听力课堂TED音频栏目主要包括TED演讲的音频MP3及中英双语文稿，供各位英语爱好者学习使用。本文主要内容为演讲MP3+双语文稿:与肥胖相关的脑科学，希望你会喜欢！

【主讲人】 Mads Tang-Christensen
肥胖症研究专家
研究领域侧重了解人类的身体对同样的食物和环境有什么不同反应

【演讲主题】The brain science of obesity
科学证明肥胖症是一种受遗传和环境影响的疾病。但是大脑和肠道中有一种有助于控制食欲的分子，可以通过进一步研究帮助肥胖症患者健康减肥。

【中英文稿】
Have you ever wondered why a pair of siblings living in the same house with the same parents, with the same food, sometimes end up in opposite sides of the weight spectrum? My name is Mads and for the last 25 years, I've been studying what we eat, when we eat and how much we eat. And probably more importantly, I've been studying how each of our unique bodies responds differently to the same food and the same environment. To be more precise, I study obesity.
你是否有想过为什么一对兄弟姐妹生活在同一屋檐下，有一样的父母，吃一样的食物，有时他们的体重却会截然不同？我叫麦斯，在过去的25年里，我一直在研究我们吃的是什么，什么时候吃，以及吃多少的问题。更重要的是，我也一直在研究我们每个独特的身体， 相同环境下对同一种食物的不同反应。更准确的说，我研究肥胖问题。

During my training as an MD, PhD, I was very fascinated by a series of experiments done by Barry Levin. He took 100 rats and subjected them to high-fat feeding. After months of feeding, he ended up with a bell-shaped curve and a weight distribution with some skinny rats and some obese rats and some in the middle. What he then did was to take the skinny rats and breed them among themselves, and the heavy rats. And he bred those among themselves. And after rounds of breeding, he ended up with two distinct populations: a diet-resistant rat and an obesity-prone rat. And here's the really interesting part. Then he took the skinny or the obese, and either massively over- or underfed them. And their weight would, of course, go up and down depending on the dietary regimen. But it was as if the little bodies would remember the same old weight trajectory. So once the dietary regimen was stopped, the rats went right back to the initial weight trajectory. It was like as if you could dress up the obese rat in a skinny sheep's clothing. But the obese rat nature was still scratching to get out.
在我作为医学生與博士培训期间，我对巴里·莱文所做的一系列实验感到非常着迷。他给一百只老鼠喂高脂肪的食物。经过一个月的喂养，他最终获得一个有关体型的权重分布和钟型曲线。这个结果里包含一些瘦老鼠，一些胖老鼠和一些肥瘦適中的老鼠。接下来，他选出瘦老鼠，让他们自己繁殖。同时，他也让胖老鼠成群一起繁殖。经过几轮繁殖，他最终得到了两个不同的种群：一种不易肥胖的老鼠，和一种极易肥胖的老鼠。有趣的是，他接着给瘦老鼠和胖老鼠，或是过度喂食或者少量喂食。结果依照不同的喂食方式，老鼠的体重当然会增加或会减少。但是就像这个小小的身体会记住他们以前的体重一样，一旦停止喂食方案，老鼠就会回到他们的初始体重。就好像你把一只肥胖的老鼠放进了瘦老鼠的衣服里，胖老鼠还是会自然的想要挣脱出来。

The same thing applies to humans. If you take a thousand kids and weigh them, their weight will also be distributed in a bell-shaped curve. Some skinny, some in the middle and some heavy. We know that some of the skinny kids will remain skinny throughout life, and some of the obese kids will stay obese throughout life. You could argue that their weight, to some degree, has been predetermined. You could also argue that obesity is a disease. Wait, did I just say that obesity a disease? Yes. There's actually data and science that shows that. And I've made it my audacious life goal to come up with a solution to prevent, treat or even cure obesity. Let me explain.
同样的事情放到人类上，如果你去选一千个孩子称体重，他们的体重也会呈现出一个钟型曲线，有些孩子体型偏瘦，有些不胖不瘦，又有些偏胖。我们知道有些瘦孩子一生都会保持苗条，一些胖孩子一生都有可能会保持肥胖，你可以在某种程度上说，他们的体重已经被预先决定了。你也可以说肥胖就是一种疾病。等下，我刚刚是不是说肥胖是一种疾病？是的。确实有一些数据和科学表明这个观点。我也已经把想出一个可以预防、治疗、甚至是治愈肥胖症的办法大胆地作为我的终生目标。让我来解释一下：

