TED-Is the obesity crisis hiding a bigger problem
http://www.ted.com/talks/peter_attia_what_if_we_re_wrong_about_diabetes.html?utm_source=email&source=email&utm_medium=social&utm_campaign=ios-share
肥胖症危是否掩盖了更大的问题？
我永远忘不了那天 2006年的春天。 我还是一个外科住院医生 在约翰霍普金斯医院 应对急救电话 大约凌晨两点左右，我被急诊室叫去 看一位女病人，她得了因糖尿病而引起的 足部溃疡。 我至今还能记得当我拉开帘子看到她之后 闻到的那种肉类腐烂的味道。 显而易见这位女士病得很重 她需要住院治疗。 这是毫无疑问的。 但那时我考虑的是另一个问题 那就是，她需要截肢吗？
现在，回想起那夜， 我很后悔那天夜里面对那位女士时 心中没有带着同样的同情与悲悯 就像我平时面对其他病人那般 三天前的夜里一位27岁的新娘 因为下背疼痛来看急诊 后来她被诊断为晚期胰腺癌。 虽然我知道我对她无能为力 没办法救她。 癌症已经是末期了。 但我还是尽我所能的 做了所有能让她 舒服一点的事情。我帮她找了条毛毯 端了杯咖啡。 给她父母送咖啡。 更重要的是，我一点也不觉得这姑娘有错 很明显她对自己的病 一点责任也没有 但是为什么，仅仅过了几夜 当我站在同一个急救室并且决定 我的这位糖尿病病人需要截肢手术时 为什么我的心中带着蔑视呢？
你看，跟那位新娘不一样 这位女士有II型糖尿病 她很胖。 而且我们都知道肥胖源自 无节制的饮食和缺乏运动，对吧？ 而且我们都知道肥胖源自 无节制的饮食和缺乏运动，对吧？ 我的意思是，节食和运动很难吗？ 我看着她躺在床上，我心说 哪怕你稍微注意一点儿自己的身体 你也绝不会落到这步田地 跟一个即将给你截肢的陌生在一起 跟一个即将给你截肢的陌生在一起
为什么当时我能心安理得的责备她呢？ 我希望我不知道原因。 但是说真的，我知道。 你看，我那时年少轻狂 我自以为是的觉得 她肯定就是我想到那样。 她饮食无度，她运气不好 她得了糖尿病，基本就是这个情况。
讽刺的是，就在那会儿 我正在参与癌症的研究 黑色素瘤的细胞免疫力疗法，具体来说 在那个领域里，我被教着去质疑一切 挑战一切固有的理论成果 并且在研究中严格遵守最高的科研准则。 但当我面对糖尿病 这种致死几率高于黑色素瘤八倍的疾病时候 我从未质疑过传统的理论。 我当时真的认为糖尿病的发病机理 早有定论。
三年以后，我发现我错了。 但是这次，我自己成了病人。 尽管我每天运动三四个小时 严格遵守健康食谱 我还是体重激增并且得了 代谢综合征。 你们也许有人听说过它。 我的身体对胰岛素产生了抗性。
你们可以把胰岛素想象成一种荷尔蒙 它能控制我们的身体对摄入的食物做出反应 消耗或是储存它们。 在术语中称之为燃料分区。 缺乏足够的胰岛素是很要命的。 胰岛素抵抗，就像字面上意思一样 意味着你的细胞变得越来越不受 胰岛素的指挥正常运作。 一旦你出现胰岛素抵抗的情况 你离患糖尿病就不远了 因为胰岛素抵抗的缘故 你无法制造足够的胰岛素。 你的血糖开始升高 一系列的病例症状 会突然爆发并且可能导致心脏病 癌症，甚至老年痴呆症 或者截肢，就像几年前的那位女士一样。
我很害怕，我很快改了食谱 做了一些让大家觉得 不可思议的改变。 得益于新的食谱 尽管我锻炼得少了，我还是减掉了40磅 你们可以看到，我现在没有超重 更重要的是，我没有胰岛素抵抗症了
但是最重要的是，我陷入了 三个亟待解决的问题 为什么这件事发生在我身上呢? 我已经尽力做到无懈可击了。 如果传统的营养理论在我身上失效了 在其他人身上会怎样呢？ 通过对考虑这些问题 我着了魔一样的 希望找到肥胖和胰岛素之间 真正的关系。
现在，主流观点认为 肥胖导致了胰岛素抵抗。 依逻辑来说，如果你想治疗胰岛素抵抗 你必须减肥，对吧？ 先对付肥胖。 但是如果我们反过来想一下？ 假如肥胖并不会导致胰岛素抵抗？ 实际上，假如它只是一个征兆 一个更深层次的问题的冰山一角？ 这听起来很疯狂 因为我们很正身处 一个肥胖症泛滥的时代，不过请耐心听我解释。 假如肥胖是身体的某种应对机制 用来对付一个潜藏在细胞深处 更加凶险的问题？ 我不认为肥胖是无害的 但是我觉得肥胖在两种新陈代谢疾病中 是比较次要的那个。
大家可以把胰岛素抵抗症看作 我们身体燃料箱变小了 就像我刚刚假设的那样 正常情况下我们摄入的热量 会被适量消耗并且适量储存。 当我们得了胰岛素抵抗的时候 这个平衡就会偏离正常情况。 于是乎，当胰岛素告诉细胞 我需要你消耗一些能量，假如 细胞认为消耗太大，那些细胞就会回应到 “不了，我更想把这些能量储存起来。” 因为脂肪细胞不同于其它细胞 它没有那么多复杂的结构和组织 所以能量都被储藏在那。 因此对我们中许多人，大约7500万美国人来说 胰岛素抵抗应被视作 肥胖的成因，而非相反的， 将胰岛素抵抗归因于肥胖。
这虽然是个相当微妙的区别， 但是它的含义却是相当深刻的。 举个例子来说， 想象一下你小腿上的乌青， 那是你不小心撞上咖啡桌时留下的。 毫无疑问，这乌青疼得要命。 而且你肯定不喜欢腿上多个斑，但是我们都知道 乌青本身并不是个问题。 恰恰相反，这是对外伤的一个正常生理反应。 所有的免疫细胞都会迅速前往受伤的部位 去清理坏死细胞的碎片并且防止 感染扩散到身体其他部位。 好了，想象一下如果我们把乌青当作一个问题， 我们发展出了一个庞大的医疗体系 以及文化来对待乌青： 遮蔽霜，止疼药，等等。 而所有这一切都掩盖了一个事实 那就是人们依旧会撞到咖啡桌 如果我们可以从问题的根源入手 告诉人们注意一下 从客厅走过的时候小心咖啡桌 这会比处理撞伤来的有效果的多 正确理解事情的表象和本因 将使这个世界产生巨大的不同。 即使治标不治本，制药行业 依旧可以为股东们带来利润， 但是对于受伤的人们来说，这没有任何帮助 原因及结果。
所以我想指出的是 在我们讨论肥胖和胰岛素抵抗的问题时 把原因和结果弄反了。 在我们讨论肥胖和胰岛素抵抗的问题时 把原因和结果弄反了。 也许我们需要问问我们自己了， 有没有可能胰岛素抵抗导致了体重增加 以及随肥胖带来的并发症， 至少对于大多数人来说 有没有可能肥胖只是胰岛抵抗的一个代谢反应 相较于其他更大的威胁， 例如一些相关的疫病， 它们才是我们真正应该去担心的。
让我们来看些有暗示性的建议。 我们知道在美国有3千万肥胖症患者 并未患胰岛素抵抗。 同时，没有证据显示他们 比非肥胖症患者更容易贻患其他疾病。 恰恰相反，在美国有6百万非肥胖症患者 存在胰岛素抵抗， 而他们却被证实 易患那些我之前提到的糖尿病并发症， 同时几率较肥胖人士来的更高。 虽然现在我还不知道为什么，但是一个可能的原因是， 对他们而言，他们的细胞无法正确的 对体内多余能量做出反应。 你可以是肥胖症患者，却没患胰岛素抵抗， 或者你可以不肥胖，却患有胰岛素抵抗， 这都表明肥胖只不过是一个表征 而胰岛素抗拒才是根源。
所以如果我们斗争搞错了对象， 我们一直与肥胖战斗着，而非胰岛素抵抗？ 而且更糟的是，如果指责过胖者 其实确是在指责胰岛素抵抗的受害者？ 如果我们对于肥胖症的一些基本认识本身 就存在误差？
就我个人而言，我没有办法继续保持傲慢的态度， 让我把那种过剩的确信感放在一边。 对于这些问题的核心为何，我有我自己的认识， 同时我也愿意将它与其他人分享 我的假设是这样的，因为老有人问我 我的假设是这样的，因为老有人问我 试问，一个细胞到底在畏惧什么 当它处于胰岛素抗拒状态时。 问题的答案可能不是摄入过多的食物。 答案更有可能是摄入过量葡萄糖而导致血糖过高。 精制的谷物和淀粉 将在短时间内抬到你的血糖含量， 而且我们有理由相信 糖分将直接导致胰岛素抵抗症。 所以如果把这些生理过程也列入考虑， 我认为是大量的不断摄入 精制谷物，糖类以及淀粉类食物导致了 肥胖症和糖尿病的流行， 但其病因是胰岛素抵抗症 而不是由于暴饮暴食以及缺乏运动。
