Alshaarawy Omayma, Anthony James C
Department of Epidemiology and Biostatistics, Michigan State University, East Lansing, MI 48823, United States.
Department of Epidemiology and Biostatistics, Michigan State University, East Lansing, MI 48823, United States.
Drug Alcohol Depend. 2015 Feb 1;147:203-7. doi: 10.1016/j.drugalcdep.2014.11.017. Epub 2014 Nov 28.
Pre-clinical studies link cannabinoid-1 receptor activation to inflammation and atherosclerotic effects; anti-inflammation and immunosuppression seem to be mediated by cannabinoid-2 receptor activation. In this epidemiological study, we aim to present estimates on suspected cannabis-attributable immunomodulation as manifest in serum C-reactive protein (CRP) levels as non-specific inflammatory markers with interpretable clinical values. With strength of data from recent large nationally representative community sample surveys, the research approach illustrates value of a quantile regressions approach in lieu of the commonly used but relatively arbitrary cutpoints for CRP values.
The study population encompasses 20-59 year old participants from the National Health and Nutrition Examination Surveys, 2005-2010 (n=1115 recently active cannabis smokers and 8041 non-smokers, identified via confidential Audio Computer Assisted Self-Interviews). Age, sex, race, education, income-poverty ratio, alcohol consumption, and tobacco smoking also were measured, together with body mass index (BMI), which actually might be on a mediational path. Quantile regressions, with bootstrapping for variance estimation, made it possible to hold these covariates constant while estimating cannabis-CRP associations.
Evidence suggesting possible cannabis-attributable immunomodulation emerges at CRP levels below the median (p<0.05). Whereas BMI might help explain a cannabis link with serum CRP, but BMI-stratified analyses disclosed no appreciable variation of the cannabis-CRP relationship across BMI subgroups.
Extending pre-clinical research on cannabis-attributable immunomodulation, this study's CRP evidence points toward possible anti-inflammatory effects of cannabis smoking. More definitive evidence can be derived by combining pre-clinical research, studies of patients, and epidemiological research approaches.
临床前研究将大麻素-1受体激活与炎症和动脉粥样硬化作用联系起来；抗炎和免疫抑制似乎由大麻素-2受体激活介导。在这项流行病学研究中，我们旨在呈现对疑似大麻所致免疫调节的估计，这种调节表现为血清C反应蛋白（CRP）水平，CRP是具有可解释临床价值的非特异性炎症标志物。借助近期全国代表性社区样本调查的有力数据，该研究方法说明了分位数回归方法相对于常用但相对随意的CRP值切点的价值。
研究人群包括2005 - 2010年美国国家健康与营养检查调查中20 - 59岁的参与者（通过保密的音频计算机辅助自我访谈确定了1115名近期有大麻吸食行为者和8041名非吸食者）。还测量了年龄、性别、种族、教育程度、收入贫困率、饮酒量和吸烟情况，以及体重指数（BMI），BMI实际上可能处于中介路径上。通过分位数回归并进行自抽样以估计方差，使得在估计大麻与CRP的关联时能够保持这些协变量不变。
有证据表明，在CRP水平低于中位数时，可能出现大麻所致的免疫调节（p<0.05）。虽然BMI可能有助于解释大麻与血清CRP的联系，但按BMI分层分析显示，大麻与CRP的关系在不同BMI亚组中没有明显差异。
本研究扩展了关于大麻所致免疫调节的临床前研究，CRP证据表明大麻吸食可能具有抗炎作用。通过结合临床前研究、患者研究和流行病学研究方法，可以获得更确凿的证据。
