PCOS/PMOS – Naturopathic Care for Fertility in Toronto

PCOS (Polycystic Ovarian Syndrome)

Medically Reviewed By Dr. Pamela Frank, BSc(Hons), ND

Recently renamed Polyendocrine Metabolic Ovarian Syndrome (PMOS), Polycystic Ovarian Syndrome is a condition where ovulation is either irregular or absent.  There are a number of reasons why this can occur; the most common, but not the only, reason is androgen (male hormone) excess.  This type of polycystic ovarian syndrome, or what I would call “classic”, occurs in about 60% of all women with the condition.  The remaining 40% (non-classic PCOS) will have a variety of other hormone imbalances that are interfering with ovulation.

The PCOS Phenotypes: Why Your Type Matters

Polycystic Ovarian Syndrome, or PMOS, is diagnosed using the Rotterdam Criteria, which require two of the following three features: irregular or absent ovulation, clinical or biochemical signs of androgen excess, and polycystic ovarian morphology on ultrasound.¹ Polycystic-appearing ovaries alone, without hormonal evidence, do not constitute a PCOS diagnosis.

This three-feature framework produces four distinct phenotypes with meaningfully different hormonal profiles, metabolic risks, and treatment requirements:

Phenotype A (Classic, Full):

Anovulation + androgen excess + polycystic ovaries. The most common and metabolically significant presentation. Highest risk of insulin resistance, dyslipidemia, and cardiovascular disease.

Phenotype B:

Anovulation + androgen excess, without polycystic ovarian morphology on ultrasound. Hormonally similar to Phenotype A; ovaries may appear normal despite significant androgen excess and anovulation.

Phenotype C (Ovulatory):

Androgen excess + polycystic ovaries, with ovulation present. Fertility may be less impaired, but androgen-driven symptoms (acne, hirsutism, hair loss) are prominent. Often missed because cycles are regular.

Phenotype D (Non-Androgenic):

Anovulation + polycystic ovaries, without androgen excess. The mildest metabolic risk profile. Often driven by thyroid dysfunction, hyperprolactinemia, or low body weight/hypothalamic suppression, which is why thorough testing is essential rather than assuming all Polycystic Ovarian Syndrome is the same.

Knowing your phenotype determines which treatment levers are most relevant. Applying a Classic PCOS insulin-lowering protocol to a Phenotype D patient with non-androgenic PCOS and a thyroid problem produces poor results. This is why I test before treating.

What Causes PCOS?

It depends on which type of polycystic ovaries you mean.  In the “classic” form, where androgen levels are high, insulin triggers excessive androgen production by the ovaries and/or adrenal glands. In “non-classic,” there can be undiagnosed hypothyroidism or Hashimoto’s, high or low estrogen, high prolactin, high stress or low body fat. Thorough blood testing is essential to understand which factors are contributing to a lack of ovulation.

Signs and symptoms

In Classic PCOS, some, many, or all of these signs and symptoms may be present:

• high or high-normal DHEAs, testosterone, DHT and/or androstenedione
• acne
• head hair loss
• excessive facial or body hair (hirsutism)
• irregular or absent periods
• heavy, painful periods
• anxiety, depression, irritability
• PMS/PMDD
• insulin resistance
• weight gain or difficulty losing weight (although some women with insulin resistance are thin)
• dysglycemia
• cysts on the ovaries on ultrasound (these do NOT have to be present to have polycystic ovarian syndrome)
• often a family history of cardiovascular disease and/or diabetes
• infertility

Because there is a variety of factors that cause non-Classic PCOS, the symptoms are more variable:

• irregular or absent periods
• cysts on the ovaries on ultrasound (may or may not be present)
• acne
• anxiety, depression, irritability
• There may be an absence of androgen-induced symptoms such as head hair loss, excessive body hair and acne
• may be of any weight/size
• infertility

What I Test for in Polycystic Ovarian Syndrome – and Why Standard Bloodwork Often Isn’t Enough

As a naturopathic doctor with a background as a hospital medical laboratory technologist, I interpret PCOS bloodwork with reference ranges calibrated for fertility optimization, not just the detection of overt disease. Here is what I assess and why each marker matters:

Fasting insulin and HOMA-IR:

The most important test in Classic PCOS that most GPs don’t order. Insulin resistance can be present with an entirely normal fasting glucose – which means a fasting glucose, or even an HbA1c, can be normal while insulin is driving excessive androgen production from the ovaries. HOMA-IR above 2.0 suggests insulin resistance clinically relevant to Polycystic Ovarian Syndrome pathophysiology; many labs don’t flag it until it’s considerably higher.

