Olanzapine

What it is

Olanzapine is a synthetic thienobenzodiazepine, taken as a tablet, an orally disintegrating tablet, a short-acting intramuscular injection or a long-acting injection. It is a second-generation or “atypical” antipsychotic, and in the United States it is also sold combined with fluoxetine. It is cleared mainly by the liver, and its clearance is about 40% higher in smokers than in non-smokers.

What the research says

It reduces the symptoms of psychosis and mania, and the randomised evidence for that is strong. In a network meta-analysis of 212 trials and 43,049 participants, olanzapine was among the more effective antipsychotics (standardised mean difference 0.59 versus placebo), and in a meta-analysis of 65 relapse-prevention trials antipsychotics as a class cut one-year relapse from 64% to 27%. The same analyses show it is also the worst of the 15 drugs for weight gain, and the label's pooled data put a 7% or greater weight gain at 22.2% on olanzapine against 3% on placebo. It carries a boxed warning about increased death in elderly people with dementia-related psychosis. Off-label it is well supported for chemotherapy-induced nausea and poorly supported for anorexia nervosa.

Evidence grade: Well established.

How it works

Drug class: Second-generation (atypical) antipsychotic; a thienobenzodiazepine acting mainly as a dopamine D2 and serotonin 5-HT2 antagonist

Olanzapine blocks several brain receptors at once, most importantly dopamine D2 and serotonin 5-HT2 receptors. Blocking dopamine signalling is thought to be what reduces hallucinations, delusions and mania. It also blocks histamine, muscarinic and alpha-1 adrenergic receptors, which is the likely reason for the sedation, dry mouth and drops in blood pressure on standing. The manufacturer's own label is candid that the mechanism is not actually established. (Source 1)

Boxed warning

WARNING: INCREASED MORTALITY IN ELDERLY PATIENTS WITH DEMENTIA-RELATED PSYCHOSIS

(Source 2)

What it is used for

• Olanzapine beats placebo for acute symptoms and for preventing relapse. In the largest network meta-analysis its effect size versus placebo was 0.59, third of 15 drugs. In the CATIE effectiveness trial it had the longest time to discontinuation for any cause, though 64% of those assigned to it still stopped within 18 months. Evidence: established. (Source 3)
• Approved on three trials for acute episodes and one monotherapy maintenance trial. A Cochrane review of five long-term trials found olanzapine monotherapy reduced relapse versus placebo (RR 0.58) and was better than lithium at preventing manic relapse, but with more weight gain and more depression than lithium; its authors judged the evidence stronger for lithium as first-line maintenance. Evidence: established. (Source 4)
• The label is explicit that olanzapine on its own is not indicated for either of these; the approval is for the combination with fluoxetine, and the supporting clinical studies sit in the Symbyax label rather than this one. We did not retrieve those trials, so this entry records the regulator's position and not the underlying evidence. Evidence: limited. (Source 5)
• An approved use for the short-acting injection. The label reports somnolence in 6% on intramuscular olanzapine versus 3% on placebo during the 24-hour treatment period. We did not retrieve an independent systematic review for this use. Evidence: limited. (Source 6)
• This is the best-supported off-label use. A Cochrane review found olanzapine added to standard antiemetics roughly doubled the chance of having no nausea or vomiting, from 25% to 50%, with a number needed to treat of 5 and moderate-quality evidence. A 380-patient NEJM trial found no nausea in 74% versus 45% in the first 24 hours. The cost is sedation. Evidence: established. (Source 7)
• A 2026 systematic review found seven randomised trials in 152 patients; the meta-analysis of four trials in 91 patients gave a BMI difference of 1.68 kg/m2 favouring olanzapine that was not statistically significant, with very high heterogeneity. The authors call the evidence inconclusive. Evidence: disputed. (Source 8)

