I'm ambivalent about starting this. How do I think about it?

Ambivalence is the right starting place, not the wrong one. The medicine is one lever among several — therapy (CBT or interpersonal therapy is at least as effective as medicine for mild-moderate depression), sleep regularisation, regular movement, food, alcohol, and the conditions around you. Many people start an SSRI/SNRI when the load is too heavy to do the other work, and use the medicine to get the floor high enough to do that work. Others find the other levers are enough. Both of those stories are true, and which one is yours depends on where you're starting from and what's available to you. The choice doesn't have to be permanent. If you start and it doesn't fit, we can change course.

How long until it works, and what should the first month feel like?

First 1–2 weeks: most people notice side effects (nausea, mild anxiety or jitteriness, sleep change, sometimes a flat or numb feeling) before any benefit. This is the part that makes people stop early. The same nausea usually settles by week two. By 2–4 weeks the lift starts — sleep often shifts first, mood next, motivation last. The full effect builds over 6–12 weeks. If by week 4 nothing has moved at all, that's information — we can adjust the dose or change the drug. For people under 25, weekly check-ins for the first month are part of the plan.

What about sexual side effects? Nobody warned me.

These are common and under-discussed. Across the class, somewhere between 30% and 70% of people on an SSRI or SNRI report some change — lower libido, delayed orgasm or inability to climax, erectile changes, reduced genital sensation. This is real and not in your head. Tell me. Options: lower the dose, change the timing, change to a drug with a lower reported rate (vortioxetine is the newer agent with lower reported numbers; bupropion is sometimes added), or add a treatment break for specific occasions. A small number of people report sexual changes that persist after stopping the drug (post-SSRI sexual dysfunction, PSSD). This is an emerging concern — uncommon, not fully understood. Worth knowing about; not a reason to avoid treatment if you need it. The conversation is the most important first step.

I want to stop. How do I do it safely?

Slowly. Stopping suddenly causes discontinuation symptoms — dizziness, electric-shock sensations (often called brain zaps), nausea, flu-like feeling, irritability, vivid dreams. These can be intense and are often mistaken for the depression coming back. They aren't relapse; they're the nervous system adjusting. Paroxetine and venlafaxine are the hardest to come off — slow tapers over months are often needed, sometimes with a fluoxetine bridge (a temporary swap to long-half-life fluoxetine to make the taper easier). Fluoxetine itself self-tapers thanks to its long half-life. The Lancet Psychiatry 2024 systematic review (Henssler et al.) put the discontinuation conversation on firmer footing — these symptoms are real and the slow-taper protocols make a measurable difference. Plan the timing — don't taper through a hard life stretch.

Is this a lifelong commitment?

For most people, no. A common course is 6–12 months past full remission for a first episode, then a careful taper with regular review. For people with multiple episodes or particular risk patterns, longer treatment makes sense — and that's a conversation, not a default. Stopping is a planned decision with a slow taper and a check-in schedule, not a one-day call. Some people genuinely do better staying on long-term, and that's also a legitimate choice.

I'm worried about my teenager going on this — there's a warning about suicide.

Your concern is appropriate. The warning is real and the data behind it is worth knowing. In patients under 25, antidepressants are associated with a small increase in suicidal thoughts and behaviours in the early weeks of treatment — not in completed suicide rates at the population level, but in the symptom of suicidal ideation. The increase is small in absolute terms. Untreated depression also carries suicide risk. The way we manage this: weekly reviews for the first month, you and your teenager both know what to watch for (new or worsening agitation, withdrawal, talk of self-harm, sleep collapse), crisis numbers on the fridge (Lifeline 13 11 14, Kids Helpline 1800 55 1800, Beyond Blue 1300 22 4636), and a low threshold for an unscheduled visit. Fluoxetine has the strongest evidence base in patients under 18 and is usually the SSRI of choice in that age group. Specialist input often helps for younger patients.

I'm planning a pregnancy / I just found out I'm pregnant. What now?

Don't stop without talking to me first. The risk picture has two sides — risk of the medicine to the developing baby, and risk of untreated maternal depression (which also affects pregnancy and infant outcomes). Sertraline and escitalopram have the strongest perinatal safety data and are usually preferred when an antidepressant is needed. Paroxetine is generally avoided in pregnancy because of a first-trimester cardiac signal. For breastfeeding, sertraline and paroxetine have the lowest infant exposure. The decision is rarely 'stop the medicine' — it's usually 'which medicine, at what dose, with what monitoring'. Perinatal psychiatry input is helpful when the picture is complex.

Are some of these drugs better than others?

The Cipriani 2018 Lancet network meta-analysis ranked 21 antidepressants on efficacy and acceptability — the differences between drugs were small. The differences between people are usually larger. Choice depends on what symptoms dominate (sleep, anxiety, pain, energy), what else you take, whether you're planning pregnancy, what side effects you most want to avoid, and what worked in family members. Sertraline and escitalopram are common starting points for depression and anxiety. Duloxetine is the SNRI of choice when chronic pain is part of the picture. Vortioxetine is newer and has lower reported sexual-side-effect rates. Paroxetine and venlafaxine have the most difficult discontinuation profiles, so they're not the easiest first choices unless there's a specific reason.

