Thyroid hormone for depression

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cbrons

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Has anyone ever used T3 or T4 to treat depression? From reading the UpToDate article, it seems T3 is more highly studied for this indication.

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Done it. An odd effect is, and counter-intuitively, it can cause weight-gain. You'd expect it to do the opposite and I've seen patients gain weight from it though they also did get benefits.
 
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Has anyone ever used T3 or T4 to treat depression? From reading the UpToDate article, it seems T3 is more highly studied for this indication.

I find a disturbing number of people (often peri or post menopausal women) in the community come to me already on levothyroxine, ostensibly for sub clinical hypothyroidism, but most likely for energy/weight loss as they age, all prescribed by PMD and unable to tolerate taper. It’s always worthwhile asking how they’ve been taking it (empty stomach in am).

I’ve used T3/Cytomel on a few occasions, with mixed results. While the dosing recs on UpToDate are once daily, an endocrinologist I spoke to actually said that given pharmokinetics, it should be up to three times a day (at least as a replacement for someone deficient).
 
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I find a disturbing number of people (often peri or post menopausal women) in the community come to me already on levothyroxine, ostensibly for sub clinical hypothyroidism, but most likely for energy/weight loss as they age, all prescribed by PMD and unable to tolerate taper. It’s always worthwhile asking how they’ve been taking it (empty stomach in am).

I’ve used T3/Cytomel on a few occasions, with mixed results. While the dosing recs on UpToDate are once daily, an endocrinologist I spoke to actually said that given pharmokinetics, it should be up to three times a day (at least as a replacement for someone deficient).

Some of the people I have read advocating for it particularly strongly have asserted that results are often better when prescribing it for people who are actually mostly euthyroid if the aim is to treat what we would recognize as severe depression. That might be a justification for not necessarily dosing it in a way that our endocrinology colleagues would recognize. I would not be shocked that to the extent it was effective the time course of its effectiveness would not be isomorphic with the point at which serum plasma levels are highest.
 
I have tried Cytomel augmentation a few times. Very mixed results. Endo hates it, they never want to let me go over 10 mcg when published efficacy for depression augmentation is in the 50 mcg range. It does feedback inhibit the endogenous release of T3 and T4 which may explain both the weight gain and the Endo antipathy. It's not recommended to stay on fif more than 6 months either so it's not a long term solution. I don't try this too much anymore, I don't see enough benefit to make it worth the hassle.
 
I have tried prescribing Cytomel augmentation several times, and in each case it did not do anything (negative or positive).
 
I've tried T3 a handful of times without any patient benefit. At worst, the patients have mild hyperthyroid symptoms like tachycardia and heat intolerance.
 
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Better would be an explanation as to why psychiatrists decided to use T3 instead of T4. The only physiologic difference is the amount of weight loss your wallet experiences paying for a med that's 100x more expensive.
 
I've never used Cytomel in residency, or as a young attending, and don't plan on using it, mainly due to what @tr said. There are so many other options for when someone is a non-responder or poor responder, that it doesn't make much sense to me to mess with the thyroid, especially when Cytomel can't be prescribed chronically.
 
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Thanks for the references, but honestly I'm not convinced.

In the first study, they didn't use a placebo control and the groups in total do not look like they reached statistical significance for a difference. So they chose a cutoff value to define "responder" to make the difference significant. Also, it's likely that T3, as pointed out by splik, may be harder to blind than T4. (Shorter acting - immediate effect - hop right on out of bed.)

The second actually points out the relative lack of good evidence. Also, if it were an actual thing, you'd think we'd have clarified this "relative brain hypothyroidism due to relative inhibition of brain 5-something-or-another-iodinase" in the intervening 20 years...
 

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Thanks for the references, but honestly I'm not convinced.

In the first study, they didn't use a placebo control and the groups in total do not look like they reached statistical significance for a difference. So they chose a cutoff value to define "responder" to make the difference significant. Also, it's likely that T3, as pointed out by splik, may be harder to blind than T4. (Shorter acting - immediate effect - hop right on out of bed.)

The second actually points out the relative lack of good evidence. Also, if it were an actual thing, you'd think we'd have clarified this "relative brain hypothyroidism due to relative inhibition of brain 5-something-or-another-iodinase" in the intervening 20 years...

Or the effective mechanism is something very different from how it helps people who are more classically hypothyroid, just like propranolol''s effectiveness in relieving somatic anxiety symptoms appears to be it's central action and not at all about how well it blocks peripheral adrenergic receptors.
 
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