For all us actual depressives out there, this is really interesting

While trying to find out whether antidepressants really completely block the absorption of thyroxine as I've seen asserted a couple of times, I found this:

It's a very interesting, evidence-based article on using thyroid medications to 'supercharge' antidepressants, especially tricyclics (my antids of choice) and SSRIs.

3 Replies

  • I'm fortunate not to suffer from clinical depression, but I have been prescribed a variety of antidepressants prior to my diagnoses of hypothyroidism and pernicious anaemia, so I was intrigued by your post.

    I haven't read the full article yet (2 hours sleep last night), but it looks very interesting; a few ideas/concerns are pinging around my head already. I'll come back later with comments.

    Thanks for posting.

  • Delayed getting back here to comment... I'm afraid I can only get access to the first page of the report without being asked to sign up to the site, so my comments are limited.

    This paragraph caught my attention:

    "Subclinical hypothyroidism. Early studies such as by Howland[8] of treatment-refractory MDD suggested that thyroid hormone augmentation might correct a hypothyroid state. However, blood thyroid hormone levels are not associated with resistance to antidepressant treatment, according to studies of MDD populations.[9-10] Also, thyroid hormones’ therapeutic action in MDD appears unlikely to be related to treating subclinical hypothyroidism because patients’ euthyroid status was verified in all adjuvant studies since 1980."

    I think any reliance on blood levels of thyroid hormone in assessing resistance to ADs and as a method of verifying euthyroid status is inherently problematic. We know they are not a reliable indicator of intracellular thyroid hormone status.

    "Close interaction between thyroid hormones and the noradrenergic system also has been examined. Brain T3 is primarily localized in the central noradrenergic systems, with axonal anterograde transport of T3 from the locus ceruleus. T3 is processed and accumulated in the noradrenergic system, carried via axonal transport, then delivered from nerve cell bodies to its neuronal targets.[5,7] T3 thus functions as a coneurotransmitter with norepinephrine."

    T3 transport in the brain is not a subject I know anything about, so I find this very interesting, particularly from the point of view of someone who also has PA and is B12 deficient, with consequent neurological and cognitive problems. My interpretation - and I hope it's sound - is that axonal transport of T3 in the brain will be compromised by the damage ensuing from B12 deficiency.

    I'm sceptical about the other statements and conclusions further down the page, extrapolated from a number of studies, because some of the studies appear to be based on the administration of very short courses of T3, before its effects can be properly assessed, and the rapid titration of large doses of T3.

    I'm still absorbing the other information on p.1, so can't comment for now. Very interesting though - thanks!

  • Interesting article. I do know that Some SSRI's increase the conversion rate of T4 to T3.

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