SSRIs and SNRIs

SSRIs and SNRIs — patient guide

By Dr HB Lo, FACRRM Reviewed 24 May 2026 22 min read

Prescribed for: Depression · Generalised anxiety disorder · Panic disorder · Social anxiety disorder · Obsessive-compulsive disorder · Post-traumatic stress disorder · Premenstrual dysphoric disorder · Chronic pain (duloxetine — diabetic neuropathy and chronic musculoskeletal pain) · Menopausal hot flushes (off-label use — paroxetine, venlafaxine, desvenlafaxine)

SSRIs (sertraline, escitalopram, citalopram, fluoxetine, paroxetine, fluvoxamine, vortioxetine) and SNRIs (venlafaxine, desvenlafaxine, duloxetine) are antidepressants used for depression, anxiety, OCD, PTSD, panic, PMDD, some chronic pain conditions, and menopausal hot flushes.

Most people notice some response by 2–4 weeks and the full effect by 6–12 weeks. The first 1–2 weeks can feel worse before they feel better — nausea, jitteriness, sleep change — and that usually settles. Sexual side effects are common and worth talking about openly.

Never stop suddenly. Discontinuation symptoms — dizziness, brain zaps, flu-like feeling — are real, often mistaken for relapse, and prevented by a slow taper. Patients under 25, parents, and carers need to know about the small early rise in suicidal thoughts and the weekly review plan for the first month. Sudden severe agitation, fever, shivering, twitchy muscles — go to ED. The medicine is one lever; sleep, exercise, therapy, and food do real work alongside it.

This page covers the SSRI and SNRI antidepressant families together. Both work mainly on serotonin (SNRIs also work on norepinephrine), they share most of their safety considerations, and in everyday practice we choose between them by fit, not category. If you’re on one of the medicines listed below, this is your page.

Before we get into the detail: I want to acknowledge two things that are both true. Many people who needed this medicine waited too long to start because of stigma, family pressure, or a system that didn’t take their distress seriously. Other people were started on it after a short consult that didn’t surface the other options. Both of those experiences are real. The medicine is one lever among several — sleep, exercise, therapy, food, alcohol, and the conditions around you all do real work. What follows is the longer version of that conversation.

Find your medicine

SSRIs

Generic name	Common brand names	Strengths	How often
Sertraline	Zoloft, Eleva, Sertra, generics	50 / 100 mg	Once daily
Escitalopram	Lexapro, Esipram, Loxalate, generics	10 / 20 mg	Once daily
Citalopram	Cipramil, Talohexal, generics	10 / 20 / 40 mg	Once daily
Fluoxetine	Prozac, Lovan, Zactin, Auscap, generics	20 mg	Once daily
Paroxetine	Aropax, Paxtine, generics	20 mg	Once daily
Fluvoxamine	Luvox, Faverin, Movox, generics	50 / 100 mg	Once or twice daily
Vortioxetine	Brintellix	5 / 10 / 15 / 20 mg	Once daily

SNRIs

Generic name	Common brand names	Strengths	How often
Venlafaxine	Efexor XR, Elaxine SR, Altven XR, generics	37.5 / 75 / 150 / 225 mg	Once daily
Desvenlafaxine	Pristiq, Desfax, generics	50 / 100 mg	Once daily
Duloxetine	Cymbalta, Andepra, Druxal, generics	30 / 60 mg	Once daily

About the dose numbers. Escitalopram is roughly twice as potent per milligram as citalopram — the numbers look smaller because the drug is more concentrated. Venlafaxine becomes a more balanced serotonin-and-norepinephrine drug at doses above 150 mg, which is why we monitor blood pressure at higher doses. Desvenlafaxine is the active metabolite of venlafaxine — same family, more predictable levels.

Closely related medicines you might be on instead. Mirtazapine is often used when sedation, weight gain, or appetite stimulation are wanted. The older tricyclic antidepressants (amitriptyline, nortriptyline) are still used, particularly for chronic pain. Bupropion has a different mechanism again and is sometimes added or substituted when sexual side effects are the issue.

What it treats

SSRIs and SNRIs are prescribed for more than depression. Your reason may be one or more of:

Depression (major depressive disorder) — see the NICE NG222 (2022) and eTG Psychotropic for the evidence base.
Generalised anxiety disorder, panic disorder, social anxiety disorder — see NICE CG113.
Obsessive-compulsive disorder. Fluvoxamine, sertraline and fluoxetine have the strongest evidence here.
Post-traumatic stress disorder. Sertraline and paroxetine are on-label.
Premenstrual dysphoric disorder (PMDD). Fluoxetine is on-label; the Cochrane review supports the SSRI class effect.
Chronic pain. Duloxetine is on-label in AU for diabetic peripheral neuropathy and chronic musculoskeletal pain (Cochrane review); off-label for fibromyalgia in AU (on-label in the US and EU).
Menopausal hot flushes. Paroxetine 7.5 mg is FDA-approved in the US for this (off-label in AU; see the Stearns JAMA 2003 paroxetine trial). Venlafaxine 37.5–75 mg has strong RCT evidence in breast-cancer survivors (Loprinzi 2000) — particularly relevant if hormonal therapy isn’t an option. One important interaction: paroxetine and fluoxetine reduce the activation of tamoxifen and shouldn’t be combined with it; sertraline, escitalopram, citalopram, venlafaxine and desvenlafaxine are preferred when both are needed.
Premature ejaculation. SSRIs delay ejaculation as a class effect — modest evidence, off-label, a GP-level conversation.

