Zhou Wen, Zhou Huanqun
Department of Reproductive Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.
Front Endocrinol (Lausanne). 2025 May 20;16:1547267. doi: 10.3389/fendo.2025.1547267. eCollection 2025.
The interplay between obesity and male reproductive health, particularly concerning reproductive hormone fluctuations, is a well-documented concern. Despite varied findings on the BMI-AMH/INHB relationship, this study utilized NHANES data (1999-2004) to clarify this association, aiming to refine the assessment of obesity's effects on the reproductive hormone levels of adult male Americans.
We conducted a cross-sectional analysis involving 728 men aged 20 and older. Height and weight were measured by trained staff, and hormone levels were determined using the ELISA method. We performed weighted multiple linear regression to assess the associations between BMI and AMH/INHB, including subgroup interactions, and utilized smoothing curve fitting to analyze nonlinear relationships, along with a threshold effect analysis to evaluate key thresholds.
Participants in higher BMI quartiles showed a declining trend in AMH levels (P=0.16) and a significant reduction in INHB levels (P<0.01). A negative correlation between BMI and AMH (β: -0.15, 95%CI: -0.23 to -0.06, P<0.01) and INHB levels (β: -2.14, 95%CI: -2.98 to -1.31, <0.0001) was observed, with these correlations remaining statistically significant (AMH: β: -0.12, 95%CI: -0.23 to -0.01, <0.05; INHB: β: -1.50, 95%CI: -2.66 to -0.34, <0.05) after adjusting for relevant confounders. However, the effect size for AMH was relatively low, which may limit its clinical significance. In the fully adjusted model, the increase in BMI in Q4 was linked to decreases of 1.62 ng ml-1 in AMH and 18.20 pg ml in INHB, but these associations were not statistically significant (P>0.05). The association between BMI and AMH/INHB showed no significant interaction effects across all covariates (P>0.05 for the interaction), although negative correlations were present in most subgroups (P<0.05). While both AMH and INHB declined with increasing BMI, they displayed nonlinear relationship at key thresholds of 30.78 kg m-² (below: β=0.02, P>0.05; above: β=-0.30, P<0.05) and 33.86 kg m² (below: β=-1.24, P=0.05; above: β=-3.22, P<0.05).
BMI is associated with a relatively independent negative correlation with serum AMH and INHB levels in adult men, which is more noticeable in obese men and shows no significant interaction with other confounding factors. However, due to the low effect size of BMI/AMH, caution is needed in interpreting its clinical significance. Although we found a non-linear relationship and key thresholds between these variables, further studies with larger sample sizes are needed to confirm these findings.
肥胖与男性生殖健康之间的相互作用,尤其是关于生殖激素波动的问题,是一个有充分文献记载的关注点。尽管关于体重指数(BMI)与抗缪勒管激素(AMH)/抑制素B(INHB)关系的研究结果各异,但本研究利用美国国家健康与营养检查调查(NHANES,1999 - 2004年)数据来阐明这种关联,旨在完善对肥胖对成年美国男性生殖激素水平影响的评估。
我们对728名20岁及以上男性进行了横断面分析。由经过培训的工作人员测量身高和体重,并采用酶联免疫吸附测定(ELISA)法测定激素水平。我们进行加权多元线性回归以评估BMI与AMH/INHB之间的关联,包括亚组间相互作用,并利用平滑曲线拟合分析非线性关系,同时进行阈值效应分析以评估关键阈值。
处于较高BMI四分位数的参与者,其AMH水平呈下降趋势(P = 0.16),INHB水平显著降低(P < 0.01)。观察到BMI与AMH(β: - 0.15,95%置信区间: - 0.23至 - 0.06,P < 0.01)以及INHB水平(β: - 2.14,95%置信区间: - 2.98至 - 1.31,P < 0.0001)之间存在负相关,在调整相关混杂因素后,这些相关性仍具有统计学意义(AMH:β: - 0.12,95%置信区间: - 0.23至 - 0.01,P < 0.05;INHB:β: - 1.50,95%置信区间: - 2.66至 - 0.34,P < 0.05)。然而,AMH的效应量相对较低,这可能限制了其临床意义。在完全调整模型中,第四四分位数中BMI的增加与AMH降低1.62 ng/ml和INHB降低18.20 pg/ml相关,但这些关联无统计学意义(P > 0.05)。BMI与AMH/INHB之间的关联在所有协变量中均未显示出显著的交互作用(交互作用P > 0.05),尽管在大多数亚组中存在负相关(P < 0.05)。虽然AMH和INHB均随BMI增加而下降,但在关键阈值30.78 kg/m²(低于该阈值:β = 0.02,P > 0.05;高于该阈值:β = - 0.30,P < 0.05)和33.86 kg/m²(低于该阈值:β = - 1.24,P = 0.05;高于该阈值:β = - 3.22,P < 0.05)处呈现非线性关系。
BMI与成年男性血清AMH和INHB水平存在相对独立的负相关,在肥胖男性中更为明显,且与其他混杂因素无显著交互作用。然而,由于BMI/AMH的效应量较低,在解释其临床意义时需谨慎。尽管我们发现了这些变量之间的非线性关系和关键阈值,但需要更大样本量的进一步研究来证实这些发现。