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(单词翻译:双击或拖选)
I'll never forget that day back in the spring of 2006. I was a surgical1 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 ulcer2 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 amputation3?
Now, looking back on that night, I'd love so desperately4 to believe that I treated that woman on that night with the same empathy and compassion5 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 judgment6 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 determined7 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 diabetes8. 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 justified9 in judging her? I'd like to say I don't know. But I actually do. You see, in the hubris10 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 metabolic11 syndrome12. Some of you may have heard of this. I had become insulin-resistant13.
You can think of insulin as this master hormone14 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 lingo15. Now failure to produce enough insulin is incompatible16 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 cascade17 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 radically18, adding and subtracting things most of you would find almost assuredly shocking. I did this and lost 40 pounds, weirdly19 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 underlying20 these questions, I became almost maniacally21 obsessed22 in trying to understand the real relationship between obesity23 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 backwards24? 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 iceberg25? I know it sounds crazy because we're obviously in the midst of an obesity epidemic26, but hear me out. What if obesity is a coping mechanism27 for a far more sinister28 problem going on underneath29 the cell? I'm not suggesting that obesity is benign30, but what I am suggesting is it may be the lesser31 of two metabolic evils.
You can think of insulin resistance as the reduced capacity of ourselves to partition fuel, as I alluded32 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 deviates33 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 cellular34 machinery35 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 bruise36 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 trauma37, all of those immune cells rushing to the site of the injury to salvage38 cellular debris39 and prevent the spread of infection to elsewhere in the body. Now, imagine we thought bruises40 were the problem, and we evolved a giant medical establishment and a culture around treating bruises: masking creams, painkillers41, 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 pharmaceutical42 industry can still do very well for its shareholders43 but nothing improves for the people with bruised44 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 obese45 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 proxy46 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 arrogance47 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 glucose48: blood sugar. Now, we know that refined grains and starches49 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 physiological50 processes to work, I'd hypothesize that it might be our increased intake51 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 bias52 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 decided53 that what I can't and won't do anymore is pretend I have the answers when I don't. I've been humbled54 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 skeptical55 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 tempting56 to want an answer right now, some form of action or policy, some dietary prescription57 -- 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.
Briefly58, to address this, our research program is focused around three meta-themes, or questions. First, how do the various foods we consume impact our metabolism59, hormones60 and enzymes61, and through what nuanced molecular62 mechanisms63? Second, based on these insights, can people make the necessary changes in their diets in a way that's safe and practical to implement64? 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 sufficiently65 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.
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1
surgical
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| adj.外科的，外科医生的，手术上的 | |
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ulcer
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| n.溃疡，腐坏物 | |
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amputation
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| n.截肢 | |
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desperately
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| adv.极度渴望地，绝望地，孤注一掷地 | |
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compassion
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| n.同情，怜悯 | |
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judgment
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| n.审判；判断力，识别力，看法，意见 | |
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determined
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| adj.坚定的；有决心的 | |
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diabetes
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| n.糖尿病 | |
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justified
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| a.正当的，有理的 | |
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hubris
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| n.傲慢，骄傲 | |
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metabolic
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| adj.新陈代谢的 | |
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syndrome
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| n.综合病症；并存特性 | |
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resistant
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| adj.(to)抵抗的，有抵抗力的 | |
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hormone
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| n.荷尔蒙，激素，内分泌 | |
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lingo
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| n.语言不知所云，外国话，隐语 | |
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incompatible
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| adj.不相容的，不协调的，不相配的 | |
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cascade
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| n.小瀑布，喷流；层叠；vi.成瀑布落下 | |
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radically
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| ad.根本地，本质地 | |
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weirdly
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| 古怪地 | |
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underlying
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| adj.在下面的，含蓄的，潜在的 | |
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maniacally
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obsessed
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| adj.心神不宁的,鬼迷心窍的,沉迷的 | |
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obesity
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| n.肥胖，肥大 | |
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backwards
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| adv.往回地，向原处，倒，相反，前后倒置地 | |
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iceberg
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| n.冰山，流冰，冷冰冰的人 | |
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epidemic
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| n.流行病；盛行；adj.流行性的，流传极广的 | |
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mechanism
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| n.机械装置；机构，结构 | |
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sinister
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| adj.不吉利的，凶恶的，左边的 | |
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underneath
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| adj.在...下面，在...底下；adv.在下面 | |
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benign
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| adj.善良的，慈祥的；良性的，无危险的 | |
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lesser
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| adj.次要的，较小的；adv.较小地，较少地 | |
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alluded
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| 提及，暗指( allude的过去式和过去分词 ) | |
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deviates
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| v.偏离，越轨( deviate的第三人称单数 ) | |
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cellular
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| adj.移动的；细胞的，由细胞组成的 | |
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machinery
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| n.(总称)机械，机器；机构 | |
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bruise
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| n.青肿，挫伤；伤痕；vt.打青；挫伤 | |
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trauma
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| n.外伤，精神创伤 | |
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salvage
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| v.救助，营救，援救；n.救助，营救 | |
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debris
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| n.瓦砾堆，废墟，碎片 | |
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bruises
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| n.瘀伤，伤痕，擦伤( bruise的名词复数 ) | |
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painkillers
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| n.止痛药( painkiller的名词复数 ) | |
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pharmaceutical
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| adj.药学的，药物的；药用的，药剂师的 | |
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shareholders
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| n.股东( shareholder的名词复数 ) | |
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bruised
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| [医]青肿的，瘀紫的 | |
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obese
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| adj.过度肥胖的，肥大的 | |
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proxy
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| n.代理权，代表权；（对代理人的）委托书；代理人 | |
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arrogance
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| n.傲慢，自大 | |
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glucose
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| n.葡萄糖 | |
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starches
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| n.淀粉( starch的名词复数 )；含淀粉的食物；浆粉v.把（衣服、床单等）浆一浆( starch的第三人称单数 ) | |
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physiological
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| adj.生理学的，生理学上的 | |
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intake
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| n.吸入，纳入；进气口，入口 | |
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bias
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| n.偏见，偏心，偏袒；vt.使有偏见 | |
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decided
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| adj.决定了的，坚决的；明显的，明确的 | |
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humbled
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| adj. 卑下的，谦逊的，粗陋的 vt. 使 ... 卑下，贬低 | |
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skeptical
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| adj.怀疑的，多疑的 | |
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tempting
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| a.诱人的, 吸引人的 | |
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prescription
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| n.处方，开药；指示，规定 | |
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briefly
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| adv.简单地，简短地 | |
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metabolism
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| n.新陈代谢 | |
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hormones
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| n. 荷尔蒙，激素 名词hormone的复数形式 | |
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enzymes
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| n. 酶，酵素 | |
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molecular
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| adj.分子的；克分子的 | |
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mechanisms
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| n.机械( mechanism的名词复数 )；机械装置；[生物学] 机制；机械作用 | |
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implement
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| n.(pl.)工具，器具；vt.实行，实施，执行 | |
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sufficiently
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| adv.足够地，充分地 | |
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