Polycystic Ovary Syndrome (PCOS)
Clinical Snapshot
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in people with ovaries of reproductive age, arising from a heterogeneous combination of hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology (PCOM). It is diagnosed using the Rotterdam criteria — 2 of these 3 features, after excluding conditions that mimic PCOS — and the specific combination present defines 4 distinct phenotypes with different reproductive and metabolic risk. Insulin resistance with compensatory hyperinsulinemia is the central pathophysiologic driver linking PCOS's reproductive features (excess insulin amplifies ovarian androgen production and disrupts normal follicle maturation) to its long-term metabolic consequences (type 2 diabetes, dyslipidemia, cardiovascular risk) — this single mechanism is why lifestyle intervention and insulin-sensitizing therapy are foundational across every phenotype, not only the ones with obesity.[1]
This chapter is authored from the 2023 International Evidence-based Guideline for the Assessment and Management of PCOS — 254 recommendations co-produced by the American Society for Reproductive Medicine, the European Society of Human Reproduction and Embryology, the Endocrine Society, and the European Society of Endocrinology — and cross-checked against the Society of Obstetricians and Gynaecologists of Canada (SOGC) Clinical Gynaecology Committee's February 2025 position statement, which explicitly adapts the international guideline's recommendations to Canadian practice.[2] It covers diagnosis, first-line combined hormonal contraceptives, metformin for the metabolic phenotype, spironolactone for hirsutism/acne, letrozole as the current first-line ovulation-induction agent (a genuine shift away from clomiphene supported by higher live-birth rates[3]), foundational lifestyle intervention, long-term risk screening, and mental-health screening.
Recognize the Condition
The 3 core features and 4 Rotterdam phenotypes
Hyperandrogenism
Clinical (hirsutism, scored with the modified Ferriman-Gallwey scale; inflammatory acne; androgenic alopecia) and/or biochemical (elevated free testosterone or free androgen index).
Ovulatory dysfunction
Oligomenorrhea (cycles longer than 35 days, or fewer than 8 cycles/year) or amenorrhea from chronic anovulation — presents clinically as irregular bleeding and/or infertility.
Polycystic ovarian morphology (PCOM)
≥20 follicles (2-9 mm) in either ovary and/or an ovarian volume ≥10 mL on transvaginal ultrasound with a high-frequency (≥8 MHz) transducer. This follicle-count threshold was raised from the older figure of 12 in the 2023 update specifically to reduce false-positive PCOM calls on modern high-resolution equipment.[1] In adults only, an elevated anti-Müllerian hormone (AMH), using a population- and assay-specific threshold, may substitute for ultrasound.
PCOS is diagnosed when 2 of these 3 features are present, once mimicking conditions have been excluded (see Assessment & Diagnosis). Which 2 (or all 3) are present defines 4 phenotypes:
| Phenotype | Features present | Relative risk pattern |
|---|---|---|
| A | Hyperandrogenism + ovulatory dysfunction + PCOM | Most severe reproductive and metabolic phenotype |
| B | Hyperandrogenism + ovulatory dysfunction (no PCOM) | Severe reproductive/metabolic phenotype, similar to A |
| C | Hyperandrogenism + PCOM, ovulatory | Milder metabolic risk; regular cycles |
| D | Ovulatory dysfunction + PCOM, non-hyperandrogenic | Milder hyperandrogenic features; metabolic risk still present |
Other commonly seen features
- Central/abdominal obesity, or in normal-weight patients, increased visceral adiposity ("lean PCOS") — insulin resistance can be present without an elevated BMI.
- Acanthosis nigricans (velvety hyperpigmented skin, typically at the neck or axillae) — a clinical marker of insulin resistance.
- Infertility from chronic anovulation.
- Higher rates of anxiety, depression, disordered eating, and body-image concerns than the general population.
- Symptoms of obstructive sleep apnea (snoring, witnessed apnea, daytime fatigue) — more common in PCOS independent of BMI and frequently under-recognized.
