Nutrition Care and Dietetic Practice in Managing Metabolic and Endocrine Dysfunction in Polyendocrine Metabolic Ovarian Syndrome (PMOS): Implications and Opportunities in the Context of the Name Change of Polycystic Ovarian Syndrome to PMOS

Abstract

Polyendocrine metabolic ovarian syndrome (PMOS) affects 8‒13% of women across the lifespan. Those with PMOS have reduced quality of life and increased risk of comorbidities, including elevated weight, eating disorders, gestational diabetes, type 2 diabetes, and cardiovascular disease. PMOS is a major population in clinical dietetic practice, and dietary intervention is the first-line approach recommended to target metabolic risk in the international evidence-based guidelines for assessment and management of polycystic ovary syndrome (PCOS). The past name, PCOS, was ovarian-centric and did not accurately reflect the pathophysiology, endocrine, or metabolic dysfunction of the syndrome. The new name, PMOS, has been determined by a rigorous global consensus process including 56 organizations, >14,000 survey responses, and consultation with experts and patients in workshops that identified the need for accurate medical representation of the syndrome and a stigma-reducing name. Dietitians encounter patients with PMOS with increased cardiometabolic risk who also experience high rates of elevated weight, weight stigma, and eating disorders. Nutrition care of patients with PMOS often involves managing these conditions, use of anti-obesity and diabetes medications, conferring with prescribing clinicians, and navigating patient goals and preferences. Improved recognition of the metabolic risks can strengthen alignment with dietary management approaches and referral to nutrition care services as part of the multidisciplinary care needed in those with PMOS. Dietitians can play a key role in managing nutritional misinformation, supporting patient health literacy and nutritional self-management. The new name can contribute to expanded opportunities for nutritional research that targets endocrine and metabolic outcomes to improve the clinical care, health, and well-being of those living with PMOS.

Rationale for Name Change of Polycystic Ovary Syndrome to Polyendocrine Metabolic Ovarian Syndrome: Implications for Dietitians and Nutrition Care

Statement of significance.

Polyendocrine metabolic ovarian syndrome (PMOS) is the new name for polycystic ovary syndrome. This perspective paper highlights the rationale for the name change related to endocrine features and metabolic risk, and the role of nutritional management and dietetic practice, highlighting recent updates on dietary approaches, body weight, anti-obesity medications, and eating disorders in PMOS.

Polyendocrine metabolic ovarian syndrome (PMOS) is the new name for polycystic ovary syndrome (PCOS) [1]. PMOS affects 8%‒13% of women across the lifespan and is associated with an increased risk of comorbidities and reduced quality of life [[10], [11], [12], [13], [14], [15], [16], [17], [2], [3], [4], [5], [6], [7], [8], [9]]. The comorbidities include metabolic: elevated body weight, type 2 diabetes, and cardiovascular disease; psychological: anxiety, depression, and eating disorders; and reproductive: infertility, gestational diabetes, and hypertension [[10], [11], [12], [13], [14], [15], [16], [17], [2], [3], [4], [5], [6], [7], [8], [9]]. The new name was identified by the International Name Change Consortium to better reflect the pathophysiology, risk of metabolic-related comorbidities, and the multidisciplinary care needed in the management of PMOS [1,18].

Nutrition care is well established as the first-line intervention in the international evidence-based guidelines for the management of PMOS to target the metabolic, endocrine, anthropometric, reproductive, and psychological aspects of the syndrome [5,19,20]. However, the primary role of nutrition has often been overlooked in approaches to care at the clinical, patient, and health system levels because of a lack of recognition of the metabolic aspects of the disease [4,18,[21], [22], [23]]. This has contributed to a lack of integrated nutrition care, limited referral to dietitians, dietary misinformation, and patients and health care providers not being informed of the potential role of nutrition in managing metabolic and endocrine symptoms [18,21,22,24,25]. Furthermore, the clinical and patient focus is often on the reproductive-endocrine symptoms, such as fertility, menstrual cyclicity, and hirsutism, and the metabolic risks may not be prioritized in patient care [18,21,22]. Patients have been told not to be concerned about cardiometabolic risks until they plan to become pregnant or until later in life [18,22]. However, it is well established that cardiometabolic risk factors such as elevated weight, insulin resistance (IR), dyslipidemia, hypertension, and subclinical cardiovascular disease develop early among adolescents and young women with PMOS [5,[26], [27], [28], [29], [30], [31], [32], [33]]. Therefore, this window in young adulthood offers an opportunity for primary prevention, particularly in nutritional approaches to manage cardiometabolic risk. Furthermore, pregnancy is a critical period for those with PMOS as they are at increased risk of complications including gestational diabetes, hypertension, and preeclampsia [12,13,15,34]. These pregnancy complications can additionally confer greater risk of developing type 2 diabetes and cardiovascular disease [12,13,15,34]. Therefore, terminology that better reflects these metabolic risks may facilitate earlier recognition and reinforce the opportunity for dietary management as first-line care in those with PMOS [1,5,18]. The new name PMOS formally acknowledges the polyendocrine and metabolic basis of the condition and aligns with the central role of nutrition in managing metabolic risk factors [1,5,18].

