Mental health articles

Before examining the disease model it is necessary to deal with the general meaning attributed to disease. Kendall has reviewed disease definitions in psychiatry, which range from the purely subjective (for example, personal suffering) to the purely objective (for example, the presence of an identifiable pathogen). This latter interpretation tends to predominate and is defined by Scadding  as the presence of abnormal phenomena displayed by a group within a species, that sets the group apart from its species in so far as the disease places them at a biological disadvantage. In lay terms, a disease is only present if it harms the ndividual or reduces his or her capacity to reproduce. We may all feel comfortable with the idea of physical disease, such as a cancer, a damaged heart valve, or a pathogen that can be transmitted between people. We can probably also agree that these conditions do, more or less, place individuals at some sort of disadvantage.

Disease theorists similarly attribute mental disorders, or psychiatric illnesses, to physiological and chemical changes in the individual, particularly in the brain but also in other parts of the body. Thus we can understand clearly the basis for disorders of perception and cognition among say, people with dementia or those who have suffered brain injuries. Observable physiological changes in brain structure have correlates in human behaviour. The disease model extends beyond these organic conditions to explain disorders such as depression, which can be attributed to changes in serotonin levels or to some other chemical fluctuation. Similarly, schizophrenia can be attributed to chemical abnormalities, and more recently to physiological differences such as the size of the temporal lobe in the human brain. The disease model, following traditional medicine, endeavours to identify through scientific objectivity the presence of a stable phenomenon that we call ‘mental illness’. Clinical syndromes become refined into diagnoses, which are essentially codes for heterogeneous, and often unstable collections of symptoms. Objectivity in psychiatry is at best quite ‘fuzzy’, but remains the gold standard. Such a gold standard affords incredible power to its possessor. Clinical syndromes and diagnoses are codified languages, available only to those who have willingly immersed themselves in that particular paradigm. They can provide an efficient means to communicate complex phenomena, but only to those in the know. The treatment armoury of the disease theorist is also elitist, being available only to the qualified practitioner. Medicines are prescribed to balance chemical imbalances, electroconvulsive therapy is administered to shunt neural pathways into shape, positron emission tomography may be requested to check those temporal lobes and, in the most extreme of cases, pieces of the brain may be removed. A consistent criticism of the disease model is the possibility that people with mental disorders can become passive recipients of treatment and the nurse or doctor an authority on the person’s experience.

 However, this is not a consequence of the disease model per se, but reflects something of the way in which practitioners apply their knowledge. Passive receipt of care can accompany any model if practitioners fail to speak to people as people, but instead believe they are dealing with symptoms, syndromes or a collection of behavioural problems. We see no reason why the disease model cannot take account of the person behind the symptoms or syndrome, and indeed in our experience this has largely been the case, though not always so. Some commentators have questioned the validity of associations between human physiology, brain chemistry and mental disorder. In fact there are both weak and strong arguments of this type. The ‘strong’ camp rejects outright any attempt to reduce human experience to physiological and chemical structures, and tends therefore to reject the disease model. In contrast, the ‘weak’ camp acknowledges the contribution of the physical sciences to our understanding of mental disorder but maintains that they are insufficient to explain adequately the phenomenon of interest. For example, some people with schizophrenia do appear to have ventricular enlargement, but others do not (Van Horne and McManus 1992). The case for and against a physiological ‘disease’ explanation for mental disorders has been rehearsed in the academic literature. We refer readers to these to draw their own conclusions.

Tags: disease, mental disorder, models