Download A Conversation between Gary Taubes and Gretchen Rubin

A Conversation
between
Gary Taubes and
Gretchen Rubin
A Note from Gretchen Rubin:
On September 30, 2016, Gary Taubes and I talked by phone for a few hours about his new book
The Case Against Sugar.
I’m a huge fan of Gary’s work. As I describe in Better Than Before, my book about habit
change, while on vacation in March 2012, I read Gary’s book Why We Get Fat and overnight, I
changed practically everything about the way I ate. I call this form of habit change the “Strategy
of the Lightning Bolt”; Gary’s ideas hit me with the force of the lightning bolt, and my habits
changed effortlessly.
I asked him to do this interview because I want to highlight key points from his book The Case
Against Sugar. The book contains so many crucial arguments that it can be challenging for the
reader to keep track of them all. I want to help other readers experience the same lightning-bolt
of understanding that has so benefitted me.
Onward and upward—to better health.
-- Gretchen Rubin
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Gretchen: Hi Gary, thanks for doing this. Your work includes so many important points and so
many mind-blowing conclusions that as the readers, we can lose track as we go. I
wanted to have this conversation to underscore the points that stand out, to me, as
really key. To start with the bottom line: If we’re looking for the factor at the heart of
all our escalating health problems, one factor explains it. And that’s sugar.
Gary:
Yes. We’ve got these epidemics worldwide of obesity, diabetes and the chronic
diseases associate with them, which are the diseases likely to kill us.
These epidemics show up in different rates in different places. They began in the 19th
century in the U.S. and Europe, and then late in the 20th century or mid-20th century
among North America populations and Inuit populations, in the South Pacific and the
Middle East. Everywhere you look in the world, as populations become westernized,
they manifest obesity and diabetes sometimes in almost unbelievable rates.
Gretchen: It’s extraordinary to see the consistency of this pattern
Gary:
“Occam’s razor” is the principle that we should never complicate a hypothesis
beyond necessity, but rather start with the simplest possible hypothesis to explain an
observation. Here, the simplest explanation is sugar. When you add the combination
of fructose and glucose—what sugar is—to any baseline diet, the end result is obesity
and diabetes.
To sugar, I would add refined grains, which is the phenomenon I wrote about in
Good Calories, Bad Calories, but some populations—in Southeast Asia in
particular—had already been consuming significant grains. But they don’t show these
negative effects until you add sugar to that diet. Once you add sugar, you get obesity
and diabetes. Without sugar you don’t have it, or at least not at the rates that are
detectible in the population.
Gretchen: Take us through the key consequences of sugar.
Gary:
First, let’s step back for a moment and clarify what we mean by “sugar,” because
that’s been a point of confusion in this story for over a century. So when I say “sugar”
in the context of what we eat—i.e., not “blood sugar”—I mean both sucrose (the
white, powdered stuff we put in our coffee) or high-fructose corn syrup. The two are
both composed of simpler carbohydrates, roughly 50-50 combinations of glucose and
fructose. And our body deals with them both pretty much in the same way.
When you eat grains or starches, they break down upon digestion into glucose alone,
which is absorbed into your blood stream pretty quickly. That’s what stimulates
insulin secretion from the pancreas, and you get elevated levels of insulin for the next
few hours after consumption. (In fact, you start getting insulin secretion before you
even eat, just thinking about consumption, but that’s not that relevant at the moment.)
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Sugar has glucose in it, but it also has this fructose, which is what makes it so sweet,
and the fructose mostly gets metabolized in the liver.
When you consume sugar—both the fructose and the glucose together—as you do if
you drink a soda or fruit juice or eat a sugar-sweetened cereal, you’re getting the
effect of both these carbohydrates together. Even when you eat fruit, you’re getting
fructose with glucose, so you’re always going to metabolize that fructose in the liver
in the environment of the elevated blood sugar and insulin that comes about because
of the glucose. Now, the fructose in this high glucose/high insulin environment
appears to cause a condition called insulin resistance, first in the liver and then
throughout the body. And this insulin resistance phenomenon is absolutely key to
understanding both obesity and diabetes.
Gretchen: Then is it really the fructose that’s triggering the insulin resistance, or is it the
combination?
Gary:
Well, you always see the glucose and fructose in combination. So you can argue that
because glucose alone may be relatively harmless, that the problem is the fructose.
But since we always consume the fructose with the glucose, that’s an assumption.
What we know, or at least what I think we know, is that the two together in sugar are
a problem.
Gretchen: Could you eat only glucose?
Gary:
Yes, if you eat a high starch diet, or high carb, high grain diet, such as in Southeast
Asia. For poor Southeast Asians, if most calories come from rice, they’re getting most
of their calories from glucose with very little or no fructose.
Gretchen: So is it more accurate to say that eating glucose and fructose in combination leads to
insulin resistance?
Gary:
Yes.
Gretchen: And insulin resistance is a key aspect of metabolic syndrome?
Gary:
Yes. The CDC now says that about 75 million Americans have metabolic syndrome
and so are at high risk for diabetes, heart disease, and even cancer. Metabolic
syndrome is defined by a cluster of what could be called metabolic abnormalities,
starting with the fact that you’re probably getting fatter. High blood pressure is a sign
of metabolic syndrome, as is low HDL cholesterol (i.e., the “good” cholesterol), and
high triglycerides (blood fats) and a tendency to have high blood sugar. All those
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things tend to go together, plus fat accumulation—your waist is getting bigger. And
all of that goes under the diagnosis of metabolic syndrome
At the heart of it is this insulin resistance phenomenon. If you aren’t insulin resistant,
you’re not going to be diagnosed with metabolic syndrome.
As it happens, it’s tough for physicians to test specifically for insulin resistance. You
have to do the test in the doctor’s office and it takes time. Your doctor can’t just take
a blood sample and send it off to the lab. The other tests that can be done quickly:
your doctor can weigh you, measure your waist circumference, and take your blood
pressure. Your doctor can take a blood sample to measure HDL and triglycerides, and
all this is quick and easy. And if the results are not where they’re supposed to be,
these are all signs that the patient is insulin resistant. Although your doctor will tell
you that you have metabolic syndrome.
Gretchen: Insulin resistance is the gateway to all of the negative consequences?