Global process in the name change and core dietetic practice principles

Stakeholder surveys found >80% of patients and health care providers considered the name PCOS confusing, stigmatizing, or inaccurate, particularly regarding ovarian, endocrine, and metabolic features [18]. Support for a name change with terminology that more accurately represented the medical aspects of the syndrome and a stigma-reducing name was proposed and agreed on by 86% of stakeholders [1,18]. In addition, a name that helped to facilitate diagnosis and multidisciplinary management of the disease was deemed critical for improved health care in those living with PMOS [18]. A global name change consortium was established and a rigorous consensus process including 56 organizations, 14,360 survey responses, and expert-patient workshops [1]. The process prioritized core principles relevant to dietetic practice, including scientific metabolic and physiological accuracy, evidence-based research and management, clear communication, avoidance of stigma, cultural-ethnic appropriateness, and patient-focused care [1,35]. Removing “cyst” and an ovarian-centric frame was deemed important to communicate more accurately to patients and health care providers the pathophysiology of the syndrome [1,36]. Including the term “metabolic” was proposed to facilitate patient and physician awareness of the scope of metabolic manifestations that can be supported by nutritional intervention [1,5]. The preferred name PMOS was agreed on by consensus in 96% of stakeholders in the final workshop to accurately reflect the multisystem endocrine and metabolic nature of the condition [1]. In addition, the new name aligned with international primary prevention population guidelines for dietary approaches in managing cardiometabolic risk, obesity, diabetes, and cardiovascular disease [[37], [38], [39]].

The name change process is accompanied by a comprehensive multistep global advocacy and implementation plan that is underway to update evidence-based guidelines and educational health care resources across disciplines [1]. The implementation plan includes a coordinated global outreach via the global name change consortium to update health systems, research institutions, funding bodies, and disease classification systems (including international classification of diseases coding), and is supported by a global transition period and continuous evaluation [1]. There will be educational opportunities for patients and health care providers to learn more about the rationale for the name change and how this can support referral to nutrition care [1]. Steps to include PMOS in international disease classification codes are in progress, and the transition to a new code is dependent on the timeline for revisions to the current ICD and adoption by health care jurisdictions [1,40].

Diagnostic criteria and intersection of endocrine and metabolic pathways in PMOS

The diagnosis of PMOS requires ≥2 of the following: menstrual-ovulatory dysfunction, clinical or biochemical hyperandrogenemia, polyfollicular ovary morphology or elevated anti-Müllerian hormone, and exclusion of other disorders [5]. These reproductive-endocrine criteria intersect with metabolic dysfunction, cardiometabolic risk, and weight-related concerns that dietitians routinely manage in those with PMOS [5]. PMOS is associated with endocrine disruption of the hypothalamic-pituitary-ovarian axis [[41], [42], [43], [44], [45], [46]]. Increased gonadotropin-releasing hormone pulsatility and luteinizing hormone drive ovarian androgen excess [[41], [42], [43], [44], [45], [46]]. Polygenic neuroendocrine origins of PMOS can lead to altered androgen, insulin, and incretin metabolism [41,[47], [48], [49]]. Excess androgens and altered androgen metabolism, particularly in those with hyperandrogenic phenotypes, are associated with greater metabolic dysregulation of these pathways [2,[50], [51], [52], [53], [54], [55], [56]]. Collectively, metabolic dysfunction is observed in multiple organs: liver, muscle, adipose, heart, and pancreas [[41], [42], [43], [44], [45], [46]]. Nutrition care in PMOS can help manage the underlying causes of PMOS, and the scope of practice for dietitians ranges from management of elevated body weight, eating disorder behaviors, and emerging interactions with incretin therapies.

