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Hypothalamic-Pituitary-Thyroid Axis and Sympathetic Nervous System Involvement in Hyperthermia Induced by 3,4-Methylenedioxymethamphetamine (Ecstasy)
Jon E. Sprague, Matthew L. Banks, Valerie J. Cook and Edward M. Mills
The Department of Pharmaceutical and Biomedical Sciences, The Raabe College of Pharmacy, Ohio Northern University, Ada, Ohio (J.E.S., M.L.B., V.J.C.); and National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland (E.M.M.)
An acute and potentially life-threatening complication associated with the recreational use of the 3,4-methylenedioxymethamphetamine (MDMA, Ecstasy) is hyperthermia. In the present study, Sprague-Dawley rats treated with MDMA (40 mg/kg s.c.) responded with a significant increase (maximal at 1 h) in rectal and skeletal muscle temperatures that lasted for at least 3 h post-treatment.
Hypophysectomized (HYPO) and thyroparathyroidectomized (TX) animals treated with MDMA (40 mg/kg s.c.) did not become hyperthermic and in fact displayed a significant hypothermia. The HYPO and TX animals were also resistant to the serotonergic neurotoxic effects of MDMA assessed by serotonin measurements 4 to 7 days later in the striatum and hippocampus. MDMA (40 mg/kg s.c.) induced a significant increase in thyroxine levels 1 h post-treatment. Thyroid hormone replacement in TX animals returned the hyperthermic response seen after MDMA.
Prazosin, an 1-antagonist (0.2 mg/kg i.p.), administered 30 min before MDMA significantly attenuated the MDMA-induced increase in rectal temperature, but had no effect on skeletal muscle temperature. Cyanopindolol, a 3-antagonist (4 mg/kg s.c.), administered 30 min before MDMA (40 mg/kg s.c.) significantly attenuated the increase in skeletal muscle temperature, but had no effect on the rise in rectal temperature.
The combination of prazosin and cyanopindolol resulted in an abolishment of MDMA-induced hyperthermia. The mechanisms of thermogenesis induced by MDMA seem to result from an interaction between the hypothalamic-pituitary-thyroid axis and the sympathetic nervous system, wherein mechanisms leading to core and skeletal muscle hyperthermia after MDMA exposure seem to be differentially regulated by 1- and 3-adrenergic receptors.
...MDMA (40 mg/kg s.c.) induced a significant increase in thyroxine levels 1 h post-treatment. Thyroid hormone replacement in TX animals returned the hyperthermic response seen after MDMA.
This is indeed interesting. I've known a few people over the years who have had thyroid problems and have also used MDMA frequently. They definitely are among the heaviest sweeters while on the drug. I've also wondered about speed and the possible thyroid toxins (iodo-compounds, aziridines etc) produced via the pseudo methods. However, thyroid complaints are quite common, and I've usually been shot down in flames when I've suggested such things.
But as thyroid is influenced by pituitary and pituitary influenced by hypothalamus, and we've known for some time MDMA hyperthermia is induced by (5HT) actions on the hypothalamus, I've always been a bit inclined to think MDMA could affect thyroid function. If someone had a predisposition to a thyroid condition, it makes sense that they may inclined to get hotter, and therefore incur more neurological damage.
Of course if you do suffer from hyperthyroidism, you should not take any amphetamines or sympathmimetic amines anyway. The condition causes increased sensitivity and response to catcholamines, so any drug which stimulates them could also increase effects like palpitations, shortness of breath etc. Alcohol, caffeine and nictotine should be also avoided.
Thanks to Rhodium for finding the article
Here's the original article
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