Does Buspirone Cause Weight Loss? Honest Evidence Review

The honest answer: no — buspirone is essentially weight-neutral. Buspirone (brand name BuSpar, discontinued 2010; generic buspirone hydrochloride remains widely available) is a 5-HT1A partial agonist FDA-approved for the management of anxiety disorders. The FDA label lists both weight gain and weight loss as “infrequent” adverse reactions — the same low frequency tier, in opposite directions, which is the textbook signature of a weight-neutral drug. The Domecq 2015 J Clin Endocrinol Metab systematic review^[1] of drugs commonly associated with weight change does not flag buspirone. The Slee 2019 Lancet network meta-analysis^[2] of pharmacological treatments for generalised anxiety disorder analyzed 89 RCTs and 25,441 patients across 22 active drugs and did not identify weight as a buspirone-specific concern. Some individual patients report appetite changes or modest weight loss on buspirone — usually from early-treatment nausea or lightheadedness — but there is no consistent directional signal in the trial or post-marketing literature. Buspirone is not a weight-loss drug and should not be used as one. Below: the verbatim FDA label, the GAD network meta-analysis, the CYP3A4 grapefruit interaction, and how buspirone compares to SSRIs, SNRIs, benzodiazepines, MAOIs, TCAs, and stimulants on weight.

At a glance — Buspirone and weight

• Buspirone is FDA-approved for the management of anxiety disorders — not for weight loss. The label uses the original (pre-DSM-5) language “anxiety disorders or the short-term relief of the symptoms of anxiety” and the controlled-trial evidence base principally maps to generalized anxiety disorder (GAD).
• The FDA label is weight-neutral. Both “weight gain” and “weight loss” are listed as infrequent adverse reactions in the Miscellaneous system organ class — the same low- frequency tier, in opposite directions. “Anorexia” and “increased appetite” are similarly both listed as infrequent under Gastrointestinal.
• No directional signal in meta-analyses. The Domecq 2015 J Clin Endocrinol Metab systematic review^[1] of 257 trials on drugs commonly associated with weight change does not flag buspirone. The Slee 2019 Lancet GAD network meta-analysis^[2] of 89 RCTs did not identify weight as a buspirone-specific concern.
• Mechanism explains the weight-neutrality. Buspirone is a partial agonist at 5-HT1A receptors and a weak D2 antagonist. It does not bind H1 (no antihistaminic weight push like mirtazapine), does not bind muscarinic receptors (no anticholinergic weight push like paroxetine), and has no GABA-A activity (mechanistically unrelated to benzodiazepines).
• Drug-interaction watchpoints: CYP3A4 substrate. Ketoconazole, ritonavir, and grapefruit juice substantially raise buspirone levels (Lilja 1998 showed grapefruit juice increased buspirone AUC ~9-fold)^[3]. The FDA label explicitly tells patients: “avoid drinking large amounts of grapefruit juice.”
• MAOI contraindication. Co-administration of buspirone with an MAOI (or within 14 days of stopping the MAOI) is contraindicated per the FDA label — serotonin-syndrome and hypertensive-crisis risk.
• If weight is the goal, buspirone is not the tool. For obesity itself, GLP-1 receptor agonists deliver 15–21% TBWL (Wegovy −14.9% in STEP-1^[8]; Zepbound −20.9% in SURMOUNT-1^[9]) — magnitudes no anxiolytic approaches.

What buspirone is

Buspirone is the generic name for buspirone hydrochloride, originally marketed as BuSpar by Bristol-Myers Squibb starting in 1986. The brand was discontinued in 2010; the generic remains widely available as 5, 7.5, 10, 15, and 30 mg tablets. Buspirone is azapirone-class — a chemical class unrelated to benzodiazepines, barbiturates, SSRIs, SNRIs, or TCAs.

The principal mechanism of buspirone is partial agonism at the 5-HT1A serotonin receptor — both pre-synaptic somatodendritic autoreceptors (which downregulate serotonergic firing acutely) and post-synaptic 5-HT1A receptors (which mediate the anxiolytic effect). It also has modest dopamine D2 receptor antagonism and active metabolite 1-(2-pyrimidinyl)piperazine (1-PP) is a weak alpha-2 adrenergic antagonist. Critically, buspirone has:

• No affinity for GABA-A receptors. Buspirone is not a benzodiazepine and does not produce sedation, motor impairment, dependence, or withdrawal in the benzodiazepine sense. This is the principal reason it gets prescribed for GAD in patients where benzodiazepine dependence risk is a concern.
• No antihistaminic (H1) activity. H1 blockade is the mechanism behind the substantial weight gain seen with mirtazapine, doxepin, and the older sedating antihistamines. Buspirone does not have this activity.
• No anticholinergic (muscarinic) activity. Muscarinic blockade contributes to the weight-gain signal seen with paroxetine and the older tricyclic antidepressants. Buspirone does not have this activity.

