So, what is bipolar disorder?

Desire — Justin Simoni

That was no beast that stirred,
That was my heart you heard
Pacing to and fro
In the ambush of my desire.
To the music my flute let fall.
— “Neither Spirit Nor Bird” (Shoshone Love Song), trans. Mary Austin

Since some folks were asking me about this, I thought I would post a little background on what bipolar disorder is, and how it is treated. Simply, bipolar disorder is a chemical brain disorder where the brain does not properly process neurotransmitter chemicals. In bipolar, this leads to a particular problem known as: desire. Whether it’s for stuff, sex, drugs, or just to feel better, bipolars desire things much, much more than other people. We feel more deeply, want things more desperately, and sometimes, just want to do anything to turn that feeling of desire off – but we can’t, not without the right drugs to balance us out. That’s why it’s so important to get the right treatment, because this is a genetic disorder, a physical disease with a very real cause.

University of California, San Diego: External Relations: News & Information: News Releases : Health
Researchers at the University of California, San Diego (UCSD) School of Medicine have identified a specific gene that causes bipolar disorder in a subset of patients who suffer from this debilitating psychiatric illness.

Published in the June 16, 2003 issue of the journal Molecular Psychiatry, the findings indicate that a mutation in a gene that regulates sensitivity to brain neurotransmitters such as dopamine, causes bipolar disorder in as many as 10 percent of bipolar cases. The mutation in this gene, G protein receptorkinase 3 (GRK3), occurs in a portion of the gene called the promoter, that regulates when the gene is turned on.

The research team hypothesizes that this mutation causes the individual to become hypersensitive to dopamine, leading to the mood extremes that characterize biopolar disorder.

A complex and variable illness, bipolar disorder is thought to be caused by multiple genes. Although previous research has suggested candidate genes or general DNA regions where faulty genes may reside, the UCSD study is the first to pinpoint a precise gene involved in the disease.

Also known as manic depression, bipolar disorder is characterized by extreme mood states alternating between euphoric peaks and terrible depression. Current treatments help many who suffer from bipolar disorder, but physicians estimate that one-third to one-half of the 1 million bipolar patients worldwide receive little benefit from existing therapies.

“One of the major limitations in bipolar treatment is the lack of new molecular targets for drugs,” said John Kelsoe, M.D., UCSD professor of psychiatry, a psychiatrist at the San Diego VA Healthcare System, and senior author of the study. “Our hope is that discovery of genetic defects that cause bipolar disorder will lead to new drugs that can be directed to those specific genes.”

During a year of screening DNA samples from more than 400 families with bipolar disorder, the study’s first author, Thomas B. Barrett, M.D., Ph.D., assistant professor of psychiatry, UCSD and psychiatrist, San Diego VA Healthcare System, determined that there were six mutations in the promoter region of the GRK3 gene. One of these mutations, P-5, occurred three times more frequently in manic-depression patients than in non-afflicted individuals.

About dopamine, from Wikipedia:

Role in Pleasure and Motivation

Dopamine is commonly associated with the ‘pleasure system’ of the brain, providing feelings of enjoyment and reinforcement to motivate us to do, or continue doing, certain activities. Certainly dopamine is released (particularly in areas such as the nucleus accumbens and striatum) by naturally rewarding experiences such as food, sex, use of certain drugs and neutral stimuli that become associated with them. This theory is often discussed in terms of drugs (such as cocaine and amphetamines) which seem to be directly or indirectly related to the increase of dopamine in these areas, and in relation to neurobiological theories of addiction, which argue that these dopamine pathways are pathologically altered in addicted persons. The mechanism of cocaine and amphetamine is different. Cocaine is acting as dopamine transporter blocker to competively inhibit dopamine uptake to increase the lifetime of dopamine, while amphetamine is acting as a dopamine transporter substrate to competively inhibit dopamine uptake and increase the dopamine efflux via dopamine transporter.

However, the idea that dopamine is the ‘reward chemical’ of the brain now seems too simple as more evidence has been gathered. Dopamine is known to be released when unpleasant or aversive stimuli are encountered, suggesting that it is not only associated with ‘rewards’ or pleasure. Also, the firing of dopamine neurons occurs when a pleasurable activity is expected, regardless of whether it actually happens or not. This suggests that dopamine may be involved in desire rather than pleasure. Drugs that are known to reduce dopamine activity (e.g. antipsychotics) have been shown to reduce people’s desire for pleasurable stimuli, despite the fact that they will rate them as just as pleasurable when they actually encounter or consume them. It seems that these drugs reduce the ‘wanting’ but not the ‘liking’, providing more evidence for the desire theory.

Other theories suggest that the crucial role of dopamine may be in predicting pleasurable activity. Related theories argue that dopamine function may be involved in the salience (‘noticeableness’) of perceived objects and events, with potentially important stimuli (including rewarding things, but also things which may be dangerous or a threat) appearing more noticeable or more important. This theory argues that dopamine’s role is to assist decision making by influencing the priority of such stimuli to the person concerned.

In my case, I’m totally “normal” (well, most of the time) and functional these days on a wonderful drug called lamictal. I actually had to talk my shrink into prescribing this drug when I first found out about it. Now, everyone I know who is bipolar and on this drug is doing great. It literally stops the roller coaster of emotions and lets you decide how you want to feel instead of being overun by the feelings. I also occassionally take an anti-psychotic to turn off the “endless chatter” loop when the brain really gets going. This is a miserable phase where you just can’t stop thinking about things, and your mind won’t shut up. Usually I turn this off at night when I want to sleep. One of the truly nasty things that happen with bipolars is when your brain decides to keep you awake all night, you don’t get any rest, and you go into this downward spiral and eventually into a place where you’re essentially awake but dreaming – your mind acts as if everything is a dream and interprets things in that weird dream-like state, making strange connections. This is called psychosis, which is why you need to keep an anti-psychotic around if you’re bipolar and turn this off before it happens.

The other thing I use is a mood elevator called Effexor. I only take this when I’m falling into that other downward spiral known as depression, which in my case starts to rear its head as extreme crankiness and a “nothing is right” feeling. When that happens, I use Effexor to lift me back out of the mood. Between the three drugs, I’m now quite stable and in charge of my own mind and emotions.

Hey, I’m one of the lucky ones. I am smart enough and know enough to get a combination that works for me. But balancing this mix is what is so difficult about bipolar. I also generally avoid stress as much as possible in my life, since it is a huge trigger for me. People wonder at how calm I always am, and about the Tao I study, but for me, these things mean survival.

There is a lot of undiagnosed bipolar out there. If you recognize any of these kind of symptoms – an out-of-control desire for something, manic-depressive behavior, and severe emotional swings, get some help, really. You’ll feel so much better!