Antidepressants and Digestion: What to Expect

Medically reviewed and written by Dr Zeeshan Afzal (MBBS), Medical Content Lead at Welzo. Last updated: August 2026. Reading time: approximately 13 minutes.

Constipation is one of the most under-discussed side effects of antidepressant treatment. It rarely appears in the headline warnings, yet it is a frequent reason people quietly stop taking a medication that was starting to help. If your bowels have slowed since you began an SSRI, SNRI or tricyclic, you are not imagining it, and there is a well-described physiological reason for it. This guide explains why antidepressants cause constipation, which drugs are most likely to do it, how long it typically lasts, and what actually works to manage it — from NHS-aligned first-line measures through to targeted gut health support. Because the digestive tract and the brain are in constant two-way communication, understanding the gut–brain connection is central to making sense of what is happening. You may also find our broader guides on gut health in the UK and constipation relief useful alongside this article. For readers looking at supportive options, Welzo's probiotics range, Akkermansia muciniphila, Citrus Pectin Powder, Ultra Purity Berberine and Ultra Purity TUDCA are covered later in this article, with important notes on interactions. Magnesium for constipation is also discussed in detail.

Table of contents

• Key takeaways
• How common is constipation on antidepressants?
• Why antidepressants cause constipation
• Which antidepressants are most likely to cause it
• What to expect: a realistic timeline
• How to tell whether the medication is the cause
• Other digestive effects of antidepressants
• First-line management: diet, fluid, movement and routine
• Laxatives: the NHS stepped approach
• Supplements and gut support
• Talking to your prescriber about switching
• Red flags: when to seek medical help
• Special groups and situations
• Testing and investigations
• Frequently asked questions
• References

Key takeaways

• Constipation affects roughly 11% to 12.5% of people taking antidepressants in clinical trials, with around 4.7% describing it as genuinely bothersome.
• Tricyclic antidepressants (amitriptyline, nortriptyline, imipramine) are the most likely culprits because of their strong anticholinergic activity. Among SSRIs, paroxetine carries the highest constipation risk.
• The mechanism involves blockade of muscarinic acetylcholine receptors in the gut wall, altered serotonin signalling in the enteric nervous system, noradrenergic slowing of transit, and possible changes to the gut microbiome.
• Many cases settle within two to four weeks as receptors adapt. Constipation that persists beyond three to four weeks usually needs active management.
• First-line measures are dietary fibre, fluid, movement and toilet routine, followed by laxatives in a stepped approach. Osmotic laxatives such as macrogol are commonly used first.
• Never stop or reduce an antidepressant without medical advice. Abrupt discontinuation can cause withdrawal symptoms and relapse of the underlying condition.

How common is constipation on antidepressants?

The scale of antidepressant use in the UK

Antidepressants are among the most widely prescribed medicines in Britain. NHS Business Services Authority figures show that 92.6 million antidepressant items were dispensed in England in 2024/25 to an estimated 8.89 million identified patients — a 3.94% rise in items on the previous year, and the largest single BNF section in the mental health dataset.¹ Even a side effect affecting one in ten users therefore represents several hundred thousand people in England alone.

Reported rates in clinical trials

A widely cited review of antidepressant tolerability found that the overall rate of constipation across trials sits at approximately 11% to 12.5%, with about 4.7% of patients rating it as a bothersome side effect rather than a minor inconvenience.² That distinction matters: a slightly firmer stool is very different from straining, incomplete evacuation and abdominal discomfort that interferes with daily life.

A large systematic review and meta-analysis of gastrointestinal side effects across 304 studies of second-generation antidepressants confirmed that all antidepressants assessed produced higher rates of gastrointestinal side effects than placebo. Escitalopram and sertraline were the least well tolerated overall across the gastrointestinal domain, though notably they were not significantly associated with constipation. Mirtazapine emerged as the antidepressant with the fewest gut-related side effects.³

Why real-world rates may differ

Trial figures often understate the everyday experience for three reasons. First, trials typically run for six to twelve weeks, so they miss longer-term effects. Second, they usually exclude people with existing bowel disorders, older adults and those on multiple medicines — the groups most vulnerable to constipation. Third, symptoms are frequently attributed to depression itself rather than the drug, since low mood, reduced appetite, inactivity and poor fluid intake all slow the bowel independently.

It is also worth knowing that adverse events are reported at surprisingly high rates in placebo groups in antidepressant trials. Expectation shapes symptom reporting. This does not mean your constipation is imaginary — but it does mean that a careful, structured assessment is more useful than assuming causation from timing alone.

