Nutrigenetic response to omega-3 fatty acids in obese asthmatics (NOOA): rationale and methods.

Nutrigenetic response to omega-3 fatty acids in obese asthmatics (NOOA): rationale and methods.
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DOI:
10.1016/j.cct.2012.12.009
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发表时间:
2013-03
影响因子:
2.2
通讯作者:
Nemours Network for Asthma Research
Nemours Network for Asthma Research
中科院分区:
医学4区
文献类型:
--
作者:
Lang JE;Mougey EB;Allayee H;Blake KV;Lockey R;Gong Y;Hossain J;Killen K;Lima JJ;Nemours Network for Asthma Research

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不受控制的哮喘是住院和急诊室就诊的主要原因。包括肥胖、非洲血统和儿童在内的因素与哮喘严重程度增加有关。考虑到哮喘引起的高发病率,存在相对较少的药物类别来控制这种常见疾病。因此,可能需要新的治疗策略来减少哮喘对公众健康的影响。数据表明,缺乏omega-3脂肪酸的高脂肪饮食可能会促进肥胖和过度炎症,导致更严重的哮喘。补充omega-3脂肪酸的小型试验已经进行,结果令人鼓舞但不一致。在过去的试验中观察到的反应的变异性可能是由于过去的受试者的遗传学(特别是ALOX 5 rs 59439148)或其特定的哮喘表型。因此,目前正在进行“肥胖型哮喘患者对Omega-3脂肪酸的营养遗传学反应(NOOA)”试验,该试验设计为随机、双盲、安慰剂对照干预研究,以确定补充Omega-3脂肪酸是否可改善患有不受控制的哮喘的肥胖青少年和年轻成人的症状。在这里,我们报告了NOOA试验的设计和原理。参与者每天服用3.18克二十碳五烯酸和822毫克二十二碳六烯酸,或匹配的对照豆油,持续24周。哮喘控制问卷评分的变化是主要结果。次要结局包括肺功能测定、脉冲多普勒、加重率、气道生物标志物、全身炎症、白三烯生物合成和T淋巴细胞功能。NOOA可能导致一种新的治疗策略,并更好地理解饮食在哮喘发病机制中的作用。
Uncontrolled asthma is a major cause of hospitalizations and emergency room visits. Factors including obesity, African ancestry and childhood are associated with increased asthma severity. Considering the high morbidity caused by asthma, relatively few classes of drugs exist to control this common disease. Therefore, new therapeutic strategies may be needed to reduce asthma’s impact on public health. Data suggest that a high fat diet that is deficient in omega-3 fatty acids could promote both obesity and excessive inflammation, resulting in greater asthma severity. Small trials with supplemental omega-3 fatty acids have been conducted with encouraging but inconsistent results. The variability in response seen in past trials may be due to the past subjects’ genetics (specifically ALOX5 rs59439148) or their particular asthma phenotypes. Therefore, the “Nutrigenetic response to Omega-3 Fatty acids in Obese Asthmatics (NOOA)” trial is currently underway and was designed as a randomized, double-blind, placebo controlled intervention study to determine if supplemental omega-3 fatty acids improves symptoms among obese adolescents and young adults with uncontrolled asthma. Here we report the design and rationale for the NOOA trial. Participants were given either 3.18g daily of eicosapentaenoic acid and 822mg daily docosahexaenoic acid, or matched control soy oil, for 24 weeks. Change in the asthma control questionnaire score was the primary outcome. Secondary outcomes included spirometry, impulse oscillometry, exacerbation rate, airway biomarkers, systemic inflammation, leukotriene biosynthesis and T-lymphocyte function. NOOA may lead to a new therapeutic treatment strategy and greater understanding of the mechanistic role of diet in the pathogenesis of asthma.
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