While this section will focus on the universal prevention of schizophrenia, it is important to note ideas and potential strategies for selective and indicated prevention that are also in development. For example, if we could identify individuals at high risk of developing schizophrenia, then selective prevention measures might be recommended. Apart from the increased risk of psychosis in those with a positive family history, our ability to identify individuals prior to the onset of schizophrenia is still poor. The positive predictive value may be improved by combining risk factors such as those derived from longitudinal cohort studies (e.g. cognitive, behavioural and psychosocial antecedents of schizophrenia), psychophysiological measures (e.g. smooth pursuit eye movement, P300, etc.), the presence of minor physical anomalies or obstetric complications.
Selective intervention relies on efficient means of identifying those at increased risk (via single or multistage screening). The sensitivity and specificity of the screens must be balanced with the safety and efficacy of any proposed intervention.
While avoidance of illicit substances and stress management may seem to be reasonable and safe selective interventions, we lack a sufficient evidence base to guide us. The use of antipsychotic medications in prepsychotic individuals is an ethically complex issue, and one that, as yet, lacks an evidence base (Tsuang et al., 2000).
Individuals thought to be at increased risk may be a target for careful review and prompt treatment if psychosis is noted to arise, but such follow-up, however well intentioned, is not a benign intervention.
For individuals with early features of psychosis, there is a growing body of evidence showing that integrated treatments (low-dose medication, psycho-education and cognitively oriented psychological treatments) improve outcomes (McGorry and Jackson, 1999): an example of indicated prevention. Prompt treatment for those in the earliest phases of schizophrenia should improve a range of short-term outcomes, and there is much hope that indicated prevention may also translate to improved long-term outcome. Future research should help to clarify this issue (McGrath and McGlashan, 1999).
Universal interventions: the search for risk factors
Unlike the search for susceptibility genes for schizophrenia, those interested in nongenetic risk factors are not able to map the environment systematically.
Prevention of schizophrenia
- The science of prevention
- Risk factors and causes
- Barriers to the primary prevention of schizophrenia
- Preventive strategies in schizophrenia
- Selective prevention
- Indicated prevention
- Genetic factors
- Season and place of birth
- Pregnancy and birth complications
- Prenatal infection
- Nutritional factors
- Developmental risk factors: from infancy to onset
- Future directions
However, research has identified a number of pre- and perinatal candidate risk factors for schizophrenia. These include family history, season of birth, place of birth, obstetric complications, prenatal exposure to viruses and prenatal famine. Other risk factors have been identified that are more proximal to the onset of illness (e.g. Head injury, substance abuse, life events).
When assessing risk factors, it is important to consider the strength of the evidence (consistency, design rigour), the effect size associated with the exposure (odds ratios or relative risks), and the population attributable risk (PAR). The PAR is an estimate of how many cases could be prevented if a particular risk factor were eliminated (assuming that the risk factor is causally related to the outcome; Last, 1988). It should be noted that the PAR is a problematic concept. For example, the total PAR values for various risk factors could total more than 100% because of possible additive or competing effects: the measure does not take into account interactions between different risk factors. However, PAR does serve to rank order risk factors in a manner of interest to prevention research. It emphasizes the fact that small risk factors, if widely distributed among the community, may ‘cause’ more cases than rarer, but larger, risk factors. It also has to assume that risk factors are true, risk-modifying factors with causal effect.