The medical model of mental health

Welcome to The Medical Model of Mental Health

Hello and welcome! In this chapter of Applied Psychology (Issues in Mental Health), we will explore the Medical Model. Think of this topic as looking at psychological disorders through the eyes of physical medicine. Don't worry if biological concepts seem tricky at first; we will break everything down step-by-step using clear everyday analogies!

By the end of these notes, you will understand:
• The core assumptions of the medical model.
• The three main biological explanations: Biochemical, Genetic, and Brain Abnormality.
• The key research study by Gottesman et al. (2010) on familial transmission.
• Real-world biological treatments: Drug Therapy and Electroconvulsive Therapy (ECT).
• Top examiner tips to secure top marks in your OCR exams.

1. Background: Core Assumptions and Biological Explanations

What is the Medical Model?

The medical model takes a somatogenic perspective. This means it views mental disorders as physical illnesses. Just like a broken bone or diabetes has an organic, physical cause, the medical model assumes that psychological disorders stem from biological faults in our anatomy, physiology, genetics, or biochemistry. Because mental illness is seen as an organic illness, it can be diagnosed by observing clusters of symptoms and treated using biological methods.

Everyday Analogy: If your car engine sputters, a mechanic looks under the hood for broken parts, dirty fuel, or wiring faults. The medical model treats the human brain in the exact same way—looking for faulty brain wiring, chemical imbalances, or genetic blueprints.

Explanation 1: The Biochemical Explanation

Our brain communicates through billions of neurons passing chemical messengers called neurotransmitters across tiny gaps called synapses. The biochemical explanation states that mental disorders occur when neurotransmitter levels are abnormal, when reuptake mechanisms fail, or when receptor sites on the postsynaptic neuron are overly sensitive or insensitive.

• Schizophrenia and the Dopamine Hypothesis: This explanation suggests that schizophrenia is linked to an excess or hyperactivity of the neurotransmitter dopamine, or hyper-responsive dopamine receptors (such as \(D_2\) receptors), particularly in the mesolimbic pathways of the brain. This excess activity is associated with positive symptoms such as hallucinations and delusions.
• Depression and the Monoamine Hypothesis: Monoamines are a group of neurotransmitters that regulate mood, alertness, and emotion. The monoamine hypothesis argues that clinical depression is caused by depleted levels of monoamines—specifically serotonin (5-HT), noradrenaline, and dopamine in neural pathways.

Memory Trick: Remember S-N-D for the Monoamines in Depression: Serotonin, Noradrenaline, Dopamine.

Explanation 2: The Genetic Explanation

The genetic explanation proposes that vulnerability to mental disorders is passed down through our DNA. Rather than inheriting the disorder directly, individuals inherit a genetic predisposition (a higher risk).

Psychologists test this using twin studies comparing concordance rates (the probability that if one twin has the disorder, the other twin also has it):
• Monozygotic (MZ) Twins: Identical twins sharing \(100\%\) of their genes.
• Dizygotic (DZ) Twins: Non-identical (fraternal) twins sharing approximately \(50\%\) of their genes.
• Evidence: Research (e.g., Glatt et al., 2008) shows concordance rates of around \(50\%\) in MZ twins compared to approximately \(15\%\) in DZ twins for schizophrenia. Because MZ twins share twice as much DNA and have significantly higher concordance rates, this provides strong evidence for a genetic basis.

Explanation 3: Brain Abnormality (Neuroanatomy)

This explanation looks at physical structural defects or abnormal activity levels in specific brain regions.

• Schizophrenia: Neuroimaging and post-mortem studies show that individuals with schizophrenia often have enlarged lateral ventricles (fluid-filled cavities in the brain). Enlarged ventricles indicate a loss of surrounding cortical grey matter. Studies also find reductions in temporal lobe volume (e.g., Brown et al., 1986 found approximately \(6\%\) lower brain weight and enlarged ventricles in post-mortem schizophrenic brains).
• Depression: Brain scans reveal reduced volume and hypoactivity (underactivity) in the prefrontal cortex (involved in rational thinking and mood regulation) and the hippocampus (memory and emotional processing), alongside hyperactivity in the amygdala (the brain's emotional threat center).