Typical dosing starts at 7.5 mg twice daily and titrates to 20–30 mg/day in divided doses (occasionally up to 60 mg/day). Onset of anxiolytic effect is slow — usually 2–4 weeks to meaningful symptom relief, which is one reason it does not work as an acute “PRN” anxiolytic. Half-life is short (~2–3 hours) with a pharmacologically active metabolite (1-PP) that extends the functional duration.

Buspirone was FDA-approved in 1986 for the management of anxiety disorders. None of its approvals or indications has ever been for weight loss, weight management, appetite suppression, or obesity. The 5-HT1A + D2 pharmacology that defines buspirone is fundamentally different from the H1 / M1 / 5-HT2C activity that produces weight effects with most psychotropics.

What the FDA label actually says about weight

From the buspirone hydrochloride package insert (DailyMed, Mylan Pharmaceuticals), the directly weight- and intake-relevant statements:

Indications and Usage: “Buspirone hydrochloride tablets are indicated for the management of anxiety disorders or the short-term relief of the symptoms of anxiety.”

Adverse Reactions, Miscellaneous: “Infrequent were weight gain, fever, roaring sensation in the head, weight loss, and malaise.”

Adverse Reactions, Gastrointestinal: “Infrequent were flatulence, anorexia, increased appetite, salivation, irritable colon, and rectal bleeding.”

Adverse Reactions, CNS (more common): nausea (8% buspirone vs 5% placebo across pooled controlled trials in the Miscellaneous-Symptoms summary), dizziness (12% vs 3%), drowsiness (10% vs 9%), headache (6% vs 3%), lightheadedness (3% vs 2%).

Drug Interactions: “Buspirone is metabolized primarily by oxidation, which in vitro has been shown to be mediated by cytochrome P450 3A4 (CYP3A4) ... Substances that inhibit CYP3A4, such as ketoconazole or ritonavir, may inhibit buspirone metabolism and increase plasma concentrations of buspirone.”

Patient counseling: “During your treatment with buspirone hydrochloride tablets, avoid drinking large amounts of grapefruit juice.”

Contraindications: “The use of monoamine oxidase inhibitors (MAOIs) intended to treat depression with buspirone or within 14 days of stopping treatment with buspirone is contraindicated because of an increased risk of serotonin syndrome and/or elevated blood pressure.”

The label is doing something distinctive here. Most psychotropic labels either flag weight gain as “frequent” and weight loss as “infrequent” (the antidepressant pattern — paroxetine, mirtazapine) or flag weight loss as the prominent signal (the stimulant pattern — lisdexamfet- amine, bupropion). The buspirone label lists weight gain and weight loss in the same low-frequency tier under the same Miscellaneous system organ class. The Gastrointestinal section does the same for anorexia and increased appetite. This symmetry, in FDA-label nomenclature, is the closest thing to a formal “weight-neutral” designation.

Buspirone’s FDA label carries no boxed warning. The MAOI contraindication is the principal absolute contraindication. Pregnancy, lactation, renal impairment, and hepatic impairment all receive standard- section discussion, not boxed warnings.

Where to verify: the buspirone hydrochloride package insert lives on DailyMed at SetID 7c9eafb9-9ce1-4b28-900c-8fcb4b23424e (Mylan Pharmaceuticals Inc. re-label). Use DailyMed, not accessdata.fda.gov — the latter 404s silently when label revisions ship.