在我几年前减去40磅时， 我只是简单的限制了精制谷物，糖，和淀粉的摄入， 诚然这也表明我存在一些偏见， 而这些主要源自我的个人经验。 但是这并不意味着我的偏见是错误的， 更重要的是，所有这些偏见都是可以被科学验证的。 但是第一步就是要接受一种可能性 那就是我们当前关于肥胖症， 糖尿病以及胰岛素抗拒症的理解可能存在偏差 并需要被验证。 我把我的事业都赌在了这个可能性上。 现在，我把所有的时间花在了这个问题的研究上， 而且我将不会停止知道找到真正的答案。 我已经决定有一件事是我不能也不会再做的， 那就是在我不知道答案的时候却假装知道。 对所有我不知道的事情，我都相当谦虚。
在过去一年里，我很幸运 可以和国内最优秀的糖尿病和肥胖症专家团队一起研究 可以和国内最优秀的糖尿病和肥胖症专家团队一起研究 同时最好的事情莫过于， 就如亚伯拉罕?林肯将自己 置身于由对手组成的团队中 我们也做了一样的事情。 我们找来了另一个科学家团队作为竞争对手， 他们也都是极为优秀的科学家， 但却对这个流行病的核心成因有着不同的假设 有一些认为是过量的卡路里摄入 有一些认为是过量的脂肪摄入 也有些人为是过量的精制谷物和淀粉摄入。 这个由多学科， 具有高度怀疑精神以及相当聪明的研究者团队 至少同意两件事情。 其一，这个问题相当重要， 以至于我们不能再假装我们知道答案而对它视而不见。 其次，如果我们愿意去犯错误， 如果我们愿意通过科学实践探究去挑战传统观念 如果我们愿意通过科学实践探究去挑战传统观念 我们终将解决这个问题。
我知道我们都希望现在就能得到一个答案， 一些可以参照行为方式或者规则，一些饮食菜单 告诉我们该吃什么，不该吃什么， 但是如果我们想找到一个正确的答案， 我们就不得不进行严谨的科学尝试， 不然我们是给出真正的答案的。
简而言之，为了找到这个答案，我们的研究项目 主要围绕着三个方面或者问题展开。 首先，我们摄入的各种各样的食物是如何 影响我们的代谢，激素和酶的， 并且这些影响是通过何种细微的分子机制发生的？ 其二，基于这个视角， 人们有没有办法对他们的饮食做出必要的调整， 使它更安全且更易实践 最终，一旦我们找到既安全、 又能安全应用到饮食中的方法 我们又如何改变他们的习惯， 使之变得更为自然， 而非一种刻意行为？ 你知道应该去做什么并不意味着 你可以坚持这么做。 有时我们不得不给人们一些诱因 使这种坚持变得更简单，不管你信不信 这都可以经过科学研究
我不知道这个研究最终会将我带向何处， 但是对我而言，至少有一点是可以肯定地： 我们不能继续指责肥胖症和糖尿病患者 就像曾经的我那样。 他们中的大部分其实都想做正确的选择， 但前提是他们必须知道到底什么是正确的， 而且它们切实可行。 我们梦想有一天当我们的患者可以 减去多余的重量 治好胰岛素抵抗症， 因为作为医学专家， 我们已经抛开了多余的思想包袱， 并完全治好了自己的新观点抵抗症 从而使我们回归我们最初的理想： 开放的思维，抛弃那些不再有效的陈旧观念的勇气 开放的思维，抛弃那些不再有效的陈旧观念的勇气 相信科学的真理没有终点， 只有不断的进化。 忠于这条追求真理的道路 对患者和科学来说都是更好的选择 忠于这条追求真理的道路 对患者和科学来说都是更好的选择 如果肥胖只是 代谢疾病的一个替罪羊， 那么我们去指责这些替罪羊又有什么好处呢？
我有时会回想到七年前急救室的那个夜晚 我有时会回想到七年前急救室的那个夜晚 我希望我可以再和那位女士聊聊。 我想向她道歉。 我想说，作为一个医生，我提供了 我所能提供的最好的治疗， 但是最为一个人， 我让你失望了。 你需要的不是我的判定和我的鄙视。 你需要的是我的同情和怜悯， 而且无论如何，你需要的是一个医生 愿意相信 也许你没有辜负我们的医疗系统。 也许是医疗系统，包括我在内的这个医疗系统， 辜负了你。 如果你现在正在看这个演讲， 我希望你可以原谅我。
（掌声）
I'll never forget that day back in the spring of 2006. I was a surgical resident at The Johns Hopkins Hospital, taking emergency call. I got paged by the E.R. around 2 in the morning to come and see a woman with a diabetic ulcer on her foot. I can still remember sort of that smell of rotting flesh as I pulled the curtain back to see her. And everybody there agreed this woman was very sick and she needed to be in the hospital. That wasn't being asked. The question that was being asked of me was a different one, which was, did she also need an amputation?
Now, looking back on that night, I'd love so desperately to believe that I treated that woman on that night with the same empathy and compassion I'd shown the 27-year-old newlywed who came to the E.R. three nights earlier with lower back pain that turned out to be advanced pancreatic cancer. In her case, I knew there was nothing I could do that was actually going to save her life. The cancer was too advanced. But I was committed to making sure that I could do anything possible to make her stay more comfortable. I brought her a warm blanket and a cup of a coffee. I brought some for her parents. But more importantly, see, I passed no judgment on her, because obviously she had done nothing to bring this on herself. So why was it that, just a few nights later, as I stood in that same E.R. and determined that my diabetic patient did indeed need an amputation, why did I hold her in such bitter contempt?
You see, unlike the woman the night before, this woman had type 2 diabetes. She was fat. And we all know that's from eating too much and not exercising enough, right? I mean, how hard can it be? As I looked down at her in the bed, I thought to myself, if you just tried caring even a little bit, you wouldn't be in this situation at this moment with some doctor you've never met about to amputate your foot.
