Dietary fat and fatty acid consumptions and the odds of asthenozoospermia: a case–control study in China

Abstract

Abstract STUDY QUESTION Are dietary fat and fatty acid (FA) intakes related to the odds of asthenozoospermia? SUMMARY ANSWER Plant-based fat consumption was associated with decreased asthenozoospermia odds, while the consumption of animal-based monounsaturated fatty acid (MUFA) was positively related to asthenozoospermia odds. WHAT IS KNOWN ALREADY Dietary fat and FA are significant ingredients of a daily diet, which have been demonstrated to be correlated to the reproductive health of men. However, to date, evidence on fat and FA associations with the odds of asthenozoospermia is unclear. STUDY DESIGN, SIZE, DURATION The hospital-based case–control study was performed in an infertility clinic from June 2020 to December 2020. Briefly, 549 asthenozoospermia cases and 581 controls with normozoospermia were available for final analyses. PARTICIPANTS/MATERIALS, SETTING, METHODS We collected dietary data through a verified food frequency questionnaire of 110 food items. Asthenozoospermia cases were ascertained according to the World Health Organization guidelines. To investigate the correlations of dietary fat and FA consumptions with the odds of asthenozoospermia, we calculated the odds ratios (ORs) and corresponding 95% CIs through unconditional logistic regression models. MAIN RESULTS AND THE ROLE OF CHANCE Relative to the lowest tertile of consumption, the highest tertile of plant-based fat intake was inversely correlated to the odds of asthenozoospermia (OR = 0.68, 95% CI = 0.50–0.91), with a significant dose–response relation (OR = 0.85, 95% CI = 0.75–0.97, per standard deviation increment). Inversely, animal-based MUFA intake (OR = 1.49, 95% CI = 1.04–2.14) was significantly correlated to increased odds of asthenozoospermia, and an evident dose–response relation was also detected (OR = 1.24, 95% CI = 1.05-1.45, per standard deviation increment). Subgroup analyses showed similar patterns of associations to those of the primary results. Moreover, we observed significant interactions on both multiplicative and additive scales between animal-based MUFA and cigarette smoking. LIMITATIONS, REASONS FOR CAUTION Selection bias and recall bias were unavoidable in any of the observational studies. As we failed to obtain the information of trans-fatty acid (TFA) consumption, the relation of TFA intake and asthenozoospermia odds was unclear. WIDER IMPLICATIONS OF THE FINDINGS This study indicated that different sources of fat and FAs might exert different effects on the etiology of asthenozoospermia, and cigarette smoking could exacerbate the adverse effect of high animal-based MUFA intake on asthenozoospermia. Our findings provide novel evidence pertaining to the fields of prevention of asthenozoospermia through decreasing animal-derived fat and FA consumptions and smoking cessation. STUDY FUNDING/COMPETING INTEREST(S) This work was supported by the JieBangGuaShuai Project of Liaoning Province, Natural Science Foundation of Liaoning Province, Clinical Research Cultivation Project of Shengjing Hospital, and Outstanding Scientific Fund of Shengjing Hospital. All authors have no conflict of interest to declare. TRIAL REGISTRATION NUMBER N/A.