Key Takeaway for Background: The medical model views mental illness as a physical disease caused by biochemical imbalances (dopamine/monoamines), genetic predispositions (twin concordance), or structural brain abnormalities (ventricles, prefrontal cortex, hippocampus, amygdala).

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

Study Details

• Title: Disorders in offspring with two psychiatrically ill parents
• Research Method: Cohort study / secondary registry study using data from national population-based registers in Denmark (the Danish Central Psychiatric Register and Civil Registration System).
• Target Population: Approximately \(2.68\) to \(2.7\) million individuals born in Denmark who were aged \(10\) years or older by January 1, 2007.

Comparison Groups Analyzed

Gottesman et al. compared several specific groups of offspring based on parental diagnosis:
1. Two parents with Schizophrenia: \(196\) couples (\(270\) offspring).
2. One parent with Schizophrenia: \(8,006\) couples (\(13,878\) offspring) where the other parent had no psychiatric admissions.
3. Two parents with Bipolar Disorder: \(83\) couples (\(146\) offspring).
4. One parent with Bipolar Disorder: \(11,995\) offspring where one parent had bipolar and the other had no admissions.
5. General Population Control: Couples where neither parent had any psychiatric admissions.

Key Findings & Statistics

Make sure to learn these exact figures carefully for your exam!

Schizophrenia Risk in Offspring by Age 52:
• Both parents diagnosed with Schizophrenia: \(27.3\%\) risk of developing schizophrenia (rising to \(39.2\%\) for any schizophrenia-spectrum disorder, and \(67.5\%\) for any psychiatric diagnosis).
• One parent diagnosed with Schizophrenia: \(7.0\%\) risk of developing schizophrenia.
• General population (neither parent admitted): \(1.12\%\) risk of developing schizophrenia.

Bipolar Disorder Risk in Offspring:
• Both parents diagnosed with Bipolar Disorder: \(24.9\%\) risk of developing bipolar disorder (rising to \(44.2\%\) for any major psychiatric disorder).
• One parent diagnosed with Bipolar Disorder: \(4.4\%\) risk of developing bipolar disorder.
• General population: \(0.48\%\) risk.

Genetic Overlap: Offspring of parents with schizophrenia also had an elevated risk of developing bipolar disorder (\(10.8\%\)), and vice versa. This shows that severe psychiatric disorders may share common underlying genetic vulnerabilities.

Conclusions

• Having one psychiatrically ill parent increases the risk of mental illness in offspring, but having both parents affected dramatically escalates that risk (from \(7.0\%\) to \(27.3\%\) for schizophrenia).
• These findings provide powerful empirical support for the genetic component of the medical model.
• Crucial Nuance: The risk for offspring with two affected parents did not reach \(100\%\) (it was \(27.3\%\)). This proves that mental illness is not purely genetically determined. It supports the diathesis-stress model: genes create a vulnerability (diathesis), but environmental triggers/stressors are required for the illness to manifest.

Key Takeaway for Gottesman et al. (2010): Having two parents with schizophrenia raises the child's risk to \(27.3\%\) compared to \(7.0\%\) for one parent and \(1.12\%\) in the general population. While this strongly supports genetic transmission, the fact that it is well below \(100\%\) proves environmental factors also play a critical role.

3. Application: Biological Treatments

Because the medical model assumes mental disorders have biological causes, it uses biological treatments to alter the patient's physiology, brain chemistry, or neural functioning.

