View Full Version : What is the physiological basis for bipolar disorder?

02-26-13, 11:34 AM
I don't mean in terms of genetic defects but physiology. You know, what's different in the bipolar brain compared to the NT brain. I know that in ADHD, there is supposed to be a problem with dopamine reuptake, in depression it's serotonin or noepinephrine reuptake. What gives rise to our bipolar symptoms, in particular in BD II?

I've tried to read through the literature but I have to admit it's too complex and technical for me to understand. Something about sodium channels. I've also read that there is atrophy in parts of the bipolar brain and degeneration or death of neurons.

Can anyone explain it to me in really simple terms (oversimplified is fine :o)? BD 101 for dummies??

02-26-13, 03:25 PM
I'm not trying to be snarky at all, but the simplest answer is that we really don't have the faintest clue as to what the physiology of either ADHD or bipolar is, in any individual case.

I do know of people who are working in the area of genetics, looking at particular genes that code for particular ion channels, with an aim towards understanding why and how lithium might exert its therapeutic effects. That's the angle that I'm most familiar with, but I'm sure there are a gazillion others (now that you've piqued my interest, I might have to go read more. . . but only after the cotton gets removed from my brain. . .nothing like a cold, rainy day to put me completely into hibernation).

02-26-13, 05:30 PM
When I first started researching Bipolar Spectrum Disorder I ran across this video.

It talks about the treatments and underlying pathophysiology of Bipolar.

If you can sit through an hour long, thick with science video, this one is really good.

03-12-13, 10:48 AM
I personally believe its a combo of genetics and a chemical imbalance but I have no evidence to support that only a zaney opinion.

03-12-13, 12:59 PM
The thing I heard years ago when i was diagnosed was it had to do with too much dopamine, which makes absolutely no sense to me and I don't believe is true. because if it was too much dopamine, how could I also have ADHD with too little dopamine? That was the theory way back when.

All I know is it's really unknown.

03-12-13, 04:08 PM
We know almost NOTHING about the causes of bipolar disorder. Truly, I think scientists know more about the nature of deep space than the bipolar brain. It's believed to be a combination of things, some to do with the physical structures of the brain, some to do with the way the brain produces and uses neurotransmitters.

Some research ( indicates that the melatonin receptors in the eyes of people with bipolar disorder are hypersensitive, which may be part of why light/sleep cycles are so intimately linked to mood episodes, especially mania. The frontal lobes in the brain have been shown to shrink and atrophy when bipolar disorder is allowed to progress unchecked. (The good news is that brain atrophy has been shown to reverse ( when the brain is stable for long periods of time!)

Many genes may show abnormalities in bipolar disorder, including genes that impact serotonin transport, dopamine, monoamine oxidase, and BDNF. Bipolar patients have been shown to have more monoamine binding sites ( in the thalamus and brain stem (anywhere from 28-40% more, depending on location). Monoamine receptors are strongly related to mood regulation and executive functioning. That is one reason why MAOIs (monoamine oxidase inhibitors) can work well for mood stability - they inhibit the binding of MAO to the overabundance of binding sites in the brain.

This (,9171,1003065,00.html) is a really great, straight-forward, easy to read piece of an article in TIME about The Bipolar Brain. It talks about the physical structural differences in a bipolar brain vs. a NT brain.

This ( study showed that people with bipolar disorder and suicide victims both showed a decrease in inositol in the frontal cortex.

This ( study showed that grey matter deficits in the right anterior cingulate gyrus and ventral striatum put a person at risk for bipolar disorder.

This ( study showed that patients with bipolar disorder with psychosis have a decrease in RELN mRNA and GAD67 protein in the brain, which implies that RELN mRNA and GAD67 protein factor into the psychotic aspect of bipolar disorder.

This ( study showed that bipolar patients hospitalized for mania had an increase in the size of the amygdala, as well as the thalamus, pallidum, and striatum. That is in contrast to this (;jsessionid=A94662B4429CB260E18BB93CD186D3 B4.d01t03?deniedAccessCustomisedMessage=&userIsAuthenticated=false) study, which showed that adolescents with bipolar disorder had smaller amygdala measurements than NT controls.

I could go on and on, because I love to research this topic, but I'll stop here. As you can see, there are a million and one possible structural and chemical influences in the brain that correlate with bipolar disorder. Many have to do with structures in the brain related to executive function and emotional regulation, or neurotransmitters related to mood and sleep. There's no concise, easy answer to the question, and I don't think there ever will be. Very little about the brain is easy or concise.