Conclusions

Many of the findings summarized above invite a diathesis-stress view of psychopathology. According to this view, psychiatric symptoms are the end-product of a biologically based predisposition (e.g. neuroticism) interacting with aversive life experiences. While this approach has proved to be a fruitful framework for many disorders/,5,,1 it should not limit our thinking about the aetiology of psychiatric symptoms. For example, the diathesis-stress framework has often been taken to imply that biological abnormalities of symptomatic individuals are somehow more fundamental than the symptoms and therefore must precede these symptoms. In their excellent review, Harrop et al. (52> demonstrate that this line of reasoning is problematic. Even in the case of ventricular enlargements or dopamine disruptions in schizophrenia, there is the possibility that the pertinent central nervous system abnormalities are produced by schizophrenic symptoms or certain environmental factors that operate in the aetiology of schizophrenia.(53) Note that there are well-researched examples of psychological conditions resulting in biological abnormalities. Consider the learned helplessness paradigm. When animals are made helpless by inescapable shocks, they not only become passive, but also exhibit noradrenaline and serotonin depletion. (54> This implies that a certain learning history may give rise to neurotransmitter abnormalities that have traditionally been conceptualized as the causes of depression. Likewise, while positron-emission tomography scanning revealed profound brain abnormalities in obsessive-compulsive patients, these cerebral differences between patients and controls were abolished after successful behavioural treatment. (55>

Even when it is plausible to assume that a biological abnormality precedes the onset of symptoms, it is not self-evident that this abnormality plays a significant aetiological role. For example, a biologically based dysfunction (e.g. scoring low on positive affectivity) may affect the course rather than the onset of a disorder. This type of causation is known as the pathoplasty model and, compared with the widespread diathesis-stress approach, it has received too little consideration.

Perhaps, then, the benefit of psychobiology to psychiatry does not consist of grand theories about causation, but of reliable measurements of basic concepts. That is, psychobiology can inform psychiatry about fundamental personality traits, the nature of emotions, and how they relate to the brain. It can also contribute good psychophysiological and neuropsychological tools that possess diagnostic and prognostic value. In doing so, it may help to define the limits within which good theorizing must occur.

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