Interactions

• Alcohol (pharmacokinetic study): Alcohol does not change olanzapine blood levels, but taken together they make blood pressure drop further on standing, so faintness and falls become likelier. The label also advises caution with centrally acting drugs and alcohol generally. (Source 9)
• Activated charcoal (sold as a supplement and used in overdose) (pharmacokinetic study): A single gram of activated charcoal cut the amount of olanzapine absorbed by roughly 60%. Useful deliberately in overdose, but it means charcoal taken for other reasons can strip out a dose. (Source 10)
• Aluminium- and magnesium-containing antacids, and cimetidine (pharmacokinetic study): Tested and found not to matter: single doses of these antacids did not change how much olanzapine was absorbed. (Source 9)
• Tobacco smoking (pharmacokinetic study): Smoking speeds up the liver enzyme that clears olanzapine, so smokers clear it about 40% faster and reach lower levels on the same dose; stopping smoking can push levels up. (Source 11)
• Carbamazepine (pharmacokinetic study): Carbamazepine induces CYP1A2 and increases olanzapine clearance by around half, so olanzapine levels fall. (Source 9)
• Fluvoxamine (pharmacokinetic study): Fluvoxamine blocks the main enzyme that clears olanzapine, raising peak levels by 54% in female non-smokers and 77% in male smokers. (Source 12)
• Other drugs with anticholinergic (antimuscarinic) activity (label): Combining olanzapine with other anticholinergic drugs raises the risk of the gut slowing to a standstill, which can be serious. (Source 10)
• Blood pressure medicines, and levodopa or dopamine agonists (label): Olanzapine can lower blood pressure further on top of antihypertensives, and because it blocks dopamine receptors it can work against levodopa and dopamine agonists used in Parkinson's disease. (Source 13)

Stopping it

• Olanzapine is not a drug of dependence in the usual sense. In animal studies designed to look for it, olanzapine showed little or no potential for abuse or physical dependence, and the label states it has not been systematically studied in humans for abuse, tolerance or physical dependence. (Source 14)
• The real risk of stopping is relapse, and it is large. In 12 randomised trials in 1,133 adults with stabilised first-episode psychosis, 53.3% of those who discontinued relapsed by 12 months against 21.0% who continued, an absolute risk reduction of 32 percentage points from staying on treatment. (Source 15)
• Across 65 relapse-prevention trials, whether the drug was withdrawn abruptly or gradually made no significant difference to relapse risk, and the drug-placebo gap narrowed the longer the study ran. (Source 16)
• Tardive dyskinesia can improve after the drug is withdrawn, but it can also first appear after stopping, and continuing the drug can mask it. (Source 17)

What goes wrong

Antipsychotics including olanzapine increase death in elderly people with dementia-related psychosis; this is the boxed warning. (Source 2)

• Meta-analysis, Certainty not rated.
• Size: seventeen placebo-controlled trials.
• Who: elderly patients with dementia-related psychosis, largely taking atypical antipsychotics.
• How long: modal duration 10 weeks.
• Result: risk of death 1.6 to 1.7 times that on placebo; about 4.5% died on drug versus about 2.6% on placebo over a typical 10-week trial, an absolute difference of roughly 1.9 percentage points.
• Funding: not stated (FDA analysis reproduced in the label)

Over the course of a typical 10-week controlled trial, the rate of death in drug-treated patients was about 4.5%, compared to a rate of about 2.6% in the placebo group.

Clinically significant weight gain is far commoner on olanzapine than on placebo, and keeps going with long-term use. (Source 18)

• Meta-analysis, Certainty not rated.
• Size: 13 placebo-controlled monotherapy studies for the short-term figures; 2,021 patients for the long-term figure; 86 clinical trials pooled for the weight-gain table.
• Who: adults treated with olanzapine monotherapy.
• How long: median exposure 6 weeks short-term; at least 48 weeks long-term (median 573 days)
• Result: mean gain 2.6 kg versus 0.3 kg loss on placebo; ≥7% baseline weight gained by 22.2% versus 3% on placebo; ≥15% by 4.2% versus 0.3%; in long-term studies mean gain 5.6 kg and 64%, 32% and 12% gained at least 7%, 15% and 25% respectively.
• Funding: not stated (manufacturer's pooled trial data)

