Management of Obesity in Menopausal Women: Implications for Metabolic Health and Minimally Invasive Surgery

Abstract

Menopause and obesity are interrelated conditions that collectively increase the risk of cardiometabolic diseases, impair quality of life, and pose challenges to gynecologic care. In menopausal women, hormonal decline facilitates fat accumulation, while obesity exacerbates menopausal symptoms and surgical complications. This review synthesizes current evidence on the pathophysiological interplay between menopause and obesity, evaluates behavioral, pharmacological, and surgical strategies for weight management, and discusses the implications for gynecologic minimally invasive surgery (MIS). A comprehensive literature review was conducted, focusing on clinical guidelines, randomized trials, and meta-analyses concerning obesity management in midlife women. Lifestyle interventions form the cornerstone of obesity treatment, but pharmacologic agents–particularly glucagon-like peptide-1 receptor agonists and dual incretin therapies–have demonstrated superior efficacy in achieving weight loss and cardiometabolic improvements. Bariatric surgery remains the most effective long.term option for severe obesity. Minimally invasive gynecologic procedures, although technically more challenging in obese patients, remain preferable when preoperative weight optimization and multidisciplinary care are applied. A multidimensional, personalized approach to obesity management in menopausal women is critical for improving metabolic outcomes and optimizing surgical safety. Importantly, preoperative optimization of obese menopausal women enhances the feasibility and outcomes of gynecologic MIS, thereby directly addressing a core concern of gynecologic practice. The emergence of novel injectable pharmacotherapies shows great promise and warrants further investigation in this population.

INTRODUCTION

Menopause, defined as the permanent cessation of menstruation due to ovarian failure, represents a major biological transition in a woman’s life. The Stages of Reproductive Aging Workshop (STRAW) system provides a standardized framework for assessing this transition, outlining seven stages–five premenopausal (−5 to −1) and two postmenopausal (+1 and +2)–anchored at the final menstrual period (FMP, stage 0). These stages reflect progressive hormonal changes, notably declining estrogen and rising follicle-stimulating hormone (FSH), which affect menstrual regularity, ovarian reserve, and systemic physiology.[1,2]

In the early reproductive years, menstrual cycles are regular, and hormonal markers such as FSH, antimüllerian hormone, and inhibin B remain low but stable. As women progress into the late reproductive and menopausal transition stages, increasing variability in cycle length, declining ovarian reserve markers, and rising FSH levels become evident.[3] The late transition is marked by prolonged amenorrhea and the onset of vasomotor symptoms such as hot flashes. Following the FMP, early postmenopause–approximately the first 5 years–is characterized by persistent hormonal changes and peak vasomotor symptoms. In the late postmenopausal phase, long-term estrogen deficiency becomes predominant, elevating the risk of urogenital atrophy, osteoporosis, and cardiometabolic disease. By integrating menstrual patterns, hormonal biomarkers, and clinical symptoms, the STRAW system facilitates both research standardization and individualized care for midlife women.[4]

In Asian populations, including Taiwan, conventional body mass index (BMI) thresholds often underestimate obesity-related risks due to differences in body fat distribution and metabolic profiles. Data from the Nutrition and Health Survey in Taiwan indicate that while only 9.8% of men and 7.7% of women meet the BMI ≥ 30 kg/m² criterion for obesity, over 85% exceed the body fat percentage threshold (≥25% for men, ≥30% for women), highlighting the limitation of BMI alone.[5] In response, the Health Promotion Administration of Taiwan adopts lower cutoffs: BMI ≥24 for overweight and ≥27 for obesity. These align with WHO Asia-Pacific recommendations, which propose BMI ≥23 as increased risk and ≥25–27.5 as obesity for Asian populations.[6]

Waist circumference (WC), another practical measure, better reflects central obesity and its link to metabolic syndrome.[7] Cutoff values of ≥90 cm for men and ≥80 cm for women are widely endorsed by both local and international guidelines. In addition, metrics such as waist-to-height ratio (WHtR >0.5) and body fat percentage offer more precise assessments of adiposity, especially in individuals with normal BMI but high fat mass. Studies of Taiwanese cohorts confirm that these indicators more accurately predict cardiometabolic risk.[8,9] Therefore, a multidimensional approach incorporating BMI, WC, WHtR, body composition, and metabolic markers is essential for effective obesity screening and prevention strategies in Taiwan and across Asia.[10]

