Testosterone, a hormone associated with male sex characteristics, is produced by the Leydig cells within the testes. It not only helps sustain male secondary sexual traits and boost sperm generation but also increases muscle mass and bone strength, while being crucial for the normal functioning of the reproductive system and multiple organs in the body [1, 2]. Although testosterone level in male serum is highest during adolescence, they gradually decline with age and significantly decrease in old age. When testosterone level in male serum drops to 300 ng/dL, it can be diagnosed as testosterone deficiency (TD) [3]. This condition may lead to various age-related issues such as sexual dysfunction, reproductive disorders, cardiovascular diseases, and metabolic disturbances, severely affecting men’s quality of life and health [4, 5]. Reports indicate that up to 40% of men over the age of 45 in the United States experience TD, a figure anticipated to rise in the future as life expectancy continues to grow [4, 6]. Therefore, TD has become an increasingly concerning global health issue.

Obesity greatly increases the likelihood of various heart and metabolic disorders, such as coronary artery disease, high blood pressure, stroke, type 2 diabetes, high cholesterol, and gout [7]. Moreover, research indicates that obesity is linked to reduced testosterone level [8]. Additionally, the distribution of fat in the body can affect the level of testosterone. Excessive accumulation of subcutaneous fat tissue typically does not affect the body’s metabolism or the synthesis and metabolism of serum testosterone [9]. However, if obesity leads to substantial fat deposition around internal organs in the abdominal region, these adipose tissues can impede skeletal muscle function and disrupt liver metabolism. Furthermore, excessive abdominal fat accumulation interferes with organ metabolism leading to insulin resistance, inflammation, and dyslipidemia. This often results in metabolic disturbances such as high waist circumference (WC) or abdominal obesity which may contribute to decreased serum testosterone concentration [10, 11]. Obesity is closely associated with reduced testosterone level, and it is imperative to comprehend the obesity index that can forecast the risk of testosterone decline and TD.

Out of numerous indexes for obesity, body mass index (BMI) stands out as a widely accepted and commonly utilized tool to evaluate obesity [12, 13, 14]. The World Health Organization defines obesity as having a BMI $\ge$30 kg/m² primarily relevant in Western societies [15]. Some research revealed an inverse relationship between BMI and testosterone, suggesting that obese individuals are more prone to experiencing reduced testosterone level in comparison to those with a normal BMI. Nevertheless, if obese individuals undergo testosterone replacement therapy and achieve weight loss, their testosterone level will rise [16, 17]. These outcomes underscore a significant interplay linking both aspects together. However, as research progressed, it became evident that BMI is limited in its ability to directly measure the degree of obesity and distinguish between lean body mass and fat. Consequently, there is a growing consensus within the scientific community that BMI alone cannot reliably predict obesity in clinical practice, prompting the need for a new indicator to either replace or complement BMI for assessing obesity [18]. As investigations into conditions linked with obesity persistently evolve; emphasis has shifted towards abdominal visceral fat assessment offering superior insights into overall adiposity distribution patterns [19]. Due to the side effects and cost considerations associated with computed tomography (CT), magnetic resonance imaging (MRI), and dual X-ray absorptiometry (DXA), these imaging modalities are not widely applicable in clinical practice. Therefore, simple clinical anthropometric indices such as WC, waist-to-hip ratio (WHR), and waist-to-height ratio (WHtR) should be utilized as alternative or supplementary indicators to BMI for identifying metabolic diseases [19]. Even though there is an association between these alternative markers and low testosterone, the correlation of these waist-based obesity indicators with BMI may confound the observation of the link between obesity and diseases, rendering them an unreliable indicator of visceral obesity [20, 21, 22, 23]. Hence underscoring the continued necessity for novel precise markers effectively appraising visceral adipose accumulations thereby comprehensively unraveling their intricate ties with TD.

