百科问答小站 logo
百科问答小站 font logo



果糖、葡萄糖、蔗糖和淀粉在体内代谢有何不同,为什么果糖相对而言危害大? 第1页

  

user avatar   rou-zai-52 网友的相关建议: 
      

知乎上许多急于恰饭的自媒体把果糖的危害夸大了

所谓有理有据,指的是既有原理/机理解释,也有数据支持。

只有原理分析,没有数据支持,那叫猜测/推测,说服力不足。比如,尼古丁能杀癌细胞,有这个“原理”,我们能得出“抽烟可以治疗癌症”吗?

知乎上许多关于果糖的说法就是如此,只有代谢的原理,没有量化研究。外行看来好像很有道理,内行看来结论很大程度具有主观性。


葡萄糖代谢:即便严重过量也很少被转化为脂肪

果糖和葡萄糖是单糖,蔗糖是双糖,淀粉是多糖;双糖和多糖在各种酶的作用下降解为单糖,然后才能被身体使用。

葡萄糖代谢的主要器官是肌肉[77,78,79],其次是大脑,葡萄糖偏向于作为能量被使用,即便严重过量,也很少被转化为人体脂肪[12,13,14,15,18]。

葡萄糖首先在转运蛋白[16,17]的帮助下从小肠吸收,进入血液,然后被运往肌肉/肝脏等地方合成肝糖原,或者给大脑、心脏、骨骼肌等器官作为能量使用。

在(肌肉等)细胞内,葡萄糖先走糖酵解(葡萄糖转丙酮酸),然后走柠檬酸循环(转乙酰辅酶A,与草酰乙酸缩合为柠檬酸),然后被氧化成二氧化碳和水并产生能量。注意,柠檬酸循环释放的能量并不是直接用于身体细胞,而是储存在ATP(更多是磷酸原系统)中。

此外,葡萄糖除了走柠檬酸循环,还可以走戊糖磷酸途径来释放能量。这在一些实验中被证实,当使用一些抑制剂,抑制了糖酵解(阻止葡萄糖转丙酮酸),葡萄糖依然可以被氧化供能。


果糖的代谢:过量部分相对容易转化为脂肪

果糖代谢的主要在肝脏,其次是小肠和肾脏。

摄入的果糖,首先在转运蛋白glut5的帮助下进入小肠,被转化为1-磷酸果糖、葡萄糖和脂肪酸[69];小肠也有果糖代谢的相关酶,能促进果糖代谢为葡萄糖/乳酸/乳糜等[33,34,35]。

然后,果糖在转运蛋白glut2[17]的帮助下进入肠细胞和门静脉,并被运输进入肝脏;有些数据显示,摄入的果糖约85.5%进入肝脏[68]。

在肝细胞内,果糖在酶的作用下[19,20,21]被转化为1-磷酸果糖;1-磷酸果糖的去路有三条:葡萄糖、丙酮酸(乳酸)[17]和脂肪酸[22,23,24,25,26]。


除了小肠和肝脏,肾脏也是糖代谢的重要器官,早在大半个世纪之前,科学就证明了这一点。

  • 1937年发现肾脏能利用糖代谢中间产物(丙酮酸等)产生葡萄糖[72];
  • 1949年发现肾脏切除后动物的血糖快速下降[73];
  • 1978年发现大鼠的血糖有26%-46%来自肾脏[74]。

当然,肾脏也是果糖代谢重要器官[70,71]。

  • 1961年发现肾脏能处理约19%的果糖,将其转化为葡萄糖[75];
  • 1982年发现注射的果糖约20%被肾脏吸收并护理[76];
  • 1989年发现肾脏处理了果糖吸收总量的20-25%[80]。

也就是说,葡萄糖和果糖代谢的最大不同可能在于:如果过量的话(注意这个前提),葡萄糖很少被转化为脂肪;果糖相对容易促成脂肪肝和高血脂[17,24];因此,过量饮用添加糖饮料与代谢疾病、胰岛素抵抗有关[1,2,3,4,5,6,7,8,9,10]。


果糖的“危害”主要通过过量热量介导,而非其代谢方式

的确,含果糖饮料摄入与体重增加密切相关[36],也与高血压、血脂异常、痛风和心血管疾病的发病率有关[37,38,39,40,41,42]。但调整体重后,这些关联变得更弱或者消失了[43],这表明,果糖对人体的危害很大程度上是以过量热量的方式来实现的,而非其本身的代谢特性。

一项包含了14个等热量试验和两项高热量试验的大型元分析[49],作者对果糖与餐后血脂进行汇总分析表明,把果糖与其他碳水化合物进行等热量交换,不会增加餐后血脂(尽管不能100%排除这种影响)。

特别值得一提的是顶刊《BMJ》上发表的一项关于糖和体重的大型元分析,包含了从7895个实验中筛选出的30个、从9445项队列研究中筛选出的38个研究[50]。

其重要结论是:The data suggest that the change in body fatness that occurs with modifying intake of sugars results from an alteration in energy balance rather than a physiological or metabolic consequence of monosaccharides or disaccharides.