Gary:
Yes, they come together.
Of course, the ultimate manifestation of this is type 2 diabetes. Without insulin
resistance, there’s no type 2 diabetes. You can see the insulin resistance before you’re
a type 2 diabetic, but type 2 diabetes seems to be fundamentally a disorder of insulin
resistance.
Gretchen: Is it accurate to say that these effects are very much tied to the act of consuming
sugar? I mean, if you don’t consume that sugar, then you’re not going to trigger this
cascade of effects? If so, then it’s within our power to avoid those consequences.
Gary:
It gets tricky. True, sugar is the initial trigger of all of this but, say, if your mother
consumed sugar while she was young and then pregnant with you, and she became
insulin resistant, with all its sequelae—well, you’re likely to be born insulin resistant
even if you’re now living in a sugar-free or low-sugar environment.
Gretchen: Wow.
Gary:
You’re going to manifest insulin resistance even without sugar in the diet, and you
become metabolically compromised. Removing sugar might not be enough—and
probably isn’t enough—to re-set the insulin resistance. You’d need to remove all the
carbs. That’s the next step, and that’s where it really gets complicated, and where
people tend to get confused. It’s also where a lot of the pushback comes against this
way of thinking.
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People who argue that we should eat very low-carb, very low-sugar, high-fat diets in
order to be healthy—or who argue that obese and diabetic individuals should eat very
low carb, very low sugar, high fat diets in order to be healthy—are probably right.
Nevertheless, that doesn’t mean that all carbs cause the metabolic syndrome. I’d say
that initially it was caused by the addition of sugar to the population, and its trickledown effect from generation to generation.
When you look at how to fix it, you go to this next step, where you now need to
remove sugar as well as much or even all of the carbohydrates in the diet and replace
them with mostly fats, or at least healthier sources of carbohydrates—green leafy
vegetables, for instance, instead of grains.
Gretchen: The population studies you cite are so striking. The effect is so dramatic. It’s so
consistent. It’s across the globe. When sugar goes up, these negative health
consequences hit, always. And when sugar goes down, the health problems go
down—as in World War I, when sugar rationing meant less diabetes.
I mean, the world is our laboratory. We have a laboratory.
Gary:
We do. We do. And you can use that laboratory to reject a hypothesis. Just the other
day, someone argued to me that the use of growth hormone in cattle is the possible
cause of obesity. The argument is that we feed these hormones to our cattle to make
the cattle bigger, then we eat food with hormones in it, and the hormones get into us,
and we get fatter.
But immediately I think well, let’s see if we could find a population that doesn’t eat
those cattle, doesn’t consume any growth hormones, and yet we still see the same
diseases. I’m willing to bet that we could find South Pacific Island populations that
had obesity and diabetes epidemics before they ever saw hormone-laced meat.
Likewise, I’ve heard the argument that people take anti-depressants, these affect
enzymes that control fat accumulation, and when people pee them away, the
medication gets into ground-water so we’re all drinking anti-depressants that make us
overweight. But could we find epidemics of obesity and diabetes in Native American
populations, for instance, in the 1950s and 1960s? They clearly were not drinking
groundwater laced with anti-depressants.
And consider the argument that eating fat is the problem. Well, look at populations
that were already eating enormous amounts of fat before sugar was introduced. They
didn’t have any of these negative health effects until the sugar came in.
On the other hand, populations that were eating very little fat continue to eat very
little fat, and then boom, add sugar, and you get obesity and diabetes.
That’s where this sort of worldwide epidemic/laboratory comes in handy. If we could
find a population that had high levels of obesity and diabetes, but didn’t consume
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sugar, or didn’t have a recent increase in sugar consumption, that would be telling.
That might be a refutation of the sugar hypothesis, but if such a population exists,
I’ve yet to find it.
Gretchen: We hear the argument that a “calorie is a calorie,” whether it comes from orange juice
or broccoli or steak. But if we want to understand why people are gaining weight, it
turns out the effect on the body is dramatically different, depending on the kind of
food we’re eating. Right?
Gary:
What we know (and it’s been known since the 1960’s) is that fat cells very carefully
regulate how much fat they take up and how much fat they let out, when they do it,
and under stimulus from different hormones and enzymes.
So if we want to know why we get fat, the first question (I think) we should ask is
why do our fat cells get fat?
And it’s very clear that this is a hormonal, enzymatic phenomenon. By that I mean
our fat cells have enzymes that cause them to take up fat and cause them to mobilize
fat and send it out into the blood stream to be used for fuel, and those enzymes are
effectively turned on and off, or turned up or down, by hormones we secrete in
response to the foods we eat.
When you eat carbohydrates, you stimulate the hormone insulin, and insulin works on
these fat cell enzymes to store fat in these cells and keep it there. When you become
insulin resistant, your insulin levels are chronically elevated, which means you’re
storing fat far more than you’re allowing it to be mobilized. Elevated insulin works to
trap fat in the fat tissue.
When you think of obesity as a fat-trapping or fat-accumulation phenomenon, the
next question is, what might determine this trapping of fat in the fat cells?
It’s clearly a hormonal phenomenon, enzymatic phenomenon. It’s clearly related to
the hormone insulin. Insulin rises when you consume carbohydrates, and if sugar
causes insulin resistance, it’s going to create a state in which you are chronically
trapping fat in your fat tissue. You’re not mobilizing it enough, and you’re not
oxidizing (burning for fuel) enough of the fat that you do mobilize.
Gretchen: I can’t remember where I came across this metaphor, but let me try it on you. Think
of your fat cells as your ATM. When your insulin is high, it’s as if you can deposit
your cash, but you can’t get it out; the money’s there, but the machine just won’t
release the cash because your password won’t work when there’s so much insulin
around.
Then, if the insulin drops, your password works, and the ATM can release the cash.
So in either case, there’s cash in the bank, but it’s a question of how to get the
machine to release your cash. Is that one way to think about it?
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Gary:
Interesting. I haven’t heard that particular metaphor before. So in this metaphor, the
conventional—i.e., wrong—argument would say that if you want to get cash out of
the ATM, you have just have to get poor enough (go spend your money and come
back) and the ATM will happily give up its money. And what we’re saying is, no, we
want the password to work. And for that to happen, insulin must drop.
