Traditional Chinese Medicine
Vol.04 No.03(2015), Article ID:15912,9 pages
10.12677/TCM.2015.43010

Nutritional Intervention with Integrated Traditional Chinese and Western Medicine for Simple Obesity

Fanghua Ren*, Jun Cai#

Department of Clinical Nutrition, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai

Email: #caijun509@163.com

Received: Jul. 27th, 2015; accepted: Aug. 10th, 2015; published: Aug. 20th, 2015

Copyright © 2015 by authors and Hans Publishers Inc.

This work is licensed under the Creative Commons Attribution International License (CC BY).

http://creativecommons.org/licenses/by/4.0/

ABSTRACT

Simple obesity is a common nutritional and metabolic disease caused by various factors, which leads to the imbalance of energy metabolism, fat accumulation in the body and weight gain. Dietary pattern is an important factor for the occurrence and progress of simple obesity. Therefore, pattern identification as the basis for diet with modern medicine and traditional Chinese medicine may play an important role in the prevention and treatment of simple obesity.

Keywords:Simple Obesity, Integrated Traditional Chinese and Western Medicine, Nutritional Intervention

单纯性肥胖病的中西医结合营养干预

任芳华*,蔡骏#

上海中医药大学附属龙华医院,临床营养科,上海

Email: #caijun509@163.com

收稿日期:2015年7月27日;录用日期:2015年8月10日;发布日期:2015年8月20日

摘 要

单纯性肥胖病是由于多种因素引起的体内能量代谢失衡,脂肪积聚过多、体重增加所致的一种常见的营养与代谢性疾病。膳食结构模式是影响肥胖病发生和发展的重要原因。因此,综合现代医学的辨病施膳及传统中医学的辨证施膳对肥胖病的防治具有重要的理论及临床意义。

关键词 :单纯性肥胖病,中西医结合,营养干预

1. 引言

单纯性肥胖病是由于遗传、环境等特定的生物化学因子引起的一系列进食调控和能量代谢紊乱,使体内能量摄入大于消耗,能量代谢失衡,体内脂肪积聚过多、体重增加所致的一种常见营养与代谢性疾病。

据我国2004年10月卫生部、科技部、国家统计局发布的《中国居民营养与健康现状》显示,我国成人超重率为22.8%,肥胖率为7.1%,估计人数分别为2.0亿和6000多万。大城市成人超重率与肥胖现患率分别高达30.0%和12.3%,儿童肥胖率已达8.1%,应引起高度重视。与1992年全国营养调查资料相比,成人超重率上升39%,肥胖率上升97%,由于超重基数大,预计今后肥胖患病率将会有较大幅度增长[1] [2] 。一项针对全球199个国家和地区,由910万参与者组成的研究表明,1980年至2008年间,全世界人口平均BMI呈增长趋势,男性平均BMI每十年增长0.4 kg/m2,女性平均BMI每十年增长0.5 kg/m2,且不同国家地区之间差异明显,肥胖病曾一度被认为只是美国和西方世界其他高收入国家所面临的一个问题,但是现在它已成为糖尿病、心血管疾病、癌症等全球疾病负担的一个主要影响因素[3] [4] 。本文从现代医学及传统医学角度探讨单纯性肥胖病的营养干预。

2. 单纯性肥胖病的病因和病理机制

单纯性肥胖病是一种异质性疾病,病因尚未明确,是由遗传因素、环境因素及年龄因素等多种因素相互作用的结果。目前对其发生机制的研究来看,主要有 [1] :1) 遗传因素:遗传学研究表明,人类体重的变异,70%为遗传因素所致。肥胖常伴有多种基因的改变所致基因多态性,为多基因遗传。2) 环境因素:遗传因素仅增加人体对肥胖的易感性,环境因素对多种易感基因的表达是一重要促进因素。3) 年龄因素:随着年龄增长,垂体前叶功能逐渐减退、内分泌代谢功能下降,导致人体由合成代谢为主逐渐转为分解代谢为主,以致代谢失去平衡,细胞功能下降,人体体成分改变,体脂群逐渐增加、分泌异常,瘦体组织群逐渐减少,总体水分减少。4) 膳食、生活方式因素:进食过量、进食行为、体力活动减少及社会因素等都与肥胖病的发生密切相关。

由此可见,尽管单纯性肥胖病病因及病理机制尚未完全明确,但膳食结构模式是影响肥胖病发生和发展的重要原因。因此,综合现代西医学的辨病施膳及传统中医学的辨证施膳是预防和治疗单纯性肥胖病的重要方法之一。

