If you have been working with female clients for any length of time, you have almost certainly encountered a client who fits the PCOS picture: irregular cycles, acne, hair loss, excess facial or body hair, insulin resistance, weight gain, and mood dysregulation. Despite how convincing that picture might have been, though, there is a really good chance your client had not received the diagnosis.

The name polycystic ovarian syndrome (PCOS) always had a problem, which is that it pointed practitioners toward the ovaries and away from the broader metabolic and endocrine dysfunction that actually drives the condition. This knowledge gap and naming mismatch have resulted in up to 70% of affected individuals remaining undiagnosed, and, of those who did receive a diagnosis, significant dissatisfaction with the experience due to delayed diagnosis and lack of support (Teede et al., 2026; Gibson-Helm et al., 2017).

The recent renaming of PCOS as PMOS, or polyendocrine metabolic ovarian syndrome, might feel like little more than an acronym change. Alternatively, it might feel, as I know it does for many of us in the functional space, like confirmation of what we have already known for years. In either case, it is easy to view the update as insignificant. However, this rename has the potential to offer so much more: erasing the blind spots that leave many clients underassessed and underserved.

This guide is designed to help you see the full symptom constellation of PMOS and to understand the importance of a whole-body assessment. You will learn what clients with this syndrome experience, how it shows up across multiple systems, what a thorough functional assessment looks like, and where we have the greatest opportunities from a functional nutrition perspective.

What the Rename Corrects

The original PCOS diagnostic criteria, developed in the 1990s, required the presence of polycystic ovaries on ultrasound, along with at least one of the following: irregular or absent ovulation, or clinical or biochemical signs of hyperandrogenism. The name itself implied that the ovaries were the origin of the problem, but research has consistently shown otherwise.

The new name shifts the focus away from the ovaries alone to the condition’s broader systemic endocrine and metabolic features. It emphasizes the underlying pathophysiology involving interacting contributions from insulin resistance and hyperinsulinemia, neuroendocrine/hypothalamic-pituitary-ovarian (HPO) axis dysregulation, and androgen excess.

Perhaps most importantly, the name change signals to providers that an expanded awareness and more comprehensive assessment are necessary. Further, it corrects the misconception that everyone with this syndrome will have visible cystic ovaries, a common reason many have been told they did not have PCOS. Ultimately, the rename reframes the diagnosis around its interconnected endocrine and metabolic pathways, not a single anatomical finding.

Mapping the Patterns: How PMOS Shows Up Across the Body

Clients with PMOS often present with a cluster of symptoms that have been addressed individually but never connected. While none of these symptoms in isolation is specific to the disorder, together they are a strong indication that it could be present.

Being able to trace these patterns across body systems enables you to support your clients better. Not only can you target underlying drivers with more customized recommendations, but you can also recognize the presentation sooner, allowing you to refer out if you are not a diagnosing provider.

Hormonal Imbalance

What your client is experiencing

• Irregular or absent menstrual cycles
• Anovulation
• Infertility
• Unpredictable or heavy bleeding

The pattern behind it

At the center of PMOS is disrupted communication between the brain, the ovaries, and the body’s metabolic signals. A dysregulated HPO axis, along with elevated insulin, causes increased ovarian production of androgens, like testosterone, and disrupts normal follicle development (Goodarzi et al., 2011). This leads to more anovulatory cycles, causing reduced progesterone production and, as a result, relatively unopposed estrogen. It is the small follicles that remain in the ovaries, not cysts, that create the characteristic “polycystic” appearance seen on ultrasound (Joham et al., 2022).

Metabolic Health

What your client is experiencing

• Weight gain that’s difficult to lose despite diet and lifestyle changes
• Increased abdominal fat
• Energy crashes
• Carbohydrate cravings
• Blood sugar markers that appear “normal” despite signs of metabolic dysfunction

The pattern behind it

Insulin resistance is a key driver of PMOS and contributes significantly to the dysfunction that is recognized with the syndrome. Insulin stimulates the ovaries to produce testosterone, while the liver produces less sex hormone-binding globulin (SHBG). This leads to a higher amount of free, active testosterone in circulation (Goodarzi et al., 2011). Insulin resistance also promotes visceral fat, which further fuels the cycle of insulin resistance and hormonal imbalance. This does not just contribute to hormone imbalance; it has broad cardiometabolic implications, as PMOS is associated with an increased risk of type 2 diabetes, metabolic syndrome, and cardiovascular disease (Teede et al., 2023; Henney et al., 2025).

