Association of Serum Androgen Levels With Framingham Cardiovascular Risk Score in Individuals With Obesity

Association of Serum Androgen Levels With Framingham Cardiovascular Risk Score in Individuals With Obesity | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Association of Serum Androgen Levels With Framingham Cardiovascular Risk Score in Individuals With Obesity Banu Betul Kocaman, Feray Akbas This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8702626/v1 This work is licensed under a CC BY 4.0 License Status: Published Journal Publication published 07 Mar, 2026 Read the published version in BMC Endocrine Disorders → Version 1 posted 23 You are reading this latest preprint version Abstract Background Obesity is strongly associated with increased cardiovascular morbidity and mortality. Although traditional risk factors are incorporated into widely used cardiovascular risk scores such as the Framingham Risk Score, hormonal alterations accompanying obesity, particularly changes in serum androgen levels, may also contribute to cardiovascular risk. This study aimed to investigate the relationship between serum androgen levels and estimated 10-year cardiovascular risk in individuals with obesity. Methods This retrospective study included 203 adults with obesity followed in an obesity clinic over a five-year period. Demographic, anthropometric, clinical, and laboratory data were collected. Cardiovascular risk was assessed using the Framingham Risk Score, and patients were stratified into low, intermediate, and high risk categories. Associations between hormonal parameters and cardiovascular risk were evaluated using correlation analyses and multivariable linear regression models adjusted for major metabolic risk factors. Results Serum dehydroepiandrosterone sulfate (DHEAS) levels showed a significant inverse correlation with the Framingham Risk Score in the overall cohort and in both sexes (p < 0.05). In multivariable linear regression analysis adjusted for age, body mass index, HbA1c, triglycerides, total cholesterol, and LDL cholesterol, DHEAS levels remained independently associated with the Framingham Risk Score (p = 0.027). DHEAS and estradiol levels decreased across increasing cardiovascular risk categories, whereas body mass index and total testosterone did not differ among risk groups. Measures of central adiposity, including waist circumference and waist-to-hip ratio, demonstrated stronger associations with cardiovascular risk than body mass index. Conclusion Lower serum DHEAS levels are associated with higher estimated cardiovascular risk in individuals with obesity, independent of traditional metabolic risk factors when cardiovascular risk is assessed as a continuous variable. Central adiposity measures appear to be more informative than body mass index for cardiovascular risk stratification. Incorporating hormonal parameters and indices of abdominal obesity may enhance cardiovascular risk assessment in obese populations. Obesity cardiovascular risk Framingham Risk Score DHEAS androgen hormones Introduction Obesity, which is considered as a complex and multifactorial disease that negatively affects health, is defined by the World Health Organization (WHO) based on body mass index (BMI) [ 1 , 2 ]. By 2022, 2.5 billion adults aged 18 years and older were overweight, including more than 890 million living with obesity, reflecting a global trend in which the age-standardised prevalence of obesity more than doubled between 1990 and 2022 and increased across nearly all countries, affecting 94% of countries for women and all but one country for men [ 3 ]. Obesity is associated with a dramatic decrease in life expectancy for both men and women. It has been suggested that the steady increase in life expectancy seen in the last two centuries may end due to the increase in the prevalence of obesity [ 4 ]. Many epidemiological studies have shown the relationship between obesity and mortality [ 5 , 6 ]. Besides mortality, obesity is also associated with increased morbidity, and studies have shown that obesity is the number one cause of preventable disease and disability by surpassing smoking [ 7 ]. Given its versatile effects on health, it is urgently needed to take the necessary measures for the prevention, early diagnosis and treatment of obesity. The most important of obesity-related diseases are cardiovascular diseases, and obesity increases the mortality associated with cardiovascular diseases [ 8 ]. Medical, surgical, and interventional treatment methods applied after cardiovascular diseases become clinically apparent are definitive but associated with high costs. Therefore, early identification of cardiovascular disease risk and the implementation of preventive measures are of great importance. Various risk scoring systems have been developed to estimate the risk of cardiovascular diseases before they become clinically apparent, among which the Framingham Risk Score is one of the most widely used tools [ 9 ]. The Framingham Risk Score aims to estimate the 10-year risk of cardiovascular disease using eight parameters. The parameters used in this score include major risk factors such as age, sex, and the presence of diabetes; however, recent studies have also highlighted additional factors that may increase the risk of cardiovascular disease, including serum androgen hormones. It has been revealed that serum androgen levels that change with obesity affect cardiovascular risk factors [ 10 – 12 ]. Many studies have shown that coronary heart disease and cardiovascular deaths are more common in men with low testosterone levels [ 10 ]. However, some recent studies have revealed the possibility that high endogenous androgen levels may also increase the risk of coronary heart disease and death [ 11 , 12 ]. Most studies with a large number of male participants have shown that DHEAS has a negative correlation with coronary heart disease and cardiovascular disease-related mortality [ 13 – 15 ]. Given the complex hormonal alterations associated with obesity, this study was designed to explore the potential contribution of serum androgen levels to cardiovascular risk assessment in individuals with obesity. Materials and Methods The study was conducted by retrospectively reviewing medical records of patients followed in the obesity clinic of Istanbul Training and Research Hospital over a five-year period. A total of 203 patients who met the study criteria were included. The inclusion criteria were as follows: (I) being registered and followed up in the obesity clinic within the last five years, (II) having a body mass index (BMI) of ≥ 30 kg/m², and (III) being between 30 and 74 years of age. The exclusion criteria were defined as: (I) failure to meet the diagnostic criteria for obesity, (II) being younger than 30 years or older than 74 years, (III) having a diagnosis of cardiovascular diseases such as ischemic heart disease, peripheral artery disease, or cerebrovascular disease, (IV) having a history of coronary revascularization and/or carotid surgery, and (V) using medications known to affect serum androgen levels. Demographic characteristics of the patients, including age, sex, smoking status, presence of chronic disease, family history, medication use, systolic and diastolic blood pressure, waist circumference (WC), hip circumference (HC), height, weight, and BMI, were obtained from obesity clinic follow-up records. Height and weight were measured according to standard protocols at the first visit, and BMI was calculated as weight (kg) divided by height squared (m²) [ 16 ]. Waist and hip circumferences were measured using a non-elastic tape measure in the standing position, and the waist-to-hip ratio was calculated by dividing waist circumference by hip circumference [ 17 ]. Blood pressure was measured from the left arm in the seated position using a standardized sphygmomanometer after at least 5 minutes of rest. Patients were evaluated for cardiovascular disease using medical history, physical examination, resting electrocardiography, and echocardiography data, and individuals with suspected cardiovascular disease were excluded. Laboratory data were obtained from the hospital database and recorded based on the first examination. Fasting blood glucose, insulin, HbA1c, total cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, total testosterone, DHEAS, and estradiol (female patients only) levels were documented. Cardiovascular risk was assessed using an eight-parameter scoring system based on the Framingham Heart Study [ 9 ]. A 10-year cardiovascular risk score was calculated using age, sex, systolic blood pressure, antihypertensive treatment status, diabetes status, smoking status, total cholesterol, and HDL cholesterol. Only current smokers were considered smokers. The presence of diabetes was determined in two categories: patients previously diagnosed with and treated for diabetes, and/or patients who met the diagnostic criteria for diabetes according to the American Diabetes Association guidelines for the relevant period [ 18 ]. Hypertension was defined by the presence of systolic blood pressure above 140 mmHg or diastolic blood pressure above 90 mmHg and/or use of any anti-hypertensive drug [ 19 ]. Chronic disease was defined as the presence of at least one physician-diagnosed chronic condition, including diabetes mellitus, hypertension, or other chronic systemic diseases requiring ongoing medical treatment. Patients were additionally stratified into three cardiovascular risk categories based on the Framingham risk score: low risk ( 20%). Statistical analysis: Statistical analyses were performed using SPSS software. Continuous variables were assessed for normality using the Shapiro–Wilk test. Normally distributed variables were expressed as mean ± standard deviation, whereas non-normally distributed variables were presented as median (interquartile range). Categorical variables were expressed as frequencies and percentages. Comparisons between two independent groups were performed using the independent samples t-test or Mann–Whitney U test, as appropriate. Comparisons among more than two groups were conducted using one-way analysis of variance (ANOVA) or the Kruskal–Wallis test. When a statistically significant difference was observed in multiple-group comparisons, post-hoc pairwise analyses were performed using Bonferroni correction or Dunn’s test, as appropriate. Clinical, anthropometric, and laboratory parameters were compared according to diabetes status, chronic disease status, and Framingham cardiovascular risk categories. Correlations between the Framingham risk score and clinical, anthropometric, metabolic, and hormonal parameters were assessed using Spearman’s rank correlation analysis. Correlation analyses were additionally performed separately for female and male patients. Multivariable linear regression analyses were conducted to evaluate whether the associations between serum DHEAS levels and diabetes or chronic disease status were independent of age. In these models, DHEAS was included as the dependent variable, and age and other clinically relevant covariates were entered as independent variables. Additional multivariable linear regression analysis was performed to assess the independent association between DHEAS and the Framingham risk score. The Framingham risk score was included as the dependent variable, and age, BMI, HbA1c, triglycerides, total cholesterol, and LDL cholesterol were included as covariates. A p value < 0.05 was considered statistically significant. Results A total of 203 patients, 166 (81.8%) females and 37 (18.2%) males, were included in the study. The median age of the patients was 45 years [35–52], median height was 160 cm [153–162], median body weight was 105 kg [92–114.2], and median BMI was 40.8 kg/m² [36–44.5]. The median waist circumference was 120 cm [109.5–127], mean hip circumference was 129.1 ± 11.9 cm, and the median waist-to-hip ratio was 0.93 [0.88–0.94]. When BMI was classified, 32 patients (15.8%) were in the first-degree obesity group, 61 patients (30%) were in the second-degree obesity group and 110 patients (54.2%) were in the third-degree obesity group. The clinical and laboratory characteristics, including blood pressure measurements and comorbidities, are shown in Table 1 . Table 1 Laboratory findings, blood pressure measurements, and comorbidities of patients with obesity Variable Patients with obesity (n: 203) Glucose, mg/dL, median [IQR] 101 [92–114.2] HbA1c, %, median [IQR] 5.8 [5.5–6.1] Total Cholesterol, mg/dL, mean ± sd 210.3 ± 41.5 HDL Cholesterol, mg/dL, mean ± sd 49.1 ± 11.7 LDL Cholesterol, mg/dL, mean ± sd 130.3 ± 35 Triglyceride, mg/dL, median [IQR] 138 [98.7–178.2] Total Testosterone, ng/dL, median [IQR] 40.7 [24.5–51] DHEAS, µg/dL, median [IQR] 133.4 [78.9–217] Estradiol, pg/mL, median [IQR] 44 [5–82.2] Insulin, µU/mL, median [IQR] 12.4 [7.5–17.5] Framingham Risk Score, %, median [IQR] 5.7 [2.2–10.6] Systolic blood pressure, mmHg, mean ± sd 121.5 ± 12.1 Diastolic blood pressure, mmHg, mean ± sd 77.6 ± 6.6 Presence of diabetes mellitus, n (%) 59 (29.1%) Presence of hypertension, n (%) 63 (31%) Presence of chronic disease, n (%) 152 (74.9%) There were no significant differences in age or BMI between female and male patients (age: 41 [33.7–49] vs. 42 [36–51], p = 0.067; BMI: 41 [37.3–45.1] vs. 41 [40–41.5] kg/m², p = 0.393). Total testosterone and DHEAS levels, as well as Framingham risk scores, were significantly lower in female patients compared with male patients (p = 0.006, p = 0.001, p = 0.017; respectively). Comparisons of clinical characteristics, laboratory parameters, comorbidities, lifestyle factors, and cardiovascular risk profiles between female and male patients are summarized in Table 2 . Table 2 Comparison of clinical, laboratory, lifestyle characteristics, and cardiovascular risk profiles by sex Variable Female (n: 166) Male (n: 37) P value Height, cm, median [IQR] 159 [154–163] 178 [175–185] 0.000 Weight, kg, median [IQR] 105 [94.5–116.2] 131 [128.5–138] 0.000 Waist circumference, cm, mean ± sd 118.1 ± 11.7 127.6 ± 9.1 0.000 Hip circumference, cm, mean ± sd 129.1 ± 12.3 128.7 ± 10.1 0.855 Waist / hip ratio, median [IQR] 0.92 [0.88–0.94] 1.07 [1.02–1.07] 0.000 Glucose, mg/dL, median [IQR] 101 [90.7–113] 103 [97.5–103.5] 0.529 HbA1c, %, median [IQR] 5.7 [5.4–6.1] 6.1 [5.8–6.3] 0.695 Total Cholesterol, mg/dL, mean ± sd 210.9 ± 40.1 207.3 ± 47.3 0.627 HDL Cholesterol, mg/dL, mean ± sd 50.6 ± 11.8 42.1 ± 8.5 0.000 LDL Cholesterol, mg/dL, mean ± sd 130.7 ± 33.6 131.5 ± 36.6 0.897 Triglyceride, mg/dL, median [IQR] 118 [89–154.2] 164 [143.5–165.5] 0.175 Total Testosterone, ng/dL, median [IQR] 36.7 [24.4–50.1] 253 [216.3–327.4] 0.000 DHEAS, µg/dL, median [IQR] 141.5 [101.8–246.9] 234.7 [223.3–332] 0.001 Insulin, µU/mL, median [IQR] 11.9 [7.3–18.1] 18.6 [15.4–20.1] 0.013 Framingham Risk Score, %, median [IQR] 3.8 [1.7–7.5] 8.2 [5.7–20.2] 0.017 Presence of diabetes mellitus, n (%) 50 (30.1%) 9 (24.3%) 0.483 Presence of hypertension, n (%) 54 (32.5%) 9 (24.3%) 0.329 Presence of chronic disease, n (%) 126 (75.9%) 26 (70.3%) 0.475 Presence of smoking, n (%) 49 (29.5%) 17 (45.9%) 0.054 Degree of obesity, first-degree / second-degree / third-degree, n (%) 27 (16.3) / 46 (27.7) / 93 (56) 4 (10.8) / 61 (30) / 111 (54.7) 0.280 Cardiovascular risk group, low / medium / half, n (%) 118 (71.1) / 35 (21.1) / 13 (7.8) 20 (54.1) / 11 (29.7) / 6 (16.2) 0.102 A significant positive correlation was observed between the Framingham risk score and age, waist circumference, waist-to-hip ratio, systolic and diastolic blood pressure, glucose, total cholesterol, LDL cholesterol, triglycerides, insulin, and HbA1c in the overall study population (p < 0.05). In contrast, the Framingham risk score was negatively correlated with DHEAS, height, and estradiol levels (p 0.05). Correlations between the Framingham risk score, DHEAS, total testosterone, and other study parameters are presented in Table 3 . Sex-stratified analyses demonstrated that the positive correlations between the Framingham risk score and age, glucose, total