Apalowo Oladayo E, O'Dwyer Meghan, Nsubuga Edirisa J, Pylate Leah, Alardawi Abeer M, Reeder Nicole, Kiyimba Frank, Tolar-Peterson Terezie, Schilling Wes, Komakech Joel J
Department of Biochemistry, Nutrition and Health Promotion, Mississippi State University, Mississippi State, MS 39762, USA.
Department of Food and Nutrition, King Abdulaziz University, Jeddah P.O. Box 80200, Saudi Arabia.
Nutrients. 2025 Aug 14;17(16):2640. doi: 10.3390/nu17162640.
Obesity is a well-documented risk factor for cardiometabolic diseases associated with insulin resistance. However, research on its relationship with alcohol intake and stress markers, such as cortisol and α-amylase, remains limited, particularly among young adults in the general population.
This study investigated the relationship between adiposity measures, alcohol intake, and biological stress biomarkers among college students.
Participants ( = 189) completed the NIH Diet History Questionnaire II. Body composition was measured via bioelectrical impedance analysis. Salivary α-amylase (sAA) activity and cortisol (sCort) were assessed using the Salimetrics α-amylase kinetic enzyme assay and enzyme immunoassay kits, respectively. Multivariable linear regression models were used to determine the association between alcohol consumption and adiposity on biological stress biomarkers.
Among students who were overweight and obese, higher alcohol consumption increased sAA activity (β 1.52, = 0.030), with a greater effect in females (β = 2.24, = 0.012). Body fat percentage showed similar patterns with sAA activity (β = 2.20, = 0.015), with no significant effect in males. There was no significant interaction between BMI or body fat and alcohol consumption on sCort levels. However, significant main effects were observed for African Americans (β = 0.22, = 0.020) and overweight and obese status (β = -0.19, = 0.025) on male students' sCort levels. African Americans (β = 0.21, = 0.026) and young male adults within the underfat category (β = 0.35, = 0.022) also exhibited increased sCort levels.
Sex-specific patterns in physiological responses between males and females revealed stronger associations in females for sAA activity and distinct patterns in sCort levels among African American males.
肥胖是与胰岛素抵抗相关的心血管代谢疾病的一个有充分记录的风险因素。然而,关于其与酒精摄入以及应激标志物(如皮质醇和α-淀粉酶)之间关系的研究仍然有限,尤其是在普通人群中的年轻成年人中。
本研究调查了大学生中肥胖指标、酒精摄入与生物应激生物标志物之间的关系。
参与者(n = 189)完成了美国国立卫生研究院饮食历史问卷II。通过生物电阻抗分析测量身体成分。分别使用Salimetricsα-淀粉酶动力学酶测定法和酶免疫测定试剂盒评估唾液α-淀粉酶(sAA)活性和皮质醇(sCort)。多变量线性回归模型用于确定酒精消费与肥胖对生物应激生物标志物的关联。
在超重和肥胖的学生中,较高的酒精消费增加了sAA活性(β = 1.52,P = 0.030),在女性中影响更大(β = 2.24,P = 0.012)。体脂百分比与sAA活性呈现相似模式(β = 2.20,P = 0.015),在男性中无显著影响。BMI或体脂与酒精消费对sCort水平没有显著交互作用。然而,观察到非裔美国人(β = 0.22,P = 0.020)以及超重和肥胖状态(β = -0.19,P = 0.025)对男学生sCort水平有显著主效应。非裔美国人(β = 0.21,P = 0.026)以及体脂不足类别的年轻男性成年人(β = 0.35,P = 0.022)也表现出sCort水平升高。
男性和女性之间生理反应的性别特异性模式显示,女性中sAA活性的关联更强,非裔美国男性中sCort水平存在不同模式。