Online research in philosophy

The etiology of schizophrenia remains heavily contested despite extensive research, huge quantities of data, and heavy investment in time and material resources around the world. Not only is there little agreement about the causes of this most devastating of psychiatric conditions, but there is disagreement as to whether the condition exists at all as a coherent entity (Bentall 2006). Evolutionary theorists have had the added problem of explaining how a severe mental illness that causes a significant reproductive disadvantage can continue to exist in human populations, where it is claimed to have a uniform prevalence across the world. Many Darwinian formulations have suggested various forms of tradeoffs where the ..

This commentary compares clinical aspects of ketamine with the amphetamine model of schizophrenia. Hallucinations and loss of insight, associated with amphetamine, seem more schizophrenia-like. Flat affect encountered with ketamine is closer to the clinical presentation in schizophrenia. We argue that flat affect is not a sign of schizophrenia, but rather, a risk factor for chronic schizophrenia.

I begin by examining how genetics drivesschizophrenia research, and raise both familiar andrelatively novel criticisms of the evidence putativelysupporting the genetic basis of schizophrenia. Inparticular, I call attention to a set of concernsabout the effects of placentation on concordance ratesof schizophrenia in monozygotic twins, which furtherweakens the case for schizophrenia''s so-called stronggenetic component. I then underscore two criticalpoints. First, I emphasize the importance of takingseriously considerations about the complexity of bothontogenesis and the development of hereditarydiseases. The recognition of developmentalconstraints and supports is crucial, for attention todevelopment exposes the naivete of too many models ofgene action in the aetiology of disease. Secondly, Iattend to those schizophreniologists who ignoremethodological criticisms and thus presume a geneticbasis for schizophrenia, and then seek the schizophrenic genotype lacking an adequatephenotype. In response I attempt to demonstrate thenecessity of a sustained effort at characterizing thephenotype of schizophrenia as an enabling conditionfor the whole enterprise of psychiatric genetics – andfor psychiatry itself. Without the organism-levelphenotype, research at the level of genes will remainunproductive – assuming of course that research at thegenetic level is appropriate at all.

The claim that the disorganized subtype of schizophrenia results from glutamate hypofunction is enhanced by consideration of current subtypology of schizophrenia, symptom definition, interdependence of neurotransmitters, and the nature of the data needed to support the hypothesis. Careful specification clarifies the clinical reality of disorganization as a feature of schizophrenia and increases the utility of the subtype.

This commentary challenges the argument that the diathesis for hallucinations is equivalent to that for schizophrenia. Evidence against this comes from data on the prevalence of hallucinations in schizophrenia, their nonspecificity, and their relationships with moderating variables. We also highlight, however, the manner in which the Behrendt & Young (B&Y) hypothesis extends recent neuroscientific theories of schizophrenia, and its potential treatment applications.

Impairments in cognitive coordination in schizophrenia are supported by phenomenological data that suggest deficits in the processing of visual context. Although the target article is sympathetic to such a phenomenological perspective, we argue that the relevance of phenomenological data for a wider understanding of consciousness in schizophrenia is not sufficiently addressed by the authors.

A diagnosis of schizophrenia is often taken to denote a state of global irrationality within the psychiatric paradigm, wherein psychotic phenomena are seen to equate with a lack of mental capacity. However, the little research that has been undertaken on mental capacity in psychiatric patients shows that people with schizophrenia are more likely to experience isolated, rather than constitutive, irrationality and are therefore not necessarily globally incapacitated. Rational suicide has not been accepted as a valid choice for people with schizophrenia due in part to a belief that characteristic irrationality prevents autonomous decision-making. Since people with schizophrenia are often seen to lack insight into the nature of their disorder, both psychiatric and ethical perspectives generally presume that suicidal acts result directly from mental illness itself and not from second-order desires. In this article, I challenge notions of global irrationality conferred by a diagnosis of schizophrenia and argue that, where delusional beliefs are unifocal, schizophrenia does not necessarily lead to a state of mental incapacity. I then attempt to show that people with schizophrenia can sometimes be rational with regard to suicide, where this decision stems from a realistic appraisal of psychological suffering.