A CALORIE is a calorie. Eat too many and spend too few, and you will become obese and sickly. This is the conventional wisdom. But increasingly, it looks too simplistic. All calories do not seem to be created equal, and the way the body processes the same calories may vary dramatically from one person to the next.

This is the intriguing suggestion from the latest research into metabolic syndrome, the nasty clique that includes high blood pressure, high blood sugar, unbalanced cholesterol and, of course, obesity. This uniquely modern scourge has swept across America, where obesity rates are notoriously high. But it is also doing damage from Mexico to South Africa and India, raising levels of disease and pushing up health costs.

Metabolic syndrome can still be blamed on eating too much and exercising too little. But it is crucial to understand why some foods are particularly harmful and why some people gain more weight than others. Thankfully, researchers are beginning to offer explanations in a series of recent papers.

One debate concerns the villainy of glucose, which is found in starches, and fructose, found in fruits, table sugar and, not surprisingly, high-fructose corn syrup. Diets with a high “glycaemic index”, raising glucose levels in the blood, seem to promote metabolic problems. David Ludwig of Boston Children’s Hospital has shown that those on a diet with a low glycaemic index experience metabolic changes that help them keep weight off, compared with those fed a low-fat diet. This challenges the notion that a calorie is a calorie. Others, however, blame fructose, which seems to promote obesity and insulin resistance. Now a study published in Nature Communications by Richard Johnson, of the University of Colorado, explains that glucose may do its harm, in part, through its conversion to fructose.

Dr Johnson and his colleagues administered a diet of water and glucose to three types of mice. One group acted as a control and two others lacked enzymes that help the body process fructose. The normal mice developed a fatty liver and became resistant to insulin. The others were protected. The body’s conversion of glucose to fructose, therefore, seems to help spur metabolic woes.

You are what you eat, maybe

Even more intriguing is the notion that the same diet may be treated differently by different people. Four recent papers explored this theme. In one, published in Science in July, Joseph Majzoub, also of Boston Children’s Hospital, deleted in mice a gene called Mrap2. Dr Majzoub and his colleagues showed that this helps to control appetite. Surprisingly, however, even when the mutant critters ate the same as normal mice, they still gained more weight. Why that is remains unclear, but it may be through Mrap2’s effect on another gene, called Mc4r, which is known to be involved in weight gain.

The second and third papers, published as a pair in Nature in August, looked at another way that different bodies metabolise the same diet. Both studies were overseen by Dusko Ehrlich of the National Institute of Agricultural Research in France. One examined bacteria in nearly 300 Danish participants and found those with more diverse microbiota in their gut showed fewer signs of metabolic syndrome, including obesity and insulin resistance. The other study put 49 overweight participants on a high-fibre diet. Those who began with fewer bacterial species saw an increase in bacterial diversity and an improvement in metabolic indicators. This was not the case for those who already had a diverse microbiome, even when fed the same diet.

Jeffrey Gordon, of Washington University in St Louis, says these two studies point to the importance of what he calls “job vacancies” in the microbiota of the obese. Fed the proper diet, a person with more vacancies may see the jobs filled by helpful bacteria. In the fourth paper, by Dr Gordon and recently published in Science, he explores this in mice. To control for the effects of genetics, Dr Gordon found four pairs of human twins, with one twin obese and the other lean. He collected their stool, then transferred the twins’ bacteria to sets of mice. Fed an identical diet, the mice with bacteria from an obese twin became obese, whereas mice with bacteria from a thin twin remained lean.

Dr Gordon then tested what would happen when mice with different bacteria were housed together—mouse droppings help to transfer bacteria. Bacteria from the lean mice made their way to the mice with the obese twin’s bacteria, preventing those mice from gaining weight and developing other metabolic abnormalities. But the phenomenon did not work in reverse, probably due to Dr Gordon’s theory on the microbiota’s job vacancies. Interestingly, the invasion did not occur, and obesity was not prevented, when the mice ate a diet high in fat and low in fruits and vegetables. The transfer of helpful bacteria therefore seems to depend on diet.

Dr Gordon hopes to be able to identify specific bacteria that might, eventually, be isolated and used as a treatment for obesity. For now, however, he and other researchers are exposing a complex interplay of factors.

One type of calorie may be metabolised differently than another. But the effect of a particular diet depends on a person’s genes and bacteria. And that person’s bacteria are determined in part by his diet. Metabolic syndrome, it seems, hinges on an intricate relationship between food, bacteria and genetics. Understand it, and researchers will illuminate one of modernity’s most common ailments.