翻译过来就是:数据表明,随着糖摄入量的改变而发生的肥胖是由于能量平衡的改变,而不是单糖或双糖的生理或代谢结果

这些也与我们之前的文章[67]所列举的大量证据相互支持:虽然食物的种类和质量有独立影响,但总体上总热量是决定短期内减肥效果的主要因素[51,52,53];不管高脂肪饮食[54,55,56,57,58]还是传统碳水占比较大的饮食[59,60,61],热量摄入类似则减肥效果类似的[62,63,64,65,66]。


现有“果糖有害”的研究,是建立在“摄入量过分夸张”基础上的

有人列举了研究证明在摄入大量果糖后一段时间,肝脏脂肪增加了76%[81]。看上去很严重,但这个是建立在两个前提下的:

(1)果糖摄入量很夸张;

(2)总能量摄入增加了35%,并且增加部分几乎都是由果糖组成。

在该研究中,受试者摄入的果糖量是每kg瘦体重3.5g;假如一个男性75kg体重/体脂20%,那么瘦体重是60kg,那他每天摄入果糖60*3.5=210g

还有其他类似的研究也发现,果糖增加了肝脏脂肪水平[44,45],也是果糖占了总热量比例的30%以上,如果按照平均每人每日2000大卡来说,总热量30%接近700大卡,相当于175g果糖左右。

30-35%的总热量,明显是拿果糖当饭吃了,远远超出了我们平时的果糖摄入量。根据上海市营养食品质检站的估算[46],一倍470ml左右的奶茶含糖近60g。

我随手搜了一些我国的糖摄入量数据:

中国九省成人含糖饮料消费及添加糖摄入量的趋势分析--《卫生研究》2014年01期,平均每人每日13.4g糖;

2015年中国15省份儿童青少年糖摄入的研究 - 中国知网,青少年糖摄入量中位数为12.6g

我国3岁及以上居民碳酸饮料中添加糖摄入状况分析-论文-万方医学网,每日添加糖撮入量的中位数,男性15.3g女性10.1g,城市13.8g农村10.7g

中国人年均糖消费居全球倒数第七 营养专家开出吃“糖”处方,我国人年均消费8千克糖,每人日均21.9g左右。

注意,吃下去的糖一般不会全是果糖,可能还有蔗糖,所以上述数据向果糖转化时,还要打折扣。也就是说,我国居民平均每日糖摄入量10-13g左右(虽然食物中有隐形糖,但没有直接数据证明隐形糖会显著影响上述结论),这些说果糖严重造成危害的研究[44,45,81]中每日180-210g果糖摄入量,相当于我国官方统计数据的10-20倍。

需要注意的是,即便在这些强调“过量摄入果糖”的研究中[44,48],受试者们的短期血脂上升,也在正常的生理范围内。另外一些研究发现[47],当摄入果糖占每日总能量15%左右(等于75g左右,必然比官方数据翻了好几倍),也没有发现肝内脂肪含量显著变化。


正常情况下,果糖大部分成为燃料

大家都知道,葡萄糖更多是作为能量被使用(肌肉和大脑),相比之下,果糖主要肝脏代谢。一些自媒体为了博眼球,过分强调这一点,暗示果糖可能会全部留在肝脏,变成脂肪之类,危害健康。

脱离剂量讨论是不科学的,在正常情况下(非过量摄入)果糖有大约30-60%左右被氧化,还有30-50%被转为葡萄糖[28]和乳酸等,转化成脂肪的比例并不高。

至于葡萄糖,它也相对不容易使人发胖,更不是某些自媒体说的是“发胖的元凶”。

其实,人体不擅长把葡萄糖转化为脂肪;跟其他一些动物(比如猪)相比[57,58,59],人类把膳食碳水转化为自身脂肪的能力较弱。这可能是因为人类的早期祖先是灵长类动物,以树叶和果实为生,并不容易吃到大量 的碳水化合物,仅有的碳水需要给身体和大脑供能。

此外,即便要把碳水转化为脂肪,这个过程本身也十分繁琐,需要11步。

相比之下,脂肪膳食脂肪可以直接水解得到脂肪酸,省(bian)事(jie)多了。

这个观点我之前的文章[29]已经阐述过:

为什么碳水和糖才是长胖元凶,明明脂肪热量更高啊?

