For the revision of our Counseling and Psychotherapy text, Rita and I are contemplating how to integrate some neuroscience information in a balanced way. Each chapter would include a short section discussing neuroscience as it pertains to each theoretical perspective. This essay is one effort for beginning or framing the discussion.  Check it out (if you like this sort of thing) and let me know your thoughts (if you do that sort of thing).

From Biological Psychiatry to Interpersonal Neurobiology

In 1980, I (John) began my career in mental health services as a recreation therapist in a 22-bed psychiatric hospital. The patients were experiencing severe depression, manic episodes, and psychotic symptoms.

There was a large and intimidating psychiatrist (Dr. M) on the unit. Dr. M was a fan of biological psychiatry. He would smile as I engaged patients in the “Newly-Friend Game” (like the Newly-Wed Game, only better), relaxation groups, bowling nights, and ice cream socials. Occasionally Dr. M cornered me, explaining how my “cute” recreational programs had absolutely no influence on our hospitalized patients’ mental health. He waxed eloquent about brain chemistry. Never mind that the Thorazine and Haldol he prescribed had nasty side effects. Eventually, he claimed, there would be designer drugs that cured mental disorders from the inside out. Everything else was irrelevant.

I had a fresh, new bachelor’s degree in psychology. Dr. M had his M.D. He knew more than I did. Class dismissed. But it’s funny how encountering a condescending attitude can be motivating. I figured there must be a brain chemistry explanation for that too.

The chemical imbalance theory of mental disorders continued its dominance through the 1980s and 90s. Explanations for psychopathology focused on too much dopamine (causing schizophrenia) and not enough norepinephrine or serotonin (causing depression). No one really knew what caused these so-called imbalances, but biogenetic factors were the prime suspects. Although I kept silent with Dr. M, I held tight to my beliefs that social, psychological, and physical experience could be therapeutic.

Evidence slowly rolled in. While teaching a class on developmental counseling, I found a study showing that testosterone levels vary as a function of winning or losing tennis matches (Booth, Shelley, Mazur, Tharp, & Kittok, 1989). My brain (and the chemicals therein) loved this idea. If our testosterone levels could change based on competitive experiences, what other ways might human behavior influence the brain?

In 1998, while perusing research on serotonin and depression, I discovered that treadmill running increased brain serotonin in rats. The researcher described the complexity of the phenomenon:

Lipolysis-elicited release of free fatty acids displaces the binding of tryptophan to albumin and because exercise increases the ratio of circulating free tryptophan to the sum of the concentrations of the amino acids that compete with tryptophan for uptake at the blood-brain barrier level, tryptophan enters markedly in the brain compartment. (Chaoeloff, 1997, p. 58)

But my take-home message was simple: physical exercise might increase serotonin in human brains and also help alleviate depression.

Then neurogenesis came along. Neurogenesis is the creation of new brain cells. It has been long known that during fetal development, cells are created and migrate to specific places in the brain and body where they engage in their specific role and function. Cells that become rods and cones end up in the eyes, while other cells become bone, and still others end up in the cerebral cortex. In the 1980s and 1990s, everyone agreed that that neurogenesis continued during infancy, but most neuroscientists also believed that after early childhood the brain locked down and neurogenesis stopped. In other words, as adults, we only had neuronal pruning (cell death) in our future.

In the late 1980s, neuroscientists began conducting research that shook long-held assumptions about neurogenesis. For example, Jenkins and colleagues housed adult monkeys in cages where the monkeys had to use their middle finger to rotate a disc to get banana pellets. Even after a short time period (1 week) upon autopsy the monkeys had an enlarged region in their motor cortex. The conclusion: Even in adult monkeys, repeated physical behaviors stimulate neurogenesis in the motor cortex. This seemed like common sense. Not only do our brains shape our experiences, but our experiences shape the brain (literally).

As it turns out, neurogenesis slows with age, but it doesn’t stop. It continues throughout the lifespan. New learning stimulates cell birth and growth in the hippocampus (and other areas involving memory processing and storage). The “new brain research” left open the possibility that counseling and psychotherapy has the potential to stimulate neurochemical changes and cell birth in the human brain.

