Clinical Practice Guidelines for Menopause: An Executive Summary and Recommendations: Indian Menopause Society 2026.

Delayed menopause/late-onset menopause: Definition and health consequences – Refer to Section 1 36. Twin and genomic studies indicate strong heritability, while longitudinal cohort data emphasize the roles of endocrine, environmental, and life-course factors, including family history, parity, nutrition, and lifestyle determinants. [59-63] 37. Screening and management: Robust data are lacking, and the protocols remain similar to those with the natural age at menopause. The absolute risk of endometrial carcinoma in asymptomatic women remains low; therefore, routine endometrial evaluation is not recommended based solely on delayed menopause. Evaluation should be triggered by symptoms such as bleeding and tailored to individual risk factors (Grade B). [64] Premature ovarian insufficiency: Definition and diagnosis – Refer to Section 1 38. A common issue in premature ovarian insufficiency (POI) is diagnostic delay, often spanning 2–5 years. Although direct causal data are limited, strong evidence indicates that untreated POI accelerates bone loss and raises the risk of cardiometabolic and other health issues, emphasizing the importance of prompt diagnosis and hormone therapy (HT) initiation (Grade B). [65-68] 39. Comprehensive and personalized management, including informed counseling, assessment of fertility goals, optimization of general health, lifestyle modification, and HT, forms the foundation of care for women with POI. [69] 40. Systemic HRT should be initiated early after diagnosis and continued until the expected age of natural menopause (ANM) to reduce skeletal, cardiovascular, and neurocognitive sequelae and preserve quality of life (Grade B). [70-72] 41. Screening and pre-MHT workup protocols are primarily similar to those for natural menopause, with a particular focus on bone health assessment. [73] DXA should be performed at diagnosis to assess both BMD and body composition, given the high prevalence of early bone loss and sarcopenia. [73,74] 42. Although women with POI are often beyond the age of peak bone mass, their bone loss results from reversible hypoestrogenism rather than from senile bone remodeling. Therefore, Z -scores (age-matched comparisons) are preferred for diagnosis, reserving T -scores for long-term postmenopausal follow-up. [73-76] 43. Current RCT evidence supports the use of HRT versus OCP, and final comparative results are expected from the Premature Ovarian Insufficiency Study of Effectiveness of Hormonal Therapy. [77-79] 44. In asymptomatic women with POI, high-quality randomized data are limited; however, current evidence and international guidelines consistently recommend HRT to improve the quality of life and reduce the risks of bone loss, cardiovascular disease, and cognitive decline associated with prolonged hypoestrogenism until the usual ANM (Grade B). [73,80-84] 45. Androgen therapy should only be considered for select, estrogen-replete women with persistent sexual symptoms; transdermal testosterone is preferred where available, but currently, no licensed preparation for women exists in India (Grade B). [85]

133. BC: Overall, midlife weight and adiposity gain are driven mainly by aging and lifestyle rather than menopause (Grade C). [218,219] 134. However, the MT independently promotes adverse fat redistribution, with increased visceral and pericardial/epicardial fat beyond aging effects, contributing to metabolic syndrome and greater cardiometabolic risk after menopause. [220,221] 135. During the MT, estrogen deficiency accelerates bone loss (Grade A) [222] and reduces muscle mass and strength (Grade B), [223] while aging further impairs bone quality and muscle regeneration. Together, these processes especially in POI and early menopause increase the risk of osteoporosis, sarcopenia, and frailty. [224] Early lifestyle measures and, where appropriate, therapeutic interventions are essential to preserve bone and muscle health in midlife women and prevent adiposity (Grade B). [225-227] 136. Skin changes: Estrogen deficiency during and after the MT reduces collagen content in both skin and bone. [228] Loss of cutaneous collagen accelerates skin aging, wrinkling, and decreased elasticity (Grade B). [229] At the same time, hormonal imbalance with relative androgen excess after menopause may contribute to frontal balding and hirsutism in some women (Grade B). [230] 137. Metabolic changes: Refer to Section 3.

217. In women experiencing menopause at the expected age, the MT, along with aging, is associated with metabolic changes that elevate cardiovascular disease (CVD) risk. MT may be considered a window of opportunity to screen and promote preventive measures to reduce the risk of CVD. Risk factors for cardiovascular disease in women can be divided into three categories: 218. Well-established risk factors such as hypertension, dyslipidemia, diabetes, obesity, unhealthy diet, sedentary lifestyle, and smoking or tobacco use. [233] A family history of premature CVD (men <55 years, women <65 years) is a strong risk factor and accounts for a major share of Atherosclerotic CVDs (ASCVD) globally, while CKD and chronic inflammatory states further increase risk. [234] 219. Under-recognized or under-rated risk factors include psychosocial (depression and anxiety); abuse and intimate partner violence (inducing chronic stress); socioeconomic and cultural status, race, and poverty; poor health literacy; and environmental risk factors (air pollution). [233] 220. Female-specific risk factors such as POI and EM, history of polycystic ovaries (PCO), functional hypothalamic amenorrhea, radiation and chemotherapy for breast cancer, and complications of pregnancy, including preeclampsia, gestational diabetes mellitus, gestational hypertension, preterm delivery, and low-for-estimated-gestational-age birth weight. Other conditions that are not necessarily sex-specific but are female predominant, like certain autoimmune disorders, including, but not limited to, rheumatoid arthritis, systemic lupus erythematosus, and scleroderma. [233,235-237] Screening for women aged ≥35 years 221. Promote awareness and education: Educate clinicians and women that CVD is the leading cause of death in women, exceeding breast cancer mortality. [238,239] 222. Integrating menopause counselling with CVD risk screening enhances early detection and preventive intervention. [240] Risk assessment tools for the prediction of cardiovascular disease 223. The Globorisk and Reynolds risk scores are designed for CVD-naïve women. Globorisk-India estimates the 10-year probability of a first fatal or nonfatal myocardial infarction (MI) or stroke, not procedure-based events. [241] 224. The Reynolds risk score estimates the risk of major cardiovascular events (ischaemic stroke, MI, need for coronary revascularizations, or cardiovascular death) in women over 45 years of age. [242,243] 225. The Framingham Risk Score and ACC/AHA risk calculators are widely used tools; however, they have not been specifically validated or stratified for the Indian population. The QRISK3 score, used in the NHS, incorporates additional factors such as mental illness, autoimmune diseases, and CKD. It has also been applied to South Asian populations living in the United Kingdom. Globorisk-India (primary recommendation) 226. We recommend using Globorisk-India (laboratory or nonlaboratory version) as the first-line tool for women aged a35 years. After estimating baseline risk, reclassify upward if any female-specific risk enhancer is present. Manage according to the revised risk category. [241,244-252] 227. Advantages of Globorisk-India (2023): Include its calibration specifically for the Indian population, availability of both laboratory-based and nonlaboratory versions suitable for urban and rural settings, ease of use via mobile or paper-based tools, and its ability to provide more accurate, context-appropriate risk estimates than Western models. It is also cost-effective, scalable, and well-suited for integration into national women’s health and NCD screening programs. [240,241,245,246] 228. How to calculate Globorisk - India tool Access: Use the web calculator at www.globorisk.org or the validated desk/pocket chart Collect core data: Age, sex (female), systolic blood pressure (mmHg), BMI or total cholesterol, diabetes (yes/no), and smoking (yes/no) Select version: Nonlaboratory for PHC/outreach use. Laboratory-based for hospitals or specialist clinics. Access: Use the web calculator at www.globorisk.org or the validated desk/pocket chart Collect core data: Age, sex (female), systolic blood pressure (mmHg), BMI or total cholesterol, diabetes (yes/no), and smoking (yes/no) Select version: Nonlaboratory for PHC/outreach use. Laboratory-based for hospitals or specialist clinics. Interpret risk < 10% = Low → Lifestyle optimization 10%–20% = Moderate → Intensified lifestyle ± pharmacotherapy. 20% = High → Comprehensive medical management (blood pressure [BP], lipids, glycaemia). < 10% = Low → Lifestyle optimization 10%–20% = Moderate → Intensified lifestyle ± pharmacotherapy. 20% = High → Comprehensive medical management (blood pressure [BP], lipids, glycaemia). Integrate female-specific modifiers into clinical judgement: Premature or EM (<45 years) history of gestational diabetes, preeclampsia, or polycystic ovary syndrome (PCOS), autoimmune disease, hypothyroidism, or chronic inflammatory disorders. Upgrade risk category: If any one modifier → move up one tier (Low → Moderate; Moderate → High). If two or more modifiers or modifier + diabetes/dyslipidemia → move up two tiers. Document: Globorisk-India = %; upgraded due to-modifier. 229. Reynolds risk score (secondary recommendation) Reserve for women 45–80 years with no prior CVD but ambiguous results on standard scores. It incorporates hs-CRP to account for inflammation as a risk factor. Also includes familial (parental MI) factor for greater precision in borderline-risk cases. [242,243] However, the derivation cohort consisted predominantly of white, middle- to upper-socioeconomic status women, which may limit its generalizability. 230. How to calculate the Reynolds risk score Available online on these two links: https://www.mdcalc.com/calc/3932/reynolds-risk-score-cardiovascular-risk-women?utm_ https://reference.medscape.com/calculator/192/reynolds-cad-risk?utm_ Reassess every 3–5 years or when major risk factors change. 231. Atypical clinical presentation: Women often present without classic exertional chest pain. Instead, symptoms may include fatigue, breathlessness, palpitations, epigastric discomfort, nausea, dizziness, or jaw and back pain rather than retrosternal heaviness. Silent or unrecognized MI is also more common in women, particularly among the elderly and those with diabetes. [247,253] Diagnostic and management challenges 232. CVD in women is often under-recognized and under-treated. Standard diagnostic tools, electrocardiogram (ECG), stress testing, and troponin thresholds, may show lower specificity due to sex-based physiological differences. [254,255] 233. Women more frequently present with nonobstructive or microvascular coronary disease, resulting in normal angiograms despite ischemic symptoms. They have a higher prevalence of endothelial dysfunction and thrombosis, with or without plaque formation, as underlying mechanisms of acute MI. These processes contribute to microvascular ischemia. [256] 234. Hence, women experience delays in diagnosis, fewer referrals for angiography, and reduced use of guideline-directed therapy, contributing to higher short-term mortality and recurrent angina, mainly from heart failure with preserved ejection fraction. [257,258] Early recognition of cardiovascular disease in women 235. Maintain high clinical suspicion: CVD should be considered in all women of 35 years presenting with fatigue, dyspnea, palpitations, or epigastric pain, especially with risk factors such as diabetes, hypertension, dyslipidemia, obesity, EM, or family history. [238,247,253] 236. Absence of classic angina does not exclude ischemia, particularly in women with microvascular dysfunction. [247,257] 237. Identify early symptoms: Women may experience unusual fatigue, poor sleep, anxiety, or exertional breathlessness weeks before acute coronary events, often dismissed as stress or menopause related. [247,253,259] 238. Early evaluation: These prodromal symptoms warrant prompt clinical evaluation and risk screening, rather than attributing these to “stress” or “age.” [247,253,259] Optimize diagnostic strategy 239. Use high-sensitivity troponins with sex-specific cutoffs and functional test (stress echo) when ECG or treadmill tests are inconclusive. [247,257,260] 240. Coronary computed tomography angiography is to be used in false positive cases and is not a screening test. Coronary flow reserve is done during coronary angiography to assess borderline lesions. [247,257,260] 241. Computed tomography (CT) coronary artery calcification (CAC) is used to assess the extent of the calcified plaque in the coronary arteries. A higher CAC score indicates a higher risk of a coronary event. It is an established tool for stratifying cardiovascular events. It is recommended for use in patients with intermediate ASCVD risk scores or uncertain profiles to more precisely evaluate risks. [261] 242. Microvascular angina (MVA) is often grouped under the broader ischemia with non-obstructive coronary arteries category, which includes both MVA and vasospastic angina. 