cholesterol, triglycerides, and HbA1c, as well as the negative correlation with DHEAS, were present in both female and male patients. Table 3 Correlation analysis between the Framingham Risk Score, total testosterone, DHEAS, and other clinical and laboratory parameters Framingham Risk Score Total Testosterone DHEAS r p r p r p Total Testosterone 0,031 0,657 DHEAS -0,326 0,000 0,590 0,000 Age 0,780 0,000 -0,279 0,000 -0,549 0,000 Height -0,141 0,045 0,512 0,000 0,240 0,001 Weight -0,009 0,900 0,399 0,000 0,264 0,000 Waist Circumference 0,223 0,001 0,269 0,000 0,132 0,060 Hip Circumference 0,043 0,545 0,029 0,685 0,089 0,209 Waist/Hip Ratio 0,251 0,000 0,327 0,000 0,050 0,482 Body Mass Index 0,077 0,278 0,022 0,755 0,095 0,179 Systolic Blood Pressure 0,556 0,000 0,019 0,791 -0,138 0,049 Diastolic Blood Pressure 0,285 0,000 0,085 0,229 -0,075 0,285 Glucose 0,502 0,000 -0,136 0,052 -0,206 0,003 Total Cholesterol 0,413 0,000 -0,110 0,117 -0,194 0,005 HDL Cholesterol -0,010 0,889 -0,244 0,000 -0,123 0,080 LDL Cholesterol 0,336 0,000 -0,055 0,434 -0,153 0,029 Triglyceride 0,442 0,000 -0,017 0,813 -0,182 0,009 Insulin 0,140 0,048 0,199 0,005 0,150 0,034 Estradiol -0,390 0,000 0,192 0,021 0,211 0,011 HbA1c 0,540 0,000 -0,058 0,408 -0,235 0,001 Spearman correlation analysis was performed. r: correlation coefficient. Multivariable linear regression analysis was performed to evaluate the independent association between serum DHEAS levels and Framingham risk score. In the model adjusted for age, body mass index (BMI), HbA1c, triglycerides, total cholesterol, and LDL cholesterol, serum DHEAS levels were found to be independently associated with Framingham risk score (p = 0.027, β = -0.126, t = 2.224). Patients with diabetes were significantly older and had higher glucose, HbA1c, triglyceride, total cholesterol, insulin levels, and Framingham risk scores compared with those without diabetes. In addition, DHEAS levels were significantly lower in patients with diabetes. Similarly, patients with chronic disease were older and exhibited higher glucose, HbA1c, and Framingham risk scores, along with lower DHEAS levels, compared with patients without chronic disease. Comparisons of clinical, anthropometric, and laboratory parameters according to diabetes and chronic disease status are presented in Table 4 . Table 4 Comparison of clinical, anthropometric, and laboratory characteristics according to diabetes and chronic disease status Variable, median [IQR] Diabetes (+) (n: 59) Diabetes (-) (n: 144) p value Chronic disease (+) (n: 152) Chronic disease (-) (n: 51) p value Age, year 52 [43.7– 56.5] 33 [31– 39.5] 0.000 47 [37–54] 36 [31–47] 0.000 BMI, Kg/m 2 41.8 [36.6– 46.4] 40 [36– 44] 0.187 41 [36.9–45.3] 40 [35–43] 0.225 Waist/hip ratio 0.92 [0.91– 0.95] 0.92 [0.88– 0.94] 0.171 0.92 [0.89–0.94] 0.92 [0.88–0.96] 0.197 Glucose, mg/dL 123.5 [102.5– 165.2] 97 [89– 104.7] 0.000 103 [94–117] 97 [89–103] 0.002 HbA1c, % 6.4 [5.9– 7.3] 5.6 [5.4– 5.9] 0.000 5.9 [5.5–6.2] 5.6 [5.3–5.9] 0.001 Total Cholesterol, mg/dL 215 [193.5– 240.2] 202.5 [182– 228.7] 0.034 206 [184.5–235.5] 204 [182–226.5] 0.501 HDL Cholesterol, mg/dL 50 [39.7– 56.7] 48 [42– 57.7] 0.577 49 [40.5–50.9] 47 [41–56] 0.584 LDL Cholesterol, mg/dL 131.4 [108.1– 153.9] 126.5 [43.7– 147.9] 0.627 126.6 [106.6–150.6] 128.4 [109–147.3] 0.705 Triglyceride, mg/dL 161.5 [137.2– 223] 118 [91– 156.5] 0.000 139 [102.5–182] 121 [92.5–153.5] 0.068 Total Testosterone, ng/dL 32.1 [19.7– 47.3] 37.6 [25.1– 53.7] 0.191 36.1 [22.6–48] 42.3 [28.5–61.6] 0.223 DHEAS, µg/dL 106.7 [67.7– 160.9] 141.5 [80.9– 235.6] 0.024 117.4 [67.2–194.9] 164.5 [106.3–287.3] 0.001 Estradiol, pg/mL 52 [43.7– 56.5] 51 [24– 92.7] 0.009 42 [5–83.5] 50 [22–83] 0.677 Insulin, µU/mL 13.6 [8.8– 23.6] 11.2 [7.3– 16.2] 0.007 11.4 [7.5–18.2] 12.5 [8.4–16.4] 0.987 Framingham Risk Score, % 14.4 [8.1– 19.5] 2.9 [1.7– 6.2] 0.000 6.3 [2.8–12.9] 2.7 [1.4–4.1] 0.000 Data are presented as median (interquartile range). p values were calculated using the Mann–Whitney U test. In multivariable linear regression analysis adjusting for age, the association between DHEAS levels and the presence of diabetes or chronic disease was no longer statistically significant (p > 0.05), indicating that the observed unadjusted differences were largely age-dependent. Patients were stratified into three groups according to the Framingham risk score: low risk ( 20%). According to the Framingham risk score, 138 patients (68.0%) were classified as low risk, 46 patients (22.7%) as intermediate risk, and 19 patients (9.4%) as high risk. Age, waist-to-hip ratio, glucose, HbA1c, total cholesterol, triglycerides, insulin levels, and the total testosterone/estradiol ratio increased progressively with higher Framingham risk categories. In contrast, DHEAS and estradiol levels decreased as cardiovascular risk increased. No significant differences were observed in BMI, HDL cholesterol, LDL cholesterol, or total testosterone among the risk groups (Table 5 ). Table 5 Clinical and laboratory characteristics across Framingham risk groups Variable, median [IQR] Low risk (n: 138) Intermediate risk (n: 46) High risk (n: 19) p Age, year 38 [33–48] 54 [50.7–56.5] 60 [55–63] 0.000 a BMI, Kg/m 2 40 [36–44] 44 [35.8–46] 40.5 [34.8–47.6] 0.900 Waist/hip ratio 0.92 [0.88–0.94] 0.92 [0.89–0.93] 0.94 [0.91–0.97] 0.014 b Glucose, mg/dL 98 [89–106] 127 [103.7–158] 138 [103.7–209.7] 0.000 c HbA1c, % 5.7 [5.4–5.9] 6.4 [5.9–7.3] 6.4 [5.9–7.5] 0.000 d Total Cholesterol, mg/dL 203.5 [182.7–226.2] 229.5 [179.2–251.2] 207.5 [193.5–242.2] 0.010 e HDL Cholesterol, mg/dL 48 [41.7–58.2] 50 [40.7–55.2] 44 [33.7–57.7] 0.724 LDL Cholesterol, mg/dL 126.4 [108–145.3] 139.2 [107.1–164] 128 [105.4–145.2] 0.055 Triglyceride, mg/dL 121.5 [91–164.7] 148.5 [128–216.2] 174.5 [147.7–228] 0.000 f Total Testosterone, ng/dL 37.3 [24.7–53.5] 35.3 [21.1–47] 44.4 [19.1–66.9] 0.385 DHEAS, µg/dL 137.3 [87.5–237.8] 117.6 [76.4–176.7] 61 [37.5–162] 0.003 g Estradiol, pg/mL 56.5 [24–94.2] 25 [5–50.5] 5 [ 5 – 30 ] 0.001 h Insulin, µU/mL 11.4 [7.5–16.6] 10.9 [6.8–13.9] 24.7 [17.8–35.3] 0.005 i Framingham Risk Score, % 3.2 [1.7–6.1] 15 [12.1–17.7] 28.7 [24.2– 39.4] 0.000 j a : Significant post-hoc difference: low vs intermediate risk (p = 0.000) and low vs high risk (p = 0.000), b : Significant post-hoc difference: low vs high risk (p = 0.016), c : Significant post-hoc difference: low vs intermediate risk (p = 0.000) and low vs high risk (p = 0.000), d : Significant post-hoc difference: low vs intermediate risk (p = 0.000) and low vs high risk (p = 0.000), e : Significant post-hoc difference: low vs intermediate risk (p = 0.019), f : Significant post-hoc difference: low vs intermediate risk (p = 0.026) and low vs high risk (p = 0.001), g : Significant post-hoc difference: low vs high risk (p = 0.008), h : Significant post-hoc difference: low vs high risk (p = 0.003), i : Significant post-hoc difference: low vs high risk (p = 0.009) and intermediate vs high risk (p = 0.005), j : Significant post-hoc difference: low vs high risk (p = 0.003), k : Significant post-hoc difference: low vs high risk (p = 0.001). Data are presented as median (interquartile range). Overall comparisons were performed using the Kruskal–Wallis test with post-hoc pairwise analyses. Discussion In this study, we investigated the relationship between serum androgen levels and estimated 10 year cardiovascular risk assessed by the Framingham risk score in individuals with obesity. We found that serum DHEAS levels were inversely associated with the Framingham risk score in the overall cohort as well as in both sexes, and this association remained significant after adjustment for major metabolic risk factors when cardiovascular risk was analyzed as a continuous variable. In addition, DHEAS and estradiol levels decreased progressively across increasing Framingham risk categories, whereas BMI and total testosterone did not differ among risk groups. Measures of central adiposity, including waist circumference and waist-to-hip ratio, showed stronger associations with cardiovascular risk than BMI. Although DHEAS levels were lower in patients with diabetes and chronic diseases, these associations were largely explained by age-related decline. Overall, these findings suggest that hormonal alterations, particularly reduced DHEAS levels, may be linked to cardiovascular risk burden in obesity, while highlighting the importance of central adiposity over general obesity in cardiovascular risk stratification. In our study, serum DHEAS levels were associated with the estimated 10-year cardiovascular risk calculated using the Framingham risk score. DHEAS showed a significant inverse correlation with the Framingham risk score in the overall cohort as well as in both sexes. This finding suggests that lower DHEA-S levels in individuals with obesity may be accompanied by a less favorable cardiovascular risk profile. To further explore this relationship, patients were categorized into low-, intermediate-, and high-risk groups according to their Framingham risk scores. Consistent with the correlation analyses, DHEAS levels were significantly lower in the high-risk group compared with the low-risk group. However, given the complex interplay between adrenal androgens, aging, and metabolic factors, the direction and strength of this association may change after multivariable adjustment. In our study, DHEAS levels remained independently and statistically significantly associated with the Framingham risk score in a multivariable linear regression model including age, body mass index, HbA1c, triglycerides, total cholesterol, and LDL cholesterol. This result suggests that DHEAS may provide additional information for cardiovascular risk assessment in an obese population beyond traditional metabolic risk markers. The literature regarding the association between DHEAS and cardiovascular outcomes is heterogeneous. Most cross-sectional studies and prospective studies predominantly including male participants have reported an inverse relationship between DHEA-S levels and coronary heart disease as well as cardiovascular mortality [ 14 , 15 ]. Consistent with these findings, a systematic review and meta-analysis by Wu et al., including studies published up to 2017, demonstrated significantly lower DHEAS levels in individuals with coronary heart disease compared with healthy controls [ 20 ]. In contrast, a large community-based prospective cohort study of older adults reported that low DHEAS levels were associated with an increased risk of hospitalization for heart failure and all-cause mortality, while no independent association with the incidence of coronary heart disease was observed [ 21 ]. Similarly, in a prospective study by Zhao et al. involving postmenopausal women, DHEA levels were not associated with overall cardiovascular events; however, inverse associations were observed in women with heart failure with reduced ejection fraction and in postmenopausal women younger than 65 years [ 22 ]. These findings have led to the hypothesis that the role of DHEAS in cardiovascular risk may be age- and phenotype-dependent. Notably, in our study, the significant inverse association between DHEAS levels and the Framingham risk score persisted even after adjustment for age, suggesting that DHEAS may reflect an earlier, subclinical stage of cardiovascular risk prior to the development of clinically overt cardiovascular events. Although some studies have suggested that DHEAS supplementation may confer various physiological benefits, including the prevention of cardiovascular disease in older individuals, a comprehensive review by Teixeira et al. emphasized that the metabolic and cardiovascular effects of DHEA are highly dependent on dosage, menopausal status, and the individual’s underlying metabolic profile, underscoring the need for caution in its therapeutic use [ 23 , 24 ]. In contrast to interventional studies with heterogeneous outcomes, our findings reflect the association between endogenous DHEAS levels and cardiovascular risk, supporting its potential role as a biomarker rather than a therapeutic agent. In our study, total testosterone and DHEAS levels were significantly lower in female patients compared with male patients, which is consistent with the well-established sex differences in circulating androgen levels. In parallel, the Framingham risk score was also significantly lower in females than in males. Male sex has long been recognized as an independent risk factor for cardiovascular disease–related morbidity and mortality, and our findings are in line with previous large-scale studies. For instance, the TRANSCEND and ONTARGET trials reported approximately 20% lower cardiovascular risk for women than for men across all cardiovascular endpoints [ 25 ]. Sex-related differences in cardiovascular risk have been extensively investigated, and multiple biological and behavioral mechanisms have been proposed. Among these, differences in sex hormone profiles, particularly androgens, have attracted considerable attention [ 10 ]. While some studies have suggested that the increased cardiovascular risk observed in men may be partly related to genetic factors such as Y chromosome linked mechanisms [ 26 ], others have emphasized the contribution of sex-specific behaviors, visceral fat distribution, metabolic characteristics, and age-related vascular and myocardial adaptations [ 27 ]. Most studies examining the relationship between testosterone levels and cardiovascular disease have reported higher rates of coronary heart disease and cardiovascular mortality in men with low testosterone levels, suggesting that testosterone may serve as a biomarker of poor cardiovascular health [ 10 , 28 ]. However, the causal nature of this association remains unclear, and conflicting findings have also been reported. Several studies have shown no significant association between testosterone levels and cardiovascular mortality, while others have suggested that elevated endogenous androgen levels may also be associated with an increased risk of coronary heart disease [ 29 ]. In the present study, no significant correlation was observed between total testosterone levels and the Framingham risk score, either in the overall cohort or when analyses were stratified by sex. These findings support the notion that the relationship between testosterone and cardiovascular risk is complex and context dependent. The heterogeneous effects of testosterone on individual cardiovascular risk factors, differences between endogenous and exogenous testosterone exposure, and the influence of testosterone metabolites may all contribute to the inconsistent results observed across studies [ 11 , 12 ]. Moreover, conditions characterized by hyperandrogenemia, such as polycystic ovary syndrome, have also been associated with increased cardiovascular risk, further underscoring the multifaceted role of androgens in cardiovascular pathophysiology [ 30 ]. When the relationship between estradiol levels and cardiovascular risk was evaluated in female patients, a significant inverse correlation was observed between serum estradiol levels and the Framingham risk score. In addition, in analyses stratified by Framingham risk categories, estradiol levels were significantly lower in the high-risk group compared with the low-risk group. Traditionally, estrogens have been considered protective against cardiovascular disease; however, evidence accumulated over the past two decades has challenged this paradigm [ 31 , 32 ]. Large randomized trials, particularly the Women’s Health Initiative, demonstrated that combined estrogen–progestin therapy does not confer cardiovascular protection and may even increase the risk of coronary heart disease, especially during the early postmenopausal period [ 31 , 32 ]. These findings have led to a substantial decline in the use of postmenopausal hormone therapy and the development of alternative treatment strategies. Observational studies evaluating endogenous estradiol levels and cardiovascular risk have yielded inconsistent results. A population-based study from Denmark reported that lower estradiol levels were associated