Adrenal Function

What your client is experiencing

• Acne
• Increased facial or body hair (hirsutism)
• Hair loss
• Other signs of androgen excess
• Significant stress
• Elevated DHEA-S on lab testing

The pattern behind it

In up to 20-30% of people with PMOS, the adrenal glands also contribute to androgen excess, mostly through increased DHEA-S production. While the reasons for this are not fully understood, the current understanding is that the adrenal glands over-respond to their normal signal from the pituitary, producing extra androgens, which are measured as DHEA-S (Torchen et al., 2025). Chronic stress may play an additional role, since it activates the same glands but isn’t thought to be the primary driver (Benjamin et al., 2021; Lobo et al., 1983). Identifying this pattern can help explain why some clients experience significant androgen-related symptoms despite having relatively mild menstrual symptoms.

Digestive and Gut Health

What your client is experiencing

• Bloating
• Constipation
• Diarrhea
• Irregular bowel habits
• Food sensitivities
• Persistent digestive discomfort

The pattern behind it

Alterations in the gut microbiome have been associated with increased inflammation, insulin resistance, and high androgens in individuals with PMOS (Qi et al., 2019; Jin et al., 2026). The gut also affects hormone metabolism, which may further influence hormone balance (Senthilkumar et al., 2025). While not the primary driver of PMOS, the gut’s significant impact on metabolic and hormonal health makes it a priority consideration in a functional approach.

Skin

What your client is experiencing

• Jawline or cystic acne
• Oily skin
• Hirsutism
• Hair loss
• Velvety and darkened skin plaques known as acanthosis nigricans
• Recurrent painful nodules in the armpit or groin suggestive of hidradenitis suppurativa (HS)

The pattern behind it

Elevated androgen hormones increase sebum production, disrupt the skin’s cell-shedding process, and affect hair follicles, leading to acne, hirsutism, and hair loss (Ghosh et al., 2014; Zeng et al., 2020). The hallmark insulin resistance of PMOS can also increase the presence of other dermatological conditions (Housman et al., 2014). Evidence suggests an association between PMOS and HS, a chronic inflammatory skin condition. While HS is a distinct diagnosis, the two conditions frequently coexist and share common drivers, including hyperandrogenism, insulin resistance, obesity, and systemic inflammation (Phan et al., 2020; Bouadi et al., 2024).

Mood and Neurological Health

What your client is experiencing

• Anxiety
• Depression
• Mood swings
• Brain fog
• Difficulty concentrating
• Food cravings
• Executive function challenges

The pattern behind it

Anxiety, depression, brain fog, and cognitive symptoms are more prevalent in individuals with PMOS. While it is not fully understood why, research suggests factors such as insulin resistance, hyperandrogenism, altered neurotransmitter signaling, and the emotional burden of living with a chronic endocrine disorder are likely factors (Cooney et al., 2017; Huddleston et al., 2024; Perović et al. 2022; Sarkisian et al., 2023).

A Functional Assessment Goes Beyond the Ovaries

Understanding the broader endocrine nature of PMOS and the interconnectedness across systems, rather than viewing acne separately from irregular cycles and mood instability, is an important skill that allows you to support your clients better.

Standard testing often includes only a basic hormone panel and pelvic ultrasound, which are useful for diagnostic purposes, but, from a functional nutrition perspective, are insufficient for understanding the full metabolic and endocrine picture or knowing where to focus your recommendations. Tests to consider for a more comprehensive look at potential contributing factors include:

Functional Nutrition Leverage Points

Because PMOS is a multi-driver syndrome and can present differently from one client to another, our most effective recommendations will be personalized to the client and the specific imbalances identified through a thorough assessment.

Support the Metabolic Foundation

Improving insulin sensitivity is one of the highest-impact interventions for most clients with PMOS, as hyperinsulinemia is a key driver of androgen excess and many of its downstream symptoms, as well as a significant risk factor for future metabolic complications (“ACOG Practice Bulletin No. 194: Polycystic Ovary Syndrome”, 2018).

Nutrition

• Emphasize a lower-glycemic diet rich in protein, fiber, and healthy fats to reduce postprandial glucose and insulin levels (Zhang et al., 2019).
• Consider meal timing strategies, such as avoiding late-night eating, spacing meals appropriately, and consuming carbohydrates later in the meal.

