Type 2 diabetes mellitus (T2DM) is a prevalent metabolic disorder characterized by insulin resistance and insufficient insulin secretion, leading to chronic hyperglycemia (1). Global projections indicate that the number of individuals with diabetes will rise to approximately 300 million by 2025 and 693 million by 2045 (2). T2DM is frequently accompanied by a spectrum of complications that adversely affect multiple organ systems, including the cardiovascular system, eyes, kidneys, endocrine glands, and peripheral nerves (3–7). Moreover, T2DM is associated with an increased risk of cognitive impairment and emotional disorders (4–8). These complications contribute to elevated healthcare costs, reduced quality of life, and increased mortality (9). Consequently, the prevention and management of T2DM-related complications warrant significant clinical attention.

Erectile dysfunction (ED) is defined as the persistent inability to attain or maintain a penile erection sufficient for satisfactory sexual performance (10). Current evidence indicates that ED affects over 150 million men globally, with projections suggesting this figure may reach 322 million by 2025 (11). Multiple etiological factors contribute to ED, including vascular diseases, obesity, smoking, metabolic syndrome, hyperlipidemia, depression, medication side effects, diabetes mellitus, and neurological disorders (12, 13). Among these, T2DM is recognized as an independent risk factor for ED, with pathogenesis involving several interrelated mechanisms (14). The condition is commonly diagnosed using the widely adopted International Index of Erectile Function-5 (IIEF-5) questionnaire (15). According to the IIEF-5 scoring system, a score ≤21 indicates the presence of ED, with further stratification into mild (12–21), moderate (8–11), and severe (0–7) categories, while a score of 22–25 suggests normal erectile function (16, 17). ED substantially impairs men’s quality of life and self-esteem (18) and poses a considerable economic burden on healthcare systems.

Beyond its status as an independent risk factor, the association between T2DM and ED is underpinned by a complex, multifactorial pathophysiology that merits further investigation (19, 20). Chronic hyperglycemia, a hallmark of T2DM, initiates a cascade of deleterious processes (21). It promotes the formation and accumulation of advanced glycation end products (AGEs) in vascular and neural tissues, leading to endothelial dysfunction (22) and reduced bioavailability of nitric oxide (NO)—a key mediator of penile vasodilation (23). Concurrently, hyperglycemia-induced oxidative stress and chronic low-grade inflammation exacerbate endothelial and neural damage (24). Insulin resistance, another central feature of T2DM, further aggravates this process by promoting both macrovascular and microvascular complications, such as atherosclerosis and microangiopathy, which impede blood flow to the corpora cavernosa (25). Additionally, diabetic autonomic neuropathy can disrupt the intricate neural signaling essential for initiating and sustaining an erection (26). Together, these vascular, neurological, and endothelial impairments create a pathophysiological ‘perfect storm’ that fosters ED in T2DM patients, positioning ED not merely as a complication but as a potential sentinel marker of underlying systemic vasculopathy (27).

The influence of psychological comorbidities—particularly anxiety and depression—on the development and progression of ED in individuals with diabetes represents a critical yet frequently overlooked dimension in clinical management (28). T2DM itself constitutes a chronic stressor, imposing a significant psychological burden related to daily self-management demands, fears of complications, and lifestyle adjustments (29). Such psychological distress may directly contribute to ED via neuroendocrine pathways, including chronic activation of the hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system, resulting in elevated cortisol and catecholamine levels (30). These hormones can induce peripheral vasoconstriction, inhibit NO synthesis, and diminish sexual desire (31). Conversely, the onset of ED can be psychologically distressing, leading to performance anxiety, diminished self-esteem, interpersonal strain, and social withdrawal, which may further compromise glycemic control through poor treatment adherence and maladaptive coping behaviors (32). This interaction establishes a vicious, self-perpetuating cycle wherein suboptimal metabolic health exacerbates ED, ED heightens psychological distress, and psychological distress, in turn, worsens metabolic control (33). Elucidating this bidirectional relationship is therefore essential for developing integrated, patient-centered interventions aimed at breaking this cycle.

Given the substantial clinical and psychosocial impact of ED in T2DM, focused attention on this patient subgroup is imperative. In particular, systematic screening using instruments such as the IIEF-5 questionnaire, even before overt symptoms emerge, is of great importance (34). Early detection of ED and prompt intervention targeting modifiable risk factors can significantly alleviate both individual suffering and the broader societal burden (35). Accordingly, this study was designed as a cross-sectional, single-center investigation to evaluate the prevalence, associated risk factors, and clinical correlates of ED in male patients with T2DM.

