Welcome to The Medical Model: Issues in Mental Health

Welcome! This chapter is part of Component 03: Applied Psychology (H567/03) in Section A: Issues in Mental Health. Mental health can feel like a huge, daunting topic, but don't worry if this seems tricky at first—we are going to break everything down step-by-step.

What is the Medical Model?
Think of the medical model as viewing psychological disorders in the exact same way a doctor views a physical sickness (such as diabetes or a broken bone). Under this model, mental illness is seen as a somatic (physical) condition caused by physiological malfunctions within the body or brain. Because the cause is physical, the solution (treatment) is also biological.

In this chapter, we will master three core areas required by the OCR specification:
1. Background: Three biological explanations of mental illness (Biochemical, Genetic, and Brain Abnormality).
2. Key Research: The classic study by Gottesman et al. (2010) on severe mental disorders in offspring.
3. Application: Biological treatments (Drug therapies and Electroconvulsive Therapy) used to treat specific mental illnesses.

Part 1: Background — Biological Explanations of Mental Illness

The medical model proposes that psychological symptoms stem from internal physiological causes. OCR requires you to understand three specific biological explanations:

1. Biochemical Explanation

This explanation states that psychological disorders are caused by imbalances, deficiencies, or abnormal activity of neurotransmitters (the chemical messengers that transmit signals across synapses between neurons).

Example A: The Monoamine Hypothesis of Depression
Monoamines are a group of neurotransmitters that regulate mood and emotion. This hypothesis suggests depression is caused by depleted or underactive levels of monoamines:
• Serotonin (\(5\text{-HT}\)): Regulates mood, sleep, appetite, and emotional stability.
• Noradrenaline (Norepinephrine): Controls alertness, energy, and drive.
• Dopamine: Controls pleasure, motivation, and reward processing.
When levels of these monoamines are too low, the brain cannot effectively transmit mood-elevating signals, leading to classic depressive symptoms such as persistent sadness, fatigue, and anhedonia (inability to feel pleasure).

Example B: The Dopamine Hypothesis of Schizophrenia
This hypothesis links symptoms of schizophrenia to abnormal dopamine receptor transmission:
• Hyperdopaminergic activity (Excess Dopamine): High levels of dopamine transmission or an excess of dopamine \(D_2\) receptors in the subcortical mesolimbic pathway are linked to positive symptoms (e.g., auditory hallucinations and delusions).
• Hypodopaminergic activity (Deficient Dopamine): Low levels of dopamine activity in the prefrontal mesocortical pathway are associated with negative symptoms (e.g., flat affect, lack of speech, and cognitive deficits).

2. Genetic Explanation

The genetic explanation argues that mental disorders are inherited from biological parents through transmitted vulnerability genes. Most mental illnesses are polygenic (caused by many genes acting together rather than a single 'faulty' gene).

Psychologists investigate genetic transmission using three main methods:
• Family Studies: Comparing rates of illness among first-degree relatives (parents, siblings, offspring who share \(50\%\) of their genes) against distant relatives.
• Twin Studies: Comparing concordance rates between monozygotic (MZ) twins (identical, sharing \(100\%\) genetic material) and dizygotic (DZ) twins (fraternal, sharing \(50\%\) genetic material). If MZ twins show higher concordance than DZ twins, a strong genetic component is indicated.
• Adoption Studies: Comparing adoptees diagnosed with a disorder to their biological parents (nature) and adoptive parents (nurture) to isolate genetic influence from the environment.

3. Brain Abnormality Explanation

This explanation states that mental disorders are caused by structural damage, atypical neurodevelopment, or abnormal volume in specific regions of the brain.

Structural Abnormalities in Schizophrenia:
• Ventricular Enlargement: Patients with schizophrenia frequently show abnormally enlarged lateral ventricles and third ventricles (fluid-filled cavities). Enlarged ventricles mean surrounding brain tissue has degenerated or failed to develop properly.
• Grey Matter Reduction: Significant volume loss of grey matter is found in the frontal lobes, temporal lobes, hippocampus, and amygdala, impairing executive functioning, memory, and emotional regulation.

Structural Abnormalities in Major Affective Disorders (Depression):
• Volume reductions are commonly observed in the prefrontal cortex (involved in decision-making and emotional control) and the hippocampus (involved in memory processing).
• Amygdala Hyperactivation: Increased activity or altered volume in the amygdala leads to heightened emotional distress and excessive negative emotional reactions.

Memory Trick (The 3 B's of Biology):
Remember B-G-B: Biochemicals (messengers), Genetics (inheritance), and Brain structures (anatomy).

Key Takeaway for Background: The medical model views psychological distress as an organic physical problem—whether caused by out-of-balance neurotransmitters, inherited genetic risk, or physical brain abnormalities.

