Sugar consumption, metabolic disease and obesity: The state of the controversy.
Sugar consumption, metabolic disease and obesity: The state of the controversy.
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DOI：
10.3109/10408363.2015.1084990
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发表时间：
2016
影响因子：
10
通讯作者：
Stanhope KL
中科院分区：
文献类型：
--
作者：
Stanhope KL
糖消费对健康的影响仍然是一个有争议的话题。本综述的目的是讨论允许争议继续的证据和缺乏证据，以及为什么解决争议很重要。有合理的机制和研究证据支持这一建议，即过量摄入糖直接或间接地促进心血管疾病（CVD）和2型糖尿病（T2 DM）的发展。直接途径涉及果糖的不受调节的肝脏摄取和代谢，这导致肝脏脂质蓄积、血脂异常、胰岛素敏感性降低和尿酸水平升高。流行病学数据表明，果糖的这些直接影响与含果糖的糖、蔗糖和HFCS的消费有关，这些糖是主要的添加糖。添加糖的摄入与脂肪肝、血脂异常、胰岛素抵抗、高尿酸血症、心血管疾病和2型糖尿病的发生和/或患病率相关，其中许多相关性与体重增加或总能量摄入无关。有饮食干预研究，其中与对照饮食相比，人类受试者在食用高糖时表现出循环脂质增加和胰岛素敏感性降低。最近，我们的小组报告说，补充自由饮食的年轻人与饮料含有0，10，17.5或25%的每日能量需求（Ereq）作为高果糖玉米糖浆（HFCS）增加脂质/脂蛋白的危险因素心血管疾病（CVD）和尿酸的剂量反应方式。然而，缺乏在受控的能量平衡饮食方案下在健康人群中进行的无混淆研究，这些研究允许确定糖对不允许体重增加的饮食的影响。此外，最近的报告得出结论，消费含有高达30% Ereq蔗糖或HFCS的饮料没有不良影响，并且几项荟萃分析的结论表明，果糖相对于任何其他碳水化合物没有特定的不良影响。摄入过量的糖也可能通过引起体重增加和脂肪增加间接促进CVD和T2 DM的发展，但这也是一个有争议的话题。从机制上讲，果糖的消耗可能会导致能量摄入增加和能量消耗减少，因为它不能刺激瘦素的产生。大脑的功能性磁共振成像表明，与葡萄糖或果糖相比，大脑对果糖或含果糖的糖的反应不同。有流行病学研究表明，糖的摄入量与体重增加有关，也有干预研究表明，与自由采食低糖饮食相比，自由采食高糖饮食可促进体重增加。然而，没有研究比较摄入高糖或低糖、盲法、随意饮食的受试者的能量摄入和体重增加，这些饮食是为了确保两组摄入的大量营养素分布相当，纤维量相同。也几乎没有数据来确定添加糖的消费形式，如饮料或固体食物，是否会影响其促进体重增加的潜力。获得资金进行临床饮食研究将是非常具有挑战性的，这些研究需要解决这些证据缺口，特别是在通常消费的添加糖水平上。然而，填补这些证据空白可能是必要的，以支持政策的变化，这将有助于把食品环境变成一个不会促进肥胖和代谢疾病的发展。
The impact of sugar consumption on health continues to be a controversial topic. The objective of this review is to discuss the evidence and lack of evidence that allows the controversy to continue, and why resolution of the controversy is important. There are plausible mechanisms and research evidence that support the suggestion that consumption of excess sugar promotes the development of cardiovascular disease (CVD) and type 2 diabetes (T2DM) both directly and indirectly. The direct pathway involves the unregulated hepatic uptake and metabolism of fructose, which leads to liver lipid accumulation, dyslipidemia, decreased insulin sensitivity and increased uric acid levels. The epidemiological data suggest that these direct effects of fructose are pertinent to the consumption of the fructose-containing sugars, sucrose and HFCS, which are the predominant added sugars. Consumption of added sugar is associated with development and/or prevalence of fatty liver, dyslipidemia, insulin resistance, hyperuricemia, cardiovascular disease and type 2 diabetes, and many of these associations are independent of body weight gain or total energy intake. There are diet intervention studies in which human subjects exhibited increased circulating lipids and decreased insulin sensitivity when consuming high sugar compared with control diets. Most recently, our group has reported that supplementing the ad libitum diets of young adults with beverages containing 0, 10, 17.5 or 25% of daily energy requirement (Ereq) as high fructose corn syrup (HFCS) increased lipid/lipoprotein risk factors for cardiovascular disease (CVD) and uric acid in a dose response manner. However, un-confounded studies conducted in healthy humans under a controlled, energy-balanced diet protocol that allow determination of the effects of sugar with diets that do not allow for body weight gain are lacking. Furthermore, there are recent reports that conclude that there are no adverse effects of consuming beverages containing up to 30% Ereq sucrose or HFCS, and the conclusions from several meta-analyses suggest that fructose has no specific adverse effects relative to any other carbohydrate. Consumption of excess sugar may also promote the development the development of CVD and T2DM indirectly by causing increased body weight and fat gain, but this is also a topic of controversy. Mechanistically, it is plausible that fructose consumption causes increased energy intake and reduced energy expenditure due to its failure to stimulate leptin production. Functional magnetic resonance imaging of the brain demonstrates that the brain responds differently to fructose or fructose-containing sugars compared with glucose or aspartame. There are epidemiological studies which show sugar consumption is associated with body weight gain, and there are intervention studies in which consumption of ad libitum high sugar diets promoted increased body weight gain compared with consumption of ad libitum low sugar diets. However, there are no studies in which energy intake and weight gain were compared in subjects consuming high or low sugar, blinded, ad libitum diets formulated to ensure both groups consumed a comparable macronutrient distribution and the same amounts of fiber. There is also little data to determine whether the form in which added sugar is consumed, as beverage or as solid food, affects its potential to promote weight gain. It will be very challenging to obtain the funding to conduct the clinical diet studies needed to address these evidence gaps, especially at the levels of added sugar that are commonly consumed. Yet, filling these evidence gaps may be necessary for supporting the policy changes that will help to turn the food environment into one that does not promote the development of obesity and metabolic disease.