Why antidepressants cause constipation

Anticholinergic (muscarinic) blockade

This is the dominant mechanism. Bowel movement depends on acetylcholine binding to muscarinic receptors — particularly the M2 and M3 subtypes — on the smooth muscle of the intestinal wall, which triggers the coordinated contractions known as peristalsis.

Tricyclic antidepressants competitively block these receptors. So does paroxetine, which has appreciably higher muscarinic affinity than other SSRIs. The result is slower colonic transit: stool spends longer in the colon, more water is reabsorbed, and the stool becomes harder and more difficult to pass. The same receptor blockade explains why constipation so often arrives alongside dry mouth, blurred vision and urinary hesitancy — an anticholinergic cluster rather than an isolated bowel problem.

Serotonin signalling in the gut

The majority of the body's serotonin is found not in the brain but in the gastrointestinal tract, where it regulates motility, secretion and sensation through the enteric nervous system.⁴ SSRIs and SNRIs raise serotonin availability at the synapse — in the gut as well as the brain.

Because different serotonin receptor subtypes do different jobs, the net effect varies between individuals. Stimulation of 5-HT4 receptors tends to accelerate transit (which is why some people get diarrhoea, particularly on sertraline). Activation of 5-HT3 receptors drives nausea, typically in the first fortnight. But chronic elevation of serotonin can also lead to receptor desensitisation over time, and in some people the balance tips towards slowed motility. This is why two people on the same drug can have opposite bowel symptoms.

Noradrenaline and sympathetic tone

SNRIs such as venlafaxine and duloxetine also raise noradrenaline. Increased sympathetic ("fight or flight") tone diverts blood flow away from the gut and reduces digestive activity, slowing gastric emptying and intestinal transit. For people already prone to sluggish bowels, this can be enough to tip them into constipation.

Direct effects on smooth muscle ion channels

Laboratory work published in 2022 identified a further mechanism specific to tricyclics. Researchers demonstrated that TCAs inhibit TRPC4 channels in colonic smooth muscle cells, and that all TCA compounds tested significantly suppressed contractions in human colonic tissue.⁵ This is a direct pharmacological brake on the colon, independent of the anticholinergic effect — and it helps explain why tricyclics are used therapeutically in diarrhoea-predominant IBS.

Effects on the gut microbiome

A landmark screen published in Nature in 2018 tested more than 1,000 marketed drugs against 40 representative gut bacterial strains and found that 24% of drugs with human targets inhibited the growth of at least one strain in vitro.⁶ A subsequent study focused specifically on antidepressants confirmed measurable antimicrobial activity against gut commensals, including sensitivity of Akkermansia species to certain agents.⁷

These are laboratory findings, and it would be overstating the evidence to claim that antidepressants reliably cause clinically significant dysbiosis in humans. But it is biologically plausible that shifts in microbial composition contribute to altered stool form, gas and bloating in some people. If you want to understand this area more fully, our guides to gut dysbiosis, microbiome diversity and short-chain fatty acids set out the underlying science.

Putting the mechanisms together

In practice, most antidepressant-related constipation is multifactorial: a partly anticholinergic drug, given to someone whose appetite, fibre intake, hydration and physical activity have all dropped because of depression, with sleep disruption and possibly other constipating medicines in the mix. Effective management addresses all of those layers, not just the drug.

Which antidepressants are most likely to cause constipation

Tricyclic antidepressants (highest risk)

Amitriptyline, nortriptyline, imipramine, dosulepin and clomipramine have the strongest anticholinergic profiles. Constipation is common enough that it should be anticipated and pre-empted, especially in older adults and at higher doses. Note that amitriptyline is very frequently prescribed at low dose for neuropathic pain, migraine prophylaxis and IBS rather than for depression — so you may be experiencing this side effect without thinking of yourself as being "on an antidepressant".

SSRIs (variable, paroxetine highest)

Paroxetine stands apart from the other SSRIs because of its muscarinic receptor affinity, and has been associated with the highest constipation rates in this class.² Fluoxetine, citalopram, escitalopram and sertraline are more commonly linked with nausea and loose stools, particularly sertraline. Some people on SSRIs nonetheless experience constipation, and SSRIs are sometimes deliberately chosen in constipation-predominant IBS precisely because of their prokinetic tendency.

