Improvements in Sperm Motility Following Low- or High-Intensity Dietary Interventions in Men With Obesity

Abstract

Introduction: Obesity increases risks of male infertility, but bariatric surgery does not improve semen quality. Recent uncontrolled studies suggest that a low-energy diet (LED) improves semen quality. Further evaluation within a randomized, controlled setting is warranted.

Methods: Men with obesity (18-60 years) with normal sperm concentration (normal count) (n = 24) or oligozoospermia (n = 43) were randomized 1:1 to either 800 kcal/day LED for 16 weeks or control, brief dietary intervention (BDI) with 16 weeks' observation. Semen parameters were compared at baseline and 16 weeks.

Results: Mean age of men with normal count was 39.4 ± 6.4 in BDI and 40.2 ± 9.6 years in the LED group. Mean age of men with oligozoospermia was 39.5 ± 7.5 in BDI and 37.7 ± 6.6 years in the LED group. LED caused more weight loss than BDI in men with normal count (14.4 vs 6.3 kg; P < .001) and men with oligozoospermia (17.6 vs 1.8 kg; P < .001). Compared with baseline, in men with normal count total motility (TM) increased 48 ± 17% to 60 ± 10% (P < .05) after LED, and 52 ± 8% to 61 ± 6% (P < .0001) after BDI; progressive motility (PM) increased 41 ± 16% to 53 ± 10% (P < .05) after LED, and 45 ± 8% to 54 ± 65% (P < .001) after BDI. In men with oligozoospermia compared with baseline, TM increased 35% [26] to 52% [16] (P < .05) after LED, and 43% [28] to 50% [23] (P = .0587) after BDI; PM increased 29% [23] to 46% [18] (P < .05) after LED, and 33% [25] to 44% [25] (P < .05) after BDI. No differences in postintervention TM or PM were observed between LED and BDI groups in men with normal count or oligozoospermia.

Conclusion: LED or BDI may be sufficient to improve sperm motility in men with obesity. The effects of paternal dietary intervention on fertility outcomes requires investigation.

Keywords: male fertility; male reproduction; obesity; sperm quality; spermatogenesis; weight loss.

Figure 1.

Effects of dietary interventions on semen parameters in men with normal count. Bar graphs showing (A) sperm concentration (58.5 × 10⁶ ± 32.8, BDI; 53.6 × 10⁶ ± 36.4, LED; P = .73), (D) total motility (61% ± 6, BDI; 60% ± 10, LED; P = .69), and (G) progressive motility (54% ± 6, BDI; 53% ± 10, LED; P = .85) at the end of the dietary intervention in BDI groups and LED groups. Baseline and end of intervention for (B) sperm concentration (P = .12), (E) total motility (P = .02), and (H) progressive motility (P = .02) in the LED group. Baseline and end of intervention for (C) sperm concentration (P = .59), (F) total motility (P < .0001), and (I) progressive motility (P < 0.001) in the BDI group. (A, D, G) Data are presented as mean ± SD. *P < .05; ***P < .001. BDI, brief dietary intervention; LED, low-energy diet.

Figure 2.

Effects of dietary interventions on DNA fragmentation index in men with normal count. (A) Bar graph of DFI at the end of the dietary intervention between the 2 groups (18.3% [6.8]; BDI, 4.1% [8], LED; P < .001). (B) Difference in DFI before and after the dietary intervention in LED group (P = .23). (C) Difference in DFI before and after the dietary intervention in BDI group (P = .15). (D) Scatter plot of weight loss and DFI as measured at the end of the study across both groups (r = −0.56, P = .005). (A) Data are given as median with interquartile range. ***P < .001. DFI: DNA fragmentation index; BDI, brief dietary intervention; LED, low-energy diet.

Figure 3.

Effects of dietary interventions on semen parameters in men with oligozoospermia. Bar graphs of (A) sperm concentration (8.3 × 10⁶ [18.3], BDI; 3.4 × 10⁶ [13.1], LED; P = 0.12), (D) total motility (50% [23], BDI; 52% [16], LED; P = .48), and (G) progressive motility (44% [25], BDI; 46% [18], LED; P = .67) at the end of the dietary intervention in the 2 groups. Baseline and end of intervention for (B) sperm concentration (P = .82), (E) total motility (P = .02), and (H) progressive motility (P = .01) in LED group. Baseline and end of intervention for (C) sperm concentration (P = .21), (F) total motility (P = .0587), and (I) progressive motility (P = .01) in BDI group. (A, D, G) Data are given as median with interquartile range. *P < .05. BDI, brief dietary intervention; LED, low-energy diet.

Figure 4.

Effects of dietary interventions on hormonal parameters after combining the 2 studies. Bar graphs of (A) LH (3.4 ± 1.5, BDI; 3.5 ± 1.4, LED; P = .81), (D) FSH (4.2 ± 2.3, BDI; 4.6 ± 2.4, LED; P = .52), (G) testosterone (13.3 ± 3.7, BDI; 14.8 ± 5.8, LED; P = .19), and (J) SHBG (24 ± 8, BDI; 27 ± 13, LED; P = .30) at the end of the dietary intervention in BDI groups and LED groups. Baseline and end of intervention (B) LH (P = .70), (E) FSH (P = .26), (H) testosterone (P < .0001), and (K) SHBG (P < .001) in the LED group. Baseline and end of intervention for (C) LH (P < .01), (F) FSH (P = .15), (I) testosterone (P = .28), and (L) SHBG (P = .15) in the BDI group. (A, D, G, J) Data are presented as mean ± SD. **P < .01; ***P < .001. BDI, brief dietary intervention; LED, low-energy diet.