3. 单纯性肥胖病的西医营养干预

3.1. 影响总能量摄入的膳食因素

3.1.1. 能量密度

能量密度是指每克食物所含的能量,这与食品的水分和脂肪含量密切相关。食品的水分含量高则能量密度低、脂肪含量高则能量密度高。有研究表明,为了获得饱足感,人们倾向于进食固定体积或重量的食物。相应地,在能量摄入上,高能量食物往往引起被动的暴饮暴食 [5] 。而且,高能量食物通常高糖高脂肪,纤维和水分含量较低,味道可口,不宜引起饱足感,导致进食过量 [6] 。普遍认为,高脂肪饮食对于肥胖的有害影响主要是通过食物能量密度进行干预。有研究表明,减少能量密度与体重下调呈正相关[7] [8] 。大多数长期观察性研究同样证实,能量密度和体重增长密切相关[9] -[12] 。

蔬菜和水果低能量密度、高纤维、高维生素,并且是很好的抗氧化剂,对体重的控制大有裨益。尽管尚未达成一致,大部分研究倾向于认为,蔬菜和水果膳食在控制体重增长中扮演重要角色 [13] - [15] 。因此,蔬菜和水果通常用于肥胖病非药物治疗的干预因素之一。

3.1.2. 食物份量大小

大份量往往伴随着较高能量,从而导致体重的增长 [16] 。大份量食物的大规模生产及餐馆中大份量食物的供给可能是引起肥胖患病率不断上升的重要原因 [17] 。

3.1.3. 在外就餐

在我国,随着家庭成员减少、经济收入增加及大城市生活节奏的加快,在外就餐和购买现成加工食品及快餐食品的现象越来越普遍。有研究表明,在外就餐可能是引起肥胖的危险因素之一,因为大部分餐馆尤其是快餐店的膳食模式跟居家膳食模式比较,通常高脂肪、高能量、营养素密度低 [18] 。快餐食物消费增加的人群,倾向于摄入更高的能量、脂肪和含糖软饮料,而膳食纤维、蔬菜和水果的摄入量较低 [19] 。此外,餐馆食物份量往往较大,味道可口,品种各异,这些因素共同导致能量摄入的增加,进而引起肥胖 [17] 。

3.2. 膳食脂肪

膳食脂肪长期被认为是引起肥胖高发的主要高危因素,因其高能量密度、可口性和较低的饱腹感等促进能量的过量摄入 [20] 。此外,膳食脂肪代谢效率高,即产热低,相比较而言,碳水化合物和蛋白质代谢效率较低。因此,高脂膳食将会导致脂肪组织更有效地能量存储 [21] 。有研究表明,总脂肪的摄入量对近期体重增加影响甚微,但是对八年后体重的增加作用是肯定的 [22] 。另有研究表明,降低膳食中脂肪供能比例的女性,第一年体重下降明显。然而,大部分的体重下降出现反弹现象,两组之间体重下降没有明显差异 [23] 。欧洲一项大规模前瞻性队列研究证实,脂肪摄入量与长期体重和腰围改变没有必然联系 [24] 。

脂肪摄入量的增加不是问题,但消耗的脂肪类型或质量却是问题的关键。单不饱和脂肪酸和多不饱和脂肪酸含量高的食品有很多健康益处,但饱和脂肪酸和反式脂肪酸则并不利于健康 [25] - [27] 。Mozaffarian等的研究证实,反式脂肪酸与不良心脏代谢性风险有关,对胰岛素抵抗也有一定作用 [28] 。在低收入和中等收入国家中,有关反式脂肪酸摄入量的数据十分稀少,许多国家仍然没有要求对反式脂肪酸进行标记和管理。反式脂肪酸的摄入量可能会持续增加,特别是含有氢化油的进口食品可以延长食品的保质期 [29] 。

3.3. 碳水化合物相关的膳食因素

过去研究主要集中在长期高碳水化合物膳食相比高脂肪膳食,可以减少体重增加,因为碳水化合物比脂肪存储效率更低 [30] 。然而,几十年来西方国家一直削减脂肪消费,肥胖患病率却持续呈现上升趋势。不断上涨的数据似乎说明碳水化合物的摄入是导致肥胖流行的原因之一。目前没有足够的数据证实,总碳水化合物的供能比影响总能量的摄入,进而导致肥胖 [31] 。

自然界中碳水化合物种类繁多,分布广泛,功能各异,对能量摄入和人体健康有不同的影响。与肥胖相关研究涉及较多的为膳食纤维、含糖饮料、升糖指数(GI)和血糖负荷(GL)。