The mechanism is similar across all of these; the goal differs. I’ll tell you which one is yours.

The basics

Take it at the same time every day. Most are once daily. If you miss a dose, take it when you remember unless it’s nearly time for the next one — don’t double up.
Don’t stop suddenly. Discontinuation symptoms (dizziness, brain zaps, flu-like feeling) are real, often mistaken for relapse, and prevented by a slow taper. We plan stopping the same way we plan starting.
Go to ED if you develop sudden severe agitation, fever, shivering, twitchy muscles, heavy sweating, or diarrhoea after starting a new medicine — these can be signs of serotonin syndrome.
For patients under 25 and parents/carers: weekly check-ins for the first month, and a low threshold for an earlier visit. Crisis numbers below.

Everything else — the first month, side effects, sexual side effects, the integrative levers, how to stop safely — is below.

What to expect in the first month

This is the part most people aren’t warned about clearly enough. The first 1–2 weeks can feel worse before they feel better, and that’s the most common reason people stop too early.

Week 1

Nausea, especially with sertraline and venlafaxine. Often settles by week two. Taking the dose with food helps.
Mild anxiety, jitteriness, or restlessness. Counter-intuitive on an anti-anxiety medicine. Usually settles in 1–2 weeks. If it’s intense and persistent, message us — we can slow the titration.
Sleep change. Some people get vivid dreams, lighter sleep, or early waking; some get sleepier. Often settles.
Headache in the first few days, usually settling.
Loose stool or constipation.
A flat or slightly numb emotional tone in some people — usually transient.

Weeks 2–4

Side effects mostly settling.
Early signs of benefit: sleep often shifts first, then mood, then motivation.
Suicidal thoughts in patients under 25 — small early risk window; weekly review is the protective design.

Weeks 4–12

Full effect builds. By 6–12 weeks we should have a clear picture of whether this drug, at this dose, is fitting.
If nothing has moved by week 4, that’s information — we adjust dose or change drug.

How long until it works?

Most people notice some response by 2–4 weeks and full effect by 6–12 weeks. Sleep usually shifts first. Mood and motivation follow. Don’t take a snapshot at week one and decide the medicine doesn’t work — that’s the window when it’s least helpful and most disruptive.

Sick day rules

Unlike blood pressure tablets, you don’t pause SSRIs/SNRIs for a stomach bug or a fever. The dehydration sick-day rule that applies to ACE inhibitors and diuretics doesn’t apply here. Take your dose with whatever you can keep down. If you genuinely can’t keep anything down for more than 24 hours, message us — but the bigger issue is that abruptly stopping causes discontinuation symptoms within days, especially for paroxetine and venlafaxine.

Tap any section below to expand the detail.

How does it work?

SSRIs block the reabsorption (reuptake) of serotonin from the gap between nerve cells back into the cell that released it. More serotonin stays available in the synapse. SNRIs do the same thing for serotonin and for norepinephrine (noradrenaline) — venlafaxine in a dose-dependent way (the norepinephrine effect becomes meaningful above ~150 mg), duloxetine in a more balanced way across the dose range.

The simple “low serotonin equals depression” story that often gets repeated is incomplete. The actual mechanism is more nuanced — downstream changes in receptor sensitivity, slow remodelling of stress-response circuits, and (probably) effects on neuroplasticity — which is part of why these drugs take weeks rather than hours to work. We treat them as effective without claiming to fully understand why.

The duloxetine pain effect probably comes from boosting the descending pain-modulating pathway from brain to spinal cord — the same system the body uses to dampen pain naturally.

Side effects in detail

Common (usually settle in the first 2–4 weeks)

Nausea, loose stool, dry mouth.
Mild anxiety, jitteriness, restlessness in the first week.
Sleep change — vivid dreams, lighter sleep, sometimes early waking; or sleepier (fluvoxamine more often).
Headache.
Sweating (especially venlafaxine and the SNRIs).
Emotional flattening or numbing — some people describe a softer emotional range. For some this is what they wanted; for others it’s the reason they stop. Worth naming so you know it isn’t unique to you.

Common, ongoing

Sexual side effects — see the dedicated section below.
Weight changes. Paroxetine is most associated with weight gain. Sertraline and escitalopram are weight-neutral on average. Fluoxetine can cause modest short-term weight loss in some people. Long-term, weight effects vary by individual.
Mild bruising or longer bleeding from small cuts — SSRIs and SNRIs mildly affect platelet function.

