适度禁食（fasting）显然对健康有益，但如何禁食却很有讲究。目前常用的有“5+2方案”（一周5天正常饮食，2天禁食），也有“1+1方案”（每隔一天禁食），都属于“间歇禁食”（intermittent fasting），其实效果差不多。

对于大多数上班族来说，5+2方案优于1+1方案，这样就不用成天饿着肚皮有气无力地工作，周六、周日大不了躺着休息。因此，我本人也开始采用5+2方案进行间歇禁食。不过，我嫌经典的禁食太严格，饥饿感阵阵袭来很难受，我便想自己设计一个“改良”的禁食方案。

我记得禁食的要诀有两条：一是减少热量，二是降低食欲，目的是降低血清胰岛素样生长因子1（IGF-1）水平。于是，我“眉头一皱计上心来”。我想出了一个既减少热量摄入又降低食欲烦扰的“妙法”，那就是把炒好的蔬菜与煮熟的皮蛋粥或豆腐汤混合，但不同煮。这有点类似“烫饭”，我管它叫“烫粥”。

吃蔬菜的目的就是能吃饱肚子但又不会摄取太多热量，而烫粥可以“欺骗”胃-神经-内分泌系统，让食物消化得不那么快。据一个禁食电视片介绍，蛋白质可以减慢消化速度，而烫饭比吃饭喝汤的消化过程更长，因为胃的消化特点是先把水吸干，然后再消化食物。

在烫粥里面加蔬菜（纤维素）和皮蛋或豆腐（蛋白质）就能达到减少热量与降低食欲的双重目的。在已经实行该食谱的周六和周日，我并不觉得很饿，但效果如何还有待观察，关键是该食谱应能显著降低血清IGF-1水平，使身体不会成天忙于消化，而是腾出时间进行修补。

现在的禁食方案都存在一个普遍的问题，那就是未考虑肠道细菌的影响。当然，吃素本身可以“塑造”特定的菌群，但它们可能会“疯长”，不节制也会刺激免疫，导致炎症。我现在采用的办法是每晚饮用一杯红酒（酒精度14%），虽不知能否抑菌，但肯定能抗炎。如果想获得确切的抑菌效果，最好每天还吃点捣碎的蒜头。

另外，红酒中所含白藜芦醇也可以对禁食产生增效作用。白藜芦醇是SIRT1激活剂，可以促进线粒体更新和增殖，而禁食可以降低IGF-1水平，并且胰岛素和瘦素水平也随之降低，有助于细胞修复，二者结合起来相得益彰。

顺便再给各位推荐一篇有关禁食与健康的综述文章（1-s2.0-S1550413113005032-main.pdf）。虽然禁食不能包治百病，但它提到至少能减少我们患糖尿病、高血压、哮喘和类风湿性关节炎的机率，在大小鼠中证实禁食可以缓解糖尿病、心脏病、癌症和神经退行性疾病。

为什么禁食有如此多的保健作用呢？下面这张图形象地说明了禁食对人体各个组织器官的有利影响。你如果能看懂这张图，就能大致得出一个确切的答案。

为了让不懂专业的人士也能看懂这张图，我就在这里按组织器官的不同粗略总结如下：

大脑：神经网络可塑性增强，神经营养因子水平升高，神经元再生作用加速，抗压能力提高，线粒体再生活性改善，氧化应激与炎症水平降低。

血管：胰岛素、IGF-1、瘦素水平下降，酮体、脂联素和饱胀素水平升高。

心脏：副交感神经节律增强，静息心率减慢，心率变化增大，血压降低，抗压能力提高。

肝脏：胰岛素敏感性增强，肝糖原分解作用加剧，IGF-1水平降低。

肠道：能量摄入减少，炎症水平降低，细胞增殖活性减弱。

肌肉组织：胰岛素敏感性增强，分解代谢程度增大，抗压能力提高，体温下降。

脂肪组织：脂肪分解及酮体生成加速，瘦素水平下降，脂联素水平升高，炎症水平降低。

我认为，无论是节食还是间歇禁食，都可以启动机体的修复系统，有利于防止衰老相关疾病的提早发生。但是，如果严格禁食或禁食不当造成营养不良，那就会对健康造成损害，而且能把这种有害效应通过表观遗传方式传给后代。

在此提醒未婚及未生育的年轻人，若你们也想禁食，请不要严格到厌食和营养不良，否则你未来的宝宝可能很容易发胖，而且易产生胰岛素抵抗，甚至患上2型糖尿病、高血压等代谢病（见附件），千万要慎重！

Ancestral diets determine vulnerability to type 2 diabetes

Middle classes from developing countries are more susceptible than western Caucasians to obesity, type 2 diabetes and cardiovascular disease because of their ancestor's diets.