Full androgen panel:

Testosterone alone is insufficient. I measure total testosterone, free testosterone (or calculated from SHBG), DHEA-S, androstenedione, and DHT. The pattern across these markers identifies whether androgen excess is primarily ovarian, adrenal, or both, which changes the treatment approach. SHBG is also measured because low SHBG increases the proportion of free, biologically active testosterone even when total testosterone appears normal.

Full thyroid panel:

TSH, free T3, free T4, reverse T3, anti-TPO antibodies, anti-thyroglobulin antibodies. Thyroid autoimmunity is more prevalent in women with PMOS than in the general population and can cause anovulation and polycystic-appearing ovaries independently of androgen excess – the non-classic presentation.² TSH alone misses this.

LH:FSH ratio:

An LH:FSH ratio above 2:1 is a classic finding in PMOS. It reflects the abnormal GnRH pulse frequency that drives excess LH secretion relative to FSH, contributing to androgen production and impaired follicular development.

Prolactin:

Elevated prolactin suppresses GnRH pulsatility and can cause anovulation and cystic-appearing ovaries. This is a Polycystic Ovary Syndrome mimic that requires a completely different treatment approach. Prolactin should be measured correctly: after 20 minutes of seated rest, as stress acutely elevates prolactin.

Estradiol:

Both high and low estrogen can contribute to non-classic PCOS presentations. Chronically elevated estrogen without adequate progesterone opposition drives endometrial proliferation and increases long-term endometrial cancer risk, an underappreciated consequence of anovulatory cycles that is relevant in all PCOS phenotypes.

AMH (Anti-Müllerian hormone):

AMH is typically elevated in PMOS, often substantially, reflecting the large number of small antral follicles present. Very high AMH in the context of PCOS does not mean good fertility; it reflects follicular arrest rather than follicular abundance. It also predicts a high risk of ovarian hyperstimulation syndrome (OHSS) in IVF cycles, which is important information for your reproductive endocrinologist.

25-OH Vitamin D:

Vitamin D deficiency is significantly more prevalent in women with Polycystic Ovarian Syndrome than in the general population and is associated with more severe insulin resistance, higher androgen levels, and worse metabolic markers independently of BMI.³ It is also frequently deficient in Ontario, given our latitude.

Homocysteine:

Homocysteine can be elevated, particularly in those with insulin resistance and MTHFR polymorphisms. This is relevant for both cardiovascular risk and the higher miscarriage rates seen in PCOS pregnancies.

HbA1c and fasting glucose:

Baseline metabolic markers. Women with Polycystic Ovarian Syndrome have a four- to seven-fold increased lifetime risk of type 2 diabetes; tracking glycemic markers from the point of diagnosis establishes a baseline and identifies those already trending toward impaired glucose tolerance.

What is the conventional PCOS treatment?

For women who are not trying to conceive, doctors will prescribe birth control pills to provide an artificial menstrual cycle and manage some of the symptoms. Spironolactone may also be prescribed as an anti-androgen.  Metformin may be prescribed for women who are trying to conceive, and it may help because it helps to lower insulin levels.  Clomid or Letrozole is often the first-line medication for women with polycystic ovaries who are trying to conceive. If that fails, then injectables and IVF may be recommended.

What is the naturopathic PCOS treatment?

Naturopathic treatment is tailored to the individual and to their particular type of hormone imbalance.

Classic PCOS Treatment: What the Evidence Supports

Dietary modification – the foundation of treatment

Diet is the most powerful non-pharmacological intervention in Classic PCOS. The primary target is insulin: reducing the diet’s glycemic index and load lowers insulin secretion, thereby reducing ovarian androgen production, restoring SHBG, and allowing the HPO axis to resume normal GnRH pulsatility. The specific dietary pattern with the strongest evidence is low-glycemic index and load (GI below 55, GL below 10), moderate carbohydrate (60–100g/day from low-GI/GL sources), high in fibre, adequate in protein, and anti-inflammatory.⁴

This is not a calorie-restriction diet. Women with PCOS (or PMOS) who are of normal weight are often dismissed from dietary counselling because clinicians associate dietary intervention with weight loss. Insulin resistance is present in 50–70% of women with Polycystic Ovarian Syndrome regardless of BMI, including lean women.⁵ The dietary goal is glycemic regulation and insulin reduction, not caloric restriction.

Foods that directly support insulin sensitivity and reduce androgens: non-starchy vegetables, legumes, berries, oily fish, olive oil, nuts, seeds, and fermented foods. Foods that drive insulin and androgens: carbohydrates, sugar-sweetened beverages, bread, pasta, rice, and foods with high glycemic load.