243. INOCA: If a woman has typical angina symptoms but normal coronary angiography, consider MVA, ischemia caused by dysfunction of small coronary vessels rather than major blockages. [257,262] 244. Positive stress test, objective ischemia (ST depression, reversible perfusion defect, or stress-induced wall motion change) despite nonobstructive coronaries (<50%) on angiography or CT suggests INOCA. [257,262] Prevention and management of cardiovascular disease 245. TLM: Robust evidence supports the effectiveness of lifestyle interventions – particularly multifactorial programs that combine dietary modification, regular physical activity, and behavioral counselling in reducing intermediate cardiovascular risk factors in both high-risk individuals and the general population. These interventions consistently demonstrate improvements in BP, lipid profiles, body weight, and glycemic parameters, thereby contributing to both primary and secondary prevention of CVD. [263-266] 246. Lifestyle and risk factor: Smoking cessation remains the single most effective strategy. Behavioral counseling, nicotine-replacement therapy, and pharmacologic support (e.g., varenicline, bupropion) may be considered where appropriate. [267,268] 247. Body weight: Maintain or achieve an ideal body weight. A family-based, structured lifestyle modification program yields a net gain in quality of life and is cost-effective at a three-times gross domestic product per capita threshold. [269-271] 248. Physical activity: Engage in 150 min/week of moderate-intensity aerobic activity (e.g., brisk walking and cycling) or 75 min/week of vigorous-intensity activity, or an equivalent combination. [272] 249. Digital and behavioral support tools: Apps, telecoaching, and wearables can enhance adherence and behavioral outcomes; however, their long-term clinical impact remains uncertain. [273] 250. Lipid optimization: For Indian midlife women, optimal lipid targets should aim for low-density lipoprotein cholesterol (LDL-C) <130 mg/dL in low-risk and <100 mg/dL (preferably <70 mg/dL) in higher-risk groups. Triglycerides 50 mg/dL are desirable. Early initiation of statin therapy is recommended when LDL-C exceeds these thresholds, particularly in the presence of South Asian ethnicity or other female-specific risk enhancers (e.g., premature menopause and gestational diabetes). [274-277] 251. Blood pressure optimization: Midlife women should be counselled on achieving and maintaining BP 140/90 mm Hg (or >130/80 mm Hg in diabetes). [278,279] 252. Dietary approaches to stop hypertension diet: Limit sodium (<2 g/day), maintain a healthy weight, and engage in 150 min/week of moderate physical activity. These measures lower systolic BP by an average of 4–11 mmHg. [280,281] 253. Antihypertensives: Thiazide diuretics (e.g., chlorthalidone and indapamide) are the preferred first-line antihypertensive agents unless contraindicated. Angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers, and calcium-channel blockers may be added or substituted as required to achieve optimal BP control. [282] 254. Glycemic optimization: For Indian midlife women with diabetes, aim for hemoglobin A1c (HbA1C) <7% through lifestyle optimization with early pharmacologic intensification when needed. This threshold is associated with a substantial reduction in microvascular complications and improvement in overall cardiovascular outcomes (Grade A). [283-285] 255. Low-dose aspirin for primary prevention: Primary prevention in women without risk factors is not recommended at any age. Indian guidelines emphasize that, given the high burden of CVD, low-dose aspirin may be considered only in high-risk women aged 40–60 years (≥two risk factors: diabetes, hypertension, CKD, family history, high LDL/Lp(a), CAC >100) with low bleeding risk, after shared decision-making and risk assessment. [274,286,287] 256. Antioxidant, vitamin, and folate supplementation: Do not use Vitamin E, Vitamin C, multivitamin, folic acid, or B-Vitamin supplements (alone or in combination) for CVD prevention. [288] 257. Omega-3 Fatty Acids and Prescription Icosapent Ethyl (eicosapentaenoic acid 4 g / day): Do not recommend routine omega-3 supplements for CVD prevention; consider prescription-strength icosapent ethyl in statin-treated, high-risk women with triglycerides t150 mg/dL. Grade A (for icosapent ethyl) and Grade C (for routine omega-3 use). [289,290] 258. MHT is not indicated solely for primary or secondary cardioprotection (Grade A). [291-293] 259. MHT initiated early among healthy women with premature or surgical menopause may reduce the adverse consequences of prolonged estrogen deficiency on cardiometabolic health. [291,294,295]

57. The current population of India is 1,465,796,710 as of Sunday, October 19, 2025, based on Worldometer’s elaboration of the latest United Nations data. [89] This number is expected to increase to 1,679,589,259 by 2050. [89] 58. The life expectancy of Indian women has increased from 40.4 years in 1950 to approximately 73.6 years in 2023. Although India’s life expectancy has been increasing, it has generally remained below the global average. [90-92] 59. According to the UN World Population Prospects 2024 Revision (medium variant), India had approximately 46 million women aged 45–49 years in 2024 and is projected to have approximately 57 million in 2050, compared with 30 million in 2011. [89] Rising trends between 2005 and 2021 suggest an increasing burden of early ovarian aging in Indian women. [93-95] 60. Population-based Indian data (NFHS 3–5) show that the prevalence of POI is 1.5%–3% of women, while EM affects 8%-16%, with the national mean age at menopause as 46 years. [94] When surgical menopause is included, state-level data suggest an overall POI (natural + induced) prevalence of 8.7% in Telangana and 8.2% in Andhra Pradesh. [95] Regional prevalence is higher in southern and eastern states and among women with lower education, rural residence, poor nutrition, or prior tubal sterilization. [96,97] Age at menopause: Determinants and health system implications 61. The estimated mean ANM in India is 46.6 years, approximately 4–5 years earlier than that in Caucasian women, whose mean ANM averages around 51 years. [40,41,98,99] 62. ANM is largely genetically determined (50%); smoking advances its onset by approximately 1–2 years in a dose-dependent manner (Grade A). [100,101] Undernutrition, reproductive factors (nulliparity, irregular cycles, or short cycles), and lower socioeconomic or educational status are consistently associated with earlier menopause in large cohort and pooled analyses (Grade B). [102-104] Medical challenges 63. From the available Indian data, it is hypothesized that ANM predisposes women to chronic health disorders a decade earlier than Caucasian women. This earlier onset is attributed to a combination of genetic predisposition, higher central adiposity at a lower BMI, lifestyle factors, and possibly lower disease awareness, delayed diagnosis, and early ANM in women. [95,105,106] 64. Multimorbidity: It refers to having multiple chronic conditions, which also emerges earlier, with many women developing two or more chronic diseases by their mid-30s to mid-40s. [107-109] 65. NCDs: South Asian women, including those in India, experience myocardial infarction approximately a decade earlier than European women, reflecting the earlier onset and higher lifetime burden of atherosclerotic CVD in this population. [110] In India, the prevalence of CVD among adults is estimated at 11% (95% CI: 9%–12%), with markedly higher rates in urban and middle-aged women than in rural populations. [111] 66. Hypertension: The overall prevalence of hypertension in India is currently estimated at 22.6% among adults aged ≥15 years, with a higher prevalence in urban (25%) than in rural areas (21.4%). [112] Longitudinal data also indicate a rising trend, with rural prevalence increasing from approximately 34% to over 40% over a decade. Despite this, awareness, treatment, and control rates remain suboptimal, with less than one-third of individuals on treatment in most reports. [113] 67. T2DM in India shows a prevalence of 6.1% in adults aged ≥15 years, rising to nearly 20% among those aged 45 plus, and evidence suggests that Indians develop T2DM on average over a decade earlier than Caucasian populations. [114,115] The migrant population from the Indian subcontinent in the UK is known to be at a significantly higher risk of developing diabetes and CVD. [116] 68. Indian data consistently demonstrate that fragility fractures, particularly hip fractures, occur approximately a decade earlier (mean age 65–71 years) than in Western populations (>75–80 years). [117-120] 69. Cancers: Breast cancer occurs at younger ages in India: Indian hospital- and registry-based studies indicate that a large proportion of breast cancer cases in India occur in women aged 45–50 years, earlier than in the West, where the peak incidence tends to be in the 60–65 age group. [121-124] 70. In India, the median age at cervical cancer diagnosis is 55 years (range: 45–60), which is comparable to or slightly older than that in the U.S., where the median age is 50 years. This conclusion is supported by India’s Population-based Cancer Registers (PBCRs) and the U.S. Surveillance, Epidemiology, and End Results Program (SEER). [125] 71. In the U.S., the median age at endometrial cancer diagnosis is 64 years, [126] whereas Indian data indicate diagnosis in the mid-50s to early-60s. Nationwide PBCR-pooled figures are lacking, with available estimates from tertiary or regional registries. [126,127] 72. Ovarian cancer in rural central India: In the PBCR of Central Rural India (2010–2016), the age-standardized incidence rate of ovarian cancer was 4.61 per 100,000, with the majority of Indian cases (most ovarian malignancies) occurring in women aged 41–50 years. The above suggests a somewhat earlier onset age than Western populations, where the median age at diagnosis is 63 years. [128] 73. Obesity: The prevalence of obesity in India is 24%–28% among adults and is lower than that in Western populations (≥40%) in the United States. [20,129-131] However, related metabolic risks appear 5–10 years earlier than in Western populations and at lower BMI thresholds (≥23 for overweight and ≥25 for obesity), with NCDs such as T2DM and CVD emerging from the mid-30s onward. [20,129-131] 74. Health-seeking behavior: Few Indian studies on health-seeking behavior have limitations of geographical bias, sample size, and lack of cost analysis; yet, the influence of sociocultural factors is well demonstrated. Rural women demonstrate substantially lower healthcare utilization rates (25%–30%) than urban women (42%–48%). This disparity is attributed to multiple factors, including distance to healthcare facilities, financial constraints, and cultural barriers. [132] 75. Policy: Unlike the UK and Australia, India does not have a dedicated national policy on menopause. There is also limited government funding and policies for menopause-related research and program evaluations, gaps in the implementation of the National Program for Health Care of the Elderly, and a shortage of trained personnel in menopausal and geriatric medicine. [133-135] 76. Nongovernmental organizations , such as the IMS, are leading the charge in championing midlife health. IMS publishes and conducts regular community workshops, wellness camps, and public awareness programs for consumers under the “Club 35 Plus.” [136] The Federation of Obstetric and Gynecological Societies of India addresses this issue by focusing on the midlife committee. [137] 77. Social challenges: In India, key social challenges include an increasing aging population, erosion of traditional family support structures, rise of nuclear families, rural-to-urban and international migration, and a growing burden of NCDs and degenerative diseases. [138,139] 78. There is a need to retain and revive Eastern cultural strengths while integrating elements of the Scandinavian model, which emphasizes gender equity, preventive health, and state-supported well-being. [140,141] Menopause and the workplace 79. Estimates indicate that approximately 9–11.6 million women aged ≥40 years work in India, with roughly 3–3.6 million in the government sector and 6–8 million in the private sector. This highlights their significant yet under-recognized contribution to the national workforce. [142,143] Barriers in the workforce include age–gender bias, career re-entry challenges, limited networking, work–life imbalance, and overrepresentation in informal, low-paid sectors, especially rural agriculture. [144] 80. Survey data show that nearly 82% of Indian women believe menopause impacts workplace well-being and career, while 18%–26% work through symptoms or take time off without disclosure. [145] A recent systematic review found that cognitive behavioral therapy, Raja Yoga, healthy lifestyle support, and menopause awareness interventions improve the well-being of menopausal women, and individuals or organizations can combine and tailor them to their needs. [146,147] Transgender individuals and menopause 81. 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46. Early menopause (EM) is not classified as POI but signifies the physiological end of the continuum of the pathological state of accelerated ovarian aging. Both conditions share pathophysiological pathways and long-term health consequences, differing only in age threshold and severity of health outcomes. [83,84,86] 47. Women experiencing EM should be offered appropriate-dose systemic HT. While robust data are limited, observational studies and biological reasoning support HT to preserve bone health and potentially decrease the risk of cardiometabolic and neurocognitive complications associated with prolonged hypoestrogenism. 48. Therapy should be continued until the ANM, at which point the risks and benefits should be re-assessed. [80,86-88]

138. Fertility: In women aged >40 years who fail to conceive after 1–2 cycles of controlled ovarian stimulation, in vitro fertilization (IVF) should be considered early, as success with conventional stimulation is poor (Grade B). [231,232] 139. The only effective treatment for ovarian aging with markedly reduced reserve is oocyte (donor egg) IVF, which yields pregnancy rates far superior to stimulation with autologous oocytes (Grade A). [233,234] 140. Counsel women aged ≥40 years about the exponential increase in chromosomal abnormalities, miscarriage, and mosaic embryos; offer individualized Preimplantation Genetic Testing for Aneuploidy (PGT-A) counseling and interpretation in collaboration with reproductive specialists (Grade A). [235,236] 141. Preconception counseling should emphasize weight optimization, control of hypertension, diabetes, thyroid disease, and identification of obstetric risks. Women aged >40 years require individualized counseling regarding maternal and perinatal complications (Grade B). [237,238] 142. Fertility preservation should be offered to women at risk of premature or treatment-induced menopause. Oocyte and embryo cryopreservation using vitrification is an established, effective, and safe technique (Grade A). [239,240] 143. Elective oocyte freezing may be considered before the age of 38 years after individualized counseling (Grade B). [241,242]

49. Iatrogenic menopause refers to the loss of ovarian function caused by medical or surgical interventions, such as indicated or prophylactic bilateral oophorectomy, pelvic radiotherapy, chemotherapy, or ovarian ablation for malignancy. [81,84] 50. Systematic reviews suggest that hysterectomy for benign reasons, even with ovarian preservation, leads to earlier ovarian failure and menopause onset compared to women who retain their uterus (Grade B). [89-92] 51. The primary reasons for surgical menopause include both clinical and nonclinical indications. Heavy menstrual bleeding, often caused by fibroids or adenomyosis, and uterine prolapse are the most common reasons for hysterectomy in India. [93,94] 52. Nonclinical factors include lower education, poorer households, a concentration of procedures within the private sector, and limited access to conservative or minimally invasive alternatives. [95] 53. The Indian Council of Medical Research strongly warns against performing hysterectomy and surgical castration without medical indication. Every clinician must ensure a clear medical justification, document informed consent, preserve the ovaries whenever possible, and advise women on the lifelong health effects of premature estrogen loss. [96-100] 54. Women experiencing iatrogenic menopause should receive multidisciplinary care involving gynecologists, oncologists, and endocrinologists. In the absence of contraindications, physiologic-dose MHT should be initiated soon after surgery or the completion of oncologic therapy and continued until the expected ANM. 55. Early counseling, personalized risk assessment, and preventive lifestyle advice should be incorporated into all treatment pathways where ovarian failure is expected, ensuring that women receive timely information and access to fertility preservation options before gonadotoxic therapy or surgery. 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88. LET includes a range of vaginally administered estrogen products approved with the indication to treat GSM. [150] 89. Comparative trials have also demonstrated that vaginal estrogen achieves a superior local effect with lower systemic absorption than oral preparations. [126] 90. A Cochrane systematic review confirmed that all licensed local estrogen preparations are equally effective in improving the symptoms and signs of VVA compared with placebo, with no significant difference in the overall efficacy among formulations (Grade A). [123] However, 17β-estradiol appears to provide greater improvement in patient-reported symptoms. In contrast, conjugated equine estrogen (CEE) produces more marked cytological changes and a slightly higher increase in serum estradiol levels, [151] with no clinically meaningful differences in overall efficacy. Estriol (E3) is a low-potency estrogen that is not converted to 17β estradiol (E2) and has modest efficacy (Grade B). [152] 91. Doses: The various doses of LET are shown in Table 1 . Doses of local estrogen therapy 92. The doses for LET include CEEs 0.3–1.25 mg/day, estradiol 25 µg/day, and estriol cream 0.5 mg/day, depending on the severity of GSM (Grade A). [153] 93. A randomized study showed that ultra-low-dose E2 (4–10 µg) significantly improved vaginal maturation, restored vaginal pH, and reduced symptoms compared with placebo (Grade B). [154] 94. Regimen: The recommended regimen for LET consists of daily application to the lower vagina for 2–4 weeks, followed by a maintenance schedule of two to three applications per week for 2–6 months (Grade A). [150] 95. Absolute contraindications: are undiagnosed vaginal bleeding and active, untreated estrogen-sensitive malignancy (Grade A). [155-157] 96. Avoid: Hypersensitivity reactions to menopausal estrogen therapy are infrequent, with most documented cases including contact dermatitis, cyclical vulvitis, and drug eruptions. [158,159] Life-threatening events, including anaphylaxis, are infrequent and are primarily described in isolated case reports or hormone allergy reviews. [160] 97. Relative contraindications: Evidence supports a risk-stratified approach, with breast cancer survivors requiring mandatory oncology consultation, while patients with CVD or venous thromboembolism (VTE) history need individualized assessment (Grade B/C). [161-165] 98. General principles of LET use: Treatment should be started early to prevent irreversible atrophic changes (Grade B). [165-167] 99. Clinical consensus supports indefinite use when needed, based on longitudinal observational studies. However, robust safety data beyond 1 year of continuous use are limited for all available vaginal preparations (Grade B). [155,167-171] 100. A systematic review found no evidence of endometrial proliferation after 6–24 months of low-dose LET use (Grade A). [161] Transvaginal ultrasonography (TVS) and endometrial biopsy (EB) (Grade A) should be used to investigate unscheduled bleeding. [167] Progesterone supplement for endometrial protection is not needed along with the use of LET (Grade A). [165,168]