Date:July 10, 2015

Source:University of Sydney

Summary:The middle classes from developing countries are more susceptible than western Caucasians to obesity, type 2 diabetes and cardiovascular disease in today's changing environment. New research reveals this may be a result of the nutrition endured by their ancestors.Share:

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The middle classes from developing countries are more susceptible than western Caucasians to obesity, type 2 diabetes and cardiovascular disease in today's changing environment. New research published in Cell Metabolism from the University of Sydney in Australia, the National Centre for Cell Science and the DYP Medical College in Pune, India reveals this may be a result of the nutrition endured by their ancestors.

The findings in the paper titled Multigenerational Undernutrition and Diabetes could explain projections that more than 70 per cent of the global burden of type 2 diabetes will fall on individuals from developing countries by 2030.

Several studies have reported that a high-fat diet causes obesity. This latest research demonstrates that eating a 'normal' diet can make animals overweight, if their ancestors had been undernourished for several generations.

Unsurprisingly, increasing prosperity in developing countries has been accompanied by a sudden increase in caloric intake. However their populations' epigenetic makeup, whereby changing environmental factors alter how people's genes are expressed, has not compensated for these dietary changes. This means their bodies are still designed to cope with undernourishment; so they store fat in a manner that makes them more prone to obesity and its resulting diseases than populations accustomed to several generations of a 'normal' diet.

This scenario was recreated in a 12-year study of two groups of rats by Associate Professor Anandwardhan Hardikar's team at the University of Sydney and colleagues overseas. The first group was undernourished for 50 generations and then put on a normal diet for two generations. The second (control) group maintained a normal diet for 52 generations. At the end of the study it was found that when the descendants of the first group were exposed to a normal diet, this did not reverse the epigenetic modifications made by their undernourished forebears. These rats were eight times more likely to develop diabetes and multiple metabolic defects when compared to the control group.

"Their adverse metabolic state was not reversed by two generations of nutrient recuperation through a normal diet," said Associate Professor Hardikar. "Instead this newly prosperous population favoured storage of the excess nutrients as fat leading to increased obesity, cardiovascular disease and metabolic risk for diabetes when compared to their 'developed world' counterparts."

Associate Professor Hardikar said lower Vitamin B12 levels in the undernourished rats could also be an indicator of this trend.

"Human studies from Ranjan Yajnik's group at KEM Hospital in Pune, India have demonstrated that low circulating B12 and high folate levels are associated with insulin resistance and type 2 diabetes."

With increasing migration of populations from developing to affluent countries, there is a need to identify factors that minimise their risk of diabetes and obesity -- one of Australia's national health priorities.

"Hopefully further research in understanding the gut microbes, which are major producers of Vitamin B12 in our body, and/or dietary supplementation with Vitamin B12 and other micronutrients, could reduce the risk of metabolic diseases in the coming generations," says Associate Professor Hardikar.

Story Source:

The above post is reprinted from materials provided by University of Sydney. Note: Materials may be edited for content and length.

Journal Reference:

Anandwardhan A. Hardikar, Sarang N. Satoor, Mahesh S. Karandikar, Mugdha V. Joglekar, Amrutesh S. Puranik, Wilson Wong, Sandeep Kumar, Amita Limaye, Dattatray S. Bhat, Andrzej S. Januszewski, Malati R. Umrani, Amaresh K. Ranjan, Kishori Apte, Pranav Yajnik, Ramesh R. Bhonde, Sanjeev Galande, Anthony C. Keech, Alicia J. Jenkins, Chittaranjan S. Yajnik. Multigenerational Undernutrition Increases Susceptibility to Obesity and Diabetes that Is Not Reversed after Dietary Recuperation. Cell Metabolism, 2015; DOI:10.1016/j.cmet.2015.06.008