Reductionistic biological psychiatry and psychology, can at times, border on an abdication of common sense. For example, Cynthia Fu et al (2003) write:
“Our understanding of mood disorders has progressed from a notion of black bile causing melancholia to a realization that they develop from a complex interaction of genetic, psychological and social factors [this sounds reasonable, however, it is more like paying lip service to a biopsychosocial model -- as one can tell from what comes next]. That these disorders of the mind derive from some form of dysfunction of the brain is supported by evidence from clinical, neurochemical, neuroendocrine and histological studies. A high prevalence of depression has been observed in patients with neurological disorders, such as Parkinson’s and Huntington’s diseases, and in patients following stroke. This clinical evidence of secondary mood disorders (i.e., a mood disorder that is secondary to a medical/neurological disorder) indicates an underlying pathology within the brain...” (p. 131 in “Neuroimaging studies of mood disorders” contained in Neuroimaging in Psychiatry edited by Fu et al 2003 and published by Martin Dunitz).
My first reaction to this position is that it lacks common sense, i.e., patients with Parkinson’s or recovering from a CVA may very well get depressed because of the loss of health and impact on their lives. Yet, this common human reaction to significant illness is not even noted by these researchers as playing an etiologic role in a mood disorder. Secondly, from a scientific perspective, the evidence for ‘downward causation’ is much stronger than for ‘upward causation’ in the affective disorders. In fact, in order to research the latter, the person has had to be identified as high risk and followed over time or to have already developed the illness. The research on this only demonstrates correlation not causation, yet the researchers act as if it is causative.
Importantly, there is massive research demonstrating the effects of early adverse experience on mothering as well as the developing infant/child, resulting in various affective disorders (‘downwards causation’), including psychosis, later in life. One example would be the area of research with non-human primates demonstrating that manipulating conditions of security for the nursing mother results in widespread behavioral and neurobiological consequences in the infants decades after the experimental manipulation (see Sanjay Mathew & Jeremy Coplan 2004 “Animal models of social anxiety” in Social Anxiety Disorder edited by Borwin Bandelow & Dan Stein for Marcel Dekker as well as the research of Steve Suomi and colleagues). These findings are robust, replicable and, though not definitive, certainly are highly suggestive of the importance of downwards causation in behavioral analogues resembling human psychiatric disorders (e.g., social anxiety disorder, PTSD, major depression, schizophrenia spectrum disorder, etc).
Some of the consequences observed in this line of research include: social anxiety and avoidance, separation anxiety, impaired immunological functioning and affect regulation, hippocampal tissue atrophy, on MRS scans decreased NAA and increased glutamate in prefrontal areas (particularly the anterior cingulate cortex) suggestive of neurotoxicity and loss of neuronal integrity, LHPA dysfunction (greater stress reactivity), increased CRF (a stress hormone) suspected to result in neurotoxicity, dopaminergic, serotonergic and glutamatergic dysfunction. The latter is believed to be a key neurochemical in neurotoxicity (increased levels of the excitatory amino acid glutamate resulting in an excess of calcium entering the cell and bringing about apoptosis, i.e., cell death).
In addition to the above research findings, it has become increasingly clear that profound stress impairs neurogenesis (the birth of new neurons) in key neural areas (hippocampus and, perhaps, prefrontal areas). All, I repeat, all of these research findings are what are observed in neuroscience research in the schizophrenias.
Clinically, it became apparent to me recently with one of my patients diagnosed with schizoaffective disorder, the role that depressive and persecutory guilt play in his psychotic symptomatology. In regard to the latter, I highly recommend Leon Grinberg’s Guilt and Depression published in 1992 by Karnac (with such chapters as “The mentally ill person as depository of the persecutory guilt of the family and society” and “Persecutory guilt, neurosis, and psychosis,” ISPSers would find much of interest in this excellent volume). Over the span of many years (twice weekly psychotherapy sessions), I have observed a complex pattern in which my patient (I will call him Nathaniel), has systematically relived in a delusional manner all of the traumas he observed his parents go through (pseudo seizures, blood dyscrasias, anger over being rescued from death, etc). Nathaniel, I have come to believe, and have very good reasons to believe, holds himself responsible for these parental traumas.