Risk Factors
- Family history of PCOS, or of type 2 diabetes in a first-degree relative.
- Premature adrenarche.
- Low birth weight or rapid postnatal weight gain.
- Obesity/excess adiposity, which worsens both the hyperandrogenic and metabolic phenotype — though PCOS also occurs at a normal body weight.
- In-utero exposure to excess androgens.
- Valproate/valproic acid therapy — associated with a PCOS-like phenotype (menstrual irregularity, hyperandrogenism, polycystic-appearing ovaries) in some patients, particularly with use during adolescence.
- Higher reported prevalence in some populations, including South Asian ancestry, where the metabolic phenotype also tends to be more severe at a given BMI.
Red Flags & Refer
Most hyperandrogenism and irregular cycles in a reproductive-age patient is PCOS. Escalate or refer for any of the following instead of proceeding with a routine PCOS work-up:
- Rapid-onset (over months, not years) or severe virilization — clitoromegaly, significant voice deepening, rapidly progressive male-pattern balding, or a substantially elevated total testosterone (generally more than 2-3 times the upper limit of the reference range) — these suggest an androgen-secreting ovarian or adrenal tumour and need urgent imaging and specialist referral, not empiric PCOS treatment.
- Features suggesting Cushing syndrome — proximal muscle weakness, wide violaceous striae, easy bruising, a rapidly progressive centripetal weight-gain pattern — investigate for Cushing syndrome rather than attributing the picture to PCOS.
- Signs or biochemistry suggesting non-classic congenital adrenal hyperplasia not adequately explained by a screening 17-hydroxyprogesterone — refer for a corticotropin stimulation test.
- Any postmenopausal-pattern or otherwise atypical abnormal uterine bleeding, or bleeding that does not respond to standard management — investigate per usual abnormal-uterine-bleeding pathways (endometrial sampling and/or ultrasound) rather than assuming it is simply anovulatory PCOS bleeding.
- Infertility with no response after an adequate first-line ovulation-induction trial, or any patient over 35 years old who has not conceived after 6 months of regular attempts — refer for reproductive endocrinology and infertility assessment.
- Symptoms suggesting obstructive sleep apnea — refer for a sleep study; OSA is more common in PCOS independent of BMI.
- Significant psychological distress, disordered eating, or suicidal ideation identified on screening — refer for mental health assessment and treatment; do not treat mental-health screening as a formality.
Assessment & Diagnosis
Step 1 — exclude conditions that mimic PCOS
Before applying the Rotterdam criteria, rule out other causes of the same clinical picture:
- Thyroid dysfunction — TSH.
- Hyperprolactinemia — serum prolactin.
- Non-classic congenital adrenal hyperplasia — an early-morning (follicular-phase) 17-hydroxyprogesterone, particularly with a suggestive family history/ancestry or rapid-onset hyperandrogenism.
- Consider Cushing syndrome or an androgen-secreting tumour only when a red flag from the section above is present — these are not routine screening tests in a typical presentation.
Step 2 — apply the Rotterdam criteria (adults)
Diagnose PCOS when at least 2 of the following 3 are present, once mimics above are excluded: ovulatory dysfunction; clinical or biochemical hyperandrogenism; and polycystic ovarian morphology, or an elevated AMH as a substitute for ultrasound in adults.[1]
Biochemical hyperandrogenism testing
Measure total testosterone plus sex hormone-binding globulin to calculate a free androgen index, or free testosterone directly by equilibrium dialysis or LC-MS/MS where available — routine direct free-testosterone immunoassays are unreliable in this population. Draw a fasting, morning sample. A patient already taking combined hormonal contraception will have suppressed androgen levels, so a low result on therapy does not rule out PCOS; where feasible without compromising the patient's contraceptive needs, testing after a washout is more accurate.