Krakauer and Krakauer [24] devised a body shape index (ABSI) as a more accurate measure for assessing abdominal visceral obesity. Unlike BMI, which primarily reflects overall body mass and does not distinguish between fat and lean mass, ABSI is specifically designed to capture information about body shape, particularly the distribution of abdominal fat, independent of overall adiposity. In contrast to BMI, which reflects overall body fat, ABSI utilizes WC for adjusting the impact of height and weight largely independent of these variables as well as from BMI itself [25, 26]. This is crucial because visceral adipose tissue, which ABSI is thought to better reflect, is metabolically more active and strongly linked to adverse health outcomes compared to subcutaneous fat. ABSI provides a better explanation for the degree and distribution of central abdominal obesity. Clinically, ABSI has shown promise in predicting various health risks beyond what BMI or WC alone can offer. Prior research has shown a link between ABSI and ailments like high blood pressure, diabetes, and heart disease [27]. Importantly, it suggests ABSI may be a stronger predictor of mortality and certain metabolic diseases than BMI or WC, particularly because it is less confounded by factors like muscle mass and height. Furthermore, it exhibits a stronger correlation with death rates than BMI or WC individually. Moreover, the ABSI can adjust the proportion index based on the population of other groups, exhibiting only marginal discrepancies. In contrast to BMI, it is applicable across diverse populations for investigating obesity and associated conditions [28]. Therefore, investigating ABSI in the context of TD is clinically relevant because it could offer a more refined and potentially more predictive tool for identifying men at risk, compared to relying solely on BMI or WC. Nevertheless, there remains a lack of comprehensive observational or laboratory investigations exploring the link between ABSI and TD.

This research sought to investigate the link between the novel obesity indicator ABSI and testosterone level in adult American men aged 20 and above, with the objective of raising awareness about the detrimental impact of obesity on adult testosterone level and TD. This provides a fresh perspective on male reproductive health and obesity issues.

This research employed NHANES data to investigate the link between the new obesity measure ABSI and testosterone. Our findings revealed a robust negative correlation between ABSI and testosterone, as well as a positive correlation between ABSI and TD. Even after controlling for demographic characteristics, comorbidities, and dietary factors, the positive correlation remained consistent. Subgroup analysis and interaction test results demonstrated that the association between ABSI and testosterone, as well as the risk of TD, persisted across different subgroups. To our knowledge, this is the first comprehensive study investigating the link between ABSI and TD risk using nationally representative data.

ABSI was found to have a significant negative correlation with serum total testosterone levels and a positive correlation with the risk of TD. Our findings not only support the established association between traditional adiposity measures BMI and WC and TD, but more importantly, they reveal that ABSI, which is based on body size distribution, may serve as a more precise clinical predictor [30, 31, 32, 33, 34, 35, 36]. While BMI and WC primarily reflect global or regional fat accumulation, ABSI offers a more sensitive measure of the ectopic distribution of abdominal fat by integrating height, weight, and WC data. This characteristic may elucidate the stronger association observed between ABSI and testosterone compared to traditional measures in the present study. The preferential accumulation of abdominal fat may contribute to TD risk through a dual mechanism: firstly, visceral adipose tissue exhibits higher aromatase activity, potentially accelerating the conversion of testosterone to estrogen, which inhibits the function of the hypothalamic-pituitary-gonadal (HPG) axis via a negative feedback mechanism [37, 38, 39]. Secondly, central obesity, as characterized by ABSI, may be spatially linked to an imbalance in adipocytokine secretion (e.g., leptin resistance, proinflammatory factor release) [40, 41]. ABSI maintained its independent association with TD risk, suggesting that the pattern of abdominal fat distribution itself may directly influence the steroidogenic function of Leydig cells through oxidative stress and a localized inflammatory microenvironment [42]. The correlation between ABSI, testosterone, and the TD risk suggests that interventions aimed at reducing abdominal fat—such as high-intensity interval training and medications targeting visceral fat—may be more effective than traditional weight-loss strategies in enhancing gonadal function [35, 40, 43].

