I'm a clinical social worker/therapist and know a bit about bi-polar disorder and schizophrenia. My clients are all children and few have been given either diagnosis yet, although more will probably when they are older. I don't think that we really know yet whether avoiding medication increases ones chances of actual schizophrenia. One article I recently read actually suggested that taking anti-psychotics long term might prevent one from making a full recovery after a psychotic episode.
I do know that you should avoid certain psychoactive substances, most of which are illegal (LSD, uppers, etc.) and heavy alcohol use. It is also best to try to avoid super stressful situations as much as you can.
It is my understanding that many people with bi-polar disorder (and schizophrenia) don't like their medications because it makes them feel flat.
If you can get objective feedback from family or friends about your behavior in manic states it would be helpful for you to assess whether you should get treatment. You could ask them whether you are doing risky things? Are you so irritable/manic that you are antagonizing others?
My 2nd cousin once removed, Lizzie Simon has bi-polar disorder. She wrote a book, "Detour : My Bipolar Road Trip in 4-D " in which she writes about her own experiences and interviews with other individuals with bi-polar disorder. She was looking for individuals who were functioning well. Lizzie goes around the country lecturing about bi-polar disorder. You might want to check out the book or/and her website.
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.