with an increased risk of coronary heart disease and mortality [ 33 ]. In contrast, some studies have found no significant association between estradiol levels and cardiovascular events [ 34 , 35 ]. In this context, our findings suggest that lower endogenous estradiol levels may be associated with a less favorable cardiovascular risk profile in women with obesity. Differences in study populations, menopausal status, timing of hormone exposure, and the distinction between endogenous hormone levels and exogenous hormone therapy may partly explain the heterogeneous results reported in the literature. When the relationship between serum androgens and parameters included in the Framingham risk score calculation was evaluated, DHEAS levels were significantly lower in patients with diabetes compared with those without diabetes. This finding is consistent with previous studies reporting an association between hyperinsulinemia and reduced DHEAS levels, as well as lower DHEAS concentrations in individuals with diabetes [ 36 ]. Similarly, DHEAS levels were significantly lower in patients with chronic diseases compared with those without chronic diseases. The inverse association between DHEAS levels and the presence of diabetes or other chronic conditions may suggest that reduced DHEAS levels reflect an unfavorable metabolic and clinical state. However, when age was included as a covariate in multivariable regression analyses, the associations between lower DHEAS levels and the presence of diabetes or chronic disease were no longer statistically significant, indicating that these relationships were largely driven by age-related decline in DHEAS levels. Taken together, these findings suggest that lower DHEAS levels observed in patients with diabetes or chronic diseases may primarily reflect aging rather than an independent effect of these conditions. BMI classification is traditionally used in cardiovascular risk assessment, and numerous studies have demonstrated an increased risk of cardiovascular disease and related mortality with rising BMI [ 37 , 38 ]. For example, the PROCAM study reported a positive association between BMI and established cardiovascular risk factors, including LDL cholesterol, systolic and diastolic blood pressure, and total cholesterol [ 38 ]. In line with these findings, a positive correlation between BMI and the Framingham risk score was observed in female patients in our study. However, when the overall study population was analyzed, no significant correlation was detected between BMI and the Framingham risk score. These findings support previous evidence suggesting that BMI alone may not adequately capture cardiovascular risk, whereas measures of central adiposity, such as waist circumference and waist-to-hip ratio, better reflect abdominal obesity and its association with cardiovascular risk and mortality [ 39 , 40 ]. Data from the NHANES III study demonstrated that individuals with normal BMI but abdominal obesity had a two-fold higher risk of cardiovascular disease–related mortality compared with those with similar BMI but without abdominal obesity, and even higher mortality risk than individuals classified as overweight or obese based on BMI alone [ 41 ]. Consistent with these observations, our study revealed significant positive correlations between the Framingham risk score and both waist circumference and waist-to-hip ratio in the overall patient group. Furthermore, when patients were stratified according to Framingham cardiovascular risk categories, BMI did not differ significantly across low-, intermediate-, and high-risk groups, whereas waist-to-hip ratio was significantly higher in the high-risk group compared with the low-risk group. These findings further emphasize that central fat distribution, rather than overall adiposity, may play a more critical role in cardiovascular risk stratification. Taken together, our results underscore the importance of incorporating waist circumference and waist-to-hip ratio alongside BMI for a more comprehensive assessment of cardiovascular risk in individuals with obesity. This study has several limitations that should be acknowledged. First, the majority of the study population consisted of female patients, which reflects the higher rate of female attendance at obesity clinics rather than the true sex distribution of obesity in the general population. This imbalance may limit the generalizability of the findings, particularly with respect to sex-specific analyses. Second, more than half of the patients were classified as having third-degree obesity, suggesting that individuals tend to seek medical care at more advanced stages of obesity. Therefore, the results may not be fully applicable to individuals with milder degrees of obesity or to community-based populations. In conclusion, our findings indicate that lower serum DHEAS levels are associated with higher estimated cardiovascular risk in individuals with obesity, independent of traditional metabolic risk factors when cardiovascular risk is assessed as a continuous variable. In addition, measures of central adiposity, such as waist circumference and waist-to-hip ratio, were more closely related to cardiovascular risk than BMI, underscoring the limitations of BMI as a sole marker of risk. Overall, these results suggest that incorporating hormonal parameters and indices of abdominal obesity into cardiovascular risk assessment may improve risk stratification in obese populations. Further prospective studies are warranted to clarify the causal relationships and potential clinical implications of these associations. Statements and Declarations Funding: The authors received no specific grants or fellowships for the writing of this paper. Competing interests: The authors declare no competing interests. Acknowledgements: The authos thank Dr. Fettah Sametoglu for his review of the thesis and general academic support. Author contribution: All authors contributed to the study conception and design. The study design was developed by F.A.. Data collection was performed by B.B.K.. Statistical analysis was conducted by B.B.K., and data analysis was performed by B.B.K. and F.A.. The first draft of the manuscript was written by B.B.K., and critical review and substantial revisions were provided by F.A.. All authors read and approved the final manuscript. Consent for publication: Not applicable. Clinical trial number: Not applicable. Availability of data and materials: The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request. Ethical Approval and consent to participate Our study was approved by the Academic Board of the Faculty of Medicine, Health Sciences University, with decision number 184 on March 27, 2019, and by the Clinical Research Ethics Committee of Istanbul Training and Research Hospital with decision number 1799 on April 26, 2019. The research was carried out in adherence to the ethical guidelines outlined in the Declaration of Helsinki. Due to the retrospective design of the study and the use of anonymized patient data, the requirement for informed consent was waived by the Ethics Committee. References World Health Organization. Obesity: preventing and managing the global epidemic. Report of a WHO consultation. World Health Organ Tech Rep Ser. 2000;894:1–253. Hruby A, Hu FB. The epidemiology of obesity: a big picture. Pharmacoeconomics. 2015;33(7):673–689. NCD Risk Factor Collaboration (NCD-RisC). 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Obesity and overweight. https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight. Accessed 1 Mar 2024. Nishida C, Ko GT, Kumanyika S. Body fat distribution and noncommunicable diseases in populations: overview of the 2008 WHO Expert Consultation on waist circumference and waist–hip ratio. Eur J Clin Nutr. 2010;64(1):2–5. American Diabetes Association. Classification and diagnosis of diabetes: standards of medical care in diabetes—2019. Diabetes Care. 2019;42(Suppl 1):S13–S28. Mancia G, Kreutz R, Brunström M, Burnier M, Grassi G, Januszewicz A, et al. 2023 ESH guidelines for the management of arterial hypertension. J Hypertens. 2023;41(12):1874–2071. Wu TT, Gao Y, Zheng YY, Ma YT, Xie X. Association of endogenous DHEA/DHEAS with coronary heart disease: a systematic review and meta-analysis. Clin Exp Pharmacol Physiol. 2019;46(11):984–994. Jia X, Sun C, Tang O, Gorlov I, Nambi V, Virani SS, et al. Plasma dehydroepiandrosterone sulfate and cardiovascular disease risk in older men and women. J Clin Endocrinol Metab. 2020;105(12):e4304–e4327. Zhao D, Guallar E, Ouyang P, Subramanya V, Vaidya D, Ndumele CE, et al. Endogenous sex hormones and incident cardiovascular disease in postmenopausal women. J Am Coll Cardiol. 2018;71(22):2555–2566. Khaw KT. Dehydroepiandrosterone, dehydroepiandrosterone sulphate and cardiovascular disease. J Endocrinol. 1996;150:149–153. Teixeira CJ, Veras K, de Oliveira Carvalho CR. Dehydroepiandrosterone on metabolism and the cardiovascular system in the postmenopausal period. J Mol Med (Berl). 2020;98(1):39–57. Kappert K, Böhm M, Schmieder R, Schumacher H, Teo K, Yusuf S, et al. Impact of sex on cardiovascular outcome in patients at high cardiovascular risk. Circulation. 2012;126(8):934-941. Charchar FJ, Bloomer LD, Barnes TA, Cowley MJ, Nelson CP, Wang Y, et al. Inheritance of coronary artery disease in men: an analysis of the role of the Y chromosome. 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Postmenopausal women with a history of irregular menses and elevated androgen measurements at high risk for worsening cardiovascular event-free survival: results from the National Institutes of Health-National Heart, Lung, and Blood Institute sponsored Women's Ischemia Syndrome Evaluation. J Clin Endocrinol Metab. 2008 Apr;93(4):1276-1284. Epub 2008 Jan 8. Retraction in: J Clin Endocrinol Metab. 2015;100(3):1206. Manson JE, Hsia J, Johnson KC, Rossouw JE, Assaf AR, Lasser NL, et al. Estrogen plus progestin and the risk of coronary heart disease. N Engl J Med. 2003;349(6):523-534. Stefanick ML. Estrogens and progestins: background and history, trends in use, and guidelines approved by the US Food and Drug Administration. Am J Med. 2005;118:64–73. Benn M, Voss SS, Holmegard HN, Jensen GB, Tybjærg-Hansen A, Nordestgaard BG. Extreme concentrations of endogenous sex hormones, ischemic heart disease, and death in women. Arterioscler Thromb Vasc Biol. 2015;35(2):471–477. Rexrode KM, Manson JE, Lee IM, Ridker PM, Sluss PM, Cook NR, et al. Sex hormone levels and risk of cardiovascular events in postmenopausal women. Circulation. 2003;108(14):1688–1693. Barrett-Connor E, Goodman-Gruen D. Prospective study of endogenous sex hormones and fatal cardiovascular disease in postmenopausal women. BMJ. 1995;311(7014):1193–1196. Yamaguchi Y, Tanaka S, Yamakawa T, Kimura M, Ukawa K, Yamada Y, et al. Reduced serum dehydroepiandrosterone levels in diabetic patients with hyperinsulinaemia. Clin Endocrinol (Oxf). 1998;49(3):377–383. Prospective Studies Collaboration, Whitlock G, Lewington S, Sherliker P, Clarke R, Emberson J, Halsey J, et al. Body-mass index and cause-specific mortality in 900 000 adults. Lancet. 2009;373(9669):1083-1096. Schulte H, Cullen P, Assmann G. Obesity, mortality and cardiovascular disease in the Münster Heart Study (PROCAM). Atherosclerosis. 1999; 144(1):199-209. Qiao T, Luo T, Pei H, Yimingniyazi B, Aili D, Aimudula A, et al. Association between abdominal obesity indices and risk of cardiovascular events in Chinese populations with type 2 diabetes. Cardiovasc Diabetol. 2022;21(1):225. Ren Y, Hu Q, Li Z, Zhang X, Yang L, Kong L. Dose–response association between Chinese visceral adiposity index and cardiovascular disease. Front Endocrinol (Lausanne). 2024;15:1284144. Sahakyan KR, Somers VK, Rodriguez-Escudero JP, Hodge DO, Carter RE, Sochor O, et al. Normal-weight central obesity and cardiovascular mortality. Ann Intern Med. 2015;163(11):827-835. Additional Declarations No competing interests reported. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-8702626","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":590544382,"identity":"2b91d65b-ad9d-47b2-9b7d-f2a41e5f8b72","order_by":0,"name":"Banu Betul Kocaman","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAABDklEQVRIiWNgGAWjYBACAyBmBjH4eKAi/CAioYCgFgMGNpgWyQaQFgNStBgcgInjAObsZ49JF1T8SWzjOXzww88cuzzj86sTPzwwYJDnFzuAVYtlT16a9IwzBoltvG3Jkr3bkovNbrzdLAF0mOHM2QnYHXYgx0yatw2ohZ/HjIF3G3PithtnN4C0JBjcxqHl/Bugln8QLYx/t9Unbp5xdvMPvFpugGxpADmsx4yZd9vhxA38vdvw2mI5442x9YxjxsZtPMeSpWW3HU+ccYN3m0WCgQROv5jz5xjeLqiRk+3nST748e226sT+/rObb/6osJHnl8auBQuQAKuUIFY5CPAfIEX1KBgFo2AUjAAAAEZ+XUjX1IXMAAAAAElFTkSuQmCC","orcid":"","institution":"İstanbul Eğitim ve Araştırma Hastanesi","correspondingAuthor":true,"prefix":"","firstName":"Banu","middleName":"Betul","lastName":"Kocaman","suffix":""},{"id":590544384,"identity":"4af3e577-825a-4817-8913-4797963eb978","order_by":1,"name":"Feray Akbas","email":"","orcid":"","institution":"İstanbul Eğitim ve Araştırma Hastanesi","correspondingAuthor":false,"prefix":"","firstName":"Feray","middleName":"","lastName":"Akbas","suffix":""}],"badges":[],"createdAt":"2026-01-26 17:08:33","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-8702626/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-8702626/v1","draftVersion":[],"editorialEvents":[{"content":"https://doi.org/10.1186/s12902-026-02222-0","type":"published","date":"2026-03-07T15:59:36+00:00"}],"editorialNote":"","failedWorkflow":false,"files":[{"id":104251981,"identity":"061bb63e-5bf0-4bff-a53c-36e11607994f","added_by":"auto","created_at":"2026-03-09 16:16:21","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1071915,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8702626/v1/1c617388-a67e-4732-a5fa-21483614f54b.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Association of Serum Androgen Levels With Framingham Cardiovascular Risk Score in Individuals With Obesity","fulltext":[{"header":"Introduction","content":"\u003cp\u003eObesity, which is considered as a complex and multifactorial disease that negatively affects health, is defined by the World Health Organization (WHO) based on body mass index (BMI) [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. By 2022, 2.5\u0026nbsp;billion adults aged 18 years and older were overweight, including more than 890\u0026nbsp;million living with obesity, reflecting a global trend in which the age-standardised prevalence of obesity more than doubled between 1990 and 2022 and increased across nearly all countries, affecting 94% of countries for women and all but one country for men [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eObesity is associated with a dramatic decrease in life expectancy for both men and women. It has been suggested that the steady increase in life expectancy seen in the last two centuries may end due to the increase in the prevalence of obesity [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. Many epidemiological studies have shown the relationship between obesity and mortality [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. Besides mortality, obesity is also associated with increased morbidity, and studies have shown that obesity is the number one cause of preventable disease and disability by surpassing smoking [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]. Given its versatile effects on health, it is urgently needed to take the necessary measures for the prevention, early diagnosis and treatment of obesity.\u003c/p\u003e \u003cp\u003eThe most important of obesity-related diseases are cardiovascular diseases, and obesity increases the mortality associated with cardiovascular diseases [\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. Medical, surgical, and interventional treatment methods applied after cardiovascular diseases become clinically apparent are definitive but associated with high costs. Therefore, early identification of cardiovascular disease risk and the implementation of preventive measures are of great importance.