Why did I feel justified in judging her? I'd like to say I don't know. But I actually do. You see, in the hubris of my youth, I thought I had her all figured out. She ate too much. She got unlucky. She got diabetes. Case closed.
Ironically, at that time in my life, I was also doing cancer research, immune-based therapies for melanoma, to be specific, and in that world I was actually taught to question everything, to challenge all assumptions and hold them to the highest possible scientific standards. Yet when it came to a disease like diabetes that kills Americans eight times more frequently than melanoma, I never once questioned the conventional wisdom. I actually just assmed the pathologic sequence of events was settled science.
Three years later, I found out how wrong I was. But this time, I was the patient. Despite exercising three or four hours every single day, and following the food pyramid to the letter, I'd gained a lot of weight and developed something called metabolic syndrome. Some of you may have heard of this. I had become insulin-resistant.
You can think of insulin as this master hormone that controls what our body does with the foods we eat, whether we burn it or store it. This is called fuel partitioning in the lingo. Now failure to produce enough insulin is incompatible with life. And insulin resistance, as its name suggests, is when your cells get increasingly resistant to the effect of insulin trying to do its job. Once you're insulin-resistant, you're on your way to getting diabetes, which is what happens when your pancreas can't keep up with the resistance and make enough insulin. Now your blood sugar levels start to rise, and an entire cascade of pathologic events sort of spirals out of control that can lead to heart disease, cancer, even Alzheimer's disease, and amputations, just like that woman a few years earlier.
With that scare, I got busy changing my diet radically, adding and subtracting things most of you would find almost assuredly shocking. I did this and lost 40 pounds, weirdly while exercising less. I, as you can see, I guess I'm not overweight anymore. More importantly, I don't have insulin resistance.
But most important, I was left with these three burning questions that wouldn't go away: How did this happen to me if I was supposedly doing everything right? If the conventional wisdom about nutrition had failed me, was it possible it was failing someone else? And underlying these questions, I became almost maniacally obsessed in trying to understand the real relationship between obesity and insulin resistance.
Now, most researchers believe obesity is the cause of insulin resistance. Logically, then, if you want to treat insulin resistance, you get people to lose weight, right? You treat the obesity. But what if we have it backwards? What if obesity isn't the cause of insulin resistance at all? In fact, what if it's a symptom of a much deeper problem, the tip of a proverbial iceberg? I know it sounds crazy because we're obviously in the midst of an obesity epidemic, but hear me out. What if obesity is a coping mechanism for a far more sinister problem going on underneath the cell? I'm not suggesting that obesity is benign, but what I am suggesting is it may be the lesser of two metabolic evils.