Buspirone weight signal in RCT and post-marketing data

The buspirone evidence base is dominated by short-term (4– 8 week) GAD efficacy trials and longer-term safety extensions. None of these were designed with weight as a primary endpoint, and none reported a meaningful directional weight effect:

• Slee 2019 Lancet GAD network meta-analysis. The most comprehensive analysis of the GAD evidence base: 89 RCTs, 25,441 patients, 22 active drugs vs placebo. The analysis^[2] ranked buspirone in the moderate- efficacy tier (better than placebo for anxiety symptom reduction, less effective than several SSRIs and SNRIs). Tolerability dropouts on buspirone were comparable to placebo — an important finding that is consistent with the flat weight profile, since most weight-active psychotropics drive at least some tolerability dropouts.
• Domecq 2015 J Clin Endocrinol Metab systematic review. Pooled 257 RCTs of medications across drug classes for which weight-change effects had been reported. Buspirone is not on the list^[1] of drugs identified as commonly associated with weight change. This is a meaningful absence: the Domecq paper is the canonical reference for psychotropic-weight comparisons, and the absence of buspirone alongside its inclusion of SSRIs, TCAs, antipsychotics, and mood stabilizers is itself the signal.
• Post-marketing experience. The FDA label notes: “Postmarketing experience has shown an adverse experience profile similar to that given above.” Voluntary FDA Adverse Event Reporting System (FAERS) signals for buspirone are dominated by neurological (dizziness, paresthesia) and gastrointestinal (nausea) categories, not metabolic / weight categories — consistent with the label tiering.

The honest summary is that buspirone trial data is not designed to detect weight effects at high resolution. But the cleanest question — if buspirone produced a clinically meaningful weight effect in either direction, would 40 years of trial and post-marketing experience have detected it? — has an answer: yes, and it hasn’t.

Buspirone vs SSRI, SNRI, benzodiazepine, MAOI, TCA, stimulant on weight

The most useful framing for “does buspirone affect my weight” is comparative: what would the alternative anxiolytic do? The honest cross-class picture:

• SSRIs (sertraline, escitalopram, paroxetine, fluoxetine, citalopram). Heterogeneous. The Serretti 2010 J Clin Psychiatry meta-analysis^[4] of 116 studies ranked the class on a spectrum: paroxetine highest- risk for long-term weight gain; citalopram and escitalopram modestly weight-positive; sertraline roughly weight-neutral at 1 year; fluoxetine the most favorable with a small acute- phase loss signal. The Gafoor 2018 BMJ cohort^[5] of 294,719 UK primary-care adults confirmed elevated incident-rate ratios for ≥5% weight gain across SSRI users over 10 years.
• SNRIs (venlafaxine, duloxetine). Roughly weight-neutral acutely with a modest gain signal at 12+ months in the Blumenthal 2014 JAMA Psychiatry EHR cohort^[6].
• Benzodiazepines (alprazolam, lorazepam, clonazepam, diazepam). Generally weight-neutral in short-term use. Chronic use is complicated by dependence, sedation, and reduced non-exercise activity thermogenesis — effects that can indirectly drive modest gain. None of the benzodiazepine labels flag weight as a frequent adverse reaction.
• MAOIs (phenelzine, tranylcypromine). Weight gain is a well-documented MAOI class effect, particularly with phenelzine. The Domecq 2015 review^[1] identifies MAOIs among the weight-gain-associated antidepressants. Also: MAOI + buspirone is contraindicated per the buspirone label.
• TCAs (amitriptyline, nortriptyline, imipramine, clomipramine). Substantial weight gain, particularly with amitriptyline. Drives the same anticholinergic + antihistaminic mechanism that explains paroxetine’s weight signal among SSRIs.
• Stimulants (lisdexamfetamine / Vyvanse, methylpheni- date). Anorectic. Vyvanse is the only stimulant FDA-approved for a weight-related indication (moderate-to-severe binge eating disorder, not weight loss per se). See our review of Vyvanse and weight loss for the per-drug data.
• Buspirone. Weight-neutral. The 5-HT1A partial-agonist mechanism does not engage the appetite or metabolic-rate pathways that drive directional weight effects in other psychotropic classes.

Magnitude: buspirone vs other anxiolytics vs GLP-1s on weight

Cross-trial caveat: figures above are from independent trials and cohorts with different populations, designs, and durations. They cannot be used to predict individual outcomes, and they are not head-to-head comparisons. The buspirone row reflects the FDA-label tier symmetry; SSRI / MAOI / TCA values are approximate meta-analytic anchors; GLP-1 rows are the STEP-1 and SURMOUNT-1 primary endpoints.

