Pharmacology, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Nutrition-Gut-Brain Interactions Research Centre, Faculty of Health and Medicine, School of Medical Sciences, Örebro University, Örebro, Sweden.
Am J Clin Nutr. 2019 Aug 1;110(2):273-279. doi: 10.1093/ajcn/nqz104.
Globally, ∼70% of adults are deficient in intestinal lactase, the enzyme required for the digestion of lactose. In these individuals, the consumption of lactose-containing milk and dairy products can lead to the development of various gastrointestinal (GI) symptoms. The primary solution to lactose intolerance is withdrawing lactose from the diet either by eliminating dairy products altogether or substituting lactose-free alternatives. However, studies have shown that certain individuals erroneously attribute their GI symptoms to lactose and thus prefer to consume lactose-free products. This has raised the question whether consuming lactose-free products reduces an individual's ability to absorb dietary lactose and if lactose-absorbers should thus avoid these products. This review summarizes the current knowledge regarding the acclimatization of lactose processing in humans. Human studies that have attempted to induce intestinal lactase expression with different lactose feeding protocols have consistently shown lack of enzyme induction. Similarly, withdrawing lactose from the diet does not reduce intestinal lactase expression. Evidence from cross-sectional studies shows that milk or dairy consumption is a poor indicator of lactase status, corroborating the results of intervention studies. However, in lactase-deficient individuals, lactose feeding supports the growth of lactose-digesting bacteria in the colon, which enhances colonic lactose processing and possibly results in the reduction of intolerance symptoms. This process is referred to as colonic adaptation. In conclusion, endogenous lactase expression does not depend on the presence of dietary lactose, but in susceptible individuals, dietary lactose might improve intolerance symptoms via colonic adaptation. For these individuals, lactose withdrawal results in the loss of colonic adaptation, which might lower the threshold for intolerance symptoms if lactose is reintroduced into the diet.
全球范围内,约 70%的成年人肠道内缺乏乳糖酶,而乳糖酶是消化乳糖所必需的酶。在这些人群中,食用含乳糖的牛奶和乳制品会导致各种胃肠道 (GI) 症状的发生。乳糖不耐受的主要解决方法是从饮食中去除乳糖,要么完全消除乳制品,要么用无乳糖替代品替代。然而,研究表明,某些人错误地将他们的胃肠道症状归因于乳糖,因此更愿意食用无乳糖产品。这就提出了一个问题,即食用无乳糖产品是否会降低个体吸收膳食乳糖的能力,以及乳糖吸收者是否因此应该避免这些产品。这篇综述总结了目前关于人类乳糖处理适应能力的知识。人类研究尝试通过不同的乳糖喂养方案诱导肠道乳糖酶表达,但一致显示缺乏酶诱导。同样,从饮食中去除乳糖并不能减少肠道乳糖酶的表达。来自横断面研究的证据表明,牛奶或乳制品的摄入是乳糖酶状态的不良指标,这与干预研究的结果相符。然而,在乳糖酶缺乏的个体中,乳糖喂养支持结肠中乳糖消化细菌的生长,这增强了结肠中的乳糖处理,可能导致不耐受症状的减轻。这个过程被称为结肠适应。总之,内源性乳糖酶的表达不依赖于膳食乳糖的存在,但在易感个体中,膳食乳糖可能通过结肠适应改善不耐受症状。对于这些个体,乳糖的去除导致结肠适应的丧失,如果重新引入乳糖饮食,可能会降低不耐受症状的阈值。