Is there an association between body mass index (BMI) and routine semen analysis parameters in adult men? No significant correlation was found between BMI and semen parameters measured with the exception of normal sperm morphology. Multiple cross-sectional studies have found inconsistent results, with two meta-analyses finding no correlation between BMI and semen parameters. A relationship between BMI and male reproductive hormones, particularly total testosterone, has been established in several studies and a systematic review. Cross-sectional study of 511 men recruited at the time of semen analysis over 4 years (2008-2012). Men presenting for semen analysis for any reason at participating fertility clinics in Auckland, New Zealand were recruited, with BMI measured or self-reported at this time. Exclusion criteria included azoospermia and pathological conditions of male genital tract. Conventional BMI categories were used (underweight <18.5 kg/m(2), normal 18.5-24.99 kg/m(2), overweight 25.00-29.99 kg/m(2), obese ≥30 kg/m(2)). The routine semen analysis results for sperm concentration, total sperm count, sperm motility (total motility), sperm morphology, semen volume and total motile sperm (primary outcome) from one semen sample were recorded. Consent from 175 men was obtained to measure LH, FSH, estradiol, total testosterone, free testosterone and sex hormone-binding globulin (SHBG) in a blood sample (secondary outcome). Associations between BMI and these outcomes were assessed using Spearman correlation and analysis of variance, and a multiple linear regression analysis was performed. In addition, the relative risks for men having abnormal semen analysis results according to reference ranges of the World Health Organization, such as oligozoospermia, were calculated. This study has sufficient power to detect a doubling in abnormally low sperm concentration and total sperm count in overweight or obese men compared with men with normal BMI. Participation rate was not recorded. The body mass indices from measured and self-reported samples had an equivalent range of values which did not differ statistically. Median BMI was 27.1 kg/m(2) [10th-90th percentile: 22.8-32.9]. Overall, 72.8% of the study population were overweight or obese (BMI >25 kg/m(2)), while 19 men (3.72%) had a BMI of 35-40 kg/m(2) and 7 men (1%) had a BMI of >40 kg/m(2). No significant correlation was found between BMI and the semen parameters measured with the exception of normal sperm morphology (r = 0.12, P = 0.024), although this finding is derived from only 330 samples. Overweight and obese men showed no significantly increased relative risk of abnormal semen parameters. Of the reproductive hormones, significant negative relationships with BMI were found for total testosterone (r = -0.35, P = <0.0001), free testosterone (r = -0.25, P = <0.0012) and SHBG (r = -0.44, P = <0.0001). Multiple linear regression analysis also showed that BMI had a marginally significant effect on normal sperm morphology (effect estimate =0.47, P = 0.038). In addition, <2 days of abstinence was negatively associated with semen volume (effect estimate =-0.80, P = 0.0074) and summer season was negatively associated with sperm concentration (effect estimate =-14.9, P = 0.020). The power of this study is limited by the relatively small overall sample size, although it does have one of the largest proportions of obese men (23.3%) in published cross-sectional studies. The study involved samples from men attending a fertility clinic, who are likely to have a lower semen quality and higher rate of pathology compared with the general population, therefore limiting the possible generalization of this study to all adult men. Our findings are consistent with those of other cross-sectional studies as well as two meta-analyses but do disagree in part with the most recent meta-analysis (which found significant odds ratios for oligozoospermia and azoospermia with increased BMI) and with studies measuring DNA fragmentation index. Therefore a definitive conclusion on the effect of BMI on semen quality remains uncertain while our data reinforce previous findings that BMI is negatively associated with male reproductive hormones. All funding for this study was from New Zealand academic and charitable sources including: Faculty of Medical and Health Sciences, University of Auckland (New Zealand), the Mercia Barnes Trust of the Royal Australian and New Zealand College of Obstetricians and Gynaecologists and the Nurture Foundation for Reproductive Research. The authors have no conflicts of interest to declare.
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