22.2% of olanzapine-treated patients gained at least 7% of their baseline weight, compared to 3% of placebo-treated patients, with a median exposure to event of 8 weeks

Across fifteen antipsychotics, olanzapine was the worst for weight gain. (Source 3)

• Meta-analysis, Certainty not rated.
• Size: 212 trials with data for 43,049 participants.
• Who: people with schizophrenia in acute treatment.
• How long: acute-phase trials.
• Result: standardised mean difference versus placebo for weight gain ranged from -0.09 for haloperidol to -0.74 for olanzapine.
• Funding: independent — the paper's stated funding is None.

Standardised mean differences compared with placebo for weight gain varied from -0·09 for the best drug (haloperidol) to -0·74 for the worst drug (olanzapine)

Sedation and dizziness are substantially commoner on olanzapine than placebo in short-term trials. (Source 19)

• Randomized trial, Certainty not rated.
• Size: 532 olanzapine and 294 placebo patients.
• Who: patients in the acute phase of short-term placebo-controlled trials of oral olanzapine at doses ≥2.5 mg/day.
• How long: short-term acute-phase trials.
• Result: somnolence 29% versus 13%, dizziness 11% versus 4%, abnormal gait 6% versus 1%, dry mouth 9% versus 5%, constipation 9% versus 4%.
• Funding: not stated (manufacturer-submitted registration data)

Somnolence 29 13 Insomnia 12 11 Dizziness 11 4 Abnormal gait 6 1

Olanzapine used as an antiemetic probably increases somnolence and fatigue. (Source 7)

• Systematic review, Moderate certainty.
• Size: 464 participants across 5 studies.
• Who: adults with cancer receiving olanzapine as an antiemetic.
• How long: chemotherapy cycles.
• Result: somnolence and fatigue RR 2.33, 95% CI 1.30 to 4.18; anticipated absolute risk 8.2% more, 95% CI 1.9 to 18.8.
• Funding: independent (Cochrane review)

probably increases somnolence and fatigue compared to no treatment or placebo (RR 2.33, 95% CI 1.30 to 4.18; anticipated absolute risk 8.2% more, 95% CI 1.9 to 18.8; 464 participants; 5 studies; moderate-quality evidence)

Antipsychotics can cause tardive dyskinesia, a movement disorder that may be permanent. (Source 17)

• Official position, Certainty not rated.
• Size: not applicable — a label safety statement.
• Who: patients treated with antipsychotic drugs; prevalence appears highest among the elderly, especially elderly women.
• How long: risk believed to rise with duration and cumulative dose.
• Result: no rate given for olanzapine specifically; the label states it is unknown whether antipsychotics differ in their potential to cause it.
• Funding: not applicable (regulatory document)

A syndrome of potentially irreversible, involuntary, dyskinetic movements may develop in patients treated with antipsychotic drugs.

Stopping an antipsychotic after a first episode of psychosis roughly doubles relapse within a year. (Source 15)

• Meta-analysis, Certainty not rated.
• Size: 12 RCTs including 1,133 adults (60.1% male; mean age 27.3 years)
• Who: adults with stabilised first-episode non-affective psychosis.
• How long: matched time points from 1 to 24 months.
• Result: relapse at 12 months 21.0% on maintenance versus 53.3% on discontinuation; RR 0.45, 95% CI 0.35-0.57, p < 0.001, I2 = 11.1%; absolute risk reduction 6.0% at 2 months rising to 32.0% at 12 months.
• Funding: not stated in the abstract.

Relapse rates at 12 months were 21.0% and 53.3% in the maintenance and discontinuation groups, respectively.