Worth knowing about

Hyponatraemia (low sodium). Most common in older adults, in the first 2–4 weeks, particularly if also on a fluid tablet (review of SSRI hyponatraemia in older adults). Symptoms: confusion, lethargy, headache, falls, new unsteadiness. We check sodium with the routine bloods after starting if you’re over 65 or on a diuretic.
GI bleeding risk is mildly elevated (around 1.5× baseline by meta-analysis) — higher if you also take regular anti-inflammatories (ibuprofen, naproxen, diclofenac) or anticoagulants. We often add a stomach-protector (PPI) when both are long-term.
Bone density / fracture signal in older adults — mixed evidence, not strong enough to change prescribing in most cases, but worth noting if osteoporosis is part of your picture.
QT interval prolongation — particularly citalopram and escitalopram at higher doses (see the TGA product information and AMH for current dose limits). We use dose limits (citalopram max 40 mg, 20 mg if over 65 or on certain interacting drugs; escitalopram max 20 mg, 10 mg if over 65). An ECG before starting is worth doing if you have cardiac disease or take other QT-prolonging drugs.
Blood pressure rise with venlafaxine and desvenlafaxine, particularly above 150 mg venlafaxine. We check BP at follow-up.

Rare but serious — call us or go to ED

Serotonin syndrome. Agitation, fever, shivering, sweating, tremor, twitchy muscles, hyperreflexia, diarrhoea (see Beyond Blue’s antidepressant safety information and HealthDirect). Most often happens when a serotonergic drug is added to an SSRI/SNRI — see the interactions section. Stop the new drug if obvious, go to ED.
Sudden severe agitation or new suicidal thoughts, especially in the first 1–4 weeks, particularly in patients under 25. Don’t wait — message us or call a crisis line.
Unusual bleeding — black stools, blood in vomit, bruising out of proportion to bumps.
Angle-closure glaucoma — sudden severe eye pain, halos around lights, blurred vision. Rare but a medical emergency.
Allergic reaction — facial swelling, breathing difficulty, severe rash.

Sexual side effects — the conversation that often doesn’t happen

This deserves its own section because it’s the side effect patients are least likely to be asked about and most likely to live with silently.

The numbers. Across the SSRI/SNRI class, somewhere between 30% and 70% of people on treatment report some sexual change. The range is wide because studies use different definitions and many studies didn’t ask. When people are asked directly, the higher end of that range is closer to the truth.

What it looks like.

Lower libido (interest).
Delayed orgasm or being unable to climax (men and women).
Erectile changes.
Reduced genital sensation or “muted” sensation during sex.
For some people, the emotional connection during sex feels muted alongside the physical change.

This is real and not in your head. It’s also reversible for most people after stopping the drug.

What we can try.

Lower the dose if your symptoms allow.
Switch to a drug with a lower reported rate — vortioxetine is the newer agent with lower reported sexual-side-effect numbers. Bupropion (different class) is sometimes substituted or added on. I’m not saying any drug is “better” — I’m saying the side-effect profile differs and a switch is a reasonable thing to try.
Add a treatment — sildenafil or tadalafil for erectile changes works on the SSRI/SNRI cause as well as it does on other causes.
Time around it — for some people, taking the dose after the time of day sex is most likely helps. This works less well for long-half-life drugs (fluoxetine) than short-half-life ones.

Post-SSRI sexual dysfunction (PSSD). A small number of people report sexual changes that persist after stopping the drug. This is an emerging concern — uncommon, not fully understood, and being actively studied. Worth knowing about; not a reason to avoid treatment if you need it. If you’re worried about it, raise it before starting so we can plan the conversation early.

The most important step is naming it. If you don’t tell me, I can’t help you adjust. There’s no “right” answer about which trade-off to make — your sex life is yours.

Drugs, food, and alcohol

Never combine with — serotonin syndrome risk (see the eTG Psychotropic and AMH for the full interaction matrix):

MAOIs. Phenelzine, tranylcypromine, moclobemide, selegiline. Also the antibiotic linezolid (acts as an MAOI) and the dye methylene blue used in some surgeries. 14-day washout in both directions; 5 weeks for fluoxetine because of its long half-life.
St John’s wort (Hypericum). Serotonergic on its own; also reduces levels of many other medicines via CYP induction.
Tryptophan or 5-HTP supplements at higher doses.
Recreational MDMA, cocaine, methamphetamine — additive serotonergic and cardiovascular risk. Worth a non-judgemental conversation if this is part of your life.

Use cautiously — discuss with me first:

Tramadol, pethidine, fentanyl — additive serotonergic risk plus tramadol lowers seizure threshold.
Triptans (sumatriptan and others for migraine) — theoretical risk; usually manageable with awareness.
Ondansetron for nausea — short courses usually fine; flag if long-term.
Lithium — serotonergic load increases; monitor levels.
SAMe supplement — additive serotonergic load.