Part 2: Key Research — Gottesman et al. (2010)

Full Citation: Gottesman, I. I., Laursen, T. M., Bertelsen, A., & Mortensen, P. B. (2010). Severe mental disorders in offspring with 2 psychiatrically ill parents. Archives of General Psychiatry, \(67(3)\), 252–257.

Aim of the Study

To calculate the cumulative risk (morbid risk) of developing schizophrenia, bipolar affective disorder, or any other severe psychiatric illness in offspring where:
1. Both parents had been admitted/diagnosed with the disorder (dual-mating couples).
2. One parent had been admitted/diagnosed.
3. Neither parent had been admitted/diagnosed (general population baseline comparison).

Methodology and Design

• Study Type: Retrospective, secondary population-based cohort study.
• Data Source: National civil registers in Denmark, specifically the Danish Civil Registration System linked with the Danish Psychiatric Central Register.
• Sample Size: Approximately \(2.68\text{ million}\) individuals born in Denmark who were alive in 1968 or born between 1968 and 1997, who had an identifiable mother and father, and were aged 10 or older by January 1, 2007.

Key Cohort Groups

• Group 1 (Dual-diagnosed Schizophrenia): Offspring with two parents diagnosed with schizophrenia (\(N = 270\) from 196 couples).
• Group 2 (One parent Schizophrenia): Offspring with one parent diagnosed with schizophrenia (\(N = 7,001\)).
• Group 3 (General Population Reference): Offspring with neither parent diagnosed with schizophrenia (\(N = 2,239,551\)).
• Group 4 (Dual-diagnosed Bipolar): Offspring with two parents diagnosed with bipolar disorder (\(N = 146\) from 83 couples).
• Group 5 (One parent Bipolar): Offspring with one parent diagnosed with bipolar disorder (\(N = 15,996\)).

Key Findings (Cumulative Risk by Age 52)

Schizophrenia Risk:
• Both Parents Diagnosed: \(27.3\%\) of offspring developed schizophrenia (this rose to \(39.2\%\) when including any schizophrenia-spectrum diagnosis, and approx. \(67.5\%\) for any psychiatric diagnosis).
• One Parent Diagnosed: \(7.0\%\) of offspring developed schizophrenia (approx. \(11.9\%\) for any mental disorder).
• Neither Parent Diagnosed: \(1.12\%\) of offspring developed schizophrenia (approx. \(14.1\%\) for any mental disorder).

Bipolar Disorder Risk:
• Both Parents Diagnosed: \(24.9\%\) of offspring developed bipolar disorder (approx. \(36.0\%\) for any mood disorder, and \(44.2\%\) for any psychiatric diagnosis).
• One Parent Diagnosed: \(4.4\%\) of offspring developed bipolar disorder.
• Neither Parent Diagnosed: \(0.48\%\) (approx. \(0.63\%\)) of offspring developed bipolar disorder.

Conclusions

1. Direct Genetic Transmission: Having two parents with a severe psychiatric disorder dramatically increases the risk for the offspring compared to having one parent or no parents affected.
2. Genetic Overlap (Pleiotropy): Offspring of parents with bipolar disorder also showed elevated rates of schizophrenia, and vice versa. This indicates shared genetic vulnerability and questions whether strict categorical boundaries in diagnostic manuals (DSM/ICD) reflect biological reality.
3. Support for Diathesis-Stress: Because the risk for dual-diagnosed parents was \(27.3\%\) and not \(100\%\), genetic inheritance provides vulnerability, but environmental factors (stressors) must be required to trigger the disorder.

CRITICAL EXAM WARNING: Common Mistakes to Avoid with Gottesman (2010):
Mistake 1: Calling this a "twin study." It is NOT a twin study! It is a population-based cohort register study using national registers.
Mistake 2: Saying Gottesman proved mental illness is "100% genetic." The concordance is \(27.3\%\), which proves that environment still plays a huge role.
Mistake 3: Writing vague terms like "higher chance" instead of learning the key comparative figures (\(27.3\%\) vs \(7.0\%\) vs \(1.12\%\)).

Key Takeaway for Gottesman et al. (2010): The risk of developing schizophrenia jumps from \(1.12\%\) (general population) to \(7.0\%\) (one parent) to \(27.3\%\) (both parents), demonstrating significant genetic transmission alongside environmental influence.

Part 3: Application — Biological Treatments of Mental Disorders

In the exam, you must be able to describe and evaluate at least one biological treatment for a specific mental disorder. Biological treatments directly target physical, neurochemical, or electrical processes in the body.

