相同质量100g肥肉和100g碳水，哪个更长肉？ 第1页

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小结

1、主流科学界的结论：决定肥胖的主要饮食因素是总热量，次要才是食物种类

2、如果热量不足，碳水和脂肪都不会让人长胖；

3、如果热量超标，脂肪比碳水更令人发胖；

4、就算没有胰岛素，人照样可以长胖，条条大路通肥胖，只要热量足够。

结论：“相同的额外热量，脂肪比碳水更容易让人发胖”。

一、总热量定胜负

1、主流学术界的结论非常明确：宏观上，肥胖主要取决于总热量

（1）国际运动营养学会（ISSN—The International Society of Sports Nutrition ）2017年的声明[1]：减肥主要靠热量差，低脂和低碳饮食效果类似。

声明中还提到：“目前为止，高碳和低碳饮食的对比研究中，只要总热量摄入相同，低碳饮食没能带来更高的减脂效果[3,4,5,6,7,8]，除极少数研究例外[2]”。

（2）美国国家脂肪协会2019年也发表过声明，同样提出低碳/极低碳水饮食并不比其他饮食更适合用于减肥[9]；

（3）一项包含了107个相关研究的大型元分析[2]得出：减肥的效果不是因为饮食中的碳水减少，而是因总热量减少；另一项包含19个研究进行了荟萃分析的结论是，只要总热量相等，低碳与常规饮食的减肥效果一样[11]。大多数研究都得出类似结论[12,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40]。

（4）甚至于，对115名2型糖尿病人的研究也发现[13]，低碳高脂饮食（碳水14%/脂肪58%）与低脂高碳饮食（53%碳水/30%脂肪）带来的体重减轻和血糖控制效果类似。

2、食物种类的影响也明显存在，但是相对于总热量的影响较为次要一些。

证据表明，同样是碳水，来自于水果、谷物、粗粮、奶制品中的碳水与2型糖尿病风险是负相关，而甜食、甜饮料则正相关[47,48,49,50,51]；增加水果/蔬菜/全谷类/豆类/家禽和鱼类的摄入，减少精制碳水/土豆/红肉/加工肉类，可能会降低冠心病的风险[53]。

护士健康研究对148.4万人随访接近20年的数据（1984-2008年）表明，高碳水化合物摄入量与二型糖尿病风险无关（相对风险-2%），高淀粉升高相应风险23%、高纤维降低相应风险20%、谷物降低相应风险29%、水果降低相应风险21%[52]；

小结：总热量过高才是肥胖的主要原因，而非胰岛素和碳水。

二、如果热量过剩，脂肪比碳水更至胖

在不运动的状态下，如果热量吃超了，脂肪比碳水更令人发胖。

《美国临床营养学杂志》有一项研究[105]，将35名正常和肥胖的受试者随机分配到持续15天【同等热量】的高碳水化合物（55%碳水）或高脂肪（50%脂肪）饮食中。

在前14天，调整了饮食量，保持他们的体重不变。第15天受试者在代谢房中静坐呆23小时，并吃了【同等热量的】超量的饮食。结果高碳水组的热量盈余约为1338千焦，高脂肪组热量盈余约为1728千焦。

所以原文结论是，对于经常久坐的人来说，长期食用高碳水化合物可以稍微少长胖一些。

三、脂肪比碳水更至胖的原因一：糖缓冲系统

1、人有糖缓冲系统，没有脂肪缓冲系统，吃的糖先存起来，吃的脂肪直接长胖

人体的糖缓冲系统主要由肝脏和肌肉构成，它们像海绵一样，可吸收许多的糖，存起来。特别是骨骼肌，它是人体处理葡萄糖的主要器官[43,44,45]。葡萄糖一旦进入肌肉，就会被合成大分子肌糖原储存其中，作为肌肉的备用能量，不会再被身体挪作他用，也不会转化为脂肪。