Anti-inflammatories and blood thinners:

NSAIDs (ibuprofen, naproxen, diclofenac, celecoxib) — increased GI bleeding risk. Paracetamol is preferred. If you need regular NSAIDs, we often add a stomach protector (PPI).
Anticoagulants (warfarin, apixaban, rivaroxaban) and antiplatelets (aspirin, clopidogrel) — bleeding risk. Manageable with awareness and monitoring.

Specific drug-drug interactions worth knowing about:

Tamoxifen + paroxetine or fluoxetine — these SSRIs reduce tamoxifen’s activation and should be avoided in women on tamoxifen for breast cancer. Sertraline, escitalopram, citalopram, venlafaxine, desvenlafaxine are preferred.
Codeine + paroxetine or fluoxetine — codeine becomes a much weaker painkiller because conversion to morphine is blocked.
Warfarin + fluoxetine, fluvoxamine or paroxetine — can raise INR; check more often after starting or changing dose.
Clozapine + fluvoxamine — significant interaction; specialist-managed only.
Theophylline, caffeine + fluvoxamine — fluvoxamine raises their levels; trial reducing caffeine after starting if you get jittery.

Alcohol. Additive sedation and slowed coordination. More importantly, regular drinking worsens depression and anxiety over time, disrupts sleep architecture (which itself worsens mood), and undermines the work the medicine is doing. Minimise during titration; honest review at follow-up.

Caffeine. Can worsen early anxiety, tremor and sleep disruption — trial reducing intake if these emerge after starting.

Food. No specific food restrictions. Take with food if nausea is a problem.

Generic substitution at the pharmacy. Generics are bioequivalent — they work the same. If the pharmacist offers a cheaper generic, that’s fine. Brand-name changes don’t change the dose.

Monitoring

Phone or in-person check-in 1–2 weeks after starting, and again at 4 weeks. Earlier if you’re under 25 or have significant risk factors — usually weekly for the first month in that group.
Blood test 2–4 weeks after starting if you’re over 65, on a diuretic, or have lower body mass — checks sodium (hyponatraemia risk).
BP check at follow-up if you’re on venlafaxine or desvenlafaxine, particularly at higher doses.
ECG before starting citalopram or escitalopram if you have cardiac disease, electrolyte issues, or take other QT-prolonging drugs.
Then every 3–6 months for the first 12 months, longer intervals after that if things are stable.
Message us if you: start a new medicine (including over-the-counter and supplements), develop new agitation or suicidal thoughts, get unexplained dizziness or unsteadiness, or want to stop.

Stopping or pausing — discontinuation in detail

This is one of the surfaces where the conversation most often falls short. Take it seriously.

Discontinuation syndrome is real. When you stop an SSRI/SNRI — particularly suddenly — your nervous system can produce a cluster of symptoms within days:

Dizziness, unsteadiness, vertigo.
“Brain zaps” — brief electric-shock sensations, often triggered by eye movements.
Nausea, flu-like feeling, headache.
Vivid dreams, sleep disruption.
Irritability, mood swings, returning anxiety or low mood.

These are often mistaken for the depression coming back. They aren’t relapse; they’re the nervous system adjusting. The 2024 Lancet Psychiatry systematic review (Henssler et al.) put the discontinuation conversation on firmer footing — these symptoms are real and slow tapers reduce them.

The taper. A reasonable starting plan for most people is reducing the dose by ~25% every 2–4 weeks. For people who’ve been on the medicine a long time, are on paroxetine or venlafaxine, or have had a difficult experience stopping before, slower is better — sometimes 10% reductions every 4 weeks, sometimes even slower at the bottom of the dose. The last few milligrams are often the hardest.

Drug-specific notes (see the RANZCP mood disorders guideline and Black Dog Institute for practical tapering frameworks):

Fluoxetine self-tapers because of its long half-life — usually stops cleanly over 1–2 weeks of half-dosing, sometimes alternate days.
Paroxetine and venlafaxine have the worst discontinuation profiles. A common move is the fluoxetine bridge — swap to fluoxetine, stabilise, then taper fluoxetine. This is mainstream practice but it’s a conversation about whether your situation needs it.
Vortioxetine discontinuation is reported to be milder, but the principle of tapering still applies.

When to do it. Not in the middle of a hard life stretch. Plan for a stable window. Pregnancy, planned surgery, major work transitions and grief are not the right time.

How long do you stay on? A common course is 6–12 months past full remission for a first episode, then a careful taper with review. For multiple episodes or specific risk patterns, longer is reasonable. The decision is yours, made with me, based on where you are — not a default rule.

Suicidality risk in patients under 25 — what to know

The TGA and the FDA both carry warnings about a small increase in suicidal thoughts and behaviours in patients under 25 in the early weeks of antidepressant treatment (TGA notice; NPS MedicineWise).

What this means in practice.

The risk is real but small in absolute terms. Population-level studies have not shown an increase in completed suicide rates — the signal is in suicidal ideation and self-harm, not death.
Untreated depression also carries suicide risk. “Don’t treat” is not the safer default.
The most reliable protection is a structured plan: weekly review for the first month, both patient and parent/carer knowing what to watch for, low threshold for an unscheduled visit, crisis numbers easily accessible.