Gretchen: Yes, using the password (having your insulin drop) is the way to get the
cash out of the bank.
Gary:
And that’s done by restricting the carbohydrates you consume, getting rid of the
sugar, maybe replacing them with fat. In the successful weight loss diet, carbohydrate
restriction is lowering insulin. If you can lower insulin, you’re going to mobilize fat
from your fat cells and your body is going to burn that for fuel and you’re going to
get leaner.
Gretchen: So when insulin is lower, the fat cells release the fat and it can be burned?
Gary:
Yes, insulin effectively orchestrates all this. If you want to store fat, raise insulin. If
you want to use fat for fuel, lower insulin.
Getting back to the ATM metaphor, insulin is the factor that controls whether the
password works. Being poor isn’t enough. Being rich isn’t enough. To get the ATM
to give you cash so you can then spend it, you need the password—which is getting
your insulin levels low enough.
Gretchen: So the idea that “a calorie is a calorie” isn’t true, because in fact, what we’re eating
shapes the hormonal environment, and that hormonal environment determines what
happens in the fat cells.
Gary:
Exactly. The body doesn’t just pay attention to “calories.” The body responds to
different macronutrients differently.
Gretchen: We often hear the argument that “People are overweight because they’re lazy and
they eat too much.” Gluttony and sloth. You argue against the proposition that the
right way for people to lose weight is just to move more and eat less.
Gary:
Yes, clearly you can find obese people who are hungry all the time, eat a lot, and
don’t want to exercise. We can find lean people like that, too, but we don’t care about
them because they’re lean. So the question is are they fat because they’re hungry and
eat a lot and don’t exercise? Or is the causality reversed: maybe something about
being predisposed to get fat makes you hungrier and sedentary. And, clearly, if
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someone had a disorder that made it difficult to burn for fat for fuel and tended to trap
fat calories in their fat cells, they wouldn’t be able to use those fat calories for energy,
so they might be hungrier and less motivated to expend energy in physical activity.
You can think of it as though they’re being starved by their fat tissue which is hording
the calories they consume. Getting back to the ATM metaphor, it’s like having an
ATM that won’t give you cash. If the money you earn is locked away in your bank
where you can’t access it, you’ll spend less and, well, want more than you would if
the ATM was a little more forthcoming.
Now let’s let go of that metaphor.
So if your fat tissue is being instructed to accumulate calories and store it as fat,
which is what insulin does, and you can’t access those calories, you’re going to have
fewer calories to spend. So you’re going to be hungrier, in effect, then you would be
if insulin was low and you could access your fat stores. You’re going to want to be
more sedentary, too.
This has been demonstrated in dozens of animal experiments of obesity. Trigger the
fat cells to take up fat, and you’ll get the gluttony and/or sloth that we’ve come to
blame human obesity on.
Gretchen: It’s ironic. A person might look at someone who’s overweight and think, “Well, this
person has tons of energy to burn, because they have all that fat accumulation, which
represents energy storage.” But again, it’s the ATM without the code. It’s not that the
energy isn’t there, but it’s not useful to that person, who’s actually in a state of
needing more, or needing to preserve.
Gary:
Yes, the simplest way of thinking about it is that they’re keeping their insulin levels
elevated.
That’s the result of the combination of the foods they’re eating and their genotype—
their genetic inheritance. A lean person can eat foods that a person predisposed to get
fat can’t eat. That’s a concept that seems very simple, but it’s exceedingly difficult to
get it across to physicians or researchers who believe the simplistic “calories in,
calories out” idea.
Gretchen: Some people say “If sugar is bad, it’s because it’s ‘empty calories.’” But you’re
arguing, “No. It’s much worse than zero. It’s not just that it’s not doing us any good,
it’s actually hurting us.”
Gary:
Yes. This simplistic concept of the “energy balance” has been exceedingly beneficial
to the sugar industry. If we get fat merely because we take in more calories than we
expend, that implies that the only characteristic of a food that influences our body
weight is the caloric content, which implies that a “calorie is a calorie is a calorie.” It
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doesn’t matter what you eat, there’s no difference between orange juice or broccoli or
steak or anything else. But there’s a tremendous difference, and it’s very much not all
about the calories.
Gretchen: It follows from this that it’s healthy to eat fat, and people find that idea very hard to
accept. We’ve been so trained to think that we should take all the fat out of our diets,
with egg-white omelets, fat-free yogurt, etc. Is it true that we’ll be healthier if we ate
more fat (not trans fats) generally?
Gary:
Yes, that would be the implication.
We’ve had a perfect storm of bad nutritional wisdom. Not only did we insist that all
calories are alike when it comes to weight gain (not true), we insisted fat was
responsible for heart disease (not true). If you believe dietary fat is the cause of heart
disease, your solution is to eat a low-fat diet, and when you take fat out of your diet,
you replace that fat with carbohydrates. Now you’re eating a diet that’s going to drive
up insulin—and that’s going to make you fatter.
If you’re fat and want to be lean, you have to cut back on carbohydrates—particularly
sugars and refined grains—and you have to replace those calories with something,
ideally fats. Now you’re eating a high fat diet that’s supposed to kill you. But the
science behind the “high fat leads to heart disease” is terrible.
That’s what I mean by a “perfect storm of bad nutritional wisdom.” Most people still
believe it, most physicians still believe that.
Gretchen: Yes. Like the school programs that say, “To make the kids healthier, we’ll give them
fat-free milk, but they don’t like that, so we’ll give them fat-free chocolate milk
instead.” No fat, tons of sugar. A terrible idea.
Gary:
It’s crazy, but that’s how we have described, defined a healthy diet in the past.
Gretchen: You touch on another key misconception: that exercise is a good way to lose weight.
There are many, many excellent reasons to exercise in terms of health, but exercise is
not a good way to lose weight.
Gary:
The misconception is that if you simply burn off the energy, your fat tissue will
happily give it up and oxidize it. We’ll go back to our ATM metaphor. It’s like
thinking that if you get poor enough—if you just go out and spend even more
money—your ATM will happily give up the cash. So to get more money out of your
ATM, you only have to spend more money around town so that you have less in your
wallet. The ATM doesn’t work like that, and your fat cells don’t work like that.
