Why we get fat -- with Gary Taubes

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I'm Andrea Sanford from diet dr.com and
I'm here with the famous science
journalist Gary Taubes author offer a
very influential book called good
calories bad calories as well as why we
get fat and what to do about it so
thanks for being here ako andreas so
could we start by could you just give
like you I know you have so much to say
on the subject but could you give a
short summary of the answer to that
question why do we get help what should
we do love it ok I'm going to give the
short answer to the why we don't get fat
first we don't get fat because we too
much and exercise too little so this is
not just an issue of calories in versus
calories out somehow we just can't quite
get the right balance and the excess is
going in our fat tissue and the argument
that I make in the book which is based
on the way pre-world War two European
researchers saw this is that um you know
obesity is not an eating disorder it's a
fat accumulation disorder there's too
much fat on your body and if you look at
what regulates fat you know if we had
somebody walking down the street it was
eight feet tall had a growth defect that
doctors first thing they do is go geez I
wonder where the tumor is in his
hypothalamus it's making them secrete
too much growth hormone excuse me in
this pituitary gland on his hypothalamus
he's going to secrete too much growth
home and that's why he's growing you
know it's like you want to know what
regulates growth so what regulates
growth of fat tissue well fundamentally
it's the hormone insulin and if it's
hormone insulin then the problem is the
carbohydrates in our diet because they
more or less regulate our insulin levels
and so that's sort of your null
hypothesis that's what we should believe
until we have remarkable evidence to
reject it so why do we get fat because
the carbs we literally cause us to
secrete too much insulin through a
variety of mechanisms not just the same
mechanism and if we're secreting too
much insulin then we're storing calories
as fat the insulins locking way it's
suppressing fatty acid oxidation and the
lean tissue the net result is you get
fatter you get rid of the carbs you get
lean
that's sort of the simplest possible
explanation for this problem right so
what should we should do that's well so
they considering that if you remove the
carbs from the diet and you replace them
with the one nutrient that doesn't
stimulate insulin secretion which is fat
you should get thinner and lo and behold
we have make a hundred and fifty or
history of very successful low
carbohydrate diet books that remove the
carbohydrates and replace them with fat
I'm going back to the 1860s maybe that's
not the Queen Siddhartha maybe it's not
a coincidence so it's sort of you know
just on that level that's a pretty good
reason to believe and then of course
this is and you don't have to take my
word for it anyone could try it for
themselves it's a great thing about
weight problems it's not like if you're
trying to get a diet to prevent heart
disease excuse me you have to do it for
40 or 50 years and you still don't know
when you get the heart attack or don't
whether the diet did it when you have a
symptom excess weight you can do the
intervention remove the carbs add back
fat instead and see what happens and a
if nothing happens in six months and
either I'm wrong or it doesn't work for
you we don't know which but certainly
one of the two is true but if it does
work it doesn't actually even matter if
I'm right you know it's one of these
things where you can actually test it
yourself and see if by paying attention
to human biology and the physiological
regulation of your fat tissue if that's
actually the secret to losing weight
getting rid of the fat you've
accumulated so it's easy to test for
yourself and a lot of people are doing
that I'm sure right now a lot of people
are doing it yeah and a lot of people I
mean again it's hard to tell from the
person like our perspective you probably
get emails from people you have these
wonderful successful emails excuse me
you get a look of those I I mean again
it's hard to quantify a lot like this
dean ornish get a lot of them that's
always an interesting question I I want
to say Dean do you get the kinds of
emails I do where people say you know
thank you I've been Toby
for 30 years I'd struggle and couldn't
understand and then finally you know I
ready to print them out to see you after
because well you also have to did the
type do they get a different type you
know because that's the problem with it
recently there's a very influential New
York Times used to be a food writer now
he's a health writer Mark Bittman mark
is wonderful cookbooks the kind of
vegetarian Lean bent in his diets and he
recently did a couple of blogs we talked
about how when he gave up dairy products
and milk his health improved remarkably
so the first blog talked about all the
reasons you know how what happened with
him personally and how great this was
then he got you know hundreds of
comments an email saying the same thing
happened to me and then his second
column was look how universal this