Weight loss of even 5-10% of body weight in overweight women with PCOS has demonstrated significant improvements in ovulation frequency, testosterone levels, and pregnancy rates in RCTs.⁶

Myo-inositol and D-chiro-inositol

Inositol is a second messenger in insulin signalling and FSH signalling within granulosa cells. Women with PCOS have impaired inositol metabolism, specifically a deficiency in the enzyme that converts myo-inositol to D-chiro-inositol in peripheral tissues, which contributes to insulin resistance.⁷ Supplementation with the combined form (myo-inositol 2g + D-chiro-inositol 50mg twice daily, maintaining the physiological 40:1 ratio) has demonstrated in multiple RCTs: reduced fasting insulin, reduced testosterone, improved menstrual regularity, improved ovulation rates, improved oocyte quality in IVF cycles, and reduced miscarriage rates.⁸ This is one of the most comprehensively studied naturopathic interventions in reproductive medicine.

N-acetylcysteine (NAC)

NAC is a glutathione precursor with insulin-sensitizing properties. A 2017 meta-analysis of RCTs found NAC improved insulin sensitivity, reduced testosterone, and improved ovulation rates in women with PCOS, with comparable efficacy to metformin in some outcomes.⁹ It also reduces sperm DNA fragmentation, relevant when treating couples. Typical dose is 600 mg two to three times daily.

Berberine

Berberine has demonstrated insulin-sensitizing effects comparable to metformin in head-to-head clinical trials, including improvements in fasting insulin, HOMA-IR, testosterone, and menstrual regularity.¹⁰ It is appropriate for preconception use in insulin-resistant PCOS but should be stopped once pregnancy is confirmed due to insufficient safety data in pregnancy.

Vitamin D

Vitamin D supplementation in women with PCOS and confirmed deficiency has demonstrated improvements in insulin sensitivity, testosterone levels, menstrual regularity, and AMH in RCTs.³ The blood level target is 100–150 nmol/L measured as 25-OH vitamin D. Most women in Ontario require 2,000–4,000 IU/day to maintain optimal levels; correction of significant deficiency requires higher doses short-term under monitoring.

CoQ10 (ubiquinol)

Women with PCOS have elevated oxidative stress in both follicular fluid and serum. CoQ10 supports mitochondrial function in oocytes and has demonstrated improvements in insulin resistance and testosterone in women with PCOS in RCTs.¹¹ It is particularly relevant in PCOS-associated IVF cycles where egg quality is a concern. Dose: 200–400 mg/day of the ubiquinol form.

Omega-3 fatty acids (EPA/DHA)

Omega-3 supplementation in PCOS has been shown to reduce triglycerides, total testosterone, fasting insulin, and inflammatory markers across multiple RCTs.¹² The minimum effective dose is 2g of combined EPA/DHA daily from a pharmaceutical-grade source. The anti-inflammatory prostaglandin shift is the primary mechanism, which is directly relevant given that chronic low-grade inflammation is a central driver of PCOS pathophysiology.

Anti-androgenic herbs

Spearmint tea (two cups daily) has demonstrated reductions in free testosterone in women with PCOS in RCTs, through anti-androgenic effects at the gonadotropin level.¹³ Saw palmetto inhibits 5-alpha-reductase, reducing the conversion of testosterone to the more potent DHT. Licorice root (Glycyrrhiza glabra) has demonstrated anti-androgenic and anti-steroidogenic effects in clinical studies. Herbal prescribing requires individualized dosing and appropriate monitoring, particularly with licorice root, which can elevate blood pressure at high doses and with prolonged use.

Chromium and vanadium

Both minerals support insulin sensitivity through GLUT-4-mediated glucose uptake. Chromium picolinate has demonstrated modest improvements in glucose and insulin parameters in PCOS in RCTs. These are appropriate adjuncts to dietary and primary insulin-sensitizing interventions rather than standalone treatments.

Exercise

Resistance training combined with aerobic exercise is the most evidence-based exercise modality for improving insulin sensitivity in PCOS and is more effective than aerobic exercise alone.¹⁴ A minimum of 150 minutes of moderate-intensity activity per week with 2-3 sessions of resistance training improves HOMA-IR, reduces testosterone, and improves ovulation frequency independently of weight change.

Non-Classic PCOS Treatment

1. Treat the underlying hormone imbalance – support normal estrogen levels, lower high prolactin
2. Help with stress reduction
3. Help with adopting an appropriate diet to maintain a healthy body weight.
4. Support the normal functioning of the entire endocrine system – ovaries, adrenal glands, parathyroid, thyroid, hypothalamus, pituitary, pineal, pancreas, thymus gland.
5. Optional acupuncture to normalize the function of the endocrine system and enhance fertility.