Common risk factors contributing to reduced or insufficient testosterone include not only obesity but also advanced age, smoking habits, hypertension as well as obesity-related conditions. Subgroup analysis within ABSI reveals that age along with hypertension serves as a significant regulatory element for testosterone insufficiency across all subgroups. Consistent with previous research, smoking and alcohol consumption have been associated with testosterone decreases and the risk of TD [44, 45]. Among non-drinkers, each additional unit of ABSI is linked to a lower decrease in testosterone levels and reduced risk of hypogonadism compared to heavy drinkers. Furthermore, non-smokers and former smokers exhibit a lesser degree of testosterone decline and decreased risk of hypogonadism when compared to smokers. The mechanisms underlying these associations involve heightened concentrations from prolonged alcohol intake stimulating hypothalamus-pituitary-adrenal axis activity thereby inducing inflammation alongside oxidative stress while concurrently inhibiting HPG axis function resulting in decreased production rates within hepatic sex hormone-binding globulin (SHBG) ultimately culminating in lowered serum concentrations [46, 47]. Furthermore, tobacco exposure emerges as another pertinent contributor towards diminished Testosterone; it has been shown capable even among rodent models [48]. Smoking elevates hepatic testosterone metabolism, leading to reduced testosterone level [49]. Additionally, the cigarette metabolite cotinine disrupts the equilibrium between total antioxidant capacity and ROS production, resulting in heightened levels of active oxygen, oxidative stress, increased lipid peroxidation, diminished antioxidant activity, and amplified toxic effects on Leydig cells with consequent impairment of testosterone synthesis [50, 51]. In summary, chronic smoking coupled with excessive alcohol usage fosters accruals pertaining to ROS elevation alongside augmented lipid peroxidation thus interfering with pathways governing biosynthesis consequently depleting circulating hormone quantities whilst elevating risks associated with TD. Conversely, individuals afflicted by comorbidities such as hypertension, diabetes and hypercholesterolemia have a lesser decrease in their testosterone level per unit of ABSI and a diminished likelihood of developing TD. Furthermore, obesity can also contribute to metabolic disturbances that precipitate the onset of diabetes and high cholesterol. Patients with diabetes frequently encounter insulin resistance, hyperlipidemia and elevated cholesterol levels—all of which are notable risk factors for TD [1, 9]. Despite these factors increasing the likelihood of TD, individuals with comorbid conditions such as hypertension, diabetes and hypercholesterolemia may prioritize lifestyle and dietary management, enhanced physical activity and weight control [52]. Meanwhile, our data collection on subjects with hypertension, diabetes and hypercholesterolemia includes individuals who are undergoing medication for reducing their blood pressure, glucose level and cholesterol level. These medication variables may attenuate the observed correlation between ABSI and TD. Naturally, future cohort studies are imperative for further elucidating the interplay between these factors in individuals with hypertension diabetes and elevated cholesterol level.

Currently, researchers have identified numerous indicators related to obesity, such as BMI, WC, WHR and WHtR. These indicators are utilized for assessing the degree of obesity and investigating the correlation between obesity and disease risk [23]. However, these indicators are not comprehensive in detecting the degree of obesity and phenotypes. Their associations and predictive strengths vary across different diseases [23, 53, 54]. For instance, BMI fails to differentiate between fat and muscle mass or reflect body fat distribution. Therefore, in the assessment of testosterone deficiency risk among obese patients, a supplementary index is essential alongside BMI or WC. ABSI is a recently introduced parameter that incorporates WC, body weight, and height to characterize body shape [24]. From a statistical perspective, ABSI differs from height, BMI and WC by better reflecting visceral fat accumulation degree and fat distribution associated with endocrine and metabolic disorders compared to traditional body measurement indices. Our study demonstrates a negative correlation between ABSI and TD. Moreover, regardless of BMI strata within each subpopulation group ABSI consistently correlates with TD risk. Interestingly enough previous research has shown an inverse relationship between ABSI and lean mass [55]. Modified ABSI also exhibits a positive association with fat mass index but a negative association with appendicular skeletal mass index [56]. Additionally, several studies indicate high sensitivity of ABSI in predicting metabolic disease risk but low specificity/accuracy suggesting it may not be suitable as a standalone indicator for detecting metabolic disease risk [57]. Nevertheless, recent research from Japan evaluated the combination of ABSI, BMI and non-alcoholic fatty liver disease (NAFLD) risk, finding that combining BMI with ABSI significantly outperforms individual predictive abilities of BMI or ABSI alone and further improves NAFLD risk prediction [29].