我们举2个典型证据:注射25g葡萄糖后,只有0.5%-2%被转化为脂肪组织中的脂肪[30];即便长期吃高碳水饮食,葡萄糖合成脂肪酸的量也很少,对于肥胖者来说大约有10g/天[31],非肥胖受试者不超过几克/天[32]。

关于果糖代谢的定量研究,到底有%多少的果糖被氧化,%转化为脂肪,这些我在另一篇回答中已经列举了大量数据进行详细分析:


扩展阅读

肉崽:人到底是怎样长胖的?

肉崽:瘦的人都有怎样的饮食习惯?

肉崽:不健身直接吃蛋白粉会怎么样?

肉崽:为什么碳水和糖才是长胖元凶,明明脂肪热量更高啊?

肉崽:当代年轻人为什么尿酸会高?

肉崽:为什么都说增肌要碳水?

肉崽:健身增肌的原理是什么?


References

1. Campos V.C., Tappy L. Physiological handling of dietary fructose-containing sugars: implications for health. Int. J. Obes. 2016;40:S6–S11.

2. Schwarz J.M., Noworolski S.M., Wen M.J., Dyachenko A., Prior J.L., Weinberg M.E., Herraiz L.A., Tai V.W., Bergeron N., Bersot T.P., et al. Effect of a high-fructose weight-maintaining diet on lipogenesis and liver fat. J. Clin. Endocrinol. Metab. 2015;100:2434–2442.

3. Stanhope K.L., Schwarz J.M., Keim N.L., Griffen S.C., Bremer A.A., Graham J.L., Hatcher B., Cox C.L., Dyachenko A., Zhang W., et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J. Clin. Investig. 2009;119:1322–1334.

4. Aeberli I., Gerber P.A., Hochuli M., Kohler S., Haile S.R., Gouni-berthold I., Berthold H.K., Spinas G.A., Berneis K. Low to moderate sugar-sweetened beverage consumption impairs glucose and lipid metabolism and promotes inflammation in healthy young men: A randomized controlled trial. Am. J. Clin. Nutr. 2011;94:479–485.

5. Bantle J.P., Raatz S.K., Thomas W., Georgopoulos A. Effects of dietary fructose on plasma lipids in healthy subjects. Am. J. Clin. Nutr. 2000;72:1128–1134.

6. Chong M.F., Fielding B.A., Frayn K.N. Mechanisms for the acute effect of fructose on postprandial lipemia. Am. J. Clin. Nutr. 2007;85:1511–1520.

7. Couchepin C., Lê K.A., Bortolotti M., da Encarna?ao J.A., Oboni J.B., Tran C., Scheneiter P., Tappy L. Markedly blunted metabolic effects of fructose in healthy young female subjects. Diabetes Care. 2008;31:1254–1256.

8. Parks E.J., Skokan L.E., Timlin M.T., Dingfelder C.S. Dietary sugars stimulate fatty acid synthesis in adults. J. Nutr. 2008:1039–1046.

9. Stanhope K.L., Bremer A.A., Medici V., Nakajima K., Ito Y., Nakano T., Chen G., Fong T.H., Lee V., Menorca R.I., et al. Consumption of fructose and high fructose corn syrup increase postprandial triglycerides, LDL-cholesterol, and apolipoprotein-B in young men and women. J. Clin. Endocrinol. Metab. 2011;96:E1596–E1605.

10. Tran C., Jacot-Descombes D., Lecoultre V., Fielding B.A., Carrel G., Lê K.-A., Schneiter P., Bortolotti M., Frayn K.N., Tappy L. Sex differences in lipid and glucose kinetics after ingestion of an acute oral fructose load. Br. J. Nutr. 2010;104:1139–1147.

11. Aeberli I., Hochuli M., Gerber P.A., Sze L., Murer S.B., Tappy L., Spinas G.A., Berneis K. Moderate amounts of fructose consumption impair insulin sensitivity in healthy young men: A randomized controlled trial. Diabetes Care. 2013;36:150–156.

12. Kaori Minehira, Vincent Bettschart, Hubert Vidal, Nathalie Vega, Véronique Di Vetta, Valentine Rey, Philippe Schneiter, Luc Tappy.Effect of Carbohydrate Overfeeding on Whole Body and Adipose Tissue Metabolism in Humans.Obes Res. 2003 Sep;11(9):1096-103.

13. K Minehira 1 , N Vega, H Vidal, K Acheson, L Tappy.Effect of carbohydrate overfeeding on whole body macronutrient metabolism and expression of lipogenic enzymes in adipose tissue of lean and overweight humans.Int J Obes Relat Metab Disord. 2004 Oct;28(10):1291-8.

