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The historical survey ended with the triumph of the medical model — the view that mental disorders are illnesses with biological causes. This lesson opens that model up and examines its engine room: the three families of biological explanation that the medical model offers for why disorders arise. It asks what is going wrong in the body and brain of a person with depression, schizophrenia or a phobia, and answers in three ways — through biochemistry (the neurotransmitters serotonin and dopamine), through genetics (inherited vulnerability), and through brain abnormality (differences in structure and function). These are the "Background" strand of the medical-model topic in the OCR Issues in Mental Health section; the "Key research" strand is Gottesman et al.'s genetic study (next lesson but one), and the "Application" strand is biological treatment (the lesson after). Understanding the explanations here is what lets you understand why the treatments in the next lessons take the form they do — if the problem is biochemical, the solution is a drug that alters biochemistry.
| This lesson covers | OCR H567 Component 03, Section A topic | AO focus |
|---|---|---|
| Biochemical explanation: neurotransmitters (serotonin, dopamine) | Medical model of mental illness — biochemical explanation (Background) | AO1; AO3 evaluation |
| Genetic explanation: heritability and vulnerability | Medical model — genetic explanation | AO1; AO2 |
| Brain-abnormality explanation: structure and function | Medical model — brain-abnormality explanation | AO1; AO3 |
| Strengths and limitations of the biological approach to disorder | Medical model — evaluation | AO3 |
The specification is referenced descriptively throughout; consult the official OCR H567 specification document for the exact published wording. This lesson develops AO1 (the three biological explanations), AO2 (applying them to specific disorders) and AO3 (evaluating the strengths and limitations of biological explanation, including the reductionism and cause-versus-effect problems). Precise figures are taught qualitatively where certainty is not warranted; consult primary sources for exact statistics.
The medical model rests on a single organising analogy: mental disorder is like physical disease. Just as diabetes arises from a malfunction of insulin regulation and pneumonia from an infection, so — on this view — depression, schizophrenia and anxiety arise from malfunctions of the body's own machinery: its chemical messengers, its inherited blueprint, its neural hardware. The three explanations below are the three places the model looks for that malfunction. They are not mutually exclusive; a disorder may involve genes that shape brain development that in turn alters neurotransmission. But they are conceptually distinct, and OCR expects you to treat each in its own right.
A word on the shared assumptions before we begin. All three explanations locate the cause of disorder inside the individual's biology, they treat disorder as a deviation from healthy physiological functioning, and they imply that appropriate treatment is physical — a drug, or an intervention on the brain. These assumptions are the model's strengths (they make disorder testable and treatable) and, as critics argue, its limitations (they can ignore the person's life, relationships and circumstances). Keep the assumptions in view; they are where AO3 lives.
A little background on how neurons communicate makes the biochemical account intelligible. The brain is a network of billions of nerve cells, or neurons, that signal to one another. Within a single neuron the signal is electrical, travelling down the length of the cell; but between neurons there is a gap, and here the signal becomes chemical. When the electrical impulse reaches the end of one neuron, it triggers the release of neurotransmitter molecules, which cross the gap and bind to specially shaped receptor sites on the receiving neuron, either making it more likely to fire (excitation) or less likely (inhibition). After acting, the neurotransmitter is cleared away — broken down by enzymes or, more commonly for our purposes, reabsorbed back into the releasing neuron by a process called reuptake, ready to be used again. This whole cycle — release, binding, clearance — is the level at which psychiatric drugs act, and it is why understanding the biochemical explanation is the key that later unlocks how antidepressants and antipsychotics work. If communication between neurons depends on the right amount of the right chemical reaching the right receptors, then too much or too little of a neurotransmitter, or too few or too many receptors, will disturb the circuits those neurons form, and the behaviours and experiences those circuits support.