一般人肝可容纳100g左右糖。有数据称骨骼肌储存糖的能力是12g/kg肌肉，所以普通人一般肌肉能存400g左右的糖。这些内容在各类教材上都有。

但是，人体没有脂肪缓冲系统。人吃下去的脂肪先在小肠消化，然后由肠细胞合成为甘油三酯，被脂载蛋白运输入血，全部吸收。

2、正常情况下人体对膳食脂肪会吸收95%左右，极少排泄

许多自媒体为了吸引眼球喜欢写类似于“吃肥肉不长胖，吃碳水才长胖”，一种理由就是人会排泄多余脂肪，碳水通过胰岛素使人发胖。这个问题下有些评论区也有人说脂肪大于多少多少g就排泄了。

这种说法纯属扯蛋。任何一本生理/生物/营养方面的教材上都写的清清楚楚：脂肪从消化道进入血液循环，没有排泄这一说。

3、不纠结于各类特殊情况，不钻牛角尖

有些人说，吃了过多脂肪导致消化不良、从肠道排泄；或者有疾病导致脂肪从肠道排泄[46]，这些都属于特殊情况，没有讨论意义。如果要扯特殊情况，吃成糖尿病之后碳水大部分从尿液排泄了，吃100g碳水可能只获得10-30g甚至更少。

值得一提的是中/短链脂肪，它们不会被储存，会被分解供能。但是它们也是热量，还是会间接导致人发胖。人体每天都要无时无刻分解脂肪来供能，有了这些中短链脂肪酸，人体可以减少分解自身的脂肪。再加上中/短链脂肪酸在一般食物中占比较少，没必要钻这个牛角尖。

四、脂肪比碳水更至胖的原因二：碳水会额外燃烧，脂肪不会

原因是，当摄入多余碳水时，身体会燃烧掉一部分；当摄入多余脂肪时身体不会燃烧它们。

早期的研究已经证实了上述观点：34名非糖尿病男性经过了10天测试，前4天限制食物，从第5天开始让他们放开吃，这导致他们摄入过多总热量（32%-54%）。结果发现碳水化合物摄入增加导致了额外的碳水化合物氧化（燃烧），但脂肪摄入增加不导致额外脂肪氧化[102]。

另一项研究的结论也一样：28名印第安土著妇女同样进行上述测试，前4天限制食物，从第5天开始让放开吃[103]。这导致她们摄入过多总热量，蛋白质摄入增加约11%，脂肪摄入增加约40%，碳水摄入增加约49%。过量摄入碳水化合物可导致碳水化合物氧化增加（r=0.51），而过量脂肪摄入则导致脂肪氧化减少（r=-0.53）。

两个研究，不同性别，不同人群，不同民族，不同体重，结论却相同：当总热量超标时，碳水摄入增加提升碳水的氧化（燃烧）水平；脂肪摄入增加则不提升脂肪的氧化水平。

这就是为什么，kevin等人观察到，摄入超量碳水化合物期间，受试者24小时的能量消耗增加了840大卡/日[104]。考虑到普通人每日的总热量消耗平均是2000千卡，相当于增加了35%的代谢，这个值相当可观。

这印证了我们之前的观点：如果热量吃超了，超标的部分是碳水，身体储存的脂肪没有那么多；而如果超量部分是脂肪，身体几乎是照单全收。所以则更令人发胖。

五、为什么碳水摄入增加会导致碳水氧化增加？

1、摄入碳水刺激胰岛素分泌，胰岛素促进碳水“燃烧”

生理上，胰岛素有3个主要生理作用：

（1）促进肌肉和肝脏吸收碳水（所谓的先补充糖库）；

（2）【促进碳水糖酵解】（所谓“燃烧”掉一些）

（3）敦促脂肪细胞摄取葡萄糖和脂肪酸（所谓长胖）。

（还有抑制脂肪分解等，就不铺开说了）

关于第二点，在不同的生理和营养教材上都有描述，说法都相同，是共识，不是什么新鲜观点。

2、胰岛素如何促进碳水燃烧？答案是通过一种酶：PDC

多数情况下，人把碳水作为主要能量来源。

我们“燃烧”碳水释放能量，给ATP充能，细胞再利用ATP的能量。在运动强度低、或者静息状态，我们有充足的氧气供应，此时我们对碳水进行“有氧氧化”：也就是俗称的三羧酸循环（也叫柠檬酸循环，TC循环）。