\u003c/p\u003e \u003cp\u003eVarious risk scoring systems have been developed to estimate the risk of cardiovascular diseases before they become clinically apparent, among which the Framingham Risk Score is one of the most widely used tools [\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]. The Framingham Risk Score aims to estimate the 10-year risk of cardiovascular disease using eight parameters. The parameters used in this score include major risk factors such as age, sex, and the presence of diabetes; however, recent studies have also highlighted additional factors that may increase the risk of cardiovascular disease, including serum androgen hormones. It has been revealed that serum androgen levels that change with obesity affect cardiovascular risk factors [\u003cspan additionalcitationids=\"CR11\" citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]. Many studies have shown that coronary heart disease and cardiovascular deaths are more common in men with low testosterone levels [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. However, some recent studies have revealed the possibility that high endogenous androgen levels may also increase the risk of coronary heart disease and death [\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e, \u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]. Most studies with a large number of male participants have shown that DHEAS has a negative correlation with coronary heart disease and cardiovascular disease-related mortality [\u003cspan additionalcitationids=\"CR14\" citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e]. Given the complex hormonal alterations associated with obesity, this study was designed to explore the potential contribution of serum androgen levels to cardiovascular risk assessment in individuals with obesity.\u003c/p\u003e"},{"header":"Materials and Methods","content":"\u003cp\u003e The study was conducted by retrospectively reviewing medical records of patients followed in the obesity clinic of Istanbul Training and Research Hospital over a five-year period. A total of 203 patients who met the study criteria were included. The inclusion criteria were as follows: (I) being registered and followed up in the obesity clinic within the last five years, (II) having a body mass index (BMI) of \u0026ge;\u0026thinsp;30 kg/m\u0026sup2;, and (III) being between 30 and 74 years of age. The exclusion criteria were defined as: (I) failure to meet the diagnostic criteria for obesity, (II) being younger than 30 years or older than 74 years, (III) having a diagnosis of cardiovascular diseases such as ischemic heart disease, peripheral artery disease, or cerebrovascular disease, (IV) having a history of coronary revascularization and/or carotid surgery, and (V) using medications known to affect serum androgen levels.\u003c/p\u003e \u003cp\u003eDemographic characteristics of the patients, including age, sex, smoking status, presence of chronic disease, family history, medication use, systolic and diastolic blood pressure, waist circumference (WC), hip circumference (HC), height, weight, and BMI, were obtained from obesity clinic follow-up records. Height and weight were measured according to standard protocols at the first visit, and BMI was calculated as weight (kg) divided by height squared (m\u0026sup2;) [\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e]. Waist and hip circumferences were measured using a non-elastic tape measure in the standing position, and the waist-to-hip ratio was calculated by dividing waist circumference by hip circumference [\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e]. Blood pressure was measured from the left arm in the seated position using a standardized sphygmomanometer after at least 5 minutes of rest. Patients were evaluated for cardiovascular disease using medical history, physical examination, resting electrocardiography, and echocardiography data, and individuals with suspected cardiovascular disease were excluded.\u003c/p\u003e \u003cp\u003eLaboratory data were obtained from the hospital database and recorded based on the first examination. Fasting blood glucose, insulin, HbA1c, total cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, total testosterone, DHEAS, and estradiol (female patients only) levels were documented.\u003c/p\u003e \u003cp\u003eCardiovascular risk was assessed using an eight-parameter scoring system based on the Framingham Heart Study [\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]. A 10-year cardiovascular risk score was calculated using age, sex, systolic blood pressure, antihypertensive treatment status, diabetes status, smoking status, total cholesterol, and HDL cholesterol. Only current smokers were considered smokers. The presence of diabetes was determined in two categories: patients previously diagnosed with and treated for diabetes, and/or patients who met the diagnostic criteria for diabetes according to the American Diabetes Association guidelines for the relevant period [\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e]. Hypertension was defined by the presence of systolic blood pressure above 140 mmHg or diastolic blood pressure above 90 mmHg and/or use of any anti-hypertensive drug [\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e]. Chronic disease was defined as the presence of at least one physician-diagnosed chronic condition, including diabetes mellitus, hypertension, or other chronic systemic diseases requiring ongoing medical treatment.\u003c/p\u003e \u003cp\u003ePatients were additionally stratified into three cardiovascular risk categories based on the Framingham risk score: low risk (\u0026lt;\u0026thinsp;10%), intermediate risk (10\u0026ndash;20%), and high risk (\u0026gt;\u0026thinsp;20%).\u003c/p\u003e \u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eStatistical analysis:\u003c/h2\u003e \u003cp\u003eStatistical analyses were performed using SPSS software. Continuous variables were assessed for normality using the Shapiro\u0026ndash;Wilk test. Normally distributed variables were expressed as mean\u0026thinsp;\u0026plusmn;\u0026thinsp;standard deviation, whereas non-normally distributed variables were presented as median (interquartile range). Categorical variables were expressed as frequencies and percentages.\u003c/p\u003e \u003cp\u003eComparisons between two independent groups were performed using the independent samples t-test or Mann\u0026ndash;Whitney U test, as appropriate. Comparisons among more than two groups were conducted using one-way analysis of variance (ANOVA) or the Kruskal\u0026ndash;Wallis test. When a statistically significant difference was observed in multiple-group comparisons, post-hoc pairwise analyses were performed using Bonferroni correction or Dunn\u0026rsquo;s test, as appropriate.\u003c/p\u003e \u003cp\u003eClinical, anthropometric, and laboratory parameters were compared according to diabetes status, chronic disease status, and Framingham cardiovascular risk categories.\u003c/p\u003e \u003cp\u003eCorrelations between the Framingham risk score and clinical, anthropometric, metabolic, and hormonal parameters were assessed using Spearman\u0026rsquo;s rank correlation analysis. Correlation analyses were additionally performed separately for female and male patients.\u003c/p\u003e \u003cp\u003eMultivariable linear regression analyses were conducted to evaluate whether the associations between serum DHEAS levels and diabetes or chronic disease status were independent of age. In these models, DHEAS was included as the dependent variable, and age and other clinically relevant covariates were entered as independent variables. Additional multivariable linear regression analysis was performed to assess the independent association between DHEAS and the Framingham risk score. The Framingham risk score was included as the dependent variable, and age, BMI, HbA1c, triglycerides, total cholesterol, and LDL cholesterol were included as covariates.\u003c/p\u003e \u003cp\u003eA p value\u0026thinsp;\u0026lt;\u0026thinsp;0.05 was considered statistically significant.\u003c/p\u003e \u003c/div\u003e"},{"header":"Results","content":"\u003cp\u003eA total of 203 patients, 166 (81.8%) females and 37 (18.2%) males, were included in the study. The median age of the patients was 45 years [35\u0026ndash;52], median height was 160 cm [153\u0026ndash;162], median body weight was 105 kg [92\u0026ndash;114.2], and median BMI was 40.8 kg/m\u0026sup2; [36\u0026ndash;44.5]. The median waist circumference was 120 cm [109.5\u0026ndash;127], mean hip circumference was 129.1\u0026thinsp;\u0026plusmn;\u0026thinsp;11.9 cm, and the median waist-to-hip ratio was 0.93 [0.88\u0026ndash;0.94]. When BMI was classified, 32 patients (15.8%) were in the first-degree obesity group, 61 patients (30%) were in the second-degree obesity group and 110 patients (54.2%) were in the third-degree obesity group.\u003c/p\u003e \u003cp\u003eThe clinical and laboratory characteristics, including blood pressure measurements and comorbidities, are shown in Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eLaboratory findings, blood pressure measurements, and comorbidities of patients with obesity\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"2\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eVariable\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003ePatients with obesity (n: 203)\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGlucose, mg/dL, median [IQR]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e101 [92\u0026ndash;114.2]\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHbA1c, %, median [IQR]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e5.8 [5.5\u0026ndash;6.1]\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTotal Cholesterol, mg/dL, mean\u0026thinsp;\u0026plusmn;\u0026thinsp;sd\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e210.3\u0026thinsp;\u0026plusmn;\u0026thinsp;41.5\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHDL Cholesterol, mg/dL, mean\u0026thinsp;\u0026plusmn;\u0026thinsp;sd\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e49.1\u0026thinsp;\u0026plusmn;\u0026thinsp;11.7\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLDL Cholesterol, mg/dL, mean\u0026thinsp;\u0026plusmn;\u0026thinsp;sd\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e130.3\u0026thinsp;\u0026plusmn;\u0026thinsp;35\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTriglyceride, mg/dL, median [IQR]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e138 [98.7\u0026ndash;178.2]\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTotal Testosterone, ng/dL, median [IQR]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e40.7 [24.5\u0026ndash;51]\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDHEAS, \u0026micro;g/dL, median [IQR]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e133.4 [78.9\u0026ndash;217]\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eEstradiol, pg/mL, median [IQR]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e44 [5\u0026ndash;82.2]\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eInsulin, \u0026micro;U/mL, median [IQR]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e12.4 [7.5\u0026ndash;17.5]\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eFramingham Risk Score, %, median [IQR]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e5.7 [2.2\u0026ndash;10.6]\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSystolic blood pressure, mmHg, mean\u0026thinsp;\u0026plusmn;\u0026thinsp;sd\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e121.5\u0026thinsp;\u0026plusmn;\u0026thinsp;12.1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDiastolic blood pressure, mmHg, mean\u0026thinsp;\u0026plusmn;\u0026thinsp;sd\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e77.6\u0026thinsp;\u0026plusmn;\u0026thinsp;6.6\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePresence of diabetes mellitus, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e59 (29.1%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePresence of hypertension, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e63 (31%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePresence of chronic disease, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e152 (74.9%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eThere were no significant differences in age or BMI between female and male patients (age: 41 [33.7\u0026ndash;49] vs. 42 [36\u0026ndash;51], p\u0026thinsp;=\u0026thinsp;0.067; BMI: 41 [37.3\u0026ndash;45.1] vs. 41 [40\u0026ndash;41.5] kg/m\u0026sup2;, p\u0026thinsp;=\u0026thinsp;0.393). Total testosterone and DHEAS levels, as well as Framingham risk scores, were significantly lower in female patients compared with male patients (p\u0026thinsp;=\u0026thinsp;0.006, p\u0026thinsp;=\u0026thinsp;0.001, p\u0026thinsp;=\u0026thinsp;0.017; respectively).\u003c/p\u003e \u003cp\u003eComparisons of clinical characteristics, laboratory parameters, comorbidities, lifestyle factors, and cardiovascular risk profiles between female and male patients are summarized in Table\u0026nbsp;\u003cspan refid=\"Tab2\" class=\"InternalRef\"\u003e2\u003c/span\u003e.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab2\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eComparison of clinical, laboratory, lifestyle characteristics, and cardiovascular risk profiles by sex\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"4\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eVariable\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eFemale (n: 166)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eMale (n: 37)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eP value\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHeight, cm, median [IQR]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e159 [154\u0026ndash;163]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e178 [175\u0026ndash;185]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e0.000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eWeight, kg, median [IQR]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e105 [94.5\u0026ndash;116.2]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e131 [128.5\u0026ndash;138]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e0.000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eWaist circumference, cm, mean\u0026thinsp;\u0026plusmn;\u0026thinsp;sd\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e118.1\u0026thinsp;\u0026plusmn;\u0026thinsp;11.7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e127.6\u0026thinsp;\u0026plusmn;\u0026thinsp;9.1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e0.000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHip circumference, cm, mean\u0026thinsp;\u0026plusmn;\u0026thinsp;sd\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e129.1\u0026thinsp;\u0026plusmn;\u0026thinsp;12.3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e128.7\u0026thinsp;\u0026plusmn;\u0026thinsp;10.1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.855\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eWaist / hip ratio, median [IQR]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.92 [0.88\u0026ndash;0.94]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e1.07 [1.02\u0026ndash;1.07]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e0.000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGlucose, mg/dL, median [IQR]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e101 [90.7\u0026ndash;113]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e103 [97.5\u0026ndash;103.5]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.529\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHbA1c, %, median [IQR]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e5.7 [5.4\u0026ndash;6.1]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e6.1 [5.8\u0026ndash;6.3]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.695\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTotal Cholesterol, mg/dL, mean\u0026thinsp;\u0026plusmn;\u0026thinsp;sd\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e210.9\u0026thinsp;\u0026plusmn;\u0026thinsp;40.1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e207.3\u0026thinsp;\u0026plusmn;\u0026thinsp;47.3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.627\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHDL