IB Psychology HLTopic 1 — Prevention and TreatmentPaper 1 & 2Biological approach~9 min read
Drug Treatments for Depression
If you accept the monoamine hypothesis, the treatment writes itself: raise serotonin activity and the symptoms should ease. That is exactly what antidepressants try to do, and for a lot of people it works. The interesting question is what the evidence really shows, and what it quietly leaves out.
📘 What you need to know
Biological treatments target brain chemistry. Antidepressants are the most widely prescribed drug therapy for MDD.
SSRIs (selective serotonin reuptake inhibitors) block the reuptake of serotonin, leaving more of it in the synaptic cleft. Fluoxetine and citalopram are common examples.
SNRIs work similarly but raise noradrenaline as well as serotonin, and are considered more effective for some patients. Duloxetine and venlafaxine are examples.
This treatment follows directly from the monoamine hypothesis: low or irregular serotonin is linked to depressive symptoms, so restoring balance should reduce them.
Kroenke et al. (2001) compared three SSRIs in 573 patients over nine months and found all three worked about equally well.
Drug therapy is cheap and widely available, unlike CBT, which needs trained therapists and often has long waiting lists.
The central criticism: drugs hold symptoms at bay without addressing the root causes, so MDD may return.
Two families of antidepressant
Type
What it does
Examples
SSRIs
Prevent serotonin being reabsorbed into the presynaptic neuron, so more stays in the synaptic cleft
Fluoxetine, citalopram
SNRIs
Do the same for serotonin and also increase noradrenaline, which suits some patients better
Duloxetine, venlafaxine
If you have already covered the neurotransmitter page, you know the mechanism — the reuptake pump is blocked, so the serotonin already released gets more time at the receptors. Say it in one sentence here and spend your words on the evidence instead.
Research support: Kroenke et al. (2001)
Aim: to compare the effectiveness of three SSRIs — paroxetine, fluoxetine and sertraline — in treating MDD.
Participants: 573 patients with MDD from 37 clinics across the USA. 84% were Caucasian, 13% Black and 3% other; 79% were female and 21% male, aged 19–96 with a mean age of 46. All had been clinically recommended for SSRI treatment.
Procedure: participants completed a baseline assessment by telephone and were randomly assigned to one of the three SSRIs, roughly 190 per group. Treatment lasted nine months. At 1, 3, 6 and 9 months each participant completed a 36-item Mental Component Summary Score measuring MDD symptoms, plus self-reports on social and work functioning, physical health, sleep, memory and pain.
Results: 79% completed the full nine months. Improvement was similar across all three drugs, at 15–17 points on the summary score. Depressive symptoms fell from 74% at baseline to 32% at three months and 26% at nine months.
Conclusion: SSRIs are effective for MDD, and the three drugs tested performed at similar levels.
The shape of this chart is the argument. A big early drop is what supporters point to; the flat second half, and the missing control group, are what critics point to.
The gap in the design. All 573 patients received an SSRI. There was no placebo condition and no no-treatment condition, so the study can tell you the three drugs perform similarly, but it cannot tell you how much of the improvement came from the drug rather than from time, expectation or the attention of a clinical trial.
Evaluation
Strengths
Reduced hospitalisation. Antidepressants have allowed many people to manage symptoms outside hospital, which means more freedom and autonomy.
Cheap and accessible. Compared with CBT, which needs trained therapists, takes longer and often involves waiting lists, drug therapy reaches far more people.
Randomised and standardised. Kroenke used random allocation, a large sample across 37 clinics and repeated standardised measures, which is a genuinely strong design for a comparison study.
It supports the underlying theory. If SSRIs help, that is at least consistent with serotonin playing a role in MDD.
Limitations
The placebo debate. Some clinicians argue the effects of SSRIs are little better than a placebo, and studies without a placebo group cannot settle it.
The monoamine hypothesis itself is uncertain. Depression is probably not a single disorder with one cause but a cluster of conditions with many underlying biological and psychological factors.
Symptoms, not causes. Drug therapy holds symptoms at bay without addressing the root cause, so MDD may return once treatment stops.
Side effects. These drugs act directly on the brain, so a clinician needs to monitor the patient for harmful consequences.
Sample bias. 79% of Kroenke’s participants were female and 84% were Caucasian, which limits generalisation.
EXAM QUESTION
Evaluate one biological treatment of one disorder. [22]
Step 1: link the treatment to the theoryMonoamine hypothesis leads to SSRIs. One sentence on the reuptake mechanism.Step 2: describe SSRIs and SNRIs with examplesSerotonin only vs serotonin and noradrenaline.Step 3: use Kroenke with the numbers573 patients, random allocation, nine months, 74% down to 26%, three drugs equally effective.Step 4: evaluate the evidence and the approachNo placebo group, sample bias, side effects, symptoms not causes, and the placebo debate more widely.Best conclusion: effective for many, but not a cure, and best combined with therapy
Link to concepts
Responsibility
Drug therapy can be effective, but because it works directly on the brain and does not address root causes, the prescribing clinician carries a duty to monitor for side effects and to keep the whole person in view rather than the symptom list alone.
Change
MDD is not stable. Life events, hormonal changes and illness can bring it on or lift it. That means a drug may be the right treatment at one point in someone’s life and the wrong one at another, and it is an argument for considering the whole person rather than taking the biologically reductionist route every time.
💡 Exam tip
Name the drug class, the mechanism and two actual drug names. Specificity scores.
The missing placebo group in Kroenke is the single best evaluation point on this page.
Quote the drop as a sequence (74 to 32 to 26) rather than a single number. The shape tells a story.
Do not repeat the whole synapse explanation. One sentence, then move to the evidence.
Comparing with CBT on cost and waiting lists is a strength of drug therapy, and it sets up the treatment-comparison essay.
Avoid giving anything that reads like medical advice. Describe research findings, not what someone should take.
⚠ Common mix-up
Saying SSRIs cure depression. They manage symptoms; relapse is possible after stopping.
Mixing SSRIs and SNRIs. SNRIs act on noradrenaline as well.
Treating Kroenke as evidence that SSRIs beat placebo. There was no placebo group.
Forgetting the drop-out. 79% completed, meaning around a fifth did not, and we do not know how they were doing.
Confusing “equally effective” with “highly effective”. The three drugs matched each other; that is a different claim.
Ignoring the sample composition. Mostly female and mostly Caucasian is a real generalisation limit.
Up next: Drug Treatments for Nicotine Addiction — a different logic entirely. Instead of correcting a chemical shortage, the drug replaces the addictive substance with a safer version of itself.
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