By Dr David Laing Dawson
When science tries to understand human behaviour it can develop methodologies to look at multiple levels of our organization. These levels could range from subatomic particles to the behaviour of tribes, nations, the population of the entire world.
Within the medical sciences we are interested in the behaviour of cells, of neurochemistry, and, at the other end of this chain, the experiences and behaviour of individual humans.
Behaviour can be observed, and observed within different contexts, and under specified situations. Internal experiences require self reporting within a social context, and self reporting is notoriously unreliable. (Imagine asking Donald Trump what he is thinking and feeling, and why he is having these thoughts and feelings, and whether he has written many books.)
Until quite recently the behaviour of brain cells, of neurochemistry, could only be studied by measuring the rise and fall of various metabolites in blood and urine.
And between these extremes (human behaviour and the rise and fall of metabolites in blood and urine) there existed an enormous black box containing the interaction of chemistry, cells, neurons, organs within the brain, systems of arousal and perception, systems of neural organization, complex biochemical and electrical feedback systems….
With EEGs, CT Scans, MRI’s, Pet scans, molecular biology, genome mapping, our new ability to at least see which parts of the brain are active (metabolizing, using glucose and oxygen) and which are dormant when we talk, listen to music and/or hallucinate, that Black Box has shrunk. But it is still there.
Behaviour is a visible product of a long complex chain of events from cell activity, neurohormone production, arousal and filtering systems, inhibiting and stimulating feedback loops.
Ritalin is a stimulant. Yet when given to a boy with ADHD it usually slows him down. So my best guess here is that with ADHD our stimulant is stimulating an inhibitory mechanism.
Like many medications, the power of Chlorpromazine (Largactil) to quell psychosis was discovered by accident. This time in France. Heinz Lehmann brought it to Canada to use in a trial at The Douglas Hospital. It worked dramatically, but why and how it worked is another question. Following the methodologies mentioned above it was first determined that chlorpromazine and drugs developed within the same family affected the neurochemical, neurotransmitter, dopamine. From this arose the dopamine hypothesis of schizophrenia.
But we have since learned that each mental illness is the product of long, complicated pathways from neuron to dendrite to neuron to behaviour (sometimes through long chains and multiple pathways), and that different medications can affect the final behavioural outcome by affecting different parts of that chain, sometimes by stimulating production of a neurohormone, sometimes by emulating a neurohormone, sometimes by inhibiting a neurohormone, sometimes by blocking the transmission of a neurohormone, and sometimes by inhibiting the degradation of a neurohormone (hence the SSRI’s – Selective Serotonin Reuptake Inhibitors)
With the modern technologies we can describe with accuracy what exactly each drug does at a neuronal, biochemical level. But there remains a black box between that level and the actual observed behaviour. Though it is getting smaller and smaller and easily bridged with hypotheses.
But psychosis is not simply too much dopamine, nor depression inadequate serotonin. Although medically altering those two neurochemicals (neurotransmitters) does affect (usually) the chain of electrical/molecular events that leads to psychosis and depression.