Key takeaways
PCOS is not one single disease but a spectrum: there are different forms with varying hormonal and metabolic causes, which explains why symptoms can differ greatly from one woman to another.
Two ways to classify it:
→ phenotypes A/B/C/D (based on medical criteria: androgens, ovulation, ovaries)
→ functional subtypes (based on the dominant cause: insulin, inflammation, adrenal glands, post-pill).
4 major functional types of PCOS:
→ insulin-resistant (the most common, linked to blood sugar and metabolism)
→ inflammatory (linked to chronic inflammation)
→ adrenal (linked to stress and adrenal hormones)
→ post-pill (temporary after stopping hormonal contraception).
The key challenge: personalizing care: identifying your type of PCOS makes it possible to tailor treatment (diet, lifestyle, medical care) and improve symptoms in a targeted way.
What are the 4 different types of PCOS?
You have probably heard of PCOS (polycystic ovary syndrome) and may be wondering about the four profiles that make it up. It is important to understand that PCOS is not a “single” diagnosis: it is a spectrum of hormonal and metabolic manifestations.
The 4 types of PCOS are now described in the scientific literature: the insulin-resistant form (in about 65% of patients1), the post-pill form (15% to 20% of cases2), the inflammatory form (30% to 35%3), and the adrenal form (10% to 15%4). Each of these subtypes involves specific mechanisms of androgen excess, inflammation, or metabolic dysfunction.
Two classification approaches: medical phenotypes (A/B/C/D) and functional subtypes
In clinical practice and research, two major methods are used to structure PCOS:
Medical phenotypes A, B, C, and D, based on the presence or absence of three diagnostic criteria:
- hyperandrogenism (clinical or biochemical),
- ovulatory dysfunction (irregular cycles or anovulation)
- polycystic ovarian morphology on ultrasound.
Functional subtypes, which seek to explain PCOS through underlying mechanisms: ovarian sensitivity to gonadotropins, dominant metabolic profile (insulin resistance, inflammation, etc.).
They explain the dominant cause of PCOS:
- Insulin-resistant PCOS
- Inflammatory PCOS
- Adrenal PCOS
- Post-pill PCOS
In practice, the A/B/C/D phenotypes are most often used to make a standardized diagnosis, and the analysis is then refined through the physiological subtype in order to offer personalized treatment.
| Phenotype | Hyperandrogenism | Ovulatory dysfunction | Polycystic ovaries | Metabolic risk | Associated functional profile |
|---|---|---|---|---|---|
| A (Complete) | Yes | Yes | Yes | High (insulin resistance, abdominal obesity, risk of metabolic syndrome up to 60%) | High ovarian response to LH |
| B (Non-PCO) | Yes | Yes | No | High (insulin resistance in 50%) | “Metabolic” profile |
| C (Ovulatory) | Yes | No (regular cycles) | Yes | Intermediate (moderate cardiovascular risk) | Predominant hyperandrogenism |
| D (Non-hyperandrogenic) | No | Yes | Yes | Low to moderate | “Mild” or atypical form |
The four PCOS phenotypes
To better support each patient, it is essential to detail these four configurations according to the Rotterdam criteria:
Phenotype A (Complete)
This profile brings together all three criteria: hyperandrogenism, anovulation, and polycystic morphology. It is the most frequently reported form, accounting for nearly 40% of cases7. Clinical signs include persistent acne, hirsutism, and irregular cycles. Metabolically, abdominal weight gain and insulin resistance are seen in 70% to 80% of patients1. Fertility may be impaired, sometimes requiring more intensive ovarian stimulation.
Phenotype B (Non-PCO)
In this case, hyperandrogenism and ovulatory dysfunction are present, but without a polycystic appearance on ultrasound. This profile represents about 20% of patients. Despite the absence of visible cysts, metabolic disorders (insulin resistance, overweight) are comparable to those seen in phenotype A, highlighting the importance of personalized follow-up.
Phenotype C (Ovulatory)
This subgroup combines hyperandrogenism and cysts, while maintaining regular cycles. It affects nearly 25% of diagnosed women. Skin symptoms (acne, mild hirsutism) are predominant, while fertility often remains preserved. Metabolic monitoring is still recommended, however, as 30% may develop insulin resistance over the long term.
Phenotype D (Non-hyperandrogenic)
The so-called “mild” form includes 15% of patients. The ovaries are polycystic and cycles are irregular, without clinical or biochemical hyperandrogenism. The metabolic profile is generally close to normal, but gynecological and endocrine follow-up is needed in cases of pregnancy planning or circulatory complications. Some women also report occasional tingling, generally linked to hormonal imbalances.
Functional subtypes of PCOS
Insulin-resistant PCOS
In this subtype, insulin resistance is at the core of the mechanism. According to a 2018 meta-analysis, 65% of patients with PCOS have clinically significant insulin resistance. Hyperinsulinemia leads to an overproduction of androgens, worsening anovulation and weight gain.
Specific symptoms
- Abdominal weight gain even with a moderate diet.
- Excessive hunger or difficulty losing weight despite effort.
- Acne and hirsutism (facial or body hair).
- Frequent fatigue and non-restorative sleep attempts.
- Acanthosis nigricans (darkened skin areas on the neck and underarms).
Diagnosis
The workup includes fasting blood glucose, fasting insulin, HbA1c, and often a glucose tolerance test. The HOMA-IR score helps assess the severity of insulin resistance. Clinical examination looks for an increased waist circumference (> 88 cm) and signs of hyperandrogenism.
