It's not gluttony. It's genetics. Why our moralizing misses the point.

    Despite receiving a MacArthur genius award for her work in Alabama "forging an inspiring model of compassionate and effective medical care in one of the most underserved regions of the United States," Regina Benjamin's qualifications to be surgeon general have been questioned. Why? She is overweight. "It tends to undermine her credibility," Dr. Marcia Angell, former editor of The New England Journal of Medicine, said in an interview with ABC News. "I do think at a time when a lot of public-health concern is about the national epidemic of obesity, having a surgeon general who is noticeably overweight raises questions in people's minds."

    It is not enough, it seems, that the obese must suffer the medical consequences of their weight, consequences that include diabetes, heart disease, and cancer, and that cause nearly 300,000 deaths in the United States each year. They must also suffer the opprobrium heaped on them by people like Angell or Rep. James Sensenbrenner （R-WI）, who advised the obese to "Look in the mirror because you are the one to blame." In our society, perhaps no group is more stigmatized than the obese.

    The abuse is nothing new, of course. Four hundred years ago, Shakespeare had Prince Hal hurl a barrage of insults at Falstaff, calling him "fat-witted," "horseback-breaker," and a "huge hill of flesh." But Shakespeare had an excuse. In his time essentially nothing was known about the real reasons that people are fat. Today we have no such excuse. Modern medical science has gone a long way toward explaining the causes of obesity, and the bottom line is clear: obesity is not a personal choice. The obese are so primarily as a result of their genes.

    Genetic studies have shown that the particular set of weight-regulating genes that a person has is by far the most important factor in determining how much that person will weigh. The heritability of obesity-a measure of how much obesity is due to genes versus other factors-is about the same as the heritability of height. It's even greater than that for many conditions that people accept as having a genetic basis, including heart disease, breast cancer, and schizophrenia. As nutrition has improved over the past 200 years, Americans have gotten much taller on average, but it is still the genes that determine who is tall or short today. The same is true for weight. Although our high-calorie, sedentary lifestyle contributes to the approximately 10-pound average weight gain of Americans compared to the recent past, some people are more severely affected by this lifestyle than others. That's because they have inherited genes that increase their predisposition for accumulating body fat. Our modern lifestyle is thus a necessary, but not a sufficient, condition for the high prevalence of obesity in our population.

    Over the past decade, scientists have identified many of the genes that regulate body weight and have proved that in some instances, different variants of these genes can lead a person to be fat or thin. These genes underlie a weight-regulating system that is remarkably precise. The average person takes in a million or more calories per year, maintaining within a narrow range over the course of decades. This implies that the body balances calorie consumption with calorie expenditure, and does with a precision greater than 99.5 percent. Even the most vigilant calorie counter couldn't compete, if for no other reason than that the calorie counts on food labels are often off by 10 percent or more.

    The genes that control food intake and metabolism act to keep weight in a stable range by creating a biological force that resists weight change in either direction. When weight is gained, hunger is reduced. When weight is lost, the unconscious drive to eat is stimulated and acts to return weight to the starting point. Moreover, the greater the amount of weight that is lost, the greater the sense of hunger that develops. Thus, when the obese lose large amounts of weight by conscious effort, their bodies fight back even more strongly by increasing hunger and reducing energy expenditure. If you think it is hard to lose 10 to 20 pounds （and it is）, try to imagine what it would feel like to lose many tens or even hundreds of pounds.

    肥胖不是因為貪婪的暴食，而是因為個體基因決定的。為什么我們在評判胖人時忘記這一點呢？

    盡管Regina Benjamin因在阿拉巴馬州的工作使得"在美國最缺乏醫療的地區鑄造了令人欣慰鼓舞的愛心高效醫療體系"被授予麥克阿瑟天才獎（MacArthur genius award）,但她成為衛生局局長的資格遭到了質疑。這是為什么呢？她超重了。"就這個理由似乎就破壞了她的信譽",作為The New England Journal of Medicine期刊的前任編輯Marcia Angell博士說，"我的確認為，當對公眾健康的擔憂集中于在美國日益擴展的肥胖問題時，人們就會對明顯超重的衛生局局長進行質疑。"

    肥胖者必須遭受著超重帶來的疾病如糖尿病，心臟病，癌癥等，由此肥胖每年導致近300,000美國人死亡，似乎這還不算，他們還得承受著很多人堆積在他們身上的冷嘲熱諷，羞辱責罵，像是Angell or Rep. James Sensenbrenner （R-WI）曾經就建議肥胖者"照照鏡子就知道你們該罵".在我們的社會，估計沒有任何群體會像胖人們一樣被歧視虐待了。

    當然，肥胖不是個新問題。早在400年前，莎士比亞筆下的Hal王子就被刻畫地不斷地諷刺Falstaff,并稱呼他為"愚笨的胖子","害苦坐騎的胖子"和"山堆的肥肉".但是莎士比亞是有理由這樣做的，因為在他那個時代世人完全不曉得導致肥胖的真正原因。而今我們不應該有任何理由。當代醫學科技已經在探索肥胖原因方面發展很多了，最重要的一點很清楚：肥胖不是個人選擇的，而是基因的作用。

    基因學研究顯示：個體帶有的體重調節基因是決定其體重的最重要因素。肥胖的可遺傳性---一種測量基因和其他因素導致肥胖多少的方法--就和身高的可遺傳性一樣起作用，它對導致肥胖的作用甚至比已經接受的像心臟病和乳癌的基因的遺傳作用還要大的多。隨著過去200年中營養攝入的不斷提高，美國人的平均身高已經提高了很多，但是還是會有基因的作用決定著人們不同的高矮。體重其實也是一樣。盡管我們由于高卡路里攝入，久坐的生活方式導致了近年來美國人的平均體重比過去將近漲了10磅，但是總是有些人比其他人更多的受到這種生活方式的影響而變胖。這是因為他們遺傳了讓他們傾向于累積脂肪的基因。我們的現代不良生活方式是個必然因素導致肥胖，但并不是致使我們整體人口數量中肥胖人口快速蔓延的全部原因。

    在過去的十年里，科學家識別了體重調節基因并且證明了不同傾向的基因可以決定一個人的胖瘦。這些基因含有一個精確的體重調節系統。一般平均下來一個人一年要攝入一百萬甚至更多的卡路里，但是在幾十年里體重卻一直保持在變化幅度很小的范圍中。這就顯示了身體自身平衡用卡路里消耗抵消了卡路里的攝入，這一抵消程度都超過了99.5%.就是最危險的很多卡路里攝入量也不能抗擊住這中平衡系統，如果不是這種基因作用，那食品標簽上的卡路里都得降10%甚至更多才能保持這樣的體重。

    這個控制從食物中吸收的熱量和新陳代謝功能以達到保持體重的基因創造出了一種可以避免體重變化的生理力量。當體重增加時，饑餓感降低。當體重減少時，食欲被無意識得激發，開始扭轉局勢使體重回歸。而且，體重減得越多，饑餓感越強烈。所以，當肥胖患者有意識的努力減下了體重時，他們的身體就更強烈的激發出提高食欲和降低能量消耗的戰斗力。所以，如果你覺查到減掉10磅甚至20磅是很困難的，那么設想一下，要減掉幾十磅甚至幾百磅會是什么感受！