315. Estrogen decline during menopause leads to alterations in the gut, vaginal, and urinary microbiota, which disrupts mucosal immunity, epithelial integrity, and microbial diversity (Grade A). [368] 316. Diets rich in fibre, fermented foods, and probiotics may support microbial diversity and estrogen metabolism (Grade B). [369-372] Local estrogen therapy helps restore vaginal Lactobacillus dominance (Grade A). [373] R EFERENCES Rocca WA, Grossardt BR, Shuster LT. Oophorectomy, menopause, estrogen treatment, and cognitive aging: Clinical evidence for a window of opportunity. Brain Res 2011;1379:188-98. Waliszewska-Prosół M, Grandi G, Ornello R, Raffaelli B, Straburzyński M, Tana C, et al . Menopause, perimenopause, and migraine: Understanding the intersections and implications for treatment. Neurol Ther 2025;14:665-80. Wang Y, Mishra A, Brinton RD. 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Available from: https://www.who.int . [Last accessed on 2025 Oct 10]. Vajaranant TS, Pasquale LR. Estrogen deficiency accelerates aging of the optic nerve. Menopause 2012;19:942-7. Freeman EE, Muñoz B, Bressler SB, West SK. Hormone replacement therapy, reproductive factors, and age-related macular degeneration: The Salisbury eye evaluation project. Ophthalmic Epidemiol 2005;12:37-45. Youngblood H, Schoenlein PV, Pasquale LR, Stamer WD, Liu Y. Estrogen dysregulation, intraocular pressure, and glaucoma risk. Exp Eye Res 2023;237:109725. Prokai-Tatrai K, Zaman K, Kapic A, Hogan K, Sanchez-Rodriguez G, Silverio AE, et al . Retina-targeted 17β-estradiol by the DHED prodrug rescues visual function and actuates neuroprotective protein networks after optic nerve crush in a rat model of surgical menopause. Int J Mol Sci 2025;26:1846. Lee HJ, Yu EH, Jeong YH, Joo JK. 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125. Nutritional supplementation: Combined calcium + Vitamin D supplementation (1000–1200 mg Ca + 800–1000 IU D 3 /day) reduces hip and total fracture risk in older adults (Grade A). [150-153] 126. Calcium: Supplements are used to correct calcium and Vitamin D deficiency and form an integral part of established osteoporosis management to achieve a total of 1000–1200 mg/day (Grade A). [154] The risk of cardiovascular events, including calculi, is not observed with the recommended doses of calcium (Grade A). [155,156] 127. Calcium supplements should be individualized, limited to ≤500 mg per dose, 800–1200 mg/day total, and spaced from interfering nutrients or drugs. Dietary restriction is not advised, and excessive intake (>2500 mg/day) should be avoided (Grade A). [56,150] 128. Vitamin D: Vitamin D deficiency is widespread across India, with prevalence estimates around 20%–100%, higher among women and residents of northern and eastern zones due to limited sun exposure and cultural clothing practices (Grade A). [157,158] 129. Vitamin D is obtained from sunlight, fortified foods, and supplements, but most Indians receive inadequate sun exposure, and current food fortification levels are insufficient to meet the RDA. 130. According to ICMR-NIN (2024) and Food Safety and Standards Authority of India standards, fortified edible oil provides approximately 110–160 IU/day, while fortified milk provides 200 IU/day, assuming average adult intake of 25–30 g oil + 250 mL milk/day, together covering only about two-thirds of the RDA. [157,159,160] Hence, supplementation is advisable in high-risk groups (indoor workers, elderly, obese, or malabsorptive states). 131. Gupta’s review underlines that even apparently healthy Indians show low serum 25(OH)D levels, supporting universal supplementation, initial correction followed by maintenance dosing until widespread and effective food fortification becomes a reality (Grade B). [157,161] 132. Measurement of serum 25(OH)D is recommended in individuals at risk of Vitamin D deficiency, including those with osteoporosis, fragility fractures, malabsorption, chronic kidney or liver disease, obesity, or limited sun exposure. Routine screening of the general population is not recommended (Grade A). [134,135] 133. Cholecalciferol is preferred for the correction and maintenance of Vitamin D deficiency; aim for a serum 25(OH)D level of 40–60 ng/mL. Doses ≤4000 IU/day are safe; toxicity occurs with >10,000 IU/day (Grade B). [162,163] 134. Cholecalciferol (Vitamin D 3 ) is available in oral tablets, capsules, granules, nanoemulsions, and spray forms, typically in doses of 1000 IU, 2000 IU, and 60,000 IU. 135. Intramuscular preparations (300,000–600,000 IU per ampoule) are cost-effective and particularly useful in patients with malabsorption, poor adherence, or intolerance to oral therapy. However, they may cause injection-site discomfort and yield variable serum 25(OH)D levels. 136. The choice between daily and bolus dosing remains debated. The Endocrine Society (USA) recommends daily dosing for physiological mimicry, yet adherence challenges are common with long-term daily use. [135] 137. Bolus regimens, weekly or monthly, are supported by Vitamin D’s long half-life and comparable ability to sustain 25(OH)D and PTH levels over time, as excess Vitamin D is stored in adipose tissue and released gradually. 138. Thus, daily, weekly, or monthly schedules may be selected based on patient preference, likelihood of adherence, and clinical context, provided the cumulative dose remains within recommended limits. [135,137,164] Management 139. Vitamin D deficiency (<20 ng/ml/<50 nmol/L): cholecalciferol (Vitamin D3), 60,000 IU/orally once a week for 12 weeks, preferably with milk or 2000 IU/day. 140. Vitamin D insufficiency (20–30 ng/ml/50–75 nmol/L): cholecalciferol (Vitamin D3), 60,000 IU/orally once a week for 8 weeks, preferably with milk or 2000 IU/day. 141. One IM injection of 600,000 IU is given to correct the deficiency (not to be repeated for 3 months and may be given after confirmation of persistent low Vitamin D levels). 142. Caution: Always combine with adequate calcium intake (dietary or supplemental) for bone benefits. Higher doses may be required in obesity, malabsorption, and chronic kidney disease. 143. All regimes are to be followed by maintenance therapy. 144. Maintenance therapy: Cholecalciferol 60,000 IU once a month in summer or twice a month in winter. Vitamin D supplements of 2000 IU/day, or Injection of Cholecalciferol 300,000 IU IM, twice a year or 600,000 IU IM once a year, [78,136,165] or exposure to sunlight in the recommended time and duration. 145. Calcitriol (0.25–0.5 μg/day) and Alfacalcidol are indicated only in chronic renal or hepatic disease with impaired Vitamin D activation. Their use mandates monitoring of calcium and renal function due to the risk of hypercalcemia, hypercalciuria, and nephrocalcinosis (Grade A). [166,167] 146. Vitamin K supplementation: 180–350 μg/day of Vitamin K2-7 may be considered along with calcium, magnesium, Vitamin D, and a balanced diet. The current RDA (WHO/FAO) of 65–80 μg/day is considered inadequate. Suggested intake is ≥100 μg/day throughout life, with higher doses when indicated. Vitamin K supports both bone health and cardiovascular health in women with osteoporosis (Grade C). [168] Pharmacological management of postmenopausal osteoporosis: Prevention versus treatment 147. Prevention refers to interventions aimed at halting or slowing bone loss in postmenopausal women with low bone mass (T-score between −1.0 and −2.5) and increased fracture risk. Treatment refers to the use of pharmacological agents to reduce fracture risk in women with established osteoporosis (T-score <−2.5 or presence of a fragility fracture). [78] Indications for pharmacotherapy The clear indications for pharmacotherapy are a history of fragility fractures, osteoporosis defined by DXA, and low bone mass with 10-year HF probability >3% OR a 10-year major OP fracture probability >20% (FRAX). 148. Categorization according to risk of fracture: Management is based on the concept of stratifying women into low, intermediate, high, or very high-risk categories according to BMD and clinical risk factors [ Table 3 ]. 149. In the absence of DXA: Treatment decisions are based on the outcomes of FRAX and OSTA [ Table 3 ]. 150. Choice of medication: depends on fracture risk level, drug-related (risk-benefit), patient profile (age, years since menopause, symptoms, and comorbidities), and environment-related factors (economics and social). 151. Patients should be educated about PMO and its treatment and empowered to participate in shared decision-making to improve adherence. Oral health and the warning signs of atypical femoral fractures are discussed. 152. Calcium and Vitamin D cotherapy is mandatory to optimize outcomes (Grade A). [78,169] 153. There are no direct head-to-head randomized trials comparing the fracture-reduction efficacy of different osteoporosis drugs; available evidence is derived primarily from placebo-controlled studies and indirect comparisons. Details of individual drug efficacy, safety, and indications are summarized in the accompanying tables (Grade B). [121] 154. Refer to endocrinologist / specialist: Special groups such as the premenopausal woman, breast cancer survivors on endocrine therapy, those with secondary causes of osteoporosis, very high risk for fracture, and nonresponders to treatment. Options of pharmacotherapy 155. Very high risk for fracture: specialist referral should be considered. The indications are the presence of single but essential clinical risk factors, such as a recent vertebral fracture (within the last 2 years), ≥2 vertebral fractures (whenever they have occurred), BMD T-score ≤−3.5, and treatment with high-dose glucocorticoids (≥7.5 mg/day of prednisolone or equivalent over 3 months). 156. Refer urgently given rapid loss in bone post initiation of glucocorticoids; while waiting, offer intravenous zoledronate as a first-line treatment option following a HF (Grade A). [169,170] 157. Teriparatide, abaloparatide, or romosozumab are first-line treatment options in postmenopausal women at very high fracture risk, particularly in those with vertebral fractures (Grade A). [121,133,171,172] 158. High risk for fracture: In EM (within 10 years of menopause) – first line of management is MHT/or bisphosphonates/denosumab. The second line includes teriparatide, abaloparatide, or romosozumab, particularly in those at risk for vertebral fractures. In late menopause (>10 years postmenopause), the first-line management is bisphosphonates/denosumab. The second line includes teriparatide, abaloparatide, or romosozumab, particularly in those at risk for vertebral fractures. 159. Intermediate risk for fracture: In EM (within 10 years of menopause) – first line of management is MHT/or bisphosphonates. In case of contraindications, intolerance, or patient preference for ease and compliance, denosumab may be offered. In late menopause (>10 years postmenopause), bisphosphonates is preferred. In cases of contraindications, intolerance/treatment failure, or patient preference for ease and compliance, denosumab may be offered. 160. Low risk of fracture: TLM Follow-up, monitoring, and duration 161. Follow - up: Patients should be monitored every 3–6 months initially for 2–3 visits, and thereafter annually for clinical assessment, evaluation of adherence, and monitoring of adverse effects. 162. Monitoring should include symptom review, assessment of compliance, health status, and fall risk, secondary causes, maintain calcium and Vitamin D status/drug-specific laboratory investigations, and periodic BMD measurement every 1–2 years where feasible (Grade A). [133] 163. During bisphosphonate or denosumab therapy report any oral symptoms such as dental mobility, pain, or swelling any unexplained thigh, groin, or hip pain, and if such symptoms develop, the femur should be imaged. 164. Investigations during therapy Teriparatide: Serum calcium and creatinine at 1 month and every 6 months Denosumab: Serum calcium and 25-hydroxy-Vitamin D before each 6-monthly injection Zoledronic acid : Renal function and calcium before each annual infusion Alendronate: Symptom review and adherence every 6–12 months. [121] Teriparatide: Serum calcium and creatinine at 1 month and every 6 months Denosumab: Serum calcium and 25-hydroxy-Vitamin D before each 6-monthly injection Zoledronic acid : Renal function and calcium before each annual infusion Alendronate: Symptom review and adherence every 6–12 months. [121] 165. Bone turnover markers: In selected clinical situations and research settings, markers of bone turnover may be used to monitor treatment response and adherence. Recommended markers include serum C-terminal telopeptide (CTX) for bone resorption and serum procollagen type I N-terminal propeptide (PINP) for bone formation. [133] Use markers for bone resorption when on antiresorptives and use bone formation markers when on anabolic agents. After baseline, for resorption markers repeat at three or 6 months and for formation markers at 6 months after treatment has been initiated. Timing of sample: morning (before 9 am) after an overnight fast for CTX and anytime for PINP. 166. We suggest that DXA should be repeated on the same machine to monitor the response to osteoporosis therapy. Interpretation of serial BMD results must account for measurement precision and least significant change (LSC) to distinguish true change from random variation (Grade B). [173] 167. The lumbar spine (L1–L4) is the preferred primary site for BMD monitoring, with the hip (total hip and femoral neck) serving as the secondary site. Both sides should be measured routinely for comprehensive treatment monitoring. [173] 168. Most established osteoporosis therapies produce only modest increases in BMD, and their antifracture efficacy is only partly explained by these changes. Stabilization of BMD without further decline is a marker of effective treatment and reflects reduced bone turnover and fracture risk (Grade A). [133] 169. Nonresponse to osteoporosis therapy may result from poor adherence, inadequate calcium or Vitamin D status, unrecognized secondary osteoporosis, interfering medications, or suboptimal drug selection and monitoring strategies. Identification and correction of these factors are essential before changing therapy (Grade C). [133] 170. Duration of therapy has to be individualized depending on the patient’s profile, drug used, and response to treatment. Oral bisphosphonates (alendronate, ibandronate, and risedronate) for at least 5 years, zoledronate for at least 3 years, and then reassess fracture risk. Longer durations of treatment, for at least 10 years with oral and 6 years with zoledronate, in special situations. Teriparatide for 24 months (can be given only once in a lifetime), abaloparatide for 18 months, and romosozumab for 12 months. Denosumab safety and efficacy have been established for 10 years. For MHT: shared decision-making for an extended period of use. Sequential osteoporosis therapies 171. Sequential therapy in osteoporosis involves strategically transitioning between different classes of medications to optimize bone health outcomes throughout a patient’s treatment journey. 