SNRIs

Venlafaxine and duloxetine occupy a middle position. Nausea and dry mouth are the most frequently reported gut effects, with constipation reported at moderate rates, likely reflecting the noradrenergic contribution described above.

Mirtazapine and other agents

Mirtazapine has the most favourable gastrointestinal profile in meta-analysis, mainly associated with increased appetite rather than gut upset.³ Constipation is still listed among its possible effects. Bupropion, agomelatine, vortioxetine and trazodone each have distinct profiles that your prescriber can discuss with you.

Comparative summary

This table summarises general patterns from published tolerability data. Individual responses vary considerably, and it is not a substitute for a discussion with your prescriber.

What to expect: a realistic timeline

Days 1 to 14

Gastrointestinal side effects appear early — usually within the first two weeks — which is precisely when adherence is most fragile. Nausea and appetite change often dominate initially. Constipation may build more gradually as transit slows.

Weeks 2 to 6

Nausea driven by 5-HT3 receptor activation commonly settles within seven to fourteen days as those receptors desensitise. Anticholinergic constipation is less reliably self-limiting: it may improve, but it can also persist while the drug is continued at the same dose. Most clinicians would expect to see improvement by week three or four if the effect is going to settle spontaneously.

Beyond three months

If constipation is still present after three to four weeks despite good first-line measures, it is reasonable to treat it as an established side effect requiring active management — either ongoing laxative therapy, a dose adjustment, or a switch to an agent with a lower anticholinergic burden. Persistent, untreated constipation is a common driver of people stopping effective treatment, which is a far worse outcome than managing the side effect.

How to tell whether the medication is the cause

The single most useful tool is the Bristol Stool Chart, developed at Bristol Royal Infirmary in 1997 and now standard in NHS practice. Types 1 (separate hard lumps) and 2 (lumpy, sausage-shaped) indicate constipation; type 3 or 4 is the target. Our full guide to the Bristol Stool Chart explains how to use it properly.

To build a useful picture for your GP, track for two weeks:

• Frequency — how many bowel movements per week
• Form — Bristol type for each
• Effort — straining, sensation of incomplete emptying, need for manual assistance
• Timing relative to the medication — did symptoms start within days to weeks of starting or increasing the dose?
• Associated anticholinergic symptoms — dry mouth, blurred vision, urinary hesitancy point strongly towards a drug effect
• Other medicines — see below

Other medicines that commonly contribute

Antidepressants are rarely the only factor. Opioid painkillers, calcium-channel blockers, antihistamines, some antipsychotics, aluminium-containing antacids and iron are all recognised contributors. Our guides on iron supplements and constipation, long-term omeprazole effects and metformin and stomach side effects cover the most common culprits. Bring a full medication list, including over-the-counter products, to any review.

Other digestive effects of antidepressants

Constipation is one of a cluster. You may also encounter:

• Nausea — the most common gut side effect of SSRIs and SNRIs, usually settling within two weeks. Taking the dose with food often helps.
• Diarrhoea or loose stools — more typical of sertraline and fluoxetine.
• Dry mouth — very common with TCAs and paroxetine; often accompanies constipation.
• Bloating and trapped wind — slowed transit allows more fermentation time in the colon. See our guides on trapped wind relief and foods that cause bloating.
• Appetite and weight change — in either direction, depending on the agent.
• Reflux and indigestion — reported with several agents; our acid reflux guide may help.

If you have pre-existing IBS, antidepressants can shift your symptom pattern. Our articles on IBS types and supplements for IBS are worth reading alongside this one.

First-line management: diet, fluid, movement and routine

Fibre

UK guidance recommends around 30 g of fibre per day for adults, yet average intake sits well below this. Increase gradually over two to three weeks — a sudden jump often worsens bloating and wind, especially when transit is already slow. Aim for a mix of soluble fibre (oats, psyllium, pulses, apples, linseed) and insoluble fibre (wholegrains, vegetable skins, nuts).

Practical resources: high-fibre foods in the UK, how to increase fibre safely, and the 30 plants a week approach to plant diversity. Fermented and prebiotic foods also play a role — see prebiotic foods and fermented foods.

Fluid

Fibre without adequate fluid can make matters worse, particularly with bulk-forming agents. Aim for six to eight glasses of fluid daily unless you have been advised to restrict fluids. Dry mouth from anticholinergic medication is a helpful prompt — if your mouth is dry, your colon is likely to be too.

Physical activity

Movement stimulates colonic motility. Depression often reduces activity substantially, compounding the drug effect. Even a daily twenty-minute walk makes a measurable difference for many people, and has independent benefits for mood.