Warning signs that need same-day contact.

New or worsening agitation.
New withdrawal from people who matter to them.
Talk of self-harm, hopelessness, being a burden, wanting to disappear.
Sleep collapse with significant mood change.
Giving things away, sudden calm after a period of distress.

Crisis numbers — put these on the fridge.

Lifeline 13 11 14 (24/7)
Beyond Blue 1300 22 4636 (24/7)
Kids Helpline 1800 55 1800 (24/7, ages 5–25)
Suicide Call Back Service 1300 659 467 (24/7)
13YARN 13 92 76 (24/7, for Aboriginal and Torres Strait Islander people)
000 for immediate danger.

Drug choice in under-18s. Fluoxetine has the strongest evidence base in patients under 18 and is usually the SSRI of choice in that age group. Sertraline and fluvoxamine are on-label for paediatric OCD. Other SSRIs and SNRIs are off-label in patients under 18 and are usually specialist-initiated.

Pregnancy and breastfeeding

The decision is rarely “just stop the medicine.” Both treated and untreated depression carry risk in pregnancy, and the conversation has two sides.

If you’re planning a pregnancy, tell me before trying. We can review which drug you’re on, and switch if your current one isn’t the best fit for pregnancy (perinatal antidepressant safety systematic review).

The picture:

Sertraline and escitalopram — strongest perinatal safety data. Usually preferred when an antidepressant is needed in pregnancy.
Paroxetine — generally avoided. First-trimester cardiac-malformation signal (mostly small septal defects, absolute risk small). Cat D in the AU classification.
Other SSRIs/SNRIs — case-by-case.
Untreated maternal depression carries its own risks — preterm birth, low birth weight, postnatal depression, impaired bonding. Stopping isn’t automatically the safer choice.

Late pregnancy. Some neonates have transient adjustment symptoms in the first days after birth (jitteriness, mild respiratory changes). Usually self-limited; the paediatric team is aware.

Breastfeeding. Most SSRIs are reasonable. Sertraline and paroxetine have the lowest infant exposure. Fluoxetine and citalopram have higher infant exposure because of long half-lives or higher transfer. The decision is rarely “don’t breastfeed” — it’s usually “choose the SSRI with the most reassuring data for this dyad.”

Perinatal psychiatry input is genuinely helpful when the picture is complex. Ask for it; it’s not a sign anything is wrong.

Cost

Most SSRIs and SNRIs are PBS-listed without restriction; vortioxetine is PBS-listed under streamlined Authority for major depression.

From 1 January 2026, the PBS co-payment is:

General patient: up to $25.00 per script
Concession card holder: up to $7.70 per script

Generic versions cost the same as branded ones at PBS pricing and work the same. Your actual charge may be lower if the medicine is under co-payment, or higher if you choose a brand with a premium. Confirm with your pharmacist.

Paroxetine 7.5 mg for hot flushes is off-label in AU and not PBS-subsidised — you pay full cost if you choose this option.

The integrative view

Most patients I see want to do everything they reasonably can alongside the medicine. This is the longer version of that conversation. The principle: the medicine is one lever among several. For mild-to-moderate depression and anxiety, the other levers do as much work as the drug. For severe depression, the drug often clears the floor enough that the other levers become possible.

Strong evidence — these reliably help

These are interventions where the data is solid enough that I’d discuss them with any patient considering or already on an SSRI/SNRI.

Psychotherapy — CBT and interpersonal therapy in particular. For mild-to-moderate depression, therapy is at least as effective as medicine alone and the benefits last longer after stopping. For moderate-to-severe depression, the combination of medicine and therapy outperforms either alone. Medicare rebates apply to a limited number of sessions under a Mental Health Treatment Plan. If you’re only doing the medicine, you’re doing less than half the available work.
Aerobic exercise. The Cochrane review (Cooney et al.) showed exercise has a measurable antidepressant effect; in some studies effect sizes were comparable to medication in mild-to-moderate depression. 150 minutes/week of brisk walking, cycling, swimming or equivalent. Compound benefit with medication (Cipriani 2018 antidepressant network meta-analysis provides the medication-effect baseline for comparison).
Resistance training 2–3 sessions/week. Independent benefit on top of aerobic.
Sleep regularisation. Disrupted sleep both causes and worsens depression and anxiety. Consistent sleep timing, dark cool room, screens out of bed, light exposure in the morning. If you snore, have witnessed pauses in breathing, or are tired despite enough time in bed — get a sleep study. Treating obstructive sleep apnoea is a depression intervention.
Reducing alcohol. Regular drinking worsens depression and anxiety over time and disrupts sleep architecture. Cutting back is one of the more reliable mood interventions.
Mediterranean-pattern eating — the SMILES trial (Jacka 2017) showed a Mediterranean dietary intervention as an add-on to usual care had a meaningful effect on depression. Vegetables, fruit, whole grains, legumes, nuts, fish, olive oil; less ultra-processed food and added sugar.
Social connection. Loneliness behaves like a clinical risk factor in its own right. One sustained connection that feels real does more than ten low-quality ones.