phenomenon is and my argument is you
know he could have talked about how
meeting space aliens had improved this
Crohn disease and he had gotten
thousands emails saying I met space
aliens and they improved my Crohn's
disease too we should because there's
such a strong selection bias you'll find
everything yeah it's just you so you can
find out maybe meeting space aliens does
improve Crohn's disease in which case if
you can find one you could find out for
yourself but it could be a placebo
effect it could be a delusion maybe the
Crohn's disease just happened to go in
remission when you met the space alien
so but for that you need a randomized
control trial to find out if it works
for you even if it is a placebo effect
who cares when it comes to low carb
diets there are a few good randomized
controlled trials right there are a lot
of good randomized control trials and oh
I don't know how good they are because
they tend to be fish I do know how good
they are they're not very good but under
the caveat that they tend to be free
living studies so somebody will you know
get two hundred subjects randomize them
into two groups or three groups I'm
going to be giving the Atkins book and
some counseling and want to be given
Ornish's book and some counseling and
want to be given like the aah a
pamphlets American Heart Association
pamphlets in it
they'll be sent off into the world the
problem is they don't particularly stay
on the diets but you still almost
universally see greater weight loss with
the carbohydrate restricted diet and
better health markers but our heart
disease risk factors on this diet that's
supposed to kill you so it's a really
good sign even though the compliance is
terrible in these Stud I mean looks to
be terrible again usually the
researchers don't document how bad it is
but if you look at how weight changes
triglycerides other biological markers
of for instance carbohydrate consumption
HDL in particular it's a pretty good
sign that by the end of the studies
everyone's pretty much collapsed back to
whatever they were eating when it
started so it's basically it's hard to
tell someone to eat in a specific way
send them home and expect them to do
that for carriers I don't know how hard
it is it's an interesting problem
because you're one of the if you don't
really understand why the diets work you
know so say you got five thousand
smokers and you wanted to test the best
way for them to quit and you were
testing like nicotine patches versus
nicotine gum versus cold turkey but you
didn't really believe cigarettes were
bad for you you probably have a higher
failure rate on all three methods and
they might all appear to be pretty much
equal because everyone would go back to
smoking as opposed to being able to
graphically illustrate to these people
that the cigarettes are killing them and
now you're still gonna have a pretty
high failure rate but there is my future
but you have a fighting chance so in
these studies one of the problems is
that they don't really know why the
diets were there's no understanding
among the researchers if what's really
happening here they're not making the
argument look to you guys carbohydrates
are making you fat we know this beyond
the shadow of a down and to you guys we
got a fat is making you fat we know this
beyond the shot of it down and the only
way you're ever going to be lean is
never to eat fat again the only way
you're ever going to be leanest every
carb
again if you can convey that with equal
sincerity and equal passion to both
groups because let's say if you're the
researcher and you only believe the carb
story then you're going to be really
convincing to the carb people but you're
going to be less convincing when you're
making it up to the fat people and so
you're going to get a better effect in
the carb group just because you can have
a better intervention and one of the
things you have to do in these
randomized controlled trials is balance
interventions the difficult thing to do
these studies and so you have to take
someone who believes that the healthiest
diets are low fat diets to convey that
message to your low fat group somebody
believes that the healthiest diets are
low carb diets convey that message but
the low carb guy might be better
we should have exotic with you in one
arm and either one is you know there
well that's kind of what you need except
that what if Dean is better more
convincing than I am they never know
what if I'm more convincing than Dean
then we're going to get in a benefit in
the low carb group because I'm a more
convincing communicator these studies
are very hard to do but still they do
show trendy but when they're done anyway
they tend you know and again it's not
just the better weight loss but and in
the first six weeks to two months when
people are really sticking to the low
carb diet and they usually give an
advice at F two months I can start
adding carbs back while they're in
what's called the induction phase their
weight is plummeting then they start
adding the carbs back and they start
plateauing and then their weight starts
creeping up again again it could be
similar saying we want you to quit
smoking so we're going to go cold turkey
