
==== Front
Sci Rep
Sci Rep
Scientific Reports
2045-2322
Nature Publishing Group UK London

39261605
72157
10.1038/s41598-024-72157-w
Article
Association between composite dietary antioxidant index and erectile dysfunction among American adults: a cross-sectional study
Zhu Huajun 1
Chen Si 2
Ye Qianyi 2
Lin Weilong 2
Li Taibiao 2
Xu Zhengyuan 2
Huang Zhuangcheng huangzc1991@126.com

2
1 https://ror.org/0269fty31 grid.477955.d Department of Pharmacy, Shaoxing Second Hospital, Shaoxing, 312000 Zhejiang China
2 grid.411679.c 0000 0004 0605 3373 The First Affiliated Hospital of Shantou University Medical College, Medical College of Shantou University, Shantou, 515041 China
11 9 2024
11 9 2024
2024
14 2123013 3 2024
4 9 2024
© The Author(s) 2024
2024
https://creativecommons.org/licenses/by-nc-nd/4.0/ Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.
Erectile dysfunction (ED) is closely related to oxidative stress, and antioxidant is a treatment and prevention method for erectile dysfunction. The Compound Dietary Antioxidant Index (CDAI) represents the overall dietary antioxidant intake of the human body. However, the link between CDAI and ED is unclear. The objective of this research was to examine the linkage between CDAI and ED. The research utilized information collected from the National Health and Nutrition Examination Survey (NHANES) spanning the years 2001 to 2004. To assess the association between CDAI and ED, the analysis employed weighted multivariate logistic regression along with weighted restricted cubic splines (RCS). Additionally, subgroup interaction analysis was conducted to confirm the findings. In this investigation, 3184 adults from the U.S., all above the age of 20, were part of the study cohort, with 863 of them identified as having ED. Adjustments for potential confounding variables revealed that the odds ratio (95% confidence interval) of CDAI associating with ED was 0.95 (0.92–0.99; P = 0.01). Besides, compared to the lowest tertile, the highest tertile of CDAI was associated with a lower risk of ED (0.63 [0.46–0.88]; P = 0.01). The application of weighted restricted cubic splines (RCS) analysis delineated a nonlinear inverse relationship between CDAI levels and the probability of ED. Subgroup analysis further demonstrated that the association between CDAI and ED remained consistent across subgroups. This cross-sectional analysis revealed a significant correlation, indicating that elevated levels of CDAI are closely linked with a lower likelihood of ED.

Keywords

Compound dietary antioxidant index (CDAI)
Erectile dysfunction (ED)
NHANES
Dietary antioxidant
Cross-sectional research
Subject terms

Urogenital diseases
Diseases
Urology
issue-copyright-statement© Springer Nature Limited 2024
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pmcIntroduction

Erectile dysfunction (ED) is characterized by the persistent difficulty in obtaining or sustaining an erection adequate for gratifying sexual activity1. An epidemiological survey found that the prevalence of ED in 30-year-old adult men was 19.2%2. Moreover, with the increase of age, the prevalence of ED gradually increased3. The physiological process of achieving an erection is governed by the equilibrium of blood inflow and outflow in the penile tissue, and ailments that alter the penile blood circulation frequently result in ED4. Atherosclerosis and diabetes are two common diseases that may lead to ED4. Concurrently, various research findings suggest that conditions such as hypercholesterolemia, high blood pressure, and coronary artery disease might elevate the likelihood of experiencing ED5–7. In addition, some poor lifestyle habits such as smoking, drinking alcohol, and lack of physical activity may also increase the risk of ED8. Recent research increasingly indicates that oxidative stress and molecular inflammation are significant contributors to the pathophysiological mechanisms underlying ED9,10.

