The discovery of the obesity gene in humans offered evidence that chronic① weight gain is the consequence of a mismatch between nature and nurture. Simplistic explanations， such as blaming obesity on a drop in fat consumption， ignore scientific reality. In countries like India and China， obesity was virtually unknown until the introduction of a high-fat， Western-style diet.
One well-known reason for this is that dietary② fat converts to body fat more efficiently than does protein or carbohydrate， but scientists have uncovered what appears to be an equally important factor. Some researchers in universities are investigating the possibility that high levels of fat and fructose are mucking③ up our brain chemistry， and thereby muting the signals that would normally tell us to put down the fork. These signals are produced by peptides， which are regulated by a number of hormones. Under normal conditions these hormones help maintain a stable body weight by adjusting levels of the peptides④ that control eating. But a diet loaded with fat and fructose hampers the regulation of these hormones. Complicating matters still further is that the brain loses its ability to respond to these hormones as body fat increases—so the oese are doubly penalized.
Other researchers are finding evidence that constant exposure to fat and sugar can cause some humans to crave them as they do an addictive drug. A Princeton University psychologist showed that rats fed a high sugar diet were， when the sugar was removed， thrown into a state of anxiety similar to that seen in withdrawal from morphine or nicotine. Sarah Leibowitz， a neurobiologist， believes that frequent exposure to fatty foods may configure the brain to crave still more fat. She has shown in animal studies that galanin， a brain peptide that simulates eating behavior and decreases energy expenditure， increases when the animal eats a high-fat diet.
There are many factors contributing to the explosion of obesity in the United States， and the world， but the radical changes in the composition of our diet are first among them. While scientific work in this arena⑤ is in its infancy， it’s already clear that varying the amount of fat and other nutrients in the diet affects brain chemistry by activating certain genes， and this in turn directs our dietary preferences. By submitting ourselves to a steady dose of highly processed， sweet， high-fat foods， we have unwittingly entered into a dangerous experiment， the long term consequences of which are only now beginning to surface.
① chronicadj. (病)慢性的；长期的，不断的；习惯性的
② dietaryadj. 饮食的； 饮食的规定
③ muckvt. 【主英】【口】把……弄得一团糟，打乱
④ peptiden. 缩氨酸
⑤ arenan. (古罗马圆形剧场中央的)角斗场，竞技场； 【喻】竞争场所
人类肥胖原因新探
人类肥胖基因的发现提供了证据，从生物学的角度，证明了慢性体重增长是营养和身体本能不协调的结果。把肥胖归咎于脂肪消耗减少这样的解释过于简单，且忽略了科学实质。在许多国家，如印度或中国，直到引进了高脂肪西式饮食，肥胖症这个概念才为人所知。
一个广为人知的原因是，食物中的脂肪比蛋白质或碳水化合物更易转化为身体中的脂肪。不过科学家发现一个看来同等重要的因素。一些大学学者在研究是否过量的脂肪和果糖会扰乱我们大脑中的化学物质，从而防碍大脑在正常情况下发出让我们放下餐叉的信号。这些信号通常是由缩氨酸产生的。而这些缩氨酸由很多荷尔蒙调节着。正常情况下，这些荷尔蒙调节控制进食的缩氨酸的水平从而有利于维持稳定的体重。不过含有过量脂肪和果糖的食物影响了这些荷尔蒙的调节功能。而且当身体脂肪增加的时候，大脑失去了对这些激素作出反应的能力——所以肥胖的人就更加容易肥胖。
另外一些研究人员正在寻找证据证明持续食用脂肪和糖会导致人们想吃更多的脂肪和糖，就像吸毒上瘾一样。普林斯顿大学的一位心理学家指出，经常喂食高糖食物的老鼠，在没有糖吃的时候，就会显得很焦虑，跟停止服用吗啡或烟碱时十分相似。神经生物学家萨拉·莱博维茨认为，频繁食用脂肪含量高的食物，会使大脑有想要更多脂肪的思维模式。她对动物进行的研究显示，当动物食用高脂肪食物的时候，甘丙肽，一种刺激进食并减低能量消耗的大脑缩氨酸增加了。
导致美国和全世界肥胖人口剧增现象有很多因素，不过饮食结构的彻底改变当数头号原因。尽管科学家在这一领域的研究还处于初期，但已清楚地表明如果改变进食脂肪和其他营养物的数量就可以通过激活某些基因而影响大脑里的化学物质，从而指导着我们的进食取向。由于我们一直吃一定量的精加工高脂肪高糖食物，实际上我们已经在不知不觉中做了一个危险的实验，其长期后果现在才显露出来。
