Ask HN: Beating depression with or without anti-depressants?

I would try them. They probably have side effects, they did for me. But the side effects are definitely not worse than that pit in the stomach. At least for me. Exercise has also been effective at ameliorating some of my anxiety/depression.

Unfortunately, psychiatry / psychology is currently barely a science. It still doesn’t have a repeatable theoretical model yet for some odd reason there are people who treat it as a science with real laws. Will it mature one day into a real science? Sure, but it’s dependent on several other fields maturing so it won’t be overnight. Consequently, I don’t blame anyone for doing more research or going with alternatives, especially since the economics of mental healthcare also go against the welfare of those who need it.

> PLEASE do not read any of these people's advice. Talk to a MEDICAL PROFESSIONAL, preferably a DOCTOR. DO NOT trust your mental health to strangers on the internet, be it reddit, or hacker news, or whatever.

I find this comment so overused, ignorant and dismissive. In my city it can take months to get a 20 minute appointment with a specialized doctor, while the internet is full of useful and scientific information and helpful people. That isn't even saying if the doctor really understands your problem or just dismisses it (had that often enough), like you dismiss other people's anecdotes. What are people supposed to do while they are waiting for an appointment for months with acute issues? I'd rather spend days myself and read the same information that a doctor (hopefully) would read in order to work on the problem before it gets worse or kills me.

So yes, try to talk to a medical professional at least once if you have the chance. If not or if it does not help, keep doing what you need to do and try to get the best information that you can find.

I have also found vitamin D to be important for my mental health. In the past I found probiotics extremely helpful for my mood as well, though lately they haven't seemed to effect me much (seems to have changed after I had a course of antibiotics, so perhaps the reason they had been effective was related to an interaction with some bacteria?)

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