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sophiaria

Latuda for Major Depressive Disorder??

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I have a severe unipolar depressive disorder that is resistant to many medications. Nothing really has worked (Wellbutrin, Abilify, sertraline, Prozac, desvenlafaxine /Pristiq). My doctor prescribed me Latuda which is a bipolar/antipsychotic. Although I got alarmed and I told her so immediately, she convinced me that this could help me blah blah blah. However, I'm still worried, my psychologist (not a medical doctor obviously) too got alarmed once found out, although she said she doesn't know much about this medication, the fact that it's antipsychotic for a person who's severely down and lethargic (me) is concerning. 

I'm currently on Pristiq (150mg), Latuda (20->40mg), and Adderall. I have not yet seen any effects.

Has anyone here been prescribed Latuda for severe depression, how was your experience? Any suggestions, warning, or tips?

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Contrary to what one may believe about antipsychotics in general, Latuda and some other antipsychotics have a dose-dependent effect wherein certain dose ranges may be stimulating, some you may not feel anything, and some you may feel a bit sedated. With Latuda, generally low doses are stimulating (20-40 mg), moderate doses tend to be innocuous (40-60 mg), and high doses may be a little on the sedating side (80-160 mg).

Try not to be alarmed by the name of the class of medication. There are many mechanisms of action that provide benefits for depressive symptoms. 5-HT1A partial agonism causes downstream dopamine release, 5-HT2A antagonism causes dopamine release in the pyramidal neurons in the prefrontal cortex (I believe), and 5-HT7 antagonism not only helps with serotonin release and subsequently depression, but can help with memory/learning as well as regulating circadian rhythm. 5-HT7 antagonism is Latuda's strongest mechanism of action. The dopamine D2 antagonism occurs on both sides of the neuron: presynaptically it antagonizes the autoreceptors with high affinity, which disinhibits dopamine release, while postsynaptically, it has a more rapid dissociation rate from the D2 neurons and hence doesn't block the effects of dopamine stimulation as much as other antipsychotics might.

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