3 ms·

This is absolutely fascinating to me. Is there any hypothesis as to why this is? I think its a damn shame where the conversation on depression is going. Depres

This is absolutely fascinating to me. Is there any hypothesis as to why this is? I think its a damn shame where the conversation on depression is going. Depression is tested and diagnosed by a questionnaire (presumably well-designed, with redundancies to make it robust). Antidepressants are serotonin reuptake inhibitors, a drug inspired by a monoamine hypothesis now discarded. We still prescribe them because they modestly lower the score on an observer rating scale better than placebo. If you take an SSRI, it should be bioavailable instantly! Why does depression take months to recover from? With this all said, all severely depressed people should get medical treatment; moderately depressed people should consider trying it. I also don't want to strawman medicine, science or psychiatry, and claim that they think we are serotonin vessels. They acknowledge all the stuff I said above. I just don't know if its communicated to the layman or the media, especially when we see horrendous, exponentially growing rates like this.

Nasrudith 7y ago
Speaking from experience at the very lowest you can "shut down" lacking motivation to do anything. The thing is mood and motivation are shockingly separate and antidepressants are a "try and see what fits". So if it combos to improved motivation while still feeling suicidal that is a bad combination. As for the why biochemically it not certain but it involves longer cycles. Ketamine is one faster acting hope but it isn't widely used from other concerns.
fucking_tragedy 7y ago
Administration of antidepressants initiates with up-regulation of target receptor sites along with many, many non-target receptor sites. Over time, those target receptors down-regulate and that is what is theorized to contribute to the antidepressant effect. The period of initial antidepressant use and its associated up-regulation of receptors can increase activation, anxiety and akathisia, a feeling of intense physical discomfort and restlessness, with many people finding the anxiety and akathisia to be inescapable. One receptor associated with this is the 5HT2C subtype, which is not a targeted receptor, but still is activated as a side-effect of SSRI therapy. It's hypothesized that people might harm themselves in order to decrease or escape the discomfort they feel while beginning antidepressants. Another hypothesis is that the anxiety and activation might drive someone who is struggling with suicidal thoughts to act upon them before the antidepressant's therapeutic effects kick in. One of the reasons Prozac is approved for minors is 1) it has an extremely long half-life such that a missed dosed isn't the end of the world and 2) it antagonizes the 5HT2C receptor site, theoretically minimizing activation, anxiety and akathisia associated with starting an antidepressant regimen.

Nasrudith 7y ago

Speaking from experience at the very lowest you can "shut down" lacking motivation to do anything. The thing is mood and motivation are shockingly separate and antidepressants are a "try and see what fits". So if it combos to improved motivation while still feeling suicidal that is a bad combination. As for the why biochemically it not certain but it involves longer cycles. Ketamine is one faster acting hope but it isn't widely used from other concerns.

fucking_tragedy 7y ago

Administration of antidepressants initiates with up-regulation of target receptor sites along with many, many non-target receptor sites. Over time, those target receptors down-regulate and that is what is theorized to contribute to the antidepressant effect. The period of initial antidepressant use and its associated up-regulation of receptors can increase activation, anxiety and akathisia, a feeling of intense physical discomfort and restlessness, with many people finding the anxiety and akathisia to be inescapable. One receptor associated with this is the 5HT2C subtype, which is not a targeted receptor, but still is activated as a side-effect of SSRI therapy. It's hypothesized that people might harm themselves in order to decrease or escape the discomfort they feel while beginning antidepressants. Another hypothesis is that the anxiety and activation might drive someone who is struggling with suicidal thoughts to act upon them before the antidepressant's therapeutic effects kick in. One of the reasons Prozac is approved for minors is 1) it has an extremely long half-life such that a missed dosed isn't the end of the world and 2) it antagonizes the 5HT2C receptor site, theoretically minimizing activation, anxiety and akathisia associated with starting an antidepressant regimen.