一卡路里就是一卡路里。如果吃得多消耗得少，就會變胖并且體弱多病。這是傳統(tǒng)認識。但人們漸漸發(fā)現(xiàn)這種認識過于簡單。所有的熱量不是平等產(chǎn)出的，值得注意的是，不同的人的身體在處理相同熱量時反應也是各不相同的。

令人驚訝的是，一項有關新陳代謝綜合癥的最新研究顯示，其并發(fā)癥包括高血壓、高血糖、高膽固醇，當然還有肥胖。這種現(xiàn)代病魔已經(jīng)遍及美國，因為美國肥胖率極高。另外，墨西哥、南非、印度等地由于患病率增加，醫(yī)療費用高漲，飽受其害。

新陳代謝綜合癥可以歸咎于過度飲食，缺乏鍛煉。但關鍵的是，要搞懂為什么有些食物危害性特別大，為什么有些人比別人胖。幸運的是，研究人員在最近的一系列論文中進行了解釋說明。

其中一種觀點認為這種危害源于淀粉食品中的葡萄糖、水果中的果糖、蔗糖和高果糖玉米糖漿。高血糖指數(shù)食物增加了血液中的含糖量，引發(fā)了新陳代謝問題。波士頓兒童醫(yī)院的大衛(wèi)·路德維希醫(yī)生指出，相比低脂肪飲食，低血糖飲食會改善新陳代謝，幫助患者減肥。這對一卡路里就是一卡路里觀念無疑是個挑戰(zhàn)。然而，還有些人把問題歸咎于果糖，認為果糖造成了肥胖和胰島素抗性�？屏_拉多大學博士理查德·約翰遜近日發(fā)表在《自然通訊》的文章解釋說，葡萄糖的危害一部分是通過轉化成果糖產(chǎn)生的。

約翰遜博士及其同事曾用老鼠做了水和葡萄糖飲食試驗。老鼠分三組，一組為控制組，另外兩組為對照組，對照組進行缺酶喂養(yǎng)，酶能幫助身體處理果糖。結果控制組老鼠變胖并產(chǎn)生胰島素抗性。另外兩組則沒發(fā)生這種情況。因此，身體在葡萄糖到果糖轉化中，會誘發(fā)新陳代謝問題。

吃什么或許就會有什么樣的身體

一個更有趣的觀念是同一飲食習慣對不同的人會產(chǎn)生不同的效果。最近的4篇論文探究了這個話題。其中一篇是《科學》雜志7月份刊載的，作者是約瑟夫·馬吉祖布，同樣來自波士頓兒童醫(yī)院，他刪除了老鼠的Mrap2基因。馬吉祖布博士及其同事表示這樣能控制老鼠食欲。然而令人驚奇的是，即使基因突變生物體與控制組老鼠吃得食物一樣，它們的體重還是增加得更多。原因尚不清楚，但有可能是Mrap2的缺失影響了基因Mc4r，因此人們認為Mc4r也與體重增加誘因有關。

第二篇和第三篇論文于8月份同時發(fā)表在《自然》，它們從另一種角度進行了研究——相同飲食習慣下，不同人產(chǎn)生的新陳代謝。這兩項研究都是在法國國家農(nóng)業(yè)研究所研究員Dusko Ehrlich監(jiān)管下進行的。其中一項實驗檢查了近300名丹麥受試者的體內細菌，發(fā)現(xiàn)腸內微生物多樣性越豐富，新陳代謝綜合癥跡象越少，包括肥胖和胰島素抗性。另一項研究中49名超重者進行高纖維飲食，他們開始時體內細菌種類比較少，后來細菌多樣性增加，新陳代謝問題有所改善。這項實驗中受試者體內微生物原來不具有多樣性，甚至飲食也與實驗不同。

來自圣路易斯華盛頓大學的杰弗里·戈登表示，這兩項研究表明胖人體內微生物區(qū)的“職位空缺”作用非常重要。適當?shù)娘嬍晨赡茉黾尤梭w內的有益細菌，從而填補空缺的職位。第四個實驗論文由戈登博士最近發(fā)表在《科學》雜志，他也是用老鼠做實驗。為了控制遺傳因素的影響，戈登博士找了4對人類雙胞胎，一組肥胖，一組纖瘦，他收集了他們的糞便，然后把人類雙胞胎基因移植到老鼠身上。老鼠飲食完全相同，從肥胖型雙胞胎移植基因的老鼠變胖了，而從纖瘦型雙胞胎移植基因的老鼠仍然偏瘦。

然后戈登博士對喂養(yǎng)在一起的帶有不同細菌的老鼠進行了測驗，發(fā)現(xiàn)老鼠糞便能傳播細菌。源于偏瘦型老鼠的細菌成功轉移到了帶有肥胖型雙胞胎細菌的老鼠身上，從而阻止了這些老鼠變胖，并引發(fā)了其他新陳代謝異常。但細菌沒有反向轉移，這可能由于戈登博士的職位空缺理論。有趣的是，當老鼠進行高脂肪、少水、少蔬菜飲食時，細菌轉移沒有發(fā)生，也未能阻止肥胖。因此這種有益的細菌轉移似乎取決于飲食。

戈登博士希望能夠認識到特定的細菌，并最終能把它分離出來，以治療肥胖。但現(xiàn)在，他與其他研究人員正在探索不同因素之間復雜的相互作用。

不同的卡路里新陳代謝方式可能互不相同。但是特定的飲食習慣所產(chǎn)生的影響取決于一個人的基因和體內細菌。而一個人的體內細菌一定程度上又取決于飲食習慣。新陳代謝綜合癥似乎使食物、細菌和遺傳交織在一起。只有搞懂其中復雜的聯(lián)系，研究員才能解釋現(xiàn)代通病中的肥胖問題。