Diagnosis in adolescents
Apply stricter criteria in adolescents, given how common physiologic multi-follicular ovaries and cycle irregularity are in the first few years post-menarche: require both hyperandrogenism (clinical or biochemical) and irregular menstrual cycles meeting adolescent-specific duration criteria based on time since menarche. Do not use PCOM on ultrasound to diagnose PCOS in adolescents — it is not specific enough at this age.[1] An adolescent who does not fully meet these criteria but has risk features should be labelled "at increased risk" and reassessed at the transition to adult criteria, rather than definitively diagnosed or definitively excluded.
Metabolic screening at diagnosis
Insulin resistance with compensatory hyperinsulinemia is the pathophysiologic driver of PCOS, but routine fasting insulin or HOMA-IR testing is not recommended for either diagnosis or monitoring — clinically available insulin assays are not standardized and have limited clinical validity in this context.[1] Screen instead for the downstream metabolic consequences directly:
- A 75 g oral glucose tolerance test is preferred over HbA1c or fasting glucose alone — it is more sensitive for detecting glucose intolerance in PCOS specifically. Repeat every 1-3 years, or sooner with additional risk factors (obesity, a family history of type 2 diabetes, or a personal history of gestational diabetes).
- Fasting lipid profile at diagnosis.
- Blood pressure at every visit.
- Weight, BMI, and waist circumference.
Endometrial and psychological screening at diagnosis
Assess the menstrual pattern to identify chronic anovulation with unopposed estrogen exposure (see Special Populations for endometrial-protection management), and screen every patient for anxiety and depressive symptoms with a regionally validated tool, plus body-image and disordered-eating concerns — screen at diagnosis and repeat based on clinical judgement, risk factors, and life events, including the perinatal period.[1]
Treatment Targets
- Restore regular ovulatory cycles and prevent unopposed-estrogen-driven endometrial hyperplasia.
- Control hyperandrogenic symptoms — hirsutism, acne, and androgenic alopecia — to the patient's own goals.
- Achieve ovulation and pregnancy when fertility is desired.
- Improve insulin sensitivity and metabolic parameters to reduce long-term type 2 diabetes and cardiovascular risk.
- Support mental health — screen for and treat anxiety, depression, and disordered eating.
- Achieve realistic, health-focused weight/lifestyle goals, recognizing that even a modest (5-10%) weight loss meaningfully improves ovulation, metabolic parameters, and quality of life without requiring a specific target BMI.
Choose Initial Treatment
Foundation for every patient
1st line, all phenotypes structured lifestyle intervention (diet and exercise) — recommend for every patient with PCOS regardless of BMI or which track below is also used, since it improves ovulation, metabolic parameters, and psychological outcomes even without reaching a specific weight target.[1]
Not seeking pregnancy — menstrual regulation and/or hyperandrogenism
1st line a combined hormonal contraceptive (any low-dose formulation, 20-30 mcg ethinyl estradiol equivalent) — regulates cycles, protects the endometrium from unopposed estrogen, and improves hirsutism/acne. Current evidence does not show one progestin to be clearly superior to another for hirsutism specifically, so progestin choice can be individualized.[4]
Alternative when contraception is not needed, or a COC is contraindicated/declined cyclic or continuous oral progestin to induce regular withdrawal bleeding and protect the endometrium, without the hyperandrogenism benefit of a COC.
Add, or use instead of a COC, for the metabolic phenotype metformin — consider in every adult with PCOS and a BMI ≥25 kg/m2 for metabolic benefit, and as an alternative for menstrual cycle regulation in a patient who cannot or does not want to use a COC.[1]
Hirsutism/acne inadequately controlled by a COC alone after an adequate (at least 6 month) trial add an anti-androgen — spironolactone is the preferred agent.[4]
Never start spironolactone, or any anti-androgen, without effective contraception already in place — every anti-androgen carries a teratogenic risk of feminizing a male fetus, and must not be used (or must be stopped immediately) in a patient who could become pregnant without reliable contraception. A COC pairs naturally with spironolactone, since it supplies both the contraception and an added mechanism against hirsutism.