3.3.1. 膳食纤维

膳食纤维是指不能被人体消化道酵素分解的多糖类及木植素。它通过多种生理机制控制人体体重 [32] :其一,高纤维食物与低纤维食物相比较,因其比重小、体积大、低能量密度和可口性使人有饱腹感,有利于减肥;其二,膳食纤维,特别是可溶性膳食纤维,能增加食物粘滞度,在肠内形成凝胶,减缓胃肠排空,刺激胃肠激素释放,从而产生饱腹感而减少能量摄入,控制体重;此外,膳食纤维可形成机械屏障,阻止小肠内消化酶对脂肪、淀粉等宏量营养素的消化吸收。有研究表明,高膳食纤维食物中糖类消化吸收缓慢,降低餐后血糖反应,增加饱腹感,因此可改善胰岛素抵抗,影响燃料分区利于脂肪氧化。多数研究证实,膳食纤维在体重控制方面的有益作用 [33] [34] 。

3.3.2. 含糖饮料

过去的几十年,世界各地添加糖的消费量急剧增加,这些添加糖主要以糖饮料的形式出现。糖饮料能够促进体重增加,因为它们不会产生高水平的饱腹感。当卡路里以液体的形式摄入时,它们不能被随后进餐的卡路里摄入量减少所补偿,从而导致了能量摄入增加,以及正向能量平衡。糖饮料导致T2DM的患病风险增高,这是通过诱导体重增加以及升糖作用造成的,而后者是因为食用大量的可迅速吸收的糖以及果糖代谢作用所导致的 [35] 。大量流行病学研究已经表明,糖饮料摄入和体重增加或肥胖 [36] [37] 、T2DM [38] 以及冠心病有着很强的关联 [39] [40] 。

一项针对4629名中国成年人进行的调查数据表明,20%的男性每天饮用两至三瓶含糖饮料 [41] 。在一项随机临床试验中,用非卡路里饮料替换卡路里饮料6个月,可导致体重减轻2.0%~2.5% [42] 。综合来看,以上数据均表明,限制饮用含糖饮料可减少肥胖及其相关慢性病的患病率。

3.3.3. 升糖指数和血糖负荷

升糖指数(GI)是衡量食物引起餐后血糖反应的一项有效生理学参数,即食物餐后2小时血浆葡萄糖曲线下面积与等量葡萄糖餐后2小时血浆葡萄糖曲线下面积比值。血糖负荷(GL)将摄入碳水化物的数量和质量结合起来,可对实际提供的食物或总体膳食模式的血糖效应进行定量测定,即GI × 碳水化合物含量(克)/100。高GI高GL的膳食模式对超重或肥胖人群的不利影响更加显著,这些人群更易出现胰岛素抵抗 [43] [44] 。低GI或GL膳食模式可以控制体重增长,刺激减重 [45] 。这是因为进食低GI或GL膳食后引起的轻度血糖和胰岛素反应可获得较高的满足感和饱腹感,导致能量摄入减少 [46] ,进而重新调节能量分区使脂肪贮存减少 [47] ,限制静息代谢率的下降 [48] [49] 。精制的碳水化合物有较高的升糖指数(GI)和血糖负荷(GL)值,并且食用这些碳水化合物会产生快速血糖波动。美国的研究数据表明,精制碳水化合物的摄入和肥胖及T2DM患病风险有关 [50] 。针对三项大型前瞻性人群进行的研究表明,对长期体重增加贡献最大的是薯片和土豆,它们和精制谷物、糖以及含糖饮料具有类似的GI和GL [51] 。

3.4. 蛋白质摄入

蛋白质相比其他等能量的宏量营养素有更高的饱腹感,因此更高的蛋白质摄入可减少总能量的摄入。另外,蛋白质产能效应高,能量消耗增加。过去几十年,蛋白质的绝对摄入量或是占总能量摄入比都相对稳定,而肥胖的患病率上升显著 [52] [53] 。尽管之前多数研究数据不支持这一假设:蛋白质在肥胖的发展中扮演重要角色,近期研究认为,蛋白质摄入与肥胖呈负相关 [54] [55] 。也有学者提出“蛋白质杠杆假设” [56] ,即人体膳食蛋白质摄入量必需维持在一定水平,当摄入蛋白丰富的膳食后,更少量脂肪和糖类的摄入即可维持人体总能量的需求,否则为了维持体内蛋白水平,需要摄入更多的能量。