Lifestyle

• Incorporate regular physical activity, including aerobic and resistance exercise, to improve insulin sensitivity, body composition, and cardiometabolic health (Kite et al., 2019).

Supplementation

• Evidence shows that berberine, cinnamon, vitamin D, and myo- and D-chiro-inositol may contribute to improvements in insulin sensitivity for this population (Zamani et al., 2022; Heshmati et al., 2021; Wu et al., 2026; Duan et al., 2026).
• N-acetylcysteine (NAC) may improve insulin sensitivity and other metabolic and endocrine outcomes in females with PMOS (Liu et al., 2023).

Support Healthy Androgen Balance

While addressing upstream metabolic dysfunction has a significant impact on reducing androgens, additional strategies may help reduce related symptoms.

Nutrition

• Spearmint tea has demonstrated some anti-androgenic effects in females with PMOS (Grant, 2010).

Lifestyle

• Minimize unnecessary exposure to endocrine-disrupting chemicals to support overall hormone balance (Lemogne et al., 2025).

Supplementation

• Zinc may improve androgen-associated symptoms such as hirsutism and hair loss (Jamilian et al., 2016).
• In some trials, resveratrol has demonstrated reductions in testosterone and DHEA-S in females with PMOS (Ali Fadlalmola et al., 2023).

Support Endocrine Resilience

Sleep and stress influence metabolic health, inflammation, and overall endocrine function.

Lifestyle

• Prioritize sufficient, restorative sleep, as poor sleep is associated with worsened insulin resistance, metabolic dysfunction, and HPA axis dysregulation (Sondrup et al., 2022; Guyon et al., 2014).
• Address chronic stress through practices that resonate with your client, such as mindfulness, breathwork, counseling, or simply increasing joyful activities. While stress is not considered a root cause of PMOS, minimizing it can support overall endocrine and metabolic health.

Supplementation

• Adaptogenic herbs such as ashwagandha, rhodiola, or holy basil may improve the stress response and increase resilience (Tóth-Mészáros et al., 2023; McKinney et al., 2026).

Support Gut Health and Reduce Inflammation

While the gut is not considered a primary driver of PMOS, research suggests it could play a much larger role in the development and progression of the condition, and that improving gut health can support insulin sensitivity, inflammation, and hormone balance (Li et al., 2025).

Nutrition

• Increase dietary fiber from vegetables, legumes, nuts, seeds, and whole grains to support a healthy microbiome and estrogen metabolism.
• Follow an anti-inflammatory diet that emphasizes omega-3-rich foods, colorful vegetables, polyphenol-rich foods, and minimizes processed foods and refined carbohydrates (Liu et al., 2026).
• Emphasize liver- and gallbladder-supportive foods, such as beets and leafy greens, to support bile flow, an important route of elimination for estrogen.
• Identify and remove food sensitivities that may be contributing to systemic inflammation.

Supplementation

• If present, address dysbiosis and consider targeted microbiome support, such as probiotics and short-chain fatty acids, which can reduce inflammation and support metabolic health.
• Consider calcium D-glucarate, DIM, or sulforaphane to support estrogen metabolism, if indicated.
• Omega-3 fatty acids can support insulin sensitivity and may also improve androgen and inflammatory markers in those with PMOS (Moslehi et al., 2023).

The Long Game: Why Early Identification and Support Matter

PMOS is not a condition that disappears at the end of a person’s reproductive years. Clients with PMOS have a significantly increased long-term risk of developing type 2 diabetes, cardiovascular disease, metabolic syndrome, non-alcoholic fatty liver disease, and mood disorders. With potential outcomes like these, it is easy to see that the benefits of the rename extend far beyond clarifying the diagnosis (Allen et al., 2022).

This seemingly simple nomenclature change offers an opportunity to look wider, assess deeper, and intervene earlier. Practitioners who recognize these PMOS patterns early, assess their clients comprehensively, and support the fundamental drivers are doing more than managing symptoms; they are intervening at a point in the trajectory where meaningful, lasting change is possible.

FAQ

These frequently asked questions expand on the key clinical concepts discussed in this article and provide additional context for practitioners evaluating polycystic ovarian metabolic syndrome (PMOS).

What is polycystic ovarian metabolic syndrome (PMOS)?

PMOS is a systemic endocrine and metabolic condition involving interconnected dysfunction across multiple physiological systems. Rather than being defined solely by the appearance of the ovaries, PMOS reflects the interaction of insulin resistance and hyperinsulinemia, HPO axis dysregulation, and androgen excess.