Seeking pregnancy — anovulatory infertility, no other infertility factor identified
1st line letrozole — produces higher ovulation and live-birth rates than clomiphene and is now the preferred first-line ovulation-induction agent, a genuine shift from the older clomiphene-first approach.[3][5]
Alternative clomiphene citrate, alone or combined with metformin — reasonable when letrozole is not available, not tolerated, or declined; combining metformin with either agent may improve outcomes specifically in a patient with a BMI ≥30 kg/m2.[1]
2nd line, specialist-directed gonadotrophin therapy or laparoscopic ovarian drilling, reserved for ovulation-induction-agent failure — both require specialist monitoring given the risk of multiple gestation and, with gonadotrophins, ovarian hyperstimulation syndrome.
Confirm the patient is not pregnant before starting each letrozole or clomiphene cycle — both are contraindicated once pregnancy is confirmed.
Metabolic phenotype not adequately controlled by lifestyle alone
Anti-obesity pharmacotherapy (a GLP-1/GIP receptor agonist, orlistat, or another agent) can be considered using the same BMI/comorbidity eligibility criteria and agent selection used outside PCOS — see the dedicated Obesity clinical guideline for full pharmacotherapy selection, dosing, and monitoring; it is not duplicated here.
Non-Pharmacologic Treatment
- Structured lifestyle intervention (a reduced-calorie diet plus regular physical activity, ideally with behavioural support) is foundational therapy for every phenotype — even a 5-10% weight loss meaningfully improves ovulation rates, insulin sensitivity, and psychological well-being, and the benefit does not require reaching a specific target BMI.[1]
- Regular physical activity (at least 150 minutes/week of moderate intensity, per general population guidance) supports both the metabolic and mental-health goals of treatment.
- Psychological therapy (cognitive behavioural therapy or similar) — offer as first-line treatment for a patient who screens positive for anxiety, depression, disordered eating, or significant body-image distress, alongside or instead of pharmacotherapy for these symptoms.[1]
- Cosmetic hair-removal methods (laser epilation, electrolysis, or topical eflornithine cream for facial hair specifically) are useful adjuncts to, not substitutes for, systemic anti-androgen therapy for hirsutism — combining a cosmetic method with systemic treatment gives a faster, more complete response than either alone.
- Sleep evaluation and, where indicated, referral for sleep-apnea assessment.
- Smoking-cessation support, given the added cardiovascular risk on top of PCOS's own metabolic phenotype.
- Natural health products: myo-inositol (commonly dosed 4 g/day, often split into two 2 g doses, sometimes combined with D-chiro-inositol in a 40:1 ratio) is used by some patients for cycle regulation and metabolic symptoms; current Canadian guidance concludes the evidence for a meaningful effect on ovulation, clinical pregnancy, or live-birth rates remains limited, with insufficient evidence to recommend a specific product or dose — present it as an option with uncertain benefit rather than an evidence-based alternative to metformin or letrozole.[2]
Special Populations
Pregnancy
Stop spironolactone (and any anti-androgen) as soon as pregnancy is confirmed or suspected — it carries a teratogenic risk of feminizing a male fetus. Letrozole and clomiphene are both contraindicated once pregnancy is confirmed; confirm a negative pregnancy test before starting each treatment cycle. Whether to continue metformin once pregnancy is confirmed after ovulation-induction therapy is individualized and typically specialist-directed — evidence for a benefit from continuing metformin specifically to prevent pregnancy complications, beyond its role in glycemic management, is not conclusive. Screen early for gestational diabetes, given the baseline glucose-intolerance risk in PCOS.
Breastfeeding
Metformin is compatible with breastfeeding, with minimal transfer into breast milk. Spironolactone has limited breastfeeding safety data and is generally avoided when a non-hormonal or topical alternative (e.g., eflornithine, cosmetic hair removal) can control symptoms instead. Follow standard postpartum contraceptive-selection guidance (not specific to PCOS) for COC timing while breastfeeding.
