[SkyPuncher]

> Sometimes they can help, but they can also cause really strange side effects, like increasing the possibility of suicide

FWIW, my understanding is this has little to do with the drugs and mostly to do with the recovery process.

In a deep depression, you might have suicidal thoughts, but lack the will to take action on those thoughts (because depression takes away your motivation). As you a person comes out of depression, they tend to recover their motivation before their suicidal thoughts dissipate. This creates a situation where a person with suicidal thoughts now has motivation - which means they have the potential motivation to take action on their suicidal thoughts.

The important nuance of this is anti-depressants don't necessarily make your suicidal thoughts _more_ suicidal. In fact, it's likely, anti-depressants are making your suicidal thoughts _less_ severe. However, they do increase your motivation before they can fully eliminate suicidal thoughts.

I'm not saying you should take an anti-dpressant willy-nilly. It's just BS to be fear mongering like this without considering why this situation happens.

[heavyset_go]

In the beginning of SSRI consumption, it causes initial 5HT2C upregulation and activation, which can directly cause feelings of anxiety, dread, hopelessness, and restlessness/akathisia[1]. Over time, however, the body down regulates 5HT2C in response to its activation, and those symptoms tend to dissipate.

In a way, yes, there can be feelings induced that can provide the motivation and energy to go through with suicidal thoughts, but those unpleasant emotions aren't exactly triggered by an inherent will to die. Those who experience akathisia sometimes feel like the only way to rid themselves of the feeling is to end their lives.

I point this out because it might seem, or feel to those experiencing it themselves, that those suicidal thoughts are organic and what the person really wants, but they tend to be exacerbated directly by medication and can get better with time. I also point it out because there are ways to sidestep 5HT2C activation with different medications or combinations, it doesn't necessarily have to be inevitable.

[1] https://en.wikipedia.org/wiki/Akathisia

[oaktrout]

I didnt find any info on 5HT2C in the linked source above, not saying what you've said isn't true, just that I was interested and didn't find much info.

[heavyset_go]

Here's Wikipedia's summary, there are sources cited in the article[1]:

> Research indicates that some suicide victims have an abnormally high number of 5-HT2C receptors in the prefrontal cortex.[13] Agomelatine, which is a 5-HT2C and 5-HT2B antagonist as well as a MT1 and MT2 agonist, is an effective antidepressant.[14][15] It has been called a norepinephrine-dopamine disinhibitor because antagonism of 5-HT2C receptors by agomelatine results in an increase of dopamine and norepinephrine activity in the frontal cortex. Conversely, many SSRIs (but not fluoxetine, which is a 5-HT2C antagonist[16]) indirectly stimulate 5-HT2C activity by increasing levels of serotonin in the synapse although the delayed mood elevation that is usually typical of SSRIs is usually paralleled by the downregulation of the 5-HT2C receptors.[17] Many atypical antipsychotics block 5-HT2C receptors, but their clinical use is limited by multiple undesirable actions on various neurotransmitters and receptors. Fluoxetine acts as a direct 5-HT2C antagonist in addition to inhibiting serotonin reuptake, however, the clinical significance of this action is variable.[16] Several tetracyclic antidepressants, including mirtazapine, are potent 5-HT2C antagonists; this action may contribute to their efficacy.

> An overactivity of 5-HT2C receptors may contribute to depressive and anxiety symptoms in a certain population of patients. Activation of 5-HT2C by serotonin is responsible for many of the negative side effects of SSRI and SNRI medications, such as sertraline, paroxetine, venlafaxine, and others. Some of the initial anxiety caused by SSRIs is due to excessive signalling at 5-HT2C. Over a period of 1–2 weeks, the receptor begins to downregulate, along with the downregulation of 5-HT2A, 5-HT1A, and other serotonin receptors. This downregulation parallels the onset of the clinical benefits of SSRIs. 5-HT2C receptors exhibit constitutive activity in vivo, and may retain the ability to influence neurotransmission in the absence of ligand occupancy. Thus, 5-HT2C receptors do not require binding by a ligand (serotonin) in order to exhibit influence on neurotransmission. Inverse agonists may be required to fully extinguish 5-HT2C constitutive activity, and may prove useful in the treatment of 5-HT2C-mediated conditions in the absence of typical serotonin activity.

[1] https://en.wikipedia.org/wiki/5-HT2C_receptor#Function