4. 单纯性肥胖病的中医营养干预

4.1. 肥胖的病因、病机

肥胖之名自古有之,最早记载见于《内经》,《素问·异法方宜论》:“其民华食而脂肥。”《素问·通评虚实论》:“甘肥贵人,则膏粱之疾也。”《素问·奇病论》:“此肥美之所发也,此人必数食甘美而多肥也。”说明肥胖的发生与饮食不节、先天禀赋等多种因素有关。《灵枢·卫气失常》曰:“人有脂,有膏,有肉。黄帝曰:别此奈何?伯高曰:肉坚,皮满者,脂;不坚,皮缓者,膏。皮肉不相离者,肉。……膏者,多气而皮纵缓,故能纵腹垂腴。肉者,身体容大。脂者,其身收小”,把肥胖分为脂型、膏型、肉型3种类型,并指出,膏人肥胖而皮肉松弛,脂人肥胖而皮肉紧敛,肉人肥胖而肌肉满壮。

现代中医对肥胖病的定义为:肥胖病是指因嗜食肥甘,喜静少动,脾失健运,痰湿脂膏积聚,导致形体发胖,超乎常人,并伴困倦乏力等为主要表现的形体疾病 [57] 。病机总属阳气虚衰、痰湿偏盛。脾气虚弱则运化转输无力,水谷精微失于输布,化为膏脂和水湿,留滞体内而致肥胖;肾阳虚衰,则血液鼓动无力,水液失于蒸腾气化,血行迟缓,水湿内停,而成肥胖。本病多属本虚标实之候。本虚是指脾肾气虚,或兼心肺气虚;标实为痰湿膏脂内停,兼有水湿、血瘀、气滞等。朱丹溪首次提出“肥白人多痰湿”的观点。《景岳全书·杂证谟·非风》:“何以肥人反多气虚?……肥人者,柔胜于刚,阴胜于阳者也,且肉以血成,总属阴类,故肥人多有气虚之证。”叶天士指出:“夫肌肤柔白属气虚,外似丰溢,里真大怯,盖阳虚之体,惟多痰多湿……”,进一步阐明肥胖病乃属本虚标实之候,阳气虚衰为本,痰湿偏盛为标。”王琦教授 [58] 长期从事中医体质学说的研究,认为形体肥胖之人体质多偏于痰湿质。有研究证实,痰湿质是代谢综合征发病的内在基础,代谢综合征是肥胖人群痰湿体质的必然趋势 [59] 。

4.2. 辨证施膳

辨证施膳是在辨证论治的基础上提出的。辨证论治是中医治疗的基本原则和特色,即在临床治疗时要根据病人的寒热虚实,结合病人自身体质,以及气候、环境等因素,综合分析,从而辨别出属于何种“证候”,根据不同证候选择处方用药。而形成证候的内在基础是体质。饮食结构和营养状况对体质有明显的影响。

整体观念是中医学理论体系的主要特点之一,这种观念同样适用于中医食疗学,并提出“药食同源”学说 [60] ,认为食物和药物之间并无绝对的分界线,饮食物各有不同的成分或四气五味,而人之五脏六腑,各有所好,脏腑之精气阴阳,需五味阴阳和合而生。正如《金匮要略》:“所食之味,有与身相宜,有与身为害。若得宜则益体,害则成疾。”长期的饮食习惯和固定的膳食品种质量,日久可因体内某些成分的增减等变化而影响体质,进而形成不同的证型。如嗜食肥甘厚味可助湿生痰,形成痰湿体质;嗜食辛辣则易化火伤阴,形成阴虚火旺体质;过食生冷寒凉则损伤脾胃,产生脾气虚弱体质;饮食无度,久则损伤脾胃,可形成形盛气虚体质;贪恋醇酒佳酿,湿热在中,易伤肝脾。饮食疗法是中医食疗方法之一,所以也应遵循“辨证施治”的原则,只是食物的性味温和,使用安全,因人、因时、因地辨证用膳。

有研究表明 [61] ,采用中医辨证食疗 + 低血糖指数食物处方 + 低热量饮食干预组体质指数、体内脂肪量下降明显优于低热量饮食组。辨证施膳可明显改善痰湿体质超重人群痰湿体质计量积分,对代谢性疾病的预防有一定意义 [62] 。

5. 总结

营养干预是防治单纯性肥胖病的重要途径之一,结合现代医学的辨病施膳模式及传统医学的辨证施膳模式,在西医选择的食物品种中,再用中医理论辩证分型地加以挑选,对肥胖病的治疗效果更显著。所有食疗处方,都必须保证营养素的种类齐全和数量充足,并且要达到平衡,这是食谱的共性;而具体用哪种食物来提供营养素,要辨证,从食用者的具体情况来选择,这是食谱的个性。但国内文献资料较少,仍缺乏高质量大样本数据的支持,这将是今后研究的重点。

综上,加强以依从性较高的辨病施膳(食谱共性)与辨证施膳(食谱个性)相结合的单纯性肥胖病综合性防治研究具有深远的医学价值和社会学意义。

文章引用

任芳华,蔡 骏. 单纯性肥胖病的中西医结合营养干预
Nutritional Intervention with Integrated Traditional Chinese and Western Medicine for Simple Obesity[J]. 中医学, 2015, 04(03): 54-62. http://dx.doi.org/10.12677/TCM.2015.43010

参考文献 (References)

  1. 1. 蔡威, 主编 (2013) 临床营养学. 复旦大学出版社, 上海.

