Selegine would be the best to try to increase DA, correct?
Also buspirone is a pretty harmless med I've found with a side effect that makes you feel uncomfortable if you take too much. But it does work for anxiety, especially if it's serotonim related.
I mostly go for pleasures like drugs, fast driving, risk taking. How could one gauge serotonin?
You can do a 24hour urine test, for the serotonin metabolite; 5-HT1AA ; get your GP/Doc to order it.
I routinely get this and the metanephrine/normetanephrine test done; just to be sure I'm at where I want to be - every 3 months.
Serotonin is an extremely over rated chemical, and though it has anti-depressant properties, the irony, is the receptors that produce this effect also tend to be the same receptors that are heterodimerized with autoreceptors or neurokinin, e.g 5-HT1A, say yet, buspar producing anxiolytic and even some anti-depressant effects.
Interestingly, the serotonin synthesis inhibitor ; p-chlorophenylylanine - doesn't induce depression in all of the studies..so there must clearly be more involved than just serotonin..and again, comes back to the individual in question.
I also believe social status is an overlooked factor in depression , especially for men...
If you have no ambition or place then this creates a psychological loop that leads to depression.
Same thing with testosterone levels. They are generally higher in people who CHOOSE to self-motivate themselves into success, they drive themselves into reward and success and then this burst of dopamine further stimulates testosterone...which is why the people that rarely ever run into hormone imbalance issues generally.
1.) Are successful in some way shape or form, or at least have some notoriety.
2.) Keep in shape and lean. (body fat increases estrogen) this also correlates to motivation as people concerned about mental health and cognitive function also usually work out to create synergism.
Neuropsychopharmacology. 1999 Aug;21(2 Suppl):24S-27S.
Sleep and serotonin: an unfinished story.
Abstract
Serotonin (5-HT) was first believed to be a true neuromodulator of sleep because the destruction of 5-HT neurons of the raphe system or the inhibition of 5-HT synthesis with p-chlorophenylalanine induced a severe insomnia which could be reversed by restoring 5-HT synthesis. However the demonstration that the electrical activity of 5-HT perikarya and the release of 5-HT are increased during waking and decreased during sleep was in direct contradiction to this hypothesis. More recent experiments suggest that the release of 5-HT during waking may initiate a cascade of genomic events in some hypnogenic neurons located in the preoptic area. Thus, when 5-HT is released during waking, it leads to an homeostatic regulation of slow-wave sleep.
PMID:
10432485
[PubMed - indexed for MEDLINE]
Edited by Area-1255, 01 January 2015 - 04:01 PM.