它的大致步骤是这样的：

对于有基础知识的同学来说，这个图很熟悉，so easy。因为每个医学生都要背这个循环，好的老师会教会你如何轻松背诵。

但没有基础知识的同学就要崩溃了：完全看不懂。别急，它只是看起来复杂，简化一下就这样：

如图上所示，葡萄糖在人体内经过一些复杂而繁琐的反应，被转化为丙酮酸；丙酮酸氧化为乙酰COA[77]，然后进入三羧酸循环彻底氧化分解，得到为二氧化碳、水和能量。

这样，大家就好理解PDC是什么了：PDC就是那个把丙酮酸氧化为乙酰COA的关键性角色，它叫丙酮酸脱氢酶复合物，英文名Pyruvate Dehydrogenase Complex。

这是它的照片：

PDC是糖酵解中的一种关键酶（的复合物）[78]。

肌肉处理、消耗葡萄糖，很大程度需要依赖并激活PDC[93]。PDC与全身最大摄氧量有很强的相关性[73,74,75]，有运动经验的人比久坐的人更能氧化碳水/丙酮酸，而得到更多的能量。

那这和本文的关系在于，吃了碳水后分泌胰岛素，胰岛素能提升PDC活性[92,101,102]；PDC活性提高了，碳水氧化增加，热量损耗增加。

92. Constantin-Teodosiu D, Constantin D, Stephens F, Laithwaite D, Greenhaff PL. The role of FOXO and PPAR transcription factors in diet-mediated inhibition of PDC activation and carbohydrate oxidation during exercise in humans and the role of pharmacological activation of PDC in overriding these changes. Diabetes. 2012;61:1017–1024.

101. Y Sakamoto, T Kuzuya.Stimulation of pyruvate dehydrogenase activity by insulin-dextran complex in mouse adipose tissue.iochem Biophys Res Commun. 1979 May 14;88(1):37-43. doi: 10.1016/0006-291x(79)91693-0.

102. M Cardell 1 , B K Siesjö, T Wieloch.Changes in pyruvate dehydrogenase complex activity during and following severe insulin-induced hypoglycemia.J Cereb Blood Flow Metab. 1991 Jan;11(1):122-8.

在这一点上上，文献和教材当然是同步的。因为好的书、教材就是文献的汇总和整理。

也就是说，作为多余热量时，碳水会有所损失，但脂肪不会——这就是为什么如果吃多了，脂肪比碳水更胖人。这才是题主的问题中真正包含的有价值回答信息，这才是我要写这个回答的目的。

六、高脂肪饮食还抑制PDC活性，抑制碳水燃烧

康斯坦丁等人证实，高脂肪饮食激活了PDK，抑制PDC的活性，减少了碳水的氧化[93]。Peters等人报告，3天的高脂肪饮食后没，PDK活性增加，碳水氧化减少[100]。这当然不是孤证，相应证据还有很多[87,88,89,90,91,94,5,96,97,9899]。

为什么高脂肪饮食会抑制PDC的活性呢？因为高脂肪饮食可以激活另一些酶（PDK），PDK会抑制PDC的活性，从而促进肥胖、糖尿病、非酒精性脂肪肝[79,80,81,82]。

如果对动物使用药物抑制PDK，则PDC的活性增加，碳水化合物燃烧增加，脂肪肝减弱[83]；如果对动物进行基因编辑，让动物体内减少或者不产生PDK，则动物的葡萄糖氧化增加、糖耐受和胰岛素敏感性明显提高、体重减轻、肥胖程度下降、脂肪肝减少/改善[84,85,86]。

PDK对PDC的抑制机理就不细说了，下图（蓝圈）给大家看一眼即可。

七、只要脂肪吃够，哪怕没有胰岛素照样长胖

胰岛素不是长胖的必要条件。

知乎上许多人持有一种观点：觉得人长胖必须得有胰岛素参与，没有胰岛素人不能合成脂肪。

对于持有这种观点（没有胰岛素不能合成脂肪、不会长胖）的人，我觉得他们的脑袋里装的都是大头针和图钉。

因为胰岛素根本就不是合成脂肪的必要或前提条件。没有胰岛素，人体一样可以把膳食中吸收进血液的脂肪运输到脂肪组织，长胖，完全不影响。

证据在生理学上。

乙酰化刺激蛋白（acylation stimulation protein，简称ASP）[54]，它是脂肪细胞分泌的一种因子。科研认为ASP储存脂肪的作用与胰岛素相当[59]。