1. Pharmacotherapy (Drug Therapy)

A. Drug Treatment for Depression: SSRIs (Selective Serotonin Reuptake Inhibitors)
• Examples: Fluoxetine (Prozac), Citalopram, Sertraline.
• How they work (Biological Mechanism): Under normal conditions, serotonin is released from the presynaptic neuron, binds to postsynaptic receptors, and is then reabsorbed by the presynaptic cell via the serotonin transporter (SERT) protein (a recycling process called reuptake). SSRIs selectively block this SERT reuptake pump.
• Effect on Symptoms: Serotonin remains in the synaptic cleft for longer and continues to stimulate postsynaptic receptors. Over several weeks, this enhanced neurotransmission improves mood, elevates energy, and relieves depressive symptoms.
• Other antidepressant classes: SNRIs (Serotonin-Noradrenaline Reuptake Inhibitors), TCAs (Tricyclics), and MAOIs (Monoamine Oxidase Inhibitors).

B. Drug Treatment for Schizophrenia: Antipsychotics
• Typical Antipsychotics (First-Generation, e.g., Chlorpromazine, Haloperidol):
- Mechanism: Act as strong dopamine \(D_2\) receptor antagonists in the mesolimbic pathway, binding to dopamine receptors without activating them, blocking excess dopamine transmission.
- Target Symptoms: Highly effective at reducing positive symptoms (e.g., hallucinations, delusions).
- Side Effects: Risk of extrapyramidal motor symptoms, tremors, and tardive dyskinesia.
• Atypical Antipsychotics (Second-Generation, e.g., Clozapine, Risperidone, Olanzapine):
- Mechanism: Transiently bind to dopamine \(D_2\) receptors with rapid dissociation, while also acting as antagonists at serotonin \(5\text{-HT}_{2\text{A}}\) receptors.
- Target Symptoms: Reduces both positive and negative symptoms (e.g., emotional flattening, social withdrawal) with a lower risk of motor side effects.

2. Electroconvulsive Therapy (ECT)

• Indication: Reserved for severe, life-threatening, treatment-resistant depression or acute catatonia.
• Procedure: Administered under general anesthesia and muscle relaxants. Electrodes are placed either unilaterally (one side of the head) or bilaterally (both sides). An electric current of approximately \(70\text{--}130\text{ volts}\) is passed through the brain for \(20\text{--}60\text{ seconds}\) to induce a brief, controlled generalized therapeutic seizure.
• Biological Mechanism: The induced seizure triggers a massive release of monoamine neurotransmitters (serotonin, dopamine, noradrenaline) and stimulates neuroplasticity in the hippocampus and prefrontal cortex.
• Side Effects: Temporary retrograde/anterograde memory loss and acute confusion.

Part 4: Evaluating the Medical Model & Biological Treatments

When writing 10-mark or 15-mark evaluative answers, use these structural strengths and weaknesses:

Strengths of the Medical Model & Treatments

• High Scientific Rigour: Relies on objective, empirical measurement techniques such as MRI scans, PET scans, genome sequencing, and vast register studies (e.g., Gottesman et al., \(N \approx 2.68\text{ million}\)).
• High Practical Applicability: Biological treatments (like SSRIs or antipsychotics) act relatively quickly compared to talk therapies, allowing acute patients to manage symptoms and lead functional lives.
• De-stigmatisation: Framing mental illness as an organic physical sickness (like asthma or diabetes) relieves patients of moral blame or guilt.

Weaknesses of the Medical Model & Treatments

• Biological Determinism & Reductionism: Reduces complex human emotional experiences to chemical formulas and neural wiring, ignoring social triggers, family dysfunction, trauma, and poverty.
• Palliative, Not Curative: Drug therapies manage and suppress symptoms while the patient takes the medication; they do not address underlying cognitive or environmental root causes (leading to high relapse rates upon cessation).
• Side Effects and Ethical Issues: Drugs can produce severe physiological side effects (weight gain, motor tremors, sexual dysfunction), and historical treatments like ECT carry risks of memory loss.

Quick Review: Checklist for Exam Success

Before sitting your exam on Section A: Issues in Mental Health, ensure you can answer YES to each of these points:

• Can you explain the difference between the Monoamine Hypothesis and the Dopamine Hypothesis?
• Can you describe brain abnormalities in schizophrenia (enlarged ventricles, grey matter loss) and depression (hippocampus/prefrontal cortex volume reductions)?
• Do you know the precise morbid risk figures from Gottesman et al. (2010): \(27.3\%\) for dual-ill schizophrenia parents vs \(7.0\%\) for one parent vs \(1.12\%\) for clean baseline?
• Can you explain the difference between typical and atypical antipsychotics?
• Do you remember that cognitive therapies like CBT belong to Alternatives to the Medical Model and must NOT be used when asked for biological treatments?