HPA axis reboot?

[adreno]

I have read that avanza/mirtazapine has cortisol lowering effects, so probably why it helps some with insomnia.
Its commonly mentioned that we have high night time cortisol which is why many of us have sleep issues but i think our total 24 hour cortisol output would probably be low, although i havent had this sort of testing done. At night i dont think our cortisol is excessively high but just high enough to bugger our sleep?? its the 3 bears thing, too hot, too cold and just right. I think finding that just right part will be apart of helping us sleep naturally as well as waking in the morning with some pep in our step.

Right, mirtazapine lowers cortisol. I think we can not say anything in general about our diurnal cortisol. Some have low (flat) throughout the day and night, whereas other others might have a skewed rhythm, with too low in morning and too high at night. Mine was flat all the way both times I tested. Strangely though, I had a lot of (physical) energy on mirtazapine, although mentally it felt like I was lobotimized. Perhaps because it enhances NE release.

 

[Ema]

"Studies demonstrate that the neurotransmitter serotonin acts as a stimulant of the hypothalmo-pituitary-adrenocortical axis (Fuller 1981), thereby producing excesses of body steroids. Serotonin, if not the specific substance, is apparently one of those substances in the brain that stimulates the adrenals.

Elevated levels of CRF, cortisol and ACTH are evidence of both stress and depression, yet animal studies with SSRIs showed that they increased the levels of ACTH, cortisol and prolactin (Stark et al. 1985; Lesieur et al. 1985 & Jones, Hillhouse and Burden in Frontiers in Neuroendocrinology, Vol. 4).

Studies also demonstrate that serotonin levels correspond with the daily rise and fall pattern of corticosteroid secretion. One single dose of 30mg of Prozac doubles cortisol levels (Petraglia et al. 1984)."

If the adrenals are weak due to primary adrenal insufficiency or an autoimmune attack, eventually they will no longer be able to respond to the demand for increased cortisol by the antidepressant. And then everything really starts to fall apart.

Ema

 

[adreno]

"Studies demonstrate that the neurotransmitter serotonin acts as a stimulant of the hypothalmo-pituitary-adrenocortical axis (Fuller 1981), thereby producing excesses of body steroids. Serotonin, if not the specific substance, is apparently one of those substances in the brain that stimulates the adrenals.

Elevated levels of CRF, cortisol and ACTH are evidence of both stress and depression, yet animal studies with SSRIs showed that they increased the levels of ACTH, cortisol and prolactin (Stark et al. 1985; Lesieur et al. 1985 & Jones, Hillhouse and Burden in Frontiers in Neuroendocrinology, Vol. 4).

Studies also demonstrate that serotonin levels correspond with the daily rise and fall pattern of corticosteroid secretion. One single dose of 30mg of Prozac doubles cortisol levels (Petraglia et al. 1984)."

If the adrenals are weak due to primary adrenal insufficiency or an autoimmune attack, eventually they will no longer be able to respond to the demand for increased cortisol by the antidepressant. And then everything really starts to fall apart.

Ema

This is incorrect.

Here's an example of a clinical trial in which an SSRI lowered cortisol output:

Compared with placebo-treated patients, SSRI-treated patients had a significantly greater reduction in both peak and total cortisol. This reduction in cortisol was limited to patients with elevated (above the median) baseline cortisol, in whom SSRI-treated patients showed substantially greater reduction in cortisol than did placebo-treated patients.

http://www.ncbi.nlm.nih.gov/pubmed/20808146

As I said, it depends on the baseline level before the treatment. SSRIs will not "deplete the adrenals". This is just nonsense.

 

[adreno]

But perhaps I was wrong about PTSD. In this study, cortisol was again decreased by SSRIs:

Treatment resulted in a decrease of salivary cortisol levels on all time points on a diurnal curve. Despite similar stress perception, cortisol response to the cognitive stress challenge resulted in a 26.5% relative decrease in stress-induced salivary cortisol with treatment. These results suggest that successful treatment with SSRI in chronic PTSD is associated with a trend for a decrease in baseline diurnal cortisol and with reduced cortisol reactivity to stress.

http://www.ncbi.nlm.nih.gov/pubmed/16891570

 

[adreno]

Another example of an SSRI calming down an hyperactive HPA axis:

Citalopram increases glucocorticoid-mediated negative feedback on the HPA axis after as little as 4 days of treatment. This effect could be due to an increased function of the corticosteroid receptors. Our findings further support the notion that one of the mechanisms by which antidepressants exert their therapeutic effects is by normalizing HPA axis hyperactivity in depressed patients.

http://www.ncbi.nlm.nih.gov/pubmed/15179544

 

[Ema]

This is incorrect.

