14 medications later, T3 thyroid hormone gave a 33% remission rate for bipolar + a 84% improvement rate

cs3000

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Along with all the studies on thyroid helping depression
1st one is a retrospective study that gives insight into a beneficial & curative effect for bipolar too , fitting with another trial
The charts of patients treated with T3 in a private clinic during the period of 2002–2006 were reviewed.
This study was a retrospective chart review of patients treated in a private clinic between 2002 and 2006. The charts of 125 patients with bipolar II disorder and 34 patients with bipolar disorder NOS were reviewed.
Patients had been unsuccessfully treated with an average of 14 other medications before starting T3.
At an average dose of 90.4 mcg (range 13 mcg–188 mcg) the medication was well tolerated.
None of the patients experienced a switch into hypomania, and only 16 discontinued due to side effects. Improvement was experienced by 84%, and 33% experienced full remission.
Very few patients experienced worsening depression, and none experienced a switch into hypomania on T3. A high percentage of patients experienced improvement on T3, and approximately one third went into remission

a trial using increased does of t4 only (less effective signalling than adding t3) until response gained
Levothyroxine was added to the baseline medication regimen, and the dosage was increased until clinical response occurred or until side effects precluded further increase. While patients were taking levothyroxine, scores on both depressive and manic symptom rating scales decreased significantly compared with baseline.
This improvement was due to the clear-cut response of depressive symptoms in 10 of 11 patients, with manic symptoms responding in five of the seven patients who exhibited them during baseline evaluation.
Four patients then underwent single- or double-blind placebo substitution; three patients relapsed into either depression or cycling. Treatment response did not depend on previous thyroid status. In 9 of 10 responsive patients, supranormal circulating levels of free thyroxine were necessary to induce clinical response. Side effects were minimal, and there were no signs or symptoms of levothyroxine-induced hypermetabolism.
 
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