Hello and welcome back to Module 5, Schizophrenia and Schizophrenia Spectrum Disorders. This is Lecture 3, Models for Understanding Schizophrenia. It may not surprise you to learn there's an enormous amount of research investigating the biological basis of schizophrenia. While no clear cause or causes have been identified, biological research has nonetheless shed light on biological components of this disorder. Twin studies and family studies have demonstrated a genetic element to this disorder. Specifically, the more closely related a person is to someone with schizophrenia, the higher their risk for developing the disorder. For example, if one identical twin is diagnosed with schizophrenia, there's a 48 percent chance the other identical twin will develop it as well. However, if one fraternal twin has schizophrenia, there is only a 17 percent chance the other fraternal twin will develop it. Defects in several genes have been implicated in schizophrenia. In fact researchers have found 281 gene defects altogether. Scientists believe schizophrenia is associated with many different possible combinations of gene defects. Before we move on to other areas of biological research, it is important to point out that identical twins share the same genetic makeup yet nonetheless, their concordance rate for schizophrenia is only 48 percent. What does this mean? Clearly, there's something more going on than simply genetics that leads to the development of the disorder in some individuals but not in others. Specifically, the impact of the environment and life stressors. Be sure to keep this in mind for the rest of this discussion. The dopamine hypothesis has been a very influential theory of the cause of schizophrenia for well over 50 years. According to this theory, neurons using the neurotransmitter dopamine fire too often. As a result there's too much dopamine being sent to receiving neurons producing the symptoms of schizophrenia. The dopamine hypothesis theory originated from the accidental discovery that a class of medications called phenothiazines significantly reduce the symptoms of the disorder. The phenothiazines were used in the 1950s as antihistamines to treat the symptoms of people's allergies. In the process doctors found the medications improve the symptoms of schizophrenia. A closer look at these medications found that they act to reduce the levels of dopamine in the brain. Working backward, researchers then concluded that schizophrenia must result from high levels of dopamine. Newer medications however, act on serotonin as well as dopamine, which raises questions about the dopamine hypothesis. Additional support for the dopamine hypothesis of schizophrenia comes from research and other areas. For example, people with a neurological disorder called Parkinson's disease take a medication called L-Dopa to treat the symptoms. L-Dopa raises the levels of dopamine in the brain. If too much L-Dopa is taken, psychotic symptoms develop. Amphetamines are a class of drugs that stimulate the brain by raising dopamine activity. Research has found that people who take high doses of amphetamines also develop symptoms of psychosis. Well, it's clear that dopamine plays a critical role in schizophrenia. The additional involvement of serotonin complicates the picture. Also, not all people with schizophrenia improve when they take medications that lower their dopamine levels. Dopamine may be an important piece of the puzzle, but there are many more pieces. Research has looked at other potential biological components to schizophrenia besides genetic factors and dopamine. A prevailing theory known as the diathesis stress model of schizophrenia, asserts that the disorder begins with a biological disposition, such as the gene defects we discussed earlier, but that in order for someone to develop the illness, this predisposition must be activated by some stressor, or negative event. Poor nutrition, problems during fetal development, birth complications, immune reactions, exposure to environmental toxins, living in poverty, family dysfunction, severe stress, as well as exposure to viruses in utero have all been suggested as events that may activate an underlying predisposition for schizophrenia. Is there any alternative to the biological model for understanding the development of schizophrenia? The short answer is not really. No. In the 1950s, a popular psychoanalytic theory claimed that cold rejecting parents, primarily mothers, were to blame for the development of schizophrenia in their children. The term schizophrenogenic, or schizophrenia creating mother emerged from this theory. While this psychoanalytic theory became famous for a long time, there is no research support for it. Cognitive behavioral theorists have proposed a theory for how learning may interact with a biological vulnerability to schizophrenia. They've developed the misinterpretation explanation. These theorists accept that on a fundamental level, schizophrenia has a biological basis, and that the brains of people with the disorder do in fact produce unreal physical sensations and strange thoughts. The CBT model goes on to state that more symptoms of schizophrenia emerge when the person seeks to make sense of these experiences. First, the person seeks confirmation from friends and family that their experiences are real. When others deny the reality of these experiences, the person then begins to suspect that other people are hiding the truth from them. From that point forward, the person begins to reject all feedback from other people about their experiences and behavior. Instead, turning more deeply inward and embracing the reality of the symptoms their brains are producing. As this process unfolds, their symptoms become increasingly severe and debilitating. As you can now see, the prevailing model for schizophrenia is a biological one. However, it is very important to note that in spite of the accumulation of biological research, the findings are complex and ultimately inadequate to explain the origins of this disorder. The CBT theory offers a model for the ways in which learning and relationships may interact with a biological vulnerability to cause the disorder to develop. There is much that remains unknown about this complex and often devastating disorder. In the next lecture, we will discuss treatment interventions for schizophrenia.
