Ultimately I think my intellectual productivity (and quality of life, happiness level, interestingness, et cetera) is better when I'm manic and I'd like to take advantage of that, but I feel obligated to see how Algernon's principle applies
People who are experiencing mania or hypomania often exhibit overconfidence, impulsiveness, and irritability, and often make poor decisions.
Hmuh, in the evolutionary environment where there's not much intellectual work to do these would be enough to somewhat punish mania, but in modern society I think that the increased cognitive performance of manic states is probably a stronger factor... in which case Algernon's law need not be feared. But maybe there are other detriments related to personal health?
I was looking at a hypothesis that bipolar disorder is probably due to problems with neocortical sodium-potassium pump activity cyclically decreasing and thus allowing increased resistance, which increases neuronal excitability by the square of the resistance. According to what I've read on Wikipedia it seems that agonizing Gi proteins would inhibit cAMP production and therefore downregulate sodium pump activity (this was the most tenuous part, and the reference was unintelligible) and increase neuronal excitability. But 5-HT1A (a type of Gi protein) agonists have been shown to be useful for improving symptoms of schizophrenia, which is typically thought of as resulting from increased neuronal excitability. Sign error? What's up? I don't have any model of the underlying mechanisms, and only vaguely know what words like 'downregulate' mean.
ETA: But apparently http://en.wikipedia.org/wiki/Risperidone , a 5-HT2A agonist, also supposedly mitigates symptoms of schizophrenia, which is weird because it increases neuronal excitation. It seems that the flawed assumption is that schizophrenia has something to do with 5-HT-caused neuronal excitability.
Thus it seems like maybe you can reduce bipolar tendencies by taking 5-HT1A antagonists, and schizophrenia is its own separate problem that is perhaps solved by taking a D2 antagonist. 5-HT2A agonists increase neuronal excitation which may interact somehow with the the 5-HT1A antagonists. I'm still confused.
There's this other problem where if the main reason D2 and 5-HT1A work is by decreasing neuronal excitability that might just be because sedate people are more similar to each other than manic people, but the kind of neuronal excitability that makes people manic and the kind that makes people schizoid are qualitatively different, and hence the difference in receptors being important. It could be that 5-HT2A agonists and 5-HT1A antagonists increase and decrease neuronal excitability respectively, but in different ways such that they're not countervailing.