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  • 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 assumed 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