Elevated BMI, weight gain trajectories, and clinical implications for dietitians

Many individuals with PMOS experience greater lifetime weight gain and higher BMI (in kg/m²), which may arise from dysregulated neuroendocrine-energy balance beyond the influence of diet and lifestyle [4,51,57,58]. Increased adiposity in childhood and adolescence is common, and those with PMOS often experience progressive and increased weight gain into adulthood [4,57,58]. These energy regulation pathways may involve altered gastrointestinal incretins and normal inhibitory feedback to the hypothalamic energy-feeding center, contributing to weight gain [[59], [60], [61], [62]]. Hyperleptinemia and leptin resistance due to increased adiposity contribute further to alterations in hypothalamic energy regulation, including energy expenditure, resting metabolic rate, thermogenesis, feeding behaviors, and appetite and satiety pathways [[59], [60], [61],63]. The intrinsic dysregulation between energy balance and body weight is complex in PMOS [4,51,57,58]. This is where dietitians can assist in communicating to patients the many factors that impact body weight in PMOS, beyond simply reducing energy-in and increasing energy-out [5].

The metabolic syndrome has a 2‒3-fold higher prevalence in adolescents and adults with PMOS, predisposing these individuals to an increased risk of diabetes and cardiovascular disease [3,7,26,50,53,55,[64], [65], [66], [67], [68], [69]]. The metabolic syndrome risk factors of central obesity with increased waist circumference, hypertension (blood pressure >130 mmHg), high fasting glucose >5.6 mmol/L, high triglycerides >1.7 mmol/L, and low HDL cholesterol <1.0 mmol/L increase the risk of diabetes and cardiovascular disease by 2‒4-fold in those with PMOS [3,7,26,50,55,[64], [65], [66], [67], [68], [69]]. IR (and compensatory hyperinsulinemia) is often observed in the metabolic syndrome and affects ∼35‒80% of those with PMOS [[70], [71], [72]]. IR amplifies weight gain, endocrine, reproductive, and metabolic dysfunction in those with PMOS [[70], [71], [72]]. IR also impacts 75% of lean individuals with PMOS, highlighting the inherent dysregulation of insulin metabolism in those with PMOS [70,71]. The cause of IR may be intrinsic (within tissues; genetic or epigenetic origin) or acquired/extrinsic (diet and lifestyle, systemic metabolic dysfunction) in PMOS [41,73,74]. IR and hyperinsulinemia can further contribute to hyperandrogenemia via altered ovarian and adrenal androgen synthesis pathways [[42], [43], [44],46]. IR can also contribute to adiposity and inflammation, further exacerbating PMOS symptoms, weight gain, and cardiometabolic risk [4,63,75]. Higher BMI together with IR has been shown to worsen reproductive, metabolic, cardiovascular, psychological, and dermatologic outcomes [4,5,70,76]. Overall, those with elevated weight are at increased risk of metabolic complications, including IR, dyslipidemia, hypertension, metabolic dysfunction-associated steatotic liver disease, type 2 diabetes, and cardiovascular disease [4,5,70,76]. Therefore, elevated weight is a potential modifiable risk factor that can be effectively targeted with nutritional management in PMOS [[5], [6], [7], [77], [78], [79], [8],[77], [78], [79], [8], [80], [81], [82]].

Diet, lifestyle, and behavioral management: current evidence and scope for dietetic practice

Evidence-based research has shown that diet and lifestyle interventions (with a focus on physical activity) can improve central adiposity, acquired/extrinsic IR, lipid profiles, androgens, and overall quality of life [5,20,69,[83], [84], [85], [86]]. Dietitians play a key role in educating and implementing these evidence-based nutrition approaches and often simultaneously manage misinformation on diets and nutraceutical supplements to treat PMOS symptoms [5]. The focus in nutritional management of PMOS is to encompass healthy eating, physical activity, and behavior strategies to optimize body composition and weight management [5]. It is key to mitigate nutritional misinformation and support patients in how best to achieve healthy eating habits, including portion control, regular meals, and avoiding unduly restrictive and nutritionally unbalanced diets [5,69,84].

