Levothyroxine desensitation?

[sleepycat6]

I'm new to Levo. I have not been officially diagnosed as Hypothyroid, despite having longterm depression & some vague related symptoms (like fatigue, dry skin).

I'm curious if anyone knows if the effects of taking Levothyroxine longterm are similar to antidepressants in the way of de-regulation? Or desensitation?

For example: Long-term use of SSRIs results in a down regulation of postsynaptic serotonin receptors, and receptors may remain in their hypoactive state... (so taking antidepressants long term comes with a risk that you may be unable to quit and will be dependent on taking them for life.) Otherwise, many people must continue to increase the dosage until they stop working altogether.

My question is, as someone who is not fully "Hypothyroid" - will taking Thyroid meds render my body incapable of producing thyroid hormones altogether? Are there any cases where people take Thyroid meds short term, or is it always for life?

[SlowDragon Administrator]

Levothyroxine doesn’t “top up “ failing thyroid, it replaces it

So most people when adequately treated on levothyroxine will eventually be on (or near) full replacement dose

If your thyroid wasn’t damaged by autoimmune thyroid disease, in theory you could slowly reduce and then stop levothyroxine

In practice, most people when prescribed levothyroxine already have some degree of thyroid damage, and this usually gets worse over time

[jimh111]

High doses of thyroid hormone that suppress TSH (reduce it close to zero) over a period of several months or more can ‘down-regulate the axis’ which means TSH stays low and doesn’t recover. This would lead to a need for permanent thyroid medication.

If the thyroid is healthy thyroid hormone therapy will gradually atrophy the thyroid but it usually recovers over time when the thyroid tablets are discontinued. Sometimes a thyroid is partially damage and so thyroid tablets may supplement the remaining thyroid. However, in autoimmune hypothyroidism where the thyroid is gradually destroyed patients may be fine on a supplementary dose for some time but eventually need a full replacement dose.

There are cases of temporary hypothyroidism, perhaps the most common being post partial thyroiditis where a woman’s thyroid is inflamed for many months after giving birth but it recovers in time.

Hypothyroidism can also be caused by insufficient TSH stimulation of the thyroid. This can be caused by severe illness, starvation and depression. This is why I suggest you get TSH, fT3 and fT4 measured, in case your thyroid hormones are on the low side in spite of what appears to be sufficient TSH stimulation. TSH can have various molecular structures and they are not all active, this is not picked up by the TSH assay.

[radd]

sleepycat6,

As soon as Levothyroxine is added there will be change to the HPT axis and thyroid signalling. The level of change & chance of reversal is dependant upon multiple factors such as the functional workings of the thyroid gland, other glands & bodily systems, the amount medicated, other medications and nutritional status.

For example medicating Levothyroxine with inadequate iron or a dose which takes FT4 levels over range risks encouraging elevated RT3 which in turn negatively alters other body mechanisms.

T4 is a pro-hormone that requires conversion to active hormone T3. Because depression can negatively influence enzymes (deiodinases) that works in convertion of T4 to T3 & cellular activity, when medicating for depression it is more commonly seen for T3 to be added as is itself a neurotransmitter as well as a hormone, and its short life ensures quick uptake and easier titivation of tiny amounts. This also carries the same levels of change to thyroid signalling but in a slightly different way.