In this study, a single center, cross-sectional survey was conducted on the probability of developing ED in 208 male T2DM patients. The relationship between ED and related clinical indicators, as well as risk factors, were analyzed. The findings showed that mild ED was more common in T2DM patients, while moderate and severe ED were less common. T2DMED patients were older, with higher PEDT scores and diabetic vasculopathy. In addition, the higher the age and Fins level, the more likely T2DM patients were to develop ED. HbA1C, age and education level affected the severity of ED, with higher levels of LDL, age, high risk of diabetic vasculopathy indicating more severe ED. The more severe the ED and higher PEDT scores in T2DM patients, the more severe their anxiety and depression. The more anxious T2DM patients were, the worse their sexual experienced. T2DM patients experienced an increase in anxiety levels with the duration of T2DM. As the level of anxiety increased in T2DM patients, ED became more severe. Our finding of significantly higher PEDT scores in the T2DMED group suggests a greater burden of ejaculatory complaints or dissatisfaction among these men. It should be noted that while the PEDT score indicates symptoms, it does not equate to a formal clinical diagnosis of premature ejaculation, which requires a specific cutoff and clinical evaluation. This association may reflect shared neurovascular, psychological, or medication-related etiologies common to both ED and ejaculatory dysfunction in the context of T2DM.

Previous research showed that the prevalence of ED in T2DM in China was 64.2% (42). In this study, the prevalence of ED in male T2DM patients was 67.8%. The prevalence of mild ED was 57.2%, moderate ED was 5.3%, and severe ED was 5.3%. In T2DM patients, right PWV and left PWV levels were elevated when compared with T2DM patients. PWV was considered as a biomarker of early atherosclerosis injury, and was related to atherosclerotic heart disease (43, 44). The severity of ED increased with the increase of PWV, which suggested that aortic sclerosis might affect ED (45). The population of this study was T2DM patients, and it was found that PWV in ED patients was higher than T2DM patients. It was speculated that in T2DM population, PWV might also be a marker of early atherosclerosis. However, this study had not conducted a relevant investigation on patients’ coronary heart disease, so this speculation needed further research and confirmation. ABI is the most commonly used non-invasive examination for detecting peripheral arterial diseases (46). A positive correlation between the severity of ED and left ABI was found in this study. Therefore, it was speculated that the more severe the ED, the higher the probability of peripheral arterial disease in these patients. Right ABI did not show positive correlation with ED, which might be due to insufficient sample size in this study.

In previous study, a positive correlation between ED and psychological distress was found in T2DM patients using the Symptom Checklist-90 (SCL-90) (47). In this study, there were negative correlations between IIEF-5 scores and HAMA scores, HAMD scores. There were differences in HAMA scores between T2DMED and T2DM patients. It was believed that the occurrence of ED in T2DM was related to the social and psychological status of patients. Abnormal blood lipids, especially lipoprotein levels, were associated with an increased risk of ED in T2DM (48). The results of binary logistic analysis conducted in this study suggested that TC, TG, and LDL levels did not affect the development of ED in T2DM. The results of Spearman correlation analysis showed a correlation between LDL and ED severity. Additionally, high-density lipoprotein (HDL) and lipoprotein (Lpa) were not included as risk factors for analysis in this study. Research has shown that the course of T2DM, poor blood glucose control, older age, and higher BMI were associated with the incidence of ED in T2DM patients (49). In this study, age had a positive impact on the development of ED in T2DM patients, and the severity of ED was positively correlated with age. In addition, age might predict the likelihood of ED in T2DM patients. However, this study did not find any correlation or influence between blood glucose levels, T2DM course, BMI and ED, possibly due to the older age of the subjects, low HbA1C levels, and better control of FBG levels.

Differences in depression status were found between the T2DMED and T2DM groups, and it was believed that depression status could predict the occurrence of ED (50). This study showed similar results, namely that there were negative correlations between IIEF-5 scores and HAMA scores, HAMD scores in T2DM patients. HAMA scores negatively affected IIEF-5 scores. Therefore, it was believed that social psychological states such as anxiety and depression could affect T2DMED patients, providing further clinical evidences for psychological intervention in the treatment of T2DMED. Kiskac’s study did not show a relationship between umALB and ED, and found a statistically significant relationship between HbA1C and the severity of ED (51), which was consistent with the findings in this study. However, there was controversy over whether there was a correlation between umALB, HbA1C, and ED, and more clinical studies were needed to verify it. Research had shown that higher levels of education might increase the incidence of ED in T2DM patients (42), while the results of this study showed no statistical correlation between education level and ED in T2DM patients. Further sample size expansion was needed to verify the relationship between the two factors.

Our finding that elevated fasting insulin (Fins) is an independent risk factor for ED in T2DM patients offers a novel and significant insight into the pathophysiology of T2DMED, extending beyond the traditional focus on hyperglycemia. This association underscores the pivotal role of insulin resistance and hyperinsulinemia in diabetic vasculopathy and endothelial dysfunction. Hyperinsulinemia may contribute to ED through several mechanisms: 1) It is a known promoter of vascular smooth muscle cell proliferation and atherosclerosis, thereby compromising penile arterial inflow; 2) It can stimulate sympathetic nervous system activity, leading to increased vasoconstriction; 3) It may directly impair endothelial NO synthase (eNOS) function and reduce NO production; and 4) It is closely linked to increased visceral adiposity and the secretion of pro-inflammatory adipokines, fostering a systemic inflammatory state detrimental to vascular health. This result suggests that in clinical practice, assessing insulin resistance status, perhaps through indicators like HOMA-IR, might help identify T2DM patients at a higher risk for ED even before overt vascular complications arise. It also implies that therapeutic strategies aimed at improving insulin sensitivity, such as specific pharmacological agents (e.g., GLP-1 receptor agonists, pioglitazone) and intensive lifestyle modification, may have dual benefits in improving both metabolic control and sexual function, a hypothesis that merits prospective interventional studies.

