This paper examines the multifactorial causes of schizophrenia, one of the most severe chronic mental illnesses. Drawing on research in genetics, neurobiology, and environmental psychology, the paper explains how no single factor alone produces the disorder. Instead, genetic predisposition — evidenced by twin and family studies — interacts with prenatal brain development abnormalities and environmental stressors such as urban living, birth trauma, and family dysfunction. The paper also addresses the difficulty clinicians face in disentangling causal factors and discusses how a healthy family environment can serve as a protective buffer even for those at high genetic risk.
Schizophrenia is one of the most severe chronic mental illnesses an individual can face over the course of his or her lifetime. People with schizophrenia can suffer a wide range of debilitating symptoms, including hearing voices that are not really there, feeling as if their thoughts are being controlled by outside forces, fearing that their minds can be read against their will, or exhibiting other paranoid symptoms that alienate them from the rest of society. Schizophrenics often find it difficult to organize their thoughts and communicate with other people; instead, they may speak in jumbled and disordered phrases (Spearing, 2002).
Schizophrenia is fairly rare. Approximately 1 percent of the population develops schizophrenia, affecting more than 2 million Americans per year. Schizophrenics are found all over the world. Although there is much that modern research does not yet know about schizophrenia, what is known illustrates the complex interplay of genetics, environment, and physiology in the development of this mental disorder (Spearing, 2002). In an effort to shed light on the condition, geneticists are trying to trace the heritable factors that contribute to schizophrenia. "Several regions of the human genome are being investigated to identify genes that may confer susceptibility for schizophrenia. The strongest evidence to date leads to chromosomes 13 and 6 but remains unconfirmed" (Spearing, 2002). Most evidence suggests that several genes or combinations of genes contribute to a predisposition to develop schizophrenia.
Prenatal difficulties — such as fetal starvation, maternal viral infections, birth complications, and a variety of fetal and maternal stressors — can also raise an individual's chance of developing schizophrenia later in life. Although a predisposition may be identified, there is no way to conclusively predict whether a given person will develop the disorder; there is no way to demonstrate that the disorder will surface until the individual has begun to show symptoms. Psychologists and psychiatrists must also guard against mistaking the symptoms of schizophrenia for those of other disorders, such as the manic stage of bipolar disorder (Spearing, 2002).
Schizophrenic symptoms usually become obvious to others when an individual enters his or her first psychotic episode. There is often a clear dissociation from reality on the part of the patient. A state of psychosis may result in hallucinations, strange sensory perceptions, or paranoid delusions. These symptoms may also precipitate alterations in personality and customary behavior. An individual may withdraw from society or use strange phrases. A lack of appropriate emotion, or immobility to the point of catatonia, is witnessed in some sufferers. This withdrawal may arise because the individual is struggling to cope with hallucinations or other symptoms, or as a result of paranoia. Children as young as five can exhibit symptoms of schizophrenia, though these cases are rare (Spearing, 2002).
Schizophrenia affects men and women with equal frequency. However, the disorder often appears earlier in men — usually in the late teens or early twenties — than in women, who are generally affected in their twenties or early thirties (Spearing, 2001). Although the specific symptoms vary from person to person, research consistently demonstrates that schizophrenia has a genetic causation. People who have a close relative with schizophrenia are much more likely to develop the disorder than those who have no relatives with the illness. Twin studies, which researchers often use to examine the possibility of genetic causation of psychiatric disorders, show: "a monozygotic (identical) twin of a person with schizophrenia has the highest risk — 40 to 50 percent — of developing the illness. A child whose parent has schizophrenia has about a 10 percent chance. By comparison, the risk of schizophrenia in the general population is about 1 percent" (Spearing, 2002). To name just one example, the younger son of the famous recovered schizophrenic mathematician John Nash also developed schizophrenia (Nasar, 2001).
However, the illness is still relatively rare, and simply coming from a family with a strong predisposition to develop schizophrenia does not automatically mean that a person will be affected. "If, for example, you have an aunt or uncle who developed schizophrenia, then your risk (on average) is estimated at approximately 3% (and therefore there is a 97% probability you won't get schizophrenia). Even for the situation where one parent has schizophrenia, the risk is estimated at 13% for a child — which means there is an 87% probability that the person will not develop schizophrenia" (Corcoran et al., 2004). Such evidence supports the notion that no single gene or chromosomal abnormality causes schizophrenia, unlike a clearly monogenic illness such as hemophilia, which can be traced fairly easily from generation to generation.
In addition to its genetic dimension, schizophrenia may also have a strong physical component rooted in brain development. "Developmental neurobiologists funded by the National Institute of Mental Health (NIMH) have found that schizophrenia may be a developmental disorder resulting when neurons form inappropriate connections during fetal development. These errors may lie dormant until puberty, when changes in the brain that occur normally during this critical stage of maturation interact adversely with the faulty connections. This research has spurred efforts to identify prenatal factors that may have some bearing on the apparent developmental abnormality" (Spearing, 2002). Such an explanation seems plausible, but it does not fully explain why males — who enter puberty later — experience symptoms earlier than females, or why some prepubescent children develop schizophrenia.
Birth trauma, malnutrition during infancy, and other physical factors can increase the tendency of someone with a genetic predisposition to develop the disease. On brain scans, schizophrenia appears to leave a biological trace. Many people with schizophrenia show enlargement of the fluid-filled cavities called ventricles in the interior of the brain, as well as decreased metabolic activity in certain brain regions. However, no specific brain abnormality has been found in all people with schizophrenia, nor do these characteristics occur exclusively in individuals with this illness (Spearing, 2002). "Microscopic studies of brain tissue after death have also shown small changes in the distribution or number of brain cells in people with schizophrenia. It appears that many — but probably not all — of these changes are present before an individual becomes ill, and schizophrenia may be, in part, a disorder in the development of the brain" (Spearing, 2002).
"Urban stress, birth trauma, and maternal factors"
"Adoption studies and family environment as buffer"
"Limits of causal attribution in clinical research"
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