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演讲者：Mads Tang-Christensen
演讲题目: The brain science of obesity
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?
你有没有想过，为什么一对兄弟姐妹和同样的父母住在同一所房子里，吃着同样的食物，有时会在体重谱的另一边？
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.
我叫Mads，在过去的25年里，我一直在研究我们吃什么，什么时候吃，吃多少。也许更重要的是，我一直在研究我们每个独特的身体如何对相同的食物和环境做出不同的反应。更确切地说，我研究肥胖。
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.
在我接受医学博士和博士培训期间，我对巴里·莱文所做的一系列实验非常着迷。他给100只老鼠喂食高脂肪食物。经过几个月的喂食，他最终形成了一个钟形曲线，体重分布在一些瘦老鼠和一些肥胖老鼠中间。
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.
然后，他把这些瘦小的老鼠带到一起，让它们和笨重的老鼠一起繁殖。他在他们中间培育他们。经过一轮又一轮的繁育，他最终得到了两个截然不同的种群：一个是耐饮食的老鼠，另一个是容易肥胖的老鼠。这是真正有趣的部分。
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.
然后，他选择了瘦子或肥胖者，要么大量过量或不足喂养他们。当然，它们的体重会根据饮食习惯上下波动。但这就好像这些小小的身体会记住同样古老的重量轨迹。因此，一旦停止饮食方案，大鼠就会回到最初的体重轨迹。这就好像你可以把肥胖的老鼠穿上一件紧身的羊皮衣服。但是肥胖的老鼠仍然在抓挠着想要出去。
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.
同样的道理也适用于人类。如果你给一千个孩子称重，他们的体重也会呈钟形曲线分布。一些瘦，一些在中间和一些沉重。我们知道，一些瘦小的孩子一生都会保持瘦小，而一些肥胖的孩子一生都会保持肥胖。你可以说它们的重量在某种程度上是预先确定的。
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.
你也可以说肥胖是一种疾病。等等，我刚才是不是说肥胖是一种疾病？对事实上有数据和科学证明了这一点。我已经把想出一个预防、治疗甚至治愈肥胖的解决方案作为我大胆的人生目标。让我解释一下。
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.
20世纪80年代初和90年代，肥胖被认为是一个潜在的全球问题，这一全球性问题的严重程度导致世卫组织在90年代末宣布肥胖为全球流行病。我可能不必告诉你为什么。糖尿病、高血压、心血管疾病、甚至某些癌症、骨关节炎的发病率较高，与抑郁症等精神疾病有明显联系。
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.
因此，随着肥胖人数的增加，患这些疾病的人数也在增加。如今，超过50%的美国成年人患有肥胖症或超重。从健康的角度来看，这是毁灭性的。但这不仅仅是美国的问题。肥胖人数激增已使肥胖成为全球健康问题。
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.
医学界内外的许多人认为肥胖不是一种疾病。他们认为肥胖是一种疾病，一种由吃得太多而运动太少引起的疾病。事实上，很多肥胖患者也这么认为。他们认为自己的体重百分之百是自己的错，这会导致自责和自卑，甚至可能导致羞耻或压力饮食，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.
但是肥胖是一种疾病的科学证据在哪里呢？嗯，从医学角度来说，有很多方法来定义疾病，但我只举三个例子。作为一个会损害你的功能和减少预期寿命的过程——肥胖，检查一下。你可以将疾病定义为一个使你更容易感染其他疾病或导致疾病的过程。
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.
肥胖，检查。或者你可以将疾病定义为导致功能损害的遗传损伤，比如染色体上的基因复制。有明确的证据表明，单基因突变可导致肥胖，例如，瘦素缺乏和POMC缺乏。我们还有两个和三个导致肥胖的基因。我的预测是，到2030年，我们将能够通过个体的基因构成来解释大多数肥胖。因此，肥胖作为一种疾病，通过这一措施，检查。
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.
让我说清楚。几十年来，我们人类拥有相同的基因。就在最近，肥胖已经成为一个更大的问题。那我们怎么解释呢？一个明显的事实是食物，特别是高热量食物，更容易获得。通过快餐或大杯软饮料来摄入你每天所需的全部卡路里相对容易，也相对便宜。
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.
所以基因确实起了作用，但环境也起着巨大的作用。某些社区的卡路里过剩是一个相对较新的现象，我们的基因还没有完全适应。在盛宴和饥荒的历史上，基因选择让我们更好地应对饥荒，这是有道理的。饥饿是不好的，但你也可以说肥胖是不好的。如果肥胖是一种疾病，那么我们如何预防、治疗甚至治愈它呢？我相信大脑掌握着关键。
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.
我一直着迷于大脑离散部分的小电信号如何导致大的行为变化。我对大脑的研究使我找到了胰高血糖素样肽1，简称GLP-1。GLP-1是一种激素和信号分子，在肠道和大脑中产生。大脑与肠道沟通，肠道与大脑沟通。是的，没错。你的肚子和你的大脑实际上是相连的。
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.
我们的研究使我们发现GLP-1对控制我们是否进食区域的神经细胞有影响。因此，例如，如果我们增加GLP-1的水平，身体进食或过量进食的欲望就会被关闭。GLP-1作为汽车油箱中的满信号。我花了数年甚至数十年的时间绘制GLP-1的电路图，以及GLP-1如何与其他信号分子和激素相互作用。
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.
所有这些因素共同作用，控制食物摄入、体重和饮食行为。这一切意味着什么？今天，我们已经设计和研究了这种分子，所以我们现在有了一种可以显著减肥的分子。
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.
显然，GLP-1不是全部答案。我们和其他人已经发现了许多激素和其他信号分子，它们也是调节食物摄入和体重的关键。
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.
最终，这些信号分子和激素可能比GLP-1更重要。所以我们有很多事情要做。我们还有很多东西要探索。所以这还不是结束。这甚至还不是开始到结束。但这也许是开始的结束。
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.
今天，地球上可能会有一场严重的体重危机，但好消息是我们走上了正确的道路。我们现在为肥胖患者提供了解决方案，下一步将是更好地了解肥胖患者面临的问题。
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. Thank you.
更好地理解基因和环境是如何相互作用的。最后，了解所有这些因素是如何结合在一起并决定我们的体重的。然后，也许就在那时，我们将能够为患有肥胖症的人提供预防、治疗甚至治愈的方法，就像我们为任何其他慢性病所努力的那样。这仍然是我们大胆的人生目标。非常感谢。
Remark：一切权益归TED所有，更多TED相关信息可至官网www.ted.com查询！
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