Oxidative stress is characterized by the accumulation of reactive oxygen species (ROS), which is caused by too much oxidant due to an imbalance between oxidants and antioxidants11. The imbalance between antioxidant capacity and oxidative reaction may directly or indirectly lead to cell damage12. An animal model study using radiation to induce ED in mice suggests that oxidative stress plays an important role in the development of ED13. Additionally, oxidative stress is known to precipitate vascular endothelial dysfunction and atherosclerosis14, both of which are recognized as underlying factors in ED. Consequently, the use of antioxidant therapy emerges as a potential new approach in treating ED15,16. Dietary intake is an important source of exogenous antioxidants, which provides an effective auxiliary function for the antioxidant system of the body. Daneshzad et al. found that daily dietary intake of antioxidants can increase antioxidant defense and reduce oxidative stress by increasing plasma antioxidant levels17. A study by Zhang et al. showed that dietary antioxidants can increase antioxidant capacity and improve penile blood flow and erectile activity in ED patients18. Recently, a cross-sectional study showed that high levels of dietary lycopene consumption reduced the risk of ED19. And previous research has shown that lycopene is a kind of nutrient have anti-inflammatory and antioxidant properties20.

The composite dietary antioxidant index (CDAI) constitutes a scoring framework established by Wright et al.21. It integrates a spectrum of dietary antioxidants—such as vitamins A, C, E, selenium, zinc, and various carotenoids—to evaluate the aggregate antioxidant capacity of an individual’s dietary intake. Previous studies have shown that higher CDAI reduces the risk of hypertension and depression and may reduce the risk of diabetic nephropathy in patients with diabetes22–24. Yet, investigations delving into the potential link between the CDAI and ED are absent from the current body of research. Hence, our goal was to elucidate the connection between dietary antioxidant capability and ED by examining the association using datasets from the National Health and Nutrition Examination Survey (NHANES).

Methods

Study population

The NHANES is a recurrent survey overseen by the Centers for Disease Control and Prevention (CDC), with its research protocols receiving approval from the National Health Statistics Research Council Center. This initiative aims to evaluate the well-being and nutritional state of both adults and children across the United States, encompassing diverse health and nutrition assessments and securing written informed consent from all participants.

Because NHANES data on the erectile function questionnaire only existed from 2001 to 2004, this study included NHANES data from 2001 to 2004, which included 4116 men (≥ 20 years of age) who completed the erectile function questionnaire. Simultaneously, we applied a set of exclusion criteria: (a) individuals without dietary antioxidant data (n = 241); (b) those with a prostate cancer diagnosis (n = 101); (c) subjects with missing survey information on body mass index(BMI) (n = 93), level of education (n = 1), recreational activity (n = 1), smoking or alcohol use (n = 8), marital status (n = 2), cardiovascular disease (n = 1), and hypertension (n = 3). After applying these criteria, the study encompassed a total of 3665 participants. The flow chart of participant inclusion is depicted in Fig. 1.Fig. 1 The selection process of NHANES 2001–2004. ED erectile dysfunction, BMI body mass index, CVD cardiovascular disease.

Exposure variable

In this study, the CDAI was considered to be the primary exposure variable. Information on individual intake levels for six dietary antioxidants (vitamin A, vitamin C, vitamin E, zinc, selenium, and carotenoids) was obtained from the NHANES Day 1 and Day 2 dietary interview questionnaires, which were designed to record participants’ total dietary intake over two discrete 24-h periods. Initial dietary assessment was conducted on the first day by face-to-face interview, and the second day dietary assessment was conducted by telephone follow-up 3–10 days later. It is important to note that the estimates of dietary antioxidants were based solely on food sources of daily intake and did not include antioxidants obtained through dietary supplements or medications. The nutritional value of all diet items is provided by the USDA’s Dietary Research Food and Nutrition Database (FNDDS) (https://fdc.nal.usda.gov), which provides nutritional profiles of each food reported in NHANES. Dietary antioxidant intake in the diet was calculated using the results of dietary interviews over an average of 2 days (this value was used only available on the first day). For evaluating cumulative exposure to antioxidants through diet, we employed an adapted version of CDAI originally formulated by Wright et al.21,25.