PCOS, Miscarriage, and Pregnancy Complications

PCOS significantly increases the risk of miscarriage, gestational diabetes, and pregnancy-induced hypertension. These are risks that persist even after conception is achieved and that warrant active management through pregnancy.

Miscarriage rates in women with PCOS are estimated at 30-50% per pregnancy in some studies, substantially higher than the general population rate of 10–20%.¹⁵ The mechanisms are multiple: hyperinsulinemia disrupts endometrial receptivity and early placentation; elevated androgens alter the endometrial immune environment; chronic low-grade inflammation impairs trophoblast invasion; and LH hypersecretion may compromise oocyte and embryo quality in the periovulatory period.

NAC combined with folic acid has demonstrated statistically significant reductions in miscarriage rates in women with PCOS compared to folic acid alone in an RCT – one of the few naturopathic interventions with direct miscarriage reduction evidence in this population.⁹ Continuing insulin-sensitizing treatment (dietary modification, inositol) through the first trimester supports endometrial and placental function during the period when miscarriage risk is highest.

For women with PCOS who have experienced recurrent pregnancy loss, a comprehensive workup beyond the PCOS diagnosis itself is warranted — antiphospholipid antibodies, thyroid antibodies, and homocysteine in particular. See the recurrent miscarriage page → for full details.

PCOS and Coming Off the Pill

Many women are first prescribed the pill in their teens or twenties for PCOS-related symptoms – irregular cycles, acne, or hirsutism – without receiving a formal diagnosis or understanding of the underlying condition. The pill manages these symptoms effectively while it is being taken, but does not address the insulin resistance and androgen excess driving them. When the pill is stopped to attempt conception, PCOS symptoms and anovulation often return, sometimes more prominently than before.

Women in this situation frequently present with their first recognized PCOS symptoms in their late 20s or 30s, having been on the pill since adolescence, with no cycle data and no prior investigation. The clinical priority is establishing which PCOS phenotype they have, measuring current metabolic and hormonal status, and building a treatment protocol before or concurrent with conception attempts.

The pill also depletes several nutrients directly relevant to PCOS management and preconception health, including folate, B6, B12, magnesium, and zinc, which need to be repleted in the post-pill preconception period. See the hormonal birth control and fertility page → for full details on post-pill preconception preparation.

Frequently Asked Questions About Infertility and PCOS

Can I get pregnant naturally with PCOS?

Many women with PCOS conceive naturally once the underlying hormonal and metabolic imbalances are addressed. The primary obstacle to natural conception in PCOS is anovulation, and anovulation is directly treatable through insulin sensitization, androgen reduction, and hormonal rebalancing. The specific treatment approach depends on which PCOS phenotype you have, which requires testing to establish.

How does PCOS affect fertility?

PCOS impairs fertility primarily through disrupted ovulation. In Classic PCOS, elevated insulin drives excessive androgen production, which disrupts normal GnRH pulsatility and prevents the LH surge required for ovulation. In non-classic presentations, anovulation may be driven by thyroid dysfunction, hyperprolactinemia, or inadequate estrogen. Conception requires ovulation; restoring regular ovulation is the central fertility goal in PCOS management.

Does PCOS affect egg quality?

Yes. Women with PCOS have elevated oxidative stress in follicular fluid, which impairs oocyte mitochondrial function and increases the risk of chromosomal errors in eggs. In IVF cycles, women with PCOS may retrieve many eggs but have a lower proportion of mature, high-quality eggs than the quantity alone suggests. Antioxidant supplementation – CoQ10, melatonin, vitamin C, vitamin E – directly addresses this mechanism.

Is PCOS the cause of my irregular periods?

PCOS is a common cause of irregular or absent periods, but not the only one. Hypothyroidism, hyperprolactinemia, hypothalamic amenorrhea (related to low body weight, excessive exercise, or chronic stress), and premature ovarian insufficiency can all cause irregular cycles and polycystic-appearing ovaries on ultrasound without meeting the full diagnostic criteria for PCOS. This is why testing, not assumption, is the correct starting point.

Will I need Letrozole for PCOS?

Not necessarily. Ovulation induction with Letrozole is a medical intervention with a role in PCOS management, particularly when natural approaches have not produced ovulation within a reasonable timeframe or when there is time pressure. Naturopathic treatment targets the hormonal and metabolic drivers of anovulation and may restore spontaneous ovulation without requiring ovulation induction. If medical ovulation induction is pursued, naturopathic preparation optimizes the follicular environment and endometrial receptivity around each cycle.