172. The optimal sequential therapy approach requires individualized assessment based on fracture risk, prior treatment history, patient factors, and long-term treatment goals, with anabolic-first strategies providing the strongest evidence base for maximizing bone health outcomes. [174] 173. Anabolic to antiresorptive sequences (preferred) : an anabolic agent (teriparatide or romosozumab) followed by an antiresorptive (bisphosphonate or denosumab) to maintain BMD gains and ensure long-term fracture protection (Grade B). [121,175] 174. Antiresorptive to antiresorptive sequences: Bisphosphonate to denosumab transition 175. Denosumab discontinuation is most critical: requires mandatory sequential therapy due to rapid bone loss, delay/lack of an alternate treatment 6 months after the last denosumab dose, and rebound fracture risk. Denosumab must always be followed by a bisphosphonate, either zoledronate or alendronate, in patients with adequate renal function. [176-178] 176. Hormone-based sequential approaches: Estrogen/MHT/raloxifene-to-bisphosphonate transitions when HRT is discontinued due to age or contraindications. 177. Between-anabolic agent transitions: Recent evidence suggests superior efficacy with the teriparatide to romosozumab sequence. 178. Combination regimens are typically reserved for very high-risk patients (e.g., multiple prior fractures, extremely low BMD, and imminent fracture risk). 179. Duration of concurrent therapy varies ; anabolic agents are limited to 12–24 months, while antiresorptives continue per standard maintenance protocols. Monitor for hypercalcemia, orthostatic hypotension (with PTH analogues), and ensure strict adherence to dosing intervals. 180. Tailoring combination therapy requires multidisciplinary assessment, balancing fracture risk reduction with cost, safety, and patient preferences. [179] Teriparatide + Denosumab Combination. [180] Hormone Replacement + Bisphosphonate Combinations. [181] Menopause hormone therapy 181. MHT may be considered as a first-line treatment in younger postmenopausal women (<60 years or within 10 years of menopause) who are at intermediate and high fracture risk after full risk assessment, provided there are no contraindications (Grade A). [182-188] 182. Continued use after 60 years is a shared decision based on an individual risk–benefit analysis. [182-188] 183. Tibolone may be preferable to MHT in symptomatic menopausal women with mammographically dense breast tissue (Grade A). [189,190] 184. MHT should not be started solely for bone protection after 10 years of menopause (Grade B). [191,192] 185. Raloxifene is a selective estrogen receptor modulator approved for the prevention and treatment of PMO, mainly with evidence for vertebral fracture and/or breast cancer, especially where bisphosphonates or other agents are unsuitable. No benefit for HF reduction. [193] 186. Primary ovarian insufficiency (POI) and EM: HT should be offered to women with POI and EM, and it can be recommended until the age of natural menopause (Grade B). [194-196] Menopause hormone therapy versus bisphosphonates 187. Both MHT and bisphosphonates effectively reduce osteoporotic fracture risk, but their clinical roles differ according to menopausal stage, risk category, and symptom profile (Grade A). [133,184,186,197,198] 188. Bisphosphonates do not confer the systemic short- or long-term health benefits of MHT in eligible women, particularly regarding cardiometabolic, urogenital, cognitive, and overall quality-of-life outcomes (Grade B). [133,184,186,197,198] 189. Bisphosphonates demonstrate additional systemic benefits, including reduced postfracture mortality, lower risk of bone metastases and recurrence in postmenopausal breast cancer, anti-inflammatory effects, and possible cardiovascular and survival advantages in older adults. These effects are most consistent in postmenopausal women and fracture survivors. [170,199-202] Refer to Flowcharts 1 and 2 for assessing and managing bone health. Algorithm for assessing and managing bone health Management after fracture

101. Tibolone: Significantly improved vaginal atrophy and cytology in comparison with placebo. [172] 102. Selective estrogen receptor modulators (SERMs): Ospemifene is currently the only approved oral treatment for GSM, with agonist activity on the vaginal epithelium and antagonist activity in breast and endometrial tissue (Grade A). [173,174] 103. Significantly, unlike other SERMs, ospemifene has not been associated with an increased risk of breast or endometrial cancer (EC), and available safety data suggest no excess risk of VTE. [175] Ospemifene may, therefore, be considered in women with a history of breast or EC, provided active treatment is complete and decisions are individualized. [176,177] 104. Postmenopausal women with GSM reported higher satisfaction and adherence for ospemifene compared to vaginal estrogen therapy, besides a lower number of missed doses in the treatment of moderate to severe GSM. [178] 105. Dehydroepiandrosterone (DHEA): is administered intravaginally once daily at bedtime. Within the vaginal mucosa, DHEA is locally converted into both estrogens and androgens (testosterone, androstenedione, and dihydrotestosterone), thereby improving epithelial maturation, vaginal pH, lubrication, and sexual function (Grade A). [179] 106. Lifestyle modifications such as smoking cessation, regular sexual activity, and pelvic floor exercises may help maintain urogenital health and reduce GSM severity (Grade B). [180] 107. Nonhormonal options are for women with mild GSM and/or willing to avoid HT or in high-risk individuals with a history of hormone-sensitive malignancy, such as breast cancer or EC. 108. Nonhormonal treatments, including vaginal moisturizers, lubricants, hyaluronic acid preparations, physical therapy, and energy-based therapies like laser, have demonstrated varying degrees of efficacy in symptom relief and QOL improvement. [181] 109. Vaginal lubricants can be recommended for the subjective symptom improvement of dyspareunia (Grade B). [182,183] Vaginal moisturizers can be offered for vaginal dryness and dyspareunia (Grade B). [184] Use vaginal lubricants, moisturizers, and hygiene products with physiologic pH and low osmolality (≤380 mOsm/kg); avoid high-osmolality products that exceed World Health Organization (WHO) recommendations, as they may irritate the epithelium and increase the infection risk (Grade B). [185] 110. Intravaginal phytoestrogens (isoflavone/genistein gels) may be considered a short-term, effective alternative to vaginal estrogen for GSM symptom relief (Grade B). [186-188] 111. Laser therapy: High-quality randomized trials are still required to provide definitive guidance on the efficacy and safety of vaginal laser therapy for various gynecological conditions (Grade C). [189-193] 112. Conclusion on management of GSM: LET, vaginal DHEA, vaginal moisturizers, and oral ospemifene have demonstrated efficacy in improving symptoms of GSM (Grade A). [193] 113. For women with contraindications to regular dose LET, effective nonhormonal alternatives, including hyaluronic acid and ultra-low-dose local estriol, are safe and beneficial (Grade B). [194,195] 114. Current evidence does not support the efficacy of energy-based therapies, vaginal or systemic testosterone, vaginal oxytocin, or oral SERMs such as raloxifene or bazedoxifene for the treatment of GSM (Grade C/D). [193]

196. Definition (Refer to Section 1). The incidence of postmenopausal bleeding (PMB) is 10%. Women <50 years of age with PMB have a <1% chance of having EC, which increases to 24% in women more than 80 years. [330,331] 197. About 90% of the women with EC present with PMB. Therefore, all women with PMB should undergo prompt evaluation (Grade A). [330,332,333] 198. About 60%–80% of women presenting with PMB will have atrophic changes of the endometrium and/or the vaginal-urogenital tract. [334,335] 199. A detailed clinical and drug history should be obtained, as several over-the-counter herbal agents such as ginseng, soy, and red clover may induce vaginal bleeding due to phytoestrogenic effects (Grade C). [336] 200. A thorough general, pelvic, and rectovaginal examination should be performed to exclude nonuterine causes of bleeding, such as cervical, vaginal, vulval, urinary, or anal pathology, as well as atrophic vaginitis (Grade C). [337] 201. Women presenting with PMB should undergo TVS as the first-line investigation. [338,339] 202. TVS should include double-layer endometrial thickness (ET) measured as the maximum anteroposterior thickness of the double endometrial echo in the long axis (sagittal). Assess morphology by the echotexture (homogeneous vs. heterogeneous), focal or cystic areas, regularity of the endometrial–myometrial junction, and endocavitary fluid. Power Doppler mapping to evaluate the endometrial and sub-endometrial vascular pattern. [339] 203. Three-dimensional TVS is adjunctive and only provides moderate accuracy in assessing endometrial volume and focal abnormalities, but shows no consistent advantage over standard two-dimensional TVS for predicting EC (Grade B). [340,341] 204. SIS is complementary and offers high diagnostic accuracy for detecting focal intrauterine lesions, such as polyps and submucous fibroids, in women with PMB; however, it does not replace TVS-based ET triage for endometrial carcinoma and cannot substitute for histologic sampling for definitive diagnosis. [342] 205. In women presenting with PMB and no other high-risk factors, a TVS with an ET threshold between 3 and 5 mm provides a high negative predictive value for endometrial malignancy. However, assessment should include endometrial morphology, Doppler findings, and individual risk factors (Grade B). [336,337-340] 206. In women with p53-abnormal (p53abn) molecular subtype endometrial carcinoma, reliance on the standard ET cutoff ≤4 mm may lead to missed diagnoses, with false-negative rates reported up to 25% (Grade B). [343] 207. Women presenting with a first episode of PMB who have any of the following risk factors should undergo both TVS and endometrial sampling: obesity, diabetes, hypertension, tamoxifen use, increasing years since menopause, history of polyps, smoking, family history of EC, poor image definition, focal echogenicity, diffuse heterogeneity, or persistent bleeding (Grade B). [338,344] 208. Low-risk women (ET ≤3–4 mm, clearly defined homogeneous echo pattern, normal morphology and color Doppler, and good image quality) whose bleeding has ceased may be managed conservatively with shared decision-making and repeat TVS or biopsy only if bleeding recurs (Grade B). [339,344] 209. All women should receive documented counseling regarding the need for follow-up and to promptly report red-flag symptoms such as recurrent bleeding, abnormal discharge, pelvic pain, or unexplained weight loss (Grade A). [339,345] 210. In postmenopausal women at low risk for EC, presenting with global (nonfocal) endometrial pathology on imaging, an outpatient endometrial sampling using a suction device (e.g., Pipelle) (unless cervical stenosis or patient noncooperative) is an acceptable, low-cost, first-line diagnostic tool (Grade B). [346,347] 211. Office/outpatient, hysteroscopy-directed biopsy is a gold standard for diagnosing endometrial lesions. [348] 212. Hysteroscopy may be offered as the preferred diagnostic test in postmenopausal women with persistent or recurrent bleeding, focal/heterogeneous endometrial pathology on ultrasound, inadequate or nonrepresentative Pipelle/aspiration sampling, or poor-quality/uninterpretable TVS diagnostic accuracy over blind sampling (Grade B). [296,349] 213. It reduces unnecessary major surgery; this is especially relevant in India, where (i) endometrial polyps account for a large share of recurrent PMB and (ii) outpatient hysteroscopy is increasingly feasible in tertiary and many secondary centers at low cost without general anesthesia (Grade B). [296] 214. When the histopathology report from endometrial sampling is inconclusive, inadequate, or nonrepresentative, the woman should be re-evaluated with transvaginal TVS to assess ET and morphology (Grade A). [339,350] 215. If subsequent TVS reveals a thin endometrial stripe and the vaginal bleeding has ceased, no further invasive evaluation is necessary; a close follow-up strategy is advised (Grade B). [337] 216. Persistent bleeding or an unsatisfactory/poor-quality TVS necessitates further evaluation by pelvic MRI when malignancy is still suspected (Grade B) and an outpatient hysteroscopic evaluation if not done as the primary procedure (Grade B). [337] 217. Recurrent PMB is defined as any episode of vaginal bleeding occurring ≥6 weeks after the resolution of an initial episode of PMB (Grade C). [351] Reassessment is warranted, as up to 4%–5% may subsequently reveal EC or premalignant pathology. Endometrial polyps account for approximately one in four cases of PMB. 218. In women with recurrent PMB after an initial negative evaluation, a first-line investigation should focus on tests with high accuracy for focal intrauterine disease (such as outpatient hysteroscopy) because up to 20% may have endometrial polyps, and up to 4%–5% may reveal EC or premalignant pathology (Grade B). [337,352,353] 219. Asymptomatic postmenopausal women with thick endometrium: There is currently no clear ET threshold that can predict the risk of malignant transformation. [354-356] 220. Postmenopausal women without bleeding, no additional risk factors, and global endometrial thickening ≤11 mm on transvaginal ultrasonography do not require invasive endometrial investigation (Grade B). [335,355] In asymptomatic postmenopausal women, an ET >11 mm should prompt an EB (Grade B). [355] In an asymptomatic woman, the decision to biopsy if the ET is between 3/4 and 11 mm should depend on the patient’s individual risk factors, endometrial morphology, and power Doppler findings (Grade C). [355,356] 221. Women with or without PMB who are at increased risk for EC should be educated about early symptoms such as abnormal or recurrent vaginal bleeding, discharge, pelvic pain, or weight loss, and the importance of long-term follow-up even after a negative initial evaluation (Grade B). [356] 222. PMB in tamoxifen users – Refer to Section 5. 223. PMB in MHT users – Refer to Section 6.