Moderate evidence — likely helpful

Mindfulness-Based Cognitive Therapy (MBCT) — Cochrane-level evidence for preventing relapse in recurrent depression (see also Black Dog Institute resources). Particularly relevant if you’ve been depressed before.
Omega-3 (EPA-predominant), 1–2 g EPA/day — meta-analyses show a small adjunctive effect. EPA:DHA ratio above 60:40. Discuss if you’re on blood thinners.
Bright light therapy — strong evidence in seasonal-pattern depression; modest evidence in non-seasonal depression.
Vitamin D — supplement to a level of 75–100 nmol/L if low. General health benefit; mood effect modest in isolation but worth correcting.
Magnesium — small RCT signal in mild-moderate depression. Food first (leafy greens, nuts, seeds, legumes, dark chocolate).

Limited but worth knowing

Saffron (Crocus sativus), 30 mg/day — multiple small RCTs in mild-moderate depression have shown effect sizes comparable to fluoxetine. The trials are small and short, but the signal is consistent. Reasonable to trial as a stand-alone in mild depression or as an adjunct — discuss timing if combining with an SSRI/SNRI (serotonergic load is theoretically additive though not strongly reported in trials).
L-methylfolate 7.5–15 mg/day — adjunctive evidence in partial responders, particularly with low/borderline folate or known MTHFR variants. Mixed RCT data; reasonable trial in the right context.
SAMe — modest standalone evidence; combining with SSRI/SNRI adds serotonergic load. Discuss before starting.

Avoid alongside SSRIs/SNRIs

St John’s wort — both a serotonergic agent and a strong inducer of CYP enzymes that reduces levels of many other medicines (see HealthDirect). Useful in mild depression as monotherapy; not safe to add to an SSRI/SNRI.
5-HTP and tryptophan supplements at higher doses — additive serotonergic risk.

A note on the “anti-antidepressant” online conversation

There is a real online conversation that says SSRIs are over-prescribed, addictive, and harmful — and a real online conversation that says they’re lifesaving and under-used. Both stories contain truth and both contain distortion. The discontinuation syndrome is real and was minimised for years. The drugs also keep many people alive who wouldn’t be without them. Hold both. The most useful position is neither for nor against; it’s a clear-eyed conversation about whether this particular drug, at this particular dose, is fitting you — and the willingness to change course when it isn’t.

Track these between now and your next visit

Mood, sleep, energy, anxiety — a brief daily note (one or two words) is enough. Patterns matter more than single days.
Side effects — when they started, whether they’re settling.
Sexual changes — bring them up; we’ll address them.
For patients under 25 (and parents/carers) — any new agitation, withdrawal, talk of self-harm, sleep collapse → contact us same day.
Anything else you’ve started — over the counter, supplements, herbal products.

Bring the list to your review.

This is general information, not personal medical advice. Every patient is different. Decisions about your medicines — which one, what dose, when to stop, what to combine with — are made with the doctor who prescribed them. If anything on this page appears to contradict advice from your treating doctor, follow your doctor; they have context about your situation that this page cannot.
Reading this page does not establish a doctor-patient relationship with Dr Hoebing Lo. If you are not a current patient, please discuss your medicines with your own GP, specialist, or pharmacist.
About the integrative content. The lifestyle, dietary, therapy and complementary recommendations on this page summarise current published research. Effect sizes are approximations from clinical studies — your individual response will vary, and real-world results are commonly smaller than trial results because day-to-day life differs from study conditions. Supplements and herbal products are not interchangeable with prescribed medication and can interact with it. Talk to your doctor and pharmacist before starting any new supplement, herbal product, or significant change in diet.
Mental-health crisis. If you are in immediate danger or thinking about ending your life, call 000, go to your nearest emergency department, or call Lifeline 13 11 14, Beyond Blue 1300 22 4636, Kids Helpline 1800 55 1800, Suicide Call Back Service 1300 659 467, or 13YARN 13 92 76. All of these are free, confidential and available 24 hours a day.
Currency. This page reflects clinical practice as of the last-reviewed date. Medicine evolves; specific details may date between reviews. Pricing shown is indicative; confirm with your pharmacist.
No commercial relationships. Dr Hoebing Lo has no financial or commercial relationship with the manufacturer of any medicine, brand, or supplement mentioned on this page.
Emergencies. If you have sudden severe agitation with fever, shivering and twitchy muscles (possible serotonin syndrome); sudden severe eye pain with blurred vision (possible angle-closure glaucoma); facial swelling or breathing difficulty; or signs of significant bleeding, call 000 or go to your nearest emergency department. Do not wait, and do not message us first.

Frequently asked questions

I'm ambivalent about starting this. How do I think about it?

