Preventing Schizophrenia

We wear seat belts when we drive in a car,  so that we are protected if we get in an accident.  When we are out in the sun, we wear sunscreen to protect our skin from the harmful effects of ultraviolet light.  We know not to smoke cigarettes because it increases the likelihood that we will develop lung cancer.

Are there similar preventative measures we can take to prevent schizophrenia?  Are there ways by which we can slow the development of this devastating illness?

Prevention of an illness can take two forms:  primary and secondary prevention. The goal of primary prevention is to prevent new cases of a disorder from ever developing.  One way we can do this with schizophrenia is improving prenatal and obstetric care.  Pregnancy and birth complications have been linked to schizophrenia.  Clinicians   and   researchers   speculate   that   by improving health and nutrition in pregnant women,  we may prevent the development of schizophrenia in their offspring.

There is a tremendous benefit from this approach,  and there are no disadvantages.  By improving prenatal care,  we improve the health of the mother and the baby and increase the likelihood that both will be safe and healthy.  Improving prenatal care is unlikely to cause any harm to the mother or the fetus.  Still, because schizophrenia is caused by a whole host of factors, there is no guarantee that a child born to a mother who was healthy during pregnancy will not develop schizophrenia.

The goal of secondary prevention is to identify those who are most at risk of developing schizophrenia and treat them early.

This approach is problematic and has been the subject of great controversy.  How does one identify someone at risk for schizophrenia?  Can this be done with any degree of accuracy?

Relatives of schizophrenia patient are at risk,  but not all relatives will develop the disorder.  Another way researchers identify at-risk individuals is with a questionnaire that measures risk for psychosis.  The questionnaire measures thoughts and behaviors that have been found to be indicators of future psychotic symptoms.  Research has shown that 20 percent to 45 percent of people who score highly on this scale will eventually develop full-blown psychosis.  The biggest problem with the secondary prevention approach is that it yields too many false positives.

Concepts of Prevention
The focus on psychosis as the core defining quality of schizophrenia (i.e., the reality distortion emphasis from Schneinderian firts-rank symptoms through DMS-IV) has led some workers to confuse early intervention with prevention. For example, Falloon described treating early psychotic manifestations, and patients who did not progress to full diagnostic criteria were considered instances of prevention.

This is more appropriately viewed as muting the severity of expression rather than prevention. Others have hypothesized secondary and tertiary prevention associated with early intervation. Here the hope is that the more effective management of the first episode will have long-lasting beneficial effects on the disease process. However, because effective psychosocial and antipsychotis drug therapies are not known to alter the course of cognitive and negative symptom pathologies, it seems doubtfull that disease progression per se is prevented.

Ata theoretical level, it is crucial to distinguish the prevention of adverse epiphenomena from the prevention of disease progression. For example, an effective early intervention might help a young patient avoid hospitalization, finish high school, and obtain a job. This may leave the person substantially better off in occupational and social outcomes that would have been the case if social relationships were interrupted by hospital care and stigmatizing symptoms, and high school failure restricted job opportunities. This example illustrated why the clinical prudence argument is strong, whereas ths disease progression argument remains speculative.

The most important prevention challenge is to reduce the number of cases of schizophrenia in the population. In the absence of precise knowledge of etiopathophysiologic pathwaws to schizophrenia, primary prevention is based on risk factors. At times the datat are sufficiently robust to be considered by individuals.

Individuals who have schizophrenia, or who have a twin or even a first-degree relative with the disease, may wish to understand heritability data in order to make childbearing decisions. But less understandable and less robust risk factors are not likely to influence childbearing behavior. It is doubtful whether anyone avoids winter birth with schizophrenia prevention in mind, and men are not likely to consider the increased risk of mutations associated with advancing paternal age. Altogether missing are markers that are highly informative of an individual’s risk.

At present, with tongue in cheek, we can advise the woman anticipating pregnancy to secure a negative family history, avoid first-trimester starvation, second-trimester influenza, birth complications, and mate with a young man timing inception to avoid a winter birth (or summer birth in the deficit form of schizophrenia is of concern).

Early clinical intervention and prevention in schizophrenia
William S. Stone, Stephen V. Faraone, Ming T. Tsuang

In this case,  a false positive is saying that people will develop schizophrenia when they will not.

So   far,  researchers   who   take   the   secondary   prevention approach have suggested prescribing low doses of antipsychotic medications to those who are most at risk for developing the illness.

That means that they give medication to people who have not developed actual symptoms.  As you might imagine,  this can be problematic and complicated.  Some argue that it is unethical to give medication to people who are not sick.  Antipsychotic medications are not without side effects and may cause longterm health problems.  In addition,  it may be stigmatizing to be diagnosed and/or treated for a mental illness.  A person who is told he or she is at risk for schizophrenia might actually become anxious or depressed.

Current research is exploring the costs and benefits of early treatment for schizophrenia.  So far,  the results are inconclusive.

The social and economic benefits of schizophrenia prevention are enormous.  It is likely that this research will continue well into the future.

Prevention timing
Prevention programs for schizophrenia can aim to improve host resistance (i.e. providing neuroleptics prophylactically), behavioral change (i.e., improved attention and processing), or environmental change (i.e., peer relationships). In each of the categories we can aim at immediate reduction in risk or may use an early inoculation model, sometimes with boosters, that seeks to influence host resistance prior to or during mayor periods of risk. In the broad field of prevention of mental disorder and substance abuse, there have been successful prevention programs in both of these general categories of immediate reduction or early inoculation, and both are potentially useful for the prevention of schizophrenia as well. Timing of an intervation will depend on the strength of risk factors across time and on the theory of change underlying the target mediators.

Early clinical intervention and prevention in schizophrenia
William S. Stone, Stephen V. Faraone, Ming T. Tsuang

Heather Barnett Veague, Ph.D.
Heather Barnett Veague attended the University of California, Los Angeles, and received her Ph.D. in psychology from Harvard University in 2004. She is the author of several journal articles investigating information processing and the self in borderline personality disorder. Currently, she is the Director of Clinical Research for the Laboratory of Adolescent Sciences at Vassar College. Dr. Veague lives in Stockbridge, Massachusetts, with her husband and children.

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