  2. 2. 中华人民共和国卫生部 (2004) 中国居民营养与健康现状. 中国心血管病研究杂志, 12, 919-922.

  3. 3. Finucane, M.M., Stevens, G.A., Cowan, M.J., et al. (2011) National, regional, and global trends in body-mass index since 1980: Systematic analysis of health examination surveys and epidemiological studies with 960 country-years and 9•1 million participants. The Lancet, 377, 557-567. http://dx.doi.org/10.1016/S0140-6736(10)62037-5

  4. 4. Misra, A. and Khurana, L. (2008) Obesity and the meta-bolic syndrome in developing countries. The Journal of Clinical Endocrinology & Metabolism, 93, s9-s30. http://dx.doi.org/10.1210/jc.2008-1595

  5. 5. Woods, S.C., Seeley, R.J. and Cota, D. (2008) Regulation of food intake through hypothalamic signaling networks involving mTOR. Annual Review of Nutrition, 28, 295-311. http://dx.doi.org/10.1146/annurev.nutr.28.061807.155505

  6. 6. Rolls, B.J. (2009) The relationship between dietary energy density and energy intake. Physiology & Behavior, 97, 609- 615. http://dx.doi.org/10.1016/j.physbeh.2009.03.011

  7. 7. Ello-Martin, J.A., Roe, L.S., Ledikwe, J.H., et al. (2007) Dietary energy density in the treatment of obesity: A year- long trial comparing 2 weight-loss diets. The American Journal of Clinical Nutrition, 85, 1465-1477.

  8. 8. Ledikwe, J.H., Rolls, B.J., Smiciklas-Wright, H., et al. (2007) Re-ductions in dietary energy density are associated with weight loss in overweight and obese participants in the PREMIER trial. The American Journal of Clinical Nutrition, 85, 1212-1221.

  9. 9. Savage, J.S., Marini, M. and Birch, L.L. (2008) Dietary energy density predicts women’s weight change over 6 y. The American Journal of Clinical Nutrition, 88, 677-684.

  10. 10. Bes-Rastrollo, M., van Dam, R.M., Martinez-Gonzalez, M.A., et al. (2008) Prospective study of dietary energy density and weight gain in women. The American Journal of Clinical Nutrition, 88, 769-777.

  11. 11. Iqbal, S.I., Helge, J.W. and Heitmann, B.L. (2006) Do energy density and dietary fiber influence subsequent 5-year weight changes in adult men and women? Obesity, 14, 106-114. http://dx.doi.org/10.1038/oby.2006.13

  12. 12. Du, H., van der A, D.L., Ginder, V., Jebb, S.A., Forouhi, N.G., Wareham, N.J., et al. (2009) Dietary energy density in relation to subsequent changes of weight and waist circumference in European men and women. PLoS ONE, 4, e5339. http://dx.doi.org/10.1371/journal.pone.0005339

  13. 13. He, K., Hu, F.B., Colditz, G.A., Manson, J.E., Willett, W.C. and Liu, S. (2004) Changes in intake of fruits and vegetables in relation to risk of obesity and weight gain among mid-dle-aged women. International Journal of Obesity, 28, 1569-1574. http://dx.doi.org/10.1038/sj.ijo.0802795

  14. 14. Vioque, J., Weinbrenner, T., Castelló, A., Asensio, L. and de la Hera, M.G. (2008) Intake of fruits and vegetables in relation to 10-year weight gain among Spanish adults. Obesity, 16, 664-670. http://dx.doi.org/10.1038/oby.2007.121

  15. 15. Buijsse, B., Feskens, E.J., Schulze, M.B., Forouhi, N.G., Wareham, N.J., Sharp, S., et al. (2009) Fruit and vegetable intakes and subsequent changes in body weight in European populations: Results from the project on diet, obesity, and genes (DiOGenes). The American Journal of Clinical Nutrition, 90, 202-209. http://dx.doi.org/10.3945/ajcn.2008.27394

  16. 16. Rolls, B.J. (2003) The supersizing of America: Portion size and the obesity epidemic. Nutrition Today, 38, 42-53. http://dx.doi.org/10.1097/00017285-200303000-00004

  17. 17. Diliberti, N., Bordi, P.L., Conklin, M.T., Roe, L.S. and Rolls, B.J. (2004) Increased portion size leads to increased energy intake in a restaurant meal. Obesity Research, 12, 562-568. http://dx.doi.org/10.1038/oby.2004.64