In the early 1980s and 1990s, obesity was considered a potential global problem, a global problem of a magnitude that led WHO in the end of 1990s to declare obesity a global pandemic. And I probably don't have to tell you why. Higher rates of diabetes, hypertension, cardiovascular disease, even some cancers, osteoarthritis and a clear link to mental conditions such as depression. So as the number of obese individuals grew, so did the number of people suffering from these diseases. Today, more than 50 percent of the US adult population are living with obesity or overweight. From a health perspective, that is devastating. But it's not only a US problem. The obesity surge has made obesity a global health problem.
在1980年代和1990年代初期，肥胖被认为是潜在的全球问题，一个巨大的全球问题。这个问题让世卫组织在1990年代后期宣布肥胖是一个全球大流行病。我可能不需要告诉你为什么。大量的糖尿病，高血压，心血管疾病，甚至是一些癌症和骨关节炎，以及与抑郁等精神状况的明确联系。 所以随着肥胖人数的增加，受这些疾病困扰的人数也在增加。如今，有超过百分之五十的美国成年人正处于肥胖和超重的情况。从健康的角度看，这个数据是毁灭性的。然而，这并不仅仅是美国的问题，肥胖潮已经成为了全球的健康问题。

Many inside and outside the medical community believe obesity is not a disease. They believe that obesity is a condition, a condition brought about by too much eating and too little exercise. As a matter of fact, a lot of people living with obesity think that too. They believe that their weight is 100 percent their own fault, which can lead to self-blame and low self-esteem, and perhaps even shame or stress eating, which is both heartbreaking, as well as counterproductive.
许多医学界内外的机构相信肥胖并不是疾病。他们相信肥胖只是一种状况，一种吃太多和缺少锻炼的状况。事实上，很多肥胖的人也同样这么认为。他们相信他们的超重完全都是他们自己的错误，这样的想法会导致他们自责并且没有自信，甚至会引起羞愧和压力下暴食，这既令人心碎，又适得其反。

But where is the scientific proof that obesity is a disease? Well, medically speaking, there's many ways to define disease, but let me give you just three examples. As a process that impairs your functionality and reduces life expectancy -- obesity, check. You can define disease as a process that leaves you more susceptible to other diseases or causes disease. Obesity, check. Or you can define disease as a genetic impairment that leads to functional impairment, like, for instance, a duplication of genes on chromosomes. There is clear evidence that a single gene mutation can lead to obesity, such as, for instance, leptin deficiency and POMC deficiency. We also have two-three genes leading to obesity. And it's my prediction that we, by the year 2030, will be able to explain most obesity by the genetic makeup of the individual. So obesity as a disease by this measure, check.
但关于肥胖是一种病的科学证明在哪里？从医学上说，有很多种方式可以定义疾病，但是让我和你说三个例子，第一，疾病是一个损害你身体的功能和减少寿命的过程——肥胖，是的！你可以把疾病定义为一个让你有更大的机会患上别的疾病的过程，肥胖，是的！又或者你可以定义疾病为一种遗传缺陷，从而导致身体机能缺陷。比如说，染色体上基因的重复。有明确的证据表明，单一基因的突变会导致肥胖，例如瘦素和阿黑皮素原的缺陷。我们也有二至三个基因导致肥胖。我预测在2030年的时候，我们可以用个体的基因组成 来解释大部分的肥胖问题。所以通过这个方法验证，肥胖确实是一种疾病。