What the evidence supports

Olanzapine was more effective than placebo for acute schizophrenia symptoms and ranked third of fifteen antipsychotics. (Source 3)

• Meta-analysis, Certainty not rated.
• Size: 212 trials with data for 43,049 participants.
• Who: people with schizophrenia or related disorders in acute treatment, excluding predominant negative symptoms, concomitant medical illness, treatment resistance and stable patients.
• How long: acute-phase trials.
• Result: standardised mean difference versus placebo 0.59, 95% credible interval 0.53-0.65, behind clozapine 0.88 and amisulpride 0.66.
• Funding: independent — the paper's stated funding is None.

All drugs were significantly more effective than placebo. The standardised mean differences with 95% credible intervals were: clozapine 0·88, 0·73-1·03; amisulpride 0·66, 0·53-0·78; olanzapine 0·59, 0·53-0·65

Continuing an antipsychotic after stabilisation cut one-year relapse from 64% to 27%. (Source 20)

• Meta-analysis, Certainty not rated.
• Size: 116 reports from 65 trials, 6,493 patients.
• Who: people with schizophrenia stabilised on an antipsychotic, then continued or withdrawn.
• How long: relapse between 7 and 12 months.
• Result: relapse 27% on drug versus 64% on placebo; RR 0.40, 95% CI 0.33-0.49; number needed to treat to benefit 3, 95% CI 2-3; readmission 10% versus 26%, NNTB 5.
• Funding: German Ministry of Education and Research.

Limit of this finding: One number in this passage is impossible as printed: the weight-gain risk ratio is given as "RR 2·07, 95% CI 2·31-3·25", and a confidence interval cannot exclude its own point estimate. The interval as published is wrong somewhere. The relapse figures quoted here are unaffected, but do not read the weight-gain interval in the same passage as a reliable estimate.

Antipsychotic drugs significantly reduced relapse rates at 1 year (drugs 27%vs placebo 64%; risk ratio [RR] 0·40, 95% CI 0·33-0·49; number needed to treat to benefit [NNTB] 3, 95% CI 2-3).

In a head-to-head effectiveness trial against four other antipsychotics, olanzapine had the longest time before patients stopped taking it. (Source 21)

• Randomized trial, Certainty not rated.
• Size: 1,493 patients randomised at 57 US sites; 1,432 received at least one dose.
• Who: adults with chronic schizophrenia.
• How long: up to 18 months.
• Result: discontinuation for any cause 64% on olanzapine versus 75% perphenazine, 82% quetiapine, 74% risperidone, 79% ziprasidone; time to discontinuation significantly longer than quetiapine (P<0.001) and risperidone (P=0.002)
• Funding: publicly funded (NIMH CATIE trial)

The time to the discontinuation of treatment for any cause was significantly longer in the olanzapine group than in the quetiapine (P<0.001) or risperidone (P=0.002) group, but not in the perphenazine (P=0.021) or ziprasidone (P=0.028) group.

Added to standard antiemetics, olanzapine roughly doubled the chance of getting through chemotherapy without nausea or vomiting. (Source 7)

• Systematic review, Moderate certainty.
• Size: 561 participants across 3 studies for the primary outcome, within a review of 14 RCTs and 1,917 participants.
• Who: adults with solid tumours having highly or moderately emetogenic chemotherapy.
• How long: chemotherapy cycles; most studies dosed over several days.
• Result: no nausea or vomiting rose from 25% to 50%; RR 1.98, 95% CI 1.59 to 2.47; number needed to treat for an additional beneficial outcome 5, 95% CI 3.3 to 6.6.
• Funding: independent (Cochrane review)

Olanzapine probably doubles the likelihood of no nausea or vomiting during chemotherapy from 25% to 50% (risk ratio (RR) 1.98, 95% confidence interval (CI) 1.59 to 2.47; 561 participants; 3 studies; solid tumours; HEC or MEC therapy; moderate-quality evidence) when added to standard therapy.

