Colineaux Hélène, Neufcourt Lola, Delpierre Cyrille, Kelly-Irving Michelle, Lepage Benoit
EQUITY Team, CERPOP, INSERM, 37 Allees Jules Guesde, 31062, Toulouse, France.
Epidemiology Department, CHU Toulouse, 37 Allees Jules Guesde, 31062, Toulouse, France.
Emerg Themes Epidemiol. 2023 Mar 23;20(1):2. doi: 10.1186/s12982-023-00121-6.
The principal aim of this study was to explore if biological differences between men and women can be explained by gendered mechanisms.
We used data from the 1958 National Child Development Study, including all the living subjects of the cohort at the outcome collection wave (44-45 years). We explored several biomarkers as outcomes: systolic blood pressure, triglycerides, LDL cholesterol, HbA1c, CRP, and cortisol. Three conceptualizations of gender have been used to define methodological strategies: (a) Gender as an individual characteristic; (b) Gender as an effect of sex on socio-behavioural characteristics; (c) Gender as an interaction between sex and the social environment, here the early-life social environment. We estimated the total effect of sex and the proportion of total effect of sex at birth eliminated by gender, measured by 3 different ways according to these 3 concepts, using g-computation.
The average level of each biomarker was significantly different according to sex at birth, higher in men for cardiometabolic biomarkers and higher in women for inflammatory and neuroendocrine biomarkers. The sizes of the differences were always smaller than one standard deviation but were larger than differences due to early-life deprivation, except for CRP. We observed gender mechanisms underlying these differences between men and women, even if the mediation effects were rarely statistically significant. These mechanisms were of three kinds: (1) mediation by socio-behavioural characteristics; (2) attenuation by gendered mechanisms; (3) interaction with early social environment. Indeed, we observed that being born into a deprived rather than non-deprived family increased metabolic and inflammatory biomarkers levels more strongly in females than in males.
The biological differences between men and women seem to not be purely explained by biological mechanisms. The exploration of gender mechanisms opens new perspectives, in terms of methodology, understanding and potential applications.
本研究的主要目的是探讨男性和女性之间的生物学差异是否可以通过性别机制来解释。
我们使用了1958年全国儿童发展研究的数据，包括该队列在结局收集波次（44 - 45岁）时所有在世的受试者。我们将几种生物标志物作为结局进行探讨：收缩压、甘油三酯、低密度脂蛋白胆固醇、糖化血红蛋白、C反应蛋白和皮质醇。性别有三种概念化方式用于定义方法策略：（a）性别作为个体特征；（b）性别作为性别对社会行为特征的影响；（c）性别作为性别与社会环境（此处为早期生活社会环境）之间的相互作用。我们估计了性别的总体效应以及出生时性别的总体效应中被性别消除的比例，根据这三个概念，使用g计算以三种不同方式进行测量。
根据出生时的性别，每种生物标志物的平均水平存在显著差异，心脏代谢生物标志物男性较高，炎症和神经内分泌生物标志物女性较高。差异的大小总是小于一个标准差，但除C反应蛋白外，均大于因早期生活贫困导致的差异。我们观察到了男女之间这些差异背后的性别机制，即使中介效应很少具有统计学意义。这些机制有三种：（1）通过社会行为特征进行中介；（2）被性别机制减弱；（3）与早期社会环境相互作用。实际上，我们观察到出生在贫困家庭而非非贫困家庭中，女性的代谢和炎症生物标志物水平升高的幅度比男性更大。
男性和女性之间的生物学差异似乎不能单纯由生物学机制来解释。对性别机制的探索在方法、理解和潜在应用方面开辟了新的视角。