The biochemical explanation proposes that disorders arise from imbalances — too much or too little activity — of the brain's chemical messengers, the neurotransmitters. A neurotransmitter is a chemical released from one neuron across the tiny gap (the synapse) to bind to receptors on the next, either exciting or inhibiting it. Communication between neurons is therefore chemical, and if the levels or activity of these chemicals are disturbed, the brain circuits they serve will behave abnormally. Two neurotransmitters are central to the OCR content.
Two neurotransmitters recur throughout this section, and it is worth knowing that each does far more in the brain than the single disorder it is most associated with, which is part of why the simple one-neurotransmitter-per-disorder story is an oversimplification. Serotonin, though famous for its link to mood, is also involved in sleep, appetite, digestion and aspects of social behaviour; dopamine, though famous for its link to psychosis, is central to movement, motivation and the brain's reward system. This breadth has two implications a strong answer can draw out. First, it helps explain why drugs that target these systems produce such a wide range of side effects — an SSRI that raises serotonin to lift mood also affects the serotonin involved in sleep, appetite and sexual function, hence the characteristic side-effect profile you meet in the treatment lesson. Second, it cautions against reading "low serotonin equals depression" or "high dopamine equals schizophrenia" as tidy equations, since a chemical that does so many jobs is unlikely to map cleanly onto a single disorder. The neurotransmitters are better thought of as widely-used signalling molecules whose disturbance can ripple through many systems at once, which is exactly why the refined, region-specific versions of the hypotheses are more credible than the original blanket claims.
Serotonin is a neurotransmitter involved in the regulation of mood, sleep, appetite and emotion. The dominant biochemical account of depression — the monoamine (serotonin) hypothesis — proposes that depression is associated with low levels or low activity of serotonin (and related monoamines such as noradrenaline) in the brain. The strongest single piece of supporting evidence is pharmacological: the antidepressant drugs that lift mood in many patients — the selective serotonin reuptake inhibitors (SSRIs) you will study in the treatment lesson — work by increasing the availability of serotonin in the synapse (by blocking its reabsorption). If raising serotonin improves mood, the reasoning runs, then low serotonin must have been part of the problem. This is elegant, but note the logical caution examiners reward: that a drug which raises serotonin helps does not prove that low serotonin caused the depression — the reasoning runs backwards from treatment to cause, and the picture is now known to be more complicated than a simple "chemical imbalance".
Dopamine is a neurotransmitter involved in movement, motivation, reward and the processing of salience — how much significance we attach to stimuli. The classic biochemical account of schizophrenia is the dopamine hypothesis, which in its original form proposed that the positive symptoms of schizophrenia (hallucinations, delusions) are associated with excess dopamine activity, particularly overactivity of dopamine transmission in certain brain pathways. Again the strongest support is pharmacological, and it runs in two directions: the antipsychotic drugs that reduce positive symptoms are dopamine antagonists (they block dopamine receptors), while drugs that increase dopamine (such as amphetamines, and the L-dopa given for Parkinson's disease) can induce psychotic-like symptoms. Refined versions of the hypothesis distinguish where dopamine is too high or too low — excess in some subcortical pathways (linked to positive symptoms) but deficient transmission in prefrontal regions (linked to negative and cognitive symptoms) — a more nuanced picture that a strong answer can acknowledge.
The evolution of the dopamine hypothesis is itself instructive about how biological explanations develop and why they should be held with appropriate tentativeness. The original, simple version — "schizophrenia is caused by too much dopamine" — was attractive precisely because it was clean and fitted the early drug evidence. But it ran into difficulties. It struggled to explain the negative symptoms (avolition, flat affect), which if anything seemed associated with under-activity in some regions; it could not easily account for why antipsychotics block dopamine receptors within hours yet take weeks to relieve symptoms, echoing the same delayed-onset puzzle seen with antidepressants; and it did not fit the fact that the newer atypical drugs, which are effective, act substantially on serotonin as well as dopamine. The response was not to abandon the hypothesis but to refine it — hence the modern picture of regionally specific dopamine dysregulation, with too much in some pathways and too little in others, and of dopamine as one player in a more complex neurochemical system rather than the sole culprit. This trajectory — a bold simple claim, confronted by anomalies, revised into something more qualified — is characteristic of a genuinely scientific explanation, and it is a point in the medical model's favour on the psychology-as-a-science debate: unlike an unfalsifiable theory, the dopamine hypothesis could be, and was, corrected by evidence. But it is equally a caution against teaching or believing the simple version as settled fact.