Here's an example of a clinical trial in which an SSRI lowered cortisol output:

http://www.ncbi.nlm.nih.gov/pubmed/20808146

As I said, it depends on the baseline level before the treatment. SSRIs will not "deplete the adrenals". This is just nonsense.

Since when are studies nonsense?

The study you posted refers to patients with an elevated cortisol level to start. Eventually those using SSRIs with adrenal insufficiency or HPA axis dysfunction will have LOW cortisol and continuing to use SSRIs can cause a terrible crash or possibly even an adrenal crisis.

You have to understand and differentiate between the populations.

Ema

 

[Ema]

Another example of an SSRI calming down an hyperactive HPA axis:

http://www.ncbi.nlm.nih.gov/pubmed/15179544

This study further proves my point. Thanks for posting it!

It clearly states that antidepressants increase cortisol at first and then can cause low cortisol when used chronically.

Ema

 

[adreno]

Eventually those using SSRIs with adrenal insufficiency or HPA axis dysfunction will have LOW cortisol and continuing to use SSRIs can cause a terrible crash or possibly even an adrenal crisis.

Excuse me, I must have missed the reference to the claim that SSRIs can cause an adrenal crises? Which studies were you referring to? I haven't seen any.

I am not talking about treating Addison's with SSRIs. Someone asked about the effects of antidepressants on cortisol levels, and I have tried to answer that. I am not recommending any treatment.

 

[adreno]

This study further proves my point. Thanks for posting it!

It clearly states that antidepressants increase cortisol at first and then can cause low cortisol when used chronically.

Ema

You misinterpret the results. As I said, acutely serotonin will stimulate cortisol release, but as the receptors start to become tolerant, less cortisol is released. This has got nothing to do with adrenals being depleted, or having an adrenal crisis. This all goes back to the belief in "adrenal fatigue", and that the adrenals can somehow be worn out. But I am going to stop debating this with you, clearly there is no point. Everyone can make up their own minds from the data.

 

[Ema]

I am not talking about treating Addison's with SSRIs. Someone asked about the effects of antidepressants on cortisol levels, and I have tried to answer that. I am not recommending any treatment.

Unfortunately many people with Addison's and HPA axis dysfunction are treated with SSRI antidepressants and often as a first line treatment. This can be devastating. Low cortisol can progress to an adrenal crisis which is well documented and can be deadly.

SSRIs increase serotonin which increases cortisol and eventually leads to lower overall levels in those with adrenal insufficiency and HPA dysfunction.

This includes quite a few members of the ME/CFS population as well as endocrine dysfunction is typically encountered in our disease.

Those who don't know their adrenal status should exercise extreme caution when using antidepressants of this and related classes and be aware of the risks that may not be apparent until after used for some period of time. This may also be the reason people feel that antidepressants "poop out" after a while and stop working...the adrenals simply can't be stimulated any longer.

Ema

 

[lavonia]

I want to mark this thread and reread it later. There are a lot of articles on opiates and HPA disruption. It varies a lot depending on the person (ie probably on the status of their adrenal glands, neurotransmitters to begin with).
I might have some more relevant comment after I read up this and reread some of my saved med studies.

Going to post this on Tramadol Induced Adrenal Insufficency
http://hal.archives-ouvertes.fr/docs/00/66/08/93/PDF/PEER_stage2_10.1007%2Fs00228-011-0992-9.pdf

It seems relevant to this conversation. I have the same symptoms and similar lab numbers to person in the above study. I pulled Tramadol (opiate and SNRI) slowly over time. It was a wonderful drug when I started taking it. However, over time the adrenal dysfunction got worse and worse. I'm not off of it long enough to say it was specifically caused by the tram, but we will see over time. Opiates definitely made the problem worse, the higher amount of opiate intake, the more my blood pressure would plummet. Going to 90/45 at worse, sitting. Never could get a read on it standing. From the drop, I've gone from standing once a day to 6 times a day, even exercising some.
I would from an experience standpoint and from reading say that there is a definite link between opiate use and cause for caution concerning the adrenals.

With the SSRI, I'd always had trouble with those as well. Never functioned well on them. That's why I chose Tram over an SSRI for severe nerve pain. I'd be curious to see what's happening under the hood, so to speak but I don't know. I'm going to read over some material and see what I think.

Thanks for the article links.