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Citalopram is one of the most prescribed antidepressants worldwide, including in the UK (1). It belongs to the SSRI (Selective Serotonin Reuptake Inhibitor) family of drugs, which were developed as a safer and more tolerable alternative to older antidepressants like MAOIs (Monoamine Oxidase Inhibitors) and TCAs (Tricyclic Antidepressants).
In practice, however, the differences between these drug classes can be more theoretical than clear-cut. While SSRIs tend to have better tolerability and lower dropout rates, they also come with their own distinct side effects—particularly gastrointestinal and cardiovascular—which makes direct comparisons with MAOIs and TCAs complex (2, 3).
Since all types of antidepressants carry a risk of side effects, the role of pharmacogenomic testing is becoming increasingly important in helping to tailor treatment to the individual.
Pharmacogenomic (PGx) testing can help predict how you might respond to citalopram, a commonly prescribed SSRI used to treat depression and anxiety. Genetic differences in how your body processes medications can affect both how well the drug works and the likelihood of side effects. Understanding these variations allows for more personalised—and safer—prescribing decisions.
If you're taking other medications or supplements—especially those that increase serotonin levels, like tryptophan or St. John’s Wort—it's important to let your GP or pharmacist know. Combining citalopram with these substances can increase serotonin levels too much and may lead to a serious condition known as serotonin syndrome (3).
SSRIs, including citalopram, have been associated with an increased risk of suicidal thoughts during the first four weeks of treatment (2, 10, 11). This is especially important for children, adolescents, and their carers to be aware of. These symptoms usually wear off over time, and the treatment often becomes very effective.
Explore PGX for Mental HealthCitalopram for mood and anxiety
Citalopram is commonly prescribed to help manage mood and anxiety-related conditions. It belongs to a class of antidepressants known as SSRIs (Selective Serotonin Reuptake Inhibitors), which work by increasing serotonin levels in the brain—a chemical linked to mood regulation.
Your doctor may have recommended citalopram to treat conditions such as (5):
Depressive illness
Panic disorder
How and when to take it
For Depressive Illness
Adults: Start with 20 mg once daily. This can be increased up to a maximum of 40 mg per day, usually adjusted at 3–4 week intervals (4).
Elderly: Typically 10–20 mg once daily, with a maximum of 20 mg per day (4).
If you're using oral drops:
Adults: Start with 16 mg once daily. The dose may be increased up to 32 mg per day at 3–4 week intervals (4).
Elderly: 8–16 mg daily, with a maximum of 16 mg.
For Panic Disorder
Adults: Start with 10 mg once daily. The usual dose is 20–30 mg, with a maximum of 40 mg per day (4).
Elderly: Start with 10 mg daily, with a maximum of 20 mg.
If you're using oral drops:
Adults: Start with 8 mg daily. The usual dose is 16–24 mg daily, with a maximum of 32 mg (4).
Elderly: Start with 8 mg daily, with a maximum of 16 mg per day.
SSRIs like citalopram are generally considered safe, but some people may be more prone to serious side effects due to genetic differences. Pharmacogenomic (PGx) testing can help identify individuals at higher risk of rare but important reactions such as serotonin syndrome, prolonged QT interval, or hyponatremia. These complex syndromes are more commonly associated with SSRIs than with older antidepressants, so it’s important to be aware of the signs and seek medical attention if they arise.
Serotonin syndrome (5) is a potentially serious and fast-developing condition. It can begin within one hour of starting a new medicine or drug combination in about 30% of cases—or within six hours in 60% of cases. The symptoms relate to changes in brain function, muscle reflexes, and automatic body functions:
Brain function: Agitation, confusion, anxiety, hypomania, hypervigilance, seizures, or coma
Muscle reflexes: Tremors, poor coordination, myoclonus (involuntary rhythmic jerks)
Autonomic functions: Sweating, fast heart rate, diarrhoea, fever, or dangerously high body temperature (over 40°C)
You don’t need to have all of these symptoms to be diagnosed with serotonin syndrome. While some cases are mild, the condition can become life-threatening and must be treated urgently.
Citalopram is one of the SSRIs most strongly associated with prolonged QT interval, a heart rhythm disturbance (2, 3). Symptoms may include:
Palpitations
Feeling faint or actually fainting
Light-headedness
Weakness
In some cases, seizures
Risk factors for prolonged QT interval (7) include:
Female sex
Older age
Recent conversion from atrial fibrillation using QT-prolonging drugs
Taking multiple medications that prolong QT interval
Electrolyte imbalances (e.g. low potassium, magnesium, or calcium)
Diuretic use
Liver or kidney dysfunction
Slow heart rate (bradycardia)
Genetic predisposition (e.g. silent long QT syndrome)
Underlying heart disease (heart failure, previous heart attack, or thickened heart muscle)
Digitalis therapy
If you experience symptoms of a prolonged QT interval, seek immediate medical attention.
Hyponatremia (8) is a condition where sodium levels in the blood drop too low, which can happen with SSRIs like citalopram. Symptoms vary depending on how quickly and how severely sodium levels fall.
Severe cases can cause brain swelling (oedema), leading to vomiting, reduced consciousness, or coma.
Milder cases may cause mood changes, confusion, or unusual behaviour.
Even mild hyponatremia can be dangerous and should be addressed quickly.
If you notice any of these symptoms, contact a healthcare provider without delay.
Apart from rare but serious side effects, citalopram may also cause more common reactions, which vary from person to person. These can include:
Anxiety
Changes in appetite (increase or decrease)
Joint pain
Chronic fatigue
Difficulty concentrating
Dry mouth
Pharmacogenomic differences may partly explain why some people experience these symptoms more strongly than others.