You can think of insulin resistance as the reduced capacity of ourselves to partition fuel, as I alluded to a moment ago, taking those calories that we take in and burning some appropriately and storing some appropriately. When we become insulin-resistant, the homeostasis in that balance deviates from this state. So now, when insulin says to a cell, I want you to burn more energy than the cell considers safe, the cell, in effect, says, "No thanks, I'd actually rather store this energy." And because fat cells are actually missing most of the complex cellular machinery found in other cells, it's probably the safest place to store it. So for many of us, about 75 million Americans, the appropriate response to insulin resistance may actually be to store it as fat, not the reverse, getting insulin resistance in response to getting fat.
This is a really subtle distinction, but the implication could be profound. Consider the following analogy: Think of the bruise you get on your shin when you inadvertently bang your leg into the coffee table. Sure, the bruise hurts like hell, and you almost certainly don't like the discolored look, but we all know the bruise per se is not the problem. In fact, it's the opposite. It's a healthy response to the trauma, all of those immune cells rushing to the site of the injury to salvage cellular debris and prevent the spread of infection to elsewhere in the body. Now, imagine we thought bruises were the problem, and we evolved a giant medical establishment and a culture around treating bruises: masking creams, painkillers, you name it, all the while ignoring the fact that people are still banging their shins into coffee tables. How much better would we be if we treated the cause -- telling people to pay attention when they walk through the living room -- rather than the effect? Getting the cause and the effect right makes all the difference in the world. Getting it wrong, and the pharmaceutical industry can still do very well for its shareholders but nothing improves for the people with bruised shins. Cause and effect.
So what I'm suggesting is maybe we have the cause and effect wrong on obesity and insulin resistance. Maybe we should be asking ourselves, is it possible that insulin resistance causes weight gain and the diseases associated with obesity, at least in most people? What if being obese is just a metabolic response to something much more threatening, an underlying epidemic, the one we ought to be worried about?
Let's look at some suggestive facts. We know that 30 million obese Americans in the United States don't have insulin resistance. And by the way, they don't appear to be at any greater risk of disease than lean people. Conversely, we know that six million lean people in the United States are insulin-resistant, and by the way, they appear to be at even greater risk for those metabolic disease I mentioned a moment ago than their obese counterparts. Now I don't know why, but it might be because, in their case, their cells haven't actually figured out the right thing to do with that excess energy. So if you can be obese and not have insulin resistance, and you can be lean and have it, this suggests that obesity may just be a proxy for what's going on.
So what if we're fighting the wrong war, fighting obesity rather than insulin resistance? Even worse, what if blaming the obese means we're blaming the victims? What if some of our fundamental ideas about obesity are just wrong?
Personally, I can't afford the luxury of arrogance anymore, let alone the luxury of certainty. I have my own ideas about what could be at the heart of this, but I'm wide open to others. Now, my hypothesis, because everybody always asks me, is this. If you ask yourself, what's a cell trying to protect itself from when it becomes insulin resistant, the answer probably isn't too much food. It's more likely too much glucose: blood sugar. Now, we know that refined grains and starches elevate your blood sugar in the short run, and there's even reason to believe that sugar may lead to insulin resistance directly. So if you put these physiological processes to work, I'd hypothesize that it might be our increased intake of refined grains, sugars and starches that's driving this epidemic of obesity and diabetes, but through insulin resistance, you see, and not necessarily through just overeating and under-exercising.
When I lost my 40 pounds a few years ago, I did it simply by restricting those things, which admittedly suggests I have a bias based on my personal experience. But that doesn't mean my bias is wrong, and most important, all of this can be tested scientifically. But step one is accepting the possibility that our current beliefs about obesity, diabetes and insulin resistance could be wrong and therefore must be tested. I'm betting my career on this. Today, I devote all of my time to working on this problem, and I'll go wherever the science takes me. I've decided that what I can't and won't do anymore is pretend I have the answers when I don't. I've been humbled enough by all I don't know.
For the past year, I've been fortunate enough to work on this problem with the most amazing team of diabetes and obesity researchers in the country, and the best part is, just like Abraham Lincoln surrounded himself with a team of rivals, we've done the same thing. We've recruited a team of scientific rivals, the best and brightest who all have different hypotheses for what's at the heart of this epidemic. Some think it's too many calories consumed. Others think it's too much dietary fat. Others think it's too many refined grains and starches. But this team of multi-disciplinary, highly skeptical and exceedingly talented researchers do agree on two things. First, this problem is just simply too important to continue ignoring because we think we know the answer. And two, if we're willing to be wrong, if we're willing to challenge the conventional wisdom with the best experiments science can offer, we can solve this problem.
I know it's tempting to want an answer right now, some form of action or policy, some dietary prescription -- eat this, not that — but if we want to get it right, we're going to have to do much more rigorous science before we can write that prescription.
Briefly, to address this, our research program is focused around three meta-themes, or questions. First, how do the various foods we consume impact our metabolism, hormones and enzymes, and through what nuanced molecular mechanisms? Second, based on these insights, can people make the necessary changes in their diets in a way that's safe and practical to implement? And finally, once we identify what safe and practical changes people can make to their diet, how can we move their behavior in that direction so that it becomes more the default rather than the exception? Just because you know what to do doesn't mean you're always going to do it. Sometimes we have to put cues around people to make it easier, and believe it or not, that can be studied scientifically.
I don't know how this journey is going to end, but this much seems clear to me, at least: We can't keep blaming our overweight and diabetic patients like I did. Most of them actually want to do the right thing, but they have to know what that is, and it's got to work. I dream of a day when our patients can shed their excess pounds and cure themselves of insulin resistance, because as medical professionals, we've shed our excess mental baggage and cured ourselves of new idea resistance sufficiently to go back to our original ideals: open minds, the courage to throw out yesterday's ideas when they don't appear to be working, and the understanding that scientific truth isn't final, but constantly evolving. Staying true to that path will be better for our patients and better for science. If obesity is nothing more than a proxy for metabolic illness, what good does it do us to punish those with the proxy?
Sometimes I think back to that night in the E.R. seven years ago. I wish I could speak with that woman again. I'd like to tell her how sorry I am. I'd say, as a doctor, I delivered the best clinical care I could, but as a human being, I let you down. You didn't need my judgment and my contempt. You needed my empathy and compassion, and above all else, you needed a doctor who was willing to consider maybe you didn't let the system down. Maybe the system, of which I was a part, was letting you down. If you're watching this now, I hope you can forgive me.