14. Sj6str~Sm L: Carbohydrate stimulated fatty acid synthesis de novo in human adipose tissue of different cellular types. Acta Med Scand 194:387, 1973b

15. Per Bj6rntorp and Lars Sj6str6m.Carbohydrate Storage in Man: Speculations and Some Quantitative Considerations.From the Clinical Metabolic Laboratory, Department of Medicine L Sahlgren's Hospital, University of Gothenburg, Gothenburg, Sweden.Address reprint requests to Per BjOrntorp, Clinical Metabolic Laboratory, Department of Medicine L Sahlgren's Hospital, University of Gothenburg, Gothenburg, Sweden.

16. Zheng Y., Scow J.S., Duenes J.A., Sarr M.G. Mechanisms of glucose uptake in intestinal cell lines: Role of GLUT2. Surgery. 2012;151:13–25.

17. Tappy L., Lê K.-A. Metabolic effects of fructose and the worldwide increase in obesity. Physiol. Rev. 2010;90:23–46.

18. P Bj?rntorp, P Berchtold, J Holm, B Larsson.The glucose uptake of human adipose tissue in obesity.Eur J Clin Invest. 1971 Sep;1(6):480-5.

19. Caliceti C., Calabria D., Roda A., Cicero A. Fructose intake, serum uric acid, and cardiometabolic disorders: A critical review. Nutrients. 2017;9:395.

20. Herman R.H., Stifel F.B., Greene H.L., Herman Y.F. Intestinal metabolism of fructose. Acta Med. Scand. 1972;192:19–25.

21. Froesch E.R. Fructose metabolism in adipose tissue. Acta Med. Scand. Suppl. 1972;542:37–46.

22. Cox C.L., Stanhope K.L., Schwarz J.M., Graham J.L., Hatcher B., Griffen S.C., Bremer A.A., Berglund L., McGahan J.P., Havel P.J., et al. Consumption of fructose-sweetened beverages for 10 weeks reduces net fat oxidation and energy expenditure in overweight/obese men and women. Eur. J. Clin. Nutr. 2012;66:201–208.

23. Schwarz J.M., Noworolski S.M., Wen M.J., Dyachenko A., Prior J.L., Weinberg M.E., Herraiz L.A., Tai V.W., Bergeron N., Bersot T.P., et al. Effect of a high-fructose weight-maintaining diet on lipogenesis and liver fat. J. Clin. Endocrinol. Metab. 2015;100:2434–2442.

24. Stanhope K.L., Schwarz J.M., Keim N.L., Griffen S.C., Bremer A.A., Graham J.L., Hatcher B., Cox C.L., Dyachenko A., Zhang W., et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J. Clin. Investig. 2009;119:1322–1334.

25. Sevastianova K., Santos A., Kotronen A., Hakkarainen A., Makkonen J., Silander K., Peltonen M., Romeo S., Lundbom J., Lundbom N., et al. Effect of short-term carbohydrate overfeeding and long-term weight loss on liver fat in overweight humans. Am. J. Clin. Nutr. 2012;96:727–734. doi: 10.3945/ajcn.112.038695. [PubMed] [CrossRef] [Google Scholar]

26. Adiels M., Taskinen M.R., Packard C., Caslake M.J., Soro-Paavonen A., Westerbacka J., Vehkavaara S., H?kkinen A., Olofsson S.O., Yki-J?rvinen H., et al. Overproduction of large VLDL particles is driven by increased liver fat content in man. Diabetologia. 2006;49:755–765.

27. Sun SZ, Empie MW . Fructose metabolism in humans - what isotopic tracer studies tell us. Nutr Metab 2012; 9: 89.

28. V C Campos & L Tappy.Physiological handling of dietary fructose-containing sugars: implications for health.International Journal of Obesity volume 40, pages S6–S11 (2016)

29. 为什么碳水和糖才是长胖元凶,明明脂肪热量更高啊?

30. P Bj?rntorp, P Berchtold, J Holm, B Larsson.The glucose uptake of human adipose tissue in obesity.Eur J Clin Invest. 1971 Sep;1(6):480-5.

31. Sj6str~Sm L: Carbohydrate stimulated fatty acid synthesis de novo in human adipose tissue of different cellular types. Acta Med Scand 194:387, 1973b

32. Per Bj6rntorp and Lars Sj6str6m.Carbohydrate Storage in Man: Speculations and Some Quantitative Considerations.From the Clinical Metabolic Laboratory, Department of Medicine L Sahlgren's Hospital, University of Gothenburg, Gothenburg, Sweden.Address reprint requests to Per BjOrntorp, Clinical Metabolic Laboratory, Department of Medicine L Sahlgren's Hospital, University of Gothenburg, Gothenburg, Sweden.