  18. 18. Zoumas-Morse, C., Rock, C.L., Sobo, E.J. and Neuhouser, M.L. (2001) Children’s patterns of macronutrient intake and associations with restaurant and home eating. Journal of the American Dietetic Association, 101, 923-925. http://dx.doi.org/10.1016/S0002-8223(01)00228-0

  19. 19. Bowman, S.A. and Vinyard, B.T. (2004) Fast food con-sumption of US adults: Impact on energy and nutrient intakes and overweight status. Journal of the American College of Nutrition, 23, 163-168. http://dx.doi.org/10.1080/07315724.2004.10719357

  20. 20. Hill, J.O., Melanson, E.L. and Wyatt, H.T. (2000) Die-tary fat intake and regulation of energy balance: Implications for obesity. Journal of Nutrition, 130, 284S-288S.

  21. 21. Maffeis, C., Schutz, Y., Grezzani, A., Provera, S., Piacentini, G. and Tato, L. (2001) Meal-induced thermogenesis and obesity: Is a fat meal a risk factor for fat gain in children? The Journal of Clinical Endocrinology and Metabolism, 86, 214-219.

  22. 22. Field, A.E., Willett, W.C., Lissner, L. and Colditz, G.A. (2007) Dietary fat and weight gain among women in the nurses’ health study. Obesity, 15, 967-976. http://dx.doi.org/10.1038/oby.2007.616

  23. 23. Howard, B.V., Manson, J.E., Stefanick, M.L., Beresford, S.A., Frank, G., Jones, B., Rodabough, R.J., Snetselaar, L., Thomson, C., Tinker, L., Vitolins, M. and Prentice, R. (2006) Low-fat dietary pattern and weight change over 7 years: The women’s health initiative dietary modification trial. JAMA, 295, 39-49. http://dx.doi.org/10.1001/jama.295.1.39

  24. 24. Forouhi, N.G., Sharp, S.J., Du, H., van der A, D.L., Halkjaer, J., Schulze, M.B., Tjonneland, A., Overvad, K., Jakobsen, M.U., Boeing, H., Buijsse, B., Palli, D., Masala, G., Feskens, E.J., Sorensen, T.I. and Wareham, N.J. (2009) Dietary fat intake and subsequent weight change in adults: Results from the European prospective investigation into cancer and nutrition cohorts. The American Journal of Clinical Nutrition, 90, 1632-1641. http://dx.doi.org/10.3945/ajcn.2009.27828

  25. 25. Mozaffarian, D., Micha, R. and Wallace, S. (2010) Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: A systematic review and meta-analysis of randomized controlled trials. PLoS Medicine, 7, e1000252. http://dx.doi.org/10.1371/journal.pmed.1000252

  26. 26. Mente, A., de Koning, L., Shannon, H.S. and Anand, S.S. (2009) A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Archives of Internal Medicine, 169, 659-669. http://dx.doi.org/10.1001/archinternmed.2009.38

  27. 27. Appel, L.J., Sacks, F.M., Carey, V.J., Obarzanek, E., Swain, J.F., Miller, E.R., et al. (2005) Effects of protein, monounsaturated fat, and carbohydrate intake on blood pressure and serum lipids: Results of the OmniHeart randomized trial. JAMA, 294, 2455-2464. http://dx.doi.org/10.1001/jama.294.19.2455

  28. 28. Mozaffarian, D., Katan, M.B., Ascherio, A., Stampfer, M.J. and Willett, W.C. (2006) Trans fatty acids and cardiovascular disease. New England Journal of Medicine, 354, 1601-1613. http://dx.doi.org/10.1056/NEJMra054035

  29. 29. Hu, F.B., Liu, Y. and Willett, W.C. (2011) Preventing chronic diseases by promoting healthy diet and lifestyle: Public policy implications for China. Obesity Reviews, 12, 552-559. http://dx.doi.org/10.1111/j.1467-789x.2011.00863.x

  30. 30. Astrup, A., Grunwald, G.K., Melanson, E.L., Saris, W.H. and Hill, J.O. (2000) The role of low-fat diets in body weight control: A meta-analysis of ad libitum dietary intervention studies. International Journal of Obesity, 24, 1545-1552. http://dx.doi.org/10.1038/sj.ijo.0801453

  31. 31. Ma, Y., Olendzki, B., Chiriboga, D., Hebert, J.R., Li, Y., Li, W., Campbell, M., Gendreau, K. and Ockene, I.S. (2005) Association between dietary carbohydrates and body weight. American Journal of Epidemiology, 161, 359-367. http://dx.doi.org/10.1093/aje/kwi051

  32. 32. Pereira, M.A. and Ludwig, D.S. (2001) Dietary fiber and body-weight regulation. Observations and mechanisms. Pediatric Clinics of North America, 48, 969-980. http://dx.doi.org/10.1016/S0031-3955(05)70351-5

  33. 33. Liu, S., Willett, W.C., Manson, J.E., Hu, F.B., Rosner, B. and Colditz, G. (2003) Relation between changes in intakes of dietary fiber and grain products and changes in weight and development of obesity among middle-aged women. American Journal of Clinical Nutrition, 78, 920-927.

