You are viewing a free preview of this lesson.
Subscribe to unlock all 10 lessons in this course and every other course on LearningBro.
If the medical model is right that disorders are biological malfunctions, then it follows that the way to treat them is to correct the biology — and that is exactly what biological treatments try to do. This lesson is the Application strand of the medical-model topic in the OCR Issues in Mental Health section: having explained the biological causes of disorder (biochemical, genetic, brain-abnormality), we now examine how the model treats one disorder biologically. The main vehicle is drug therapy — the antidepressants (chiefly SSRIs) used for depression and the antipsychotics used for schizophrenia — together with electroconvulsive therapy (ECT) where it remains relevant. For each, we ask how it works (its mechanism, which flows directly from the neurotransmitter explanations of the previous lessons), how well it works (effectiveness), and what it costs (side effects), before evaluating the biological approach to treatment as a whole. The through-line to hold onto is that the treatment is the explanation made practical: SSRIs raise serotonin precisely because low serotonin is the proposed cause of depression.
| This lesson covers | OCR H567 Component 03, Section A topic | AO focus |
|---|---|---|
| Drug therapy for depression: SSRIs (mechanism) | Medical model — biological treatment of one disorder (Application) | AO1; AO2 relating treatment to explanation |
| Drug therapy for schizophrenia: antipsychotics (mechanism) | Medical model — biological treatment | AO1; AO2 |
| Electroconvulsive therapy (ECT) where relevant | Medical model — biological treatment | AO1; AO3 |
| Effectiveness, side effects and evaluation of biological treatment | Medical model — evaluation of treatment | AO3 |
The specification is referenced descriptively throughout; consult the official OCR H567 specification document for the exact published wording. This lesson develops AO1 (the biological treatments and their mechanisms), AO2 (applying a treatment to a novel case and linking it to the biological explanation) and AO3 (evaluating effectiveness, side effects and the broader strengths and limitations of biological treatment). Drug classes and mechanisms are given accurately; where exact efficacy figures are uncertain they are taught qualitatively.
It is worth registering at the outset just how transformative the arrival of effective psychiatric drugs was, because the historical scale of the change is itself part of any fair evaluation. Before the 1950s there was no medication that reliably reduced the core symptoms of severe mental illness; the great asylums were, in large part, custodial institutions housing people for whom little could be done. The introduction of the first antipsychotics in the 1950s, and of antidepressants shortly after, changed this at a stroke: for the first time, symptoms that had seemed intractable — the hallucinations and delusions of psychosis, the paralysing despair of depression — could be substantially dampened by a tablet. This was the pharmacological engine of deinstitutionalisation, the movement discussed in the historical lesson that emptied the asylums and moved patients into community care, which simply would not have been possible without drugs to control symptoms outside the hospital. Whatever the limitations discussed below, this history establishes the baseline for evaluation: biological treatment did not merely add a modest option to an existing toolkit; it made possible a wholesale change in how societies care for the severely mentally ill. An answer that weighs the drugs' side effects and their tendency to manage rather than cure should set those genuine costs against this genuinely revolutionary benefit.
Drug therapy (chemotherapy in the psychiatric sense — psychoactive medication) is the flagship biological treatment. Its rationale is simple and follows directly from the biochemical explanation: if a disorder is associated with too little or too much of a neurotransmitter, then a drug that raises or lowers that neurotransmitter's activity should relieve the symptoms. Because the treatment targets the proposed cause, drug therapy is the clearest expression of the medical model in action. We take one disorder — depression — as the primary worked example (the OCR content requires the biological treatment of one disorder), and treat antipsychotics for schizophrenia and ECT more briefly for contrast.
The most widely prescribed antidepressants are the selective serotonin reuptake inhibitors (SSRIs) — drugs such as fluoxetine (Prozac), sertraline and citalopram. Their mechanism follows precisely from the serotonin hypothesis of depression. Normally, after serotonin is released into the synapse and acts on the receiving neuron, it is reabsorbed (reuptake) into the releasing neuron and recycled, ending its action. SSRIs block this reuptake: they inhibit the transporter that reabsorbs serotonin, so serotonin remains in the synapse longer and continues to stimulate the receiving neuron. The selective in the name signals that they act mainly on serotonin, sparing other systems, which gives them a more favourable side-effect profile than older antidepressants. The result — after a delay of some weeks, which is itself a clue that the story is more complex than a simple chemical top-up — is, for many patients, a lifting of mood.
