Dept. of Addictive Behavior and Addiction Medicine, Central Institute of Mental Health (CIMH), University of Heidelberg, Mannheim, Germany.
Horm Behav. 2011 Jun;60(1):58-64. doi: 10.1016/j.yhbeh.2011.02.013. Epub 2011 Mar 3.
Preclinical and clinical data suggest modulating effects of appetite-regulating hormones and stress perception on food intake. Nicotine intake also interferes with regulation of body weight. Especially following smoking cessation gaining weight is a common but only partially understood consequence. The aim of this study was to examine the interaction between smoking habits, the appetite regulating hormone leptin, negative affectivity, and stress vulnerability on eating behavior in a clinical case-control study under standardized conditions. In a large population-based study sample, we compared leptin and cortisol plasma concentrations (radioimmunoassay) between current tobacco smokers with high cognitive restraint and disinhibition in eating behavior and smokers scoring low in both categories as assessed with the Three Factor Eating Questionnaire (TFEQ; Stunkard & Messick, 1985). As a measure for smoking effects on the stress axis, the saliva cortisol concentrations were compared before and after nicotine smoking. Additionally, stress perception was assessed with the Perceived Stress Scale (PSS), symptoms of depression and anxiety with the Beck Depression Inventory (BDI) and the State Trait Anxiety Inventory (STAI). In smokers showing high cognitive restraint and disinhibition we found significantly higher leptin concentrations than in the group of smokers scoring low in both categories. Furthermore there was a significant group difference in saliva cortisol concentrations after nicotine intake. Smokers showing high cognitive restraint and disinhibition were also characterized by significantly higher scores in the STAI, the PSS and the BDI. Our results suggest that smokers with a pathological eating behavior show an impaired neuroendocrine regulation of appetite and are prone to experience higher levels of stress and negative affectivity. This interaction of behavioral and neuroendocrinological factors may constitute a high risk condition for gaining weight following smoking cessation.
临床前和临床数据表明,食欲调节激素和压力感知对食物摄入有调节作用。尼古丁的摄入也会干扰体重的调节。尤其是在戒烟后,体重增加是一种常见但部分尚未被理解的后果。本研究的目的是在标准化条件下,通过临床病例对照研究,检测吸烟习惯、食欲调节激素瘦素、负性情感和压力易感性对进食行为的相互作用。在一项基于大样本的研究中,我们比较了当前吸烟者中高认知约束和饮食行为中抑制作用的高瘦素和皮质醇血浆浓度(放射免疫测定),以及在饮食行为中这两个类别得分较低的吸烟者。作为吸烟对压力轴影响的测量指标,比较了尼古丁吸烟前后的唾液皮质醇浓度。此外,使用感知压力量表(PSS)评估压力感知,使用贝克抑郁量表(BDI)和状态特质焦虑量表(STAI)评估抑郁和焦虑症状。在表现出高认知约束和抑制作用的吸烟者中,我们发现瘦素浓度明显高于两个类别得分较低的吸烟者。此外,在尼古丁摄入后,唾液皮质醇浓度也存在显著的组间差异。表现出高认知约束和抑制作用的吸烟者,在 STAI、PSS 和 BDI 中的得分也明显更高。我们的研究结果表明,表现出病理性进食行为的吸烟者存在食欲的神经内分泌调节受损,并且更容易体验到更高水平的压力和负性情感。这种行为和神经内分泌因素的相互作用可能构成戒烟后体重增加的高风险条件。