Cholesterol, mg/dL, mean\u0026thinsp;\u0026plusmn;\u0026thinsp;sd\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e50.6\u0026thinsp;\u0026plusmn;\u0026thinsp;11.8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e42.1\u0026thinsp;\u0026plusmn;\u0026thinsp;8.5\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e0.000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLDL Cholesterol, mg/dL, mean\u0026thinsp;\u0026plusmn;\u0026thinsp;sd\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e130.7\u0026thinsp;\u0026plusmn;\u0026thinsp;33.6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e131.5\u0026thinsp;\u0026plusmn;\u0026thinsp;36.6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.897\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTriglyceride, mg/dL, median [IQR]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e118 [89\u0026ndash;154.2]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e164 [143.5\u0026ndash;165.5]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.175\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTotal Testosterone, ng/dL, median [IQR]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e36.7 [24.4\u0026ndash;50.1]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e253 [216.3\u0026ndash;327.4]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e0.000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDHEAS, \u0026micro;g/dL, median [IQR]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e141.5 [101.8\u0026ndash;246.9]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e234.7 [223.3\u0026ndash;332]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e0.001\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eInsulin, \u0026micro;U/mL, median [IQR]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e11.9 [7.3\u0026ndash;18.1]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e18.6 [15.4\u0026ndash;20.1]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e0.013\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eFramingham Risk Score, %, median [IQR]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e3.8 [1.7\u0026ndash;7.5]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e8.2 [5.7\u0026ndash;20.2]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e0.017\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePresence of diabetes mellitus, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e50 (30.1%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e9 (24.3%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.483\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePresence of hypertension, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e54 (32.5%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e9 (24.3%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.329\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePresence of chronic disease, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e126 (75.9%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e26 (70.3%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.475\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePresence of smoking, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e49 (29.5%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e17 (45.9%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.054\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDegree of obesity, first-degree / second-degree / third-degree, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e27 (16.3) / 46 (27.7) / 93 (56)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e4 (10.8) / 61 (30) / 111 (54.7)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.280\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCardiovascular risk group, low / medium / half, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e118 (71.1) / 35 (21.1) / 13 (7.8)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e20 (54.1) / 11 (29.7) / 6 (16.2)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.102\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eA significant positive correlation was observed between the Framingham risk score and age, waist circumference, waist-to-hip ratio, systolic and diastolic blood pressure, glucose, total cholesterol, LDL cholesterol, triglycerides, insulin, and HbA1c in the overall study population (p\u0026thinsp;\u0026lt;\u0026thinsp;0.05). In contrast, the Framingham risk score was negatively correlated with DHEAS, height, and estradiol levels (p\u0026thinsp;\u0026lt;\u0026thinsp;0.05). No significant correlations were found between the Framingham risk score and the remaining parameters (p\u0026thinsp;\u0026gt;\u0026thinsp;0.05). Correlations between the Framingham risk score, DHEAS, total testosterone, and other study parameters are presented in Table\u0026nbsp;\u003cspan refid=\"Tab3\" class=\"InternalRef\"\u003e3\u003c/span\u003e. Sex-stratified analyses demonstrated that the positive correlations between the Framingham risk score and age, glucose, total cholesterol, triglycerides, and HbA1c, as well as the negative correlation with DHEAS, were present in both female and male patients.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab3\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 3\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eCorrelation analysis between the Framingham Risk Score, total testosterone, DHEAS, and other clinical and laboratory parameters\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"9\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c6\" colnum=\"6\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c7\" colnum=\"7\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c8\" colnum=\"8\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c9\" colnum=\"9\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\" morerows=\"1\" rowspan=\"2\"\u003e\u0026nbsp;\u003c/th\u003e \u003cth align=\"left\" colspan=\"2\" nameend=\"c3\" namest=\"c2\"\u003e \u003cp\u003eFramingham Risk Score\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/th\u003e \u003cth align=\"left\" colspan=\"2\" nameend=\"c6\" namest=\"c5\"\u003e \u003cp\u003eTotal Testosterone\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/th\u003e \u003cth align=\"left\" colspan=\"2\" nameend=\"c9\" namest=\"c8\"\u003e \u003cp\u003eDHEAS\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003er\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003ep\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003er\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c6\"\u003e \u003cp\u003ep\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/th\u003e \u003cth align=\"left\" colname=\"c8\"\u003e \u003cp\u003er\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c9\"\u003e \u003cp\u003ep\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTotal Testosterone\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0,031\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0,657\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDHEAS\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e-0,326\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0,590\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAge\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0,780\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e-0,279\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e-0,549\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHeight\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e-0,141\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e0,045\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0,512\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e0,240\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e \u003cp\u003e\u003cb\u003e0,001\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eWeight\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e-0,009\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0,900\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0,399\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e0,264\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eWaist Circumference\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0,223\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e0,001\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0,269\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e0,132\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e \u003cp\u003e0,060\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHip Circumference\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0,043\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0,545\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0,029\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0,685\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e0,089\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e \u003cp\u003e0,209\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eWaist/Hip Ratio\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0,251\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0,327\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e0,050\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e \u003cp\u003e0,482\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eBody Mass Index\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0,077\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0,278\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0,022\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0,755\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e0,095\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e \u003cp\u003e0,179\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSystolic Blood Pressure\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0,556\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0,019\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0,791\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e-0,138\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e \u003cp\u003e\u003cb\u003e0,049\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDiastolic Blood Pressure\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0,285\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0,085\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0,229\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e-0,075\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e \u003cp\u003e0,285\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGlucose\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0,502\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e-0,136\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0,052\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e-0,206\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e \u003cp\u003e\u003cb\u003e0,003\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTotal Cholesterol\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0,413\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e-0,110\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0,117\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e-0,194\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e \u003cp\u003e\u003cb\u003e0,005\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHDL Cholesterol\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e-0,010\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0,889\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e-0,244\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e-0,123\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e \u003cp\u003e0,080\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLDL Cholesterol\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0,336\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e-0,055\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0,434\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e-0,153\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e \u003cp\u003e\u003cb\u003e0,029\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTriglyceride\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0,442\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e-0,017\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0,813\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e-0,182\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e \u003cp\u003e\u003cb\u003e0,009\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eInsulin\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0,140\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e0,048\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0,199\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e\u003cb\u003e0,005\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e0,150\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e \u003cp\u003e\u003cb\u003e0,034\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eEstradiol\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e-0,390\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0,192\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e\u003cb\u003e0,021\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e0,211\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e \u003cp\u003e\u003cb\u003e0,011\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHbA1c\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0,540\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u003cb\u003e0,000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e-0,058\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0,408\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e-0,235\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c9\"\u003e \u003cp\u003e\u003cb\u003e0,001\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"9\" nameend=\"c9\" namest=\"c1\"\u003e \u003cp\u003e\u003cem\u003eSpearman correlation analysis was performed. r: correlation coefficient.\u003c/em\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eMultivariable linear regression analysis was performed to evaluate the independent association between serum DHEAS levels and Framingham risk score. In the model adjusted for age, body mass index (BMI), HbA1c, triglycerides, total cholesterol, and LDL cholesterol, serum DHEAS levels were found to be independently associated with Framingham risk score (p\u0026thinsp;=\u0026thinsp;0.027, β = -0.126, t\u0026thinsp;=\u0026thinsp;2.224).\u003c/p\u003e \u003cp\u003ePatients with diabetes were significantly older and had higher glucose, HbA1c, triglyceride, total cholesterol, insulin levels, and Framingham risk scores compared with those without diabetes. In addition, DHEAS levels were significantly lower in patients with diabetes. Similarly, patients with chronic disease were older and exhibited higher glucose, HbA1c, and Framingham risk scores, along with lower DHEAS levels, compared with patients without chronic disease.\u003c/p\u003e \u003cp\u003eComparisons of clinical, anthropometric, and laboratory parameters according to diabetes and chronic disease status are presented in Table\u0026nbsp;\u003cspan refid=\"Tab4\" class=\"InternalRef\"\u003e4\u003c/span\u003e.