它通过激活甘油三酯合成酶，促进脂肪细胞获得更多的脂肪酸[69]。跟胰岛素一样，它还能抑制抑制脂肪分解酶的活性（如HSL），减少脂肪分解[60]。

肥胖和高血脂体内ASP水平增加[59,62]，ASP和腰臀比正相关（ASP水平越高，腰围越大）

ASP会响应于脂肪摄入。进食高脂肪食物后，乳糜微粒（半消化的食物脂肪微粒）能会刺激APS生成增加10-20倍，并且ASP水平升高与血脂升高正相关[63,64]。

注意，ASP可以独立于胰岛素发挥作用[61]，所以我们说，不需要胰岛素，人体一样可以长胖。

有趣的是，类似于胰岛素抵抗这样的概念，ASP也可以被抵抗，ASP促进腹部脂肪堆积的能力会随肥胖逐渐变弱[65,66,67]，ASP抵抗也被视为代谢综合征中的一种表现[69]。ASP在血脂异常[69]、多囊卵巢[70]、肾病[71]、非酒精性脂肪性肝[72]、胰岛素抵抗、肥胖和冠心病、心血管疾病中都发挥了一定作用[55,56]，心肌梗死期间ASP的激活和刺激也被关注[57,58]。

八、题外话

仔细的看，我们所有的探讨前提都是“超出同样的热量”。实际上，由于高脂肪饮食具有抑制食欲的作用，往往总热量摄入低于正常饮食。

那这就意味着高脂肪低碳（或者生酮）饮食更利于常人减肥吗？

这没有答案。

1、高脂肪饮食具有抑制食欲的好处，但是它难以坚持。大量数据表明，低碳/生酮饮食是所有饮食方案中退出率最高的。结果大概率是爆碳、复胖——一夜回到解放前，比减肥之前更糟糕；

2、低碳/生酮饮食还有许多安全性方面的问题：酮作为一种酸性物质，会降低血液的PH值，这就需要考验人的酸碱缓冲系统。对于一些人能承受，而对于另一些遗传条件的人，可能会变成酸中毒甚至昏迷死亡，这有大量的案例；

3、生酮饮食对某些人群可能损伤肝、肾和骨密度，长期癫痫生酮的儿童肾结石发病率比正常人同高接近30倍，这些也需要引起注意；

4、医学上，低碳和生酮饮食已经被证实纳入治疗手段。这被很多生酮商用来做广告，但这不代表安全，更不代表适合大众自己操作：砒霜和吗啡也都是医学治疗手段。

扩展阅读

不健身直接吃蛋白粉会怎么样？

“肌肉在休息的时候超量生长”，其中关于“休息”的定义是睡觉吗？

当代年轻人为什么尿酸会高？

肉崽：训练后需要拉伸吗？（一）

肉崽：训练后需要拉伸吗？（二）

肉崽：训练后需要拉伸吗？（三）

肉崽：训练后需要拉伸吗：参考文献（1-200）

肉崽：训练后需要拉伸吗：参考文献（200-323）

肉崽：被误解最多的健美训练要素（一）：轻重量精确刺激肌肉

肉崽：被误解最多的健美训练要素（二）：慢速动作

肉崽：被误解最多的健美训练要素（三）：孤立训练

肉崽：被误解最多的健美训练要素（四）：变换动作给予肌肉新刺激

肉崽：被误解最多的健美训练要素（五）：依据肌纤维类型针对训练

肉崽：“8-12次最佳增肌次数范围” 其实是个伪命题

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8. Hall K, Guo J. Obesity Energetics: Body Weight Regulation and the Effects of Diet Composition. Gastroenterology. 2017;152(7):1718-27.

