Polyendocrine Metabolic Ovarian Syndrome (PMOS), previously known as Polycystic Ovary Syndrome (PCOS), is the most common endocrine disorder affecting women of reproductive age globally. Although the name PMOS has been proposed to better represent the pathophysiology of the condition, the clinical presentation remains unchanged. The updated terminology reflects a broader and more comprehensive understanding of the metabolic and endocrine dysfunction driving PMOS rather than the isolated ovarian involvement in this condition.¹^-³

PMOS Pathophysiology

PMOS is not simply a dysfunction of the ovary, but a multifactorial endocrine disorder.¹^,² Insulin resistance, independent of body size, is a key upstream driver of PMOS in individuals with and without a genetic predisposition to ovarian enzyme dysfunction.² Chronically elevated insulin contributes to PMOS through several mechanisms, including:

• Stimulating ovarian androgen production
• Reducing hepatic production of sex hormone-binding globulin (SHBG) 
• Increasing biologically available androgens
• Contributing to altered follicular development and ovulatory dysfunction through disrupted hypothalamic-pituitary-ovarian (HPO) axis signaling

Altered luteinizing hormone (LH) signaling often accompanies this disrupted HPO axis communication, further stimulating ovarian androgen production and perpetuating the hyperandrogenic cycle.² Together, these physiologic changes impair normal follicle maturation and contribute to many of the hallmark features of PMOS, including irregular menstrual cycles, anovulation, acne, hair changes, fertility challenges, and broader metabolic symptoms. ¹^-³

Although ovarian androgen production is often emphasized in PMOS, adrenal androgen excess may also contribute to the syndrome in a subset of patients.¹^,² The adrenal glands produce dehydroepiandrosterone (DHEA) and its sulfated storage form, DHEA-S, which can serve as upstream precursors for downstream androgen production in peripheral tissues. This phenotype is sometimes described as adrenal PMOS. Stress, inflammation, and blood sugar dysregulation can commonly increase DHEA production through hypothalamic-pituitary-adrenal (HPA) axis signaling. Adrenal PMOS may also arise in patients whose adrenal glands are naturally hyperresponsive to normal ACTH signaling. Increased adrenal androgen output may contribute to hyperandrogenic symptoms such as acne, hirsutism, scalp hair thinning, and menstrual irregularity even when ovarian androgen markers appear more normal.¹^,²

Because PMOS is strongly tied to insulin and broader endocrine function, long-term management should consider not only reproductive outcomes but also long-term cardiometabolic risks, such as type 2 diabetes and cardiovascular disease.³ Lifestyle interventions, including individualized approaches to diet, movement, sleep, and stress management, remain foundational.

Signs and Symptoms of PMOS

Clinical presentation can vary considerably, but the following are some of the most common signs and symptoms of PMOS.

Menstrual and Ovulatory Changes (often appear early)

• Irregular cycle length
• Long cycles (>35 days)
• Missing or infrequent periods (fewer than 6–9 per year)
• Anovulatory cycles
• Difficulty identifying predictable fertile windows
• Light or heavy menses
• Polycystic ovaries on ultrasound (in some, not all)

Changes in the menstrual cycle may occur before other symptoms emerge and can impact overall reproductive health and fertility.

Hyperandrogenic Skin and Hair Manifestations

• Persistent or adult acne
• Increased facial or body hair growth (hirsutism)
• Scalp hair thinning
• Oily skin
• Seborrheic changes

These features are often driven by elevated androgens and altered androgen metabolism.

Metabolic Symptoms

• Weight gain or weight loss resistance
• Central adiposity
• Hyperglycemia and/or hyperinsulinemia
• Blood sugar fluctuations
• Increased appetite and cravings
• Fatigue

Many patients seeking care for weight gain associated with PMOS ultimately demonstrate underlying insulin resistance.

Diagnosis of PMOS

The International Evidence-Based Guideline for the Assessment and Management of PCOS 2023 recommends that diagnosis requires the presence of 2 out of the following 3 criteria, and exclusion of conditions such as hypothyroidism, hyperprolactinemia, and non-classic congenital adrenal hyperplasia that may present with similar clinical features.³

The criteria include:

• Clinical or biochemical hyperandrogenism
• Ovulatory dysfunction
• Findings of polycystic ovaries on ultrasound or elevated AMH levels

In adolescents, both hyperandrogenism and ovulatory dysfunction must be present and ultrasound and AMH testing are not recommended in this population.^3,4

How DUTCH Testing Can Add Clinical Insight in PMOS

DUTCH testing is not a diagnostic test for PMOS and should not replace established diagnostic criteria. However, for providers using hormone testing, the DUTCH test offers an at-home hormone testing option to provide additional information that supports a more individualized treatment plan for patients with PMOS. The DUTCH test not only measures hormone production but also evaluates metabolism patterns that offer key insights into a patient’s clinical presentation.   