224. The WHO defines QOL as “an individual’s perception of their position in life in the context of the culture and value system in which they live and in relation to their goals, expectations, standards, and concerns.” It encompasses various aspects of well-being, including physical, mental, emotional, social, and material health, as well as capabilities and the ability to participate in life events (Grade A). [357] 225. Validated tools to evaluate QOL: General– Global QOL is for a broad assessment of an individual’s overall well-being, including physical, psychological, social, cultural, and environmental dimensions. Moreover, health-related QOL (HRQOL) focuses on the impact of health status, disease, or treatment on physical, mental, and social functioning (Grade A). [358,359] 226. Work-related tools: Work Productivity and Activity Impairment (WPAI) for workplace productivity and Work Ability Index as occupational functioning tools (Grade B). [360,361] 227. When evaluating drug therapies, in addition to safety and efficacy, it is essential to assess the drug’s effect on QOL (Grade A). [362-364] 228. Moderate-to-severe VMSs (hot flashes and night sweats) are among the strongest determinants of reduced HRQOL in midlife women, affecting sleep quality, emotional well-being, daily functioning, and sexual health (Grade A). [365,366] 229. Sleep disturbance and psychological well-being are consistently reported as the most affected domains, followed by work productivity and sexual function (Grade A). [365-367] 230. The QOL domain most affected by bothersome vulvovaginal symptoms is sexual function, impacting 40% of women (Grade A). [368,369] 231. Metabolic diseases, CVD, cancers, fractures, and UI can severely impair QOL, affecting physical, psychological, and social domains. [370-373] 232. Studies using the WPAI scale have shown that hot flashes and night sweats impair daily activities more than working activities (Grade B). [374,375] 233. Indian studies consistently show that menopausal symptoms significantly impair HRQOL in both rural and urban women, affecting physical, psychological, vasomotor, and urogenital domains (Grade B). [376-384] 234. Menopause health education improves QOL and symptom control in menopausal women. Trusted educational programs facilitate emotional and physical well-being (Grade A). [381,385] Lifestyle changes such as exercise and yoga improve QOL. Exercise has been shown to reduce VMS severity and enhance QOL, although future rigorous randomized controlled trials are needed to establish optimal exercise prescription principles (Grade A). [61,386-388] 235. PFMT significantly improves HRQOL in women with GSM, with benefits for urinary symptoms, sexual health, and overall well-being (Grade A). [389] 236. MHT improves QOL in symptomatic menopausal women, mainly through relief of VMS, sleep, and psychological well-being (Grade A). [24,390-393] 237. 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Akrishti Gupta Alka Kumar Anjan Pyal Anita Kant Annil Mahajan Anita Shah Asha Kapadia Asif Sultan Atul Munshi Bipasa Sen Bina Tandon B Chandrashekar Reddy Chellamma VK Cherunur Ambuja Ch Ratna Kishore CH Trivedi Duru Shah Hara P Pattanaik Hepshiba Khurabani Jagmeet Madan Jaideep Malhotra Jignesh Shah Jyotika Desai Jyoti Hak Jyoti M Shah Jyothi Unni K Madhulika Agarwal Lakshmi Ratna Madhu Babu Madhukar Reddy Mala Raj Maninder Ahuja Monal Shah Navneet Takkar Neelam Agarwal Nidhi Gupta C Nikhileshwar Reddy N. Vivek Padma Kurada Pooja Shah Prem Blaise Rejula Pushpa Sethi Rama A Vaidya Rashmi Shah Rashmi Banerjee Ravi R Hebballi Rohit Raina Saroj Srivastava Sabahat Rasool Sai Deepak Yaranagula Sai Praveen Haranath Saket Kumar Sharad Kumar Sheela Mane Shobhana Mohandas Smrity Shailly Bagde Sonia Malik Sudha Sharma Sunila Khandelwal Suvarna Khadilkar Tanmaya Talukdar Thanuja Mannava Tripti Nagaria Tushar Patel Usha Rani Poli Urvashi Prasad Jha Urvashi Yavalkar Vishal R Tandon Yashodhara Pradeep

190. Sarcopenia: It is a progressive and generalized skeletal-muscle disorder characterized by low muscle strength and low muscle quantity or quality, with or without impaired physical performance. It is associated with increased risk of falls, fractures, disability, and mortality. [118,203,204] 191. According to the South-West Asia Group for Sarcopenia (SWAG-SARCO) definition, developed specifically for South Asia, sarcopenia is identified by a reduction in any two of the following: muscle function, strength, or mass. [205,206] 192. In India, the prevalence of sarcopenia in older adults is 39%–44% and 19% can have severe sarcopenia. [207,208] Screening tools 193. Calf Circumference (CC) and SARC-F questionnaire are the initial tools. 194. Primary: Measure CC as a part of the initial clinical evaluation. CC is a validated, simple, noninvasive, cost-effective anthropometric measure with high sensitivity and specificity for sarcopenia screening and correlates well with muscle mass (Grade B). [209-211] 195. CC has been validated as a screening tool in Indian studies, with ≤32 cm (women) as key thresholds for identifying sarcopenia risk (sensitivity 100%, specificity 60%, NPV 100%, accuracy 80%). [212] 196. CC should be interpreted with caution in individuals with high or low BMI, as adiposity can affect measurements. Adjusted cut-offs or correction factors may be used. 197. Protocol: Measure right calf, standing position, noncompressing tape, largest circumference; note edema/obesity [209] (consider + 1 cm threshold in obese adults as per Thai data). [211] 198. India-specific (CC ≤32 cm (women) is a strong screen (Sn 100%, NPV 100%); confirm positives with strength/mass tests. [212] 199. The Asian Working Group for Sarcopenia and the SWAG-SARCO recommend calf-circumference cut-offs of 34 cm for men and 33 cm for women. The European Working Group on Sarcopenia in Older People-2 uses 31 cm as a universal proxy measure. [118,203,205] Thai community cohorts: validate 33 cm (women) and suggest + 1 cm for obese adults to improve accuracy. [211] 200. SARC-F questionnaire: It is a self-administered questionnaire, which has five components, including strength, assistance in walking, rising from a chair, climbing stairs, and falls. It is a simple, inexpensive, and convenient method for screening for sarcopenia risk. It has low-to-moderate sensitivity and very high specificity for predicting low muscle strength. SARC-F score: A 3-level score range of 0–2 points for each item. The total score range is 0–10, with scores ≥4 indicating sarcopenia risk. [213] 201. SARC-CalF: SARC-CalF adds a calf measurement to the SARC-F questionnaire to make screening more reliable. A score of 11 or above indicates probable sarcopenia. In women, a calf circumference of 33 cm or less adds 10 points to the score. This combined tool detects sarcopenia better than SARC-F alone, both in the community and in clinics. [214,215] 202. Diagnosis: AEWGSOP recommends the use of grip strength or a chair stand to measure muscle function with specific cutoff points for each test. 203. Grip strength: Handgrip strength is the most widely used method for measuring muscle strength. This test requires 5 min and a well-calibrated handheld dynamometer. Method-six measures should be taken, three with each arm. Ideally, patients should be encouraged to squeeze as hard as possible for 3–5 s during the measure; the highest of the six measurements is reported as the final result. [216] 204. Chair stand test: It is also known as Chair Rise Test. It assesses lower extremity muscle function. This test requires 1–2 min and uses only a straight-back chair without armrests and a stopwatch. Method - The subject is first asked to stand from a sitting position without using their arms. If they can perform the task, they are then asked to stand up and sit down five times, as quickly as possible, with arms folded across their chests. The time taken to complete five stands is recorded. A chair-stand time >15 s for five rises or low handgrip strength (<16 kg in women; <27 kg in men) indicates reduced muscle strength or possible sarcopenia. [118] Other diagnostic methods 205. Assessment of physical performance includes gait speed measurement and the Short Physical Performance Battery (SPPB), incorporating the timed up-and-go test, 400-m walk, or long-distance corridor walk for endurance evaluation. A gait speed of 0.8 m/s suggests poor physical performance in adults aged over 60 years. 206. Assessment of muscle mass by DXA/Bioelectrical Impedance Analysis. BIA, where feasible. Appendicular skeletal muscle index cutoff used in Indian women is <5.0 kg/m2. [217,218] 207. Case-finding strategy: Suspect sarcopenia in all women in the geriatric age group.Screening: SARC-F or SARC-CalF may be used for initial screening. A positive screen should prompt an objective assessment. Muscle strength assessment: Handgrip strength (preferred) or the Chair Stand Test may be used.Severity assessment: Gait speed, Short Physical Performance Battery (SPPB), Timed Up and Go Test (TUGT), and 400-m walk test.Muscle mass assessment: DXA orBioelectrical Impedance Analysis. [205] 208. Balance: In postmenopausal women, impaired balance and postural instability arise from age-related neuromuscular decline (vision, proprioception, reaction time, and muscle strength). Estrogen deficiency may affect muscle coordination and proprioceptive control, and there is limited data on its effects on vestibular signaling (Grade B). [219] 209. These factors collectively increase fall risk, a major determinant of forearm, hip, and other fragility fractures (Grade B). [220] 210. Preventive strategies should emphasize strength, balance training, and fall-risk screening, with MHT reserved for bone protection rather than balance improvement. [221,222] 211. Screening for balance impairment in postmenopausal women should include simple functional assessments, such as the Timed Up and Go test, Functional Reach Test, and one-leg stand, combined with a structured evaluation of fall risk factors (Grade A). [222-225] 212. Frailty: Prevalence ranged from 14.5% in Uttarakhand to 41.3% in Arunachal Pradesh. [226] 213. Frailty is a multicausal clinical syndrome characterized by a decrease in strength, endurance, and reduction in physiological processes, increasing an individual’s susceptibility to the development of dependency and/or death. [227] 214. Diagnosis: The Fried’s frailty phenotype tool includes five items: unintentional weight loss (4.5 kg or more over the past year), exhaustion (self-reported), low physical activity, weakness (low grip strength), and walking speed. Individuals with two deficits are considered prefrail, and those with three or more deficits are classified as frail. [228] 215. Management: Sarcopenia and frailty are reversible with early multimodal intervention. The most robust evidence supports progressive resistance training, adequate dietary protein (1.0–1.5 g/kg/day), and Vitamin D sufficiency. Pharmacologic options play only an adjunct role (Grade B). [229,230] 216. Management of postmenopausal women with balance impairment should incorporate a multifactorial fall prevention approach combining individualized exercise therapy, medication review, vision correction, and footwear optimization consistent with global evidence-based recommendations. [231,232]

4. Theories: The timing hypothesis proposes that menopause hormone therapy (MHT) is most effective when initiated during the late MT or early postmenopausal years, whereas delayed initiation beyond this window may offer diminished benefit or even adverse cardiovascular outcomes. [8] 5. This concept is supported by the Early versus Late Intervention Trial with Estradiol (ELITE) and builds upon Clarkson’s “timing hypothesis” derived from animal models and Hodis’ subsequent clinical translations. [9-11] 6. Analyses of robust pre-Women’s Health Initiative (WHI) and reanalysis of WHI data supported by the Danish Osteoporosis Study (DOPS) reinforced the understanding of the “critical window of opportunity.” [12-15] 7. Brinton’s “healthy cell bias” theory proposes that estrogen exerts protective and reparative effects only in metabolically healthy and functionally competent cells. In contrast, estrogen signaling may become ineffective or even detrimental in aged or metabolically compromised tissues. [16,17] 8. The timing hypothesis and Brinton’s healthy cell bias theory explain the variability in MHT outcomes across cardiovascular, neurological, musculoskeletal, and metabolic domains. 9. These models emphasize that both the timing of initiation and the metabolic health of target tissues determine estrogen’s benefit–risk profile, refining the understanding of its context-dependent actions and guiding individualized therapeutic decisions. [18-20] 10. MHT: Initiating MHT within 10 years of menopause or before the age of 60 years is associated with reduced all-cause mortality and cardiovascular events, supporting a “window of opportunity” effect; this benefit is not observed with later initiation (Grade A). [21-24] 11. Therapeutic lifestyle management (TLM): Adopting healthy lifestyle measures can enhance the benefits of HT, mitigate metabolic, cardiovascular, and cognitive risks, and may extend the “window of opportunity” by maintaining cell health and reducing end-organ vulnerability (Grade B). [25-28] 12. Education: Interventions, including structured therapeutic lifestyle programs, menopausal education, and coping skills training, significantly reduce symptom burden, improve quality of life (QOL), and enhance adaptation, serving as effective adjuncts to MHT (Grade B). [29,30]

115. UI, an involuntary urine leakage, affects >50% of postmenopausal women and is a significant social problem. 116. There are five types of UI: stress, urge, mixed, overflow, and functional incontinence. Urge and mixed incontinence predominate in the older population. [196-198] 117. Diagnosis: Initial evaluation and diagnosis of a woman with UI can be based on symptoms alone to initiate conservative treatment. [198] 118. Urodynamics is not routinely recommended and is reserved for complicated UI requiring surgery to rule out mixed causes of voiding dysfunction (Grade A). [140,199,200] 119. Routine renal/bladder imaging or cystoscopy is not indicated in the initial evaluation of uncomplicated UI or overactive bladder. These investigations should be performed only in refractory, recurrent, or complex cases (Grade A). [201-203] 120. Management: Pelvic floor muscle training (PFMT), whether supervised or home-based, is recommended as first-line therapy for stress UI (SUI) and mixed incontinence (Grade B). [204,205] 121. All types of pelvic floor therapy are effective for SUI. At this point, no single therapy is superior to another (Grade B). [204] 122. Available interventions are PFMT, vaginal cone, biofeedback, electrical muscle stimulation, radiofrequency, and electroacupuncture. [204]

1. Women may present to a menopause clinic with menstrual disturbances, menopausal symptoms, or for a routine health check-up, and may also be identified opportunistically during other healthcare visits. [1] Refer to Figure 1 for an initial assessment. Physician’s approach to evaluate a woman at 35 years or older. MT: Menopause transition, FMP: Final menstrual period, PM : Post menpopause 2. Clinical examination should follow a holistic, preventative, and diagnostic approach, extending beyond isolated menopausal symptoms to identify both hidden and obvious noncommunicable diseases (NCDs). [2-4] 3. Age-related biological changes, along with lifestyle and socioeconomic factors, require customized risk assessment and long-term management strategies. Components of clinical evaluation 4. History and physical examination: Take a thorough history, including menstrual, reproductive, sexual, psychosocial, and family history. Perform the general and systemic physical examinations, as well as breast and pelvic examinations. Measure the Body Mass Index (BMI), waist circumference, and calf circumference. 5. Symptom assessment tools: Record menopausal symptoms using a validated scale. Menopause-related symptoms may be documented using the Menopause Rating Scale (MRS). [5,6] Refer to Table 1 . Menopause Rating Scale The percentage of symptoms at each visit is documented to assess the severity of symptoms and to follow up on the effectiveness of treatment. No problems 0%-4%; Mild problems 5%-24%; Moderate problems 25%-49%; Severe problems 50%-95%; Complete problems 95%-100% The degree of symptoms is documented in the boxes to assess severity and the follow-up for treatment effectiveness. The total MRS score is calculated, and menopausal symptoms are classified as None: 0–4; Mild: 5–8; Moderate: 9–16; Severe: 17 plus. 6. Based on the MRS outcome, the Female Sexual Function Index [FSFI-6 Refer to Table 2 ] for sexual health assessment, Insomnia Severity Index [ISI Refer to Table 3 ] for sleep disturbances, Patient Health Questionnaire [PHQ-4 Refer to Table 4 ] for psychological health, and s-Moca for dementia screening are documented as needed. [7-10] Sexual health-Female Sexual Function Index - 6 Form Total score=30. A score of ≤19 suggests dysfunction Sleep: Insomnia Severity Index, 7-item questionnaire Total Score: 28 cut-offs: 0–7: No clinically significant insomnia, 8–14: Sub threshold insomnia, 15–21: Moderate insomnia, ≥22: Severe insomnia Psychological Health, Patient Health Questionnaire-4, past 2 weeks Each item scored 0–3; Total Score: 0–12 ≥6 suggests clinically relevant psychological distress Risk stratification tools for diseases 7. Breast: A woman may be categorized into low, moderate, or high risk according to her risk of developing invasive breast cancer using the Gail Model, the limitation being that it has not been validated in India ( https://www.cancer.gov/bcrisktool ). 