In a placebo-controlled phase 3 trial, olanzapine added to a three-drug antiemetic regimen markedly increased the proportion with no nausea. (Source 22)

• Randomized trial, Certainty not rated.
• Size: 380 evaluable patients (192 olanzapine, 188 placebo)
• Who: chemotherapy-naive patients receiving cisplatin ≥70 mg/m2 or cyclophosphamide-doxorubicin.
• How long: 10 mg daily on days 1 through 4, outcomes to 120 hours.
• Result: no nausea 74% versus 45% at 0-24 hours (P=0.002), 42% versus 25% at 25-120 hours (P=0.002), 37% versus 22% overall (P=0.002); complete response 64% versus 41% overall (P<0.001)
• Funding: publicly funded (National Cancer Institute)

Limit of this finding: The published abstract gives exactly P=0.002 for all three nausea comparisons even though the gaps between olanzapine and placebo are very different (29, 17 and 15 percentage points). That is the journal's own text. Treat the three p-values as showing that each comparison favoured olanzapine, not as three independently precise figures.

The proportion of patients with no chemotherapy-induced nausea was significantly greater with olanzapine than with placebo in the first 24 hours after chemotherapy (74% vs. 45%, P=0.002), the period from 25 to 120 hours after chemotherapy (42% vs. 25%, P=0.002), and the overall 120-hour period (37% vs. 22%, P=0.002).

What the evidence does not support

Most patients stopped olanzapine within 18 months even though it outlasted the comparators. (Source 21)

• Randomized trial, Certainty not rated.
• Size: 1,432 patients who received at least one dose.
• Who: adults with chronic schizophrenia.
• How long: up to 18 months.
• Result: 64% of those assigned to olanzapine discontinued; 74% across all five arms.
• Funding: publicly funded (NIMH CATIE trial)

Overall, 74 percent of patients discontinued the study medication before 18 months (1061 of the 1432 patients who received at least one dose): 64 percent of those assigned to olanzapine

For weight restoration in anorexia nervosa the pooled effect was not statistically significant. (Source 8)

• Meta-analysis, Very low certainty.
• Size: 7 RCTs with 152 patients identified; meta-analysis of 4 studies with 91 patients.
• Who: patients with anorexia nervosa.
• How long: not stated in the abstract.
• Result: mean difference in BMI 1.68 kg/m2, 95% CI 0.82 to 4.18, p = 0.19, I2 = 94%.
• Funding: not stated in the abstract.

Limit of this finding: The paper's own numbers do not fit together. A 95% confidence interval of 0.82 to 4.18 does not include zero, which cannot go with a p-value of 0.19, and the interval is not centred on the stated difference of 1.68. The contradiction is in the published paper, not in the transcription. Also note that although seven trials with 152 patients were found, the pooled estimate rests on just 4 studies with 91 patients. The honest reading is that this analysis does not establish that olanzapine produces weight gain in anorexia nervosa.

Meta-analysis of 4 studies (91 patients) showed a mean difference in BMI of 1.68 kg/m² (95% CI: 0.82, 4.18) in favor of olanzapine but not statistically significant (p = 0.19), with high heterogeneity (I² = 94%).

Olanzapine added to a mood stabiliser did not clearly prevent mood relapse in bipolar disorder, and did not beat lithium or valproate overall. (Source 23)

• Systematic review, Certainty not rated.
• Size: 5 trials, 1,165 participants; the pooled relapse comparison used 2 studies with 460 participants.
• Who: people with bipolar affective disorder in long-term treatment.
• How long: long-term maintenance trials.
• Result: relapse into mood episode RR 0.68, 95% CI 0.43 to 1.07, p = 0.09 (not significant); olanzapine monotherapy versus placebo alone RR 0.58, 95% CI 0.49 to 0.69, p<0.00001.
• Funding: independent (Cochrane review)

Limit of this finding: The two intervals in this passage sit oddly together: the pooled result from two studies (460 people) has a wide interval, 0.43 to 1.07, while a single trial drawn from inside that pool is reported with a much narrower one, 0.49 to 0.69. A single study normally gives a wider interval than the pool containing it, not a narrower one. Do not read the single-trial figure as the more certain of the two.

