Fernander Anita F, Shavers Vickie L, Hammons George J
Behavioral Science Department, College of Medicine, University of Kentucky, Lexington, KY, USA.
Addiction. 2007 Oct;102 Suppl 2:43-57. doi: 10.1111/j.1360-0443.2007.01954.x.
To articulate a broader, multi-causal model that incorporates psychosocial and environmental factors that can differ systematically across racially classified social groups (RCSGs) and impact biological pathways related to the development of tobacco-related diseases.
This paper is built upon a review of the existing scientific literature on selected biopsychosocial factors (diet/nutrition, obesity, alcoholic intake, psychosocial stress, occupational/environmental exposures and exposure to other diseases and illnesses) and tobacco use in examining the biological contributions to differences in tobacco-related health outcomes among RCSGs.
Recent work has focused on RCSG genetic variations as a possible explanation for differences in tobacco-related health disparities. It is argued in this paper that, given the genetic heterogeneity 'within' RCSGs, it is unlikely that across RCSG genetic variations are likely to be the major source of differences impacting biological pathways in tobacco-related health outcomes. The evidence shows that results, even at the level of within-population genetic variations, have been limited and often inconsistent. A conceptual framework is proposed to account for biological pathways related to the development of tobacco-related diseases.
Determinants of tobacco-related health disparities are not understood clearly. The contribution of biological factors may be important. Current efforts to determine biological differences in tobacco use and related diseases among RCSGs have focused primarily on genetic variations. However, this approach has limitations. An alternative biopsychosocial framework that examines the potential biological mechanisms through which life experiences and behavior might affect tobacco use and health outcomes in these population groups is needed, including those of life-style (e.g. diet/nutrition, obesity, physical exercise, alcohol consumption), psychosocial (e.g. stress and coping), occupational/environmental exposures and the presence of other diseases/illnesses.
构建一个更广泛的多因果模型，纳入心理社会和环境因素，这些因素在按种族分类的社会群体（RCSGs）中可能存在系统性差异，并影响与烟草相关疾病发展相关的生物学途径。
本文基于对现有科学文献的综述，这些文献涉及选定的生物心理社会因素（饮食/营养、肥胖、酒精摄入、心理社会压力、职业/环境暴露以及接触其他疾病）和烟草使用，以研究RCSGs中烟草相关健康结果差异的生物学贡献。
近期的研究工作聚焦于RCSG基因变异，将其作为烟草相关健康差异的一种可能解释。本文认为，鉴于RCSGs内部的基因异质性，跨RCSG的基因变异不太可能是影响烟草相关健康结果生物学途径差异的主要来源。证据表明，即使在人群内部基因变异水平上，结果也很有限且往往不一致。本文提出了一个概念框架来解释与烟草相关疾病发展相关的生物学途径。
烟草相关健康差异的决定因素尚未完全明确。生物学因素的贡献可能很重要。目前确定RCSGs中烟草使用及相关疾病生物学差异的努力主要集中在基因变异上。然而，这种方法存在局限性。需要一个替代性的生物心理社会框架，来研究生活经历和行为可能影响这些人群烟草使用和健康结果的潜在生物学机制，包括生活方式（如饮食/营养、肥胖、体育锻炼、饮酒）、心理社会（如压力与应对）、职业/环境暴露以及其他疾病的存在情况。