Older classes exist and are worth knowing for contrast. Tricyclic antidepressants and monoamine oxidase inhibitors (MAOIs) also raise monoamine levels but by different mechanisms and with more side effects and dietary restrictions, which is why SSRIs became first-line for most patients.
The delayed onset of the antidepressants deserves a closer look, because it is both clinically important and a genuine puzzle for the simple chemical-imbalance story. If depression were straightforwardly a shortage of serotonin in the synapse, and an SSRI raises synaptic serotonin within hours of the first dose, we would expect mood to lift almost immediately. It does not. Patients typically feel no benefit for two to four weeks, and sometimes longer, even though the drug is boosting serotonin from day one. This mismatch tells us that the therapeutic effect cannot simply be the raised serotonin; something slower must be happening downstream — adaptations in the number and sensitivity of receptors, changes in gene expression within neurons, or gradual effects on the growth and connectivity of brain cells in mood-regulating regions. The practical consequence is that patients must be warned to persist through an initial period in which they feel no better (and may even feel worse, given early side effects) before improvement arrives — a common reason people abandon treatment prematurely. The theoretical consequence is that the "low serotonin causes depression" account, while a useful first approximation, is now widely regarded as incomplete, and the honest teaching position is that antidepressants clearly help many people while the precise reason they help is still being worked out.
A point that repays emphasis is that SSRIs did not become first-line because they are dramatically more effective than the older tricyclics and MAOIs — in head-to-head terms the classes are broadly comparable at relieving depression. They became first-line because they are safer and better tolerated, and this is itself a lesson about how drug treatment is judged. The older tricyclics are dangerous in overdose, a grave concern in a population that by definition includes people at risk of suicide, and the MAOIs require patients to avoid certain foods (those rich in tyramine, such as mature cheese and some cured meats) on pain of dangerous surges in blood pressure. SSRIs, acting more selectively, carry neither of these hazards to the same degree, so a doctor can prescribe them more freely and a patient can take them more safely. The general principle — that the tolerability and safety of a treatment can matter as much as its raw efficacy, because a safer drug is one people will actually take and survive — is exactly the kind of evaluative nuance that lifts an answer above a simple "do they work?" analysis.
For schizophrenia, the main drug treatment is the antipsychotics, whose mechanism follows from the dopamine hypothesis. Typical (first-generation) antipsychotics (such as chlorpromazine and haloperidol) are dopamine antagonists: they block dopamine (particularly D2) receptors, reducing dopamine transmission and thereby dampening the positive symptoms — hallucinations and delusions — that excess dopamine is thought to produce. Atypical (second-generation) antipsychotics (such as clozapine, risperidone and olanzapine) act on dopamine but also on other systems (notably serotonin), and were developed to treat a broader range of symptoms with, in some respects, fewer motor side effects. Because the drug's action (blocking dopamine) mirrors the proposed cause (excess dopamine), antipsychotics are, like SSRIs, the explanation turned into treatment.
| Disorder | Drug class | Mechanism | Neurotransmitter target |
|---|---|---|---|
| Depression | SSRIs | Block reuptake, so serotonin stays in the synapse longer | Serotonin (increased) |
| Schizophrenia | Typical antipsychotics | Block dopamine (D2) receptors | Dopamine (reduced) |
| Schizophrenia | Atypical antipsychotics | Act on dopamine and serotonin systems | Dopamine and serotonin |
Electroconvulsive therapy (ECT) is a biological treatment in which a small, controlled electric current is passed through the brain to induce a brief, controlled seizure, under general anaesthetic and with a muscle relaxant, typically over a course of several sessions. Historically it was used widely and sometimes crudely; modern ECT is administered carefully and is reserved mainly for severe depression that has not responded to drugs or psychological therapy, or where a rapid response is needed (for example, where a person is severely suicidal or not eating). Its precise mechanism is not fully understood — it is thought to alter neurotransmitter activity and neural functioning broadly — which is itself an evaluative point. ECT can be effective for severe, treatment-resistant depression, and for some patients it works when nothing else has; but it carries risks, notably memory loss (especially of events around the time of treatment), and it remains controversial precisely because it is a physical intervention whose workings are unclear and whose history includes misuse.