Option A: Drug Therapy (Pharmacotherapy)

1. Biological Treatment for Depression: SSRIs
• Example: Selective Serotonin Reuptake Inhibitors (e.g., Fluoxetine/Prozac, Citalopram).
• Biological Mechanism: Normally, after serotonin is released into the synaptic cleft and binds to postsynaptic receptors, it is reabsorbed back into the presynaptic neuron by a transporter protein called the Serotonin Transporter (SERT). SSRIs selectively block this reuptake transporter. As a result, serotonin remains in the synaptic cleft longer and repeatedly stimulates postsynaptic receptors, compensating for depleted monoamine levels and elevating mood.
• Other antidepressant classes: Monoamine Oxidase Inhibitors (MAOIs) and Tricyclics (TCAs).

2. Biological Treatment for Schizophrenia: Antipsychotics
• Typical (First-Generation) Antipsychotics: (e.g., Chlorpromazine, Haloperidol). These act primarily as dopamine \(D_2\) receptor antagonists. They bind to dopamine receptors on the postsynaptic membrane without activating them, blocking dopamine from binding and reducing positive symptoms like hallucinations.
• Atypical (Second-Generation) Antipsychotics: (e.g., Clozapine, Risperidone). These antagonise both dopamine \(D_2\) receptors and serotonin \(5\text{-HT}_{2\text{A}}\) receptors. They help alleviate positive symptoms while carrying a lower risk of severe motor/extrapyramidal side effects.

Option B: Electroconvulsive Therapy (ECT)

• Used for: Severe, life-threatening, or treatment-resistant depression where medication has failed.
• Procedure: The patient is given a general anaesthetic and a muscle relaxant. Electrodes are placed on the scalp (either unilaterally or bilaterally), and a controlled electrical current is passed through the brain.
• Mechanism: The electric shock induces a brief bilateral seizure lasting approximately \(20\) to \(50\) seconds. This seizure alters neurotransmitter receptor sensitivity and stimulates neuroplasticity across mood-regulating brain pathways.

Key Takeaway for Biological Treatments: Biological treatments directly modify neurobiology. Antidepressants (SSRIs) block serotonin reuptake, antipsychotics block dopamine (\(D_2\)) receptors, and ECT induces controlled seizures to reset neurochemical pathways in severe cases.

4. Pitfalls, Exam Traps & How to Avoid Them

• Trap 1: Mixing up topics. Remember that Topic 2 is The Medical Model (Gottesman et al.). Do not mix this up with Topic 1 (Historical Context / Rosenhan) or Topic 3 (Alternatives to the Medical Model / Szasz).
• Trap 2: Misquoting the Gottesman statistics. Examiners frequently spot students confusing the one-parent and two-parent figures. Be precise: Two parents with schizophrenia = \(27.3\%\), One parent = \(7.0\%\), General population = \(1.12\%\).
• Trap 3: Claiming disorders are \(100\%\) genetic. If schizophrenia were entirely genetic, the risk for a child with two affected parents would be \(100\%\). The fact that it is \(27.3\%\) proves that genetic transmission is powerful, but environmental triggers (diathesis-stress) are also necessary.
• Trap 4: Being too vague about treatments. Never write "the patient takes happy pills" or "they take medication to fix their brain." Always name the specific drug class (e.g., SSRIs or Typical Antipsychotics) and explain the biological mechanism (e.g., blocking presynaptic reuptake transporters or antagonising \(D_2\) receptors).

Quick Revision Checklist

• Can you define the somatogenic perspective?
• Can you explain the dopamine hypothesis for schizophrenia and the monoamine hypothesis for depression?
• What are the twin concordance rates for schizophrenia (\(\sim 50\%\) MZ vs \(\sim 15\%\) DZ)?
• What brain structural abnormalities are linked to schizophrenia (enlarged ventricles, \(\sim 6\%\) brain weight reduction) and depression (prefrontal cortex, hippocampus, amygdala)?
• Can you state the key percentages from Gottesman et al. (2010) (\(27.3\%\), \(7.0\%\), \(1.12\%\))?
• Can you explain step-by-step how SSRIs or Antipsychotics work at the synapse?