Ambivalence is the right starting place, not the wrong one. The medicine is one lever among several — therapy (CBT or interpersonal therapy is at least as effective as medicine for mild-moderate depression), sleep regularisation, regular movement, food, alcohol, and the conditions around you. Many people start an SSRI/SNRI when the load is too heavy to do the other work, and use the medicine to get the floor high enough to do that work. Others find the other levers are enough. Both of those stories are true, and which one is yours depends on where you're starting from and what's available to you. The choice doesn't have to be permanent. If you start and it doesn't fit, we can change course.
How long until it works, and what should the first month feel like?

First 1–2 weeks: most people notice side effects (nausea, mild anxiety or jitteriness, sleep change, sometimes a flat or numb feeling) before any benefit. This is the part that makes people stop early. The same nausea usually settles by week two. By 2–4 weeks the lift starts — sleep often shifts first, mood next, motivation last. The full effect builds over 6–12 weeks. If by week 4 nothing has moved at all, that's information — we can adjust the dose or change the drug. For people under 25, weekly check-ins for the first month are part of the plan.
What about sexual side effects? Nobody warned me.

These are common and under-discussed. Across the class, somewhere between 30% and 70% of people on an SSRI or SNRI report some change — lower libido, delayed orgasm or inability to climax, erectile changes, reduced genital sensation. This is real and not in your head. Tell me. Options: lower the dose, change the timing, change to a drug with a lower reported rate (vortioxetine is the newer agent with lower reported numbers; bupropion is sometimes added), or add a treatment break for specific occasions. A small number of people report sexual changes that persist after stopping the drug (post-SSRI sexual dysfunction, PSSD). This is an emerging concern — uncommon, not fully understood. Worth knowing about; not a reason to avoid treatment if you need it. The conversation is the most important first step.
I want to stop. How do I do it safely?

Slowly. Stopping suddenly causes discontinuation symptoms — dizziness, electric-shock sensations (often called brain zaps), nausea, flu-like feeling, irritability, vivid dreams. These can be intense and are often mistaken for the depression coming back. They aren't relapse; they're the nervous system adjusting. Paroxetine and venlafaxine are the hardest to come off — slow tapers over months are often needed, sometimes with a fluoxetine bridge (a temporary swap to long-half-life fluoxetine to make the taper easier). Fluoxetine itself self-tapers thanks to its long half-life. The Lancet Psychiatry 2024 systematic review (Henssler et al.) put the discontinuation conversation on firmer footing — these symptoms are real and the slow-taper protocols make a measurable difference. Plan the timing — don't taper through a hard life stretch.
Is this a lifelong commitment?

For most people, no. A common course is 6–12 months past full remission for a first episode, then a careful taper with regular review. For people with multiple episodes or particular risk patterns, longer treatment makes sense — and that's a conversation, not a default. Stopping is a planned decision with a slow taper and a check-in schedule, not a one-day call. Some people genuinely do better staying on long-term, and that's also a legitimate choice.
I'm worried about my teenager going on this — there's a warning about suicide.

Your concern is appropriate. The warning is real and the data behind it is worth knowing. In patients under 25, antidepressants are associated with a small increase in suicidal thoughts and behaviours in the early weeks of treatment — not in completed suicide rates at the population level, but in the symptom of suicidal ideation. The increase is small in absolute terms. Untreated depression also carries suicide risk. The way we manage this: weekly reviews for the first month, you and your teenager both know what to watch for (new or worsening agitation, withdrawal, talk of self-harm, sleep collapse), crisis numbers on the fridge (Lifeline 13 11 14, Kids Helpline 1800 55 1800, Beyond Blue 1300 22 4636), and a low threshold for an unscheduled visit. Fluoxetine has the strongest evidence base in patients under 18 and is usually the SSRI of choice in that age group. Specialist input often helps for younger patients.
I'm planning a pregnancy / I just found out I'm pregnant. What now?

Don't stop without talking to me first. The risk picture has two sides — risk of the medicine to the developing baby, and risk of untreated maternal depression (which also affects pregnancy and infant outcomes). Sertraline and escitalopram have the strongest perinatal safety data and are usually preferred when an antidepressant is needed. Paroxetine is generally avoided in pregnancy because of a first-trimester cardiac signal. For breastfeeding, sertraline and paroxetine have the lowest infant exposure. The decision is rarely 'stop the medicine' — it's usually 'which medicine, at what dose, with what monitoring'. Perinatal psychiatry input is helpful when the picture is complex.
Are some of these drugs better than others?

The Cipriani 2018 Lancet network meta-analysis ranked 21 antidepressants on efficacy and acceptability — the differences between drugs were small. The differences between people are usually larger. Choice depends on what symptoms dominate (sleep, anxiety, pain, energy), what else you take, whether you're planning pregnancy, what side effects you most want to avoid, and what worked in family members. Sertraline and escitalopram are common starting points for depression and anxiety. Duloxetine is the SNRI of choice when chronic pain is part of the picture. Vortioxetine is newer and has lower reported sexual-side-effect rates. Paroxetine and venlafaxine have the most difficult discontinuation profiles, so they're not the easiest first choices unless there's a specific reason.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.