Does PCOS go away after pregnancy?

PCOS does not resolve after pregnancy. The underlying metabolic and hormonal tendencies persist after delivery, and women with PCOS have increased lifetime risks of type 2 diabetes, cardiovascular disease, and endometrial cancer compared to women without PCOS. Ongoing management of insulin resistance and androgen excess after pregnancy and through perimenopause is relevant to long-term health, not just fertility.

Can PCOS cause miscarriage?

Yes. Women with PCOS have significantly higher miscarriage rates than the general population, estimated at 30–50% in some studies, driven by hyperinsulinemia, chronic inflammation, androgen excess, and endometrial immune dysregulation. Addressing these factors before and during early pregnancy is directly relevant to pregnancy maintenance, not just to conception.

Updated PCOS or PMOS and Fertility Research Citations

1. Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril. 2004;81(1):19–25. PMID: 14711538
2. Arduc A, et al. High prevalence of Hashimoto’s thyroiditis in patients with polycystic ovary syndrome. Endocr Res. 2015;40(4):204–210. PMID: 25822940
3. Fatemi Naini A, et al. Effect of vitamin D supplementation on metabolic and endocrine parameters in PCOS women. Gynecol Endocrinol. 2022. PMID: verify before publishing
4. Barrea L, et al. Source and amount of carbohydrate in the diet and inflammation in women with polycystic ovary syndrome. Nutrients. 2019;11(11):2795. PMID: 31731609
5. Stepto NK, et al. Women with polycystic ovary syndrome have intrinsic insulin resistance on euglycaemic–hyperinsulaemic clamp. Hum Reprod. 2013;28(3):777–784. PMID: 23293219
6. Palomba S, et al. Lifestyle interventions in PCOS: a systematic review. Reprod Biomed Online. 2018;37(2):184–201. PMID: 29898884
7. Unfer V, et al. Inositols in PCOS: myth or reality? A systematic review. Reprod Biomed Online. 2020;40(2):305–312. PMID: 31901312
8. Monastra G, et al. The use of inositol(s) isomers in the treatment of polycystic ovary syndrome. Arch Gynecol Obstet. 2017;295(5):1297–1301. PMID: 28367605
9. Thakker D, et al. N-acetylcysteine for polycystic ovary syndrome: a systematic review and meta-analysis. J Obstet Gynaecol Res. 2015;41(4):479–489. PMID: 25494321
10. Li MF, et al. Therapeutic effect of berberine on metabolic diseases. Biomed Pharmacother. 2018;99:284–292. PMID: 29334657
11. Pirola CJ, Gianotti TF. Coenzyme Q10 in PCOS. Mol Aspects Med. 2022;83:101001. PMID: verify before publishing
12. Khani B, et al. Effect of omega-3 fatty acids on androgen profile and menstrual status in women with polycystic ovary syndrome. Iran J Reprod Med. 2011;9(2):131–136. PMID: 25530727
13. Grant P. Spearmint herbal tea has significant anti-androgen effects in polycystic ovarian syndrome. Phytother Res. 2010;24(2):186–188. PMID: 19585478
14. Kogure GS, et al. Effects of resistance exercise on the musculoskeletal system in PCOS women. J Strength Cond Res. 2016. PMID: verify before publishing
15. Palomba S, et al. Miscarriage in women with polycystic ovary syndrome: a systematic review and meta-analysis. Hum Reprod Update. 2021;27(5):844–861. PMID: 33943024

PCOS Research

These are just a couple of studies that demonstrate the benefit of naturopathic treatment for Polycystic Ovarian Syndrome.

PCOS, BMI and Fertility

A study looking at the connection between body mass index (BMI) and fertility found that a higher than normal BMI was an independent negative factor for many aspects of fertility. These negative effects were more profound in those with severe obesity and with PCOS.   Source: The effect of female body mass index on in vitro fertilization cycle outcomes: a multi-center analysis. 2018.  Journal of Assisted Reproduction and Genetics, 1-11.

Acupuncture, TCM and PCOS

In a randomized controlled study, 60 patients were assigned to a control or observational group where they were given acupuncture combined with Chinese medicine for 3 cycles. Acupuncture combined with Chinese medicine was found to improve the endocrine levels and insulin resistance of PCOS as well as increased pregnancy rates.  Source: [Acupuncture and Chinese medicine of artificial cycle therapy for insulin resistance of polycystic ovary syndrome with phlegm damp type and its mechanism]. Zhongguo Zhen Jiu. 2017 Nov 12;37(11):1163.