  34. 34. Du, H., van der A, D.L., Boshuizen, H.C., Forouhi, N.G., Wareham, N.J., Halkjaer, J., Tjonneland, A., Overvad, K., Jakobsen, M.U., Boeing, H., Buijsse, B., Masala, G., Palli, D., Sorensen, T.I., Saris, W.H. and Feskens, E.J. (2009) Dietary fiber and subsequent changes in body weight and waist circumference in European men and women. American Journal of Clinical Nutrition, 91, 329-336. http://dx.doi.org/10.3945/ajcn.2009.28191

  35. 35. Malik, V.S., Popkin, B.M., Bray, G.A., Despres, J.P. and Hu, F.B. (2010) Sugar-sweetened beverages, obesity, type 2 diabetes mellitus, and cardiovascular disease risk. Circulation, 121, 1356-1364. http://dx.doi.org/10.1161/CIRCULATIONAHA.109.876185

  36. 36. Mozaffarian, D., Hao, T., Rimm, E.B., Willett, W.C. and Hu, F.B. (2011) Changes in diet and lifestyle and long-term weight gain in women and men. New England Journal of Medicine, 364, 2392-2404. http://dx.doi.org/10.1056/NEJMoa1014296

  37. 37. Malik, V.S., Willett, W.C. and Hu, F.B. (2009) Sugar-sweetened beverages and BMI in children and adolescents: Reanalyses of a meta-analysis. American Journal of Clinical Nutrition, 89, 438-489. http://dx.doi.org/10.3945/ajcn.2008.26980

  38. 38. Malik, V.S., Popkin, B.M., Bray, G.A., Despres, J.-P., Willett, W.C. and Hu, F.B. (2010) Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: A me-ta-analysis. Diabetes Care, 33, 2477-2483. http://dx.doi.org/10.2337/dc10-1079

  39. 39. Fung, T.T., Malik, V., Rexrode, K.M., Manson, J.E., Willett, W.C. and Hu, F.B. (2009) Sweetened beverage consumption and risk of coronary heart disease in women. American Journal of Clinical Nutrition, 89, 1037-1042. http://dx.doi.org/10.3945/ajcn.2008.27140

  40. 40. de Koning, L., Malik, V.S., Kellogg, M.D., Rimm, E.B., Willett, W.C. and Hu, F.B. (2012) Sweetened beverage consumption, incident coronary heart disease and biomarkers of risk in men. Circulation, 125, 1735-1741. http://dx.doi.org/10.1161/CIRCULATIONAHA.111.067017

  41. 41. Ko, G.T., So, W.-Y., Chow, C.-C., Wong, P.T., Tong, S.D., Hui, S.S., et al. (2010) Risk associations of obesity with sugar-sweetened beverages and lifestyle factors in Chinese: The “better health for better Hong Kong” health promotion campaign. European Journal of Clinical Nutrition, 64, 1386-1392. http://dx.doi.org/10.1038/ejcn.2010.181

  42. 42. Tate, D.F., Turner-McGrievy, G., Lyons, E., Stevens, J., Erickson, K., Polzien, K., et al. (2012) Replacing caloric beverages with water or diet beverages for weight loss in adults: Main results of the choose healthy options consciously everyday (CHOICE) randomized clinical trial. American Journal of Clinical Nutrition, 95, 555-563. http://dx.doi.org/10.3945/ajcn.111.026278

  43. 43. Sun, Q., Spiegelman, D., van Dam, R.M., Holmes, M.D., Malik, V.S., Willett, W.C. and Hu, F.B. (2010) White rice, brown rice, and risk of type 2 diabetes in US men and women. Archives of Internal Medicine, 170, 961-969. http://dx.doi.org/10.1001/archinternmed.2010.109

  44. 44. Villegas, R., Liu, S.M., Gao, Y.-T., Yang, G., Li, H.L., Zheng, W. and Shu, X.O. (2007) Prospective study of dietary carbohydrates, glycemic index, glycemic load, and inci-dence of type 2 diabetes mellitus in middle-aged Chinese women. Archives of Internal Medicine, 167, 2310-2316. http://dx.doi.org/10.1001/archinte.167.21.2310