Weight management is dependent on the patient’s goals and may include maintaining weight, preventing weight gain, or achieving weight loss [5]. Evidence shows that in those with higher body weight, diet and lifestyle interventions that reduce weight by 5%‒10% of total body weight can have significant metabolic, reproductive, and psychological benefits [5,69,84,86]. Weight gain, body shape, and image are highly ranked issues for patients and health care professionals caring for those with PMOS [22,24,87,88]. One of the challenges in the new name is a potential perceived emphasis on metabolic dysfunction associated with elevated body weight, and body weight being assigned as the primary cause of PMOS. This may create misinformation and patient dissatisfaction with the new name. Dietitians may counter this by providing education and support to patients on the complexity of body weight regulation in PMOS and navigating diet therapy strategies to focus on metabolic health with the patient [5].

Emerging evidence suggests metabolic responsiveness to diet interventions varies in individuals and may be dependent on PMOS phenotype [[89], [90], [91]]. There is no conclusive evidence to support any one type of diet composition or nutraceutical for improvement in anthropometric, metabolic, hormonal, and psychological outcomes [5,84,86,92]. Rather, diet interventions following population guidelines to promote metabolic health and/or to target body weight management include a range of healthy eating approaches to meet food preferences, nutritional adequacy, and sustainability [5,20,76,93]. Recent meta-analyses of randomized clinical trials in PMOS show several dietary approaches, including Dietary Approaches to Stop Hypertension (DASH), Mediterranean, and low-carbohydrate diets, can positively impact body weight and cardiometabolic outcomes [20]. Intermittent fasting and time-restricted eating trials have shown potential to improve weight, metabolic, hormonal, and inflammatory profiles [94]. However, further robust studies using these interventions in defined PMOS phenotypes are needed. This is an area where dietitians may need to counter misinformation and support patients who are interested in these nutritional approaches [95]. It is important to note that these fasting and time-restrictive interventions may not be appropriate in those with underlying eating disorders or disordered eating patterns [95]. Co-development of dietary approaches with the patient can support nutrition literacy, self-efficacy, and motivation in reaching body weight and metabolic health goals [5,69,84,96,97]. Recognizing PMOS as a metabolic condition can strengthen the understanding of patients and health care providers of the effectiveness of dietary management and the importance of referral to nutrition care support.

Weight stigma, eating disorders, and disordered eating in PMOS

Recognition of metabolic dysfunction in PMOS may help support a broader appreciation of the role of physiology, behavior, and psychosocial determinants of health and a move away from weight-centric models of care. Nutritionists and dietitians need to navigate significant weight discrimination and stigma that has been widely experienced in those with PMOS [88,98]. Weight stigma has been shown to worsen metabolic and psychological outcomes and can lead to poorer health behaviors [[100], [101], [102], [103], [104], [105], [99]]. Experienced and perceived weight stigma mediates feelings of body shame, anxiety, depression, and altered eating and exercise behaviors [59,[102], [103], [104]]. Dietitians are recommended to use weight-neutral, inclusive practices that promote acceptance and respect of body size diversity, including shared decision-making, cultural sensitivity, psychosocial support, and family engagement to optimize adherence to diet and lifestyle interventions [5]. Weight-inclusive care that promotes a healthy lifestyle without a focus on intentional weight loss has been shown to support motivation, sustainable changes, and improvements in metabolic and mental health outcomes [98]. It is important to acknowledge that higher weight is a risk factor for PMOS and comorbidities; however, it is only one indicator of overall health [5,84]. Several steps can be taken by dietitians to address weight stigma in clinical practice, including raising awareness, investing in professional weight stigma education, asking patients for permission to discuss and measure weight, and using terminology such as “higher weight” instead of “overweight or obese.” In addition, sharing with a patient that monitoring weight can help with ongoing metabolic risk assessment and assessment of the effectiveness of nutrition interventions, particularly in those seeking intentional weight loss [5].