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Your overweight isn’t being caused by being sedentary, and becoming physically
active isn’t the cure.
Also, exercise makes you hungry. You give up some fat as you exercise, but as soon
as you’re done, your fat tissue is going to restock those calories, which means you’re
going to be hungry. This has been clear for as long as humans have existed: physical
activity increases appetite.
Yet, somehow we assume that obese people can be physically active, and move as
much as light people, and they’re not going to respond by being hungrier, or if they
do respond, they’re supposed to control the hunger by willpower. It’s not the solution.
The studies very clearly show that exercise has little to no effect on weight, as does a
world of obese people who do manual labor for a living.
Gretchen: Is it true that one of the positive effects of exercise is that it tends to make people
more insulin sensitive?
Gary:
It is true. My understanding, though, is that that’s a short-term phenomenon, perhaps
36 hours. I once discussed the relevant research with a Case Western physiologist
who had been studying this phenomenon since the 1960s. As he explained it to me,
physical activity tends to deplete the glycogen stores in your liver and muscle cells.
(Glycogen is the storage form of carbohydrates.) After you exercise, your body wants
to replete those stores.
Just as your fat tissue want to replete the fat calories that you’ve given up, your liver
and muscle cells want to replete the glycogen stores that they’ve been forced to give
up. Now a key thing that insulin does is tell your muscle and liver cells to take up
glucose and use it for glycogen storage and fuel. Since these cells now want to take
up glucose, they make this process very easy and you appear to be very sensitive to
insulin. As soon as your cells replete their glycogen stores, this sensitivity to insulin
goes away, because now your body doesn’t have to do that and it takes as much
insulin as it used to. One way to think about it is that you remain insulin sensitive
until you’ve had enough carbohydrates to replete glycogen. If you follow-up your
exercise with a plate of pasta or even a Gatorade, that’s going to happen very quickly.
Gretchen: Here’s a question. When we’re eating food, do calories matter at all, does amount
matter at all?
Gary:
What I’m saying is that it doesn’t do much good to think in terms of calories. It’s one
way to access the quantity of a food you’re consuming, but what you care about is the
effect of that food on this hormonal milieu. This in turn will determine whether your
body stores calories or burns them, which then determines how much you want to
consume and how much it takes to feel satiated.
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Gretchen: Right. I get that.
What about this? Let’s say I have a serving of full-fat Greek yogurt that I bought at
the grocery store, but I also have my special gourmet version that has triple fat. I eat
that triple-fat serving. Would the effect on my body be the same for both servings, or
would it be different because the triple fat has even more fat? Or are you saying that,
in the end, I wouldn’t eat the triple fat because it would make me so full, or that I’d
eat less later in the day…?
Gary:
Is this triple fat yogurt rhetorical or is this a real thing?
Gretchen: I’m making it up. Though I would definitely eat it if I could, because I’m such a
believer in your arguments!
Gary:
What we want to know is what effect these foods have on the hormonal milieu. Does
it stimulate fat storage and the trapping of fat and fat calories? If it doesn’t, then
you’re unlikely to get fat eating them, even if you force yourself to eat more than you
want. If you eat them without forcing and just eat to satiety, you won’t store excess
calories and fats. That would go into your fat tissue as it’s supposed to after meals,
and they’ll come back out afterwards to be used for fuel and energy.
You should reach a balance between your appetite and your fat storage such that you
are eating to satiety, and you think of it as eating in moderation, but you’re eating in
moderation because you have the full availability of the calories that go into your fat
tissue and come back out. As long as these foods don’t trigger this process by which
fat is trapped in the fat cells, you’ll be able to eat them to satiety without getting fat—
most people. Again, this gets complicated because other hormones affect fat storage
as well, particularly in women, as they get older.
Gretchen: That’s the basic framework?
Gary:
Yes. If you force yourself to eat more than you really want, if you ate a stick of butter
every day, you could probably hack the system to store more calories as fat, but
you’re forcing it to do so. Even then, you’re not going to become 50 or 100 pounds
obese. You might put on 5 or 10 pounds. I’m speculating that you can force yourself
to gain. When you stop the forcing, those 5 or 10 excess pounds will go away, they’ll
be burned for fuel.
Gretchen: I’d be curious to hear your view of the argument that we should try to have long
periods every day where we don’t eat. Some people say we should try to limit our
eating to within a certain fairly narrow span of hours.
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I suppose this would be healthy because during that non-eating time, insulin can drop,
and all these mechanisms can come into play. Is that right? Is this proven?
Gary:
Well, say you’re going without eating for 18 hours. You skip dinner and go from
lunch today to breakfast tomorrow without eating in between. This is the kind of
thing that now goes under the term “intermittent fasting.”
So one question is whether going 18 hours between meals, say, twice a week, will
make you healthier? I know people who say it does. I also know people who say they
went on low-carb diets, their weight plateaued, still at a higher level than they
preferred, and when they took up intermittent fasting, they started losing weight
again.
Now the question is, if it works, does it work because it reduces the calories you
consume over the course of the week? Or does it work because it prolongs the period
during which your insulin is low enough that you’re mobilizing fat and oxidizing it?
Or for some other reason? The evidence fits a few different scenarios.
I find it fascinating. I’ve experimented with it myself (although not as much as I
would like) to see what happens—at least to me. Physicians I respect are now
suggesting that this is a very healthy thing to do in the long run, although I know a
few others who disagree.
My take is that there’s just not enough research on this question to tell us what we can
reasonably believe to be true, and certainly not why it works, assuming it does.
One question that I think should be asked is whether this is a way of eating that is
likely to be kept up for life. I question whether many people will keep up this practice
of skipping meals, or whether it’s just going to be last year’s fad.
For instance, because I’ve got kids and my kids are eating every night, I tend to want
to eat every meal as well with them, and so I predict it would be tough for me to keep
it up. If I didn’t have children, it might be a very simple technique. It’s surprisingly
easy to go 18 hours without food, at least if you’re not eating a lot of carbs.
Gretchen: Let’s switch gears. As I was reading The Case Against Sugar, here’s another issue
that jumped out at me: that the uneasiness that many people feel about artificial
sweeteners can be traced back to defensive actions by the sugar lobby.