Toilet routine and posture

• Respond to the urge rather than deferring it — repeatedly ignoring the call to stool blunts the reflex.
• Use the natural post-meal surge in colonic activity, strongest after breakfast.
• Raise your feet on a low stool so your knees sit above your hips, and avoid straining.
• Allow unhurried time; rushing is counterproductive.

Sleep and stress

Bowel function is closely tied to circadian rhythm and autonomic balance. Our guides on gut health and sleep and the vagus nerve and the gut explain why sleep disruption and sustained stress slow transit, and what can be done about it.

Laxatives: the NHS stepped approach

NICE Clinical Knowledge Summaries set out a stepped approach for adults, adjusted according to whether stools are hard or simply difficult to pass.⁸

Laxatives should be continued until stools are consistently soft and easy to pass, then reduced gradually rather than stopped abruptly. If two laxatives from different classes at maximum tolerated doses have failed over an adequate period, your GP may consider referral or prescription-only options such as prucalopride or linaclotide. Always check with a pharmacist before combining laxatives with other medicines.

Supplements and gut support

Supplements are an adjunct to — not a replacement for — the measures above, and they do not treat depression. Discuss anything new with your GP or pharmacist, because interactions with antidepressants are a genuine consideration.

Magnesium

Magnesium salts, particularly magnesium citrate and magnesium hydroxide, have an osmotic effect that draws water into the bowel. Magnesium is one of the more commonly used self-care options for occasional constipation. Caution is needed in kidney impairment, and magnesium can interact with certain medicines. Our guide to magnesium for constipation covers forms, dosing considerations and safety.

Probiotics

A 2022 systematic review and meta-analysis of 30 randomised controlled trials found that 57% of participants responded to probiotic treatment compared with 44% on control (RR 1.28, 95% CI 1.07–1.52), with a significant improvement in stool frequency. The effect was driven largely by Bifidobacterium lactis; probiotic mixtures did not show the same benefit, and stool consistency was not significantly changed.⁹ An earlier meta-analysis reported a reduction in whole gut transit time of 12.4 hours and an increase of 1.3 bowel movements per week.¹⁰

The evidence is therefore modest and strain-specific rather than transformative. If you want to try one, our guides on how to choose a probiotic, the best probiotics in the UK, when to take probiotics and probiotic side effects will help you choose sensibly, and our do probiotics work article gives a balanced appraisal of the evidence. You can browse the full Welzo probiotics range. Those interested in next-generation strains may want to read about Akkermansia versus conventional probiotics before considering Welzo Akkermansia.

Fibre supplements

Psyllium husk is the best-evidenced fibre supplement for constipation and is generally better tolerated than inulin in people prone to bloating — our psyllium versus inulin comparison explains why. Pectin is a soluble fibre that is fermented to short-chain fatty acids in the colon; Welzo Citrus Pectin Powder is one option, and our prebiotic supplement guide compares the main choices. Introduce any fibre supplement slowly and with plenty of water.

Supplements requiring particular caution

Two popular gut supplements deserve specific mention for anyone on antidepressants:

• Berberine — Welzo Ultra Purity Berberine is used mainly for metabolic and microbial support, but berberine inhibits several cytochrome P450 enzymes and can therefore affect the metabolism of other drugs, including some antidepressants. Read our berberine interactions guide and speak to your pharmacist before combining.
• TUDCA — Welzo Ultra Purity TUDCA is a bile acid used for liver and biliary support. Bile acids influence stool form in both directions, and our TUDCA side effects article outlines what to watch for.

Our general guide to probiotic safety is also relevant for anyone who is immunocompromised or seriously unwell.

Talking to your prescriber about switching

Do not stop or reduce your antidepressant on your own. Abrupt discontinuation can produce withdrawal symptoms and risks relapse of the condition being treated. If constipation is severe, persistent beyond three to four weeks, or affecting your willingness to continue treatment, that is a legitimate and important reason to book a review.

Options your prescriber may consider include:

• Dose review — anticholinergic effects are often dose-related.
• Timing changes — occasionally helpful for tolerability, though less so for constipation than for nausea or sedation.
• Adding a laxative — often the pragmatic first step when the antidepressant is working well for mood.
• Switching agents — moving from a tricyclic or paroxetine to an agent with lower anticholinergic burden. NICE guidance on depression in adults supports shared decision-making about tolerability when choosing and reviewing treatment.¹¹
• Reviewing the whole medication list — often the highest-yield step.