There was no statistically significant difference between olanzapine and placebo (either alone or in combination with lithium or valproate) in terms of number of participants who experienced relapse into mood episode (random effects RR 0.68, 95% CI 0.43 to 1.07, p = 0.09; 2 studies, n=460)

Whether olanzapine raises serious adverse events when used as an antiemetic remains uncertain. (Source 7)

• Systematic review, Low certainty.
• Size: 889 participants across 7 studies.
• Who: adults with cancer receiving olanzapine as an antiemetic.
• How long: chemotherapy cycles.
• Result: serious adverse events RR 2.46, 95% CI 0.48 to 12.55; absolute risk difference 0.7% more, 95% CI 0.2 to 5.2.
• Funding: independent (Cochrane review)

It is uncertain if olanzapine increases the risk of serious adverse events (absolute risk difference 0.7% more, 95% CI 0.2 to 5.2) (RR 2.46, 95% CI 0.48 to 12.55; 7 studies, 889 participants, low-quality evidence).

Where the research disagrees

Whether olanzapine's efficacy advantage is large enough to accept its metabolic harm

• Leucht and colleagues, Lancet 2013, network meta-analysis of 212 trials and 43,049 participants, meta-analysis: Antipsychotics differed substantially in side-effects, and small but robust differences were seen in efficacy. (Source 24)
• CATIE investigators, NEJM 2005, publicly funded 18-month head-to-head trial in 1,493 patients, rct: Olanzapine was the most effective in terms of the rates of discontinuation, and the efficacy of the conventional antipsychotic agent perphenazine appeared similar to that of quetiapine, risperidone, and ziprasidone. Olanzapine was associated with greater weight gain and increases in measures of glucose and lipid metabolism. (Source 25)

Whether olanzapine should be used for long-term maintenance in bipolar disorder

• US ZYPREXA prescribing information (DailyMed SPL, 2026), position: Oral ZYPREXA is indicated for the acute treatment of manic or mixed episodes associated with bipolar I disorder and maintenance treatment of bipolar I disorder. (Source 4)
• Cichon and colleagues, Cochrane review of 5 long-term trials in 1,165 participants, 2009, systematic-review: notwithstanding these positive results, the current evidence is stronger for lithium as first line maintenance treatment of bipolar disorder (Source 26)

How much

• Reference intake: Dosing is set by the prescriber, not by the reader. As a regulatory position, the US ZYPREXA label (DailyMed SPL published 16 February 2026) states oral olanzapine is given once a day without regard to meals, generally beginning with 5 to 10 mg, with a target of 10 mg/day within several days for schizophrenia in adults. (Source 27)
• Upper limit: The label does not set a single maximum. For bipolar I monotherapy it states that the safety of doses above 20 mg/day has not been evaluated in clinical trials, and for schizophrenia it notes that doses above 10 mg/day were not shown to be more efficacious. A lower 5 mg starting dose is specified for debilitated or pharmacodynamically sensitive patients. (Source 28)
• Studied: Efficacy in schizophrenia was demonstrated in a dose range of 10 to 15 mg/day in clinical trials. (Source 27)
• Studied: Short-term antimanic efficacy was demonstrated in a dose range of 5 mg to 20 mg/day over 3 to 4 weeks. (Source 28)
• Studied: CATIE randomised patients to olanzapine 7.5 to 30 mg per day for up to 18 months. (Source 29)
• Studied: The NEJM antiemetic trial gave 10 mg of olanzapine orally daily on days 1 through 4 of chemotherapy. (Source 30)

A common belief, and what the research shows

The belief: Olanzapine is a sedative for sleep or anxiety, so a small dose is harmless.