The evidence is no longer slowly rolling in—it’s popping like popcorn. Neuroscience research is as popular as Beyoncé. Whenever more evidence arrives showing how counseling and psychotherapy might be affecting brain functioning, non-medical mental health professionals get giddy. As you might suspect (or already know) occasionally we’re so excited that our statements about the implications and applications of neuroscience are way ahead of the actual scientific evidence. Counseling and psychotherapy practitioners have created new marketing terminology like “brain-based therapy” and “neurocounseling” and “interpersonal neurobiology” despite the lack of clear scientific evidence to support these terms. In some cases the birthing of this new terminology has caused lament within the neuroscience community (Satel & Lillienfeld, 2015).

Where does all this take us? As Dr. M would say, the brain is central to mood and behavior change. But now we know the reverse is also true: mood and behavior are central to brain development and change. If Dr. M were still alive, I might say, “touche” or “voila” or some other fancy and clever retort to show him that he had the directionality wrong—all these years.

But my retort would be incorrect too. The influence goes both directions at once. Even more importantly, we need to acknowledge that the relationships between and among brain structures, neurotransmitters, hormones, other chemicals, and human behaviors are still complex and mysterious. Even though journalists sometimes write with flourish about our ability to peer directly into the brain and see exactly what’s happening, that’s just not true. And to the extent we can “see” what’s happening, it appears that the brain is simultaneously functioning as a whole, as regions, as inter- and intra-cellular processes, and doing all these activities in particular sequences and all at once. Sure, as many mental health professionals will enthusiastically claim, we now know that meditation and interpersonal empathic experiences appear to stimulate the anterior insular cortex (AIC)! But it’s more complicated than that. The following excerpt from the neuroscience literature helps communicate this complexity (Mutschler, Reinbold, Wankerl, Seifritz, & Ball, 2013).

In summary, we argue that the dorsal AIC plays a pivotal role in empathy (similarly as during emotion processing and pain) by integrating sensory stimuli with its salience, possibly via connections to the cingulate cortex. This assumption is also supported by the fact that ALE-findings related to emotion and empathy for pain and also the DGR—which has been associated with cognition—overlap in the dorsal anterior insula, suggesting that these functions share a common neural substrate . . . . As mentioned above we assume that the overall role of the morphometrically identified area in the dorsal AIC related to individual differences in empathy which overlaps the DGR might be involved in integrating information which is relevant for socio-emotional and cognitive processing. Thus, we assume that empathy is not (only) related to a specific “socio-emotional” interaction area, but to a superordinate “domain-general” area, in line with concepts of empathy that include not only social and emotional, but also cognitive aspects . . . . Whether our findings in the dorsal AIC have also a relation to the “von Economo neurons” [VENs, . . .] remains to be determined. VENs have been hypothesized to play are role in social-emotional processing including empathy . . . .

This excerpt should inspire us all to pause with respect for the density and specificity of neuroscience. It should also inspire us to ramp down our expectations. If we just focus on empathy and the insula, we can see many sources of potential error: (a) much of the empathy research focuses on empathy for pain; (b) empathy is hard to measure; (c) it’s possible for a human brain to “light up” with empathy, but for the human to not express or show empathy toward someone else; (d) while empathy is generally considered a positive quality, some people use empathy to manipulate and hurt others; (e) there is brain structural and functional overlap; (f) the role of the VENs is unknown; and on and on. To use an inappropriate metaphor, it’s likely that the particular blend and balance of neurotransmitters (there may be up to 100) and hormones (there are about 50) and other cellular substances in each individual—along with structural variability—is more unique than a fingerprint on a snowflake.

In every chapter of this text Charles Luke (of Tennessee Tech) and I will share a highlight or update on neuroscience research. These highlights and updates will focus not only on the promise and potential of neuroscience to counseling and psychotherapy, but also on its limitations. A focus on limitations is needed because our ability to imagine what’s happening in the brain greatly outpaces neuroscience research. Although it’s tempting (and terribly fun), we shouldn’t let our imagination get too far in front of the science. As Dr. M might have said, “the brain offers us the greatest opportunity and potential to understand, explain, predict, and manage human behavior.” Of course it does; and it always will.