| Disorder | Neurotransmitter | Proposed abnormality | Pharmacological evidence |
|---|---|---|---|
| Depression | Serotonin (and noradrenaline) | Too little activity | SSRIs raise serotonin and lift mood |
| Schizophrenia (positive symptoms) | Dopamine | Excess activity in certain pathways | Antipsychotics block dopamine; amphetamines induce psychosis |
The genetic explanation proposes that vulnerability to mental disorder is inherited — that genes passed from parents to children raise (or lower) the risk of developing a disorder. The claim is not, in any serious version, that there is a single "schizophrenia gene" or "depression gene" that determines the disorder; it is that many genes each contribute a small increment of susceptibility, and that this genetic loading interacts with the environment (the diathesis–stress model — an inherited diathesis, or vulnerability, triggered by environmental stress). The evidence comes from three classic study designs.
Family studies examine whether disorders run in families — whether having a relative with, say, schizophrenia raises one's own risk, and whether the risk rises with the closeness of the genetic relationship. They do: the risk of schizophrenia is higher for first-degree relatives (parents, siblings, children) than for the general population, and higher still where more relatives are affected. This is exactly the design of Gottesman et al.'s (2010) prescribed key research, which measures the risk to the offspring of two ill parents.
Twin studies compare monozygotic (MZ, identical) twins, who share essentially all their genes, with dizygotic (DZ, fraternal) twins, who share about half. If a disorder is genetic, the concordance rate — the probability that if one twin has the disorder the other does too — should be substantially higher in MZ than in DZ pairs. For schizophrenia this is what is found: concordance is markedly higher in identical than in fraternal twins, strong evidence of a genetic contribution. Crucially, though, MZ concordance is well below 100% — if one identical twin has schizophrenia, the other frequently does not — which proves that genes cannot be the whole story and that environment must play a major part.
Adoption studies separate genes from environment by studying people raised apart from their biological relatives. If adopted children resemble their biological (rather than adoptive) parents in disorder risk, that points to genes rather than shared upbringing. Adoption studies of schizophrenia broadly support a genetic contribution, since adoptees' risk tracks their biological background.
Reading concordance carefully. The single most important interpretive point is that heritability is a matter of degree, and that the gap between MZ concordance and 100% is itself the evidence for environmental influence. A candidate who reports "schizophrenia is genetic" as if genes determined it has misunderstood the data; the sophisticated statement is that genes confer vulnerability which the environment may or may not convert into disorder.
There is also a subtlety about twin studies that a strong answer can raise. The whole logic of comparing identical with fraternal twins assumes that the only systematic difference between the two kinds of pair is genetic — that identical and fraternal twins share their environments to the same extent. This is the so-called equal environments assumption, and it is arguably false: identical twins, who look alike and are often treated as a unit, may share a more similar environment than fraternal twins do. If so, then part of the higher concordance in identical pairs might reflect their more similar upbringing rather than their more similar genes, which would inflate estimates of heritability. This does not overturn the genetic evidence — the effect is generally thought too small to explain the large MZ–DZ gap for schizophrenia — but it shows that even the strongest classic evidence for the genetic explanation is not airtight, and mentioning it demonstrates exactly the critical engagement examiners reward. Adoption studies are valuable precisely because they sidestep this problem, which is why converging evidence from several designs is more persuasive than any one design alone.
The brain-abnormality explanation proposes that disorders arise from differences in the structure or function of the brain — that the physical organ is built or working differently in people with a disorder. Modern brain-imaging (structural scans such as MRI and functional scans such as fMRI and PET) has made it possible to compare the brains of people with and without disorders.
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