It is one thing to hypothesize that psychological and emotional problems are associated with changes at the biological level (e.g., specific patterns of brain activity or levels of neurotransmitters) or that symptom remission is associated with biological changes. It’s another to assume that the underlying causes of mental health problems are always biological in nature and that meaningful improvements in treatment will only take place when we can directly target the relevant brain circuitry. While it may be the case that biological factors play a more significant causal role in some mental health problems (e.g., schizophrenia) than others, the assumption that the major causal factor for mental health problems is always biological is a form of simplistic reductionism.
I want to be perfectly clear that I do not question the potential value of brain science research. What I do question is the single-minded emphasis on brain science research to the virtual exclusion of all other forms of mental health research. The new NIMH paradigm for research means that the amount of funding available for the development and refinement of treatments such as psychotherapy that are not targeted directly at the brain circuitry (although they do influence it indirectly), is likely to continue to shrink. It is important to recognize that funding priorities shape the programs of research pursued by scientists, and thus the type of research findings that are published in professional journals and disseminated to the public. This in turn shapes the curricula in psychiatry and clinical psychology training programs, which shapes the way in which mental health professionals understand and treat mental health problems. It also influences healthcare policy decisions and the type of coverage provided by third party insurers.
In concrete terms, the explicit NIMH policy shift is likely to mean that despite the large and growing body of evidence demonstrating that a variety of forms of psychotherapy (e.g., cognitive therapy, interpersonal psychotherapy, psychoanalytic therapy, emotion focused therapy) are effective treatments for a range of problems, we are likely to continue to see a decreasing availability of the already diminishing resources that can provide high quality psychotherapy for those who can potentially benefit from it.
What place do the humanities have in psychiatry? One might as well ask: What place does the mind have in the brain? What place does clinical experience have in medicine? What is the utility of the empty space within the vessel?… In this article, I focus on the importance of the humanities to psychiatry, via the perennial conflict between biological psychiatry and psychodynamically oriented psychiatry. I hope to use a humanist approach to show that these “two cultures” depend on each other for balanced progress in the field…
Biological psychiatry has made truly impressive progress, yet it remains the case in 2013 that “biological psychiatrists do not hold the panacea for serious mental disorders,”particularly when standing on the lone pillar of science. The art of medicine remains a critical foundational structure in psychiatry, and both pillars are necessary for the stability of the field. One might say that the humanities and/or psychoanalytic thought helps provide science with the relevant questions on which to focus its “piecemeal work.”Put another way: the humanities provide the wonder, which science then illuminates.
It is sometimes the case that older theories are not proved false—rather, the very progress they contributed to now shows their limits.
Today we know an awful lot about schizophrenia and manic-depressive illness. An enormous amount of information has been collected about the psychological and biological expressions of these diseases — about the personal experience and outward behaviors corresponding to them, the anatomical abnormalities which show themselves in certain groups of patients and neurochemical dynamics characteristic of others — about patterns of their transmission in families and certain genetic elements involved. But this information refuses to combine into a “case” — an explanatory argument based on the available evidence: there are gaping lacunae where pieces of the puzzle are supposed to dovetail; and none of the things we know can be said to constitute the smoking gun. We still do not know what causes these diseases and thus cannot either understand their nature or cure them. After two hundred years neither of the two approaches — the biological and the psychodynamic — in which psychiatry put its hopes brought these understanding and cure any closer. Therefore, I feel justified to offer a new – radically different — approach that has never been tried.
The historical recency, the timing of the spread in different societies, and the increase in the rates of mental disease of unknown etiology indicates that it cannot be understood in terms of any universal, biological or psychological, propensity of human nature, or explained by the characteristics of the individual human organism or personality as such. The observable trends (however incredible) pertain to and distinguish between specific societies and historical periods, and therefore must be accounted for historically. …
My intention is not to prove either the biological or the psychodynamic approach to mental disease wrong, but to complement them, adding to psychiatry a necessary element which has been heretofore missing. All the findings of the biological research, specifically, should be consistent with the approach I propose and, in cases they are not, the fault would lie with the approach rather than the findings. Culture, personality, and biology are different, but not mutually exclusive realities, and for this reason cultural, psychological, and biological arguments should not be mutually exclusive.