33. Grand RJ, Schay MI, Jaksina S . Development and control of intestinal and hepatic fructokinase. Pediatr Res 1974; 8: 765–770.

34. Korieh A, Crouzoulon G . Dietary regulation of fructose metabolism in the intestine and in the liver of the rat. Duration of the effects of a high fructose diet after the return to the standard diet. Arch Int Physiol Biochim Biophys 1991; 99: 455–460.

35. Bjorkman O, Crump M, Phillips RW . Intestinal metabolism of orally administered glucose and fructose in Yucatan miniature swine. J Nutr 1984; 114: 1413–1420.

36. Te Morenga L, Mallard S, Mann J . Dietary sugars and body weight: systematic review and meta-analyses of randomised controlled trials and cohort studies. Br Med J 2013; 346: e7492.

37. Yang Q, Zhang Z, Gregg EW, Flanders WD, Merritt R, Hu FB . Added sugar intake and cardiovascular diseases mortality among US adults. JAMA Intern Med 2014; 174: 516–524.

38. Jayalath VH, Sievenpiper JL, de Souza RJ, Ha V, Mirrahimi A, Santaren ID et al. Total fructose intake and risk of hypertension: a systematic review and meta-analysis of prospective cohorts. J Am Coll Nutr 2014; 33: 328–339.

39. Hu FB, Malik VS . Sugar-sweetened beverages and risk of obesity and type 2 diabetes: epidemiologic evidence. Physiol Behav 2010; 100: 47–54.

40. Choi HK, Willett W, Curhan G . Fructose-rich beverages and risk of gout in women. JAMA 2010; 304: 2270–2278.

41. Choi HK, Curhan G . Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. Br Med J 2008; 336: 309–312.

42. Montonen J, Jarvinen R, Knekt P, Heliovaara M, Reunanen A . Consumption of sweetened beverages and intakes of fructose and glucose predict type 2 diabetes occurrence. J Nutr 2007; 137: 1447–1454.

43. Blum JW, Jacobsen DJ, Donnelly JE . Beverage consumption patterns in elementary school aged children across a two-year period. J Am Coll Nutr 2005; 24: 93–98.

44. Schwarz JM, Noworolski SM, Wen MJ, Dyachenko A, Bergeron N, Bersot TP et al. Effect of a high-fructose weight-maintaining diet on lipogenesis and liver fat. J Clin Endocrinol Metab 2015; 100: 2434–2442.

45. Lecoultre V, Egli L, Carrel G, Theytaz F, Kreis R, Schneiter P et al. Effects of fructose and glucose overfeeding on hepatic insulin sensitivity and intrahepatic lipids in healthy humans. Obesity 2013; 21: 782–785.

46. 来看看!喝一杯奶茶等于吃了多少块糖?

47. Le KA, Faeh D, Stettler R, Ith M, Kreis R, Vermathen P et al. A 4-wk high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans. Am J Clin Nutr 2006; 84: 1374–1379.

48. Egli L, Lecoultre V, Theytaz F, Campos V, Hodson L, Schneiter P et al. Exercise prevents fructose-induced hypertriglyceridemia in healthy young subjects. Diabetes 2013; 62: 2259–2265.

49. D David Wang 1 , John L Sievenpiper 2 , Russell J de Souza 3 , Adrian I Cozma 1 , Laura Chiavaroli 1 , Vanessa Ha 1 , Arash Mirrahimi 4 , Amanda J Carleton 5 , Marco Di Buono 6 , Alexandra L Jenkins 7 , Lawrence A Leiter 8 , Thomas M S Wolever 8 , Joseph Beyene 9 , Cyril W C Kendall 10 , David J A Jenkins 8.Effect of fructose on postprandial triglycerides: a systematic review and meta-analysis of controlled feeding trials.Atherosclerosis. 2014 Jan;232(1):125-33.

50. Lisa Te Morenga, research fellow12, Simonette Mallard, research assistant1, Jim Mann, professor123.Dietary sugars and body weight: systematic review and meta-analyses of randomised controlled trials and cohort studies.BMJ 2013; 346

51. Carol F Kirkpatrick 1 , Julie P Bolick 2 , Penny M Kris-Etherton 3 , Geeta Sikand 4 , Karen E Aspry 5 , Daniel E Soffer 6 , Kaye-Eileen Willard 7 , Kevin C Maki 8.Review of current evidence and clinical recommendations on the effects of low-carbohydrate and very-low-carbohydrate (including ketogenic) diets for the management of body weight and other cardiometabolic risk factors: A scientific statement from the National Lipid Association Nutrition and Lifestyle Task Force.J Clin Lipidol. Sep-Oct 2019;13(5):689-711.e1.