8. Cardiovascular disease (CVD): 10-year probability risk of myocardial infarction/stroke based on the Globorisk India tool (use the web calculator at www.globorisk.org or the validated desk/pocket chart) and/or Reynolds Risk Score ( www.mdcalc.com/calc/3932/reynolds-risk-score-cardiovascular-risk-women?utm ). Refer to Section 3 CVD. 9. Skeletal health: Risk assessment for osteoporosis may be done by OSTA/FRAX ( http://www.shef.ac.uk/FRAX ). Refer to Section 3 on osteoporosis. 10. Muscle health is evaluated using the SARC-calf, a 6-item questionnaire. Refer to Section 3 sarcopenia. 11. The results for risk assessment for diseases are documented in Table 5 . The risk status is categorized as low, moderate, or high risk for disease. Comprehensive chart for documenting the risk score for noncommunicable diseases over 5/10 years and lifetime results WHO: World Health Organization, ISH: International Society of Hypertension, FRAX: Fracture risk assessment tool, SCORE: Simple calculated osteoporosis risk estimation 12. Record the presence of GSM by noting the most bothersome symptoms and the vaginal pH with a narrow range litmus paper. Recommended laboratory and imaging investigations 13. Baseline tests: Complete blood count, urine routine, fasting glucose/glycated hemoglobin, lipid profile, thyroid-stimulating hormone. 14. Cancer screening: Pap smear, stool for occult blood, mammography/ultrasound of the breast. 15. Reproductive Health: Vaginal pH and TVS. 16. Others: Dental and eye check-up. 17. Investigations should be individualized based on clinical findings. The investigations listed in Table 6 should be chosen judiciously, depending on the woman’s history and examination. Tests performed solely on indication FSH: Follicle-stimulating hormone, OCPs: Oral contraceptive pills, LFT: Liver function tests, ECG: Electrocardiogram, 2D Echo: Two-dimensional echocardiography, CVD: Cardiovascular disease, 25, OH Vitamin D: 25-hydroxy Vitamin D, VMI: Vaginal saturation index, USG: Ultrasonography Individualized health plan 18. Each woman needs a personalized health management plan for menopause. Management planning is based on the information obtained by history, clinical examination, the use of risk assessment tools, and the results of the investigations. Refer to Tables 7 and 8 . Management plan for women without menopausal symptoms NCD: Noncommunicable disease, CVD: Cardiovascular disease, VTE: Venous thromboembolism Management plan for women with menopausal symptoms (vasomotor symptoms/genitourinary syndrome of menopause/bone health) NCD: Noncommunicable disease, MHT: Menopausal hormone therapy, CVD: Cardiovascular disease, VTE: Venous thromboembolism 19. Based on the symptom profile, women can generally be categorized as either symptomatic or asymptomatic. 20. Based on the health profile, they are further classified as low risk, moderate risk, or high risk to personalize care and treatment decisions. 21. Counseling: The aims of counseling include addressing women’s questions and concerns, educating patients, and boosting their confidence in making decisions. [11-13] If a therapy is selected, the patient and clinician should agree on the goals, risks, and benefits, and a tentative duration of use. The skill of medical counseling and translating statistics into simple language is a vital part of consultation. 22. The classification of the frequency of drug reactions as per the WHO and the Council for International Organizations of Medical Sciences is shown in Table 9 . [14] Classification of frequency of drug reactions Source: RCOG Clinical Governance Advice. RCOG: Royal College of Obstetricians and Gynecologists Therapeutic lifestyle modification 23. Indian Mantra for Menopausal Health [ Figure 2 ]: The literal meaning of mantra is “tool or instrument of thought.” This word originates from the most ancient Vedic text, the Rigveda. [15] The Indian Mantra for menopause well-being 24. Dietary therapy: The ICMR, NIN (2024) recommends “My Plate for the Day” for adults with a caloric intake of 2000 Kcal. Emphasize the traditional Indian dietary patterns with a balance of different food groups. [16] Refer to Table 10 . Nutritional plan for a sedentary woman 25. Free sugars include all sugars added to foods or drinks, as well as the sugars naturally found in honey, syrups, jaggery, fruit juices, and fruit concentrates. It excludes the sugars naturally present in whole fruits, vegetables, or plain milk. [16,17] 26. Keep “free sugars” to <5% of your daily energy intake, which is about five teaspoons (25 g) of sugar each day. Ideally, aim for under 5% (around three teaspoons or 15 g), as strongly advised to lower adiposity, type 2 diabetes, CVD, and mortality. [16,17] 27. One teaspoon of sugar, honey, or jaggery is equivalent to 4 g. A small glass (200 ml) of sweetened soft drink or packaged fruit juice contains 5–7 teaspoons of sugar. Indian sweets such as gulab jamun and laddoo often contain 8–12 teaspoons of sugar. [16] 28. Prioritize food sources for calcium intake exceeding 800 mg daily and ensure Vitamin D repletion through 1000–2000 IU daily or 60,000 IU monthly, or by daily exposure of arms, legs, or face to sunlight for 20 min between 11 AM and 2 PM to meet the RDA. Refer to Section 3. 29. Complete tobacco cessation and alcohol minimization are among the most effective, evidence-based strategies (Grade A) [18-21] for protecting postmenopausal women against breast, oral, and lung cancers, liver disease, and osteoporosis, endorsed worldwide by major health authorities. [18-21] 30. Exercise therapy: Physical activity and exercise help maintain a healthy weight, enhance bone density, coordination, and balance, and improve muscle strength and joint mobility. It also improves lipid profiles, alleviates genitourinary issues, reduces depression, and encourages better sleep. [22-24] 31. Exercise should incorporate aerobic, muscle-strengthening, breathing, and balance activities. Engage in 30 min of moderate-intensity physical activity, mainly 5 days a week. Muscle-strengthening activities should be included at a minimum of 2 days per week. The duration of physical activity depends on the goal; 30 min per day improves fitness and lowers the risk of chronic diseases; 60 min per day helps prevent weight gain and maintain metabolic health; 60–90 min per day helps prevent weight regain after weight loss. 32. Mind–body exercise therapy is a physical activity combining movement, mental focus, and controlled breathing. It is frequently used to enhance flexibility, strength, and balance while also encouraging relaxation and alleviating stress. 20–30 min daily can support psychological well-being, improve sleep, and help reduce vasomotor symptoms. [25-27] 33. Yoga therapy of ≥8 weeks duration improves vasomotor, psychological, and quality of life outcomes in perimenopausal women (Grade B). [28-34] 34. Sleep therapy: Proper sleep scheduling and maintaining a regular sleep-wake schedule are crucial. Consistently going to bed and waking up at the same times helps synchronize the circadian rhythm. [35,36] Avoid stimulants: Limiting caffeine, nicotine, and alcohol for at least 4–6 h before bedtime can enhance sleep onset and quality. Avoid using your bed for activities such as watching television, using smartphones, or reading to reinforce the connection between bed and sleep. Avoid stimulating activity close to bedtime: Exercise or heavy meals should be avoided within 2 h of sleep onset. Create a restful environment: Dim lighting, a quiet room, and a cool temperature (18°C–21°C) enhance sleep quality. Engaging in prayer, meditation, gratitude journaling, or positive thought exercises before sleep reduces cognitive arousal and nighttime repetitive negative thinking (rumination). Avoid spending too much time in bed: Limiting bedtime to the actual sleep duration helps improve sleep efficiency. [35,36] 35. Therapy to enhance emotional well-being: Emotional well-being during menopause is affected by biological, psychological, and social factors. Strong social connectedness and perceived emotional support are associated with better quality of life and lower anxiety, through their influence on biological, psychological, and social determinants of health. [37-39] 36. Maintaining a healthy BMI: Losing weight and maintaining it were associated with a reduced breast cancer risk for women aged 50 years and older in The Nurses’ Health Study and The Health Professionals Follow-Up Study (Grade B). [40-42] 37. Immunization: For the schedule for adult immunization. [43] Refer to Table 11 . Schedule of vaccines for adults (Association of Physicians of India 2024) PPSV 23: Pneumococcal polysaccharide vaccine 23, PCV 23: Pneumococcal conjugate vaccine 23, IM: Intramuscularly, SC: Subcutaneously, LAIV: Live-attenuated influenza vaccine, HCPs: Healthcare Professionals, CKD: Chronic kidney disease Nonhormonal therapies 38. Complementary and alternative treatments should be approached cautiously as the evidence remains limited. 39. Awareness should be raised about phytoestrogens and lycopene-rich foods (18–24 mg daily) in the Indian diet (Grade C). [44-47] 40. In the Indian context, it is highly advisable to validate the effects of locally used herbs and phytoestrogen-containing formulations for menopausal symptom management using modern clinical research methods, including RCTs and phytochemical standardization. 41. Herbal remedies such as Shatavari, Ashoka, and Soy isoflavones may show promise in managing menopausal symptoms, but clinical use should remain cautious until validated through rigorous Indian RCTs and regulatory quality controls. In India, herbal and nutraceutical products are not regulated for potency, purity, or quality. [48-50] Nonprescription-based therapies 42. Cognitive behavioral therapy (CBT): CBT is a structured, goal-focused form of psychotherapy. It helps individuals manage problems by altering unhelpful thoughts and behavior patterns. Emerging evidence supports CBT as a strong recommendation for managing vasomotor symptoms (VMS) (Grade A). [51-57] 43. Hypnosis is a form of mind–body therapy that uses guided relaxation, focused attention, and suggestion to induce a heightened state of awareness. It reduces hot-flash frequency and severity by approximately 60%–70% and improves sleep and quality of life in postmenopausal women. It can be an adjunct or alternative to pharmacological therapy for vasomotor symptoms (Grade B). [58-60] Nonhormonal prescription therapies 44. Nonhormonal therapies, including SSRIs SNRIs, and certain anticonvulsants, although less effective than menopausal hormone therapy (MHT), can relieve VMS. They are recommended when MHT is contraindicated, not preferred, or used as supplementary treatment (Grade A). [61] 45. Evidence from randomized controlled trials supports the efficacy of SSRIs (paroxetine, escitalopram, fluoxetine, sertraline), SNRIs (venlafaxine, desvenlafaxine, and duloxetine) (Grade A), [61-63] and gabapentinoids (gabapentin and pregabalin) in alleviating vasomotor symptoms (Grade B). [61-63] 46. Clinical trials typically assess SSRIs/SNRIs or gabapentin over a short period (8–12 weeks); further use should be based on individual benefit, tolerability, and preference, with gradual discontinuation. 47. Neurokinin-3 (NK3) receptor antagonists, such as fezolinetant (approved by the Food and Drug Administration [FDA] in 2023) and elinzanetant (approved by the FDA in 2025), represent a nonhormonal therapy for VMS. 48. In a meta-analysis, fezolinetant 45 mg once daily was statistically significantly more effective than other non-HTs in reducing the frequency and severity of moderate-to-severe VMS and showed at least comparable or superior effects on symptom severity versus most nonhormonal agents (Grade A). [64,65] 49. Elinzanetant 120 mg/day, a dual NK-1/NK-3 receptor antagonist, has demonstrated significant reductions in the frequency and severity of moderate-to-severe VMS and related sleep disturbance in postmenopausal women. [66] 50. For women suffering mainly from insomnia, select gabapentin, while for those with primarily mood disorders, opt for fluoxetine and paroxetine. Low-dose venlafaxine was as effective as low-dose estradiol in controlling VMS. [67] In breast cancer patients, fluoxetine and paroxetine should be avoided as they may interfere with the effectiveness of tamoxifen. [68] Menopause hormone therapy – An overview 51. Most long-term and randomized data on MHT come from international studies. Hence, when interpreting this data in India, one should account for local epidemiological differences, such as an earlier ANM and distinctive patterns of breast cancer, CVD, metabolic risk, and osteoporosis seen in Indian women. [69-76] 52. MHT should be prescribed for accepted indications, in appropriately selected women, with an understanding that secondary benefits alone do not constitute a sufficient indication for therapy. Types, terminology 53. Hormone therapy (HT) in menopause medicine is an umbrella term that covers various treatment approaches (estrogen alone or in combination with progestogen and androgens). [71-77] 54. Types: Estrogen therapy (ET)- 17 beta estradiol (E2)/conjugated equine estrogen (CEE)/estriol/estradiol valerate (EV)/estetrol. Combined estrogenestradiolini therapy (EPT)- The commonly used progesterones in EPT are micronized progesterone (MP), dydrogesterone (DYD), and the levonorgestrel-releasing intrauterine system (LNG). Selective estrogen receptor modulators (SERMs) -The available SERMS in India are tibolone and raloxifene. Androgen therapy for women is not available in India. 55. Treatment terminology: Based on the pharmacokinetics of HT, as well as the individual’s age and health profile, the following terminology is recommended (Grade C). [71-77] 56. Estrogen replacement therapy/hormone replacement therapy (ERT/HRT): replicates the estrogen environment of premenopausal women as in premature ovarian insufficiency (POI) and early menopause (EM). It has no contraceptive effect. 57. Estrogen additive therapy (EAT/MHT): complements endogenous postmenopausal estrogen with exogenous estrogen, tailored to meet the indication for HT as in the management of menopause within 10 years of menopause. [77] 58. Estrogen maintenance therapy (EMT): which involves continuing the therapy beyond 10 years of menopause. 59. Oral contraceptive pills (OCPs): are hormonal preparations containing either combined estrogen–progestin (usually including ethinyl estradiol, and in some cases, 17 beta estradiol, EV, or estetrol) or progestin alone, used primarily for contraception and for the regulation of menstrual and hormonal disorders. 60. During MT, low-dose combined oral contraceptives (COCs) can ease vasomotor and mood symptoms, may support bone health, and decrease the risk of colorectal cancer (Grade B). [78-82] COCs offer effective contraception, help regulate irregular bleeding, and lower the risk of endometrial and ovarian cancers (Grade A). [81,82] 61. Although no definitive randomized trials to date compare continuous versus cyclic OCP use specifically in women during the MT expert guidance and reviews support shortened or eliminated hormone-free intervals with continuous or extended use to reduce VMS and abnormal bleeding, as learnt from continuous combined HT users. [78,80,83-86] 62. Checklist before prescribing MHT: Before starting MHT, every woman should undergo a comprehensive clinical evaluation and personalized risk assessment (Grade A). [87-90] Counseling must include potential benefits, risks, and alternatives. A documented, written informed consent is highly recommended as part of shared decision-making and medico-legal safety. Refer to Figure 3 . Hormone Therapy Consent Form 63. The concept of precision medicine in prescribing systemic MHT emphasizes individualized therapy, where treatment is tailored to each woman and may change over time as her age, risk profile, symptoms, and health status evolve. 64. The six right principles for prescribing systemic MHT are to select the right woman, right age, right hormone, right regimen, right route, and right dose. 65. Right woman: The classical indications for postmenopausal MHT that have consistently withstood the test of time, supported by evidence from multiple randomized clinical trials and meta-analyses, are the beneficial effects of estrogens on moderate-to-severe VMS and urogenital atrophy. [91-97] In eligible women at risk for fracture, MHT may be considered after full risk assessment (Grade A). [95.96] HT is strongly recommended for women with POI and should be offered to women with EM until they reach ANM (Grade A). [98-102] 66. Right age: MHT has the most favorable benefit-to-risk profile when started within roughly 10 years of menopause. For starting later than 10 years after menopause or in women over 60, the benefit-to-risk ratio becomes less favorable, and shared decision-making is crucial. It is not recommended for women >20 years postmenopause. [77,103-110] 67. Right hormone: Estrogen. Both CEE and 17 β-estradiol effectively relieve vasomotor symptoms (Grade A). [111,112] 68. Oral CEE favorably alters HDL and Lp(a) levels but raises triglycerides, C-reactive protein (CRP), and clotting factors due to hepatic first-pass effects. Use CEE for lean, low-risk women; prefer 17 β-estradiol (oral or transdermal) for those with cardiovascular and metabolic risks (Grade B for selection). [106,107,113-119] 69. EV is a synthetic ester of 17 β-estradiol that is quickly hydrolyzed to estradiol following oral or parenteral administration. Its clinical efficacy and safety are comparable to those of other oral estrogens for symptom relief and bone protection, although large RCTs are lacking. [120-123] 70. Progesterone: The choice of a progestogen to accompany systemic ET should be based on endometrial safety, systemic risk profile, tolerability, route preference, and cost-effectiveness. [124-127] 71. All approved progesterones effectively prevent estrogen-induced endometrial hyperplasia when used at the correct dose and duration, tailored to individual needs based on estrogen potency and route. 