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab4\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 4\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eComparison of clinical, anthropometric, and laboratory characteristics according to diabetes and chronic disease status\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"8\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c6\" colnum=\"6\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c7\" colnum=\"7\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c8\" colnum=\"8\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eVariable, median [IQR]\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eDiabetes (+) (n: 59)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eDiabetes (-) (n: 144)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003ep value\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eChronic disease (+) (n: 152)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c6\"\u003e \u003cp\u003eChronic disease (-) (n: 51)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c7\"\u003e \u003cp\u003ep value\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colspan=\"1\" nameend=\"c8\" namest=\"c8\"\u003e\u0026nbsp;\u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAge, year\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e52 [43.7\u0026ndash; 56.5]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e33 [31\u0026ndash; 39.5]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e0.000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e47 [37\u0026ndash;54]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e36 [31\u0026ndash;47]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e0.000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"1\" nameend=\"c8\" namest=\"c8\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eBMI, Kg/m\u003csup\u003e2\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e41.8 [36.6\u0026ndash; 46.4]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e40 [36\u0026ndash; 44]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.187\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e41 [36.9\u0026ndash;45.3]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e40 [35\u0026ndash;43]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e0.225\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"1\" nameend=\"c8\" namest=\"c8\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eWaist/hip ratio\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.92 [0.91\u0026ndash; 0.95]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.92 [0.88\u0026ndash; 0.94]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.171\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.92 [0.89\u0026ndash;0.94]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.92 [0.88\u0026ndash;0.96]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e0.197\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"1\" nameend=\"c8\" namest=\"c8\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGlucose, mg/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e123.5 [102.5\u0026ndash; 165.2]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e97 [89\u0026ndash; 104.7]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e0.000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e103 [94\u0026ndash;117]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e97 [89\u0026ndash;103]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e0.002\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"1\" nameend=\"c8\" namest=\"c8\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHbA1c, %\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e6.4 [5.9\u0026ndash; 7.3]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e5.6 [5.4\u0026ndash; 5.9]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e0.000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e5.9 [5.5\u0026ndash;6.2]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e5.6 [5.3\u0026ndash;5.9]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e0.001\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"1\" nameend=\"c8\" namest=\"c8\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTotal Cholesterol, mg/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e215 [193.5\u0026ndash; 240.2]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e202.5 [182\u0026ndash; 228.7]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e0.034\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e206 [184.5\u0026ndash;235.5]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e204 [182\u0026ndash;226.5]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e0.501\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"1\" nameend=\"c8\" namest=\"c8\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHDL Cholesterol, mg/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e50 [39.7\u0026ndash; 56.7]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e48 [42\u0026ndash; 57.7]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.577\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e49 [40.5\u0026ndash;50.9]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e47 [41\u0026ndash;56]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e0.584\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"1\" nameend=\"c8\" namest=\"c8\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLDL Cholesterol, mg/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e131.4 [108.1\u0026ndash; 153.9]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e126.5 [43.7\u0026ndash; 147.9]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.627\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e126.6 [106.6\u0026ndash;150.6]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e128.4 [109\u0026ndash;147.3]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e0.705\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"1\" nameend=\"c8\" namest=\"c8\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTriglyceride, mg/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e161.5 [137.2\u0026ndash; 223]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e118 [91\u0026ndash; 156.5]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e0.000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e139 [102.5\u0026ndash;182]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e121 [92.5\u0026ndash;153.5]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e0.068\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"1\" nameend=\"c8\" namest=\"c8\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTotal Testosterone, ng/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e32.1 [19.7\u0026ndash; 47.3]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e37.6 [25.1\u0026ndash; 53.7]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.191\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e36.1 [22.6\u0026ndash;48]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e42.3 [28.5\u0026ndash;61.6]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e0.223\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"1\" nameend=\"c8\" namest=\"c8\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDHEAS, \u0026micro;g/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e106.7 [67.7\u0026ndash; 160.9]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e141.5 [80.9\u0026ndash; 235.6]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e0.024\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e117.4 [67.2\u0026ndash;194.9]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e164.5 [106.3\u0026ndash;287.3]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e0.001\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"1\" nameend=\"c8\" namest=\"c8\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eEstradiol, pg/mL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e52 [43.7\u0026ndash; 56.5]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e51 [24\u0026ndash; 92.7]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e0.009\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e42 [5\u0026ndash;83.5]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e50 [22\u0026ndash;83]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e0.677\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"1\" nameend=\"c8\" namest=\"c8\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eInsulin, \u0026micro;U/mL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e13.6 [8.8\u0026ndash; 23.6]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e11.2 [7.3\u0026ndash; 16.2]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e0.007\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e11.4 [7.5\u0026ndash;18.2]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e12.5 [8.4\u0026ndash;16.4]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e0.987\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"1\" nameend=\"c8\" namest=\"c8\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eFramingham Risk Score, %\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e14.4 [8.1\u0026ndash; 19.5]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e2.9 [1.7\u0026ndash; 6.2]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e0.000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e6.3 [2.8\u0026ndash;12.9]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e2.7 [1.4\u0026ndash;4.1]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e0.000\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"1\" nameend=\"c8\" namest=\"c8\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"8\" nameend=\"c8\" namest=\"c1\"\u003e \u003cp\u003e\u003cem\u003eData are presented as median (interquartile range). p values were calculated using the Mann\u0026ndash;Whitney U test.\u003c/em\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eIn multivariable linear regression analysis adjusting for age, the association between DHEAS levels and the presence of diabetes or chronic disease was no longer statistically significant (p\u0026thinsp;\u0026gt;\u0026thinsp;0.05), indicating that the observed unadjusted differences were largely age-dependent.\u003c/p\u003e \u003cp\u003ePatients were stratified into three groups according to the Framingham risk score: low risk (\u0026lt;\u0026thinsp;10%), intermediate risk (10\u0026ndash;20%), and high risk (\u0026gt;\u0026thinsp;20%). According to the Framingham risk score, 138 patients (68.0%) were classified as low risk, 46 patients (22.7%) as intermediate risk, and 19 patients (9.4%) as high risk. Age, waist-to-hip ratio, glucose, HbA1c, total cholesterol, triglycerides, insulin levels, and the total testosterone/estradiol ratio increased progressively with higher Framingham risk categories. In contrast, DHEAS and estradiol levels decreased as cardiovascular risk increased. No significant differences were observed in BMI, HDL cholesterol, LDL cholesterol, or total testosterone among the risk groups (Table\u0026nbsp;\u003cspan refid=\"Tab5\" class=\"InternalRef\"\u003e5\u003c/span\u003e).\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab5\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 5\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eClinical and laboratory characteristics across Framingham risk groups\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"5\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eVariable, median [IQR]\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eLow risk (n: 138)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eIntermediate risk (n: 46)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eHigh risk (n: 19)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003ep\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAge, year\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e38 [33\u0026ndash;48]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e54 [50.7\u0026ndash;56.5]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e60 [55\u0026ndash;63]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u003cb\u003e0.000\u003c/b\u003e\u003csup\u003e\u003cb\u003ea\u003c/b\u003e\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eBMI, Kg/m\u003csup\u003e2\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e40 [36\u0026ndash;44]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e44 [35.8\u0026ndash;46]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e40.5 [34.8\u0026ndash;47.6]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.900\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eWaist/hip ratio\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.92 [0.88\u0026ndash;0.94]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.92 [0.89\u0026ndash;0.93]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.94 [0.91\u0026ndash;0.97]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u003cb\u003e0.014\u003c/b\u003e\u003csup\u003e\u003cb\u003eb\u003c/b\u003e\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGlucose, mg/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e98 [89\u0026ndash;106]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e127 [103.7\u0026ndash;158]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e138 [103.7\u0026ndash;209.7]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u003cb\u003e0.000\u003c/b\u003e\u003csup\u003e\u003cb\u003ec\u003c/b\u003e\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHbA1c, %\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e5.7 [5.4\u0026ndash;5.9]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e6.4 [5.9\u0026ndash;7.3]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e6.4 [5.9\u0026ndash;7.5]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u003cb\u003e0.000\u003c/b\u003e\u003csup\u003e\u003cb\u003ed\u003c/b\u003e\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTotal Cholesterol, mg/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e203.5 [182.7\u0026ndash;226.2]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e229.5 [179.2\u0026ndash;251.2]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e207.5 [193.5\u0026ndash;242.2]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u003cb\u003e0.010\u003c/b\u003e\u003csup\u003e\u003cb\u003ee\u003c/b\u003e\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHDL Cholesterol, mg/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e48 [41.7\u0026ndash;58.2]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e50 [40.7\u0026ndash;55.2]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e44 [33.7\u0026ndash;57.7]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.724\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLDL Cholesterol, mg/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e126.4 [108\u0026ndash;145.3]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e139.2 [107.1\u0026ndash;164]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e128 [105.4\u0026ndash;145.2]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.055\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTriglyceride, mg/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e121.5 [91\u0026ndash;164.7]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e148.5 [128\u0026ndash;216.2]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e174.5 [147.7\u0026ndash;228]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u003cb\u003e0.000\u003c/b\u003e\u003csup\u003e\u003cb\u003ef\u003c/b\u003e\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTotal Testosterone, ng/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e37.3 [24.7\u0026ndash;53.5]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e35.3 [21.1\u0026ndash;47]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e44.4 [19.1\u0026ndash;66.9]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.385\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDHEAS, \u0026micro;g/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e137.3 [87.5\u0026ndash;237.8]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e117.6 [76.4\u0026ndash;176.7]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e61 [37.5\u0026ndash;162]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u003cb\u003e0.003\u003c/b\u003e\u003csup\u003e\u003cb\u003eg\u003c/b\u003e\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eEstradiol, pg/mL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e56.5 [24\u0026ndash;94.2]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e25 [5\u0026ndash;50.5]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e5 [\u003cspan additionalcitationids=\"CR6 CR7 CR8 CR9 CR10 CR11 CR12 CR13 CR14 CR15 CR16 CR17 CR18 CR19 CR20 CR21 CR22 CR23 CR24 CR25 CR26 CR27 CR28 CR29\" citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR30\" class=\"CitationRef\"\u003e30\u003c/span\u003e]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u003cb\u003e0.001\u003c/b\u003e\u003csup\u003e\u003cb\u003eh\u003c/b\u003e\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eInsulin, \u0026micro;U/mL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e11.4 [7.5\u0026ndash;16.6]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e10.9 [6.8\u0026ndash;13.9]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e24.7 [17.8\u0026ndash;35.3]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u003cb\u003e0.005\u003c/b\u003e\u003csup\u003e\u003cb\u003ei\u003c/b\u003e\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eFramingham Risk Score, %\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e3.2 [1.7\u0026ndash;6.1]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e15 [12.1\u0026ndash;17.7]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e28.7 [24.2\u0026ndash; 39.4]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u003cb\u003e0.000\u003c/b\u003e\u003csup\u003e\u003cb\u003ej\u003c/b\u003e\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"5\" nameend=\"c5\" namest=\"c1\"\u003e \u003cp\u003e\u003cb\u003ea\u003c/b\u003e: Significant post-hoc difference: low vs intermediate risk (p\u0026thinsp;=\u0026thinsp;0.000) and low vs high risk (p\u0026thinsp;=\u0026thinsp;0.000), \u003cb\u003eb\u003c/b\u003e: Significant post-hoc difference: low vs high risk (p\u0026thinsp;=\u0026thinsp;0.016), \u003cb\u003ec\u003c/b\u003e: Significant post-hoc difference: low vs intermediate risk (p\u0026thinsp;=\u0026thinsp;0.000) and low vs high risk (p\u0026thinsp;=\u0026thinsp;0.000), \u003cb\u003ed\u003c/b\u003e: Significant post-hoc difference: low vs intermediate risk (p\u0026thinsp;=\u0026thinsp;0.000) and low vs high risk (p\u0026thinsp;=\u0026thinsp;0.000), \u003cb\u003ee\u003c/b\u003e: Significant post-hoc difference: low vs intermediate risk (p\u0026thinsp;=\u0026thinsp;0.019), \u003cb\u003ef\u003c/b\u003e: Significant post-hoc difference: low vs intermediate risk (p\u0026thinsp;=\u0026thinsp;0.026) and low vs high risk (p\u0026thinsp;=\u0026thinsp;0.001), \u003cb\u003eg\u003c/b\u003e: Significant post-hoc difference: low vs high risk (p\u0026thinsp;=\u0026thinsp;0.008), \u003cb\u003eh\u003c/b\u003e: Significant post-hoc difference: low vs high risk (p\u0026thinsp;=\u0026thinsp;0.003), \u003cb\u003ei\u003c/b\u003e: Significant post-hoc difference: low vs high risk (p\u0026thinsp;=\u0026thinsp;0.009) and intermediate vs high risk (p\u0026thinsp;=\u0026thinsp;0.005), \u003cb\u003ej\u003c/b\u003e: Significant post-hoc difference: low vs high risk (p\u0026thinsp;=\u0026thinsp;0.003), \u003cb\u003ek\u003c/b\u003e: Significant post-hoc difference: low vs high risk (p\u0026thinsp;=\u0026thinsp;0.001).\u003c/p\u003e \u003cp\u003e\u003cem\u003eData are presented as median (interquartile range). Overall comparisons were performed using the Kruskal\u0026ndash;Wallis test with post-hoc pairwise analyses.\u003c/em\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eIn this study, we investigated the relationship between serum androgen levels and estimated 10 year cardiovascular risk assessed by the Framingham risk score in individuals with obesity. We found that serum DHEAS levels were inversely associated with the Framingham risk score in the overall cohort as well as in both sexes, and this association remained significant after adjustment for major metabolic risk factors when cardiovascular risk was analyzed as a continuous variable. In addition, DHEAS and estradiol levels decreased progressively across increasing Framingham risk categories, whereas BMI and total testosterone did not differ among risk groups. Measures of central adiposity, including waist circumference and waist-to-hip ratio, showed stronger associations with cardiovascular risk than BMI. Although DHEAS levels were lower in patients with diabetes and chronic diseases, these associations were largely explained by age-related decline. Overall, these findings suggest that hormonal alterations, particularly reduced DHEAS levels, may be linked to cardiovascular risk burden in obesity, while highlighting the importance of central adiposity over general obesity in cardiovascular risk stratification.\u003c/p\u003e \u003cp\u003eIn our study, serum DHEAS levels were associated with the estimated 10-year cardiovascular risk calculated using the Framingham risk score. DHEAS showed a significant inverse correlation with the Framingham risk score in the overall cohort as well as in both sexes. This finding suggests that lower DHEA-S levels in individuals with obesity may be accompanied by a less favorable cardiovascular risk profile. To further explore this relationship, patients were categorized into low-, intermediate-, and high-risk groups according to their Framingham risk scores. Consistent with the correlation analyses, DHEAS levels were significantly lower in the high-risk group compared with the low-risk group. However, given the complex interplay between adrenal androgens, aging, and metabolic factors, the direction and strength of this association may change after multivariable adjustment. In our study, DHEAS levels remained independently and statistically significantly associated with the Framingham risk score in a multivariable linear regression model including age, body mass index, HbA1c, triglycerides, total cholesterol, and LDL cholesterol. This result suggests that DHEAS may provide additional information for cardiovascular risk assessment in an obese population beyond traditional metabolic risk markers.\u003c/p\u003e \u003cp\u003eThe literature regarding the association between DHEAS and cardiovascular outcomes is heterogeneous. Most cross-sectional studies and prospective studies predominantly including male participants have reported an inverse relationship between DHEA-S levels and coronary heart disease as well as cardiovascular mortality [\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e, \u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e]. Consistent with these findings, a systematic review and meta-analysis by Wu et al., including studies published up to 2017, demonstrated significantly lower DHEAS levels in individuals with coronary heart disease compared with healthy controls [\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e]. In contrast, a large community-based prospective cohort study of older adults reported that low DHEAS levels were associated with an increased risk of hospitalization for heart failure and all-cause mortality, while no independent association with the incidence of coronary heart disease was observed [\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e]. Similarly, in a prospective study by Zhao et al. involving postmenopausal women, DHEA levels were not associated with overall cardiovascular events; however, inverse associations were observed in women with heart failure with reduced ejection fraction and in postmenopausal women younger than 65 years [\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e]. These findings have led to the hypothesis that the role of DHEAS in cardiovascular risk may be age- and phenotype-dependent. Notably, in our study, the significant inverse association between DHEAS levels and the Framingham risk score persisted even after adjustment for age, suggesting that DHEAS may reflect an earlier, subclinical stage of cardiovascular risk prior to the development of clinically overt cardiovascular events.\u003c/p\u003e \u003cp\u003eAlthough some studies have suggested that DHEAS supplementation may confer various physiological benefits, including the prevention of cardiovascular disease in older individuals, a comprehensive review by Teixeira et al. emphasized that the metabolic and cardiovascular effects of DHEA are highly dependent on dosage, menopausal status, and the individual\u0026rsquo;s underlying metabolic profile, underscoring the need for caution in its therapeutic use [\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e, \u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e]. In contrast to interventional studies with heterogeneous outcomes, our findings reflect the association between endogenous DHEAS levels and cardiovascular risk, supporting its potential role as a biomarker rather than a therapeutic agent.\u003c/p\u003e \u003cp\u003eIn our study, total testosterone and DHEAS levels were significantly lower in female patients compared with male patients, which is consistent with the well-established sex differences in circulating androgen levels. In parallel, the Framingham risk score was also significantly lower in females than in males. Male sex has long been recognized as an independent risk factor for cardiovascular disease\u0026ndash;related morbidity and mortality, and our findings are in line with previous large-scale studies. For instance, the TRANSCEND and ONTARGET trials reported approximately 20% lower cardiovascular risk for women than for men across all cardiovascular endpoints [\u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eSex-related differences in cardiovascular risk have been extensively investigated, and multiple biological and behavioral mechanisms have been proposed. Among these, differences in sex hormone profiles, particularly androgens, have attracted considerable attention [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. While some studies have suggested that the increased cardiovascular risk observed in men may be partly related to genetic factors such as Y chromosome linked mechanisms [\u003cspan citationid=\"CR26\" class=\"CitationRef\"\u003e26\u003c/span\u003e], others have emphasized the contribution of sex-specific behaviors, visceral fat distribution, metabolic characteristics, and age-related vascular and myocardial adaptations [\u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eMost studies examining the relationship between testosterone levels and cardiovascular disease have reported higher rates of coronary heart disease and cardiovascular mortality in men with low testosterone levels, suggesting that testosterone may serve as a biomarker of poor cardiovascular health [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e, \u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e]. However, the causal nature of this association remains unclear, and conflicting findings have also been reported. Several studies have shown no significant association between testosterone levels and cardiovascular mortality, while others have suggested that elevated endogenous androgen levels may also be associated with an increased risk of coronary heart disease [\u003cspan citationid=\"CR29\" class=\"CitationRef\"\u003e29\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eIn the present study, no significant correlation was observed between total testosterone levels and the Framingham risk score, either in the overall cohort or when analyses were stratified by sex. These findings support the notion that the relationship between testosterone and cardiovascular risk is complex and context dependent. The heterogeneous effects of testosterone on individual cardiovascular risk factors, differences between endogenous and exogenous testosterone exposure, and the influence of testosterone metabolites may all contribute to the inconsistent results observed across studies [\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e, \u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]. Moreover, conditions characterized by hyperandrogenemia, such as polycystic ovary syndrome, have also been associated with increased cardiovascular risk, further underscoring the multifaceted role of androgens in cardiovascular pathophysiology [\u003cspan citationid=\"CR30\" class=\"CitationRef\"\u003e30\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eWhen the relationship between estradiol levels and cardiovascular risk was evaluated in female patients, a significant inverse correlation was observed between serum estradiol levels and the Framingham risk score. In addition, in analyses stratified by Framingham risk categories, estradiol levels were significantly lower in the high-risk group compared with the low-risk group. Traditionally, estrogens have been considered protective against cardiovascular disease; however, evidence accumulated over the past two decades has challenged this paradigm [\u003cspan citationid=\"CR31\" class=\"CitationRef\"\u003e31\u003c/span\u003e, \u003cspan citationid=\"CR32\" class=\"CitationRef\"\u003e32\u003c/span\u003e]. Large randomized trials, particularly the Women\u0026rsquo;s Health Initiative, demonstrated that combined estrogen\u0026ndash;progestin therapy does not confer cardiovascular protection and may even increase the risk of coronary heart disease, especially during the early postmenopausal period [\u003cspan citationid=\"CR31\" class=\"CitationRef\"\u003e31\u003c/span\u003e, \u003cspan citationid=\"CR32\" class=\"CitationRef\"\u003e32\u003c/span\u003e]. These findings have led to a substantial decline in the use of postmenopausal hormone therapy and the development of alternative treatment strategies.\u003c/p\u003e \u003cp\u003eObservational studies evaluating endogenous estradiol levels and cardiovascular risk have yielded inconsistent results. A population-based study from Denmark reported that lower estradiol levels were associated with an increased risk of coronary heart disease and mortality [\u003cspan citationid=\"CR33\" class=\"CitationRef\"\u003e33\u003c/span\u003e]. In contrast, some studies have found no significant association between estradiol levels and cardiovascular events [\u003cspan citationid=\"CR34\" class=\"CitationRef\"\u003e34\u003c/span\u003e, \u003cspan citationid=\"CR35\" class=\"CitationRef\"\u003e35\u003c/span\u003e]. In this context, our findings suggest that lower endogenous estradiol levels may be associated with a less favorable cardiovascular risk profile in women with obesity. Differences in study populations, menopausal status, timing of hormone exposure, and the distinction between endogenous hormone levels and exogenous hormone therapy may partly explain the heterogeneous results reported in the literature.\u003c/p\u003e \u003cp\u003eWhen the relationship between serum androgens and parameters included in the Framingham risk score calculation was evaluated, DHEAS levels were significantly lower in patients with diabetes compared with those without diabetes. This finding is consistent with previous studies reporting an association between hyperinsulinemia and reduced DHEAS levels, as well as lower DHEAS concentrations in individuals with diabetes [\u003cspan citationid=\"CR36\" class=\"CitationRef\"\u003e36\u003c/span\u003e]. Similarly, DHEAS levels were significantly lower in patients with chronic diseases compared with those without chronic diseases. The inverse association between DHEAS levels and the presence of diabetes or other chronic conditions may suggest that reduced DHEAS levels reflect an unfavorable metabolic and clinical state. However, when age was included as a covariate in multivariable regression analyses, the associations between lower DHEAS levels and the presence of diabetes or chronic disease were no longer statistically significant, indicating that these relationships were largely driven by age-related decline in DHEAS levels. Taken together, these findings suggest that lower DHEAS levels observed in patients with diabetes or chronic diseases may primarily reflect aging rather than an independent effect of these conditions.