(Applause)
肥胖症危是否掩盖了更大的问题？
我永远忘不了那天 2006年的春天。 我还是一个外科住院医生 在约翰霍普金斯医院 应对急救电话 大约凌晨两点左右，我被急诊室叫去 看一位女病人，她得了因糖尿病而引起的 足部溃疡。 我至今还能记得当我拉开帘子看到她之后 闻到的那种肉类腐烂的味道。 显而易见这位女士病得很重 她需要住院治疗。 这是毫无疑问的。 但那时我考虑的是另一个问题 那就是，她需要截肢吗？
现在，回想起那夜， 我很后悔那天夜里面对那位女士时 心中没有带着同样的同情与悲悯 就像我平时面对其他病人那般 三天前的夜里一位27岁的新娘 因为下背疼痛来看急诊 后来她被诊断为晚期胰腺癌。 虽然我知道我对她无能为力 没办法救她。 癌症已经是末期了。 但我还是尽我所能的 做了所有能让她 舒服一点的事情。我帮她找了条毛毯 端了杯咖啡。 给她父母送咖啡。 更重要的是，我一点也不觉得这姑娘有错 很明显她对自己的病 一点责任也没有 但是为什么，仅仅过了几夜 当我站在同一个急救室并且决定 我的这位糖尿病病人需要截肢手术时 为什么我的心中带着蔑视呢？
你看，跟那位新娘不一样 这位女士有II型糖尿病 她很胖。 而且我们都知道肥胖源自 无节制的饮食和缺乏运动，对吧？ 而且我们都知道肥胖源自 无节制的饮食和缺乏运动，对吧？ 我的意思是，节食和运动很难吗？ 我看着她躺在床上，我心说 哪怕你稍微注意一点儿自己的身体 你也绝不会落到这步田地 跟一个即将给你截肢的陌生在一起 跟一个即将给你截肢的陌生在一起
为什么当时我能心安理得的责备她呢？ 我希望我不知道原因。 但是说真的，我知道。 你看，我那时年少轻狂 我自以为是的觉得 她肯定就是我想到那样。 她饮食无度，她运气不好 她得了糖尿病，基本就是这个情况。
讽刺的是，就在那会儿 我正在参与癌症的研究 黑色素瘤的细胞免疫力疗法，具体来说 在那个领域里，我被教着去质疑一切 挑战一切固有的理论成果 并且在研究中严格遵守最高的科研准则。 但当我面对糖尿病 这种致死几率高于黑色素瘤八倍的疾病时候 我从未质疑过传统的理论。 我当时真的认为糖尿病的发病机理 早有定论。
三年以后，我发现我错了。 但是这次，我自己成了病人。 尽管我每天运动三四个小时 严格遵守健康食谱 我还是体重激增并且得了 代谢综合征。 你们也许有人听说过它。 我的身体对胰岛素产生了抗性。
你们可以把胰岛素想象成一种荷尔蒙 它能控制我们的身体对摄入的食物做出反应 消耗或是储存它们。 在术语中称之为燃料分区。 缺乏足够的胰岛素是很要命的。 胰岛素抵抗，就像字面上意思一样 意味着你的细胞变得越来越不受 胰岛素的指挥正常运作。 一旦你出现胰岛素抵抗的情况 你离患糖尿病就不远了 因为胰岛素抵抗的缘故 你无法制造足够的胰岛素。 你的血糖开始升高 一系列的病例症状 会突然爆发并且可能导致心脏病 癌症，甚至老年痴呆症 或者截肢，就像几年前的那位女士一样。
我很害怕，我很快改了食谱 做了一些让大家觉得 不可思议的改变。 得益于新的食谱 尽管我锻炼得少了，我还是减掉了40磅 你们可以看到，我现在没有超重 更重要的是，我没有胰岛素抵抗症了
但是最重要的是，我陷入了 三个亟待解决的问题 为什么这件事发生在我身上呢? 我已经尽力做到无懈可击了。 如果传统的营养理论在我身上失效了 在其他人身上会怎样呢？ 通过对考虑这些问题 我着了魔一样的 希望找到肥胖和胰岛素之间 真正的关系。
现在，主流观点认为 肥胖导致了胰岛素抵抗。 依逻辑来说，如果你想治疗胰岛素抵抗 你必须减肥，对吧？ 先对付肥胖。 但是如果我们反过来想一下？ 假如肥胖并不会导致胰岛素抵抗？ 实际上，假如它只是一个征兆 一个更深层次的问题的冰山一角？ 这听起来很疯狂 因为我们很正身处 一个肥胖症泛滥的时代，不过请耐心听我解释。 假如肥胖是身体的某种应对机制 用来对付一个潜藏在细胞深处 更加凶险的问题？ 我不认为肥胖是无害的 但是我觉得肥胖在两种新陈代谢疾病中 是比较次要的那个。
大家可以把胰岛素抵抗症看作 我们身体燃料箱变小了 就像我刚刚假设的那样 正常情况下我们摄入的热量 会被适量消耗并且适量储存。 当我们得了胰岛素抵抗的时候 这个平衡就会偏离正常情况。 于是乎，当胰岛素告诉细胞 我需要你消耗一些能量，假如 细胞认为消耗太大，那些细胞就会回应到 “不了，我更想把这些能量储存起来。” 因为脂肪细胞不同于其它细胞 它没有那么多复杂的结构和组织 所以能量都被储藏在那。 因此对我们中许多人，大约7500万美国人来说 胰岛素抵抗应被视作 肥胖的成因，而非相反的， 将胰岛素抵抗归因于肥胖。
这虽然是个相当微妙的区别， 但是它的含义却是相当深刻的。 举个例子来说， 想象一下你小腿上的乌青， 那是你不小心撞上咖啡桌时留下的。 毫无疑问，这乌青疼得要命。 而且你肯定不喜欢腿上多个斑，但是我们都知道 乌青本身并不是个问题。 恰恰相反，这是对外伤的一个正常生理反应。 所有的免疫细胞都会迅速前往受伤的部位 去清理坏死细胞的碎片并且防止 感染扩散到身体其他部位。 好了，想象一下如果我们把乌青当作一个问题， 我们发展出了一个庞大的医疗体系 以及文化来对待乌青： 遮蔽霜，止疼药，等等。 而所有这一切都掩盖了一个事实 那就是人们依旧会撞到咖啡桌 如果我们可以从问题的根源入手 告诉人们注意一下 从客厅走过的时候小心咖啡桌 这会比处理撞伤来的有效果的多 正确理解事情的表象和本因 将使这个世界产生巨大的不同。 即使治标不治本，制药行业 依旧可以为股东们带来利润， 但是对于受伤的人们来说，这没有任何帮助 原因及结果。
所以我想指出的是 在我们讨论肥胖和胰岛素抵抗的问题时 把原因和结果弄反了。 在我们讨论肥胖和胰岛素抵抗的问题时 把原因和结果弄反了。 也许我们需要问问我们自己了， 有没有可能胰岛素抵抗导致了体重增加 以及随肥胖带来的并发症， 至少对于大多数人来说 有没有可能肥胖只是胰岛抵抗的一个代谢反应 相较于其他更大的威胁， 例如一些相关的疫病， 它们才是我们真正应该去担心的。
让我们来看些有暗示性的建议。 我们知道在美国有3千万肥胖症患者 并未患胰岛素抵抗。 同时，没有证据显示他们 比非肥胖症患者更容易贻患其他疾病。 恰恰相反，在美国有6百万非肥胖症患者 存在胰岛素抵抗， 而他们却被证实 易患那些我之前提到的糖尿病并发症， 同时几率较肥胖人士来的更高。 虽然现在我还不知道为什么，但是一个可能的原因是， 对他们而言，他们的细胞无法正确的 对体内多余能量做出反应。 你可以是肥胖症患者，却没患胰岛素抵抗， 或者你可以不肥胖，却患有胰岛素抵抗， 这都表明肥胖只不过是一个表征 而胰岛素抗拒才是根源。
所以如果我们斗争搞错了对象， 我们一直与肥胖战斗着，而非胰岛素抵抗？ 而且更糟的是，如果指责过胖者 其实确是在指责胰岛素抵抗的受害者？ 如果我们对于肥胖症的一些基本认识本身 就存在误差？
就我个人而言，我没有办法继续保持傲慢的态度， 让我把那种过剩的确信感放在一边。 对于这些问题的核心为何，我有我自己的认识， 同时我也愿意将它与其他人分享 我的假设是这样的，因为老有人问我 我的假设是这样的，因为老有人问我 试问，一个细胞到底在畏惧什么 当它处于胰岛素抗拒状态时。 问题的答案可能不是摄入过多的食物。 答案更有可能是摄入过量葡萄糖而导致血糖过高。 精制的谷物和淀粉 将在短时间内抬到你的血糖含量， 而且我们有理由相信 糖分将直接导致胰岛素抵抗症。 所以如果把这些生理过程也列入考虑， 我认为是大量的不断摄入 精制谷物，糖类以及淀粉类食物导致了 肥胖症和糖尿病的流行， 但其病因是胰岛素抵抗症 而不是由于暴饮暴食以及缺乏运动。
在我几年前减去40磅时， 我只是简单的限制了精制谷物，糖，和淀粉的摄入， 诚然这也表明我存在一些偏见， 而这些主要源自我的个人经验。 但是这并不意味着我的偏见是错误的， 更重要的是，所有这些偏见都是可以被科学验证的。 但是第一步就是要接受一种可能性 那就是我们当前关于肥胖症， 糖尿病以及胰岛素抗拒症的理解可能存在偏差 并需要被验证。 我把我的事业都赌在了这个可能性上。 现在，我把所有的时间花在了这个问题的研究上， 而且我将不会停止知道找到真正的答案。 我已经决定有一件事是我不能也不会再做的， 那就是在我不知道答案的时候却假装知道。 对所有我不知道的事情，我都相当谦虚。