52. H J van Wyk, R E Davis, J S Davies.A critical review of low-carbohydrate diets in people with Type 2 diabetes.Diabet Med. 2016 Feb;33(2):148-57.

53. Alan A Aragon 1 , Brad J Schoenfeld 2 , Robert Wildman 3 , Susan Kleiner 4 , Trisha VanDusseldorp 5 , Lem Taylor 6 , Conrad P Earnest 7 , Paul J Arciero 8 , Colin Wilborn 6 , Douglas S Kalman 9 , Jeffrey R Stout 10 , Darryn S Willoughby 11 , Bill Campbell 12 , Shawn M Arent 13 , Laurent Bannock 14 , Abbie E Smith-Ryan 15 , Jose Antonio16.International society of sports nutrition position stand: diets and body composition.J Int Soc Sports Nutr. 2017 Jun 14;14:16.

54. Cardillo S, Seshadri P, Iqbal N. The effects of a lowcarbohydrate versus low-fat diet on adipocytokines in severely obese adults: three-year follow-up of a randomized trial. Eur Rev Med Pharmacol Sci 2006; 10: 99–106.

55. Buchwald H, Avidor Y, Braunwald E et al. Bariatric surgery: asystematic review and meta-analysis. JAMA 2004; 292: 1724–1737.

56. S. J. Hallberg et al., Diabetes Ther. 9, 583–612(2018).

57. B. S. Lennerz et al., Pediatrics 141, e20173349(2018).

58. Nassib Bezerra Bueno 1 , Ingrid Sofia Vieira de Melo, Suzana Lima de Oliveira, Terezinha da Rocha Ataide.Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term weight loss: a meta-analysis of randomised controlled trials.Br J Nutr. 2013 Oct;110(7):1178-87.

59. Vivian L Veum, Johnny Laupsa-Borge, ?yvin Eng, Espen Rostrup, Terje H Larsen, Jan Erik Nordrehaug, Ottar K Nyg?rd , J?rn V Sagen, Oddrun A Gudbrandsen, Simon N Dankel, Gunnar Mellgren.Visceral adiposity and metabolic syndrome after very high-fat and low-fat isocaloric diets: a randomized controlled trial.Am J Clin Nutr. 2017 Jan;105(1):85-99."

60. Long Ge et al. Comparison of dietary macronutrient patterns of 14 popular named dietary programmes for weight and cardiovascular risk factor reduction in adults: systematic review and network meta-analysis of randomised trials.BMJ. 01 April,2020.

61. D Papamichou, D B Panagiotakos, C Itsiopoulos.Dietary patterns and management of type 2 diabetes: A systematic review of randomised clinical trials.Nutr Metab Cardiovasc Dis. 2019 Jun;29(6):531-543.

62. Gary D Foster 1 , Holly R Wyatt, James O Hill, Brian G McGuckin, Carrie Brill, B Selma Mohammed, Philippe O Szapary, Daniel J Rader, Joel S Edman, Samuel Klein.A randomized trial of a low-carbohydrate diet for obesity.N Engl J Med. 2003 May 22;348(21):2082-90."

63. Tingting Dong, Conceptualization, Data curation, Formal analysis, Software, Writing – original draft, Writing – review & editing,1 Man Guo, Data curation, Formal analysis,2 Peiyue Zhang, Data curation,1 Guogang Sun,Conceptualization,1 and Bo Chen, Writing – review & editing1.The effects of low-carbohydrate diets on cardiovascular risk factors: A meta-analysis.PLoS One. 2020; 15(1): e0225348."

64. Lukas Schwingshackl,corresponding author1 Anna Chaimani,2,3,4 Georg Hoffmann,5 Carolina Schwedhelm,1 and Heiner Boeing1.A network meta-analysis on the comparative efficacy of different dietary approaches on glycaemic control in patients with type 2 diabetes mellitus.Eur J Epidemiol. 2018; 33(2): 157–170.

65. Ole Snorgaard,1 Grith M Poulsen,2 Henning K Andersen,3 and Arne Astrup2.Systematic review and meta-analysis of dietary carbohydrate restriction in patients with type 2 diabetes.BMJ Open Diabetes Res Care. 2017; 5(1): e000354.

66. Alain J. Nordmann, MD, MSc; Abigail Nordmann, BS; Matthias Briel, MD; Ulrich Keller, MD;William S. Yancy, Jr, MD, MSH; Bonnie J. Brehm, PhD; Heiner C. Bucher, MD, MPH.Effects of Low-Carbohydrate vs Low-Fat Diets on Weight Loss and Cardiovascular Risk Factors,A Meta-analysis of Randomized Controlled Trials.Arch Intern Med. 2006;166:285-293

67. 一天吃一顿饭会瘦吗?