Briefly, the intake of each of the six dietary antioxidants was normalized using the gender-specific average across all participants and then divided by the gender-specific standard deviation. Subsequently, the CDAI was calculated by summing the standardized values of the six dietary antioxidants (as below).CDAI=∑i=16eachintake-meanSD.

Outcome variable

ED was gauged using a direct question from the Massachusetts Male Aging Study (MMAS)26, which asks, “How would you rate your ability to get and maintain an erection adequate for satisfactory sexual activity?” The response options included “always or almost always,” “usually,” “sometimes,” or “never.” The reliability of this straightforward method for assessing ED is comparable to that of the International Index of Erectile Function (IIEF)26. For the purposes of this questionnaire, those who reported being “sometimes” or “never” able to maintain an erection were categorized as having ED, whereas those who indicated they were “usually” or “always or almost always” able were categorized as not having ED.

Covariates

Beyond the primary outcomes measured, we also factored in several covariates for a comprehensive analysis: age categorized as under 40, between 40 and 59, and 60 or older; racial groups identified as white, black, and other; marital status classified into married/living with partner, and single/divorced/widowed; educational attainment segmented into less than high school, high school or equivalent, and college or above; body mass index (BMI) divided into two groups: under 30.00, 30.00 or more; smoking status categorized as never, former, or now; drinking status identified as never, former, or now; levels of recreational activity classified as vigorous, moderate, or inactive; and presence of health conditions such as hypercholesterolemia, cardiovascular disease (CVD), hypertension, and diabetes, each classified as yes or no. In addition, testosterone levels (low, normal, unknown) and total daily energy intake were also included as covariates.

Statistical analysis

Considering the intricate multistage stratified sampling method utilized by NHANES to represent the U.S. populace, we applied the prescribed sample weights according to NHANES directives and conducted weighted analyses to refine the precision of the data. Demographic details are presented as the weighted average plus or minus the standard error (SE) for continuous measures, and as the weighted proportion for categorical measures. The baseline characteristics correlated with ED status were assessed using the survey-weighted linear regression for continuous variables and the survey-weighted chi-square tests for categorical variables. To determine the adjusted odds ratios (OR) and 95% confidence intervals (CI) of ED in relation to the CDAI tertiles, we employed weighted logistic regression models. Four distinct weighted multiple logistic regression models were constructed: model 1 with no variable adjustment; model 2 adjusted for age and race; model 3 included adjustments for age, race, BMI, marital status, education, smoking status, drinking status, recreational activities, testosterone levels, and total daily energy intake; Model 4 additionally accounted for hypertension, diabetes, hypercholesterolemia, and cardiovascular disease. Moreover, weighted restricted cubic splines (RCS) were used to explore the dose–response correlation between dietary niacin intake and ED risk. Subsequent stratification by factors like age, race, BMI, smoking status, drinking status, recreational activities, hypertension, diabetes, hypercholesterolemia, and CVD, along with interaction analyses, were performed to investigate varying associations across subgroups. At the same time, we performed sensitivity analyses to exclude participants who had taken medications that could affect erectile function (such as PDE5 inhibitors, steroids, sex hormones, antipsychotics, and antidepressants) in the previous 30 days, and then performed multivariate logistic regression analyses to validate the association between CDAI and ED risk. All statistical evaluations in this study were conducted using R software (version 4.2.3), considering a bilateral P-value of < 0.05 as statistically significant.

Result

Characteristics of participants

Table 1 displays that our study encompassed 3,665 individuals, with an ED prevalence of 26.77%. The CDAI was notably reduced in participants with ED in comparison to those without [0.11 (0.18) vs 1.15 (0.16), P < 0.0001]. It was observed that men experiencing ED were typically older, in a marriage or cohabitating, possessed a higher level of education, exhibited increased BMI, consumed alcohol currently, engaged in less physical activity, and were more likely to have hypercholesterolemia, CVD, hypertension, and diabetes (all P < 0.001). In addition, participants with ED had a lower total daily energy intake than those without ED [2195.21 (49.56) vs 2645.25 (30.05), P < 0.0001].Table 1 Baseline characteristics of the study population.