EVIDENCE-BASED CLINICAL ALGORITHM IN TAIWAN

An evidence-based algorithm for obesity management begins with screening individuals with BMI ≥24 or WC ≥90 cm (men) or ≥80 cm (women). For BMI ≥27 with comorbidities or ≥2 cardiovascular risk factors, intensive lifestyle therapy is recommended. For BMI ≥37.5 or ≥32.5 with comorbidities, consider pharmacotherapy, psychological support, and bariatric evaluation. Reassess every 3–6 months and escalate treatment if needed.[10]

PATHOPHYSIOLOGY OF OBESITY – ENERGY HOMEOSTASIS AND GUT–BRAIN AXIS

The pathophysiology of obesity is intricately linked to disruptions in energy homeostasis, primarily mediated through the gut–brain axis. This neuroendocrine communication system integrates signals from the gastrointestinal tract, adipose tissue, and circulating hormones, and relays them to the central nervous system to regulate appetite, satiety, and energy balance. Genetic and epigenetic factors, along with neuropeptide hormone feedback, influence the sensitivity and responsiveness of this axis. In obesity, dysregulation of the gut–brain axis results in altered signaling patterns that promote increased hunger and diminished satiety. Key hormones involved in this process include leptin, which normally inhibits appetite, and ghrelin, which stimulates food intake; both exhibit resistance or abnormal levels in individuals with obesity.[11] Furthermore, obesity-induced metabolic adaptations, including changes in microbial composition and inflammatory signaling, can impair hormonal feedback loops and reinforce weight regain following weight loss. This maladaptive response underscores the chronic and relapsing nature of obesity, highlighting the need for therapeutic strategies that target the gut–brain axis to restore homeostatic control of energy intake.[12,13]

MENOPAUSE AND OBESITY: A BIDIRECTIONAL RELATIONSHIP

The relationship between menopause and obesity is complex and bidirectional, involving dynamic hormonal, metabolic, and symptomatic interactions. Obesity has been shown to influence the timing of menopause, with adipose tissue acting as an extragonadal site for estrogen production through aromatization. This peripheral estrogen source may delay ovarian senescence, and population-based studies suggest that higher BMI is associated with later age at menopause. Conversely, women with low BMI (<18.5 kg/m²) are at increased risk for earlier menopause, likely due to insufficient estrogenic support from adipose tissue.[14,15] However, the association between adiposity and menopause timing remains inconsistent across studies, with lifestyle, genetic, and metabolic confounders contributing to variability in findings.

Once menopause occurs, the decline in estrogen levels precipitates a cascade of physiological changes that promote adiposity. Reduced estrogen disrupts fat metabolism by decreasing resting energy expenditure, increasing appetite, and facilitating central fat accumulation–particularly in the abdominal region.[14,15] These shifts in body composition are characterized by increased fat mass and concurrent reductions in lean muscle mass, thereby elevating the risk of insulin resistance, dyslipidemia, and other metabolic complications.[16]

Obesity, in turn, exacerbates the symptomatic burden of menopause. Higher BMI is associated with more severe vasomotor symptoms (e.g., hot flashes), joint pain, sleep disturbances, and genitourinary discomfort. Moreover, obesity contributes to hormonal dysregulation, increasing the prevalence of anovulatory cycles and abnormal uterine bleeding. It also compromises overall health-related quality of life and has been linked to a heightened risk of hormone-sensitive malignancies, including breast and endometrial cancers, through sustained estrogen exposure and chronic low-grade inflammation.[15]

Obesity is strongly associated with a range of cardiovascular and metabolic comorbidities due to both pathophysiological alterations and mechanical stress. Excess adiposity contributes to the development of conditions such as type 2 diabetes, hypertension, asthma, osteoarthritis, obstructive sleep apnea, and cardiovascular disease (CVD). Epidemiological data demonstrate significantly higher cardiovascular event rates among individuals with obesity (BMI 30–39.9 kg/m²) compared to those with normal BMI–20.21 versus 13.72 per 1000 person-years in men and 9.97 versus 6.37 in women–highlighting the elevated risk even in the absence of traditional CVD risk factors.[17,18] A key contributor to these adverse outcomes is visceral adipose tissue, which functions as an active endocrine organ secreting proinflammatory cytokines and adipokines, promoting chronic low-grade systemic inflammation. Moreover, obesity-related fat accumulation and its abnormal distribution induce structural and mechanical changes that exacerbate comorbid conditions. For example, increased pharyngeal soft tissue mass predisposes individuals to obstructive sleep apnea, whereas elevated joint loading accelerates the progression of osteoarthritis. Together, these mechanisms illustrate how obesity serves as both a systemic inflammatory condition and a biomechanical burden, significantly amplifying chronic disease risk and disability.