68. Francey C., Cros J., Rosset R., Creze C., Rey V., Stefanoni N., Schneiter P., Tappy L., Seyssel K. The extra-splanchnic fructose escape after ingestion of a fructose-glucose drink: An exploratory study in healthy humans using a dual fructose isotope method. Clin. Nutr. ESPEN. 2019;29:125–132.

69. Lee H.J., Cha J.Y. Recent insights into the role of ChREBP in intestinal fructose absorption and metabolism. BMB Rep. 2018;51:429–436.

70. Krebs HA, Lund P: Formation of glucose from hexoses, pentoses, polyols and related substances in kidney cortex. Biochem J 98: 210–214, 1966

71. Bowman RH: Gluconeogenesis in the isolated perfused rat kidney. J Biol Chem 245: 1604–1612, 1970

72. Benoy MP, Elliott KA: The metabolism of lactic and pyruvic acids in normal and tumour tissues: Synthesis of carbohydrate. Biochem J 31: 1268–1275, 1937

73. Cohn C, Kolinsky M: Effect of blood sugar levels and insulin lack on gluconeogenesis by the kidney of the dog. Am J Physiol 156: 345–348, 1949

74. Kida K, Nakajo S, Kamiya F, Toyama Y, Nishio T, Nakagawa H: Renal net glucose release in vivo and its contribution to blood glucose in rats. J Clin Invest 62: 721–726, 1978

75. Salomon LL, Lanza FL, Smith DE: Renal conversion of fructose to glucose. Am J Physiol 200: 871–877, 1961

76. Björkman O, Felig P: Role of the kidney in the metabolism of fructose in 60-hour fasted humans. Diabetes 31: 516–520, 1982

77. DeFronzo R.A., Jacot E., Jequier E., Maeder E., Wahren J., Felber J.P. The effect of insulin on the disposal of intravenous glucose. Results from indirect calorimetry and hepatic and femoral venous catheterization.Diabetes.1981;30:1000–1007.

78. Ferrannini E, Simonson DC, Katz LD, Reichard G, Jr, Bevilacqua S, Barrett EJ, Olsson M, DeFronzo RA. The disposal of an oral glucose load in patients with non-insulin-dependent diabetes.Metabolism.1988;37:79–85.

79. Biolo G, Declan R, and Wolfe RR. Physiologic hyperinsulinemia stimulates protein synthesis and enhances transport of selected amino acids in human skeletal muscle. J Clin Invest 95: 811–819, 1995.

80. Bjorkman O, Gunnarsson R, Hagstrom E, Felig P, Wahren J . Splanchnic and renal exchange of infused fructose in insulin-deficient type 1 diabetic patients and healthy controls. J Clin Invest 1989; 83: 52–59.

81. Lê, K.-A., et al., Fructose overconsumption causes dyslipidemia and ectopic lipid deposition in healthy subjects with and without a family history of type 2 diabetes. The American journal of clinical nutrition, 2009. 89(6): p. 1760-1765.



user avatar   a-rong-enzyme 网友的相关建议: 
      

深度分析一下。

在看郑爽的一些相关事件的时候,我有一种强烈的感觉,郑爽是一个非常复杂且混乱的人。

她呈现给大众一个非常极端的两面,一面是令人怜惜的恋爱脑形象,一面是利用别人的心机girl。

换句话说,率真、义无反顾是她,冷漠、富有心机也是她。

当这极端的两面化为一个人时,大众就会感觉很困惑,难以理解她的各种迷惑行为。

她的这种极端性和两面性,都源于她和其家人固有的一系列的人际关系模式:

第一层次:“爱你的前提是你要对我有用”,“利用你是爱你的一种方式”;

第二层次:“我在感情里可以肆无忌惮地利用你”;

第三层次:“为了爱你(用你),我可以连自己都不放过”。

有网友总结,郑爽为张翰整容,为胡彦斌写书,给张恒送孩子。

看起来是傻女人为爱痴缠,其实这里的“爱”,本质上还是一种利用。

当年她跟张翰的恋情里,单方面公布分手,还自爆为爱整容。

为爱整容是真的,但以此为由给张翰施压也是真的。

对外宣称是因为跟张翰在一起自卑而整容,再单方面宣布分手,无疑是塑造弱势形象,给张翰施加愧疚感,以此来达到她的情感目的。

如果说把他们爱的纠缠叫做套路和利用,有些过度解读,那么分手后,不断炒作前任的行为就越发体现了她的情感模式:“爱就是工具”。

跟胡彦斌分手后,一边是郑爽爸爸出面说胡彦斌是花心大萝卜的渣男,一边郑爽又写书,表示对胡彦斌的留恋:“这是唯一想让我写进书里,关于爱情的人”;

