“Emerging Technologies to Improve Care,” read the name of the session in my program book. I waltzed in late, trying to shake myself awake, prepared to make a hasty exit.
“The way psychiatrists practice right now,” I heard one of the panelists say, “is all trial and error.”
Suddenly, I was wide awake. I flipped through my program for the name of the speaker - Jay Lombard MD, chief scientific officer at a Norfolk company called Genomind. Its website says:
Many patients complain of mood disturbances, including depression and anxiety. However, despite the commonality of these complaints, there is significant biochemical heterogeneity regarding the etiology of mood disorders, which may account for the high rate of treatment failures or adverse side effects.
OK, here’s the English translation. A depression is not just a depression. There are many biological-environmental causes, which makes one-size-fits-all treatments such as antidepressants not only a joke, but lamentably bad medicine.
Dr Lombard reeled off some of the same genes I listed in yesterday’s piece. A quick review:
Serotonin transporter gene: Regulates serotonin reuptake. A variation results in a hyperactive amygdala that results in over-reaction to stimulae, with downstream anxiety, depression, and other conditions.
BDNF: Regulates cell maintenance and survival, neural growth and connectivity. A variation results in inefficiencies in these processes, leading to moodiness and anxiety.
COMT: Breaks down dopamine. A variation impacts signaling in a way that raises the risk of schizophrenia.
MAO-A: Breaks down dopamine. A variation results in a hyperactive amygdala and low-responding cortical areas, resulting in difficulties controlling impulses, leading to aggressive behavior.
In addition, Dr Lombard noted three more, namely:
DRD2: Antipsychotics bind to this receptor. A variation results in poor binding and a bad med response.
Methylfolic acid gene: Breaks down folic acid. A variation results in B vitamin deficiencies that may lead to depression.
Calcium channel gene: Regulates the intake of calcium into the neuron. A variation results in too much calcium which ramps up excitability, with risk of bipolar, schizophrenia, and treatment-resistant depression.
So - maybe if we can pinpoint the actual physical malfunction that is contributing to our bad moods and behaviors, we can target our treatments accordingly. This would represent a quantum leap over our current mindset of throwing meds at diagnostic labels.
Daniel Hoffman MD, president and chief medical officer at the Denver-based CNS Response, put it this way: “The world wants buckets of symptom clusters and it doesn’t work.” He quoted Thomas Insel, head of the NIMH to the effect that the DSM is 100 percent reliable but zero percent valid.
In other words, doctors may all be in agreement on what schizophrenia or bipolar may look like, but they may also be unanimously wrong. “Why we’re spending so much time on the DSM-5 is beyond me,” he went on to say.
Instead of symptom clusters, we need to be looking at neurological outcomes that correlate to specific parts of the brain. Otherwise, “we are doing harm.”
He wasn’t through. Citing STAR*D (which most unequivocally demonstrated the limited efficacy of antidepressants), he observed: “What Pharma told us about these meds didn’t pan out.”
Maybe you can see where this is going, real diagnostics based on bio-markers: A saliva kit to tease out problematic genes, a blood test to differentiate bipolar from schizophrenia, qEEG to read brain waves. All of these are just about ready for prime time. The biggest issue is getting the insurance companies to reimburse.
About one third of patients diagnosed with ADHD, said Dr Hoffman, don’t have the neuropathology for it. Kids with ADHD have very specific EEG patterns. But we don’t give up on the non-ADHD kid. In essence, we are looking for “the right drug for the right brain.”
What a novel thought.
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