Why ECT is contentious. ECT sharpens the central tension of biological treatment. On one hand there is real evidence that it helps some severely ill people, sometimes rapidly and life-savingly. On the other, its mechanism is poorly understood, it can impair memory, and its coercive historical associations (evoked vividly in popular culture) fuel objections. A strong answer treats it neither as barbarism nor as a simple cure, but as a last-line option whose use must weigh serious benefits against serious costs.
ECT is a revealing case for the broader ethics of biological treatment because it forces two genuinely competing goods into open conflict. On one side is the imperative to relieve suffering and preserve life: for a person who is severely, dangerously depressed — not eating, actively suicidal, and unresponsive to weeks of medication and therapy — a treatment that can work within days may quite literally be life-saving, and to withhold it out of squeamishness could itself be a grave harm. On the other side are the values of autonomy and informed consent and the duty to avoid harm, given that ECT carries a real risk of memory loss and that its mechanism remains poorly understood. The tension becomes most acute in the rare cases where a severely ill person lacks the capacity to consent, so that the question of treating them without consent arises — precisely the coercive scenario that Szasz warned against, now with a physical intervention on the brain at stake. There is no formula that dissolves this conflict; what good practice demands is a careful, case-by-case weighing of the severity of the risk to the patient against the seriousness of the intervention, the fullest possible involvement of the patient in the decision, and a genuine reckoning with the fact that both acting and not acting carry moral costs. That ECT can be defended in extremis and is open to serious ethical objection is not a contradiction to be resolved but the very shape of the dilemma, and recognising this is the mark of a mature answer.
Evaluating a treatment means asking honestly how well it works and what it costs — the heart of AO3 on this topic.
Drug therapies are, for many patients, genuinely effective: antidepressants relieve depression and antipsychotics reduce positive symptoms for a substantial proportion of those who take them, and they have transformed the management of severe mental illness — antipsychotics were central to the deinstitutionalisation that emptied the asylums. But the picture is not uniform. Drugs do not work for everyone; response varies; relapse is common when medication stops; and there is debate about how much of the benefit, especially in milder depression, reflects the placebo effect rather than the pharmacological action. The delayed onset of SSRIs and the fact that raising serotonin within hours does not lift mood for weeks both suggest the "chemical imbalance" story is incomplete. Effectiveness is therefore real but partial and contested.
All biological treatments carry side effects, and these are a major evaluative and ethical issue. SSRIs can cause nausea, insomnia or drowsiness, sexual dysfunction, and — a serious concern flagged by regulators — a possible increase in suicidal thoughts in a minority, particularly younger patients, early in treatment. Antipsychotics, especially typical ones, can cause distressing movement disorders (extrapyramidal effects such as tremor and rigidity, and, with long-term use, tardive dyskinesia — involuntary repetitive movements that can be irreversible); atypicals reduce these but can cause substantial weight gain and metabolic problems, and clozapine carries a rare but dangerous blood disorder requiring monitoring. Side effects are not a footnote: they cause real suffering and are a leading reason patients stop taking medication, which then risks relapse.
Because side effects are unpleasant and benefits can feel less tangible than costs, non-compliance (patients not taking medication as prescribed) is a serious practical problem, especially in schizophrenia where the illness itself can undermine insight. There are also concerns, for some drug classes, about dependency and difficult withdrawal. A treatment that works only if taken, and is unpleasant to take, faces a genuine adherence challenge — which is one reason the application strands of Component 03 value strategies that improve compliance.
Subscribe to continue reading
Get full access to this lesson and all 10 lessons in this course.