Why some patients notice modest weight loss on buspirone

Patient forums include genuine reports of small weight loss on buspirone, particularly in the first 4–8 weeks. None of these are inconsistent with a population-level weight-neutral signal. The mechanisms:

• Early-treatment nausea and lightheadedness. The buspirone label reports nausea at 8% vs 5% placebo and dizziness at 12% vs 3% placebo across pooled controlled trials. Both are most common in the first 1–4 weeks and resolve as the gut and vestibular systems adapt. While present, they can modestly suppress intake — usually 1–3 kg over 4–8 weeks for the patients who experience them.
• Anxiety-related comfort-eating attenuation. A subset of GAD patients use food (particularly carbohydrate- dense food) as an anxiety-management strategy. Effective anxiolysis — regardless of mechanism — can attenuate this behavior, producing modest weight loss that is mediated by the anxiety treatment, not by buspirone per se. SSRI patients describe the same pattern. The pharmaco- dynamics of buspirone do not directly cause this effect.
• Concurrent lifestyle changes. People who start an anxiolytic frequently also start therapy, mindfulness practice, exercise programs, or dietary changes. Attribution to the drug specifically is easy and often partially incorrect.
• Confounding with discontinued benzodiazepines. Many patients switch from a chronic benzodiazepine to buspirone — the benzodiazepine taper itself can produce modest weight loss as sedation-related reduced activity reverses, and the buspirone gets credit for the effect.

Symmetric mechanisms produce occasional modest weight gain in other patients: appetite normalization from successful anxiety treatment, fluid-related changes, concurrent dietary shifts. Neither direction dominates at the population level.

Drug-interaction watchpoints

Buspirone is a CYP3A4 substrate. The clinically meaningful interactions cluster around drugs that inhibit or induce CYP3A4:

• Grapefruit juice. The Lilja 1998 Clin Pharmacol Ther study^[3] in healthy volunteers showed that 200 mL of grapefruit juice three times daily for two days increased buspirone AUC roughly nine-fold and Cmax roughly four-fold. The mechanism is gut-wall CYP3A4 inhibition by furanocoumarins in grapefruit. The FDA label tells patients explicitly to avoid large amounts of grapefruit juice.
• Strong CYP3A4 inhibitors. Ketoconazole, itraconazole, ritonavir, clarithromycin, and erythromycin substantially raise buspirone exposure. The label recommends using a lower buspirone dose (2.5 mg twice daily) when co-prescribing strong CYP3A4 inhibitors.
• CYP3A4 inducers. Rifampin, phenytoin, phenobarbital, carbamazepine, and dexamethasone reduce buspirone exposure and may require a buspirone dose increase. The label notes that buspirone exposure can drop dramatically with rifampin co-administration.
• MAOIs (contraindicated). Phenelzine, tranylcypromine, isocarboxazid, and selegiline at MAOI-doses should not be combined with buspirone. Wait 14 days between discontinuation of an MAOI and initiation of buspirone (or vice versa). Risk: serotonin syndrome, hypertensive crisis.
• Other serotonergic agents. Buspirone can be combined with SSRIs and SNRIs and is in fact commonly prescribed as an SSRI augmentation strategy — though patients on multiple serotonergic agents should be monitored for serotonin syndrome, particularly during titration.
• GLP-1 receptor agonists. No FDA-label pharmacokinetic interaction between buspirone and semaglutide, tirzepatide, liraglutide, or orforglipron. GLP-1s are peptides cleared peptide-style, not via CYP enzymes. Overlapping early nausea is the principal practical issue.

What to do if weight changes during buspirone therapy

Weight changes during buspirone treatment usually have causes other than the drug itself — but they still warrant clinical attention. A reasonable framework:

• Timing matters. Weight loss in the first 4–8 weeks is most often nausea/dizziness-related and resolves as tolerance develops. Weight changes after month 3–4 (in either direction) on stable buspirone dosing are unlikely to be drug-driven and should prompt the same differential diagnosis (thyroid, malabsorption, depression, GI disease, dietary change) you would consider in any patient.
• Rule out the easy confounders. Concurrent lifestyle changes, new medications (particularly steroids, antipsychotics, and mirtazapine for sleep), changes in alcohol intake, and changes in physical activity all dwarf buspirone’s direct weight effect.
• If clinically significant weight change persists. Refer to the prescribing clinician. Buspirone is not typically the agent to swap for weight reasons — given its weight-neutral profile, switching to another anxiolytic rarely improves the picture and may worsen it (SSRI, mirtazapine, and TCA all have less favorable weight profiles).
• If weight loss is the primary goal. Buspirone is not the tool. GLP-1 receptor agonists, Contrave (bupropion / naltrexone), phentermine / topiramate, and (where appropriate) bariatric procedures are the evidence-based weight-loss interventions. The Bollinger 2025 Dig Dis Sci study^[10] found that comorbid mood and anxiety disorders did not attenuate metabolic-pharmaco- therapy weight outcomes, which is reassuring for buspirone- treated GAD patients who are also pursuing weight management.
• Never stop buspirone abruptly to chase weight changes. Buspirone does not produce the dramatic discontinuation syndromes of SSRIs (particularly paroxetine) or benzodiazepines, but anxiety relapse is common and generally not worth the trade-off if the drug is doing its job.

How buspirone differs from MAOIs, TCAs, and stimulants

A frequent source of confusion: buspirone is in none of the classes that have established weight effects.

• Buspirone is not an antidepressant. Monotherapy buspirone is not FDA-approved for depression and does not reliably treat it. Buspirone is occasionally used off-label as an augmentation agent in partial SSRI responders for depression — the STAR*D trial included a buspirone augmentation arm — but it is not a primary antidepressant.
• Buspirone is not a benzodiazepine. No GABA-A activity. No sedation in the benzodiazepine sense (drowsiness rate is 10% buspirone vs 9% placebo). No dependence or withdrawal syndrome of clinical significance. No reliable acute anxiolysis — buspirone takes 2–4 weeks to work, so it cannot be used as a PRN agent the way alprazolam or lorazepam can.
• Buspirone is not an MAOI. Buspirone is in fact contraindicated with MAOIs (serotonin syndrome, hypertensive crisis risk). MAOIs themselves carry a robust weight-gain signal, particularly phenelzine; buspirone does not.
• Buspirone is not a TCA. No tricyclic structure, no muscarinic or histamine blockade, no cardiac conduction effects of comparable magnitude. TCAs (especially amitriptyline) carry substantial weight-gain signals; buspirone does not.
• Buspirone is not a stimulant. Buspirone is not anorectic and does not produce stimulant-class weight loss. Patients seeking pharmacological appetite suppression for weight loss are not buspirone candidates.

Important contraindications and warnings

• MAOI co-administration (absolute contraindication). Buspirone with phenelzine, tranylcypromine, isocarboxazid, selegiline (at MAOI doses), linezolid, or methylene blue is contraindicated. 14-day washout required when switching.
• Known hypersensitivity to buspirone. Absolute contraindication.
• Severe hepatic or renal impairment. Buspirone is not recommended in severe hepatic or renal impairment; AUC increases substantially and the label specifies caution.
• Serotonin syndrome (monitoring). The label states: “Patients should be monitored for emergence of serotonin syndrome.” Risk is highest when buspirone is combined with other serotonergic agents (SSRIs, SNRIs, tramadol, triptans, linezolid, MAOIs).
• Pregnancy and lactation. Buspirone is FDA Pregnancy Category B (older nomenclature). Animal studies do not show teratogenicity at typical exposures; human data are limited. Lactation: small amounts excreted in milk — discuss risks/benefits with prescriber.
• No boxed warning. Unlike most antidepres- sants (which carry the FDA suicidality boxed warning in young adults) and most benzodiazepines (concomitant-opioid warning), the buspirone label has no boxed warning.

Why this question matters (anxiety and obesity overlap)

Anxiety disorders and obesity are bidirectionally linked. The Luppino 2010 meta-analysis^[7] pooled 15 longitudinal studies covering 58,745 participants and found that obesity at baseline increased the odds of incident depression and anxiety by ~55%, and depression / anxiety at baseline increased the odds of incident obesity by ~58%. Many GAD patients are also managing weight; many weight-loss-seekers carry meaningful anxiety symptoms.

Among anxiolytics, buspirone is uniquely weight-neutral. For a GAD patient where weight is a meaningful clinical concern and where buspirone is a clinically appropriate anxiolytic, the drug pairs well with active weight- management strategies — including GLP-1 receptor agonists — without adding pharmacological pressure in either direction. The Bollinger 2025 Dig Dis Sci paper^[10] confirmed that comorbid mood and anxiety disorders did not attenuate weight-management outcomes on metabolic pharmacotherapy — an important data point for patients worried that anxiety treatment will undermine a weight-loss regimen.