  45. 45. Ludwig, D.S. (2003) Dietary glycemic index and the regulation of body weight. Lipids, 38, 117-121. http://dx.doi.org/10.1007/s11745-003-1040-x

  46. 46. Ball, S.D., Keller, K.R., Moyer-Mileur, L.J., Ding, Y.W., Do-naldson, D. and Jackson, W.D. (2003) Prolongation of satiety after low versus moderately high glycemic index meals in obese adolescents. Pediatrics, 111, 488-494. http://dx.doi.org/10.1542/peds.111.3.488

  47. 47. Stevenson, E.J., Williams, C., Mash, L.E., Phillips, B. and Nute, M.L. (2006) Influence of high-carbohydrate mixed meals with different glycemic indexes on substrate utilization during subsequent exercise in women. American Journal of Clinical Nutrition, 84, 354-360.

  48. 48. Pereira, M.A., Swain, J., Goldfine, A.B., Rifai, N. and Ludwig, D.S. (2004) Effects of a low-glycemic load diet on resting energy expenditure and heart disease risk factors during weight loss. JAMA, 292, 2482-2490. http://dx.doi.org/10.1001/jama.292.20.2482

  49. 49. Du, H., van der A, D.L. and Feskens, E.J. (2006) Dietary gly-caemic index: A review of the physiological mechanisms and observed health impacts. Acta Cardiologica, 61, 383-397. http://dx.doi.org/10.2143/AC.61.4.2017298

  50. 50. Gross, L.S., Li, L., Ford, E.S. and Liu, S. (2004) Increased con-sumption of refined carbohydrates and the epidemic of type 2 diabetes in the United States: an ecologic assessment. American Journal of Clinical Nutrition, 79, 774-779.

  51. 51. Mozaffarian, D., Hao, T., Rimm, E.B., Willett, W.C. and Hu, F.B. (2011) Changes in diet and lifestyle and long-term weight gain in women and men. New England Journal of Medicine, 364, 2392-2404. http://dx.doi.org/10.1056/NEJMoa1014296

  52. 52. Norris, J., Harnack, L., Carmichael, S., Pouane, T., Wakimoto, P. and Block, G. (1997) US trends in nutrient intake: The 1987 and 1992 national health interview surveys. American Journal of Public Health, 87, 740-746. http://dx.doi.org/10.2105/AJPH.87.5.740

  53. 53. Cavadini, C., Siega-Riz, A.M. and Popkin, B.M. (2000) US ado-lescent food intake trends from 1965 to 1996. Archives of Disease in Childhood, 83, 18-24. http://dx.doi.org/10.1136/adc.83.1.18

  54. 54. Due, A., Toubro, S., Skov, A.R. and Astrup, A. (2004) Effect of nor-mal-fat diets, either medium or high in protein, on body weight in overweight subjects: A randomised 1-year trial. In-ternational Journal of Obesity, 28, 1283-1290. http://dx.doi.org/10.1038/sj.ijo.0802767

  55. 55. Halkjaer, J., Tjonneland, A., Thomsen, B.L., Overvad, K. and So-rensen, T.I. (2006) Intake of macronutrients as predictors of 5-y changes in waist circumference. American Journal of Clinical Nutrition, 84, 789-797.

  56. 56. Simpson, S.J. and Raubenheimer, D. (2005) Obesity: The protein leverage hypo-thesis. Obesity Reviews, 6, 133-142. http://dx.doi.org/10.1111/j.1467-789X.2005.00178.x

  57. 57. 中华人民共和国技术监督局 (1997) 中华人民共和国国家标准•中医临床诊疗术语疾病部分. 中国标准出版社, 北京, 6.

  58. 58. 王琦 (1995) 中医体质学. 中国医药科技出版社, 北京, 161.

  59. 59. 崔博乐, 李怡, 张军, 米逸颖 (2009) 论肥胖与代谢综合症的中医学认识. 北京中医药, 1, 32-33.

  60. 60. 王会梅, 徐桂华, 王丹文 (2008) 中医食疗的理论与应用. 辽宁中医药大学学报, 4, 69-71.

  61. 61. 陈艳鸿, 叶艳彬 (2006) 低血糖指数食物结合中医食疗对单纯性肥胖症的治疗效果. 中国现代医药杂志, 5, 15-18.

  62. 62. 冯志海, 彭扣芝, 单留峰 (2012) 辨证施膳对社区痰湿型体质超重人群影响的研究. 中国中医基础医学杂志, 11, 1276-1282.

  63. NOTES

    *第一作者。

    #通讯作者。

期刊菜单