In summary, menopause and obesity reciprocally reinforce one another. Menopause promotes adiposity through hormonal decline, whereas excess adipose tissue alters reproductive endocrinology, symptom expression, and disease risk. Understanding this interplay is critical to informing individualized prevention and management strategies for midlife women, emphasizing weight control, lifestyle interventions, and symptom-focused care to mitigate long-term health consequences.

CLINICAL EVALUATION FRAMEWORK FOR OBESE WOMEN DURING THE MENOPAUSAL TRANSITION

The comprehensive assessment of women living with obesity during the menopausal transition requires an integrated approach that includes detailed anamnesis, physical examination, and relevant laboratory testing. Clinical history should focus on dietary habits, physical activity levels, weight evolution since the premenopausal period, ongoing treatments, and the use of weight-promoting medications. Additional psychosocial and medical factors–such as mental stress, endocrine or psychiatric disorders, and weight-related stigma–must also be explored. The presence of obesity-related comorbidities (e.g., CVD, sleep apnea) and a family history of metabolic or oncologic diseases are important components of the diagnostic workup.[19,20,21]

Physical examination should assess anthropometric measures (weight, height, BMI, WC), blood pressure, and clinical signs indicative of endocrine or metabolic abnormalities, such as acanthosis nigricans, goiter, hirsutism, striae, and proximal muscle weakness. Complementary laboratory investigations are essential and typically include general biochemistry (e.g., glucose, creatinine, and uric acid), lipid profile (triglycerides, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol), insulin, thyroid-stimulating hormone, liver function tests, and electrocardiography. Optional evaluations may include body composition analysis, polysomnography for sleep-disordered breathing, hepatic ultrasound, and referrals to nutritionists, endocrinologists, or psychiatric specialists when indicated.

By integrating obesity management into routine gynecological care, gynecologists can significantly impact the overall health and well-being of menopausal women. This multidisciplinary approach not only supports individualized, evidence-based care but also promotes early intervention and prevention of long-term cardiometabolic complications in this high-risk population.

HORMONE THERAPY FOR OBESE MENOPAUSAL WOMEN

Menopausal hormone therapy (MHT) remains the most effective treatment for vasomotor symptoms and the prevention of osteoporosis. Beyond symptom relief, estrogen also influences fat metabolism and insulin sensitivity. According to the 2019 Taiwan Menopause Society consensus statement,[22] appropriate indications for MHT include severe climacteric symptoms and increased risk of fragility fractures, whereas contraindications encompass a history of breast or endometrial cancer, unexplained vaginal bleeding, active liver disease, uncontrolled hypertension, and previous thromboembolic disorders. In obese women, individualized risk–benefit assessment is essential, particularly in the presence of cardiometabolic comorbidities.

Current cardiovascular guidelines emphasize careful risk stratification before initiating MHT. Evidence from the Women’s Health Initiative and subsequent meta-analyses indicates that MHT is safest when started in women younger than 60 years or within 10 years of menopause onset, especially when using transdermal estrogen formulations.[23,24,25] In obese women, who are at increased baseline risk of venous thromboembolism and CVD, transdermal preparations are preferred over oral therapy due to their lower thrombotic risk profile. Both the 2020 American Heart Association scientific statement and the North American Menopause Society recommend that baseline cardiovascular evaluation—such as atherosclerotic cardiovascular disease scoring and assessment of hypertension, diabetes, and lipid status–should guide therapeutic decision-making.[26]

GYNECOLOGIC MINIMALLY INVASIVE SURGERY AND THE IMPACT OF OBESITY

Obesity significantly influences the safety and efficacy of gynecologic minimally invasive surgeries (MISs), including laparoscopy and hysteroscopy. Excess abdominal fat increases technical difficulty, limits visualization, prolongs operative time, and raises the risk of anesthesia-related complications. Moreover, obese patients are more prone to intraoperative injuries, surgical site infections, and postoperative venous thromboembolism.[27,28,29]

Despite these challenges, MIS remains preferable over open surgery due to lower overall complication rates, faster recovery, and reduced wound morbidity. Recent advances in surgical instrumentation, energy devices, and robotic-assisted systems have improved the feasibility of MIS in obese women.[30] Proper patient selection, experienced surgical teams, and optimized preoperative weight management are essential for reducing perioperative risks.

