
In contrast to thyroid hormone that was utilized for weight reduction,
DNP did not affect
nitrogen discharge and hence was hypothesized to cause fat as opposed to lean muscle
loss. The subsequent surplus heat generation resulted in uncontrolled hyperthermia after
collapse of thermoregulatory homeostasis, which leads to critical illness and
mortality.
After a couple of years of its use, numerous harmful effects,
including noxious hyperthermia, hepatotoxicity, growth of cataracts, and some instances of
agranulocytosis were documented. As additional adverse symptoms were reported, DNP was banned
and categorized as very dangerous and not fit for human ingestion by the Federal Drug
Administration in 1938.
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