While the technological advancements of recent decades allow us to map the human genome and look at the brain on the molecular level, the enormous amount of data that has been amassed is virtually useless for psychiatrists trying to diagnose their sick patients because the assumed biological causes of schizophrenia and manic-depressive illness have not been found. No brain abnormalities that are specific to either illness or present in all cases have been identified. Nevertheless, the experts who study and treat schizophrenia and manic-depressive illness (MDI) keep the faith (quite literally) that a breakthrough is just around the corner.
For years, genetic research has appeared to be the most promising of the recently opened avenues, but the excitement seems unwarranted by the findings. The relatively large number of chromosomal regions which may be implicated in susceptibility for bipolar disorder means that hope of finding a specific bipolar gene or even a small number of genes must be given up. Some researchers think the way to go is to narrow the search by looking for genes associated with specific aspects of the disease. Of course, this further refinement is only possible because of the huge variation in symptoms and experiences of those who fall under the MDI/bipolar umbrella, and we are once again reminded of the difficulty of defining what this illness or group of illnesses even is. Furthermore, even the distinction between schizophrenia and MDI seems to collapse in light of the genetic linkage data. In Manic-Depressive Illness: Bipolar Disorders and Recurrent Depression(2nd Edition), Drs. Frederick Goodwin and Kay Redfield Jamison write:
While the search for predisposing genes had traditionally tended to proceed under the assumption that schizophrenia and bipolar disorder are separate disease entities with different underlying etiologies, emerging findings from many fields of psychiatric research do not fit well with this model. Most notably, the pattern of findings emerging from genetic studies shows increasing evidence for an overlap in genetic susceptibility across the traditional classification categories. (49)
Genetic studies in the schizophrenia research community lead to pretty much the same hypothesis as with bipolar: genetic susceptibility is most likely polygenic, meaning dependent on the total number of certain genes which may contribute to vulnerability. It must be noted that genetic vulnerability is a condition, not a cause of schizophrenia and bipolar – something else must be acting on this vulnerability. In one way or another, this fact is usually noted in the literature that deals with genetic data, but it is often obscured by a tone of confidence which suggests the information may be more meaningful and explanatory than it truly is.
Even when a specific gene has been well studied across illnesses, its usefulness in understanding genetic susceptibility may be extremely limited. Some studies in both schizophrenia and MDI have found an increased risk of illness for those who possess the short form of the serotonin transporter promoter gene 5-HTT. The thing is, each of us has two copies of this gene, and over two-thirds of us have one long and one short form, meaning that having the normal variant of the gene is the risk factor! If most of us possess a gene which puts us at risk for an illness which only a small minority of people have, then this particular trait is obviously not much of a causal explanation.
In the Wall Street Journal today, Shirley S. Wang reports on a new study published today in The Lancet, which “provides early evidence that several disorders thought to be distinct appear to have some genetic overlap, and it may help in one day diagnosing mental illness based on faulty biological processes, and not just on behavioral symptoms.”
The study compared the genes of some 33,000 people with schizophrenia, bipolar disorder, major depression, autism or attention-deficit hyperactivity disorder, and also compared them with a group of nearly 28,000 controls. It “identified several regions of the genome that were associated with all five diseases.”
In Mind, Modernity, Madness, Liah Greenfeld came to a similar conclusion that viewing manic-depressive illness and schizophrenia as distinct illnesses, each with its own biological causes, is wrong. Instead, she argues that they should be placed on a continuum of the complexity of the will-impairment caused by the anomie inherent in modern culture. This argument, linking mental illness to individuals’ (varied) response to the pressures of modern society, could also explain why “the findings don’t mean that an individual with one or more of these gene variants has or will develop the condition,” as the Wall Street Journal article–and the authors of the study–conclude.