Robotic surgery has emerged as a promising option for obese, menopausal women undergoing gynecologic procedures. Its enhanced three-dimensional visualization and wristed instruments may help surgeons overcome technical challenges related to excess adipose tissue, potentially improving operative precision and safety. Retrospective studies support this view, reporting lower conversion rates to open laparotomy and reduced intraoperative blood loss, particularly among patients with higher BMI. These findings highlight the potential advantages of robotic systems in this high-risk population.[31] Nevertheless, the current evidence remains incomplete. Randomized controlled trials specifically addressing obese menopausal women are still lacking, and meta-analyses of general hysterectomy cases have not consistently shown superiority of robotic surgery over conventional laparoscopy in terms of operating time, blood loss, or overall complication rates.[32,33] In addition, robotic procedures are associated with higher costs, and in some reports, longer operative times. Taken together, while robotic surgery appears to offer meaningful advantages in technical feasibility and perioperative management, further prospective studies are warranted to confirm whether these benefits translate into improved long-term outcomes.

Thus, comprehensive obesity management in menopausal women not only improves metabolic health but also enhances surgical safety and outcomes in gynecologic procedures.

BEHAVIORAL AND NUTRITIONAL FOUNDATIONS OF OBESITY MANAGEMENT IN MENOPAUSAL WOMEN

Effective obesity management, particularly in menopausal women, necessitates a multifaceted strategy that incorporates behavioral intervention, physical activity, and nutritional optimization.[34] Behavioral change interventions form the foundation of long-term weight control by helping patients set health goals and adopt sustainable habits in areas such as nutrition, exercise, sleep, and stress management. Core behavioral techniques–such as self-monitoring, goal-setting, stimulus control, cognitive restructuring, and relapse prevention–enhance treatment adherence. Behavioral therapy also targets the neurocognitive regulation of hunger and satiety, addressing maladaptive eating behaviors such as stress eating, rapid eating, and portion distortion. Personalized healthy habit formation, adapted to individual clinical, psychological, and cultural contexts, is particularly important in menopausal women, where adequate protein intake plays a critical role in preserving lean mass and preventing sarcopenia.[34]

Structured behavioral programs are guided by counseling frameworks such as the 5As (Assess, Advise, Agree, Assist, and Arrange),[34,35] which facilitate shared decision-making and help personalize the patient journey. Intensive lifestyle interventions, defined as at least 14 sessions within 6 months, are recommended to achieve meaningful weight loss outcomes. Physical activity is central to this strategy, with guidelines suggesting 150–300 min of moderate-intensity aerobic exercise per week and strength training at least two to three times weekly.[36,37] Wearable devices and activity trackers can enhance adherence and engagement. Exercise provides wide-ranging benefits including reductions in visceral adiposity, WC, and inflammatory markers, while improving musculoskeletal strength, bone density, and physical function–thereby preventing osteoporosis and frailty in postmenopausal women.

Nutritional strategies complement behavioral and physical interventions by promoting a sustainable caloric deficit–typically 500–750 kcal/day–and emphasizing the reduction of ultra-processed foods and portion sizes.[38,39] Evidence-based dietary patterns such as the Mediterranean and Dietary Approaches to Stop Hypertension diets are strongly recommended due to their cardiometabolic benefits.[40] The Mediterranean diet, in particular, is associated with improvements in blood pressure, lipid profiles, insulin sensitivity, and reductions in cardiovascular risk. Diet plans should be individualized based on food preferences, medical conditions, and sociocultural factors to maximize adherence and long-term effectiveness.[41]

In summary, comprehensive obesity management in menopausal women requires an integrative approach that emphasizes behavior modification, regular physical activity, and personalized dietary interventions. These pillars not only support sustainable weight loss but also improve metabolic health, functional capacity, and quality of life across the menopausal transition.