1. Expanded Androgen Assessment

DUTCH evaluates both parent and downstream androgen metabolites. This broader view highlights not just androgen production, but androgen metabolism, which can influence hyperandrogenic states in PMOS.

One of the challenges in assessing hormones in PMOS is that circulating testosterone does not always reflect tissue-level androgen activity, and this is where 5α-androstanediol becomes clinically interesting. 5α-androstanediol is a downstream metabolite formed from intracellular 5α-DHT, our most potent androgen metabolite. Because 5α-DHT largely remains inside cells, direct measurement may not fully capture biologically relevant androgen activity; 5α-androstanediol, however, serves as a measurable and clinically useful downstream marker of intracellular androgen metabolism.⁵

Research summarized in DUTCH’s White Paper on 5α-androstanediol highlights several observations regarding 5α-androstanediol:⁵

• Women with androgen excess symptoms—including acne, hirsutism, menstrual irregularities, scalp hair loss, and PCOS—often demonstrate elevated 5a-androstanediol
• Elevations may occur even when total testosterone remains within reference range
• Changes in 5α-androstanediol may parallel symptom improvement
• 5a-androstanediol may function as a more sensitive marker of androgenic effects than some traditional androgen measurements alone

2. Ovulation Assessment Through Progesterone Production

Because oligo- and anovulation occur in PMOS, progesterone metabolite assessment can provide insight into whether ovulation occurred as well as relative luteal hormone production.

Due to infrequent ovulation, progesterone is often low, leaving patients with PMOS in a relative estrogen dominant state. 

3. Cortisol and Adrenal Pattern Assessment

Because adrenal output can contribute to PMOS phenotypes, evaluating cortisol patterns may offer insight into HPA axis function, especially if adrenal androgen production is elevated. The key adrenal evaluations on the DUTCH test include:

• Diurnal free cortisol rhythm
• Total cortisol output
• Cortisol clearance patterns

In this case, this patient has elevated free cortisol and DHEA production, indicating that there may be excess adrenal output contributing to her androgen excess. Stress reduction, anti-inflammatories, blood sugar regulation, and grounding adaptogens may all be helpful supports here in lowering cortisol and adrenal androgen production, which may alleviate symptoms related to PMOS. 

4. Estrogen Production and Metabolism

Patients with PMOS may have elevated estrogens due to high androgens and peripheral conversion. Evaluating estrogen levels and metabolism may be particularly helpful in the setting of infrequent ovulation and lower progesterone exposure due to long-term risk of endometrial hyperplasia and cancer.

For example, given this patient’s high estradiol and low-end methylation activity, she may benefit from methylation supports to assist with more efficient phase 2 estrogen clearance. We can also see that progesterone is low and that ovulation has not occurred in this case; anovulation is a common occurrence in PMOS, and one of the goals of treatment in PMOS is to support regular ovulation.  

In Summary

PMOS is increasingly recognized as a complex condition shaped by reproductive, metabolic, and endocrine physiology rather than isolated ovarian dysfunction. While conventional laboratory assessment remains foundational, the DUTCH test may provide additional insight into hormone production and metabolism patterns that influence the clinical presentation. For healthcare providers managing PMOS, evaluating androgen metabolism, ovulatory status, and HPA axis function together on the DUTCH test may provide a more comprehensive understanding of a patient's presentation and help inform a more targeted, individualized treatment plan.

References

1. Azziz R, Carmina E, Chen Z, et al. Polycystic ovary syndrome. Nat Rev Dis Primers. 2016;2:16057. doi:10.1038/nrdp.2016.57 
2. Rosenfield RL, Ehrmann DA. The pathogenesis of polycystic ovary syndrome: the hypothesis of PCOS as functional ovarian hyperandrogenism revisited. Endocr Rev. 2016;37(5):467-520. doi:10.1210/er.2015-1104 
3. Teede HJ, Tay CT, Laven J, et al. Recommendations from the 2023 International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome. Fertil Steril. 2023;120(4):767-793. doi:10.1016/j.fertnstert.2023.07.025
4. Shukla A, Choudhary A. Polycystic ovarian syndrome. In: StatPearls [Internet]. StatPearls Publishing; updated January 2025. Accessed June 23, 2026. https://www.ncbi.nlm.nih.gov/books/NBK459251/
5. Jaferi A. 5α-Androstanediol in women: a marker of androgen status in women. Precision Analytical Inc; 2024. Accessed June 29, 2026. https://dutchtest.com/api/files/file/5a-Androstanediol%20in%20Women.pdf