This particularly struck me, because I drink a lot of diet soda. People constantly tell
me, “Artificial sweeteners are so bad for you.” I had a very smart friend say to me,
“Oh, it’s much healthier to drink a regular Coke than to drink a Diet Coke.” I always
say, “Where’s your evidence?” I’ve never seen any convincing evidence—certainly
the evidence against sugar is much, much stronger than the evidence against artificial
sweetener.
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Gary:
You always have to think about the trade-off. If sugar causes insulin resistance and
leads to obesity, diabetes, heart disease, etc., and if some people find it virtually
impossible to live without their sweets, and artificial sweetener lets them give up
sugar, the trade-off is, “What are the risks and benefits of sugar, compared to the risks
and benefits of artificial sweeteners?”
From what I’ve seen in the research, for that trade-off, artificial sweeteners are much
better—or much less bad—than sugar.
In The Case Against Sugar, I recount how the sugar industry went after cyclamates
and saccharin, which were the competition in the 1960s. The sugar industry
succeeded at painting these artificial sweeteners as carcinogens and getting the FDA
to ban cyclamates. As such, it surely fueled the fear of artificial sweeteners.
Ideally, the goal should be to get rid of your sweet tooth. Getting rid of your sweet
tooth altogether should make it easier to avoid consuming sugar in the future, or when
you’re particularly hungry or just particularly tempted. So my fear with artificial
sweeteners is not so much that they’ll shorten your life, but make it easier to fall back
into the habit of consuming sugar.
Gretchen: The less sugar you eat, the less you crave it. At least that’s true for me.
Gary:
It’s interesting. One likely phenomenon that I’ve never really written about (but
maybe should) is a likely explanation for why people who are obese or predisposed to
be obese would crave carbohydrates and sugar more than someone who is naturally
lean. The obese people tend to be insulin resistant, which means that their insulin is
going to be elevated. This insulin is not only preventing their fat cells from
mobilizing fat, it’s signaling the other cells in their body to burn carbohydrates
(glucose) for fuel. So for someone who’s insulin resistant, carbohydrates are their
primary source of fuel. Even when their blood sugar is dropping and they should be
burning fat instead, their body wants to continue to burn carbs.
Now these people also tend to secrete too much insulin, and this will happen even
before they eat, when they’re just thinking about eating. This is called the “cephalic
phase” insulin response, and it’s like a Pavlovian phenomenon. If I start thinking
about eating some delicious bread pudding, I’m not just going to salivate, my
pancreas is going to start secreting insulin to prepare my body to deal with that bread
pudding as I eat it. The more predisposed we are to put on weight, and the more
insulin resistant we are, the greater this response will be.
So now let’s imagine two people, a naturally lean person and a person predisposed to
get fat, and they both walk by a bakery. They smell the freshly baked bread and the
sweets and they’ll experience entirely different levels of cravings based on how their
bodies respond to the stimulus—the cephalic phase insulin response in particular.
A lean person might have a relatively mild response—“Mmm, that smells good,” and
he or she just keeps walking. The obese person or the person predisposed to gain
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weight will have a much different response: the delicious smell will trigger a
hormonal response—insulin—that works to lock up fat calories and lower blood
sugar, and suddenly that person is almost literally starving, and starving for
carbohydrates. The insulin is in effect emptying their blood stream of available fuels.
The lean person walks by the bakery proud of his or her willpower. The obese person
or the person predisposed to obesity can’t resist walking in, buying the bread or
sweets, and eating it. And then feels guilty for not being able to eat in moderation. It’s
physiology driving behavior, not the other way around.
Gretchen: In culture, we put a lot of emotional or character weight on that response—on
whether they walk in to the bakery or walk on by.
Gary:
We see it as willpower or a lack thereof.
Gretchen: People say things like “You’re eating because you’re an emotional eater” or “You
don’t have any willpower.” But in fact, these folks are experiencing something that’s
very concrete. It’s a physical response to things happening in their bodies.
Back to the issue of artificial sweeteners. I’ve heard the argument that artificial
sweeteners cause an insulin response. My sister Elizabeth is a type 1 diabetic, and she
told me, “I’ve never had an insulin response to artificial sweeteners.” But is that a
thing?
Gary:
The last time I reviewed this literature, it was at best ambiguous. It’s possible. It’s
possible, for instance, that a person has a cephalic phase response to thinking about
drinking a diet Coke, or some people do. This is where you need to do well-controlled
randomized control trials.
Most of the evidence about the effect of artificial sweeteners is observational. It’s
observed that people who drink a lot of diet sodas tend to be heavier than people who
don’t, but then you ask, “Who tends to drink diet soda?” People who are predisposed
to gaining weight, who are trying to keep their weight in control and still have their
sodas.
Gretchen: Let’s talk about the glycemic index and fructose. This is important, but it’s confusing.
Gary:
Yes. So the glycemic index measures how much your blood sugar goes up in
response to consuming a set amount of a particular food. The catch is that this
response varies from person to person, and the glycemic index of a particular food
naturally varies depending on the context of the other foods with which it’s eaten.
Say you’ve got white flour, and you make a high-fat croissant out of it. That flour is
going to have a lower glycemic index than if you bake it into lower-fat white bread.
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We don’t actually know the long-term consequences of the variations. If you have the
same food in a fat-rich meal, you’re going to have a lower glycemic index, but does
that mean you’re going to be healthier in a long run from eating it rather than the
lower fat version? We don’t actually know.
Gretchen: Right. I’m wondering, are you better off eating toast with butter or just dry toast? Are
you better off eating high-fat ice cream or low-fat ice cream?
Gary:
The answer is that we don’t really know. Or at least I don’t really know. I could
imagine the scenario in which the high-fat ice cream is healthier, because it’s got all
that fat, to reduce the glycemic index.
Gretchen: It would digest more slowly?
Gary:
Yes, it will digest more slowly. The carbs will get into your bloodstream more
slowly. The rise in blood sugar would be slowed. It could be great but,
simultaneously, you’re still going to store that fat, because of the insulin that’s still
being secreted. Store the fat first. Maybe this lower blood sugar and the lower insulin
still don’t balance out the fat storage that results from storing the fat first.