As a result of his omnipotent guilt feelings, he has made several serious suicide attempts. His delusions involved escaping to a superior race of beings, leaving earthlings behind and developing cures for serious medical illnesses in order to bring about immortality (to cure the damage he feels he inflicted upon his parents by being born). Nathaniel’s internal world is littered with damaged and dying parental objects (see the work of Henri Rey- Rey, H. (1994). Universals of Psychoanalysis in the Treatment of Borderline and Psychotic States: Space-Time and Language Factors. London: Free Association Books), which he holds himself responsible for. Along with this ‘little history’ of individual lives is the interaction with the cultural ‘big history (thanks to Francoise Davoine and Jean Max Guadlierre for cogently drawing our attention to this). In Nathaniel’s case, it is the massive effects of the Holocaust on his father.
Grinberg (1990) called our attention to the disturbances in the sense of identity and structure of the self, caused by such processes as splitting pathological projective identification and failure to work through mourning. One of Grinberg’s contributions to a deeper understanding of this phenomenon is his distinction between persecutory and depressive guilt. He defined these terms as follows:
“The individual may respond to an experience of loss with a guilt in which anxiety and retaliation phantasies predominate, forming the type of guilt that I have called persecutory guilt. This guilt corresponds with the functioning of labile ego with a very strict superego, and occurs in states of depression in which envy and aggressive impulses predominate; these incline towards manic reparations and, in my opinion, would form part of the emotions of the paranoid-schizoid position. On the other hand, depressive guilt appears later, with a more mature and integrated ego that can feel pain, responsibility, and a genuine wish for object reparation; it would correspond with the guilt of the depressive position described by M. Klein (1940). Both types of guilt can also be experienced in relation to one’s own self” (p. 177).
Grinberg (1992) thought that persecutory guilt plays a significant role in all neurotic and psychotic conditions. In mania, Grinberg believed, there was an attempt to counteract the influence of persecutory guilt, which appeared as an absolute denial of it, along with strong feelings of omnipotence. Denial is used to reduce the danger of persecutors and also to diminish the importance of good objects, but this very denial tends to increase their persecutory guilt even more. Grinberg saw mania as not just a defensive state, but having a particular mental organization of its own:
“...mania, with its extreme mechanisms of denial, omnipotence, and derealization is not only a defensive counterpart to anxieties and persecutory and depressive guilt but also a regressive state with very particular characteristics with respect to the functioning of the ego and its relationship with the object” (p. 101).
Grinberg (1990) described the pathological consequences of a failure in caregiver containment:
“The baby, as well as looking for the satisfaction of his nutritional needs, projects his affects of fear and pain on to the breast of his mother with the hope of feeling loved and understood, and therefore, receiving these feelings back again detoxicated and stripped of their intolerable painful quality, if the breast fulfills this function, it gives him meaning. If it is absent, the fear born of the phantasy of having destroyed it implies not only that he will cease to exist, since without the breast he cannot live, but also that the meaning, as though it were material, has ceased to exist.” (p. 181)
With the psychoanalytic situation in mind, Grinberg (1997) had this to say of containment:
“The analyst not only has to contain the projections he receives but must also be capable of detoxifying them – that is of stripping them of their pathogenic elements and returning them through appropriately timed interpretations, the basis of this attitude would be an acceptance of invasion by these projections and of all the consequences, so as to be able to share and feel on a basis of consubstantiality with the patient the affects continued within them, whatever their nature (murderous hatred, death anxiety, catastrophic terror, and the like), AS IF THEY WERE PART OF THE ANALYST’S OWN SELF [what Searles & Benedetti have referred to as “therapeutic symbiosis”]. It is a matter of offering one’s entire availability, mental space and time for all the mental time and space required by the patient, with their different affective contents. In other words, the analyst has to experience in his own personality a transformation that will allow him to reach a state of convergence with the anxiety, grief, hate, delusion or hallucination experienced by the analysand.” (p. 11)
Brian Koehler PhD
New York University
80 East 11th Street #339
New York NY 10003
212.533.5687
brian_koehler@psychoanalysis.net