Adolescents
A combined hormonal contraceptive remains 1st line for menstrual regulation and hyperandrogenism in an adolescent who meets diagnostic criteria; consider metformin for an adolescent with overweight/obesity and confirmed metabolic risk. Avoid over-medicalizing an adolescent who does not fully meet the stricter adolescent diagnostic criteria (see Assessment & Diagnosis) — label as "at increased risk" and reassess at the transition to adult criteria rather than committing to a definitive, lifelong PCOS diagnosis prematurely.
Renal impairment
Metformin is contraindicated at an eGFR under 30 mL/min/1.73m2, and requires dose reduction and caution between 30-45; hold before an iodinated-contrast procedure per standard practice. Use spironolactone with caution, or avoid, in significant renal impairment given the added hyperkalemia risk.
Monitoring & Follow-Up
Reassess menstrual regularity and hyperandrogenic symptoms only after an adequate trial of the chosen therapy — allow at least 6 months before judging a COC or spironolactone trial for hirsutism/acne inadequate, since the visible hair-growth response is slow. Repeat the 75 g OGTT every 1-3 years based on individual risk factors, and recheck blood pressure and lipids at routine follow-up visits. Reassess weight, BMI, and waist circumference, and revisit lifestyle-intervention goals, at each visit rather than only at diagnosis. Rescreen for anxiety, depression, and disordered eating periodically — at minimum with any significant life event, including the perinatal period, and whenever new symptoms are reported, not only at the initial visit.[1] In a patient with chronic anovulation who is not on a COC or cyclic progestin, ask specifically about the bleeding pattern at every visit and manage per the endometrial-protection options above rather than allowing prolonged unopposed-estrogen exposure to go unaddressed. For a patient undergoing ovulation induction, reassess after each cycle (dose escalation for letrozole/clomiphene per the Drug Tables schedule) and refer for specialist reproductive-endocrinology input if pregnancy has not occurred after an adequate multi-cycle trial (commonly around 5-6 cycles).
Common Errors to Avoid
- Ordering a fasting insulin level or calculating HOMA-IR to diagnose or monitor insulin resistance in PCOS — these assays are not standardized and are not recommended for routine clinical use.
- Diagnosing PCOS in an adolescent using PCOM on ultrasound alone — normal physiologic multi-follicular ovaries are common at this age, and PCOM is not a valid diagnostic criterion in adolescents.
- Assuming hirsutism and irregular cycles are routine PCOS without checking for a red flag (rapid-onset/severe virilization, markedly elevated testosterone, Cushingoid features) that should trigger a tumour or Cushing syndrome work-up instead.
- Starting spironolactone, or any anti-androgen, without first confirming effective contraception is in place.
- Defaulting to clomiphene as the first ovulation-induction agent out of habit — letrozole is now the preferred first-line option given its higher live-birth rate.
- Treating cyproterone acetate/ethinyl estradiol as an interchangeable, risk-free COC choice rather than a specific option with an elevated VTE signal that should be reserved and counselled on explicitly.
- Ordering fasting glucose or HbA1c alone for metabolic screening — a 75 g OGTT detects glucose intolerance in PCOS that these tests can miss.
- Skipping anxiety/depression/disordered-eating screening because the visit is focused on cycles, hirsutism, or fertility — mental-health comorbidity in PCOS is common and frequently under-recognized.
- Leaving chronic anovulation with unopposed estrogen exposure unaddressed for months at a time without a plan for endometrial protection.
- Judging a COC, spironolactone, or letrozole trial a failure before an adequate duration or cycle count has actually elapsed.
Clinical Decision Algorithm
Drug Tables
How to use this table: Doses are adult doses and require patient-specific confirmation, including renal/hepatic adjustment. Every anti-androgen row assumes effective contraception is already in place — see Choose Initial Treatment. Select any drug name to open its complete Pharmasist Drug Database page.
