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Re: Which antidepressants are 'less' activating? Mtom

Posted by linkadge on August 7, 2021, at 10:50:56

In reply to Re: Which antidepressants are 'less' activating?, posted by Mtom on August 6, 2021, at 18:20:09

Hi,

You raised many good points in the discussion of SSRIs vs. TCAs.

In terms of cardiac safety, there are two things to consider. The first is the norepinephrine reuptake inhibition which can increase heart rate and/or blood pressure, the second is the sodium channel inhibition. For the first effect, many newer antidepressants (venlafaxine, milnacipran, bupropion, duloxetine etc.) inhibit norepinephrine reuptake too. Venlafaxine seems to be particularly bad at raising blood pressure. Blood pressure monitoring is important in these cases.

The second effect of the TCAs is the inhibition of sodium channels. My understanding is that this effect is only really problematic in the higher / overdose situations. Again, many non-TCA drugs (i.e. antiepileptics, lithium) block sodium channels and (depending on the dose) can alter heart rhythm. Also, it is more problematic in people taking other sodium channel blockers or with genetic defects (i.e. Brugada syndrome which affects sodium channels).

Nortriptyline generally has a wide cardiac safety index in spite of some ability to block sodium channels. Also, it has been studied extensively in helping patients with post heart attack related depression. It has also been studied quite a bit in elderly with depression. It appears particularly good at treating depression related to Parkinson's disease or other comorbidities. There have been studies showing that apathy (from SSRIS) can be relieved by switching to (or adding) nortriptyline.

I tend to think that the 'cardiac safety' is more viewed in terms of safety in overdose. This may protect the doctor from lawsuit, and yes the patient from overdose, but denying the option may also keep the patient sick. I wonder too about some of the initial research comparing SSRIs to TCAS. There could be a heavy sponsorship bias. In a similar vein, initial studies show that the atypical antipsychotics were much more effective than the older ones. Later however, a large study (CATIE) showed that atypicals were no better than the older antipsychotics for core symptoms and caused more metabolic problems (but fewer movement related problems).

In terms of the lack of selectivity, this may cause more side effects but can also contribute to the therapeutic effect. For example, the antihistamine effects can contribute to reduced anxiety and/or improved sleep. The anticholinergic effects can help depression and/or anxiety (like scopolamine). The sodium channel blocking effects can reduce anxiety (similar to mood stabilizer augmentation). Drugs like amitriptyline too tend to improve sleep much better than SSRIs. I tend to think that sleep disruption from SSRIs may contribute to tachyphylaxis.

At the end of the day, your doctor should be open to trying a drug from another class if you have tried sufficient SSRIs and found them to be intolerable.

The side effects from TCAs are different and (depending on your situation) may actually be preferable. For example, I noticed zero agitation or insomnia on amitriptyline (as I do on SSRIs) as well as no sexual dysfunction. I also felt MUCH less apathetic and had more energy on amitriptyline than SSRIS. I did feel a bit more spacy and had a bit of blurred vision.

At the end of the day, your doctor should be willing to try a drug from a different class, especially if the current medications are intolerable.

I left a link below to Dr. Gillman's website. He was a psychiatrist who also did research on serotonin syndrome and MAOIs. He has some good thoughts on the TCAs.

https://psychotropical.com/tca-intro/

Linkadge


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