The intersection of menopause and diabetes represents a critical yet frequently overlooked dimension of women's health. Menopause, defined as the permanent cessation of ovulation due to ovarian reserve depletion, marks a natural stage of reproductive ageing. Although typically occurring around age 51 in high-income countries, emerging but inconsistent evidence suggests that diabetes may influence the timing of menopause. For instance, women with type 1 diabetes may experience accelerated reproductive ageing, often reaching menopause before age 47. This is supported by findings from the Familial Autoimmune and Diabetes Study, which reported that women with type 1 diabetes had later menarche and earlier menopause compared with both their unaffected sisters and unrelated healthy controls, resulting in a roughly 17% (∼6-year) reduction in their reproductive lifespan.1 Proposed mechanisms for this phenomenon include chronic hyperglycaemia-induced ovarian ageing, autoimmune oophoritis, and insulin-driven follicular depletion. However, other studies report no significant difference in menopausal timing for women with type 1 diabetes, nor a clear association between glycaemic control and age at menopause. This inconsistency extends to type 2 diabetes, for which the available evidence also does not suggest a significant effect on timing.2 While the effect of diabetes on menopausal timing remains uncertain, the impact of menopause, and the associated decline in estradiol, on glucose homeostasis and other aspects of metabolism is more clearly established. Estradiol serves as a crucial metabolic regulator and its decline during menopause contributes to multiple adverse metabolic effects that elevate cardiovascular risk. These include progressive weight gain, increasing insulin resistance, redistribution of body fat to visceral areas, dyslipidaemia, and endothelial dysfunction, independent of ageing.3 Epidemiological data underscore these risks: the Women's Health Initiative found that a reproductive lifespan (menarche-to-menopause interval) shorter than 30 years was associated with a 37% greater risk of diabetes, compared with spans of 36–40 years.4 Menopausal hormone therapy (MHT) may attenuate these metabolic effects, for instance, by improving glycaemic control and potentially supporting weight regulation. A recent systematic review and meta-analysis reported an overall HbA1c-lowering effect of MHT in women with type 2 diabetes; however, data for women with type 1 diabetes remained insufficient to draw reliable conclusions.5 MHT has also been shown to have favourable, albeit modest, effects on body composition.6 Recent observational data suggest that combining MHT with incretin-based therapies enhances weight loss and glycaemic control compared with incretin monotherapy.7 Despite these findings, clinical guidance on menopause management and MHT use in women with diabetes, particularly type 1 diabetes, remains limited. Women with type 2 diabetes are half as likely to receive MHT as their non-diabetic peers, likely due to concerns about cardiovascular safety.8 Yet, a Cochrane review identified only one small study, comparing 12-month MHT effects on cardiovascular risk factors in women with type 1 and type 2 diabetes, finding no significant differences, but robust evidence supporting its long-term cardiovascular safety is lacking.9 Professional societies such as the European Society of Endocrinology (ESE) do not issue a separate diabetes-specific MHT algorithm, but consider MHT acceptable for symptomatic women with diabetes, provided there is no established cardiovascular disease or very high calculated cardiovascular risk.10 Accordingly, long-standing diabetes duration should prompt careful assessment for overt or subclinical atherosclerotic disease. Transdermal estradiol is usually preferred due to lower thromboembolic risk, and a progestogen with neutral metabolic effects (micronised progesterone or dydrogesterone) is recommended to avoid worsening of insulin resistance. However, this has yet to be validated conclusively.2, 8, 11 Similarly to women without diabetes, MHT should not be initiated solely for primary CVD prevention, and its use should still be confined to women younger than 60 years or within 10 years of menopause onset. The combination of SGLT2 inhibitors or GLP-1 receptor agonists with MHT is theoretically promising for risk mitigation but remains to be demonstrated in clinical research. Many challenges during menopause are shared by women with type 1 and type 2 diabetes. Yet, disruptions in insulin sensitivity and glucose regulation may be particularly demanding for women with type 1 diabetes, who lack endogenous insulin. Two qualitative UK surveys found that many women with type 1 diabetes experienced erratic blood glucose levels and often confused vasomotor menopausal symptoms with hypoglycaemia, leading to frequent monitoring, anxiety, fear of complications, and impaired quality of life. Nearly, 90% of respondents with type 1 diabetes reported no prior education about menopause, and more than 70% had never discussed it with their healthcare provider, underscoring a critical gap in clinician awareness and patient-provider communication regarding this important life transition.12 In this context, continuous glucose monitoring (CGM) may represent a valuable supportive tool by allowing real-time differentiation between true hypoglycaemic and menopause-related vasomotor or autonomic symptoms. Bone health represents another critical yet neglected concern. Postmenopausal women with diabetes face elevated fracture risks, with oestrogen deficiency and diabetes synergistically impairing bone density and microstructure.13 This risk may be exacerbated by weight-loss interventions, such as incretin-based medications or bariatric surgery, both disproportionately used in women and known to accelerate bone loss. When prescribing incretin-based therapies or alternative weight-loss interventions, a thorough baseline evaluation of bone health, including a DXA scan and FRAX-based fracture risk assessment, is important. In participants with established osteoporosis, bone-specific pharmacotherapy is essential. In high-risk participants without osteoporosis, concomitant preventive bisphosphonates, or where appropriate, MHT may be warranted. For all participants, core measures include resistance exercise and sufficient protein, vitamin D, and calcium intake. In summary, the intersection of menopause and diabetes, particularly its cardiometabolic implications, is clinically significant but remains critically understudied. There is an urgent need for data on contemporary MHT regimens in both type 1 and type 2 diabetes, including their safety, efficacy, and use alongside agents with proven cardiometabolic benefit. Key gaps also include the role of bone health and novel non-hormonal therapies for vasomotor symptoms. Only by addressing these gaps can we develop evidence-based guidelines to safeguard the health and quality of life for women navigating the dual challenges of diabetes and menopause. Open access publishing facilitated by Inselspital Universitatsspital Bern, as part of the Wiley - Inselspital Universitatsspital Bern agreement via the Consortium Of Swiss Academic Libraries.. This work was supported by the Swiss National Science Foundation (grant number 10000574). DS is supported by the Swiss National MD-PhD Fellowship Program of the Swiss Academy of Medical Sciences, funded by Monique Dornonville de la Cour Foundation. The authors declare no conflict of interest related to this work.
Haage et al. (Thu,) studied this question.