You can also report suspected side effects yourself through the MHRA Yellow Card scheme, which contributes to national medicines safety monitoring.¹²

Red flags: when to seek medical help

Contact your GP promptly, or seek urgent care, if you experience:

• Blood in the stool, or black, tarry stools
• Unexplained weight loss
• A persistent change in bowel habit, particularly over the age of 50
• Severe abdominal pain, vomiting, or marked abdominal distension (possible obstruction)
• No bowel movement for several days despite laxatives, especially with abdominal swelling
• A family history of bowel cancer or inflammatory bowel disease alongside new symptoms
• Iron deficiency anaemia

Severe anticholinergic constipation can, rarely, progress to acute colonic pseudo-obstruction. This is uncommon but is a recognised complication and is why persistent, severe constipation on a tricyclic should never simply be tolerated. Our guides on when to see a GP about stomach symptoms and bowel cancer screening in the UK explain the assessment pathway.

Special groups and situations

Older adults

Anticholinergic burden accumulates with polypharmacy, and older adults are more susceptible to constipation, urinary retention and confusion. Tricyclics are generally avoided where possible in this group. See our guide to gut health in older adults.

People with IBS

Low-dose tricyclics are used deliberately in diarrhoea-predominant IBS, while SSRIs are sometimes favoured in constipation-predominant IBS. Dietary approaches such as the low FODMAP diet should be undertaken with dietetic support, particularly alongside medication changes.

Pregnancy and breastfeeding

Both constipation and antidepressant use are common in pregnancy, and laxative choice is restricted. This requires individual specialist advice — do not self-treat.

Anxiety and the gut

Many people taking antidepressants are treating anxiety rather than depression, and anxiety has its own strong effects on gut motility. Our article on probiotics for anxiety reviews the emerging evidence on the microbiota–gut–brain axis.

Testing and investigations

Most antidepressant-related constipation needs no investigation beyond a careful history, medication review and examination. Where symptoms are atypical, persistent or accompanied by red flags, your GP may arrange blood tests (including thyroid function, calcium and full blood count), a faecal immunochemical test, or referral. Our guides on the gut health blood test and gut microbiome testing in the UK explain what these tests can and cannot tell you — microbiome tests in particular are not diagnostic and should not replace clinical assessment.

Frequently asked questions

Do antidepressants cause constipation?

Yes. Constipation is a recognised side effect, reported in roughly 11% to 12.5% of people in clinical trials, with about 4.7% finding it bothersome. Tricyclic antidepressants and paroxetine carry the highest risk because they block muscarinic acetylcholine receptors in the gut wall, slowing colonic transit.

How long does constipation from antidepressants last?

Many cases improve within two to four weeks as the body adapts. Anticholinergic constipation is less reliably self-limiting than antidepressant-related nausea, which usually settles within seven to fourteen days. If constipation persists beyond three to four weeks despite dietary and lifestyle measures, arrange a medication review.

Which antidepressant is least likely to cause constipation?

In meta-analysis, mirtazapine had the fewest gastrointestinal side effects overall, being mainly associated with increased appetite. Among SSRIs, sertraline and escitalopram are more often linked with loose stools than constipation. The right choice depends on your full clinical picture, so this is a conversation for your prescriber rather than a decision to make alone.

Can I take laxatives with my antidepressant?

Generally yes, and this is often the most practical solution when the antidepressant is working well. Osmotic laxatives such as macrogol are commonly used first-line for chronic constipation, with a stimulant added if stools are soft but still difficult to pass. Check with a pharmacist, as some laxatives can affect the absorption of other medicines if taken at the same time.

Will probiotics help constipation caused by antidepressants?

Possibly, but modestly. Meta-analysis found 57% of people responded to probiotics versus 44% on control, with improvements in stool frequency driven mainly by Bifidobacterium lactis strains. Probiotics are best regarded as an adjunct to fibre, fluid, movement and, where needed, laxatives — not a replacement for them.

Should I stop my antidepressant because of constipation?

No — not without medical advice. Stopping abruptly can cause discontinuation symptoms and risks relapse of depression or anxiety. Constipation is almost always manageable while continuing treatment. If it is not, your prescriber can discuss a dose change or a switch to a different agent.

Why does amitriptyline cause constipation more than other antidepressants?

