目的:膳食脂肪和脂肪酸(FA)的摄入与弱精子症的几率有关吗?
结论:植物性脂肪的摄入与弱精子症的几率降低有关,而动物性单不饱和脂肪酸(MUFA)的消耗与弱精子症的几率呈正相关。
背景:膳食脂肪和FA是日常饮食的重要成分,已被证明与男性的生殖健康有关。然而,到目前为止,关于脂肪和FA与弱精子症发生率相关的证据尚不清楚.
■基于医院的病例对照研究于2020年6月至2020年12月在不孕症诊所进行。简而言之,549例弱精子症病例和581例正常精子症对照可用于最终分析。
方法:我们通过经过验证的食物频率问卷收集了110种食物的饮食数据。根据世界卫生组织指南确定了无精症病例。探讨膳食脂肪和FA消耗与弱精子症几率的相关性。我们通过非条件逻辑回归模型计算比值比(ORs)和相应的95%CI.
结果:相对于最低三元消费,植物性脂肪摄入量的最高三元率与弱精子症的几率呈负相关(OR=0.68,95%CI=0.50-0.91),具有显着的剂量反应关系(OR=0.85,95%CI=0.75-0.97,每标准偏差增量)。相反,基于动物的MUFA摄入量(OR=1.49,95%CI=1.04-2.14)与弱精子症的几率增加显着相关,并且还检测到明显的剂量反应关系(OR=1.24,95%CI=1.05-1.45,每标准偏差增量)。亚组分析显示与主要结果相似的关联模式。此外,我们观察到以动物为基础的MUFA和吸烟之间在倍增和加性尺度上的显著相互作用。
结论:在任何观察性研究中,选择偏倚和回忆偏倚都是不可避免的。由于我们未能获得反式脂肪酸(TFA)消费的信息,TFA摄入量与弱精子症几率的关系尚不清楚。
结论:这项研究表明,不同来源的脂肪和脂肪酸可能对弱精子症的病因产生不同的影响。吸烟会加剧高动物性MUFA摄入对弱精子症的不利影响。我们的发现为通过减少动物源性脂肪和FA的消耗以及戒烟来预防弱精子症提供了新的证据。
背景:这项工作得到了辽宁省杰邦瓜帅项目的支持,辽宁省自然科学基金,盛京医院临床科研培养项目,盛京医院优秀科学基金。所有作者都没有利益冲突要声明。
背景:不适用。
OBJECTIVE: Are dietary fat and fatty acid (FA) intakes related to the odds of
asthenozoospermia?
CONCLUSIONS: 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.
BACKGROUND: 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.
UNASSIGNED: 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.
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.
RESULTS: 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.
CONCLUSIONS: 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.
CONCLUSIONS: 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.
BACKGROUND: 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.
BACKGROUND: N/A.