Background and Objectives: Cardiovascular–kidney–metabolic (CKM) syndrome reflects the interconnection between metabolic risk factors, chronic kidney disease (CKD), and cardiovascular disease (CVD). Despite increasing awareness, population-based data on CKM syndrome are limited, particularly in Europe. This study assessed the prevalence of CKM syndrome and the use of renal and cardiac biomarkers in Lithuania. Materials and Methods: Health records of 923,329 adults aged ≥40 years from the national Electronic Health Services and Cooperation Infrastructure Information System were analyzed. CKM-associated conditions (prediabetes/type 2 diabetes, obesity, CKD) and cardiovascular outcomes (atherosclerotic CVD, peripheral vascular disease, stroke, heart failure, atrial fibrillation) were identified. CKM stages were defined as stage 0 (no CKM conditions), stages 1–3 (at least one CKM condition), and stage 4 (at least one CVD diagnosis). The use of estimated glomerular filtration rate (eGFR), albumin-to-creatinine ratio (ACR) and N-terminal pro–B-type natriuretic peptide (NT-proBNP) testing was evaluated. Results: Overall, 34.8% of adults met criteria for stage 4 CKM syndrome, and 23.4% were classified as stage 1–3. Obesity (21.2%) and type 2 diabetes (17.2%) were the most common CKM-associated conditions. Heart failure (25.4%) and atrial fibrillation (14.0%) were the most common cardiovascular outcomes, with ≥2 CVD diagnoses present in 15.4% of patients. Among stage 1–3 patients, eGFR, ACR, and NT-proBNP were measured in 53.5%, 9.0%, and 4.9%, respectively. Conclusions: A third of Lithuanian adults aged ≥40 years had stage 4 CKM syndrome. The underuse of biomarker testing highlights missed opportunities for early detection. Broader implementation of biomarker testing and integrated care is warranted to slow progression of CKM syndrome and reduce cardiovascular risk.

Background/Objectives: While it is known that Hashimoto’s thyroiditis (HT), goiter, thyroid nodules, and thyroid dysfunction may affect women’s reproductive health through hormonal and metabolic mechanisms, data are limited regarding the specific impacts on female sexual function. This study evaluated sexual function in women with thyroid disorders and examined its associations with thyroid function, age, menopausal status, and body mass index (BMI). Methods: A population-based survey was conducted in Kaunas, Lithuania, within the WHO MONICA framework. A random sample of 1569 women aged 25–69 years was included in the final analysis after applying the exclusion criteria. Anthropometric measurements were taken using standardized procedures, and the BMI was calculated. Sexual function was assessed using the 19-item Female Sexual Function Index (FSFI). Thyroid structure was evaluated by a team of trained physicians using ultrasound, while thyroid function was assessed via serum analysis (ELISA-based assays for TSH, fT4, and anti-TPO antibodies). Results: Of the 1569 women analyzed, 64.1% had sexual dysfunction (SD) (FSFI ≤ 26.55). Age and BMI showed significant negative correlations with all FSFI domains, with the strongest associations for arousal, lubrication, and total FSFI score (p < 0.01). SD was more prevalent among postmenopausal (43.6%) women than in premenopausal women (22.6%, p < 0.001) and increased with a higher BMI (p < 0.001). HT was found in 28.3% of participants. Compared with the reference group, women with HT were older, had higher BMI, higher TSH levels, and more hypothyroidism (p < 0.001). SD was more common in the HT group (71.7% vs. 64.2%, p < 0.001), with significantly lower lubrication and higher pain scores. In the multivariate analysis, only goiter remained an independent predictor of SD (p = 0.04). Conclusions: In conclusion, women with HT were older; had a higher BMI; and more frequently experienced SD, particularly reduced lubrication and increased pain, compared with the reference group. Although several thyroid conditions were associated with sexual dysfunction, only goiter remained an independent predictor after adjusting for age and BMI.

Insulin resistance (IR) is recognized as a central mechanism in metabolic dysfunction, with its influence extending far beyond glucose regulation. Increasingly, IR is recognized as the Eminence Grisethe unseen but powerful driverbehind many non-communicable chronic diseases (NCDs) and the biological processes of aging. The research topic "Is insulin resistance the Eminence Grise of aging and NCDs?" brings together 12 original investigations and reviews that collectively expand our understanding of IR as a systemic, multi-organ phenomenon. These studies explore IR not only as a metabolic hallmark but as a unifying pathophysiological thread linking cardiovascular, renal, hepatic, respiratory, neurological, and psychological disorders across the lifespan. The reviewed studies explored various accessible, non-insulin-based surrogate indices (Triglyceride-Glucose [TyG], Estimated Glucose Disposal Rate [eGDR]) across aging-related diseases. Although the hyperinsulinemic-euglycemic clamp remains the most accurate method for assessing IR, its application is often limited by the complexity and constraints of clinical settings.Decades of research have established that IR contributes to a wide range of metabolic and degenerative diseases. It plays a fundamental role in the development of type 2 diabetes, dyslipidemia, non-alcoholic fatty liver disease (NAFLD), and atherosclerosis (1,2). Mechanistically, IR arises from the interplay between genetic susceptibility, ectopic lipid accumulation, mitochondrial dysfunction, chronic inflammation, and altered adipokine signaling (3). Beyond classical metabolic organs, impaired insulin signaling affects endothelial cells, neurons, and immune responses, contributing to vascular stiffness, neurodegeneration, and systemic low-grade inflammationhallmarks of aging (1-5). However, despite this well-established framework, several aspects remain underexplored. While the molecular basis of IR has been elucidated in skeletal muscle, liver, and adipose tissue, much less is known about its role in non-traditional target organs such as the lungs, kidneys, or brain. Moreover, there remains a gap in understanding the predictive and diagnostic value of emerging non-insulinbased IR indices, their relevance in acute settings, and their relationship with mental health and cognitive decline. Gaps also persist regarding pharmacological modulation, adipose-immune crosstalk, and longitudinal mechanistic studies integrating omics and imaging biomarkers. 37The papers in this address several of these gaps, validate surrogate markers, and deepen our 38 understanding of IR. 39The interplay between IR and cardiovascular disease (CVD) remains a subject of persistent inquiry.