Vulnerability to Psychopathology: A Biosocial Model

Does theory drive practice, or does practice drive theory, or does creative practicality serve as the main driver of psychotherapy and underlying psychopathology? Perhaps it is not one or another of these “hardfast” alternatives but a combination of time, sequence, place, and process that yields results helping our patients in meaningful and effective ways. To be certain, the one variable that seems to be universal is that of the therapist, regardless of theory, practice, and experience.

Professor Zuckerman’s volume focuses its attention on a biosocial model that deals with the interaction among biology-genetics, personality, and stressful events—key factors in vulnerability. This model is similar to George Engel’s pioneering work on the biopsychosocial model, which Vulnerability to Psychopathology never mentions or references.

The book has a lengthy bibliography (many items are dated) that is extensive in coverage but somewhat scattered. However, it can be useful to researchers and graduate students who need to have “a single source of information on the…history, diagnosis, prevalence, prognosis, course, outcome, comorbidity, [and] demographic characteristics” of mental disorders (from the book’s jacket), but this lengthy volume does not provide the latest information. The stress literature needs to be updated, and even the diagnostic manuals are now being further revised than is evident in the author’s discussion.

If one addresses vulnerability, more than a single chapter on discussions of individual personality disorders is needed. We know that clinical outcomes may not fit well with current or distant theories, and theories alone cannot explain results, even when results are tightly evidentially based. When dealing with prediction and vulnerability, one must examine every assumption and must base each on facts, when possible. Without bias, one must test carefully crafted predictions that are based on carefully assembled, verifiable evidence. Currently accepted disease classifications will be replaced by new categorizations with emphasis on evidence-based diagnoses and assumptions.

Van Praag addressed some of these ideas in his paper “Nosologomania: A Disorder of Psychiatry” (1). He questioned the use of alternative models instead of currently used ones. He specifically discussed the confusion of etiology and pathogenesis as well as the proliferation of new diagnoses, and he concluded that “the nosological doctrine seems to be an albatross around psychiatry’s neck” (p. 155).

Chicurel (2) highlighted neuroscientific progress in obtaining a molecular handle on how the brain controls our daily cycle of sleep and wakefulness, thus opening a new avenue of study that could lead to new theories and therapies for sleep disorders. New antidepressants hold much promise for advances in the postgenomic era. This may lead to better understanding of the factors that result in differential responses to antidepressants. Factors including nutritional status, stress, and even the social milieu can affect individual responses to selective serotonin reuptake inhibitors (3). We know little of the potential genetic and environmental factors that might influence individual responses to specific antidepressants at specific times. “The new science of pharmacogenomics can help us understand the genetic determinants of drug response, whereas the role of other environmental factors such as diet or social contact needs to systematically [be] studied” (3, p. 877). It may be that psychological factors also determine specific differential reactions to pharmacotherapeutic agents.

Haim Harari, President of the Weizmann Institute of Science, noted that “the world of computers, information systems, electronics and optics is now dominating every aspect of our lives” (4, p. 3). He also highlighted the advances in genetics that influence our health, our food, and our behavior. The Human Genome Project already is affecting our theories. The third advance that Professor Harari underlined is our increasing understanding of the brain and its relationship to brain imaging and other functional aspects of the central nervous system (CNS). These and other “revolutions” are affecting research, theory, and treatment. Gradually we are replacing “old scientific fields with new ones, enhancing our facilities” (4, p. 3), and launching new scientific and clinical adventures.

Finally, to discuss some newer findings further, the role of apoptosis in CNS degeneration and regeneration opens new avenues for clinical theory and practice. We are living in a new era of change and advance. These can and will affect our thinking, our research, and our clinical work. Let’s use the new findings so that we can more effectively benefit our patients.