Why was the name changed from polycystic ovary syndrome?

The rename shifts the focus away from the ovaries as the presumed origin of the condition and toward its broader endocrine and metabolic features. The new terminology also helps correct the misconception that everyone with the syndrome will have visible cystic ovaries on ultrasound.

Does everyone with PMOS have polycystic ovaries?

No. The article emphasizes that the characteristic appearance on ultrasound is caused by the presence of multiple small follicles rather than ovarian cysts, and not everyone with PMOS will have this appearance. The condition is better understood through its interconnected endocrine and metabolic patterns rather than a single anatomical finding.

What are some common patterns practitioners may notice in clients with PMOS?

Clients may present with symptoms affecting multiple systems that have previously been treated as separate concerns. Patterns discussed in the article include:

• Irregular or absent menstrual cycles and anovulation
• Weight gain, abdominal fat, energy crashes, and carbohydrate cravings
• Acne, hirsutism, and hair loss
• Elevated DHEA-S or other signs of androgen excess
• Bloating, constipation, diarrhea, and other digestive concerns
• Anxiety, depression, brain fog, and difficulty concentrating
• Signs of insulin resistance or broader metabolic dysfunction

How does insulin resistance contribute to PMOS?

Insulin resistance is a key driver of PMOS. Elevated insulin can stimulate the ovaries to produce more testosterone while also reducing the liver’s production of sex hormone-binding globulin (SHBG). This increases the amount of free, active testosterone in circulation. Insulin resistance can also promote visceral fat, further contributing to metabolic dysfunction and androgen excess.

Can someone have PMOS even if their blood sugar markers appear normal?

Yes. The article notes that some clients may experience signs of metabolic dysfunction even when standard blood sugar markers appear “normal.” Looking more broadly at metabolic patterns and potential insulin resistance can provide additional context when evaluating clients with other features of PMOS.

How does PMOS affect menstrual cycles and fertility?

Dysregulation of the HPO axis, combined with elevated insulin and increased androgen production, can interfere with normal follicle development and ovulation. More anovulatory cycles can lead to reduced progesterone production and relatively unopposed estrogen, contributing to irregular or absent menstrual cycles, unpredictable bleeding, and fertility challenges.

What role do the adrenal glands play in PMOS?

In approximately 20-30% of people with PMOS, the adrenal glands may contribute to androgen excess, primarily through increased DHEA-S production. The article explains that this pattern may help account for significant androgen-related symptoms in some clients who have relatively mild menstrual symptoms.

Can chronic stress contribute to androgen excess in PMOS?

Chronic stress may play an additional role in adrenal androgen production because stress activates the adrenal glands. However, the article emphasizes that stress is not considered the primary driver of PMOS. Identifying elevated DHEA-S and other patterns of adrenal involvement can help practitioners recognize when the adrenals may be contributing to a client’s symptoms.

How does gut health influence PMOS?

The gut can influence inflammation, insulin sensitivity, and hormone metabolism. Alterations in the gut microbiome have been associated with increased inflammation, insulin resistance, and higher androgen levels in individuals with PMOS. While gut dysfunction is not considered a primary driver, its influence on metabolic and hormonal health makes it an important consideration in a functional approach.

What is the estrobolome, and why does it matter?

The estrobolome is the collection of gut bacteria involved in estrogen metabolism. Changes in the gut microbiome can influence how estrogen is metabolized and eliminated, potentially affecting overall hormone balance. Supporting healthy gut function may therefore be an important component of a comprehensive approach to PMOS.

What skin conditions or symptoms may be associated with PMOS?

Elevated androgen levels and insulin resistance can contribute to several dermatological manifestations. These may include:

• Jawline or cystic acne
• Oily skin
• Hirsutism
• Hair loss
• Acanthosis nigricans
• Hidradenitis suppurativa (HS)

Can PMOS affect mood and cognitive function?

Yes. Anxiety, depression, brain fog, and other cognitive symptoms are more prevalent in individuals with PMOS. The article discusses several potential contributing factors, including insulin resistance, hyperandrogenism, altered neurotransmitter signaling, and the emotional burden of living with a chronic endocrine disorder.

What types of testing can provide a more comprehensive assessment of PMOS?

Standard diagnostic testing may include a basic hormone panel and pelvic ultrasound. From a functional nutrition perspective, additional testing may help practitioners better understand potential contributing factors. Depending on the client’s presentation, this may include:

• Salivary or serum hormone testing
• DUTCH or salivary adrenal testing
• Serum metabolic markers
• GI-MAP testing
• Food sensitivity testing
• Thyroid markers
• Inflammatory markers

What should practitioners prioritize when supporting clients with PMOS?