It’s possible that a high-carb diet with a lot of fat is worse than a high-carb diet
without a lot of fat. But that still wouldn’t mean that that the ideal diet is one that’s
low in fat. I’d still argue that the problem is the carbohydrates, because it’s the
carbohydrate content of the diet which will ultimately determine whether fat is stored
or used for fuel. Ultimately, though, the research necessary to resolve these issues—
or at least resolve them unambiguously—has never been done.
As I discuss in my book, the other critical problem with this glycemic index concept
is that the fructose in sugar doesn’t elevate blood sugar, because it’s mostly
metabolized in the liver. So it has a low glycemic index. And so, gram for gram,
sugar has a lower glycemic index than white flour and most starchy vegetables.
In the 1980s, this made researchers suggest that sugar might be relatively safe for
diabetics, when I would argue—and generations of physicians did—that it could be
the worst thing for them.
If you only focus on glycemic index, you’re only looking at one way that we
metabolize the carbohydrates in our diet. And you’re ignoring what happens to the
fructose—which is one-half of the sugar molecule—and you’re going to be misled, or
at least miss a critical part of the story.
Finally, there’s this issue of individual variation. People, and particularly diabetics,
are now experimenting with devices called continuous glucose monitors that allow
them to almost continuously monitor their own blood sugar, minute by minute. By
doing so they can see how they respond to specific foods, regardless of the glycemic
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index. These CGMs, as they’re called, confirm that the way my blood sugar responds
to a particular carbohydrate-rich food is likely to be quite different than how yours
does. For diabetics, it’s crucial to know which foods stimulate a lot of blood sugar
and require a lot of insulin, and which foods don’t.
Gretchen: Yes, my sister Elizabeth wears a monitor.
Another point in your book is just as health experts told us not to eat fat, they also
told us not to eat salt. But the research really exonerates salt, right?
Gary:
Right.
Going back to the crux of my book: if you’re insulin resistant, you’re likely to have
elevated blood pressure, or hypertension. If you’re obese, you’re likely to have high
blood pressure. If you’re diabetic, you’re likely to have high blood pressure. Heart
disease is associated with high blood pressure. The simplest way to think about this is
that if you’re insulin resistant, you’re likely to have high blood pressure. That’s a
concept that’s built into this idea of metabolic syndrome. And so the key question—to
me, anyway—is what causes the insulin resistance. That’s clearly not caused by salt.
Occam’s razor says all these things have the same cause. You look at the mechanisms
by which sugar and refined grains might elevate blood pressure, and there’s a lot of
evidence to support the idea that hypertension is caused by the same thing that causes
insulin resistance—which is most likely sugar, not salt. Yes, maybe you can reduce
your blood pressure a little by restricting salt consumption, but it’s not elevated
because of the salt. It’s elevated because of the sugar you eat. If you got rid of the
sugar (and maybe the refined grains) and resolve the underlying insulin resistance and
metabolic syndrome, the hypertension is going to go away, too. And this hypothesis is
supported by the clinical trials of low-carbohydrate diets, which almost invariably
show a reduction in blood pressure with carbohydrate and so sugar restriction.
Gretchen: To me, it’s distressing that people are so misled by bad health advice. Sure, some
people think, “I’ll eat anything I want.” But many people really try to be
conscientious. They’re working hard to make good choices. Or maybe they’re trying
to help someone else become healthier. But they’re doing it all wrong. They’re not
tackling what they need to tackle. They think the solution is more exercise, or less
salt, or no fat. And as you so convincingly show, that’s just not the solution.
Recently, I read a piece in the New York Times, “Children’s Blood Pressure Rises
with Obesity” (September 13, 2016). According to the article, this was the doctor’s
recommendation for the obese children with high blood pressure: “The focus should
include a lower-calorie diet that emphasizes vegetables, fresh fruits, fiber and nonfat
dairy; a reduction in dietary salt; regular physical exercise towards the goal 30 to 60
minutes of aerobic activity on most days; a limit of screen time and working toward a
maximum of two hours a day spent on sedentary nonacademic activities.”
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Look at this advice! It would be very tough for the children to comply, and it
wouldn’t help them lower their weight and their blood pressure.
Gary:
Yes, that’s how I see it, too. These authorities are trying to help children who are
obese, and they’re doing it by insisting that these children not only restrict their diets,
but exercise more as well. The increase in exercise is suppose to make them leaner,
but the one thing we know for sure is that it’s going to make them hungrier. So now
we have hungry kids who are supposed to eat even less than they were eating without
the exercise, and to eat these incredibly bland meals—no salt, low fat—that I would
argue are going to make their weight problem worse because of the high-carbohydrate
content. There’s so many ways in which this advice is wrong and, of course, it’s the
child who ends up paying the price.
When this advice fails, as it invariably does (the obesity epidemic, if nothing else,
tells us this advice fails), the experts are going to implicitly blame the children for not
having the willpower or maybe the “grit” necessary to do what lean kids do
naturally—eat in moderation and exercise. What they won’t do is ask themselves
whether maybe their advice is wrong, which is all I’ve been doing for the past 15
years.
Whenever I think about escaping this often thankless business of challenging the
nutrition establishment, I think of obese children and what we put them through. This
advice is that these kids are overweight because they’re watching too much TV,
they’re eating too much. But the world is full of thin children who look at screens all
day. So maybe these obese children are obese because of what the foods they’re
eating do to their hormonal milieu and how that effects whether they store calories as
fat or burn them for fuel. And this is not only encoded in their genes, but maybe
predetermined in the womb, a result to what their mothers (and grandmothers and
great-grandmothers) were eating.
Gretchen: Switching gears. Would you say that we’re better off eating as little sugar as
possible?
Gary:
Clearly. I think the less sugar we eat, the better. Sugar is the fundamental trigger.
Now, for many people, less sugar isn’t going to make them necessarily lighter, it’s
not going to reverse this excess fat problem, but it will make them healthier.
Gretchen: The problem isn’t eating the fat or the salt, or sitting on the couch, it’s sugar.
Gary:
I think sugar is both a drug and a long-term toxin. I think we get addicted to it young.
We may even be born addicted to it. Ultimately, I think everyone will be healthier
and happier if they’re not consuming it, just as I think I’m happier and healthier
getting over my cigarette addiction.