Characteristic	Total	Erectile dysfunction	P-value	
No	Yes	
Total patients	3665	2684 (73.23)	981 (26.77)		
Age (year), n (%)	 < 0.0001	
 < 40	1255 (34.24)	1178 (48.44)	77 (8.74)		
 40–59	1233 (33.64)	1036 (41.20)	197 (32.86)		
 ≥ 60	1177 (32.11)	470 (10.36)	707 (58.40)		
Race, n (%)	0.03	
 White	1994 (54.41)	1419 (73.45)	575 (78.78)		
 Black	679 (18.53)	532 (10.45)	147 (7.78)		
 Other	992 (27.07)	733 (16.10)	259 (13.44)		
Marital status, n (%)	 < 0.0001	
 Married/living with partner	2541 (69.33)	1802 (66.28)	739 (78.50)		
 Single/divorced/widowed	1124 (30.67)	882 (33.72)	242 (21.50)		
Education level, n (%)	 < 0.0001	
 Less than high school	996 (27.18)	611 (13.46)	385 (27.68)		
 High school or equivalent	915 (24.97)	714 (27.15)	201 (23.60)		
 College or above, n (%)	1754 (47.86)	1359 (59.39)	395 (48.73)		
BMI	 < 0.001	
 < 30.00	2622 (71.54)	1951 (71.57)	671 (62.87)		
 ≥ 30.00	1043 (28.46)	733 (28.43)	310 (37.13)		
Smoking status, n (%)	 < 0.0001	
 Never	1492 (40.71)	1206 (45.93)	286 (28.92)		
 Former	1179 (32.17)	693 (25.50)	486 (47.58)		
 Now	994 (27.12)	785 (28.57)	209 (23.50)		
Drinking status, n (%)	 < 0.0001	
 Never	264 (7.2)	194 (8.19)	70 (7.15)		
 Former	744 (20.3)	425 (13.29)	319 (30.13)		
 Now	2657 (72.5)	2065 (78.52)	592 (62.72)		
Recreational activity, n (%)	 < 0.0001	
 Vigorous	1257 (34.3)	1089 (44.65)	168 (18.73)		
 Moderate	1012 (27.61)	688 (27.19)	324 (38.23)		
 Inactivity	1396 (38.09)	907 (28.17)	489 (43.04)		
Hypercholesterolemia, n (%)	 < 0.0001	
 No	2334 (63.68)	1812 (66.92)	522 (48.26)		
 Yes	1331 (36.32)	872 (33.08)	459 (51.74)		
CVD	 < 0.0001	
 No	3198 (87.26)	2506 (94.70)	692 (71.80)		
 Yes	467 (12.74)	178 (5.30)	289 (28.20)		
Hypertension, n (%)	 < 0.0001	
 No	2208 (60.25)	1841 (69.80)	367 (41.76)		
 Yes	1457 (39.75)	843 (30.20)	614 (58.24)		
Diabetes, n (%)	 < 0.0001	
 No	3160 (86.22)	2462 (93.51)	698 (72.45)		
 Yes	505 (13.78)	222 (6.49)	283 (27.55)		
Testosterone, n (%)	0.001	
 Low	91 (2.16)	46 (1.65)	45 (4.43)		
 Normal	485 (12.25)	375 (12.51)	110 (11.09)		
 Unknown	3089 (85.59)	2263 (85.84)	826 (84.48)		
Total energy (Kcal), mean (s.e.)	2562.69 (26.80)	2645.25 (30.05)	2195.21 (49.56)	 < 0.0001	
CDAI, mean (s.e.)	0.96 (0.14)	1.15 (0.16)	0.11 (0.18)	 < 0.0001	
BMI body mass index, CVD cardiovascular disease, CDAI composite dietary antioxidant index.

The survey-weighted linear regression tests was used to analyze differences between continuous variables.

The survey-weighted chi-square tests were used to analyze differences between categorical variables.

