Scientific Challenge to the Bipolar Diagnosis: What It Means to Recovery

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Health Central (John McManamy)

 

Monday, July 11, 2011

Is the term, bipolar disorder, a diagnostic dinosaur? Should we just light a match to the DSM right now and start over?

I just returned from the National NAMI convention in Chicago, where, at one session in particular - Emerging Technologies to Improve Care - I found myself scribbling very fast into my notepad. The reason had less to do with emerging technologies and more to do with how our new understanding of the brain is rendering the bipolar diagnosis obsolete. As one of the presenters - Daniel Hoffman, chief medical officer of CNS Response - noted (quoting head of the NIMH Thomas Insel): “The DSM is 100 percent reliable and zero percent valid.”

What this translates to is that even though every psychiatrist in the world may agree on what bipolar disorder (sort of) looks like, it doesn’t mean it’s true. According to Dr Hoffman: “The world wants buckets of symptom clusters and it doesn’t work.”

A month ago, I returned from the Ninth International Conference on Bipolar Disorders, where I listened to a panel of experts involved with the DSM-5. As one psychiatrist I later talked to described it, the session came across as an exercise in counting angels on the head of a pin.

Granted, clustering symptoms into disease categories helps us separate out bipolar from schizophrenia from unipolar depression from borderline personality disorder (though rather badly), but how good is it at distinguishing bipolar from bipolar from bipolar? Let me explain:

On the surface, your clinical condition may appear the same as mine, but how similar are they really when we open up the hood and look inside? At the NAMI convention, Jay Lombard, chief scientific officer at Genomind, rattled off some off some prime suspect genes involved in specific brain functions, including:

SERT - the serotonin transporter gene that has been linked to how we respond to stressful life events. Those with a certain variation are far more vulnerable and less resilient. PTSD may be one outcome, depression another. And on and on ...

COMT - which is involved in the metabolism of dopamine in the prefrontal cortex. Higher enzyme activity lowers dopamine and vice-versa. Negative symptoms - cognitive dysfunction - are the core feature of schizophrenia and also figure mightily in bipolar.

DRD2 - affects how antipsychotics bind to this dopamine receptor.

MTHFRC - involves the conversion of folic acid. Failure to break down folic acid has been linked to bipolar.

Calcium channels - which regulate calcium flowing into the neuron, which in turn mediates excitability in the brain.

In addition, at another session, Jill Bolte Taylor, author of “My Stroke of Insight” mentioned the importance of GABA in keeping the excitability levels in the brain down to an acceptable threshold.

Many many many more genes affecting key brain functions can be added to this list (including the CLOCK gene that regulates circadian rhythms), but I think you have already spotted the pattern, namely our genes switch on and off certain cellular functions, which in turn affect certain neural systems, which impact how we how we think and feel and react and cope.

In other words, there is no “depression gene” or “bipolar gene” or “schizophrenia gene.” This is why it is often far more helpful to think in terms of what is really holding us back in life. Maybe the science isn’t there yet to pinpoint exactly what is wrong with us, but our own rigorous self-enquiry offers strong hints of what we need to be working on:

Having problems dealing with stress? Messed up sleep? Sluggish thinking? Tendency to get over-excited?

Maybe if we make headway in these areas of our life (using techniques such as mindfulness), our depressions and manias become a lot more manageable. Who knows? Maybe bipolar is simply the downstream effect of a bunch of stuff going on. No doubt, there will be considerable overlap between your bunch of stuff and my bunch of stuff, but there will obviously be key differences. This is why there will never be a magic one-size-fits-all treatment.

The session at NAMI offered us a look into the future, making use of already existing technologies such as EEG to suggest the right treatment for the right underlyiing condition, which is the topic of a future blog. In the meantime, now more than ever, be smart, know thyself.


Posted Jul 25 2011, 08:54 AM by Vanessa Matheny