在过去一年里，我很幸运 可以和国内最优秀的糖尿病和肥胖症专家团队一起研究 可以和国内最优秀的糖尿病和肥胖症专家团队一起研究 同时最好的事情莫过于， 就如亚伯拉罕?林肯将自己 置身于由对手组成的团队中 我们也做了一样的事情。 我们找来了另一个科学家团队作为竞争对手， 他们也都是极为优秀的科学家， 但却对这个流行病的核心成因有着不同的假设 有一些认为是过量的卡路里摄入 有一些认为是过量的脂肪摄入 也有些人为是过量的精制谷物和淀粉摄入。 这个由多学科， 具有高度怀疑精神以及相当聪明的研究者团队 至少同意两件事情。 其一，这个问题相当重要， 以至于我们不能再假装我们知道答案而对它视而不见。 其次，如果我们愿意去犯错误， 如果我们愿意通过科学实践探究去挑战传统观念 如果我们愿意通过科学实践探究去挑战传统观念 我们终将解决这个问题。
我知道我们都希望现在就能得到一个答案， 一些可以参照行为方式或者规则，一些饮食菜单 告诉我们该吃什么，不该吃什么， 但是如果我们想找到一个正确的答案， 我们就不得不进行严谨的科学尝试， 不然我们是给出真正的答案的。
简而言之，为了找到这个答案，我们的研究项目 主要围绕着三个方面或者问题展开。 首先，我们摄入的各种各样的食物是如何 影响我们的代谢，激素和酶的， 并且这些影响是通过何种细微的分子机制发生的？ 其二，基于这个视角， 人们有没有办法对他们的饮食做出必要的调整， 使它更安全且更易实践 最终，一旦我们找到既安全、 又能安全应用到饮食中的方法 我们又如何改变他们的习惯， 使之变得更为自然， 而非一种刻意行为？ 你知道应该去做什么并不意味着 你可以坚持这么做。 有时我们不得不给人们一些诱因 使这种坚持变得更简单，不管你信不信 这都可以经过科学研究
我不知道这个研究最终会将我带向何处， 但是对我而言，至少有一点是可以肯定地： 我们不能继续指责肥胖症和糖尿病患者 就像曾经的我那样。 他们中的大部分其实都想做正确的选择， 但前提是他们必须知道到底什么是正确的， 而且它们切实可行。 我们梦想有一天当我们的患者可以 减去多余的重量 治好胰岛素抵抗症， 因为作为医学专家， 我们已经抛开了多余的思想包袱， 并完全治好了自己的新观点抵抗症 从而使我们回归我们最初的理想： 开放的思维，抛弃那些不再有效的陈旧观念的勇气 开放的思维，抛弃那些不再有效的陈旧观念的勇气 相信科学的真理没有终点， 只有不断的进化。 忠于这条追求真理的道路 对患者和科学来说都是更好的选择 忠于这条追求真理的道路 对患者和科学来说都是更好的选择 如果肥胖只是 代谢疾病的一个替罪羊， 那么我们去指责这些替罪羊又有什么好处呢？
我有时会回想到七年前急救室的那个夜晚 我有时会回想到七年前急救室的那个夜晚 我希望我可以再和那位女士聊聊。 我想向她道歉。 我想说，作为一个医生，我提供了 我所能提供的最好的治疗， 但是最为一个人， 我让你失望了。 你需要的不是我的判定和我的鄙视。 你需要的是我的同情和怜悯， 而且无论如何，你需要的是一个医生 愿意相信 也许你没有辜负我们的医疗系统。 也许是医疗系统，包括我在内的这个医疗系统， 辜负了你。 如果你现在正在看这个演讲， 我希望你可以原谅我。
（掌声）
I'll never forget that day back in the spring of 2006. I was a surgical resident at The Johns Hopkins Hospital, taking emergency call. I got paged by the E.R. around 2 in the morning to come and see a woman with a diabetic ulcer on her foot. I can still remember sort of that smell of rotting flesh as I pulled the curtain back to see her. And everybody there agreed this woman was very sick and she needed to be in the hospital. That wasn't being asked. The question that was being asked of me was a different one, which was, did she also need an amputation?
Now, looking back on that night, I'd love so desperately to believe that I treated that woman on that night with the same empathy and compassion I'd shown the 27-year-old newlywed who came to the E.R. three nights earlier with lower back pain that turned out to be advanced pancreatic cancer. In her case, I knew there was nothing I could do that was actually going to save her life. The cancer was too advanced. But I was committed to making sure that I could do anything possible to make her stay more comfortable. I brought her a warm blanket and a cup of a coffee. I brought some for her parents. But more importantly, see, I passed no judgment on her, because obviously she had done nothing to bring this on herself. So why was it that, just a few nights later, as I stood in that same E.R. and determined that my diabetic patient did indeed need an amputation, why did I hold her in such bitter contempt?
You see, unlike the woman the night before, this woman had type 2 diabetes. She was fat. And we all know that's from eating too much and not exercising enough, right? I mean, how hard can it be? As I looked down at her in the bed, I thought to myself, if you just tried caring even a little bit, you wouldn't be in this situation at this moment with some doctor you've never met about to amputate your foot.
Why did I feel justified in judging her? I'd like to say I don't know. But I actually do. You see, in the hubris of my youth, I thought I had her all figured out. She ate too much. She got unlucky. She got diabetes. Case closed.
Ironically, at that time in my life, I was also doing cancer research, immune-based therapies for melanoma, to be specific, and in that world I was actually taught to question everything, to challenge all assumptions and hold them to the highest possible scientific standards. Yet when it came to a disease like diabetes that kills Americans eight times more frequently than melanoma, I never once questioned the conventional wisdom. I actually just assmed the pathologic sequence of events was settled science.