The relationship between CDAI and ED

Table 2 in our study highlights the relationship between the CDAI and ED risk, as evaluated through weighted multivariate logistic regression analysis. Our findings indicate a notable inverse correlation. Specifically, a rise in CDAI scores corresponds to a diminished likelihood of experiencing ED. This relationship is consistently observed across various models: Model 1 exhibits an OR of 0.93 (95% CI 0.90–0.96, P < 0.0001), Model 2 shows an OR of 0.94 (95% CI 0.91–0.98, P = 0.002), Model 3 presents an OR of 0.95 (95% CI 0.91–0.99, P = 0.01), and even after adjusting for all covariates in Model 4, the relationship remains statistically significant (OR 0.94; 95% CI 0.90–0.99, P = 0.01). Furthermore, when categorizing CDAI into tertiles for a more nuanced analysis, it was observed that individuals in the highest tertile (T3) exhibited a considerably reduced risk of ED compared to those in the lowest tertile (T1), across all models: model 1 (OR 0.53; 95% CI 0.40–0.69, P < 0.0001), Model 2 (OR 0.57; 95% CI 0.43–0.75, P < 0.001), Model 3 (OR 0.61; 95% CI 0.45–0.82, P = 0.01), and Model 4 (OR 0.57; 95% CI 0.39–0.82, P = 0.01). The trend across these models was statistically significant (P < 0.01). Additionally, the use of restricted cubic spline (RCS) in our analysis provided insight into the dose–response relationship between CDAI scores and ED risk. This analysis revealed a negative, non-linear association, indicating a sharp decline in ED risk with initial increases in CDAI scores, which then plateaued. This trend was statistically significant (P for overall < 0.0001; P for nonlinearity = 0.0367), as depicted in Fig. 2.Table 2 Association of CDAI and erectile dysfunction risk.

	Model 1	P-value	Model 2	P-value	Model 3	P-value	Model 4	P-value	
OR (95% CI)	OR (95% CI)	OR (95% CI)	OR (95% CI)	
CDAI	0.93 (0.90, 0.96)	 < 0.0001	0.94 (0.91, 0.98)	0.002	0.95 (0.91, 0.99)	0.01	0.94 (0.90, 0.99)	0.01	
Stratified by CDAI tertiles	
 Tertile1	1		1		1		1		
 Tertile2	0.79 (0.63, 0.99)	0.04	0.75 (0.58, 0.98)	0.04	0.81 (0.61, 1.08)	0.13	0.79 (0.57, 1.10)	0.14	
 Tertile3	0.53 (0.40, 0.69)	 < 0.0001	0.57 (0.43, 0.75)	 < 0.001	0.61 (0.45, 0.82)	0.004	0.57 (0.39, 0.82)	0.01	
P for trend		 < 0.0001		 < 0.001		0.004		0.006	
Model1: unadjusted.

Model2: adjusted for age and race education level, BMI categories, recreational activity, smoking, drinking status, testosrerone, and total energy.

Model3: adjusted for age, race, marital status.

Model4: further adjusted for CVD, hypercholesterolemia, hypertension as well as diabetes.

OR odds ratios, CI confidence intervals, CDAI composite dietary antioxidant index.

Fig. 2 Dose–response relationship analysis between CDAI and erectile dysfunction. ED erectile dysfunction, CI confidence intervals, CDAI composite dietary antioxidant index. RCS regression was adjusted for age, race, marital status, education level, BMI categories, recreational activity, smoking, drinking status, CVD, hypercholesterolemia, hypertension, diabetes, testosterone, and total energy (Model 4). The red solid line represents ORs, red shaded region represents 95% CI.

Subgroup analysis

Our study proceeded to examine the stability of the link between CDAI and the risk of ED across different participant subgroups, with the results visualized in Fig. 3. After adjusting for covariates, we found that the association between CDAI score and ED did not differ significantly within subgroups (All P for interaction > 0.05). Specifically, the association between CDAI score and ED risk was consistent across subgroups such as age, race, BMI category, smoking status, drinking status, recreational activity, hypertension, diabetes, hypercholesterolemia, and CVD.Fig. 3 Stratified associations between CDAI and erectile dysfunction. OR odds ratios, CI confidence intervals, BMI body mass index, CVD cardiovascular disease. Analyses were adjusted for age, race, marital status, education level, BMI categories, recreational activity, smoking, drinking status, CVD, hypercholesterolemia, hypertension, diabetes, testosterone, and total energy.