PHARMACOLOGICAL MANAGEMENT OF OBESITY IN MENOPAUSAL WOMEN: AN OVERVIEW

Pharmacologic therapy serves as a critical adjunct to lifestyle modifications in managing obesity among menopausal women, especially those with a BMI ≥27 kg/m² accompanied by comorbidities or BMI ≥30 kg/m². These interventions should always be integrated with a balanced hypocaloric diet, regular physical activity, and professional guidance to optimize efficacy and long-term adherence.[35]

Among available pharmacotherapies, glucagon-like peptide-1 (GLP-1) receptor agonists have demonstrated superior efficacy and safety.[42,43] Recent clinical trials of antiobesity medications have continued to yield novel and impressive results, offering groundbreaking perspectives for clinical management and patient counseling.[44,45,46] Semaglutide 2.4 mg, administered once weekly, is currently considered the first-line agent due to its favorable cardiovascular outcomes and potent weight loss effects. Tirzepatide 15 mg, a dual GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) receptor agonist, has shown the highest efficacy in clinical trials, achieving weight reductions of up to 20% along with improvements in insulin sensitivity and lipid metabolism. Liraglutide 3.0 mg, a once-daily GLP-1 agonist, remains a widely used option, particularly in high-risk populations with cardiometabolic disease.[21]

Alternative agents, such as orlistat 120 mg, which acts locally as a lipase inhibitor, and the naltrexone/bupropion fixed-dose combination (denoted N32/B360 LP), may be considered in cases where GLP-1-based therapies are contraindicated, poorly tolerated, or ineffective. Orlistat is nonsystemic but limited by gastrointestinal side effects, whereas naltrexone/bupropion acts centrally by modulating POMC neuron activity and reward-driven eating, albeit with cardiovascular monitoring considerations.[21]

MECHANISMS OF ACTION: CENTRAL AND PERIPHERAL PATHWAYS

Pharmacotherapies for obesity exert their effects through three main mechanisms: Appetite suppression, promotion of energy expenditure, and inhibition of nutrient absorption. Central agents act on hypothalamic neurons (e.g., POMC, NPY/AgRP) and reward pathways (e.g., VTA, NAc), modulating satiety and hedonic eating. Agents such as liraglutide, semaglutide, bupropion, and naltrexone act within these pathways to suppress food intake and improve behavioral control over eating.[47]

Peripherally, GLP-1 agonists delay gastric emptying, stimulate pancreatic insulin secretion, and suppress glucagon release.[44] They also enhance hepatic lipid and glucose metabolism and increase glucose uptake in adipose and muscle tissues. Orlistat, by contrast, acts within the gastrointestinal tract to inhibit lipase activity and reduce fat absorption by approximately 30%.[47]

GLUCAGON-LIKE PEPTIDE-1 AND DUAL INCRETIN-BASED THERAPIES

Liraglutide, a GLP-1 analog with 97% homology to endogenous GLP-1, has shown efficacy in improving glycemic and cardiovascular parameters while preventing progression from prediabetes. Approximately 70% of patients receiving liraglutide achieve ≥5% body weight loss. Semaglutide offers greater potency with a more convenient weekly dosing regimen. The STEP trial demonstrated superior outcomes in women (16.1% vs. 11.6% in men), with reductions in WC, glycated hemoglobin, triglycerides, and inflammatory markers.[48] Cardiovascular risk was reduced by 13% in the LEADER trial.[49]

Tirzepatide represents a next-generation incretin agent targeting both GLP-1 and GIP receptors.[50,51,52,53] It achieves the most significant weight reductions (15%–20%), enhances insulin sensitivity, and improves lipid profiles. Its efficacy and tolerability profile position it as a promising candidate for long-term obesity management in menopausal populations. Ongoing and future trials are anticipated to further expand its indications and validate its benefits in broader clinical settings.[53]

COMPARATIVE EFFICACY AND META-ANALYTIC EVIDENCE

Meta-analyses confirm the superior efficacy of GLP-1-based therapies. Liraglutide users demonstrated a 5.54-fold increased likelihood of ≥5% weight loss and a 30.4% probability of achieving ≥10% weight reduction. Semaglutide and tirzepatide outperform all agents in weight loss magnitude and cardiometabolic benefit.[34] Orlistat and naltrexone/bupropion offer moderate effects and may be used selectively.