9. 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.

10. Dena M Bravata, Lisa Sanders, Jane Huang, Harlan M Krumholz, Ingram Olkin, Christopher D Gardner, Dawn M Bravata.Efficacy and safety of low-carbohydrate diets: a systematic review.JAMA. 2003 Apr 9;289(14):1837-50.

11. Celeste E. Naude, Anel Schoonees, Marjanne Senekal, Taryn Young, Paul Garner, 4and Jimmy Volmink.Low Carbohydrate versus Isoenergetic Balanced Diets for Reducing Weight and Cardiovascular Risk: A Systematic Review and Meta-Analysis.PLoS One. 2014; 9(7): e100652

12. Michael L Dansinger 1 , Joi Augustin Gleason, John L Griffith, Harry P Selker, Ernst J Schaefer.Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial.JAMA. 2005 Jan 5;293(1):43-53.

13. Jeannie Tay, Campbell H Thompson, Natalie D Luscombe-Marsh, Thomas P Wycherley, Manny Noakes, Jonathan D Buckley, Gary A Wittert, William S Yancy Jr, Grant D Brinkworth.Effects of an energy-restricted low-carbohydrate, highunsaturatedfat/low saturated fat diet versus a high-carbohydrate, low-fat diet in type 2 diabetes: A 2-year randomized clinical trial.Diabetes Obes Metab. 2018 Apr;20(4):858-871.

14. Grant D Brinkworth 1 , Manny Noakes, Jonathan D Buckley, Jennifer B Keogh, Peter M Clifton.Long-term effects of a very-low-carbohydrate weight loss diet compared with an isocaloric low-fat diet after 12 mo.Am J Clin Nutr. 2009 Jul;90(1):23-32.

15. Alain J Nordmann 1 , Abigail Nordmann, Matthias Briel, Ulrich Keller, William S Yancy Jr, Bonnie J Brehm, Heiner C Bucher.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 Feb 13;166(3):285-93.

16. Carolyn D Summerbell 1 , Cate Cameron, Paul P Glasziou.WITHDRAWN: Advice on low-fat diets for obesity.Cochrane Database Syst Rev. 2008 Jul 16;(3):CD003640.

17. Jeannie Tay 1 , Natalie D Luscombe-Marsh 2 , Campbell H Thompson 3 , Manny Noakes 4 , Jonathan D Buckley 5 , Gary A Wittert 3 , William S Yancy Jr 6 , Grant D Brinkworth 7.Comparison of low- and high-carbohydrate diets for type 2 diabetes management: a randomized trial.Am J Clin Nutr. 2015 Oct;102(4):780-90.

18. 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."

19. Carol S Johnston 1 , Sherrie L Tjonn, Pamela D Swan, Andrea White, Heather Hutchins, Barry Sears.Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets.Am J Clin Nutr. 2006 May;83(5):1055-61.

20. 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.

21. 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.

22. Christopher D. Gardner et al. Effect of Low-Fat vs Low-Carbohydrate Diet on 12-Month Weight Loss in Overweight Adults and the Association With Genotype Pattern or Insulin Secretion: The DIETFITS Randomized Clinical Trial. JAMA, 2018; 319 (7): 667-679.

23. Alain J Nordmann 1 , Abigail Nordmann, Matthias Briel, Ulrich Keller, William S Yancy Jr, Bonnie J Brehm, Heiner C Bucher.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 Feb 13;166(3):285-93.

24. Marc-Andre Cornier 1 , W Troy Donahoo, Rocio Pereira, Inga Gurevich, Rickard Westergren, Sven Enerback, Peter J Eckel, Marc L Goalstone, James O Hill, Robert H Eckel, Boris Draznin.Insulin sensitivity determines the effectiveness of dietary macronutrient composition on weight loss in obese women.Obes Res. 2005 Apr;13(4):703-9.

25. Lisa J Moran, Henry Ko, Marie Misso, Kate Marsh, Manny Noakes, Mac Talbot, Meredith Frearson, Mala Thondan, Nigel Stepto, Helena J Teede.Dietary composition in the treatment of polycystic ovary syndrome: a systematic review to inform evidence-based guidelines.J Acad Nutr Diet. 2013 Apr;113(4):520-45.

