Bipolar I vs Bipolar II
Dividing bipolar into I and II arguably has more to do with diagnostic convenience than true biology. A University of Chicago/Johns Hopkins study, however, makes a strong case for a genetic distinction. That study found a greater sharing of alleles (one of two or more alternate forms of a gene) along the chromosome 18q21in siblings with bipolar II than mere randomness would account for.
A 2003 NMIH study tracking 135 bipolar I and 71 bipolar II patients for up to 20 years found:
- Both BP I and BP II patients had similar demographics and ages of onset at first episode.
- Both had more lifetime co-occurring substance abuse than the general population.
- BP II had “significantly higher lifetime prevalence” of anxiety disorders, especially social and other phobias.
- BP Is had more severe episodes at intake.
- BP IIs had “a substantially more chronic course, with significantly more major and minor depressive episodes and shorter inter-episode well intervals.”
Nevertheless, for many people, bipolar II may be bipolar I waiting to happen.
The DSM’s one-week minimum for mania and four-day minimum for hypomania are regarded by many experts as artificial criteria. The British Association for Psychopharmacology’s 2003 Evidence-based Guidelines for Treating Bipolar Disorder, for instance, notes that when the four-day minimum was reduced to two in a sample population in Zurich, the rate of those with bipolar II jumped from 0.4 percent to 5.3 percent.
A likely candidate for the DSM-V as bipolar III is “cyclothymia,” listed in the current DSM as a separate disorder, characterized by hypomania and mild depression. One third of those with cyclothymia are eventually diagnosed with bipolar, lending credence to the “kindling” theory of bipolar disorder, that if left untreated in its early stages the illness will break out into something far more severe later on.
The medical literature refers to bipolar as a mood disorder and the popular conception is one of mood swings from one extreme to the other. In actuality, this represents only a small part of what is visible to both the medical profession and the public, like the spots on measles. (Many of those who are bipolar, incidentally, can function untreated in the “normal” mood range for sustained periods of time.)
The cause and workings of the disorder are total terra incognita to science, though there are lots of theories. At the Fourth International Conference on Bipolar Disorder in June 2001, Paul Harrison MD, MRC Psych of Oxford reported on the Stanley Foundation’s pooled research of 60 brains and other studies:
Among the usual suspects in the brain for bipolar are mild ventricular enlargement, smaller cingulate cortex, and an enlarged amygdala and smaller hippocampus. The classical theory of the brain is that the neurons do all the exciting stuff while the glia acts as mind glue. Now science is finding that astrocytes (a type of glia) and neurons are anatomically and functionally related, with an impact on synaptic activity. By measuring various synaptic protein genes and finding corresponding decreases in glial action, researchers have uncovered “perhaps more [brain] abnormalities … in bipolar disorder than would have been expected.” These anomalies overlap with schizophrenia, but not with unipolar depression.
Dr. Harrison concluded that there is probably a structural neuropathology of bipolar disorder situated in the medial prefrontal cortex and possibly other connected brain regions.
Still, so little is actually known about the illness that the pharmaceutical industry has yet to develop a drug to treat its symptoms. Lithium, the best-known mood stabilizer, is a common salt, not a proprietary drug. Drugs used as mood stabilizers – Depakote, Neurontin, Lamictal, Topamax, and Tegretol – came on the market as antiseizure medications for treating epilepsy. Antidepressants were developed with unipolar depression in mind, and antipsychotics went into production to treat schizophrenia.
Inevitably, a “bipolar” pill will find its way to the market and there will be an eager queue of desperate people lining up to be treated. Make no mistake, there is nothing glamorous or romantic about an illness that destroys up to one in five of those who have it, and wreaks havoc on the survivors, not to mention their families. The streets and prisons are littered with wrecked lives. Vincent Van Gogh may have created great works of art, but his death in his brother’s arms at age 37 was not a pretty picture.
The standard propaganda about bipolar is that it is the result of a chemical imbalance in the brain, a physical condition not unlike diabetes. For the purposes of gaining acceptance in society, most people with bipolar seem to go along with this blatant half-truth.
True, a chemical storm is raging in the brain, but the analogy to the one taking place in the diabetic’s pancreas is totally misleading. Unlike diabetes and other physical diseases, bipolar defines who we are, from the way we perceive colors and listen to music to how we taste our food. We don’t have bipolar. We are bipolar, for both better and worse.