Three years later, I found out how wrong I was. But this time, I was the patient. Despite exercising three or four hours every single day, and following the food pyramid to the letter, I'd gained a lot of weight and developed something called metabolic syndrome. Some of you may have heard of this. I had become insulin-resistant.
You can think of insulin as this master hormone that controls what our body does with the foods we eat, whether we burn it or store it. This is called fuel partitioning in the lingo. Now failure to produce enough insulin is incompatible with life. And insulin resistance, as its name suggests, is when your cells get increasingly resistant to the effect of insulin trying to do its job. Once you're insulin-resistant, you're on your way to getting diabetes, which is what happens when your pancreas can't keep up with the resistance and make enough insulin. Now your blood sugar levels start to rise, and an entire cascade of pathologic events sort of spirals out of control that can lead to heart disease, cancer, even Alzheimer's disease, and amputations, just like that woman a few years earlier.
With that scare, I got busy changing my diet radically, adding and subtracting things most of you would find almost assuredly shocking. I did this and lost 40 pounds, weirdly while exercising less. I, as you can see, I guess I'm not overweight anymore. More importantly, I don't have insulin resistance.
But most important, I was left with these three burning questions that wouldn't go away: How did this happen to me if I was supposedly doing everything right? If the conventional wisdom about nutrition had failed me, was it possible it was failing someone else? And underlying these questions, I became almost maniacally obsessed in trying to understand the real relationship between obesity and insulin resistance.
Now, most researchers believe obesity is the cause of insulin resistance. Logically, then, if you want to treat insulin resistance, you get people to lose weight, right? You treat the obesity. But what if we have it backwards? What if obesity isn't the cause of insulin resistance at all? In fact, what if it's a symptom of a much deeper problem, the tip of a proverbial iceberg? I know it sounds crazy because we're obviously in the midst of an obesity epidemic, but hear me out. What if obesity is a coping mechanism for a far more sinister problem going on underneath the cell? I'm not suggesting that obesity is benign, but what I am suggesting is it may be the lesser of two metabolic evils.
You can think of insulin resistance as the reduced capacity of ourselves to partition fuel, as I alluded to a moment ago, taking those calories that we take in and burning some appropriately and storing some appropriately. When we become insulin-resistant, the homeostasis in that balance deviates from this state. So now, when insulin says to a cell, I want you to burn more energy than the cell considers safe, the cell, in effect, says, "No thanks, I'd actually rather store this energy." And because fat cells are actually missing most of the complex cellular machinery found in other cells, it's probably the safest place to store it. So for many of us, about 75 million Americans, the appropriate response to insulin resistance may actually be to store it as fat, not the reverse, getting insulin resistance in response to getting fat.
