Division of Rheumatology, Inflammation and Immunity, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Nutrition. 2024 Jul;123:112413. doi: 10.1016/j.nut.2024.112413. Epub 2024 Feb 28.
We assessed the joint effects of omega (n)-3 fatty acid supplementation and dietary fish intake on systemic lipid mediators of inflammation among adults.
Within VITAL, a double-blind randomized controlled trial, adults were randomized to ω-3 fatty acids (460 mg EPA + 380 mg DHA/d) or placebo. We selected participants who reported low (<1 serving/mo) baseline dietary fish intake and matched them by age, sex, race, and trial arm to participants with self-reported highest fish intake (≥3.9 servings/wk). Baseline and 1-y plasma samples were tested for 9 ω-3 fatty acid-derived lipid mediators. Multivariable linear models assessed lipid mediator changes and joint effects of ω-3 fatty acid supplementation and dietary fish intake.
Forty-eight participants with low baseline fish intake were matched to 48 with high fish intake. Mean age was 64.6 (±7.26), 50% were female, and 85% non-Hispanic white. One-year lipid mediator changes in expected directions were observed in those receiving ω-3 fatty acids versus placebo: reductions in proinflammatory mediators, PGD2, 5-HETE, and 12-HETE; increases in proresolving mediators, EPA and DHA. Larger 1-y lipid biomarker changes were seen in those with low baseline fish intake randomized to active ω-3 fatty acids for DHA, EPA, PGD2, Resolvin D1, and Resolvin D4 were observed, although no significant multiplicative interactions were detected.
Beneficial changes in circulating proresolving and proinflammatory mediators were found with 1-y of ω-3 fatty acid supplementation versus placebo for all participants, with a trend toward larger effects among those with low baseline fish intake, although interactions were not significant.
我们评估了ω(n)-3 脂肪酸补充剂和饮食中鱼类摄入量对成年人系统性炎症脂质介质的联合影响。
在 VITAL 中,一项双盲随机对照试验中,成年人被随机分配到 ω-3 脂肪酸(460mg EPA+380mg DHA/天)或安慰剂。我们选择基线饮食中鱼类摄入量低(<1 份/月)的参与者,并按年龄、性别、种族和试验臂与自我报告鱼类摄入量最高(≥3.9 份/周)的参与者进行匹配。检测基线和 1 年血浆样本中 9 种 ω-3 衍生脂质介质。多变量线性模型评估脂质介质变化和 ω-3 脂肪酸补充剂与饮食中鱼类摄入量的联合作用。
48 名基线鱼类摄入量低的参与者与 48 名鱼类摄入量高的参与者相匹配。平均年龄为 64.6(±7.26),50%为女性,85%为非西班牙裔白人。与安慰剂相比,接受 ω-3 脂肪酸治疗的患者观察到预期方向的 1 年脂质介质变化:促炎介质 PGD2、5-HETE 和 12-HETE 减少,促分解介质 EPA 和 DHA 增加。在基线鱼类摄入量低的患者中,随机分配到活性 ω-3 脂肪酸的患者中观察到更大的 1 年脂质生物标志物变化,尽管未检测到显著的乘法相互作用,但 DHA、EPA、PGD2、Resolvin D1 和 Resolvin D4 的变化更大。
所有参与者接受 1 年 ω-3 脂肪酸补充剂治疗与安慰剂相比,循环中促分解和促炎介质均发生有益变化,基线鱼类摄入量低的患者作用趋势更大,但相互作用无统计学意义。