Explore PGX for Mental HealthCitalopram’s journey through the body—how it’s absorbed, distributed, metabolised, and eliminated—is influenced by both your biology and your genes (12). These areas of research, known as pharmacokinetics and pharmacogenetics, help explain why people can respond differently to the same antidepressant.
People with CYP2C19 gene variants may need dose adjustments or an alternative medication. Pharmacogenomic testing can help reduce the trial-and-error period, improving treatment outcomes and lowering the risk of side effects.
Citalopram is absorbed in the gastrointestinal tract and reaches peak levels in the blood within 2 to 4 hours after oral administration. Genetic variations in the ABCB1 gene—which controls how substances cross the blood-brain barrier—can influence how much citalopram reaches its target in the brain.
Citalopram is mainly broken down (metabolised) by an enzyme called CYP2C19, part of the cytochrome P450 family. Genetic differences in this enzyme affect how quickly your body processes the medication:
Ultra-rapid metabolisers may clear the drug too quickly, reducing its effectiveness.
Poor metabolisers may build up higher levels of the drug, increasing the risk of side effects like nausea, dizziness, or QT prolongation.
A secondary enzyme, CYP3A4, also plays a role in citalopram metabolism and may contribute to individual differences in response.
Citalopram is eliminated mainly through the kidneys. Genetic factors affecting kidney function can alter how quickly the drug is cleared from the body—particularly in people with kidney disease or inherited differences in renal processing.
Your genetic makeup can influence how well citalopram works for you and how likely you are to experience side effects. One key gene involved is CYP2C19, which plays a major role in how citalopram is metabolised in the liver.
People with reduced CYP2C19 function may process the drug more slowly, leading to higher levels in the body and a greater risk of side effects like QT interval prolongation.
Those with ultra-rapid metabolism may break the drug down too quickly, which can make it less effective at treating depression or anxiety.
Knowing your CYP2C19 status through pharmacogenomic testing can help your doctor tailor your prescription—choosing the right dose or even a different medication to improve outcomes and reduce risks.
Other antidepressants are also influenced by genetic variations in CYP2C19 or related enzymes. This includes:
Escitalopram – another SSRI closely related to citalopram, also influenced by CYP2C19
Sertraline – an SSRI with moderate dependence on CYP pathways
Amitriptyline – a tricyclic antidepressant affected by both CYP2C19 and CYP2D6
Paroxetine – mainly metabolised by CYP2D6, another enzyme involved in antidepressant response
Pharmacogenomic testing can guide safer and more effective choices across this wider group of medications.
Explore PGX for Mental Health1. https://pmc.ncbi.nlm.nih.gov/articles/PMC8684293/#:~:text=The%20selective%20serotonin%20reuptake%20inhibitor 2. https://pmc.ncbi.nlm.nih.gov/articles/PMC5972123/ 3. https://pmc.ncbi.nlm.nih.gov/articles/PMC8395812/ 4. https://www.nice.org.uk/about/what-we-do/evidence-and-best-practice-resources/british-national-formulary--bnf 5. https://pmc.ncbi.nlm.nih.gov/articles/PMC6539562/ 6. https://www.mayoclinic.org/diseases-conditions/long-qt-syndrome/symptoms-causes/syc-20352518 7. https://pmc.ncbi.nlm.nih.gov/articles/PMC4110870/ 8. https://pmc.ncbi.nlm.nih.gov/articles/PMC10502587/ 9. https://scholar.google.pl/scholar?q=Psychiatric+Aspects+of+Hyponatremia+%E2%80%93+A+Clinical+Approach&hl=en&as_sdt=0&as_vis=1&oi=scholart 10. https://pmc.ncbi.nlm.nih.gov/articles/PMC8882171/ 11. https://www.mdpi.com/1424-8247/17/12/1714 12. https://pmc.ncbi.nlm.nih.gov/articles/PMC3349993/ 13. https://pmc.ncbi.nlm.nih.gov/articles/PMC11744214/ 14. https://www.researchgate.net/publication/232074249_Antidepressants_Pharmacological_profile_and_clinical_consequences 15. https://www.sciencedirect.com/science/article/pii/S2666915322000816 16. https://pmc.ncbi.nlm.nih.gov/articles/PMC4047306/ 17. https://www.mdpi.com/2079-7737/14/4/336 18. https://pmc.ncbi.nlm.nih.gov/articles/PMC3726062/ 19. https://pmc.ncbi.nlm.nih.gov/articles/PMC8254768/ 20. https://pmc.ncbi.nlm.nih.gov/articles/PMC5600671/ 21. https://pmc.ncbi.nlm.nih.gov/articles/PMC9628301/ 22. https://pmc.ncbi.nlm.nih.gov/articles/PMC8773150/ 23. https://pmc.ncbi.nlm.nih.gov/articles/PMC7008964/ 24. https://pmc.ncbi.nlm.nih.gov/articles/PMC4512908/ 25. https://pmc.ncbi.nlm.nih.gov/articles/PMC5044489/ 26. https://www.mdpi.com/1424-8247/17/3/280 27. https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2024.1412420/full 28. https://www.researchgate.net/publication/7988732_Side-Effect_Profile_of_Fluoxetine_in_Comparison_with_Other_SSRIs_Tricyclic_and_Newer_Antidepressants_A_Meta-Analysis_of_Clinical_Trial_Data 29. https://www.researchgate.net/publication/7510625_Drug_interactions_and_fluoxetine_A_commentary_from_a_clinician's_perspective 30. https://pmc.ncbi.nlm.nih.gov/articles/PMC10197723/ 31. https://www.researchgate.net/publication/8546695_Escitalopram_versus_citalopram_The_surprising_role_of_the_R-enantiomer 32. https://pmc.ncbi.nlm.nih.gov/articles/PMC10675869/ 33. https://pubmed.ncbi.nlm.nih.gov/17375980/