核桃（Walnuts）营养价值丰富（富含omega-3脂肪酸、抗氧化剂、维生素、膳食纤维等成分），被称为“超级食物”。

现在，来自于美国伊利诺伊大学食品科学与人类营养学助理教授Hannah Holscher带领团队找到了“超级”的潜在原因。他们发现，核桃不仅仅会影响肠道菌群以及微生物产生的次级胆汁酸（Secondary bile acids），还可以降低成年人身体内的低密度胆固醇水平，从而对心脏、新陈代谢和胃肠道产生积极的作用。这一新发现以“Walnut Consumption Alters the Gastrointestinal Microbiota, Microbially Derived Secondary Bile Acids, and Health Markers in Healthy Adults: A Randomized Controlled Trial”为题发表于《The Journal of Nutrition》期刊。

“我们发现，食用核桃可以增加分泌丁酸（有益于肠道健康的代谢物）的微生物的水平。” Hannah Holscher解释道。这一研究为解析食物与肠道微生物的互作提供了新视角。

影响肠道菌群

具体来说，Hannah Holscher团队招募了18名健康的成年人，将他们随机分成两组，分别食用0g或者42g（相当于一手掌多的核桃）核桃。研究人员会在试验开始前、结束后采集他们的排泄物和血液样本，从而分析核桃对于微生物、胆汁酸以及健康代谢标志物的影响。

结果显示，摄取核桃会增加3类细菌的浓度：Faecalibacterium、罗斯氏菌（Roseburia）和梭菌（Clostridium）。其中，梭菌负责丁酸的分泌，Faecalibacterium可以减少炎症、提高胰岛素敏感性。

影响次级胆汁酸

研究结果还表明，与对照组相比，食用核桃可以减少次级胆汁酸的浓度。而次级胆汁酸会损伤为肠道细胞。事实上，先前已有研究表明，在结直肠癌发病率较高的人群中，次级胆汁酸的含量更高。所以，控制次级胆汁酸的水平有助于肠道健康。

部分能量会被肠道微生物利用

最后，值得一提的是，该研究还解释了为什么“食用核桃所产生的卡路里少于传统认知”。

“这是因为，从核桃中获取多少能量的计算值与实际身体所吸收的能量值是不一样的。” Hannah Holscher解释道，“通常，机体只会吸收标签上约80%的核桃能量。这意味着，微生物可以获得剩余20%的卡路里、脂肪和纤维。”那么，微生物会反过来积极影响宿主，还是消极对待宿主呢？该研究提供的初步发现表明，微生物与宿主未能消化的核桃成分相互作用，并产生了积极的效果。（来源：生物探索  艾曼）

Walnut Consumption Alters the Gastrointestinal Microbiota, Microbially Derived Secondary Bile Acids, and Health Markers in Healthy Adults: A Randomized Controlled Trial

Abstract  Background  Epidemiologic data suggest that diets rich in nuts have beneficial health effects, including reducing total and cause-specific mortality from cancer and heart disease. Although there is accumulating preclinical evidence that walnuts beneficially affect the gastrointestinal microbiota and gut and metabolic health, these relations have not been investigated in humans. Objective  We aimed to assess the impact of walnut consumption on the human gastrointestinal microbiota and metabolic markers of health. Methods  A controlled-feeding, randomized crossover study was undertaken in healthy men and women [n = 18; mean age = 53.1 y; body mass index (kg/m2): 28.8]. Study participants received isocaloric diets containing 0 or 42 g walnuts/d for two 3-wk periods, with a 1-wk washout between diet periods. Fecal and blood samples were collected at baseline and at the end of each period to assess secondary outcomes of the study, including effects of walnut consumption on fecal microbiota and bile acids and metabolic markers of health. Results  Compared with after the control period, walnut consumption resulted in a 49–160% higher relative abundance of Faecalibacterium, Clostridium, Dialister, and Roseburia and 16–38% lower relative abundances of Ruminococcus, Dorea, Oscillospira, and Bifidobacterium (P < 0.05). Fecal secondary bile acids, deoxycholic acid and lithocholic acid, were 25% and 45% lower, respectively, after the walnut treatment compared with the control treatment (P < 0.05). Serum LDL cholesterol and the noncholesterol sterol campesterol concentrations were 7% and 6% lower, respectively, after walnut consumption compared with after the control treatment (P < 0.01). Conclusions  Walnut consumption affected the composition and function of the human gastrointestinal microbiota, increasing the relative abundances of Firmicutes species in butyrate-producing Clostridium clusters XIVa and IV, including Faecalibacterium and Roseburia, and reducing microbially derived, proinflammatory secondary bile acids and LDL cholesterol. These results suggest that the gastrointestinal microbiota may contribute to the underlying mechanisms of the beneficial health effects of walnut consumption. This trial was registered at www.clinicaltrials.gov as NCT01832909.

原文链接：https://academic.oup.com/jn/advance-article/doi/10.1093/jn/nxy004/4992079