72. MP and DYD maintain a neutral metabolic and vascular profile and are considered Venous thromboembolism (VTE) neutral when combined with transdermal ET (Grade A). [127-130] 73. Evidence from extensive cohort studies indicates that estrogen combined with MP or DYD does not seem to increase breast cancer risk during typical usage durations of <5 years and may pose a lower risk than regimens using synthetic progestins such as medroxyprogesterone acetate (MPA) (Grade B). [131-135] Long-term use exceeding 5–7 years requires individualized reassessment, as data beyond this period remains limited. 74. However, the National Institute for Health and Care Excellence (NICE) evidence review states that “it is unclear whether different progestogen types alter breast cancer risk.” It therefore does not currently recommend choosing progestogen solely based on breast cancer risk. [136-139] 75. A large Norwegian cohort study involving over 1.3 million women found that combined oral estrogen–progestin therapy was linked to a two-fold increase in breast cancer risk, with differences depending on the formulation. Vaginal estradiol showed no increased risk. The study did not include MP or DYD regimens, so its findings mainly relate to synthetic progestins. [135] 76. These data emphasize that breast cancer risk from MHT varies with regimen and duration, endorsing personalized treatment and regular review (Grade A). [131-135] 77. MP helps improve sleep in women with insomnia, but it can cause daytime drowsiness in some. [140,141] 78. DYD: The combination formula offers oral bioavailability, minimal sedation, and fixed-dose components, all of which improve patient adherence. [142-144] 79. LNG-IUS, 20 µg/day: offers effective endometrial protection for 5 years. It has a higher initial cost and necessitates procedural insertion. [138,145,146] 80. Right regime: available treatment options include estrogen alone, sequential combined hormone therapy (scMHT), and continuous combined hormone therapy (ccMHT) regimens. The choice of an appropriate regimen should be guided by factors such as menopausal stage, uterine status, symptomatology, and patient preferences. Refer to Figure 4 . Systemic regime depending on the stage of menopause 81. An estrogen-only regimen is recommended for women who have undergone surgical menopause. Estrogen is administered daily without interruption. [103] 82. Exceptional cases: Firm evidence is lacking; we recommend adding progestogen to estrogen in hysterectomized women who have residual endometrial tissue after endometrial ablation or supracervical hysterectomy, a history of endometriosis, and stage I endometrial carcinoma. [147-149] 83. Alternative: Tibolone 2.5 mg/day may also be considered for women without a uterus. [150,151] 84. scMHT Regimen: In women with an intact uterus, adding a progestogen is crucial to counter the proliferative effects of estrogen on the endometrium and prevent hyperplasia or carcinoma. Estrogen daily with progestogen added for 12–14 days each month is indicated for women in late MT or within 1–2 years of the FMP. Predictable withdrawal bleeding occurs at the end of each progestogen cycle. Shorter progestogen phases (<10 days) or use beyond 5 years are linked to an increased risk of endometrial cancer. [152,153] 85. Alternative: Low-dose combined OCPs may be used in early or late MT for both symptom relief and contraceptive protection (Grade A). [83,84,85] 86. ccMHT regimen: involves daily administration of estrogen and progestogen without interruption. This approach maintains consistent hormonal levels and aims to induce endometrial atrophy over time. [86,153] 87. A 2020 review suggests that scMHT with synthetic progestins, as well as either scMHT or ccMHT with MP, may be associated with a modest rise in endometrial cancer risk when progestogen exposure is insufficient. [152] This risk appears especially relevant with shorter progestogen phases, lower doses, or duration exceeding 5 years. Adequate endometrial protection requires administering progestogen for at least 12–14 days per 28-day cycle or providing continuous exposure, depending on the type of progestin, the dose, and the duration of MHT use. [135,152,153] Refer Figure 4 MHT regimes. 88. Right route: oral versus transdermal should be personalized according to cardiovascular/metabolic risk profile, clinical indications, and patient preference. [104,131,154-157] 89. Transdermal estrogen: is the preferred route of administration for postmenopausal women with metabolic or vascular risk factors such as obesity, metabolic syndrome, type 2 diabetes mellitus, hypertriglyceridemia, elevated CRP, and controlled hypertension. [117,128,129,158] 90. It is also recommended for women with migraine with aura, gallbladder disease, bowel disorders (such as irritable bowel syndrome or inflammatory bowel disease), or those who smoke, including women using hepatic enzyme–inducing medications such as phenytoin or carbamazepine. [157,159] 91. Transdermal estradiol may be beneficial for some women experiencing sexual dysfunction, as it better preserves libido and genital blood flow, whereas the oral route may reduce free testosterone and sexual desire in certain users. Evidence from randomized trials supports biological plausibility, although data are limited and the Cochrane review has not specifically investigated differences in route (Grade B). [160,161] 92. Oral estrogen: In women with low HDL, oral estrogen has a greater effect on raising HDL levels than transdermal routes and also reduces lipoprotein(a). [162,163] Oral MHT positively impacts glucose metabolism and insulin sensitivity, potentially reducing the risk of developing type 2 diabetes in women without preexisting diabetes (Grade A). [163,164] 93. Right dose: Use the appropriate, minimum, effective, and adjustable dose for symptom relief or bone protection, with dose tapering as age advances. [165,166] Low-dose and ultra-low-dose therapies effectively alleviate symptoms and help sustain bone mass [92,167,168] [Tables 12 and 13 ]. Doses of estrogen therapy CEE: Conjugated equine estrogens, EV: Estradiol valerate Types of progesterones and the required dose for preventing endometrial hyperplasia CEE: Conjugated equine estrogens, LNG: Levonorgestrel-releasing intrauterine system, MP: Micronized progesterone, DYD: Dydrogesterone, TDE: Transdermal estradiol 94. It is important to note that the precise optimal dose for each patient remains personalized, and the evidence is continually evolving. The progestogen dose should be proportional to the estrogen dose to suppress the endometrium. The evidence comparing oral and transdermal MHT regarding dose equivalence for progestogens is limited. [124,169-171] 95. Enhanced monitoring and clinical vigilance are recommended in women with persistent endometrial thickening (>5 mm), obesity (higher endogenous estrogen), or those receiving MHT for >5 years. Indications of menopausal hormone therapy: Refer to Figure 5 Flow chart to prescribe menopausal hormone therapy 96. Vasomotor symptoms: The most effective treatment for VMS is MHT during menopause transition (Grade A). [91,93,172,173] 97. Depression, Mood, and Sleep: Refer to Section 1. 98. Genitourinary syndrome of menopause: Refer to Section 2. 99. Osteoporosis: Refer to Section 3. 100. Absolute contraindications of systemic HT: Undiagnosed abnormal vaginal bleeding; known, current, suspected, or past breast cancer, estrogen-dependent cancers (endometrial, ovarian, and others); active or recent VTE; history of stroke or MI; severe active liver disease with impaired or abnormal liver function; porphyria cutanea tarda; dementia; hypersensitivity; and known or suspected pregnancy (Grade A). [92,136,157,174] 101. Relative contraindications: The presence of latent or established comorbidities requires personalized assessment, shared decision-making, and coordination within a multidisciplinary care team to ensure safe initiation and monitoring of therapy. 102. Drug Interactions: Enzyme-inducing drugs, such as rifampicin, barbiturates, and some antiepileptic drugs like phenytoin or carbamazepine, may accelerate the metabolism of (MHT) and reduce its effectiveness; clinicians should monitor and adjust accordingly (Grade B). [87] Duration of use 103. POI: HRT should be maintained until the average ANM (Grade A). [175-182] Continuation beyond the ANM should be a jointly reviewed decision, considering ongoing indications, patient preferences, and an evolving risk profile (Grade C). [98,183,184] 104. Early menopause: Continuation beyond 48–50 years may be considered on an individual basis through shared decision-making when symptomatic or for bone protection. [175-177] 105. Natural menopause: After nearly 20 years of follow-up, Women’s Health Initiative (WHI) trials showed that EPT and ET were not associated with increased all-cause, cardiovascular, or overall cancer mortality when initiated around the MT. [185-187] 106. Extended therapy beyond these durations may be justified through shared decision-making, particularly for women with recurrent VMS or for osteoporosis prevention when other therapies are unsuitable. Management should remain personalized, with an annually documented benefit–risk review and careful attention to the hormone regimen, duration, and route of administration. [135,70,188-191] 107. Local ET continues to be the primary treatment for GSM across all ages, due to its proven effectiveness and safety with minimal systemic absorption, and may need long-term use (Grade A). [190] 108. Follow-up: Review at 1–2 months after initiation to assess compliance, tolerance, and side effects; at 3 months to address unscheduled bleeding or intolerance; and annually thereafter for a comprehensive evaluation, including risk re-evaluation for NCDs and an updated benefit–risk analysis. Modify the dose or route of therapy as appropriate to the changing clinical profile of the aging woman. 109. Situations requiring immediate discontinuation of HT: New or worsening migraine and headache pattern Visual disturbances such as blurring or symptoms indicating vascular occlusion (e.g., retinal thrombosis) Jaundice or indications of liver dysfunction Persistent or significant elevation in blood pressure Furthermore, HT should be stopped 4–6 weeks prior to elective major surgery involving prolonged immobilization to reduce the risk of VTE If new breast symptoms (lump, nipple change) or unexpected bleeding occur during therapy, the appropriate evaluation should be undertaken, and the decision to continue or pause MHT is made on a case-by-case basis. Unscheduled bleeding until a diagnosis is reached Therapy may be reviewed and resumed following full recovery and a comprehensive clinical reassessment of the patient’s risk profile. New or worsening migraine and headache pattern Visual disturbances such as blurring or symptoms indicating vascular occlusion (e.g., retinal thrombosis) Jaundice or indications of liver dysfunction Persistent or significant elevation in blood pressure Furthermore, HT should be stopped 4–6 weeks prior to elective major surgery involving prolonged immobilization to reduce the risk of VTE If new breast symptoms (lump, nipple change) or unexpected bleeding occur during therapy, the appropriate evaluation should be undertaken, and the decision to continue or pause MHT is made on a case-by-case basis. Unscheduled bleeding until a diagnosis is reached Therapy may be reviewed and resumed following full recovery and a comprehensive clinical reassessment of the patient’s risk profile. 110. Common adverse effects of MHT: Fluid retention may occur in the short term. Recommend reducing dietary salt intake, maintaining adequate hydration, encouraging regular physical activity, and reviewing the estrogen dose. Persistent or troublesome edema should prompt dose reduction or a change in route. Bloating: consider switching to a low-dose transdermal estrogen; reduce the progestogen dose to the level that still protects the uterus; switch to an alternative progesterone. Breast tenderness is common during the first few months. Consider reducing the estrogen dose, switching to a different form of estrogen, or trying a different progestin. Headaches: Switching to transdermal estrogen and using the lowest effective dose often improves tolerance; some women benefit from a continuous-combined regimen. Mood changes: Lower the progestogen dose; switch progestogen; or change from systemic progestin to the LNG-IUS. [151] Nausea: Advise taking the tablet with food or at bedtime; if it persists, reduce the estrogen dose or switch to a transdermal preparation. Chloasma: recommend broad-spectrum sunscreen for women prone to it. Persistent menopausal symptoms: despite seemingly adequate MHT, reassess the diagnosis, adherence, and drug–drug interactions, especially enzyme-inducing antiepileptics and TB drugs. Then, adjust the estrogen dose or change the route, and optimize the progestogen regimen. [151,191] Bleeding: during HT is common when beginning MHT, especially within the first 3–6 months or within 3 months of adjusting the dose or route. [192] In scMHT, a scheduled withdrawal bleed is expected at the end of the progestogen phase. [192] Unscheduled bleeding, such as spotting, heavy, or persistent bleeding outside the normal phase, bleeding before completing the progestogen phase in sequential regimens, or any new bleeding after 6 months on a continuous-combined regimen, requires investigation. [192] While TVS of the endometrium is the standard first-line investigation, it may not exclude pathology in women on MHT, and endometrial sampling remains the definitive method to exclude hyperplasia or carcinoma. [192] Thick endometrium on TVS in women without bleed: After 6 months of amenorrhea, with an ET of <10 mm, and no significant risk factors for endometrial cancer, can be offered adjustments in their progestogen therapy and follow-up instead of immediate biopsy. [192] Individuals with one major or two minor risk factors for endometrial carcinoma, and with ET >4 mm on ccMHT or >7 mm on sc/ccMHT, should be offered EB. If the endometrium appears inhomogeneous, cystic, or irregular, or if bleeding recurs, EB is recommended regardless of ET measurement (Grade B). [192] 111. Stopping MHT: Discuss both abrupt and gradual taper options, taking into account the woman’s previous VMS burden, age, and tolerance. Ensure follow-up to address potential recurrence of symptoms. Symptoms recur in up to 50% of women, usually within the first few months after stopping therapy. There is no high-quality evidence that tapering the dose reduces recurrence or severity of vasomotor or other menopausal symptoms compared with abrupt cessation. [193-196] Special clinical situations: Judicious use of menopausal hormone therapy, when benefits clearly outweigh risks 112. Continuing MHT beyond 10 years from menopause or after age 60: MHT may be continued in healthy women already using low-dose transdermal estradiol with MP or DYD, provided the benefits outweigh the risks. An annual review of symptoms, breast and cardiovascular health, and any emerging contraindications is essential. [107,197-201] When risks related to cardiovascular, thrombotic, or cognitive issues emerge, nonhormonal options are preferred (Grade A). [107,187,198] 113. Vasomotor and sexual symptoms may continue into the seventh and eighth decades, and residual GSM symptoms often need ongoing treatment. Symptom-driven, personalized continuation is suitable when benefits outweigh risks. [199-201] 114. Re-starting or initiating systemic MHT beyond 10 years from menopause or after age 60 enters the early hazard window for VTE and stroke: If therapy is clinically indicated for severe symptoms, opt for transdermal 17 β-estradiol (up to 50 µg/day) with MP or DYD, as this combination is linked to lower VTE and stroke risks than oral estrogen–progestin therapy (Grade A). [107,192,202-208] The prolonged use of MHT in appropriately selected women does not raise all-cause or cardiovascular mortality and can improve quality of life. [107,192,202-208] 115. Starting systemic MHT de novo more than 20 years after menopause, usually at age 70 or older, is not recommended, owing to increased risks of coronary events, stroke, venous thrombosis, and dementia as shown in WHI and other studies (Grade A). [203] Nonhormonal options should be preferred in this group. [203] 116. For bone health after 10 years postmenopause: Nonhormonal pharmacological options, such as bisphosphonates, denosumab, or SERMs, are preferred when MHT is generally not recommended for primary osteoporosis prevention (Grade A). [204,208] 117. Systemic lupus erythematosus (SLE): Active SLE or the presence of antiphospholipid antibodies (aCL or lupus anticoagulant) significantly increases the risk of VTE and stroke. [209] Mild or stable SLE without additional thrombophilia can be safely treated with MHT. Randomized data show no significant increase in severe flares among stable SLE patients receiving MHT. [209] 118. MHT and comorbidities: Refer to Section 3. 