Management
Metformin, a first-line insulin sensitizer, improves cycle regularity and fertility. A low-glycemic-index diet rich in fiber and omega-3s, combined with 150 minutes of moderate physical activity per week, is recommended. Recent studies show that GLP-1 analogs can reduce body weight by 5% to 10%12 and improve insulin resistance.
Post-pill PCOS
In 15% to 20% of women, stopping hormonal contraception triggers a temporary phase of irregular cycles, increased androgens, and a polycystic appearance on ultrasound. This phenomenon generally lasts 3 to 6 months, while the hypothalamic-pituitary axis regains its balance.
Insulin resistance is rarely a factor here. Symptomatic support (dietary regulation, stress management) is sufficient in most cases. If symptoms persist beyond 6 months, a complete hormonal workup is necessary to rule out persistent PCOS.
Inflammatory PCOS
Low-grade inflammation is implicated in 30% to 35% of PCOS cases. Chronic activation of the immune system, measured by elevated C-reactive protein (CRP) and pro-inflammatory cytokines, promotes insulin resistance and androgen excess.
Diagnosis
In addition to the Rotterdam criteria, CRP, IL-6, and TNF-α are measured. Clinically, persistent fatigue, joint pain, digestive issues, and inflammatory acne are assessed.
Management
An anti-inflammatory diet (colorful fruits, green vegetables, omega-3s) reduces CRP by an average of 20% after 3 months. Regular use of stress-management techniques (meditation, heart-rate coherence) improves the hormonal profile.
Menopause supplements, such as inositol (2 g/day), have shown reductions in IL-6 and improved insulin sensitivity.
Our supplement [MY] ESSENTIALS METABOLISM ACTIVATORS contains Myo-inositol:
A key natural compound for cellular metabolism, it promotes better insulin sensitivity and plays an active role in hormonal regulation. Particularly useful in cases of PCOS, it helps stabilize and harmonize hormonal cycles.
Adrenal PCOS
In this form (10% to 15% of cases), overproduction of DHEA-S by the adrenal glands is predominant. Chronic stress and activation of the corticotropic axis explain this excess androgen production.
Symptoms
- Irregular cycles or amenorrhea.
- Hirsutism, acne resistant to conventional treatments.
- Anxiety, insomnia, mood disturbances.
- Weight gain that is difficult to reverse.
Diagnosis
After excluding other forms of PCOS, DHEA-S, DHEA, and 17-OHP are measured to confirm adrenal origin. A high DHEA-S level of > 7 µmol/L points toward this subtype.
Management
A lifestyle focused on sleep, stress management (yoga, sophrology), and a balanced diet can reduce DHEA-S production by 15% to 25%15. Medically, a combined estrogen-progestin pill is often used and, if necessary, metformin in cases of a high HOMA-IR index.
How can you identify your type of PCOS?
Quick symptom checklist
Type of PCOS Associated symptoms
| Type of PCOS | Associated symptoms |
|---|---|
| Insulin-resistant PCOS |
|
| Inflammatory PCOS |
|
| Adrenal PCOS |
|
| Post-pill PCOS |
|
Biological tests to request
- Fasting blood glucose
- Fasting insulin
- Metabolic tests: fasting blood glucose, insulin, HOMA-IR, HbA1c.
- Total and free testosterone
- DHEA-S (> 7 µmol/L suggesting adrenal origin)
- Inflammatory markers: CRP, cytokines (IL-6, TNF-α) if inflammatory PCOS is suspected.
- Complete hormonal panel: androgens (testosterone, DHEA-S), SHBG.
FAQ
What are the distinctive symptoms of each type of PCOS?
Insulin-resistant: abdominal weight gain, fatigue, acanthosis nigricans.
Post-pill: temporary onset or worsening of acne, hirsutism, and cycle disturbances after stopping the pill.
Inflammatory: inflammatory acne, diffuse joint pain, chronic fatigue.
Adrenal: high DHEA-S levels, anxiety, sleep disturbances, persistent hirsutism.
Can PCOS change from one type to another?
Yes. For example, PCOS initially classified as post-pill may reveal insulin resistance over the longer term, especially if metabolic factors (overweight, family history of diabetes) appear.
What tests confirm each subtype of PCOS?
Complete hormonal panel: androgens (testosterone, DHEA-S), SHBG.
Metabolic tests: fasting blood glucose, insulin, HOMA-IR, HbA1c.
Inflammatory markers: CRP, cytokines (IL-6, TNF-α) if inflammatory PCOS is suspected.
Pelvic ultrasound for the polycystic appearance of the ovaries.
By combining these data, your healthcare practitioner will be able to make a precise diagnosis and recommend the treatment best suited to your situation. If your menopause symptoms interfere with your daily life, it is essential to discuss them for appropriate care.
Sources:
- International evidence-based guideline for the assessment and management of PCOS (2023)
https://www.monash.edu/medicine/sphpm/mchri/pcos/guideline - Insulin Resistance and Polycystic Ovary Syndrome – Endocrine Reviews (2018)
https://academic.oup.com/edrv/article/39/2/105/4792933 - Epidemiology, Diagnosis, and Management of Polycystic Ovary Syndrome – Clinical Epidemiology (2014)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3872139/ - Inflammation in Polycystic Ovary Syndrome – Journal of Clinical Endocrinology & Metabolism (2011)
https://academic.oup.com/jcem/article/96/2/333/2833674 - Adrenal Hyperandrogenism in Polycystic Ovary Syndrome – Fertility and Sterility (2006)
https://www.sciencedirect.com/science/article/pii/S0015028206005093
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