Amitriptyline is a tricyclic with strong anticholinergic activity, blocking M2 and M3 muscarinic receptors on intestinal smooth muscle and reducing peristalsis. Laboratory research has also shown that tricyclics inhibit TRPC4 ion channels in colonic muscle cells, directly suppressing contractions. This dual action is why constipation is so characteristic of this class.

Can antidepressants change my gut bacteria?

Laboratory studies suggest they can. A Nature screen of over 1,000 drugs found 24% of human-targeted medicines inhibited the growth of at least one gut bacterial strain in vitro, and antidepressants specifically have shown antimicrobial activity against gut commensals in test-tube studies. Whether this translates into clinically meaningful changes in people is not yet established.

Does magnesium help with antidepressant-induced constipation?

Magnesium salts such as magnesium citrate and magnesium hydroxide have an osmotic laxative effect. They are widely used for occasional constipation, but should be used cautiously in kidney impairment and can interact with some medicines, so check with a pharmacist first.

When should I see a doctor about constipation on antidepressants?

See your GP if constipation persists beyond three to four weeks despite first-line measures, if it is severe, or at any point if you notice red flags: blood in the stool, unexplained weight loss, severe abdominal pain or vomiting, a persistent change in bowel habit over the age of 50, or no bowel movement for several days with abdominal swelling.

About the author

Dr Zeeshan Afzal (MBBS) is a UK-registered medical doctor and Medical Content Lead at Welzo. He reviews Welzo's digestive health content for clinical accuracy against current NHS, NICE and peer-reviewed sources.

Medical disclaimer

This article is for general information and does not constitute medical advice, diagnosis or treatment. It is not a substitute for consultation with a qualified healthcare professional. Never stop, start or change a prescribed medicine on the basis of information found online. If you have concerns about your medication or your bowel symptoms, speak to your GP, pharmacist or prescribing clinician. If you are experiencing a medical emergency, call 999 or attend your nearest emergency department.

References

1. NHS Business Services Authority. Medicines used in mental health – England – 2015/16 to 2024/25.
2. Kelly K, Posternak M, Alpert JE. Toward achieving optimal response: understanding and managing antidepressant side effects. Dialogues in Clinical Neuroscience. PMC3181894.
3. Oliva V, et al. Gastrointestinal side effects associated with antidepressant treatments in patients with major depressive disorder: a systematic review and meta-analysis. PubMed 33549697.
4. Oliva V, et al. (full text discussion of enteric serotonin and gastrointestinal motility). ScienceDirect.
5. Jeong B, et al. Inhibition of TRPC4 channel activity in colonic myocytes by tricyclic antidepressants disrupts colonic motility causing constipation. Journal of Cellular and Molecular Medicine, 2022. PMC9549500.
6. Maier L, et al. Extensive impact of non-antibiotic drugs on human gut bacteria. Nature, 2018. nature.com.
7. Ait Chait Y, et al. Unravelling the antimicrobial action of antidepressants on gut commensal microbes. Scientific Reports, 2020. nature.com.
8. NICE Clinical Knowledge Summaries. Constipation.
9. van der Schoot A, et al. Probiotics and synbiotics in chronic constipation in adults: a systematic review and meta-analysis of randomised controlled trials. Clinical Nutrition, 2022. PubMed 36372047.
10. Dimidi E, et al. The effect of probiotics on functional constipation in adults: a systematic review and meta-analysis of randomised controlled trials. American Journal of Clinical Nutrition. ScienceDirect.
11. National Institute for Health and Care Excellence. Depression in adults: treatment and management (NG222).
12. Medicines and Healthcare products Regulatory Agency. Yellow Card scheme.
13. NHS. Selective serotonin reuptake inhibitors (SSRIs).
14. NHS. Constipation.
15. Harvard Health Publishing. What to do when medication makes you constipated.
16. Mayo Clinic. Antidepressants: get tips to cope with side effects.

Image credits

All images are used under free licences and are not subject to commercial stock copyright.

• Digestive system diagram — BruceBlaus, Blausen Medical, via Wikimedia Commons, CC BY 3.0.
• Gut–brain axis diagram — via Wikimedia Commons, CC BY-SA 4.0.
• Fluoxetine capsules — via Wikimedia Commons, free licence.
• Bristol Stool Chart — Kyle Thompson, via Wikimedia Commons, CC BY-SA 3.0.
• Large intestine anatomy — BruceBlaus, Blausen Medical, via Wikimedia Commons, CC BY 3.0.
• Fruit, vegetables and grains — National Cancer Institute (NCI Visuals Online), public domain.