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In our society, it’s hard to do. People have to understand what this substance is doing
in their bodies to have the motivation to do it. That’s why, in the last chapter of The
Case Against Sugar, I recommend doing an experiment to see how you feel. Go three
months without sugar, and see how you feel.
Gretchen: As I’ve told you before, that’s exactly what I did. Four years ago, I read your book
Why We Get Fat, and I immediately cut out all sugar and added a bunch of fat to my
diet. I went from eating things like oatmeal, egg-white omelets, and tons of fruit to
eating eggs and bacon. As I was eating my bacon, I remember thinking, “Well, I hope
Gary Taubes is right.” I got amazing results.
Then without telling me, my father decided he’d give this way of eating a try, too.
Now, it was one thing for me to do this self-experiment, but my father was in his 70s,
overweight, got consistently bad results in his blood tests, with all indicators getting
slightly worse every year. And he was eating oatmeal for breakfast every day, eggwhite omelets, all the rest, as I’d been doing before, and he just decided he was going
to give it a try.
It was extraordinary. Literally, his cardiologist asked, “Jack, what have you been
doing?” Because the change was dramatic. Everything reversed. He lost a bunch of
weight, and he has maintained it for years, and all his other indicators are better too.
You suggest that we should just try eating this way. I so agree. I tell people, “This is
within your reach. You don’t need the Hubble Telescope to do this experiment. Try it
yourself, and just see what happens to you.” In my experience, when people try it, the
benefits are dramatic. And there’s all this delicious food to eat!
Gary:
There are probably 50 different measures of metabolic risks that would suggest that
we’re healthier eating a high-fat diet without these highly processed carbohydrates,
and specifically without sugar, than we are eating what the U.S. government
recommends. But we don’t know for sure, and so eating this way is still taking a risk.
There are people out there, nutritionists out there, who can’t imagine that a bacon
cheeseburger without the bun is a healthy thing to eat.
Gretchen: It’s hard to accept how wrong the conventional low-fat wisdom is.
Gary:
When I lived in New York, on 6th Avenue and 12th Street, I got my coffee every
morning at a bagel shop on our block. The bagel shop was full of NYU students,
virtually all of them overweight, who were ordering bagels with low-fat soy cream
cheese and their coffee lattes with low-fat soy milk. They thought they were eating a
healthy diet, that they were as lean as they possibly could be because they were eating
healthy.
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Gretchen: That’s so poignant to me. It’s not someone saying “I’m just going to have whatever I
want, carpe diem.” It’s a person who’s conscientiously making an effort to make
healthy choice—and often they’re making terrible choices.
Gary:
Right. In the paradigm I argue, you target the carbohydrates, specifically the sugars
and the refined grains and easily-digestible starches. You get rid of those, and you
replace them with mostly fat, because even if fat is unhealthy if eaten with a lot of
carbs, I’d argue it’s healthy if eaten without the carbs.
You see what happens to your body when you do that. It’s very easy to see how your
body responds, how your risk factors respond when you shift to these low carb, high
fat diets.
Gretchen: I want to read a passage from your new book that I thought was very helpful about
understanding how to think about the role of sugar.
“Lung cancer is…assuredly a multifactorial, complex disease. Most smokers will
never get lung cancer, and at least a tenth of all cases of lung cancer are unrelated to
smoking cigarettes, and yet it’s widely accepted—for very good reasons—that
smoking is the primary cause.
“Whether or not obesity and diabetes and their associated diseases are multifactorial,
complex disorders, something has to explain their connection with modern Western
diets and lifestyles and the epidemics that are both ongoing and almost ubiquitous
worldwide. What is it? We are clearly doing something different from what we did
fifty years ago, or 150 years ago, and our bodies and health reflect it. Why?” (19-20)
Gary:
Right. That’s the question. The conventional wisdom is we’re just eating too much of
everything—too many calories and too much fat—and not getting enough exercise.
I’d say we’re mainlining sugar and highly carbohydrates and that’s the problem.
Gretchen: People point to subtle environmental causes, or to newly discovered hormones, to
understand the obesity epidemic, but in fact, the big giant factor in this area is insulin.
And everyone understands insulin! It’s not controversial. Everyone agrees about the
basics of how insulin works, how it functions in the body.
Gary:
Yes, I’m arguing that the problem of obesity and diabetes was basically solved by
1960s era endocrinology, but that’s not what scientists are interested in studying
today.
The question is, why do people become fat and diabetic, and why has it happened
worldwide? What changed in our diet or lifestyle or environment that triggered this
massive epidemic of what geneticists would call the obese and diabetic phenotype?
The manifestation of obesity and diabetes in populations all around the world, all in
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the past 100 to 150 years, has been a worldwide epidemic. It’s got to be something
simple. The idea that it’s a little bit of this and a little bit of that and a little bit of this
and it’s a little bit of something in different populations is such poor science.
And if we give incorrect health advice based on tis dysfunctional science, it’s like
convicting the wrong criminal for a crime. If you put an innocent man in jail, you’re
not just doing a disservice to the innocent man—you’re leaving the guilty party free
to kill again.
People don’t realize that they’ve been eating the wrong things their whole life, and
they’ve been eating the wrong things because the research community didn’t know
how to do science correctly, how to think skeptically and critically, and then
organizations grew up to magnify the bad science and industries took advantage of
this bad science to do make profits. The obesity and diabetes epidemics are just
tremendous business for the pharmaceutical and medical fields.
Gretchen: Here’s a practical question I think a lot of readers will ask. If a person thinks, “Okay,
I’m convinced. I’m going to cut most of the sugar out of my diet, but honestly, I will
have a little sugar.” Would you say that they’re healthier to have a little bit of sugar
every day or have one big sugary treat once a week?
Gary:
The answer is I don’t know. A lot depends on the individual. A lot is programmed
genetically. Would you be better off having a little sugar every day, rather than the
shock of the single big ice cream cone? We don’t have the research necessary to say
one or the other.
But here’s something to consider. For many people, moderation just doesn’t work.
Personally, I find that if I don’t eat any sugar, I don’t think about sugar. It’s easier for
me to avoid sugar entirely than to try to eat it in moderation. Just like if I don’t smoke
any cigarettes, I’m not thinking about my next cigarette. If I don’t eat any sugar, then
it’s just something I don’t do, and I’m perfectly happy not doing it and I like my highfat meals.