Combined hormonal contraceptives
1st line for menstrual regulation and hyperandrogenism. No single progestin has been shown clearly superior for hirsutism; anti-androgenic progestins are commonly selected specifically when hirsutism is the dominant complaint.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Levonorgestrel/ethinyl estradiol | Cyclic: 1 tablet PO daily for 21 days, then 7 hormone-free days Continuous/extended-cycle: 1 tablet PO daily on a continuous or extended schedule per product labeling | Breakthrough bleeding, breast tenderness, nausea, headache; rare venous thromboembolism. | Enzyme-inducing drugs (certain anticonvulsants, rifampin, St. John's wort) may reduce contraceptive efficacy. | Standard first choice; regulates cycles and protects the endometrium. |
| Drospirenone/ethinyl estradiol | Dosing: 1 tablet PO daily for 21 days, then 7 hormone-free days | Breakthrough bleeding, mood changes, breast tenderness, hyperkalemia risk. | Additive hyperkalemia risk with ACE inhibitors, ARBs, potassium-sparing diuretics, or NSAIDs. | Anti-androgenic (antimineralocorticoid) progestin; a common choice when hirsutism is prominent. Check potassium if an additional hyperkalemia risk factor is present. |
| Cyproterone acetate/ethinyl estradiol | Dosing: 1 tablet PO daily for 21 days, then 7 hormone-free days | Breakthrough bleeding, mood changes, breast tenderness. | None significant beyond the general COC class. | The most potent anti-androgenic COC. Health Canada's safety review confirms an elevated venous thromboembolism signal relative to other COCs — reserve for hirsutism unresponsive to a standard COC, and counsel VTE symptoms (unilateral leg swelling/pain, sudden shortness of breath or chest pain) explicitly. |
Evidence note: the elevated VTE signal specific to cyproterone acetate/ethinyl estradiol is confirmed by a Health Canada summary safety review.[6]
Insulin sensitizer
Consider in every adult with PCOS and a BMI ≥25 kg/m2 for metabolic benefit; also an alternative for cycle regulation when a COC is not used, and an adjunct to ovulation induction.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Metformin | Starting dose: 500 mg PO once daily with food Titration: Increase by 500 mg weekly as tolerated Maintenance: 1500-2000 mg/day in divided doses, or extended-release once daily up to 2000 mg | GI upset (diarrhea, nausea) — dose-related and usually transient; rare lactic acidosis in significant renal impairment; long-term use associated with vitamin B12 deficiency. | Iodinated contrast media — hold before and after the procedure per standard practice given acute kidney injury risk. | Start low and titrate slowly with food to improve GI tolerability. Check eGFR before starting and periodically; contraindicated at an eGFR under 30 mL/min/1.73m2, use with caution 30-45. Consider periodic vitamin B12 with long-term use. |
Anti-androgens
For hirsutism/acne inadequately controlled by a COC alone after an adequate 6-month trial. Always combine with effective contraception given teratogenic risk.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Spironolactone | Dosing: 50-100 mg PO BID Maximum: 200 mg/day in divided doses | Menstrual irregularity if not combined with a COC, breast tenderness, hyperkalemia (chiefly with an additional risk factor). | Additive hyperkalemia risk with ACE inhibitors, ARBs, potassium-sparing diuretics, potassium supplements, or NSAIDs. | Effect on hair growth takes at least 6 months to assess. Requires effective contraception — teratogenic feminization risk to a male fetus. Routine potassium monitoring is not necessary in an otherwise healthy young patient without an independent hyperkalemia risk factor. |
| Eflornithine cream | Dosing: Apply a thin layer to affected facial areas BID, at least 8 hours apart | Local skin irritation, stinging, acne-like eruptions at the application site. | None significant — topical, minimal systemic absorption. | Topical adjunct for facial hirsutism specifically; not a substitute for systemic anti-androgen therapy. Visible benefit may take 4-8 weeks; effect reverses within about 8 weeks of stopping. |