同时也不忘展现自己的弱势形象:“支持你做任何事情,哪怕你只想玩玩感情,我都能够接受你的放纵”。

比起张翰的隐忍,胡彦斌选择用歌来抒发自己内心的涌动:

“你说的这么认真,显得我存心敷衍,这些套路的情节,苍白地上了台面”(胡彦斌自己定义为“套路”);

“你要的全拿走,剩下的我承受,留下我们的狗,别管有没有用,我怕它以后没人宠”。

在与张恒的恋情中,工具人的关系模式继续升级,这次充当工具的是两个无辜的小生命。

从郑爽录音里的态度来看,这完全不是想要成为一名母亲该有的状态。相较于上次的为爱整容,这次恐怕又是为爱“生子”。

感情好的时候,公司开着时候,张恒还有用的时候,赶紧整两个孩子让情感联结更深一点,感情吹了,就动弃养的心思。

在最新曝光的录音中,进一步证明她的内在逻辑是“孩子就是感情的工具,以后感情要是还有,孩子就重新要”。

回到前面提到的郑爽的人际关系模式:“为了爱你(用你),我可以连自己都不放过”。

作为一个女明星,在考虑要孩子的时候就应该很清楚,假如有一天感情破裂,秘密泄露,对她自己的发展会有怎样的后果,但她还是那么做了,也能看出她的极端:

一方面,可能当时真的感觉来了,爱的死去活来;另一方面,作为极度害怕被抛弃的类型,她的内心也一定极度焦虑,以至于不考虑后果地寄希望于通过孩子来避免这种焦虑。

郑爽这类女孩,其实对任何男性可能都具有致命的诱惑力。她在爱情中的义无反顾,会让你们的感情迅速拉近,并且你会被代入到她的“人生剧本”中;

而当你发现,她曾经表现出来的义无反顾和深沉的爱,其实是一种换取你更多情感价值和物质价值的手段时,你又会三观炸裂,感觉亦真亦假。

但此时,你已经在与她的纠缠中无法自拔了。

就像张恒,当郑爽提出要代孕时,他之所以会答应,一定有感动的成分(假如不是男方阴谋):“眼前这个女人一定是想跟我一辈子的,否则不会担风险要孩子。”




我们中国人常讲究要中庸,这真是大智慧,放到人的人格特征上也是如此。

如果你感觉眼前的这个男生或者女生,情绪、想法、行为都容易走极端,个性过于“分裂”,那还是尽量远离吧,因为他/她可能是一朵有毒的玫瑰。

如果我们是跟郑爽有类似的人格特点,那还是要先以自我完善和成长为主,而不是寄希望用什么东西或手段来拴住一个人或一段感情,尤其是用孩子!


我是暗涌,心理学科普作者,关注我,用心理学视角看人性!



user avatar   kuntengclinic 网友的相关建议: 
      


user avatar   floyd-liao 网友的相关建议: 
      

朋友太漂亮,那就把她拿下,性别不要卡的太死,因为要攻略美女很刺激有了目的性反而会更期待见面走在一起,我就是这么做的,所以现在这个大美女朋友不但一直和我在一起还给我钱花,我说的很粗俗很离谱可人活一次管那么多世俗规则干嘛。




  

相关话题

  C4 植物在演化上是否具有同一起源? 
  为什么有些实验室没有实验室主页? 
  气泡水和碳酸饮料是不是两回事?如果是,这两种饮料在配料和相关标准上有哪些不同? 
  哪些食物比较有营养? 
  水飞蓟素真的可以护肝吗?原理是怎样的?普通人和服用很多药的老年人有必要预防性服用吗? 
  两个由相同元素构成的不同单质能不能发生化学反应? 
  为什么人类不用比甘蔗或甜菜更甜的水果提炼糖? 
  身边有人煲汤只喝汤,煲汤的材料都是倒掉的,这是不是很浪费?营养在汤里还是在材料里? 
  转基因食物的基因是否可在人体内表达出有毒蛋白? 
  假如一个成年人体内的水含量要达到90%且尽可能正常生活,ta的身体结构需要发生哪些变化? 

前一个讨论
没读过《资本论》经济学不算入门吗?
下一个讨论
如果与鲁迅相处一个下午,你会问什么问题?





© 2024-11-25 - tinynew.org. All Rights Reserved.
© 2024-11-25 - tinynew.org. 保留所有权利