What the research shows: It is an antipsychotic with a boxed warning and a metabolic profile that is the worst of the fifteen drugs compared in the largest network meta-analysis, where the standardised mean difference for weight gain ran “from -0·09 for the best drug (haloperidol) to -0·74 for the worst drug (olanzapine)”. In the manufacturer's pooled data, 22.2% of olanzapine-treated patients gained at least 7% of their body weight against 3% on placebo, and over at least 48 weeks the mean gain was 5.6 kg. The boxed warning reports death in about 4.5% of drug-treated elderly dementia patients against about 2.6% on placebo over a typical 10-week trial. Sedation is real — somnolence 29% versus 13% on placebo — but it is a side effect, not the reason the drug exists.

Questions and answers

What is it?

Olanzapine is a prescription medicine, not a nutrient or a natural substance. It is a second-generation or atypical antipsychotic of the thienobenzodiazepine class, available as a tablet, an orally disintegrating tablet, a short-acting injection and a long-acting depot injection. In the United States it is approved for schizophrenia and for manic or mixed episodes of bipolar I disorder, and in combination with fluoxetine for certain depressive conditions. (Source 31)

What does it do in the body?

It blocks receptors in the brain, chiefly dopamine D2 and serotonin 5-HT2 receptors, and this combination is thought to be what reduces hallucinations, delusions and mania. It also blocks histamine, muscarinic and alpha-adrenergic receptors, which explains much of the sedation, dry mouth and blood pressure drops. The manufacturer's own label says plainly that the mechanism in the approved indications is unclear. (Source 1)

Is it good or bad for you?

Both, and the balance depends on the condition. For schizophrenia and mania the benefit is real and measured: continuing an antipsychotic cut one-year relapse from 64% on placebo to 27% on drug, a number needed to treat of 3. Against that sit the harms: a boxed warning for increased death in elderly people with dementia-related psychosis, the worst weight gain of fifteen antipsychotics compared head to head, somnolence in 29% versus 13% on placebo, and the risk of tardive dyskinesia. For chemotherapy nausea the trade-off is favourable and short-lived; for anorexia nervosa the evidence does not show a significant benefit. (Source 32)

How do you get more of it?

There is no food, supplement or behaviour that provides olanzapine; it is prescription-only and the dose is set by a prescriber. What trials actually used is on record: 10 to 15 mg/day for schizophrenia, 5 to 20 mg/day for acute mania, 7.5 to 30 mg/day in the CATIE effectiveness trial, and 10 mg daily on days 1 to 4 in the chemotherapy nausea trial. Blood levels for a given dose are higher in non-smokers, in women and in older people. (Source 27)

If it is harmful, what reduces it?

Olanzapine is cleared by the liver, and clearance can be deliberately increased: activated charcoal given within a few hours reduced the amount absorbed by about 60%, which is why it is used in overdose, and carbamazepine raises clearance by around 50%. Smoking also raises clearance by about 40%. In ordinary care the way to reduce exposure is for the prescriber to lower or stop the dose, bearing in mind the substantial relapse risk of stopping. (Source 10)

Why might someone be low in it or missing it?

Nobody is naturally deficient in olanzapine; it is a drug. Levels can be lower than intended for identifiable reasons: smoking raises clearance by about 40%, carbamazepine by about 50%, and activated charcoal blocks absorption. The label notes the combined effect of age, smoking and sex can be large — clearance in a young smoking man may be three times that in an elderly non-smoking woman on the same dose. (Source 11)

Which whole foods contain it or feed it?

None. Olanzapine occurs in no food and is not produced by the body. Food does not need to be timed around it either, as the label states oral olanzapine is given once a day without regard to meals. The food-adjacent items that do matter are activated charcoal, which blocks absorption, and alcohol, which worsens the drop in blood pressure on standing. (Source 27)

What happens if you do not have it?