Furthermore, the researchers conducted a study involving 11,872 Taiwanese participants aged 30 and above who have diabetes. They utilized various anthropometric indexes, including ABSI, BMI, WC, WHR, WHtR and Body Roundness Index (BRI), either individually or in combination, to predict mortality risk among the diabetic population. The findings revealed that the combined effect of BMI and ABSI on mortality risk was greater than their individual effects and surpassed the combined effects of other anthropometric measures [58]. Consequently, ABSI is likely to serve as a complementary predictor of TD risk in addition to BMI. Our study has validated these findings, demonstrating that the combined predictive ability of ABSI and BMI for TD in American adult men surpasses their individual predictive abilities. Furthermore, our results indicate that O_BMI+ABSI outperforms BMI $\times$ ABSI in predicting TD, suggesting the need for further research across a broader spectrum of metabolic diseases to confirm the superiority of combined indicators.

Our research has multiple advantages, being the first and most extensive examination of the relationship between ABSI, testosterone and TD risk. Moreover, the extensive and dependable NHANES dataset empowers us to explore potential variables that could impact the relationship between ABSI and testosterone. Additionally, we conducted subgroup analyses across diverse populations to assess the strength of the relationship between ABSI, testosterone, and TD. Our research also indicates that ABSI serves as a valuable complement to BMI in assessing obesity and its relation to TD, with their combined predictive capacity for TD risk surpassing that of either measure alone. The Youden Index maximizes the sum of sensitivity and specificity, effectively identifying a threshold that optimizes the ability of the test to correctly classify both those with and without the condition (TD in this case). This approach is particularly useful when equal weight is given to the importance of correctly identifying both true positives (those with TD) and true negatives (those without TD). Consequently, our study results hold significant public health implications for obesity management and TD prevention.

Nevertheless, this study is subject to certain constraints. Firstly, it is a cross-sectional study, precluding the establishment of a causal relationship between ABSI and TD. As the original data for this study was sourced from the NHANES database, the findings derived from the analysis are only generalizable to the US population and may not be extrapolated to other global regions. Secondly, there exist numerous potential confounding factors influencing BMI, weight-adjusted waist index (WWI), ABSI, and TD; some of these warrant further investigation by researchers. Given our inability to account for all potential confounders using the NHANES database, caution should be exercised in interpreting our results and subsequent research should validate the conclusions drawn from this study. The collection of a substantial number of questionnaires in this study encompassed dietary factors, comorbidities, and demographic information reliant on self-reporting by subjects. Consequently, introducing bias due to missing data. Furthermore, as NHANES’ medical questionnaire lacked comprehensive information on testosterone and TD symptoms/signs/comorbidities/laboratory data related to TD were not considered. TD is multifaceted beyond being merely a biochemical marker and necessitates consideration alongside other clinical conditions. However, owing to constraints within the NHANES database we could only define TD as total testosterone below 300 ng/dL; additionally lacking access to testicular examination/imaging data which could have been included as covariates in our study. Last but not least, it is important to acknowledge that the Youden Index has limitations and may not be the most appropriate threshold selection criterion in all contexts. A key limitation is that the Youden Index gives equal weight to sensitivity and specificity and does not consider the relative clinical consequences of false positives versus false negatives, or the prevalence of the condition in the population.

Another important consideration is the generalizability of our findings, which are primarily based on data from the NHANES survey, a nationally representative sample of the U.S. adult population. While NHANES provides a robust snapshot of the U.S., it is essential to acknowledge that the observed associations may not directly translate to other populations globally due to several factors.