Gretchen: Yes, I write about this in Better Than Before, my book about habit change. I call it
using the “Strategy of Abstaining.” For many people—like you and me—it’s much
easier to have no sugar than to have a little sugar. And yet moderation is held up as
the ideal.
I’ve heard from so many people who told me, “My dietician used to tell me that if I
didn’t have a cheat day every once in a while, I was going to be unhealthy. And I’m
so much happier once I heard you say that it’s okay to have none.” I’m this way
myself. It’s so, so, so much easier to have none than to have a little. You just forget
about it, there’s no temptation.
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Gary:
It’s the equivalent of saying if I never got to smoke a cigarette occasionally, I’d never
be able to cut back on smoking, and that’s ludicrous. No authority would ever
recommend such a thing. We know that something like cigarettes and alcohol, the key
thing is never to do it. You go cold turkey and stay cold turkey. Somehow, with
sweets, there’s this idea that you’ve got to allow yourself to cheat.
You can go back to animal studies in the 1930s where they demonstrate that you can
kill carb craving in animals by allowing them to eat high-fat diets, and you can kill fat
craving by allowing them to eat a high-carb diet. If that’s true in humans as well, then
the way to inhibit sugar and carb craving is to allow people to eat high fat diets. But
then they have to believe that the fat isn’t going to kill them.
Gretchen: Plus, when you’re really trying to eat fat without carbs that takes planning.
Gary:
Yes. Because if you go for the fat without the carbs, you’re getting rid of virtually all
processed foods.
This has to be kept in mind when people do clinical trials to study these phenomena.
Because processed foods have a lot of salt and sugar and refined carbohydrates and
fats, if I advise you to avoid any single one of these elements and you take my advice,
you’re going to get rid of most of them at the same time. I think this is why most
successful diets work, because one way or another, they prevent you from eating
processed foods—particularly the grains and sugars.
Then the question is: What should you really avoid? What’s really causing the
damage? Because when we eat whole foods, natural foods, we can isolate the harmful
ingredient—avoid sugar and refined grains alone, if they’re the ones that are causing
the damage.
Gretchen: Right. The question is, who’s the real culprit?
Gary:
And The Case Against Sugar argues that the real culprit is sugar.
Sugar (including, for all intents and purposes, high fructose corn syrup) is the cause
of insulin resistance. Once you become insulin resistant, you’re going to have
elevated insulin and blood sugar. You’ve now got metabolic syndrome, and you’re on
your way towards obesity, diabetes, heart disease, cancer, possibly Alzheimer’s, and
many other chronic diseases very common in western populations and very
uncommon in non-westernized population—not that non-westernized populations
exist anymore (outside of perhaps a few tribes deep in the Amazon).
What I’m arguing in this book is that the fundamental defect that’s associated,
perhaps causally, with all these chronic disease, including obesity and diabetes, is
insulin resistance, and the most likely suspect for causing this insulin resistance is the
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sugar we eat and drink. Get rid of the sugar, and you take away the trigger of all of
these disorders.
Gretchen: And the problem with sugar isn’t that it’s “empty calories.” Or that because it’s
delicious, you eat more calories than you burn. The problem is that there’s something
special about sugar and the way that it’s handled in the body.
Gary:
Yes. And particularly at the high dose of sugar we consume in modern societies, and
the speed with which we consume it. In soft drinks, juices, candies, cakes, breakfast
cereals, low-fat fruity yogurts, you name it.
Sugar has metabolic effects in the body that cause insulin resistance, and being
insulin resistant seems fundamental to all the diseases we’ve discussed. It’s not about
empty calories. It’s about the metabolic effects of these sugars.
A hundred calories of sugar does something profoundly different to your body than
100 calories of fat or 100 calories of protein. And I’m arguing that ultimately it
causes these chronic diseases.
Gretchen: At some point, you mentioned that this effect may be much more severe if you’re
drinking the sugar. Right?
Gary:
Yes, you’re maximizing the speed of delivery and so you’re maximizing the load, the
fructose load that your liver has to deal with.
In fact, I wonder how much of what’s happened worldwide was in fact caused by the
sugary beverages—the sodas and the fruit juices and the teas and the Snapples. We
thought the fruit juices were inherently healthy because, well, they’ve got all those
vitamins and nutrients in fruit, and we figured we could balance out the calories with
more exercise. But what we were doing was mainlining sugar, and even with
relatively massive amounts of exercise, I think the physiological effects eventually
catch up to you.
Gretchen: I could keep asking you questions for hours, but we’ve been talking a long time. This
has been fascinating. Thanks so much for taking me through your arguments.
Gary:
Great to talk to you.
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Gary Taubes is a health and science journalist. He is the author of several books, including Why
We Get Fat; Good Calories, Bad Calories; and most recently, The Case Against Sugar. He is a
recipient of a Robert Wood Johnson Foundation Investigator Award in Health Policy Research
and has won numerous awards for his journalism, including the International Health Reporting
Award from the Pan American Health Organization and the National Association of Science
Writers Science in Society Journalism Award three times. He is the co-founder of the Nutrition
Science Initiative (NuSI.org), a non-profit organization dedicated to funding and facilitating
nutrition research capable of resolving key controversies in the field. He was educated at
Harvard, Stanford, and Columbia. He lives in Oakland, California with his wife and two sons.
Gretchen Rubin is the author of several books, including the blockbuster New York
Times bestsellers, Better Than Before, The Happiness Project and Happier at Home. She has an
enormous readership, both in print and online, and her books have sold more than two million
copies, in more than thirty languages. On her top-ranking weekly podcast Happier with Gretchen
Rubin, she discusses good habits and happiness with her sister Elizabeth Craft. A graduate of
Yale and Yale Law School, where she was editor-in-chief of the Yale Law Journal, Gretchen
Rubin was clerking for Supreme Court Justice Sandra Day O’Connor when she realized she
wanted to be a writer. She lives in New York City with her husband and two daughters, and she
quit sugar and started eating a low-carb diet in March 2012, after reading Gary Taubes’s book
Why We Get Fat.
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