26. 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.

27. Anette Due 1 , Thomas M Larsen, Huiling Mu, Kjeld Hermansen, Steen Stender, Arne Astrup.Comparison of 3 ad libitum diets for weight-loss maintenance, risk of cardiovascular disease, and diabetes: a 6-mo randomized, controlled trial.Am J Clin Nutr. 2008 Nov;88(5):1232-41.

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31. Celeste E. Naude, Anel Schoonees, Marjanne Senekal, Taryn Young, Paul Garner, 4and Jimmy Volmink.Low Carbohydrate versus Isoenergetic Balanced Diets for Reducing Weight and Cardiovascular Risk: A Systematic Review and Meta-Analysis.PLoS One. 2014; 9(7): e100652

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38. 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."

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山东男人，180，抢答一波。

这又是一个挑动南北对立的问题，估计和那位说北方男人太高，作为劳动力不适合工业制造业经济发展的神贴一个作者。

什么时候身高成优越感了？

什么时候月匈大就成优越感了？

个体差异而已。

找对象又不是80年代集市上挑牲口，得看肩高，看牙口。

都2021年了，一个男人要是靠个头产生优越感，说明这个人基本就是个草包，长那么高个头白瞎了。

有的喜欢肤白貌美大长腿。

有的喜欢36D，锥子脸，水蛇腰。

有的喜欢小鸟依人，有的御姐控萝莉控，

还有的非得娶处女，还有的硕士以下学历不考虑。

但真没见几个执着于女孩子身高的，150—180的女孩子，我身边的北方男人都娶过。

另外，不是每个北方男人都高大魁梧，有40%的175以下。这种身高对于150—170的女士，都不算什么身高优势的。何况南方女士也有50%以上是身高高于160的。

男人最重要的是品行，修养，能力，责任感，而不是多大块头，毕竟现在农业也机械化了，重体力劳动，耐力劳动，已经占比极地了，高大魁梧，威猛彪悍，只具有审美价值和欣赏价值。

治安越来越好的今天，都市里面也不需要一个巨石强森一样的肌肉男来给予女士们安全感。

女人们也不用想太多，男人喜欢你，爱上你，想和你结婚，不会因为你个头矮点，罩杯小一个号而犹豫。

最后，这种南北对立的话题，就谈谈GDP房价和产业领域就行了。扯到男女身上，简直就是人为的撕裂。

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山东男人，180，抢答一波。

这又是一个挑动南北对立的问题，估计和那位说北方男人太高，作为劳动力不适合工业制造业经济发展的神贴一个作者。

什么时候身高成优越感了？

什么时候月匈大就成优越感了？

个体差异而已。

找对象又不是80年代集市上挑牲口，得看肩高，看牙口。

都2021年了，一个男人要是靠个头产生优越感，说明这个人基本就是个草包，长那么高个头白瞎了。

有的喜欢肤白貌美大长腿。

有的喜欢36D，锥子脸，水蛇腰。

有的喜欢小鸟依人，有的御姐控萝莉控，

还有的非得娶处女，还有的硕士以下学历不考虑。

但真没见几个执着于女孩子身高的，150—180的女孩子，我身边的北方男人都娶过。

另外，不是每个北方男人都高大魁梧，有40%的175以下。这种身高对于150—170的女士，都不算什么身高优势的。何况南方女士也有50%以上是身高高于160的。

男人最重要的是品行，修养，能力，责任感，而不是多大块头，毕竟现在农业也机械化了，重体力劳动，耐力劳动，已经占比极地了，高大魁梧，威猛彪悍，只具有审美价值和欣赏价值。

治安越来越好的今天，都市里面也不需要一个巨石强森一样的肌肉男来给予女士们安全感。

女人们也不用想太多，男人喜欢你，爱上你，想和你结婚，不会因为你个头矮点，罩杯小一个号而犹豫。

最后，这种南北对立的话题，就谈谈GDP房价和产业领域就行了。扯到男女身上，简直就是人为的撕裂。

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