In recent posts, I have been exploring the outer reaches of the theories that animate this blog, and now feel the need to hew back to my roots in clinical psychiatry upon which this whole project rests. For example, the basis of many of these ideas is my challenge to the primacy of the “pleasure principle,” which is that pro-social behavior is fundamentally goal-directed and pleasure-seeking. In “Empathy and the Laws of Affect” (Science–2011), psycho-biologist Jaak Panksepp, whose specialty is emotion, hypothesizes that there are ancient internally mediated neurochemical rewards for pro-social behavior in all mammals (such as grooming in primates). According to the pleasure principle, depression would be caused by the over-inhibition of the goal-oriented motivation centers in the brain (those mediated by dopamine). There is evidence from functional imaging studies that indeed this is the mechanism in rat depression (Ferenczi–2016), but I claim that clinical depression in humans is fundamentally different than in rats.
The evolution of human pro-social emotions go back to the formation of groups in primates some 50 million years ago. It is my contention that social group formation was accomplished by the stick and not the carrot—that is predominantly motivated by aversion to distinctly painful experiences. For example I believe that chimpanzees embrace after an altercation in order to decrease the engendered separation anxiety rather than seeking warm-and-fuzzy feelings from the hug. It was fear, not pleasure, that did the heavy lifting in the evolution of our sociality. I determined from my studies of the “major” depressions that the predominant social emotions are 1) separation anxiety, 2) the fear of being trapped at the bottom/periphery of groups and 3) the fear of banishment.
The most powerful reasons leading me to this conclusion had to do with that fact that, although trained as a Freudian, I practiced during the era in which the (surprisingly few) broad categories of drugs were discovered and first used clinically. I became fascinated with how these drugs altered patients’ subjective emotional experiences of their illness, and never failed to interrogate them about this issue. Prozac is the prime example.
In 1993, psychiatrist Peter Kramer pointed out in his popular book Listening to Prozac that patients who were considered normal but who were somewhat shy in social situations reported very positive personality changes in response to Prozac, which made them feel more socially at ease. I finally concluded that it simply decreases people’s emotional reactivity to their lives: “My children were driving me crazy and my boss is a yeller. Since taking Prozac, it all just doesn’t get to me as much.” A New York City friend called me one night from Madison Square Garden during a Knicks game upset that Prozac had turned him into an “out-of-towner”: no hysterics at the slam dunks.
I eventually concluded that the core pathological process in all mental illness is the loss of regulation of specific key social emotions (including those listed above), which results in their unrestrained pathological hyperactivity—a mechanism that can be compared to cancer. I concluded that all medical psychiatric treatments (as opposed to psychotherapy—which probably, to a degree, has this same effect) amounted to “turning the emotional volume down.”
Over the years, I have found several studies (Sackien, 1999; Azuma, 2007) that support the idea that electroconvulsive treatment (ECT) for depression is effective because of the inhibitory phase after the massive stimulation of an induced convulsive seizure. Indeed, it is thought that deep brain stimulation is effective by interrupting the chronic over-activity of an area in the frontal lobe (Mayberg–2005).
Taking a wider view, new evidence has confirmed that, indeed, the higher, more recently evolved brain structures in the outer cortex are in an inhibitory relationship with the primary emotions that spring from the more ancient brain centers (Northoff et al–2009). It is important not only in the understanding of clinical depression, but also of human nature itself that the inhibition inherent to the more recently evolved portions of our brain include the aversive anxiety-based emotions such as guilt and shame (superego) that escape into pathological hyperactivity in serious depression.
My basic clinical observation is that at the heart of mental illness is the pathological hyperactivity of the painful social emotions and that the inability to experience pleasure is secondary and reactive. A simple way to understand this is that, with the exception of mania, mental illness is the pathological hyperactivity of the “Thou Shalt Not” emotions in the mind. You see, Freud had it right all along. The mammalian pleasure principle operates in the Freudian id, the inhibition of which is what made us human from the very beginning— right through to the evolution of our own species. Then Homo sapiens evolved a brand-new layer of goal-directed behavior, called narcissism by the Freudians and vanity by everyone else. What our species brings to the 6-million hominin table is revealed in the illness of mania in an exaggerated, distorted manner.
So here are the four layers of human nature:
- Mammalian: Survival behavior motivated by pleasure principle (id).
- Primate: Id partially inhibited by fears of separation and social entrapment resulting in dominance–submission hierarchical social structure.
- Hominin: Id further inhibited by above fears + fear of banishment resulting in group authority (superego) social structure.
- Homo sapiens: Group authority overlain by pleasure-directed motivation for “self-display”(vanity) resulting in partial reemergence of id.