Two persistent myths about mental health medication deserve to be addressed before anything else.
The first: that antidepressants are happy pills that make you artificially cheerful, numb your emotions, and fundamentally change who you are. This is not how they work. People on antidepressants do not report feeling falsely happy. They report feeling less crushed. Less unable. The floor comes up; a false ceiling does not come down.
The second: that taking medication for mental health is a sign of weakness, an easy way out, or evidence that your faith is insufficient. This view - held more explicitly in some African and Caribbean communities than in others, but present in virtually all of them to some degree - keeps people suffering from treatable conditions when effective help is available. It deserves a direct, clear response.
Mental health conditions are medical conditions. They involve documented changes in brain chemistry, structure, and function. Treating them with medication is not more morally different from treating diabetes with metformin or hypertension with amlodipine than from anything else in medicine. The body has a problem. The medication helps the body address the problem.
SSRIs - the most commonly prescribed antidepressants
Selective Serotonin Reuptake Inhibitors are first-line medication for depression and most anxiety disorders. Commonly prescribed SSRIs in the UK: sertraline (Zoloft), fluoxetine (Prozac), citalopram, escitalopram (Cipralex), paroxetine (Seroxat).
What they actually do: SSRIs prevent the reabsorption (reuptake) of serotonin at the synapse between neurons, increasing its availability in the synaptic cleft. The older explanation - that depression is caused by a serotonin deficiency that SSRIs correct - has been significantly revised by research. The mechanism of therapeutic benefit is more complex and less completely understood than the serotonin story suggests. What is clear from clinical evidence is that SSRIs work for many people with depression and anxiety, even if the precise reason is incompletely understood.
What they do not do: They do not make you happy. They do not numb your emotions. They do not cause personality changes in most people. They are not addictive in the way benzodiazepines are. What people typically report is that the medication reduces the intensity and frequency of depressive or anxiety episodes - making them manageable rather than overwhelming.
The 4-6 week delay: The single most clinically important practical point. SSRIs do not work immediately. The therapeutic effect builds over 4-6 weeks. Many people stop in the first week or two, concluding that the medication does not work - before the therapeutic window has been reached. If your GP prescribes an SSRI, they should explicitly tell you: you may feel worse before you feel better in the first two weeks; the therapeutic effect develops over 4-6 weeks; do not stop without discussing with your GP.
Common early side effects (first 1-3 weeks): Nausea, headache, increased anxiety or agitation, disrupted sleep. Most of these resolve after 2-3 weeks. If they are intolerable, contact your GP rather than stopping abruptly.
Persistent side effects: Sexual dysfunction - reduced libido, delayed orgasm, or inability to orgasm - affects approximately 40-60% of people on SSRIs and does not always resolve. It is the most common reason for discontinuing SSRIs and is frequently not discussed proactively. If sexual function matters to you (and it should be assumed that it does), discuss this explicitly with your prescriber before starting. Switching to a different antidepressant (such as bupropion or mirtazapine) may help.
Stopping SSRIs: Do not stop abruptly. Discontinuation syndrome - dizziness, flu-like symptoms, electric shock sensations, mood disturbance - can be significant. Always taper gradually under GP guidance. The duration of taper depends on how long you have been on the medication.
SNRIs - a related class
Serotonin and noradrenaline reuptake inhibitors (venlafaxine, duloxetine) work on both serotonin and noradrenaline systems. Used for depression (often when SSRIs have been inadequate), anxiety disorders, and chronic pain. Similar side effect profile to SSRIs, with the addition of blood pressure effects at higher doses (venlafaxine). Discontinuation syndrome can be more pronounced.
Mirtazapine
A different mechanism from SSRIs/SNRIs - blocks certain serotonin and histamine receptors. Significant sedating effect makes it useful when insomnia accompanies depression. Weight gain is common. Useful for people who have not responded to SSRIs or who cannot tolerate their side effects.
Case study: Adaeze and the SSRI she did not want to start
Adaeze, 31, came to me with moderate depression following a difficult 18 months: job loss, relationship breakdown, and the death of her father in Nigeria which she could not travel to be present for. She was reluctant to try medication. Her church community had suggested depression was a spiritual problem requiring prayer, not medicine.
I spent time acknowledging this view without dismissing it. I explained the biology. I told her what sertraline actually does and does not do. I was explicit about the timeline and the likely early side effects. I told her that taking medication and praying were not mutually exclusive.
She started sertraline 50mg.
Week one: nausea, worse anxiety, difficulty sleeping. She called me, worried she had made the wrong decision. I told her this was expected and temporary. She continued.
Week six: "I feel like I can think again. The sadness is still there but it is not crushing me. I can function."
She used sertraline for eight months, concurrent with CBT. She tapered off at month nine and has remained well since.
"I still believe God heals," she told me. "I also believe he gave us medicine."
Antipsychotics
Antipsychotics are prescribed for schizophrenia, bipolar disorder, severe psychotic depression, and several other conditions. First-generation (typical) antipsychotics (haloperidol, chlorpromazine) have significant movement side effects. Second-generation (atypical) antipsychotics (olanzapine, quetiapine, risperidone, aripiprazole, clozapine) have fewer movement side effects but significant metabolic effects.
The metabolic side effect problem: Weight gain from olanzapine, quetiapine, and clozapine in particular is not a lifestyle consequence - it is a pharmacological effect on appetite regulation and metabolism that is often dramatic (10-20kg or more). If you are on an antipsychotic and gaining weight significantly, tell your prescriber. Switching to a more metabolically neutral antipsychotic (aripiprazole, amisulpride) may be appropriate, depending on the clinical situation.
Never stop antipsychotics suddenly. Abrupt discontinuation can trigger rapid and severe relapse of psychotic symptoms. Any change to antipsychotic medication should be done gradually under specialist supervision.
Clozapine: The most effective antipsychotic for treatment-resistant schizophrenia, with unique evidence for reducing suicide risk. Requires regular blood monitoring (weekly initially) due to risk of agranulocytosis (reduction in white blood cells). Worth the monitoring burden for the right patients.
Mood stabilisers
Lithium: The gold standard for bipolar disorder, with the most evidence for reducing both manic and depressive episodes, and the strongest evidence for reducing suicide risk in bipolar disorder. Requires regular blood level monitoring (narrow therapeutic window) and monitoring of thyroid and kidney function. Still underused due to the monitoring requirements, despite its remarkable efficacy.
Valproate (sodium valproate): Effective mood stabiliser absolutely contraindicated in pregnancy and in women who could become pregnant, due to severe risk of neural tube defects and developmental effects on the foetus. If you are a woman of childbearing potential currently on valproate, please discuss this with your doctor urgently. Alternative mood stabilisers can be used.
Sources: NICE CG90 - Depression in Adults 2022; NICE CG185 - Bipolar Disorder 2023; Cipriani A et al, The Lancet 2018 (antidepressant comparative effectiveness - comprehensive meta-analysis); Moncrieff J et al, Molecular Psychiatry 2022 (serotonin hypothesis review); Taylor D et al, The Maudsley Prescribing Guidelines in Psychiatry, 14th edition 2021; FDA valproate safety communication.
