Funny how the whole delicate neurological/neurochemical structure is so interwoven:
“…The researchers suggest that the strange defensive behavior exhibited by the enzyme-deficient mice may actually reflect a limited range of adaptive responses and lack of emotional flexibility — the mice may only have one gear for fear.”
We’ve all known people who make exaggerated choices around danger that make no sense to ourselves. (Having heard my mother and my sometime partner on the subject of my riding motorcycles, I’m pretty sure of that.) However, only at my most desperately depressed have I engaged in unsafe sex, which is the second stupidest risk I can think of (the first having nothing to do with motorcycles.)
The role of MAO-A and depressive neurotransmitters, combined with the dopamine-deficient sense of hopelessness and diminished executive function, make that make sense:
“Monoamine oxidase A is the main enzyme in the brain that breaks down serotonin, norepinephrine and dopamine…”
Which makes me think that it’s possible, in humans in vivo, to be deficient in both MAO-A and in dopamine, serotonin, etc. It would explain a lot about certain mental states, even though it seems chemically tautological at first glance to be both Big 3-deficient and MAO-A deficient. As I’ve learned, though, deficiency and dysregulation do have additive effects, they don’t cancel each other out.
I’d like to see more studies which monitor serum and brain levels of these key chemicals together, preferably in humans. Science tends to take the simplest possible approach, which is rarely the most realistic and not necessarily the most telling. It does get funded and it does make it simpler to design the studies.
I look forward to having more sophisticated thinkers (and funders) get into this branch of psychoneurology, since all these lively lovely tiny bits of info won’t come together in a meaningful way until we can look at them in concert with a higher degree of exactitude and completeness. I suppose I’ll have to be patient. And careful.