Because PMOS is a multi-driver syndrome, recommendations should be individualized based on the client’s presentation and assessment findings. The article highlights several functional nutrition leverage points:

• Supporting metabolic health and insulin sensitivity
• Supporting healthy androgen balance
• Improving endocrine resilience through sleep and stress management
• Supporting gut health and reducing inflammation
• Addressing contributing environmental and lifestyle factors

What nutritional strategies may support metabolic health in clients with PMOS?

The article recommends emphasizing a lower-glycemic diet rich in protein, fiber, and healthy fats. Practitioners may also consider meal timing strategies such as avoiding late-night eating, appropriately spacing meals, and consuming carbohydrates later in the meal.

What supplements may support insulin sensitivity in clients with PMOS?

The article identifies several supplements that may contribute to improvements in insulin sensitivity, including berberine, cinnamon, vitamin D, and myo- and D-chiro-inositol. N-acetylcysteine (NAC) may also improve insulin sensitivity and other metabolic and endocrine outcomes in females with PMOS.

How can practitioners support healthy androgen balance?

Addressing upstream metabolic dysfunction can have a significant impact on androgen levels. The article also discusses additional strategies such as spearmint tea, minimizing unnecessary exposure to endocrine-disrupting chemicals, zinc, and resveratrol when appropriate.

Why are sleep and stress management important for clients with PMOS?

Sleep and stress influence metabolic health, inflammation, and overall endocrine function. Prioritizing restorative sleep may support insulin sensitivity and HPA axis regulation, while addressing chronic stress can support broader metabolic and endocrine health. The article recommends choosing stress-management practices that resonate with the individual client.

How can practitioners support gut health in clients with PMOS?

The article recommends supporting the microbiome and reducing inflammation through strategies such as increasing dietary fiber, emphasizing colorful and polyphenol-rich foods, including omega-3-rich foods, minimizing processed foods and refined carbohydrates, and identifying food sensitivities that may contribute to inflammation. When indicated, targeted microbiome support may also be considered.

Why is early identification of PMOS important?

PMOS does not simply disappear at the end of a person’s reproductive years. The condition is associated with increased long-term risks including type 2 diabetes, cardiovascular disease, metabolic syndrome, non-alcoholic fatty liver disease, and mood disorders. Recognizing PMOS patterns early provides an opportunity to assess contributing factors and support healthier metabolic and endocrine function before more significant complications develop.

Can functional nutrition practitioners diagnose PMOS?

The article emphasizes that practitioners should recognize PMOS patterns early and refer clients out when they are not diagnosing providers. Functional nutrition practitioners can use a comprehensive assessment to identify potential contributing factors and provide appropriate nutrition and lifestyle support within their professional scope.

References

ACOG Practice Bulletin No. 194: Polycystic Ovary Syndrome. (2018). Obstetrics & Gynecology, 131(6), e157–e171. https://doi.org/10.1097/AOG.0000000000002656

Ali Fadlalmola, H., Elhusein, A. M., Al-Sayaghi, K. M., Albadrani, M. S., Swamy, D. V., Mamanao, D. M., El-Amin, E. I., Ibrahim, S. E., & Abbas, S. M. (2023). Efficacy of resveratrol in women with polycystic ovary syndrome: A systematic review and meta-analysis of randomized clinical trials. The Pan African Medical Journal, 44, 134. https://doi.org/10.11604/pamj.2023.44.134.32404

Allen, L. A., Shrikrishnapalasuriyar, N., & Rees, D. A. (2022). Long-term health outcomes in young women with polycystic ovary syndrome: A narrative review. Clinical Endocrinology, 97(2), 187–198. https://doi.org/10.1111/cen.14609

Benjamin, J. J., K, M., Koshy, T., K N, M., & R, P. (2021). DHEA and polycystic ovarian syndrome: Meta-analysis of case-control studies. PLoS ONE, 16(12), e0261552. https://doi.org/10.1371/journal.pone.0261552

Bouadi, N., Rijal, H., Jeremian, R., Li, K., Abduelmula, A., Maliyar, K., Georgakopoulos, J. R., & Yeung, J. (2024). Comorbidities and risk factors associated with hidradenitis suppurativa: A systematic review and meta-analysis. Journal of Cutaneous Medicine and Surgery, 28(4), 392–393. https://doi.org/10.1177/12034754241239252