The strong correlations between ED severity, vascular parameters (PWV, ABI), and psychological scales (HAMA, HAMD) revealed in this study have profound implications for clinical practice and future research directions. Clinically, these findings advocate for a paradigm shift in the management of male T2DM patients towards integrated, multi-disciplinary care. Routine screening for ED using simple questionnaires like the IIEF-5 should be incorporated into standard diabetes care, especially for older patients and those with poor glycemic control. Positive screens should trigger a comprehensive evaluation encompassing not only glycemic and lipid profiles but also assessments of subclinical atherosclerosis (e.g., via PWV measurement) and mental health status. Management must then be equally multifaceted: optimizing glycemic control and cardiovascular risk factors forms the foundation, but it must be complemented by targeted psychosexual counseling, cognitive-behavioral therapy for anxiety/depression, and consideration of phosphodiesterase type 5 (PDE5) inhibitors, which address both the vascular and psychological components by improving erectile confidence. For future research, longitudinal studies are urgently needed to establish causality within the observed correlations. Moreover, investigating the effects of different anti-diabetic drug classes on ED incidence and progression, exploring the role of novel biomarkers like endothelial progenitor cells or specific inflammatory cytokines, and developing tailored psycho-educational interventions for this vulnerable population are critical next steps to move from understanding associations to improving patient outcomes.

More importantly, the results suggested that HbA1c, age, and high school/vocational education level were significant risk factors affecting ED severity in the multivariable model. It is noteworthy that while the bivariate Spearman correlation between HbA1c and ED severity was not statistically significant, HbA1c became a significant predictor in the ordered logistic regression analysis after adjusting for other covariates. This indicates that the relationship between glycemic control and ED severity is more clearly discernible when accounting for potential confounders such as age, BMI, and hypertension status. In addition, a notable finding of our study was the high prevalence of ED (67.8%) in a cohort with a relatively short mean T2DM duration of 2–3 years. This suggests that ED can manifest early in the course of T2DM, potentially even preceding or coinciding with the formal diagnosis. Several factors may explain this phenomenon. First, T2DM is often preceded by a prolonged period of insulin resistance and metabolic syndrome, during which subclinical endothelial dysfunction and microvascular damage accumulate. ED may thus be an early sentinel sign of this underlying vasculopathy. Second, the pathogenesis of ED in T2DM is multifactorial; factors like suboptimal glycemic control (reflected in our cohort’s mean HbA1c >8%), concurrent hypertension, dyslipidemia, and psychological distress—all present in our population—can contribute to ED independently of, or synergistically with, diabetes duration. Third, our cohort’s mean age was mid-40s, an age where vasculogenic factors begin to significantly contribute to ED. The high prevalence highlights the importance of routine sexual health screening in all men with T2DM, regardless of disease duration.

The high prevalence of ED (67.8%) in our cohort means that the odds ratios (ORs) reported from our binary logistic regression analyses likely overestimate the strength of associations compared to risk ratios or prevalence ratios. The highly imbalanced distribution of ED severity (predominantly mild) may limit the precision of estimates for factors specifically associated with moderate-to-severe ED in our ordered logistic regression model. Future cross-sectional studies with a high outcome prevalence would benefit from employing analytical methods, such as modified Poisson regression, that generate prevalence ratios for more directly interpretable measures of association. Additionally, the duration of T2DM was calculated from the time of formal diagnosis. The potential long, undiagnosed preclinical phase of diabetes means the true duration of metabolic disturbance may be underestimated, which could influence the association between disease duration and complications like ED. Furthermore, this study did not assess hormonal parameters such as testosterone or sex hormone-binding globulin levels, which are known to influence both metabolic health and sexual function. Future studies incorporating these biomarkers would provide a more comprehensive understanding of the endocrine pathways involved in T2DM-related ED.

However, several limitations should be considered in this study. First, all participants were of Han ethnicity, limiting the generalizability of our findings to other ethnic groups. Second, we did not collect detailed data on lifestyle factors, which are known to influence both metabolic health and sexual function. Third, while we recorded major medication classes, a more granular analysis of specific antidiabetic, antihypertensive, and psychotropic medications and their doses was not performed. Fourth, although we assessed vascular parameters (PWV, ABI), we did not systematically document the presence or severity of established macrovascular or microvascular complications. Fifth, we did not measure several biomarkers implicated in endothelial dysfunction and ED.

In this study, the findings suggested that T2DM patients had a high probability of ED. The incidence rate and severity of ED in T2DM patients were related to age, glycosylated hemoglobin, vascular disease, neuropathy and other factors. Patients with T2DM had social, emotional, and cognitive barriers when developing ED, which explained the psychological reasons for ED, namely that T2DM patients with anxiety or depression were prone to developing ED. Therefore, it was suggested that clinical attention should be paid to the erectile status of male patients with T2DM, and early screening of ED population, early intervention and treatment should be carried out as far as possible.