Not taking olanzapine is not a deficiency; the question is what happens to the illness. For schizophrenia, a meta-analysis of 65 trials found that stopping antipsychotic treatment after stabilisation raised one-year relapse from 27% to 64%, and readmission from 10% to 26%. In first-episode psychosis specifically, 53.3% relapsed within 12 months after discontinuation against 21.0% who continued. For chemotherapy nausea, going without olanzapine simply means the lower nausea-free rate seen in the placebo arms, around 22 to 25%. (Source 20)

How can you test for it?

There is no routine blood test for olanzapine levels in ordinary care; what gets measured is its metabolic effect. The label directs fasting blood glucose testing at the start of treatment and periodically after, regular weight monitoring, and monitoring for symptoms of hyperglycaemia. These are reliable, standard laboratory tests, but they measure the consequences of the drug rather than the drug itself. (Source 33)

References

1. DailyMed (US National Library of Medicine), FDA Structured Product Label. ZYPREXA (olanzapine) - 12.1 Mechanism of Action (Full Prescribing Information). 2026. Read the source
2. DailyMed (US National Library of Medicine), FDA Structured Product Label. ZYPREXA (olanzapine) - BOXED WARNING (Full Prescribing Information). 2026. Read the source
3. The Lancet. Comparative efficacy and tolerability of 15 antipsychotic drugs in schizophrenia: a multiple-treatments meta-analysis.. 2013. PMID 23810019, DOI 10.1016/S0140-6736(13)60733-3. Read the source
4. DailyMed (US National Library of Medicine), FDA Structured Product Label. ZYPREXA (olanzapine) - 1.2 Bipolar I Disorder (Manic or Mixed Episodes) (Full Prescribing Information). 2026. Read the source
5. DailyMed (US National Library of Medicine), FDA Structured Product Label. ZYPREXA (olanzapine) - 1.5 ZYPREXA and Fluoxetine in Combination: Depressive Episodes Associated with Bipolar I Disorder (Full Prescribing Information). 2026. Read the source
6. DailyMed (US National Library of Medicine), FDA Structured Product Label. ZYPREXA (olanzapine) - 1.4 ZYPREXA IntraMuscular: Agitation Associated with Schizophrenia and Bipolar I Mania (Full Prescribing Information). 2026. Read the source
7. Cochrane Database of Systematic Reviews. Olanzapine for the prevention and treatment of cancer-related nausea and vomiting in adults.. 2018. PMID 30246876, DOI 10.1002/14651858.CD012555.pub2. Read the source
8. BMC Psychiatry. Olanzapine effectiveness on weight gain in anorexia nervosa patients: systematic review and meta-analysis. (Result). 2026. PMID 42157160, DOI 10.1186/s12888-026-08017-w. Read the source
9. DailyMed (US National Library of Medicine), FDA Structured Product Label. ZYPREXA (olanzapine) - 7.1 Potential for Other Drugs to Affect Olanzapine: antacids, carbamazepine, alcohol (Full Prescribing Information). 2026. Read the source
10. DailyMed (US National Library of Medicine), FDA Structured Product Label. ZYPREXA (olanzapine) - 7.1 Potential for Other Drugs to Affect Olanzapine: charcoal, anticholinergic drugs (Full Prescribing Information). 2026. Read the source
11. DailyMed (US National Library of Medicine), FDA Structured Product Label. ZYPREXA (olanzapine) - 12.3 Pharmacokinetics, Special Populations: Smoking Status, Race and Combined Effects (Full Prescribing Information). 2026. Read the source
12. DailyMed (US National Library of Medicine), FDA Structured Product Label. ZYPREXA (olanzapine) - 7.1 Potential for Other Drugs to Affect Olanzapine: inhibitors of CYP1A2 and CYP2D6 (Full Prescribing Information). 2026. Read the source
13. DailyMed (US National Library of Medicine), FDA Structured Product Label. ZYPREXA (olanzapine) - 7.2 Potential for Olanzapine to Affect Other Drugs (Full Prescribing Information). 2026. Read the source
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