Genetic Explanation of Schizophrenia

The genetic explanation proposes that schizophrenia develops due to the presence of certain genes or combinations of genes. This theory is supported by twin studies and adoption studies, which examine concordance rates - the likelihood of developing schizophrenia if a relative has the disorder.

Evidence from Gottesman's 1991 study on inheritance and twin studies shows a clear pattern: the more genes shared with a person who has schizophrenia, the higher the risk of developing the disorder. For example:

• Identical twins have a 48% risk
• Fraternal twins have a 17% risk
• First-degree relatives $parents, siblings, children$ have a 13% risk
• Second-degree relatives have a 4-6% risk
• The general population has a 1% risk

Example: If one identical twin has schizophrenia, the other twin has a 48% chance of also developing the disorder, compared to only a 17% chance for fraternal twins.

Highlight: While the genetic link is strong, no concordance rate reaches 100%, indicating that other factors beyond genetics play a role in the development of schizophrenia.

Adoption Studies and Candidate Genes

Adoption studies provide further evidence for the genetic basis of schizophrenia while also highlighting the importance of environmental factors. The Tienari et al. $1994$ study compared adopted children of schizophrenic parents with adopted children of non-schizophrenic parents. The results showed:

1. A higher rate of psychoses and severe diagnoses in the offspring of schizophrenic parents
2. The genetic effect was only manifested in the presence of a disturbed family environment
3. The impact of disturbed family relations was strongest when combined with genetic predisposition

These findings support a genetic hypothesis for schizophrenia but also emphasize the interaction between genetic and environmental factors.

Recent genetic research has identified numerous candidate genes associated with schizophrenia:

• A 2014 study by Ripke et al. found 108 distinct locations on the human genome linked to schizophrenia
• These genetic locations were primarily in regulatory regions rather than coding regions
• Geschwind noted that most schizophrenia-linked DNA interacted with genes crucial for brain development

Vocabulary: Heterogeneity - The quality of being diverse in character or content.

Highlight: The genetic basis of schizophrenia is complex, involving multiple genes and variations, which contributes to the heterogeneity of the disorder.

The Dopamine Hypothesis

The dopamine hypothesis is a prominent biological explanation of schizophrenia that focuses on the role of the neurotransmitter dopamine in the brain. This theory proposes that imbalances in dopamine activity contribute to schizophrenia symptoms. The hypothesis identifies two key aspects:

1. Hypodopaminergia: Low dopamine activity in the prefrontal cortex $mesocortical pathway$, associated with negative symptoms of schizophrenia.
2. Hyperdopaminergia: Excessive dopamine activity in the mesolimbic pathway, associated with positive symptoms of schizophrenia.

The dopamine hypothesis suggests that these imbalances may be due to:

• Variations in the number of dopamine receptors in different brain areas
• Differences in the sensitivity of dopamine receptors

Vocabulary: Neural correlate - A measurable brain function or state that corresponds with a particular mental state or behavior.

Definition: Positive symptoms are abnormal experiences or behaviors that are present in schizophrenia, such as hallucinations or delusions. Negative symptoms refer to normal behaviors or experiences that are absent or diminished in schizophrenia, such as lack of motivation or social withdrawal.

Highlight: The dopamine hypothesis provides a biological explanation of schizophrenia that links brain chemistry to specific symptoms, offering potential targets for treatment.

Evaluating the Dopamine Hypothesis

While the dopamine hypothesis offers a compelling biological explanation of schizophrenia, it's important to critically evaluate its strengths and limitations:

1. Neural Correlate: There is a correlation between brain structure/function and schizophrenia symptoms. However, correlation does not imply causation.
2. Treatment Effectiveness: Antipsychotic medications that target dopamine activity can reduce positive symptoms. This supports the hypothesis but falls into the treatment-causation fallacy.
3. Amphetamine Studies: Large doses of amphetamines, which increase dopamine activity, can induce schizophrenia-like symptoms. This provides indirect support for the dopamine hypothesis.
4. Limitations: The hypothesis doesn't fully explain all aspects of schizophrenia, particularly negative symptoms and cognitive deficits.

Example: The effectiveness of antipsychotic medications in reducing positive symptoms supports the dopamine hypothesis. However, these medications may not address the root cause of schizophrenia.

Highlight: While the dopamine hypothesis is a valuable biological explanation of schizophrenia, it's important to consider it as part of a broader, multifaceted understanding of the disorder.

Structural Brain Differences in Schizophrenia

Biological causes of schizophrenia also include structural differences in the brains of individuals with the disorder. One significant finding is the presence of enlarged ventricles in some schizophrenia patients:

• Ventricles are spaces in the brain filled with cerebrospinal fluid.
• Enlarged ventricles may indicate a loss of brain tissue in surrounding areas.

Brain imaging studies, particularly in monozygotic $identical$ twins where one twin has schizophrenia and the other doesn't, have revealed these structural differences. This research provides strong evidence for a biological explanation of schizophrenia, as it shows physical brain changes associated with the disorder.

Definition: Ventricles are cavities within the brain that are filled with cerebrospinal fluid, which helps protect and nourish the brain.

Highlight: The presence of enlarged ventricles in some schizophrenia patients provides a visible biological cause of schizophrenia, linking brain structure to the disorder.

These structural differences, along with genetic factors and neurochemical imbalances, contribute to our understanding of the biological causes of schizophrenia. However, it's crucial to remember that schizophrenia is a complex disorder influenced by both biological and environmental factors. Future research continues to explore how these various elements interact to produce the symptoms and course of schizophrenia.

The Biological Approach to Schizophrenia

The biological approach to schizophrenia examines how biological factors contribute to the development and symptoms of this complex mental disorder. This perspective is based on several key principles:

1. All psychological processes have a biological basis
2. Behavior and mental processes are governed by biological mechanisms
3. It emphasizes nature over nurture in explaining schizophrenia
4. It takes a reductionist rather than holistic view
5. It leans towards biological determinism rather than free will

The main biological factors examined in schizophrenia research include:

• Genes: The genetic code that influences an individual's traits and predispositions
• Biological structures: The physical organization and anatomy of the brain and nervous system
• Neurochemistry: The chemical processes and neurotransmitters in the brain
• Hormones: Chemical messengers that regulate various bodily functions

Vocabulary: Reductionism - The practice of analyzing complex phenomena by breaking them down into simpler, more fundamental elements.

Highlight: The biological approach to schizophrenia sits on the nature side of the nature-nurture debate, emphasizing genetic and physiological factors over environmental influences.