Common bad takes

“Buspirone is a weight-loss drug.” No. Buspirone is FDA-approved for the management of anxiety disorders, not for weight loss. The FDA label lists weight gain and weight loss as the same low-frequency tier (“infrequent”) in opposite directions — the textbook signature of a weight-neutral drug. The Domecq 2015 systematic review^[1] of drugs commonly associated with weight change does not flag buspirone.

“Buspirone is basically the same as an SSRI.” No. Buspirone is a 5-HT1A partial agonist and weak D2 antagonist. SSRIs are serotonin reuptake inhibitors. These are different targets, different pharmacology, and different clinical profiles — including different weight signals (SSRIs class-positive, buspirone neutral).

“Buspirone is just a milder benzo.” Mechanistically wrong. Buspirone has no GABA-A activity and is in no way pharmacologically related to benzodiazepines. It is not a PRN anxiolytic, has no abuse liability of clinical significance, and does not produce benzodiazepine-style withdrawal.

“Buspirone will help me lose weight from anxiety eating.” Possibly, but only indirectly. If successful anxiety treatment attenuates a comfort-eating pattern, the resulting weight change is mediated by anxiety treatment, not by buspirone’s direct pharmacology — and any anxiolytic that works for you would produce the same effect. Buspirone is not the tool to choose specifically for weight loss.

“Buspirone has a black-box weight warning.” No. Buspirone carries no boxed warning. Its principal contraindications are MAOI co-administration and known hypersensitivity.

“Grapefruit juice with buspirone is fine.” Wrong. The Lilja 1998 Clin Pharmacol Ther study^[3] showed grapefruit juice raised buspirone AUC roughly nine-fold. The FDA label tells patients explicitly to avoid large amounts. This is one of the more dramatic grapefruit-juice CYP3A4 interactions in clinical pharmacology.

Bottom line

• Buspirone is FDA-approved for the management of anxiety disorders — not for weight loss.
• Buspirone is weight-neutral. The FDA label lists weight gain and weight loss as both “infrequent” adverse reactions — the same low-frequency tier in opposite directions. Anorexia and increased appetite are similarly symmetric. The Domecq 2015 systematic review^[1] of drugs commonly associated with weight change does not flag buspirone.
• Small subsets report appetite changes or weight loss — mostly from early-treatment nausea (8% buspirone vs 5% placebo) or lightheadedness (12% vs 3% placebo). No consistent directional signal in 40 years of trial and post-marketing data.
• Mechanism explains the weight-neutrality. 5-HT1A partial agonism + weak D2 antagonism, with no H1, no muscarinic, and no GABA-A activity — the receptor systems that drive weight effects in most other psychotropic classes are uninvolved.
• Watch the CYP3A4 interactions. Grapefruit juice (9-fold AUC increase^[3]), ketoconazole, ritonavir, and similar strong CYP3A4 inhibitors substantially raise buspirone levels. CYP3A4 inducers (rifampin, phenytoin, carbamazepine) substantially reduce them.
• MAOI contraindication is absolute. Serotonin syndrome / hypertensive crisis risk. 14-day washout.
• Do not use buspirone for weight loss. If weight loss is the clinical goal, GLP-1 receptor agonists deliver 15–21% TBWL^[8][9] — magnitudes no anxiolytic approaches.

Related research

• Does Paxil cause weight loss? Honest evidence review
• Does Lexapro cause weight loss? Honest evidence review
• Does Prozac cause weight loss? Honest evidence review
• Wellbutrin XL for weight loss: how fast and how much?
• Does Vyvanse cause weight loss? Honest evidence review
• Antidepressants and weight on a GLP-1: SSRI, SNRI, mirtazapine, and bupropion class review
• GLP-1 + SSRI interactions: FDA-label review and per-drug data
• Non-GLP-1 drug weight-effect lookup tool
• GLP-1 side-effect questions answered

Important disclaimer. This article is educational and does not constitute medical advice. Buspirone is FDA-approved for the management of anxiety disorders; it is not FDA-approved for weight loss or obesity and is not used as a weight-management intervention in any major obesity guideline. Decisions about starting, stopping, or switching anxiolytics should be made with a qualified prescribing clinician who knows your mental-health history. MAOI co-administration with buspirone is absolutely contraindicated.