Evidence note: the recommendation against routine potassium monitoring in an otherwise healthy young patient on spironolactone follows the current Endocrine Society hirsutism clinical practice guideline.[4]
Ovulation induction
1st line for anovulatory infertility with no other infertility factor identified. Confirm a negative pregnancy test before starting each cycle — both agents are contraindicated once pregnancy is confirmed.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Letrozole | Cycle days 3-7 (or 2-6), cycle 1: 2.5 mg PO once daily Subsequent anovulatory cycles: Increase to 5 mg, then a maximum of 7.5 mg, PO once daily | Hot flashes, fatigue, headache, dizziness. | None significant at ovulation-induction doses. | Preferred first-line agent — higher live-birth and ovulation rates than clomiphene. Typically trialed for up to 5-6 cycles, escalating the dose each anovulatory cycle, before moving to the next line of therapy. |
| Clomiphene citrate | Cycle days 3-7 (or 2-6), cycle 1: 50 mg PO once daily Subsequent anovulatory cycles: Increase to 100 mg, then a maximum of 150 mg, PO once daily | Hot flashes, mood changes, visual disturbances (stop if these occur), antiestrogenic thinning of the endometrium. | None significant at ovulation-induction doses. | Alternative when letrozole is not available, not tolerated, or declined. Lower live-birth rate than letrozole; combining with metformin may help specifically with a BMI ≥30 kg/m2. No Pharmasist Drug Database monograph currently exists for this agent. |
Natural health product
Evidence for a meaningful effect on ovulation, clinical pregnancy, or live-birth rates remains limited; present as an option with uncertain benefit rather than an evidence-based alternative to metformin or letrozole.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Myo-inositol | Typical dosing: 4 g/day PO, often split into two 2 g doses | GI upset (mild). | None well established. | Commonly combined with D-chiro-inositol in a 40:1 ratio. No Pharmasist Drug Database monograph exists for this supplement. |
Evidence note: the current SOGC position statement concludes there is insufficient evidence to recommend a specific inositol product or dose.[2]
Note: anti-obesity pharmacotherapy (GLP-1/GIP receptor agonists, orlistat, and related agents) is not repeated here — see the dedicated Obesity clinical guideline for full pharmacotherapy selection, dosing, and monitoring.
References
- Recommendations From the 2023 International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome — Journal of Clinical Endocrinology & Metabolism (Teede HJ, Tay CT, Laven JJE, et al.). J Clin Endocrinol Metab 2023;108(10):2447-2469
- SOGC Position Statement: Inositol for the Management of Polycystic Ovary Syndrome — Society of Obstetricians and Gynaecologists of Canada, Clinical Gynaecology Committee (Antaki R, Desrosiers K, Francoeur D, Magee B, Mills K). SOGC Position Statement, February 2025
- Letrozole versus clomiphene for infertility in the polycystic ovary syndrome — New England Journal of Medicine (Legro RS, Brzyski RG, Diamond MP, et al.). N Engl J Med 2014;371(2):119-129
- Evaluation and Treatment of Hirsutism in Premenopausal Women: An Endocrine Society Clinical Practice Guideline — Journal of Clinical Endocrinology & Metabolism, Endocrine Society (Martin KA, Anderson RR, Chang RJ, et al.). J Clin Endocrinol Metab 2018;103(4):1233-1257
- No. 362-Ovulation Induction in Polycystic Ovary Syndrome — Journal of Obstetrics and Gynaecology Canada, Society of Obstetricians and Gynaecologists of Canada (Smithson DS, Vause TDR, Cheung AP). J Obstet Gynaecol Can 2018;40(7):978-987
- Summary Safety Review - DIANE-35 (Cyproterone Acetate and Ethinyl Estradiol) - Venous Thromboembolism (blood clot) — Health Canada, Drug and Health Products Portal. Health Canada Summary Safety Review
Professional reference only. Apply clinical judgment and verify patient-specific decisions against current authoritative guidance and product information.