Dietitians encounter high rates of eating disorders and disordered eating in those with PMOS, with a 2‒3-fold higher prevalence of risk of an eating disorder [6,59,[106], [107], [108], [109]]. Eating disorders and disordered eating are associated with increased emotional distress, depression, anxiety, and body dissatisfaction [[110], [111], [112], [113]]. Binge eating and bulimia nervosa are the most common eating disorders in PMOS, and these are often observed in those with higher weight [59,114]. The pathophysiological mechanisms of eating disorders in PMOS are complex, heterogeneous, and patient-specific [62,[115], [116], [117], [118], [119]]. Dysregulation of the hypothalamic neuroregulation of appetite and satiety has been proposed, and IR, leptin resistance, and hyperandrogenemia may impact regulation of these neural-circuit pathways [62,[115], [116], [117], [118], [119]]. The psychosocial contributors to eating disorders have been proposed to include weight stigma, anxiety, and depression, as these can influence feeding cues and behaviors [109,117,120]. Together, the endocrine, metabolic, and psychosocial factors can contribute to the development and perpetuation of an eating disorder or disordered eating patterns [109,117,120]. Raised awareness and screening for eating disorders and disordered eating are recommended regardless of weight [5]. For nutritionists and dietitians working with patients with PMOS, specialized eating disorder training may be needed to support best practice in weight and mental health management for effective nutrition care [5,59]. Furthermore, referral to an allied health professional who is specialized in eating disorders may be required for a full diagnostic assessment and continuing psychological care [5,59,121]. The new name PMOS provides a stronger emphasis on metabolic contributors to body weight regulation and eating behaviors, potentially supporting more physiologically informed and less stigmatizing care.

Pharmacologic obesity and diabetes treatments and the importance of nutrition care

Anti-obesity, prediabetes, and diabetes medications are commonly used in those with PMOS. Dietitians and nutritionists are required to collaborate with prescribing health care providers and support patients in the use of these medications [5,[121], [122], [123], [124], [125], [126]]. These include metformin, glucagon-like peptide-1 (GLP-1) receptor agonists (RAs) (liraglutide, semaglutide), combined GLP-1 RAs with gastrointestinal peptide (GIP) (tirzepatide), and orlistat [5,[121], [122], [123], [124], [125], [126]]. Several GLP-1 medications (that may include GIP) are approved treatments for type 2 diabetes and chronic elevated body weight (BMI >30 or BMI >27 with ≥1 other related comorbidity) by regulatory bodies, including the United States Food and Drug Administration, Health Canada Pharmaceutical Drugs Directorate, and Australian Therapeutic Goods Administration. More recently, behavioral weight loss programs prescribe GLP-1 medications to help individuals manage body weight and meet body weight goals. Dietitians play key roles in the nutritional management of the side effects, potential nutritional deficiencies, use in pregnancy, and post-therapy diet strategies to minimize potential weight regain in those with PMOS [[122], [123], [124], [125],[127], [128], [129], [130], [131], [132], [133], [134]]. Dietitians may need to provide behavioral support to patients and appropriate referral to mental health professionals, particularly among those with eating disorders and disordered eating [135,136]. Dietitians may also need to coordinate with prescribing clinicians and psychologists on the use of GLP-1 medications in the context of clinical best practices and sustainable nutrition approaches in those with PMOS [5,[123], [124], [125],127,129,[133], [134], [135], [136]].

Emerging clinical observations show that GLP-1 medications may have some limitations related to eating disorders. The use of these medications may impact symptoms of pre-existing eating disorders or disordered eating patterns, contribute to the development of an eating disorder, or negatively impact ongoing psychological treatment for an eating disorder [135,136]. Limited evidence shows GLP-1 agonists may benefit those with binge eating disorder and negatively affect those with weight suppression, including anorexia nervosa, atypical anorexia nervosa, or bulimia nervosa; however, more research is needed on the use of these medications in eating disorders [135,136]. Other clinical evidence suggests that GLP-1 agonists may increase eating restriction patterns and contribute to the development of a binge eating disorder [135,136]. Currently, GLP-1 medications are not approved for the treatment of eating disorder symptoms [135,136]. There remains limited research on the long-term impact of GLP-1 medications related to the effect of discontinuation on eating disorder symptoms, weight gain, and metabolism in different PMOS phenotypes [[122], [123], [124], [125],133,134]. Further research is also needed on dietary protein requirements and musculoskeletal effects with the aim of optimizing weight loss, preserving muscle mass, and improving metabolic outcomes in those with PMOS [127,128]. Overall, these pharmacotherapies can be beneficial in modulating the metabolic and endocrine determinants of weight in those with PMOS; however, nutritional oversight of patients using these therapies is recommended [[122], [123], [124], [125],129,134].