Cooney, L. G., Lee, I., Sammel, M. D., & Dokras, A. (2017). High prevalence of moderate and severe depressive and anxiety symptoms in polycystic ovary syndrome: A systematic review and meta-analysis. Human Reproduction, 32(5), 1075–1091. https://doi.org/10.1093/humrep/dex044

Duan, M., Yang, M., Li, C., Wu, X., Yin, X., & Zhu, H. (2026). Effects of inositol in women with polycystic ovary syndrome: An umbrella review of meta-analyses from randomized controlled trials. Frontiers in Endocrinology, 17, 1741509. https://doi.org/10.3389/fendo.2026.1741509

Ghosh, S., Chaudhuri, S., Jain, V. K., & Aggarwal, K. (2014). Profiling and hormonal therapy for acne in women. Indian Journal of Dermatology, 59(2), 107–115. https://doi.org/10.4103/0019-5154.127667

Gibson-Helm, M., Teede, H., Dunaif, A., & Dokras, A. (2017). Delayed diagnosis and a lack of information associated with dissatisfaction in women with polycystic ovary syndrome. The Journal of Clinical Endocrinology & Metabolism, 102(2), 604–612. https://doi.org/10.1210/jc.2016-2963

Goodarzi, M. O., Dumesic, D. A., Chazenbalk, G., & Azziz, R. (2011). Polycystic ovary syndrome: Etiology, pathogenesis and diagnosis. Nature Reviews Endocrinology, 7(4), 219–231. https://doi.org/10.1038/nrendo.2010.217

Grant, P. (2010). Spearmint herbal tea has significant anti-androgen effects in polycystic ovarian syndrome: A randomized controlled trial. Phytotherapy Research, 24(2), 186–188. https://doi.org/10.1002/ptr.2900

Guyon, A., Balbo, M., Morselli, L. L., Tasali, E., Leproult, R., L’Hermite-Balériaux, M., Van Cauter, E., & Spiegel, K. (2014). Adverse effects of two nights of sleep restriction on the hypothalamic-pituitary-adrenal axis in healthy men. The Journal of Clinical Endocrinology & Metabolism, 99(8), 2861–2868. https://doi.org/10.1210/jc.2013-4254

Henney, A. E., Gillespiec, C. S., Lai, J. Y. M., Schofield, P., Riley, D. R., Caleyachetty, R., Barber, T. M., Miras, A. D., Dobbie, L. J., Hughes, D. M., Alam, U., Hydes, T. J., & Cuthbertson, D. J. (2025). Risk of type 2 diabetes, MASLD and cardiovascular disease in people living with polycystic ovary syndrome. The Journal of Clinical Endocrinology & Metabolism, 110(5), 1235–1246. https://doi.org/10.1210/clinem/dgae481

Heshmati, J., Sepidarkish, M., Morvaridzadeh, M., Farsi, F., Tripathi, N., Razavi, M., & Rezaeinejad, M. (2021). The effect of cinnamon supplementation on glycemic control in women with polycystic ovary syndrome: A systematic review and meta-analysis. Journal of Food Biochemistry, 45(1), e13543. https://doi.org/10.1111/jfbc.13543

Housman, E., & Reynolds, R. V. (2014). Polycystic ovary syndrome: A review for dermatologists: Part I. Diagnosis and manifestations. Journal of the American Academy of Dermatology, 71(5), 847.e1–858. https://doi.org/10.1016/j.jaad.2014.05.007

Huddleston, H. G., Jaswa, E. G., Casaletto, K. B., Neuhaus, J., Kim, C., Wellons, M., Launer, L. J., & Yaffe, K. (2024). Associations of polycystic ovary syndrome with indicators of brain health at midlife in the CARDIA cohort. Neurology, 102(4), e208104. https://doi.org/10.1212/WNL.0000000000208104

Jamilian, M., Foroozanfard, F., Bahmani, F., Talaee, R., Monavari, M., & Asemi, Z. (2016). Effects of zinc supplementation on endocrine outcomes in women with polycystic ovary syndrome: A randomized, double-blind, placebo-controlled trial. Biological Trace Element Research, 170(2), 271–278. https://doi.org/10.1007/s12011-015-0480-7