The pharmacologic management of obesity in menopausal women requires individualized, evidence-based approaches. GLP-1 receptor agonists and dual incretin agents offer the most effective and durable outcomes. Their combination of central appetite suppression, peripheral metabolic enhancement, and cardiovascular benefit supports their prioritization. As new injectable agents undergo rigorous clinical evaluation, their evolving role in personalized obesity treatment strategies remains highly anticipated.[34]

BARIATRIC SURGERY FOR OBESITY MANAGEMENT IN MENOPAUSAL WOMEN: INDICATIONS, PROCEDURES, AND POSTOPERATIVE CONSIDERATIONS

Bariatric surgery is increasingly recognized as the most effective intervention for achieving substantial and sustained weight loss, particularly in individuals with severe obesity and associated metabolic disorders. According to the 2022 joint guidelines from the American Society for Metabolic and Bariatric Surgery and the International Federation for the Surgery of Obesity and Metabolic Disorders, surgical intervention is recommended for individuals with a BMI ≥40 kg/m², or ≥35 kg/m² with comorbidities. For Asian populations, lower BMI thresholds are used given differing body fat distribution and cardiometabolic risk profiles; surgical consideration begins at BMI ≥27.5 kg/m² with comorbidities, and BMI ≥25 kg/m² is considered clinical obesity.[54]

Common bariatric procedures include vertical sleeve gastrectomy, Roux-en-Y gastric bypass, adjustable gastric banding, and biliopancreatic diversion with or without duodenal switch. Among these, sleeve gastrectomy and gastric bypass remain the most frequently performed due to their favorable balance between efficacy and safety.[55] A laparoscopic approach is generally preferred, as it is associated with reduced perioperative complications, shorter hospital stays, and faster recovery.

In postmenopausal women, bariatric surgery not only improves body weight but also significantly enhances metabolic health and reduces the burden of obesity-related comorbidities such as type 2 diabetes, hypertension, and sleep apnea. Moreover, surgical weight loss is associated with improvements in reproductive hormone profiles, systemic inflammation, and quality of life.[21,56]

However, successful outcomes depend on structured postoperative care. Nutritional supplementation is essential to prevent micronutrient deficiencies, particularly in patients undergoing malabsorptive procedures. Regular follow-up visits should include monitoring of weight trajectory, metabolic markers, and psychosocial well-being.[57] A multidisciplinary care model–incorporating nutritionists, psychologists, endocrinologists, and bariatric specialists–is recommended to support long-term adherence and reduce the risk of complications.[56,58] Bariatric surgery represents a powerful and durable treatment option for managing obesity in menopausal women. When implemented with proper patient selection and comprehensive follow-up, it significantly improves weight, cardiometabolic risk, and overall quality of life.

In conclusion, the management of obesity in menopausal women requires a holistic, individualized strategy that integrates lifestyle modification, pharmacologic treatment, and surgical options when appropriate. The bidirectional relationship between menopause and obesity not only exacerbates metabolic and symptomatic burdens but also complicates surgical care. The rise of GLP-1 receptor agonists and dual incretin-based injectables such as semaglutide and tirzepatide represents a major advancement in nonsurgical obesity treatment, offering potent and well-tolerated options with significant cardiometabolic benefits. Ongoing and future clinical trials are expected to further validate their utility in menopausal populations. Importantly, optimizing weight before gynecologic minimally invasive procedures can enhance surgical safety, reduce perioperative risk, and improve long-term outcomes. A multidisciplinary approach–engaging gynecologists, endocrinologists, bariatric specialists, and behavioral therapists–is essential to deliver comprehensive care to this high-risk population.

Author contributions

H.W.H. and K.C.L. conducted the literature review, selection, and interpretation. C.Y.L. and Y.C.O. provided critical input during the study design and conceptual discussions. K.C.L., serving as co-corresponding author, had primary responsibility for overseeing the development of the manuscript, interpreting key findings, and supervising the drafting and revision processes. All authors contributed to the writing of the manuscript and approved the final version.

This review article was developed and adapted based on a plenary lecture delivered by K.C.L. at the 2024 Annual Meeting of the Taiwan Association of Obstetrics and Gynecology (TAOG), during the Special Symposium on Menopause.

Data availability statement

The datasets generated during and/or analyzed during the current study are publicly available.

Conflicts of interest

Dr. Kuo-Chung Lan, an editorial board member at Gynecology and Minimally Invasive Therapy, had no role in the peer review process of or decision to publish this article. All authors declared no conflicts of interest in writing this paper.

Funding Statement

Nil.