Potential challenges of the new name PMOS for patients and dietetic practice

A potential challenge with the transition to the new name is that it may create confusion for patients and nutritionists related to the diagnosis of PMOS, as the new name may suggest that metabolic aspects such as IR are now included in the diagnostic criteria. The metabolic aspects may be perceived as indicators of PMOS rather than formally meeting the specific diagnostic criteria. Retaining the term “ovarian” is accurate; however, this may require balancing this narrow anatomical focus with communication of PMOS as a multisystem disorder that requires multidisciplinary care, including nutritional management. In terms of body weight, the perception that body weight is the primary metabolic factor driving the etiology of PMOS could inadvertently lead to a refocus on weight as the most important modifiable risk factor, rather than overall metabolic health [22,88,98]. The new name may inadvertently cause a perceived shift to focus on body weight management in dietetic practice, particularly in those with elevated weight. These perceptions could contribute to experiences of weight stigma and adversely impact body image, dietary patterns, and eating behaviors in patients [59,[102], [103], [104]].

Implications of the new PMOS name for dietitians and nutrition management

Women with PMOS are a major population in current and future clinical practice for accredited nutritionists and dietitians [5,16]. Nutrition experts are also key team members in specialized obesity, diabetes, cardiovascular, eating disorder, and bariatric surgery clinics, and these operationalize nutrition as a standard of care in the management of these comorbidities [5,12]. Evidence shows that women have significant delays in diagnosis of PMOS and ≤70% of those with PMOS remain undiagnosed [18,137]. This delay in diagnosis can contribute to delayed assessment of metabolic complications and missed opportunities for early nutrition intervention [18,137]. The name change was considered an important first step in transforming multidisciplinary health care for those with PMOS [1]. The name change has significant potential to impact nutrition care and dietetic practice to improve patient care in the following ways:

• ○Improve referral pathways to dietitians in models of care that include nutrition management as first-line treatment.
• ○Earlier recognition of metabolic risks that are potentially modifiable risk factors, with nutritional management in the prevention of comorbidities.
• ○Address misinformation and non-evidence-based approaches to dietary intervention and nutraceutical supplement use.
• ○Enhance patient health literacy, self-efficacy, and understanding of why nutrition is central in managing symptoms and comorbidities.
• ○Strengthen interdisciplinary health care practice and models of care across endocrinology, obstetrics gynecology, primary care, psychology, and nutrition teams.
• ○Support nutrition care across the lifespan, including adolescence, reproductive years, menopause, and postmenopause to address metabolic risk.

In conclusion, as the PMOS term becomes integrated into guidelines, international disease coding, and patient education materials, dietitians are uniquely positioned to guide implementation of evidence-based dietary interventions and expand nutrition-metabolic research. Research priorities include identifying optimal dietary strategies, refining metabolic phenotyping, addressing weight stigma, and evaluating culturally tailored interventions in those with PMOS. The metabolic emphasis of PMOS will allow dietitians to lead research and development of integrated diet and lifestyle programs, longitudinal weight-management support, and collaboration with pharmacotherapy and reproductive medicine teams. The transition to the new naming of PMOS highlights how terminology may influence recognition of metabolic risk, referral pathways, research priorities, and patient understanding of the syndrome. Although terminology change alone will not improve outcomes, more accurate recognition of endocrine and metabolic dysfunction will strengthen opportunities for health care provider and patient education, earlier intervention to target metabolic risk, multidisciplinary models of care, and evidence-based nutrition management across the lifespan in those living with PMOS.

Author contributions

The authors’ responsibilities were as follows– DV, LM, HT, MB-K: contributed to the planning and writing of the final manuscript; DV: had primary responsibility for the final content; and all authors: read and approved the final manuscript.

Declaration of Generative AI and AI-assisted technologies in the writing process

The authors declare that no generative AI or AI-assisted technologies were used in the writing of this manuscript.

Funding

The authors reported no funding received for this study.

Conflict of interest

The authors report no conflicts of interest.