Sensitivity analysis

After excluding 320 participants who had taken PDE5 inhibitors, steroids, sex hormones, antipsychotics, and antidepressants in the past 30 days, a weighted multifactor logistic regression analysis of CDAI and ED risk was presented in Table 3. In Model 4, after adjusting for potential covariates, the risk of CDAI and ED still presents a negative correlation (OR 0.94; 95% CI 0.90–0.99, P = 0.02). Compared with T1, the risk of ED was significantly reduced in T3 group of CDAI (T3 vs T1; OR 0.54; 95% CI 0.37–0.79, P = 0.01).Table 3 Sensitivity analyses.

	Model 1	P-value	Model 2	P-value	Model 3	P-value	Model 4	P-value	
OR (95% CI)	OR (95% CI)	OR (95% CI)	OR (95% CI)	
CDAI	0.93 (0.90, 0.96)	 < 0.001	0.94 (0.91, 0.97)	0.001	0.95 (0.91, 1.00)	0.02	0.94 (0.90, 0.99)	0.02	
Stratified by CDAI tertiles	
 Tertile1	1		1		1		1		
 Tertile2	0.78 (0.62, 0.98)	0.03	0.75 (0.57, 0.98)	0.03	0.79 (0.58, 1.09)	0.14	0.80 (0.56, 1.13)	0.18	
 Tertile3	0.51 (0.38, 0.67)	 < 0.0001	0.54 (0.41, 0.71)	 < 0.001	0.57 (0.42, 0.79)	0.003	0.54 (0.37, 0.79)	0.01	
P for trend		 < 0.0001		 < 0.001		0.003		0.005	
Sensitivity analyses excluded participants taking medications that could affect erectile function.

Model1: unadjusted.

Model2: adjusted for age and race.

Model3: adjusted for age, race, marital status, education level, BMI categories, recreational activity, smoking, drinking status, testosterone, and total energy.

Model4: further adjusted for CVD, hypercholesterolemia, hypertension as well as diabetes.

OR odds ratios, CI confidence intervals, CDAI composite dietary antioxidant index.

Discussion

In our analysis of the nationwide, cross-sectional survey data derived from the NHANES, we observed a pronounced link between the CDAI and the occurrence of ED. Through both univariate and multivariate logistic regression analyses, we discerned that elevated CDAI scores were inversely related to the likelihood of ED. Additionally, a dose–response evaluation between CDAI levels and ED incidence revealed a nonlinear inverse trend. When examining various demographic and health condition strata, our subgroup assessments indicated that these factors did not alter the robustness of the CDAI–ED relationship. At the same time, sensitivity analysis also shows the stability of the research conclusions.

The causes of ED are manifold and may be caused by psychological, neurological, hormonal, arterial, or cavernous body damage27. However, it is now generally accepted that ED is primarily caused by underlying vascular causes28. Normal erection depends on NO—mediated smooth muscle relaxation of the cavernous body produced by the vascular endothelium. In cavernous smooth muscle, NO activates guanosine cyclase, increases the concentration of cyclic guanosine monophosphate acid, and ultimately leads to hyperpolarization and relaxation of smooth muscle by opening potassium channels and inhibiting calcium channels, further triggering penile erection29. Therefore, vascular endothelial dysfunction resulting in reduced endothelial production of NO appears to play a key role in erectile dysfunction30.