This is a really subtle distinction, but the implication could be profound. Consider the following analogy: Think of the bruise you get on your shin when you inadvertently bang your leg into the coffee table. Sure, the bruise hurts like hell, and you almost certainly don't like the discolored look, but we all know the bruise per se is not the problem. In fact, it's the opposite. It's a healthy response to the trauma, all of those immune cells rushing to the site of the injury to salvage cellular debris and prevent the spread of infection to elsewhere in the body. Now, imagine we thought bruises were the problem, and we evolved a giant medical establishment and a culture around treating bruises: masking creams, painkillers, you name it, all the while ignoring the fact that people are still banging their shins into coffee tables. How much better would we be if we treated the cause -- telling people to pay attention when they walk through the living room -- rather than the effect? Getting the cause and the effect right makes all the difference in the world. Getting it wrong, and the pharmaceutical industry can still do very well for its shareholders but nothing improves for the people with bruised shins. Cause and effect.
So what I'm suggesting is maybe we have the cause and effect wrong on obesity and insulin resistance. Maybe we should be asking ourselves, is it possible that insulin resistance causes weight gain and the diseases associated with obesity, at least in most people? What if being obese is just a metabolic response to something much more threatening, an underlying epidemic, the one we ought to be worried about?
Let's look at some suggestive facts. We know that 30 million obese Americans in the United States don't have insulin resistance. And by the way, they don't appear to be at any greater risk of disease than lean people. Conversely, we know that six million lean people in the United States are insulin-resistant, and by the way, they appear to be at even greater risk for those metabolic disease I mentioned a moment ago than their obese counterparts. Now I don't know why, but it might be because, in their case, their cells haven't actually figured out the right thing to do with that excess energy. So if you can be obese and not have insulin resistance, and you can be lean and have it, this suggests that obesity may just be a proxy for what's going on.
So what if we're fighting the wrong war, fighting obesity rather than insulin resistance? Even worse, what if blaming the obese means we're blaming the victims? What if some of our fundamental ideas about obesity are just wrong?
Personally, I can't afford the luxury of arrogance anymore, let alone the luxury of certainty. I have my own ideas about what could be at the heart of this, but I'm wide open to others. Now, my hypothesis, because everybody always asks me, is this. If you ask yourself, what's a cell trying to protect itself from when it becomes insulin resistant, the answer probably isn't too much food. It's more likely too much glucose: blood sugar. Now, we know that refined grains and starches elevate your blood sugar in the short run, and there's even reason to believe that sugar may lead to insulin resistance directly. So if you put these physiological processes to work, I'd hypothesize that it might be our increased intake of refined grains, sugars and starches that's driving this epidemic of obesity and diabetes, but through insulin resistance, you see, and not necessarily through just overeating and under-exercising.
When I lost my 40 pounds a few years ago, I did it simply by restricting those things, which admittedly suggests I have a bias based on my personal experience. But that doesn't mean my bias is wrong, and most important, all of this can be tested scientifically. But step one is accepting the possibility that our current beliefs about obesity, diabetes and insulin resistance could be wrong and therefore must be tested. I'm betting my career on this. Today, I devote all of my time to working on this problem, and I'll go wherever the science takes me. I've decided that what I can't and won't do anymore is pretend I have the answers when I don't. I've been humbled enough by all I don't know.
For the past year, I've been fortunate enough to work on this problem with the most amazing team of diabetes and obesity researchers in the country, and the best part is, just like Abraham Lincoln surrounded himself with a team of rivals, we've done the same thing. We've recruited a team of scientific rivals, the best and brightest who all have different hypotheses for what's at the heart of this epidemic. Some think it's too many calories consumed. Others think it's too much dietary fat. Others think it's too many refined grains and starches. But this team of multi-disciplinary, highly skeptical and exceedingly talented researchers do agree on two things. First, this problem is just simply too important to continue ignoring because we think we know the answer. And two, if we're willing to be wrong, if we're willing to challenge the conventional wisdom with the best experiments science can offer, we can solve this problem.
I know it's tempting to want an answer right now, some form of action or policy, some dietary prescription -- eat this, not that — but if we want to get it right, we're going to have to do much more rigorous science before we can write that prescription.
Briefly, to address this, our research program is focused around three meta-themes, or questions. First, how do the various foods we consume impact our metabolism, hormones and enzymes, and through what nuanced molecular mechanisms? Second, based on these insights, can people make the necessary changes in their diets in a way that's safe and practical to implement? And finally, once we identify what safe and practical changes people can make to their diet, how can we move their behavior in that direction so that it becomes more the default rather than the exception? Just because you know what to do doesn't mean you're always going to do it. Sometimes we have to put cues around people to make it easier, and believe it or not, that can be studied scientifically.
I don't know how this journey is going to end, but this much seems clear to me, at least: We can't keep blaming our overweight and diabetic patients like I did. Most of them actually want to do the right thing, but they have to know what that is, and it's got to work. I dream of a day when our patients can shed their excess pounds and cure themselves of insulin resistance, because as medical professionals, we've shed our excess mental baggage and cured ourselves of new idea resistance sufficiently to go back to our original ideals: open minds, the courage to throw out yesterday's ideas when they don't appear to be working, and the understanding that scientific truth isn't final, but constantly evolving. Staying true to that path will be better for our patients and better for science. If obesity is nothing more than a proxy for metabolic illness, what good does it do us to punish those with the proxy?
Sometimes I think back to that night in the E.R. seven years ago. I wish I could speak with that woman again. I'd like to tell her how sorry I am. I'd say, as a doctor, I delivered the best clinical care I could, but as a human being, I let you down. You didn't need my judgment and my contempt. You needed my empathy and compassion, and above all else, you needed a doctor who was willing to consider maybe you didn't let the system down. Maybe the system, of which I was a part, was letting you down. If you're watching this now, I hope you can forgive me.
(Applause)
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