Jin, S., Zhu, M., Lu, Y., Zhao, J., Zhu, J., & Fang, X. (2026). Gut microbiota and polyendocrine metabolic ovarian syndrome: An integrated gut-metabolism-endocrine-ovary axis. Experimental Biology and Medicine, 251, 11058. https://doi.org/10.3389/ebm.2026.11058

Joham, A. E., Norman, R. J., Stener-Victorin, E., Legro, R. S., Franks, S., Moran, L. J., Boyle, J., & Teede, H. J. (2022). Polycystic ovary syndrome. The Lancet Diabetes & Endocrinology, 10(9), 668–680. https://doi.org/10.1016/S2213-8587(22)00163-2

Kite, C., Lahart, I. M., Afzal, I., Broom, D. R., Randeva, H., Kyrou, I., & Brown, J. E. (2019). Exercise, or exercise and diet for the management of polycystic ovary syndrome: A systematic review and meta-analysis. Systematic Reviews, 8(1), 51. https://doi.org/10.1186/s13643-019-0962-3

Lemogne Robert, A., Oliveira Torres, E., & Jota Baptista, C. (2025). Effects of endocrine disruptive chemicals (EDCs) and therapeutic approaches to the polycystic ovary syndrome (PCOS): A current state-of-the-art. Environmental Toxicology and Pharmacology, 120, 104842. https://doi.org/10.1016/j.etap.2025.104842

Li, C., Cheng, D., Ren, H., & Zhang, T. (2025). Unraveling the gut microbiota’s role in PCOS: A new frontier in metabolic health. Frontiers in Endocrinology, 16, 1529703. https://doi.org/10.3389/fendo.2025.1529703

Liu, J., Su, H., Jin, X., Wang, L., & Huang, J. (2023). The effects of N-acetylcysteine supplement on metabolic parameters in women with polycystic ovary syndrome: A systematic review and meta-analysis. Frontiers in Nutrition, 10, 1209614. https://doi.org/10.3389/fnut.2023.1209614

Liu, S., Wang, R., Yu, W., Shi, C., Wang, X., Liu, A., & Zhang, L. (2026). Natural products in the metabolic and endocrine modulation of polycystic ovary syndrome: Current perspectives. Nutrients, 18(6), 964. https://doi.org/10.3390/nu18060964

Lobo, R. A., Granger, L. R., Paul, W. L., Goebelsmann, U., & Mishell, D. R., Jr. (1983). Psychological stress and increases in urinary norepinephrine metabolites, platelet serotonin, and adrenal androgens in women with polycystic ovary syndrome. American Journal of Obstetrics and Gynecology, 145(4), 496–503. https://doi.org/10.1016/0002-9378(83)90324-1

McKinney, E., Stewart, J., Kewalramani, R., & Singh, S. (2026). Effects of multi-herb and ashwagandha root formulas on stress modulation: A randomized, double-blind, placebo-controlled clinical study. Trials, 27(1), 205. https://doi.org/10.1186/s13063-026-09495-9

Moslehi, N., Zeraattalab-Motlagh, S., Rahimi Sakak, F., Shab-Bidar, S., Tehrani, F. R., & Mirmiran, P. (2023). Effects of nutrition on metabolic and endocrine outcomes in women with polycystic ovary syndrome: An umbrella review of meta-analyses of randomized controlled trials. Nutrition Reviews, 81(5), 555–577. https://doi.org/10.1093/nutrit/nuac075

Perović, M., Wugalter, K., & Einstein, G. (2022). Review of the effects of polycystic ovary syndrome on cognition: Looking beyond the androgen hypothesis. Frontiers in Neuroendocrinology, 67, 101038. https://doi.org/10.1016/j.yfrne.2022.101038

Phan, K., Charlton, O., & Smith, S. D. (2020). Hidradenitis suppurativa and polycystic ovarian syndrome: Systematic review and meta-analysis. The Australasian Journal of Dermatology, 61(1), e28–e33. https://doi.org/10.1111/ajd.13110

Qi, X., Yun, C., Pang, Y., & Qiao, J. (2021). The impact of the gut microbiota on the reproductive and metabolic endocrine system. Gut Microbes, 13(1), 1–21. https://doi.org/10.1080/19490976.2021.1894070

Sarkisian, K. I., Ho, L., Yang, J., Mandelbaum, R., & Stanczyk, F. Z. (2023). Neuroendocrine, neurotransmitter, and gut microbiota imbalance contributing to potential psychiatric disorder prevalence in polycystic ovarian syndrome. F&S Reports, 4(4), 337–342. https://doi.org/10.1016/j.xfre.2023.08.009