Despite our efforts to adjust for a comprehensive set of known confounders, it is essential to acknowledge the inherent limitation of observational studies in fully accounting for all potential confounding variables. Unmeasured confounders—factors that are associated with both ABSI and testosterone levels/TD risk but were not directly assessed or adequately controlled for in the NHANES dataset—could potentially influence our findings and introduce bias. For example, physical activity levels, while partially captured through general survey questions in NHANES, may not have been assessed with sufficient detail or granularity to fully account for its complex influence. Individuals with higher levels of physical activity might tend to have both lower ABSI (due to better body composition) and healthier testosterone profiles, independent of a direct causal link between ABSI and testosterone [59]. Similarly, genetic factors influencing both body fat distribution patterns (and thus ABSI) and hormonal regulation could act as unmeasured confounders. While we adjusted for race/ethnicity as a proxy for some genetic background, this is a crude measure and does not capture the full spectrum of genetic variability that might predispose individuals to certain body shapes and hormonal profiles [60]. For instance, certain genetic variants might predispose individuals to both higher visceral adiposity (potentially leading to higher ABSI) and a tendency towards lower testosterone levels, again creating an association that is not directly causal. Considering the calculation formula for ABSI, WC is positioned in the numerator and its error directly and linearly affects ABSI. Despite the large-scale nature of NHANES measurements, staff techniques, cooperation and physiological conditions of the participants, measurement timing, and equipment precision give rise to some inevitable errors in the measurements of WC, height, and weight. Underestimation of height concurrently increases BMI and decreases height terms, ultimately resulting in an underestimation of ABSI. Therefore, ABSI is more sensitive to WC error than BMI or WC alone as its calculation involves multivariable interactions. In the future, sensitivity analyses can be carried out to simulate the robustness of the association between ABSI and outcomes under different error margins. Another way to reduce the error is to verify the reproducibility of ABSI in a multicenter study and clarify its clinical application threshold.

This study has unveiled a negative linear correlation between ABSI and testosterone in U.S. male adults aged 20 and above, while also identifying a positive linear correlation between ABSI and the incidence of TD. We acknowledge that, like all observational studies, our findings are susceptible to the influence of unmeasured confounding factors, such as physical activity levels and genetic predispositions, which could partially explain the observed associations. It is important to note that, due to the cross-sectional design of our study, we have established associations, but cannot infer causal relationships between ABSI and testosterone or TD. In future applications for the prevention and management of TD, particular attention should be given to individuals aged 20–40 without hypertension. Additionally, consideration should be directed towards individuals aged 60 and older, non-Hispanic blacks, those with less than a 9th-grade education, individuals with PIR 1.7, smokers, drinkers, as well as those diagnosed with diabetes, hypertension, and hypercholesterolemia. ABSI serves as a valuable complement to BMI in assessing obesity and its association with TD. The combined use of ABSI and BMI demonstrates stronger predictive capabilities for the risk of TD compared to their individual use alone. These findings enhance our understanding of low testosterone levels related to obesity and offer fresh insights into the prevention and management of TD alongside male health. Future longitudinal studies are needed to elucidate potential causal pathways and confirm the directionality of the observed associations.

The study includes the original contributions, which are detailed in the article. For additional information, inquiries may be directed to the corresponding author.

FG and CD designed this study. FG and PL analyzed the data and wrote the original draft. All authors have contributed to the editorial changes made to the manuscript. All authors read and approved the final manuscript. All authors have participated sufficiently in the work and agreed to be accountable for all aspects of the work.

The data for this study are all from the NHANES database and do not require ethical approval. The NHANES database has been approved by the National Health Statistics Ethics Review Board in the U.S., and all participants have provided written informed consent prior to data collection.

This study was supported by the National Natural Science Foundation of China and the Natural Science Foundation of Guangdong Province (Grant Numbers: 82301796, 2025A1515012486).

The authors declare no conflict of interest.