119. Breast cancer survivors: In patients aged 40–45 years with breast cancer and secondary amenorrhea following chemotherapy, an undetectable anti-Müllerian hormone at 30 months serves as a reliable predictor of permanent menopause. [210] Refer to Section 5. 120. Benign breast diseases: Do not carry a high risk of malignancy and are not a contraindication to HT. MHT may be used with appropriate screening and vigilance (Grade C). [211,212] 121. MHT and Mammograms: Combined estrogen–progestin therapy raises mammographic breast density, resulting in higher recall rates and decreased mammographic sensitivity. About half of the increased risk of hormone-receptor-positive breast cancer associated with MHT seems to be mediated through this change in density. [213] Mammographic density usually decreases within 1–2 years after stopping therapy. Continued personalized breast imaging and monitoring are advised. [214] 122. Breast, MHT, and Cancer Risk: Women with a low and moderate baseline risk of breast cancer may be prescribed MHT based on individual needs after a comprehensive history, breast examination, use of risk assessment tools, and informed counseling. They should receive accurate, evidence-based information about MHT-related breast cancer risk (Grade A). [134,136,185,215,216] 123. In women at high risk of breast cancer and in breast cancer survivors , nonhormonal therapies are preferred for symptom relief. Systemic MHT is contraindicated due to recurrence risk, as shown in HABITS and LIBERATE trials (Grade A). [185,217-219] 124. However, in rare individual cases, HR-negative disease, long disease-free interval, intolerable symptoms, multidisciplinary consent where systemic MHT is being considered, a comprehensive risk–benefit assessment, and shared decision-making between the oncologist and menopause specialist are essential. [220,221] 125. In BRCA1/2 mutation carriers who undergo risk-reducing bilateral salpingo-oophorectomy, short-term systemic HT up to the median age of natural menopause seems safe (Grade B). [222-224] The use of HT in this context aims to prevent the consequences of premature estrogen deprivation. [222-224] Continuing systemic MHT beyond the natural age of menopause (Grade A) [222-224] is discouraged due to limited long-term safety data on breast and vascular outcomes (Grade C). [185] 126. MHT should be avoided in BRCA carriers who have had previous breast cancer and in women with significant baseline risk factors. [220] Preexisting cancers and menopausal hormone therapy 127. Decisions regarding MHT after cancer should be made through shared decision-making, involving both the patient and the treating oncologist. [225,226] Recommend offering transdermal instead of oral MHT. [227] 128. MHT is neutral: Low-grade, early-stage EC type I, cervical adenocarcinoma, epithelial ovarian cancer, germ cell tumors, hematological malignancies, local cutaneous malignant melanoma, colorectal cancer, hepatocellular cancer, BRCA 1/2 mutation carriers without cancer, most types of ovarian cancer, squamous cell carcinomas of the cervix, vaginal and vulvar squamous cell carcinoma, prolactinoma, kidney cancer, pancreatic cancer, and thyroid cancer. [225,228-231] 129. MHT is relatively contraindicated: leiomyosarcoma, EC type II, advanced metastatic malignant melanoma, gastric cancer, bladder cancer, and lung cancer (Grade B). [152,225,230,232] 130. MHT is contraindicated in women with endometrial stromal sarcoma, uterine carcinosarcoma (Grade A), ovarian cancers such as estrogen-dependent granulosa cell tumors, low-grade serous tumors, and Sertoli–Leydig tumors, as well as endometrioid ovarian tumors, cervical adenocarcinoma, meningioma, glioma, and hormone receptor-positive cancers. Gastric and bladder cancers are also contraindicated due to increased risk of recurrence or tumor stimulation (Grade B). [152,225,226,230,232] Integrated conclusions on the risks and benefits of systemic hormone therapy within 10 years of menopause, based on evidence from WHI [Refer to Tables 14 and 15 ], PEPI, KEEPS, ELITE, and DOPS Trials Based on women’s health initiative, the number of excess events on hormone therapy versus placebo per 10,000 women per year of hormone therapy Use between the age groups of 50 and 59 years. CVD: Caridovascular disease, CIOMS: Council for International Organizations of Medical Sciences, WHO: World Health Organization, VTE: Venous thromboembolism, NA: Not applicable, E + P: Estrogen +progesterone Based on Women’s Health Initiative: Fewer events on estrogen versus placebo per 10,000 women per year of hormone therapy use between the age group of 50 years and 59 years ET: Estrogen therapy, EPT: Estrogen–progestin therapy 131. The risk–benefit balance of MHT varies depending on several factors, including the woman’s age, time since menopause, baseline health status, family history of noncommunicable diseases and cancers, route of administration, and the specific regimen used. 132. Risks are reduced when therapy starts before age 60 or within 10 years of menopause, following a thorough individual risk assessment, with annual reviews to reassess indication, dose, and duration. 133. As with other long-term therapeutic interventions, careful patient selection, judicious use, and regular monitoring are essential to maximize benefits and minimize potential risks. 134. The risk–benefit balance of MHT depends on several factors, including the woman’s age, time since menopause, baseline health status, route of administration, and regimen used. Risks are minimized when therapy is started before the age of 60 or within 10 years of menopause and is reviewed annually. 135. As with other long-term therapeutic interventions, careful selection, judicious use, and regular monitoring of MHT are essential to maximize benefits and minimize potential risks. Risks of systemic therapy 136. The magnitude and type of MHT-related risks in the 50–59-year age group, including breast cancer, and stroke, are rare, with fewer than 10 cases per 10,000 women with VTE showing 11events. These risks are lower with CEE than with CEE plus MPA and are equal to or lower than those linked to obesity, a much more common and modifiable risk factor. [233-238] 137. Cardiovascular disease: Systemic therapy should not be used for primary or secondary prevention of CVD. At any age, women at high risk of CVD or with established CVD should avoid MHT (Grade A). [239] 138. VTE: MHT increases the absolute risk by 4 in 10,000 women for ERT users and 11 in 10,000 for EPT users, while in OCP users, it ranges from 3 to 15 per 10,000 woman-years (Grade A). The risk peaks during the first 1-2 years of treatment and is influenced by the oral route, obesity, smoking, thrombophilia, and age. [157,208,240,241] 139. The absolute risk of VTE is significantly higher during physiological states such as pregnancy, with 5–20 VTE cases per 10,000 deliveries, and reaches its peak in the postpartum period at 40–65 per 10,000 woman-years. [242] 140. Transdermal ET (Grade A) and natural progesterones (Grade C) may not cause VTE. Population screening for thrombophilia is not recommended before using MHT. [243,244] 141. Stroke: Unlike CVD, the timing hypothesis does not apply to stroke, as the risk appears predominantly thrombotic rather than atherosclerotic in origin. [245] 142. Standard-dose oral estrogen or combined EPT is linked to an absolute increase of 2 additional strokes per 10,000 woman-years among those aged <60 years (Grade B). [206,245] For women aged 50–54 years, the excess absolute risk is 1.5 per 10,000 woman-years, rising to 2.2 at age 59 and 2.8 at ages 60–64. [206,240,243,245-247] 143. The risk increases with estrogen dose, age, and route of administration, reaching its highest during the first 1–2 years of treatment. In contrast, low-dose (≤50 µg/day) transdermal estradiol and nonoral routes do not seem to raise stroke risk compared to nonusers (Grade C). [198] The event rate, therefore, stays very low, particularly in younger, healthy postmenopausal women using low-dose or transdermal formulations. [198] 144. MHT and breast cancer: The impact of MHT on breast cancer risk is complex, influenced by background risk, type of MHT, dose, duration of use, regimen, route of administration, and prior exposure. 145. The incremental risk associated with MHT is minimal, with an estimated increase of fewer than 1 additional case per 1000 women aged 50–59 years annually (Grade A). [185,216,219,248] This level of risk is comparable to or lower than that related to common preventable lifestyle factors such as obesity, alcohol consumption, and physical inactivity (Grade A). [185,216,219,248] 146. The increased breast cancer risk associated with CEE + MPA diminishes after discontinuation, usually returning to nonuser levels within about 3 years, particularly following short-term use. However, some elevated risk may persist after more than 5 years of use or with certain synthetic progestins (Grade A). [185,216,219,248] 147. Tumors in women using MHT are usually ER-positive and of the lobular type (Grade C). [216,248] 148. The Collaborative Group Lancet 2019 meta-analysis synthesized only observational data. These findings suggest a slight absolute increase in breast cancer risk, mainly with combined estrogen–progestin therapy, and a lower risk with estrogen-only therapy. [38] 149. According to this analysis, adopted by NICE Guidance 2020 (NG23) as a patient discussion aid for women starting MHT at around age 50 and assessed for risk between ages 50–69 years, the estimated excess breast cancer cases after 5 years of use are: [136] Continuous combined MHT: one additional case per 50 users. Sequential combined MHT: one additional case for every 70 users. Estrogen-only MHT: one additional case per 200 users. All estimates are based on observational data, mainly using oral 17 β-estradiol and synthetic progestins in older women aged 50–69 years. [137] The findings generally align with the Norwegian EBBA-Life cohort and both the studies found no increased risk with vaginal estrogen. [135] 150. In contrast, DOPS, a randomized trial in younger postmenopausal women using 17 β-estradiol ± norethisterone acetate, found no increase in breast cancer incidence or mortality and reported an overall reduction in mortality after 16 years. [131] 151. Similarly, in the WHI trial, women receiving CEE 0.625 mg experienced a statistically lower incidence of breast cancer compared with placebo, and this benefit persisted for over 20 years of extended follow-up. The combined estrogen plus progestin arm showed a modest increase in incidence, mainly limited to the duration of treatment, but no significant difference in breast cancer-specific mortality was observed (Grade A). [185] 152. When counseling women, the focus should be on absolute risks quantified in RCTs, as observational data are susceptible to residual confounding and selection bias. [249,250] Therefore, counseling should primarily depend on RCT-derived absolute risk estimates from WHI and DOPS, while recognizing supportive observational trends. This approach encourages shared decision-making and personalized risk stratification based on age, time since menopause, comorbidities, and treatment goals. 153. MHT and ovarian cancer: In absolute terms, ovarian cancer risk is a rare event with estrogen alone (CEE), the increase is by approximately 0.2 per 1000 women, 0.1 in CEE plus MPA regime, and about 1 per 1000 women with estradiol alone (Grade A). [136,187] 154. MHT and endometrial cancer: Unopposed systemic estrogen (CEE or E2 alone) in women with an intact uterus carries an absolute risk of 1–3 cases per 1000 women. [251] Continuous combined estrogen–progestin therapy (CEE + MPA) lowers endometrial cancer incidence by approximately 3–4 cases per 10,000 women-years compared to placebo. [251,252] 155. Combined oral contraceptives provide significant and lasting protection against both ovarian and endometrial cancers and should be recognized as protective factors in women’s lifetime risk assessments (Grade A). [253,254] 156. MHT and gallbladder: The use of oral estrogen-alone or combined MHT is linked to a higher risk of gallstones, cholecystitis, and cholecystectomy (Grade A). [92] Observational evidence suggests that transdermal estrogen has a lower risk of gallbladder disease compared to oral preparations, and that oral estradiol may pose a reduced risk relative to CEE. However, these differences have not been confirmed in randomized controlled trials (Grade C). [255,256] Benefits of systemic therapy 157. When initiated near menopause, systemic HT offers significant benefits beyond vasomotor relief, positively impacting metabolic health, bone density, mood, and sleep while also potentially lowering the risk of diabetes and colorectal cancer. [257-260] 158. MHT enhances QOL by providing consistent relief from vasomotor and urogenital symptoms, as well as improving sleep quality, mood, and cognitive well-being (Grade A). [261,262] Reductions in coronary events and all-cause mortality with low absolute risks of serious adverse events were noted in the WHI in the younger women. [263] 159. Androgens: Available data are of low quality and conflicting regarding the risk of breast cancer associated with androgen use. Tissue-selective hormone modulators 160. Tibolone: Tibolone is a selective tissue estrogen receptor modulator. It is a synthetic steroid compound with estrogenic, progestogenic, and androgenic properties. It exerts an estrogenic effect on bone, inhibiting bone resorption by reducing osteoclastic activity. 161. Tibolone is effective in treating VMS and improves urogenital atrophy. It improves mood and libido (Grade B). [150] It is prescribed in a single daily dose of 2.5 mg orally. A lower dose of 1.25 mg is equally effective for most indications, including osteoporosis (Grade A). [264] 162. Raloxifene is a selective estrogen receptor modulator (SERM) indicated for the prevention and treatment of postmenopausal osteoporosis, particularly in women at increased risk of breast cancer. It acts as an estrogen agonist in bone and lipid metabolism, and as an antagonist in breast and endometrial tissue. [265,266] 163. Raloxifene lowers the risk of invasive estrogen receptor–positive breast cancer by approximately 60%–70% in postmenopausal women, without stimulating the endometrium (Grade A). The recommended dose is 60 mg once daily. [264,265] 164. Bazedoxifene: a third-generation SERM, acts as an estrogen agonist on bone and lipid metabolism and as an antagonist on breast and endometrium. When combined with conjugated estrogens (CE), it forms a tissue-selective estrogen complex (TSEC) that provides symptom relief and bone protection without the need for a progestogen (Grade A). [267,268] 165. TSEC (CE + BZA) provides an effective alternative to traditional MHT for postmenopausal women with a uterus, particularly those at increased risk of breast cancer or intolerant to progestogens. However, it has a slightly increased risk of VTE and is contraindicated in women with previous VTE, breast or uterine cancer, or liver disease (Grade A). [267,268] Digital tools, artificial intelligence, and machine–learning approaches in menopause care 166. Postmenopausal women may use digital platforms (such as mobile applications, websites, search engines, and podcasts) solely for education, awareness, and symptom monitoring. [268,269] 167. These platforms should not be used to initiate, modify, or cease therapeutic interventions without a clinician’s supervision. Clinician-guided interpretation remains crucial to ensure safety, accuracy, and personalized care. [269,270] Economics of menopause management 168. Menopause imposes a measurable economic burden on women and society through decreased workplace productivity, increased healthcare utilization, and the ongoing costs of untreated chronic diseases developing in midlife. Untreated vasomotor and sleep symptoms alone have been shown to significantly reduce quality of life and work performance, leading to substantial indirect costs (Grade B). [271] 169. The Indian healthcare system remains one of the most privatized globally, characterized by low public health expenditure and substantial out-of-pocket spending, which creates significant barriers to equitable access for midlife women. Gender and socioeconomic disparities further exacerbate this burden, especially among older women with multimorbidity. [272] 170. Expanding insurance coverage for women in midlife, particularly beyond age 65, and subsidizing evidence-based preventive interventions such as bone-protective agents and cardiovascular screening would enhance equity and reduce catastrophic household expenditure in the long term. [273] 171. Integrating menopause management into national NCD and women’s health programs can lead to downstream cost savings by preventing osteoporosis, cardiovascular disease, and mental health issues through early detection and intervention. [274,275] 172. Economic evaluations and modeling studies support that targeted lifestyle counselling and risk-based preventive screening in midlife/around the menopausal transition can be cost-effective, particularly when compared with the substantial downstream costs of osteoporotic fractures and cardiometabolic events (Grade B). [276-279] 173. Setting up dedicated menopause clinics and integrating midlife health services into primary and district-level care are cost-effective, high-impact approaches to support healthy aging and reduce the long-term strain on India’s health system (Grade B). [280] R EFERENCES Lakshmi RM, Kusumalatha K, Shraddha S. 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