Senthilkumar, H., & Arumugam, M. (2025). Gut microbiota: A hidden player in polycystic ovary syndrome. Journal of Translational Medicine, 23(1), 443. https://doi.org/10.1186/s12967-025-06315-7

Sondrup, N., Termannsen, A. D., Eriksen, J. N., Hjorth, M. F., Færch, K., Klingenberg, L., & Quist, J. S. (2022). Effects of sleep manipulation on markers of insulin sensitivity: A systematic review and meta-analysis of randomized controlled trials. Sleep Medicine Reviews, 62, 101594. https://doi.org/10.1016/j.smrv.2022.101594

Teede, H. J., Khomami, M. B., Morman, R., Laven, J. S. E., Joham, A. E., Costello, M. F., Patil, M., Rees, D. A., Berry, L., Cree, M. G., Zhao, H., Norman, R. J., Dokras, A., Piltonen, T., & Global Name Change Consortium. (2026). Polyendocrine metabolic ovarian syndrome, the new name for polycystic ovary syndrome: A multistep global consensus process. The Lancet, 407(10545), 2329–2339. https://doi.org/10.1016/S0140-6736(26)00717-8

Teede, H. J., Tay, C. T., Laven, J. J. E., Dokras, A., Moran, L. J., Piltonen, T. T., Costello, M. F., Boivin, J., Redman, L. M., Boyle, J. A., Norman, R. J., Mousa, A., & Joham, A. E. (2023). Recommendations from the 2023 International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome. The Journal of Clinical Endocrinology & Metabolism, 108(10), 2447–2469. https://doi.org/10.1210/clinem/dgad463

Torchen, L. C., Wu, M., Thompson, B., & Beaudouin, A. (2025). Polycystic ovary syndrome: Origins and implications: The significance of functional adrenal hyperandrogenism in polycystic ovary syndrome across the lifespan. Reproduction, 169(6), e250091. https://doi.org/10.1530/REP-25-0091

Tóth-Mészáros, A., Garmaa, G., Hegyi, P., Bánvölgyi, A., Fenyves, B., Fehérvári, P., Harnos, A., Gergő, D., Nguyen Do To, U., & Csupor, D. (2023). The effect of adaptogenic plants on stress: A systematic review and meta-analysis. Journal of Functional Foods, 108, 105695. https://doi.org/10.1016/j.jff.2023.105695

Wu, B., & Yao, J. (2026). A meta-analysis of the effects of vitamin D supplementation on endocrine metabolic and inflammatory markers in patients with polycystic ovarian syndrome. Medicine, 105(1), e46892. https://doi.org/10.1097/MD.0000000000046892

Zamani, M., Zarei, M., Nikbaf-Shandiz, M., Hosseini, S., Shiraseb, F., & Asbaghi, O. (2022). The effects of berberine supplementation on cardiovascular risk factors in adults: A systematic review and dose-response meta-analysis. Frontiers in Nutrition, 9, 1013055. https://doi.org/10.3389/fnut.2022.1013055

Zeng, X., Xie, Y. J., Liu, Y. T., Long, S. L., & Mo, Z. C. (2020). Polycystic ovarian syndrome: Correlation between hyperandrogenism, insulin resistance and obesity. Clinica Chimica Acta, 502, 214–221. https://doi.org/10.1016/j.cca.2019.11.003

Zhang, X., Zheng, Y., Guo, Y., & Lai, Z. (2019). The effect of low carbohydrate diet on polycystic ovary syndrome: A meta-analysis of randomized controlled trials. International Journal of Endocrinology, 2019, 4386401. https://doi.org/10.1155/2019/4386401

Sara Fields, Lead Instructor

MRHP, FNTP

Sara fell in love with food and nutrition early in life and has worked in this sphere for nearly 15 years. From her work in organic farming and sustainable agriculture to gourmet and specialty foods retail, she has cultivated a passion for both culinary adventure and for nourishing food’s healing effects on our bodies and the earth.

Seeing firsthand the effects of diet on autoimmune disease and mental health, she was catapulted into a career in nutrition. Since 2014 she has worked as a Nutritional Therapy Practitioner, and in 2016 she received her certification as a Restorative Health Practitioner. The IRH program has added invaluable tools to her repertoire, allowing her to dig deeper to uncover root causes of imbalance and to ultimately help her clients improve their quality of life.

Read more about Sara