On January 1, 2012, in discussion on the psychiatry research yahoo group, I wrote: “… there is nothing inherently rewarding about dopamine, so why are behaviorists praying to a dopaminergic god of operant conditioning?”
The same can be asked about serotonin, oxytocin, and other hormones / neurotransmitters that are commonly proposed as causes of human behaviors. The link between oxytocin and “bonding” associated with love is perhaps the most commonly proposed cause and effect relationship. But love is profoundly social. How could a hormone, like oxytocin, that has no inherent social value cause anyone to think, believe, or feel like they are in love? It can’t!
I will now try again to clarify my point about the FDA Critical Path Initiative and the gene, cell, tissue, organ, organ system pathway, which I have detailed. The issue is how pharmacogenomics establishes the relative salience of sensory stimuli associated with behavior.
It is important for psychologists to understand how salience is established because treatment outcomes may sometimes depend on that understanding. When exposure to conditioned cues is not contingent on any behavioral response and occurs in absence of the reinforcer, similar cell populations respond to cues paired with sucrose versus quinine (e.g., in a strictly Pavlovian conditioning experiment). For example, single neurons in the orbitofrontal cortex of monkeys responded similarly to visual cues predicting an aversive stimulus (a puff of air) or a rewarding stimulus (liquid reward). Experiments like that one with aversive stimuli or rewards demonstrate a lack of clarity: How do differences in the molecular biology of dopamine release and cell firing populations in the nucleus accumbens translate into learning about the appetitive value of the stimulus; it’s salience?
Debates concerning the ability to distinguish between learning about rewarding stimuli and learning about aversive stimuli have been put on hold, or ignored. Nevertheless, learning is involved. Until a molecular “marker” of neuronal activation can be linked directly to the sensory stimuli that activated the genes in cells of tissue in the brain (e.g., those that are most closely linked to differences in behavior) the behaviorists have only their unexplained correlates, which say nothing about cause and effect. Rather than attempt to discuss how behaviors are learned, behaviorists focus on the analysis of the behavior.
So who is suggesting that the unexplained behavioral correlates of learned behavior be treated with talk therapy and drugs that somehow supposedly alter the complex molecular biology of the involved circuitry in the brain? The answer to that question may help to establish the hierarchal structure through which litigation can help to establish standards of care in psychology, as litigation has done for medical practice. Who suggested “rebirthing therapy,” for example? Can talking a patient’s way though simulations of their birth result in anything more than income for the psychologist?
Psychologists might want to begin to dictate theirs own standards from within their ranks. But, if not, I’m relatively certain that the standards will be set based on patient access to a rapidly expanding knowledge base that’s coming from neuroscientists, as the ASAM policy statement suggests. Litigation based on patient harm due to treatments that are not based on any current understanding of the biology of behavior is as sure to follow the current trends as have been any potentially litigious complaints. Unfortunately, a fatality related to the practice of rebirthing therapy may be what leads the way.