\u003c/p\u003e \u003cp\u003eBMI classification is traditionally used in cardiovascular risk assessment, and numerous studies have demonstrated an increased risk of cardiovascular disease and related mortality with rising BMI [\u003cspan citationid=\"CR37\" class=\"CitationRef\"\u003e37\u003c/span\u003e, \u003cspan citationid=\"CR38\" class=\"CitationRef\"\u003e38\u003c/span\u003e]. For example, the PROCAM study reported a positive association between BMI and established cardiovascular risk factors, including LDL cholesterol, systolic and diastolic blood pressure, and total cholesterol [\u003cspan citationid=\"CR38\" class=\"CitationRef\"\u003e38\u003c/span\u003e]. In line with these findings, a positive correlation between BMI and the Framingham risk score was observed in female patients in our study. However, when the overall study population was analyzed, no significant correlation was detected between BMI and the Framingham risk score. These findings support previous evidence suggesting that BMI alone may not adequately capture cardiovascular risk, whereas measures of central adiposity, such as waist circumference and waist-to-hip ratio, better reflect abdominal obesity and its association with cardiovascular risk and mortality [\u003cspan citationid=\"CR39\" class=\"CitationRef\"\u003e39\u003c/span\u003e, \u003cspan citationid=\"CR40\" class=\"CitationRef\"\u003e40\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eData from the NHANES III study demonstrated that individuals with normal BMI but abdominal obesity had a two-fold higher risk of cardiovascular disease\u0026ndash;related mortality compared with those with similar BMI but without abdominal obesity, and even higher mortality risk than individuals classified as overweight or obese based on BMI alone [\u003cspan citationid=\"CR41\" class=\"CitationRef\"\u003e41\u003c/span\u003e]. Consistent with these observations, our study revealed significant positive correlations between the Framingham risk score and both waist circumference and waist-to-hip ratio in the overall patient group.\u003c/p\u003e \u003cp\u003eFurthermore, when patients were stratified according to Framingham cardiovascular risk categories, BMI did not differ significantly across low-, intermediate-, and high-risk groups, whereas waist-to-hip ratio was significantly higher in the high-risk group compared with the low-risk group. These findings further emphasize that central fat distribution, rather than overall adiposity, may play a more critical role in cardiovascular risk stratification. Taken together, our results underscore the importance of incorporating waist circumference and waist-to-hip ratio alongside BMI for a more comprehensive assessment of cardiovascular risk in individuals with obesity.\u003c/p\u003e \u003cp\u003eThis study has several limitations that should be acknowledged. First, the majority of the study population consisted of female patients, which reflects the higher rate of female attendance at obesity clinics rather than the true sex distribution of obesity in the general population. This imbalance may limit the generalizability of the findings, particularly with respect to sex-specific analyses. Second, more than half of the patients were classified as having third-degree obesity, suggesting that individuals tend to seek medical care at more advanced stages of obesity. Therefore, the results may not be fully applicable to individuals with milder degrees of obesity or to community-based populations.\u003c/p\u003e \u003cp\u003eIn conclusion, our findings indicate that lower serum DHEAS levels are associated with higher estimated cardiovascular risk in individuals with obesity, independent of traditional metabolic risk factors when cardiovascular risk is assessed as a continuous variable. In addition, measures of central adiposity, such as waist circumference and waist-to-hip ratio, were more closely related to cardiovascular risk than BMI, underscoring the limitations of BMI as a sole marker of risk. Overall, these results suggest that incorporating hormonal parameters and indices of abdominal obesity into cardiovascular risk assessment may improve risk stratification in obese populations. Further prospective studies are warranted to clarify the causal relationships and potential clinical implications of these associations.\u003c/p\u003e"},{"header":"Statements and Declarations","content":"\u003cp\u003e\u003cstrong\u003eFunding:\u003c/strong\u003e The authors received no specific grants or fellowships for the writing of this paper.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests:\u0026nbsp;\u003c/strong\u003eThe authors declare no competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements:\u0026nbsp;\u003c/strong\u003eThe authos thank Dr. Fettah Sametoglu for his review of the thesis and general academic support.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor contribution:\u0026nbsp;\u003c/strong\u003eAll authors contributed to the study conception and design. The study design was developed by F.A.. Data collection was performed by B.B.K.. Statistical analysis was conducted by B.B.K., and data analysis was performed by B.B.K. and F.A.. The first draft of the manuscript was written by B.B.K., and critical review and substantial revisions were provided by F.A.. All authors read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication:\u0026nbsp;\u003c/strong\u003eNot applicable.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eClinical trial number:\u0026nbsp;\u003c/strong\u003eNot applicable.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials:\u0026nbsp;\u003c/strong\u003eThe datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthical Approval\u0026nbsp;\u003c/strong\u003e\u003cstrong\u003eand consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eOur study was approved by the Academic Board of the Faculty of Medicine, Health Sciences University, with decision number 184 on March 27, 2019, and by the Clinical Research Ethics Committee of Istanbul Training and Research Hospital with decision number 1799 on April 26, 2019. The research was carried out in adherence to the ethical guidelines outlined in the Declaration of Helsinki. Due to the retrospective design of the study and the use of anonymized patient data, the requirement for informed consent was waived by the Ethics Committee.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eWorld Health Organization. Obesity: preventing and managing the global epidemic. Report of a WHO consultation. World Health Organ Tech Rep Ser. 2000;894:1\u0026ndash;253.\u003c/li\u003e\n\u003cli\u003eHruby A, Hu FB. The epidemiology of obesity: a big picture. Pharmacoeconomics. 2015;33(7):673\u0026ndash;689.\u003c/li\u003e\n\u003cli\u003eNCD Risk Factor Collaboration (NCD-RisC). Worldwide trends in underweight and obesity from 1990 to 2022: a pooled analysis of 3663 population-representative studies with 222 million children, adolescents, and adults. 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J Am Coll Cardiol. 2014;64(17):1801-1810.\u003c/li\u003e\n\u003cli\u003eSanders JL, Boudreau RM, Cappola AR, Arnold AM, Robbins J, Cushman M, et al. Cardiovascular disease is associated with greater incident dehydroepiandrosterone sulfate decline in the oldest old. J Am Geriatr Soc. 2010;58(3):421-426.\u003c/li\u003e\n\u003cli\u003eWorld Health Organization. Obesity and overweight. https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight. Accessed 1 Mar 2024.\u003c/li\u003e\n\u003cli\u003eNishida C, Ko GT, Kumanyika S. Body fat distribution and noncommunicable diseases in populations: overview of the 2008 WHO Expert Consultation on waist circumference and waist\u0026ndash;hip ratio. Eur J Clin Nutr. 2010;64(1):2\u0026ndash;5.\u003c/li\u003e\n\u003cli\u003eAmerican Diabetes Association. Classification and diagnosis of diabetes: standards of medical care in diabetes\u0026mdash;2019. Diabetes Care. 2019;42(Suppl 1):S13\u0026ndash;S28.\u003c/li\u003e\n\u003cli\u003eMancia G, Kreutz R, Brunstr\u0026ouml;m M, Burnier M, Grassi G, Januszewicz A, et al. 2023 ESH guidelines for the management of arterial hypertension. J Hypertens. 2023;41(12):1874\u0026ndash;2071.\u003c/li\u003e\n\u003cli\u003eWu TT, Gao Y, Zheng YY, Ma YT, Xie X. Association of endogenous DHEA/DHEAS with coronary heart disease: a systematic review and meta-analysis. Clin Exp Pharmacol Physiol. 2019;46(11):984\u0026ndash;994.\u003c/li\u003e\n\u003cli\u003eJia X, Sun C, Tang O, Gorlov I, Nambi V, Virani SS, et al. Plasma dehydroepiandrosterone sulfate and cardiovascular disease risk in older men and women. J Clin Endocrinol Metab. 2020;105(12):e4304\u0026ndash;e4327.\u003c/li\u003e\n\u003cli\u003eZhao D, Guallar E, Ouyang P, Subramanya V, Vaidya D, Ndumele CE, et al. Endogenous sex hormones and incident cardiovascular disease in postmenopausal women. J Am Coll Cardiol. 2018;71(22):2555\u0026ndash;2566.\u003c/li\u003e\n\u003cli\u003eKhaw KT. Dehydroepiandrosterone, dehydroepiandrosterone sulphate and cardiovascular disease. J Endocrinol. 1996;150:149\u0026ndash;153.\u003c/li\u003e\n\u003cli\u003eTeixeira CJ, Veras K, de Oliveira Carvalho CR. Dehydroepiandrosterone on metabolism and the cardiovascular system in the postmenopausal period. J Mol Med (Berl). 2020;98(1):39\u0026ndash;57.\u003c/li\u003e\n\u003cli\u003eKappert K, B\u0026ouml;hm M, Schmieder R, Schumacher H, Teo K, Yusuf S, et al. Impact of sex on cardiovascular outcome in patients at high cardiovascular risk. Circulation. 2012;126(8):934-941.\u003c/li\u003e\n\u003cli\u003eCharchar FJ, Bloomer LD, Barnes TA, Cowley MJ, Nelson CP, Wang Y, et al. Inheritance of coronary artery disease in men: an analysis of the role of the Y chromosome. Lancet. 2012;379(9819):915-922.\u003c/li\u003e\n\u003cli\u003eHayward CS, Kelly RP, Collins P. The roles of gender, the menopause and hormone replacement on cardiovascular function. Cardiovasc Res. 2000;46:28\u0026ndash;49.\u003c/li\u003e\n\u003cli\u003eYeap BB, Marriott RJ, Dwivedi G, Adams RJ, Antonio L, Ballantyne CM, et al. Associations of testosterone and related hormones with all-cause and cardiovascular mortality and incident cardiovascular disease in men. Ann Intern Med. 2024;177(6):768\u0026ndash;781.\u003c/li\u003e\n\u003cli\u003eHaring R, Teng Z, Xanthakis V, Coviello A, Sullivan L, Bhasin S, et al. Association of sex steroids, gonadotrophins, and their trajectories with clinical cardiovascular disease and all-cause mortality in elderly men. Clin Endocrinol (Oxf). 2013;78:629\u0026ndash;634.\u003c/li\u003e\n\u003cli\u003eShaw LJ, Bairey Merz CN, Azziz R, Stanczyk FZ, Sopko G, Braunstein GD, et al. Postmenopausal women with a history of irregular menses and elevated androgen measurements at high risk for worsening cardiovascular event-free survival: results from the National Institutes of Health-National Heart, Lung, and Blood Institute sponsored Women\u0026apos;s Ischemia Syndrome Evaluation. J Clin Endocrinol Metab. 2008 Apr;93(4):1276-1284. Epub 2008 Jan 8. Retraction in: J Clin Endocrinol Metab. 2015;100(3):1206.\u003c/li\u003e\n\u003cli\u003eManson JE, Hsia J, Johnson KC, Rossouw JE, Assaf AR, Lasser NL, et al. Estrogen plus progestin and the risk of coronary heart disease. N Engl J Med. 2003;349(6):523-534.\u003c/li\u003e\n\u003cli\u003eStefanick ML. Estrogens and progestins: background and history, trends in use, and guidelines approved by the US Food and Drug Administration. Am J Med. 2005;118:64\u0026ndash;73.\u003c/li\u003e\n\u003cli\u003eBenn M, Voss SS, Holmegard HN, Jensen GB, Tybj\u0026aelig;rg-Hansen A, Nordestgaard BG. Extreme concentrations of endogenous sex hormones, ischemic heart disease, and death in women. Arterioscler Thromb Vasc Biol. 2015;35(2):471\u0026ndash;477.\u003c/li\u003e\n\u003cli\u003eRexrode KM, Manson JE, Lee IM, Ridker PM, Sluss PM, Cook NR, et al. Sex hormone levels and risk of cardiovascular events in postmenopausal women. Circulation. 2003;108(14):1688\u0026ndash;1693.\u003c/li\u003e\n\u003cli\u003eBarrett-Connor E, Goodman-Gruen D. Prospective study of endogenous sex hormones and fatal cardiovascular disease in postmenopausal women. BMJ. 1995;311(7014):1193\u0026ndash;1196.\u003c/li\u003e\n\u003cli\u003eYamaguchi Y, Tanaka S, Yamakawa T, Kimura M, Ukawa K, Yamada Y, et al. Reduced serum dehydroepiandrosterone levels in diabetic patients with hyperinsulinaemia. Clin Endocrinol (Oxf). 1998;49(3):377\u0026ndash;383.\u003c/li\u003e\n\u003cli\u003eProspective Studies Collaboration, Whitlock G, Lewington S, Sherliker P, Clarke R, Emberson J, Halsey J, et al. Body-mass index and cause-specific mortality in 900 000 adults. Lancet. 2009;373(9669):1083-1096.\u003c/li\u003e\n\u003cli\u003eSchulte H, Cullen P, Assmann G. Obesity, mortality and cardiovascular disease in the M\u0026uuml;nster Heart Study (PROCAM). Atherosclerosis. 1999; 144(1):199-209.\u003c/li\u003e\n\u003cli\u003eQiao T, Luo T, Pei H, Yimingniyazi B, Aili D, Aimudula A, et al. Association between abdominal obesity indices and risk of cardiovascular events in Chinese populations with type 2 diabetes. Cardiovasc Diabetol. 2022;21(1):225.\u003c/li\u003e\n\u003cli\u003eRen Y, Hu Q, Li Z, Zhang X, Yang L, Kong L. Dose\u0026ndash;response association between Chinese visceral adiposity index and cardiovascular disease. Front Endocrinol (Lausanne). 2024;15:1284144.\u003c/li\u003e\n\u003cli\u003eSahakyan KR, Somers VK, Rodriguez-Escudero JP, Hodge DO, Carter RE, Sochor O, et al. Normal-weight central obesity and cardiovascular mortality. Ann Intern Med. 2015;163(11):827-835.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-endocrine-disorders","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bend","sideBox":"Learn more about [BMC Endocrine Disorders](http://bmcendocrdisord.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bend/default.aspx","title":"BMC Endocrine Disorders","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Obesity, cardiovascular risk, Framingham Risk Score, DHEAS, androgen hormones","lastPublishedDoi":"10.21203/rs.3.rs-8702626/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8702626/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eObesity is strongly associated with increased cardiovascular morbidity and mortality. Although traditional risk factors are incorporated into widely used cardiovascular risk scores such as the Framingham Risk Score, hormonal alterations accompanying obesity, particularly changes in serum androgen levels, may also contribute to cardiovascular risk. This study aimed to investigate the relationship between serum androgen levels and estimated 10-year cardiovascular risk in individuals with obesity.\u003c/p\u003e\u003ch2\u003eMethods\u003c/h2\u003e \u003cp\u003eThis retrospective study included 203 adults with obesity followed in an obesity clinic over a five-year period. Demographic, anthropometric, clinical, and laboratory data were collected. Cardiovascular risk was assessed using the Framingham Risk Score, and patients were stratified into low, intermediate, and high risk categories. Associations between hormonal parameters and cardiovascular risk were evaluated using correlation analyses and multivariable linear regression models adjusted for major metabolic risk factors.\u003c/p\u003e\u003ch2\u003eResults\u003c/h2\u003e \u003cp\u003eSerum dehydroepiandrosterone sulfate (DHEAS) levels showed a significant inverse correlation with the Framingham Risk Score in the overall cohort and in both sexes (p\u0026thinsp;\u0026lt;\u0026thinsp;0.05). In multivariable linear regression analysis adjusted for age, body mass index, HbA1c, triglycerides, total cholesterol, and LDL cholesterol, DHEAS levels remained independently associated with the Framingham Risk Score (p\u0026thinsp;=\u0026thinsp;0.027). DHEAS and estradiol levels decreased across increasing cardiovascular risk categories, whereas body mass index and total testosterone did not differ among risk groups. Measures of central adiposity, including waist circumference and waist-to-hip ratio, demonstrated stronger associations with cardiovascular risk than body mass index.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003eLower serum DHEAS levels are associated with higher estimated cardiovascular risk in individuals with obesity, independent of traditional metabolic risk factors when cardiovascular risk is assessed as a continuous variable. Central adiposity measures appear to be more informative than body mass index for cardiovascular risk stratification. Incorporating hormonal parameters and indices of abdominal obesity may enhance cardiovascular risk assessment in obese populations.\u003c/p\u003e","manuscriptTitle":"Association of Serum Androgen Levels With Framingham Cardiovascular Risk Score in Individuals With Obesity","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-02-13 05:25:46","doi":"10.21203/rs.3.rs-8702626/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision 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