Let me be clear. We humans have had the same genes for decades. And just recently, obesity has become a bigger problem. How do we then explain that? One obvious thing is actually food, especially calorie-rich food, which is much more readily available. It's relatively easy and also relatively cheap to eat your entire daily need of calories by a fast food or big soft drinks. So genes do play a role, but the environment also plays a huge role. The overabundance of calories in certain communities is a relatively new thing, and our genes haven't quite adapted yet. In the history of feast and famine, genetic selection has prepared us much better for famine, and for good reason. Starvation is bad, but you could also argue obesity is bad. And if obesity is a disease, how do we then prevent, treat or even cure it? I believe that the brain holds the key.
让我说清楚一点，我们人类几十年来有着相同的基因，但是最近，肥胖变成了一个大问题。我们应该怎么解释呢？一个很明显的事实是食物，尤其是高卡路里的食物，更唾手可得。人们现在更容易也更便宜吃快餐和大饮料作为日常卡路里的摄取。虽然基因起了作用，但是环境也是一个很大的因素。在一些社区里，卡路里过多的食物是一项新奇的事物，并且我们的基因也未能适应。历史上的盛宴和饥荒，基因选择为我们更好的适应饥荒并且有其理由，饥荒是不好的。你可以说肥胖也是不好的。如果肥胖是疾病，我们应该怎样预防、治疗甚至治愈呢？我相信大脑是关键。

I have always been fascinated with how small electrical signals in discrete parts of the brain lead to big behavioral changes. And my study of the brain led me to Glucagon-Like Peptide 1, or GLP-1 for short. GLP-1 is a hormone and a signal molecule that is produced both in the gut and in the brain. The brain speaks to the gut and the gut speaks to the brain. Yes, that's right. Your belly and your brain are literally connected.
我一直相信大脑里离散部分的小电子信号可以导致大的行为改变。我对大脑的研究让我认识到 胰高血糖素样肽 1，或简称 GLP-1。GLP-1是一种激素和信号分子，它可以在肠道和大脑中产生。大脑和肠道相互交流。是的，你的大脑和肠道理论上是连在一起的。

Our research led us to see that GLP-1 has an effect on nerve cells sitting in areas that control whether we eat or not. So, for instance, if we increase the level of GLP-1, the body's desire to eat or overeat food gets turned off. GLP-1 serves as the full signal in your car's gas tank. I've spent years and decades mapping the circuitry of GLP-1 and how GLP-1 interacts with other signal molecules and hormones. All of these things go together and control food intake, body weight and the control of eating behavior. And what does that all mean? Well, today, we have engineered and studied the molecule, so we now have a molecule that can lead to a significant weight loss.
我们的研究使我们看到 GLP-1对神经细胞的影响，不管我们是不是在吃的时候。例如，如果我们增加GLP-1的水平，身体里想要吃或者暴食的欲望被关闭了，GLP-1就像是你汽车里油箱的充满信号。我花了几年和几十年绘制GLP-1的电路图以及GLP-1如何与其他分子和激素互动。这些事情一起控制食物的摄入，体重和饮食习惯。这一切意味着什么呢？现在我们研究并设计了分子，这个分子可以对减重有很重要的影响。

Obviously, GLP-1 is not the whole answer. We and others have discovered numerous hormones and other signal molecules that are also pivotal for the regulation of food intake and body weight. And it may end up that these signal molecules and hormones are even more important than GLP-1. So ... There's plenty for us to do. There's still plenty for us to explore. So this is not the end. It's not even the beginning to the end. But perhaps this may be the end to the beginning.
显然，GLP-1并不是问题的全部答案。我和其他人已经发现了多种激素和其他信号分子可以监管和规范食物的摄入和体重。所以，这些信号分子和激素的作用甚至会比GLP-1更重要。所以，我们还有很多的事情要去做。还有很多方面还等着我们去探索，所以研究还没有结束，这甚至还不是结束的开始。但也许是初阶段结束而已。

We may have a massive weight crisis on the planet today, but the good news is we are on the right path. We now have solutions for people living with obesity, and the next steps will be to understand even better the problems people living with obesity are facing. To understand even better how genes and environment play together. And understand, finally, how all these things come together and determine our body weight. Then, and maybe just then, we will be able to come up with a prevention, a treatment or even a cure for people living with obesity, like we strive for with any other chronic disease. And this -- this still remains our audacious life’s goal.
在这个星球上，我们可能会有很大的体重危机，但好消息是，我们在正确的轨道上，我们现在有了针对肥胖人的办法，下一步我们需要更好的了解那些有肥胖问题的人面对的是什么，为了更好地理解基因和环境如何共同发挥作用，并且理解这些事情最后是怎样结合在一起去决定我们的体重的。也许在那个时候，我们能更好的想出预防措施，以及治疗甚至是治愈肥胖人的方法，就像我们为其他慢性病努力一样。这仍然是我们无畏的人生目标。

Thank you.
谢谢。