Previous studies have shown that oxidative stress is the main cause of endothelial dysfunction31. Oxidative stress is defined as an excess of ROS or a lack of antioxidants32, and the imbalance in ROS production can lead to cell damage. During oxidative stress, a large number of ROS react with NO to form peroxynitrite, which accelerates the degradation of NO and ultimately leads to the decrease of available NO33,34. Meanwhile, peroxynitrite and superoxide can increase the incidence of endothelial cell apoptosis35. This leads to endothelial stripping, further reducing the available NO. In addition, superoxide has been reported to have a direct vasoconstrictive effect through the mobilization of calcium ions36, which may produce ED. Therefore, antioxidant therapy may help prevent and treat ED.

In this study, CDAI was calculated to include dietary nutrients such as vitamin A, vitamin C, vitamin E, zinc, selenium, and carotenoids. All of these nutrients are associated with lower levels of oxidative stress in the body. Non-enzymatic antioxidants, such as vitamins A, C, and E, can reduce the damage caused by oxidative stress37,38. Selenium binds to selenium proteins to prevent lipid peroxidation and oxidative cell damage39. Zinc is an antioxidant called mitochondrial metalloenzyme (ZnSOD)40. Carotenoids help produce antioxidant enzymes41. Although there are still relatively few studies on the relationship between CDAI and ED, the use of dietary antioxidant properties to intervene in ED has been the focus of current research. Studies by Cassidy et al. found that habitual consumption of specific foods rich in flavonoids (which have strong antioxidant properties) was associated with a reduced incidence of ED42. Gao et al. showed that higher intake of lycopene (a carotenoid) was associated with a lower prevalence of ED19. In addition, a study on NHANES showed that dietary increases in trace metals zinc and selenium also helped reduce the prevalence of ED43. Prior research has predominantly concentrated on the impact of isolated dietary antioxidants on the health of vascular endothelium. Yet, considering the synergistic effects of nutrient complexes found in foods, a holistic antioxidant intake might offer a more encompassing benefit. Indices like CDAI could serve as a measure of such comprehensive dietary antioxidant consumption. Our study’s findings reveal an inverse relationship between CDAI scores and the incidence of ED, hinting that a diet rich in a spectrum of antioxidant nutrients might play a role in both preventing and alleviating ED that stems from oxidative stress. Nonetheless, the precise biological mechanisms at play remain elusive, and further investigation is required to bridge the knowledge gap in this domain.

Our investigation presents various strengths and limitations. A significant strength is the extensive sample size that mirrors the broader national demographic, enhancing the generalizability of our findings. Additionally, the use of proper sampling weights in our analysis mitigates the potential for over-sampling bias, bolstering the credibility of our conclusions. Nonetheless, the study is not without its limitations. Given its cross-sectional design, it does not support the establishment of a causal link between CDAI and the incidence of ED. Moreover, the reliance on self-reported data from a single-question survey format in NHANES for diagnosing ED may compromise the precision of the diagnosis. In addition, the study lacked measures of relevant markers of oxidative stress in the participants. Lastly, since the erectile dysfunction data from NHANES spans only from 2001 to 2004, this constrains our capacity to affirm whether the observed associations hold true for the present-day population.

Conclusions

The results of our research indicate that high levels of CDAI could potentially lower the likelihood of ED in adults in the United States. Nevertheless, the necessity for further validation of these findings through extensive, prospective cohort studies remains crucial.

Author contributions

HZ: protocol/project development, data analysis, manuscript writing, and manuscript revision; SC: project development and data analysis; QY: project development and data analysis; WL: data collection and management, data analysis, and manuscript writing; TL: data analysis and manuscript writing; ZX: project development and data analysis; ZH: protocol/project development, data collection and management, data analysis, and manuscript writing.

Data availability

We analyzed publicly available data sets for this study. This data can be found here: https://www.cdc.gov/nchs/nhanes/index.htm.

Competing interests

The authors declare no competing interests.

Ethical approval

The studies involving human participants were approved by the National Center for Health Statistics Research Ethics Review Board, and informed consent was obtained from all participants in this study (continuation of protocol #2001-01). Participants gave informed consent to participate in the study before taking part.

Informed consent

Informed consent was obtained from all individual participants enrolled in the study.

Publisher's note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

These authors contributed equally: Huajun Zhu, Si Chen and Qianyi Ye.
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