and then after three weeks or six weeks
when you comfortably quit then you could
start smoking in moderation good luck
with that and good luck with that yeah
and yeah these are the kinds of issues I
address and why we get fat like is maybe
it's better just to stick with the quit
smoking period even if six cigarettes a
day is harmless and isn't going to give
you a lung cancer or heart disease it
could be a ticket back to smoking two
packs a day because
these you know once you open the door
you have problems until maybe for some
people complete abstinence is better but
this this idea that carbs and insulin
make you fat that's kind of
controversial still and a lot of people
are claiming that in fact insulin has
nothing to do with weight gain what do
you say about that again it's so when I
use a phrase no hypothesis like the
simplest possible hypothesis is you know
we know that insulin to a great extent
determines fat accumulation and fat
cells we know the carbohydrates to a
great extent determine in some levels I
mean other protein stimulates insulin
and actually dietary the more fat in the
diet the lower the insulin secretion we
also have this hundred some-odd your
history of the idea that carbohydrates
are fattening and the success of
carbohydrate restricted diets and so to
me that should be the null hypothesis
the hypothesis that you need remarkable
evidence to reject now you can find
studies in the literature that say
effectively anything you know one of the
advantages I had as a science writer if
it was an advantage was in my second
book was about both my first two books
were about the discovery of non existent
phenomenon with the second book that's
this cold fusion phenomena was ludicrous
on the surface was like 50 orders of
magnitude greater effect than could be
explained by physical law you know it
almost could use it as a defective
definition of impossible and yet after
one group professed to have discovered
it and another group started to try and
steal it from them other groups actually
came up with replications and they were
all wrong you know it needed really
rigorously well-done research to
demonstrate this was all just bad
science and the world is full of you
know experiments it seemed to show
something and seem to show something
else and so one of the things everyone
does including the best scientist when
you're in this business you do sort of I
believe this should be true and I can
reject these experiments this is you
know because it's just very likely they
were just done poor
little sloppy or the they were
interpreted to confirm what the
researcher thought was true when they
really didn't show one thing one way the
other on the null hypothesis the
insulins regulating fat accumulation you
know nobody really disagrees with the
role of insulin on fat aqui there are
other hormones involved obviously stress
hormones are involved texts or moans are
involved but the trigger from the diet
and you really want to get remarkable
evidence to disprove that and then the
question is what do you call remarkable
writes okay could I come up with a few
objections sure one that's often voice
is that that insulin is really a satiety
hormone that's what a lot of obesity
researchers believe if you raise insulin
you feel satiety you eat less oh yeah
and it's quite partially true and it
makes a lot of sense that in the brain
insulin is a satiety hormone if you
infuse it into this repro spinal fluid
of primates which is what these
experiments will do it will suppress
eating but it makes perfect sense that a
hormone that in the body works as an
anabolic hormone to store fuels in the
brain as a negative feedback loop to say
hey look for storing fuels that means we
could we're eating and we could you know
start the process of suppressing eating
behavior because we know we're eating
and we know we're doing the things we
want to do with the fuel that we're
getting so this makes perfect sense they
too don't preclude the other but when I
was doing my research for good calories
bad calories this idea that obesity is a
that insulin is a satiety hormones it
took the group that came up with that
idea woods and Steve woods and and I
think Don port and Michael Schwartz they
fought a terrific battle for like a
decade to get the research community to
accept it and they eventually won but
what they people forgotten the process
was that in the body and the periphery
insulin is a storage hormone you know
and it is there's no that to the point
that when I was I remember one interview
I did in my book with the head of the
Joslin Diabetes Center at Harvard
Medical School just
we are arguably the most preeminent
diabetes research center in the world
and I asked him what the role of insulin
was and he said well it's a satiety
hormone in the brain I said in it but
what about in the body
it's the fat storage hormone among other
things and if you look at you know
Johnson's diabetes textbook produced you
know published by your Diabetes Research
Center that's one of the rolls it talks
about and you have this problem with
type 2 diabetics that they get insulin
therapy they get fatter independent of
sort of increasing calorie consumption
and his response was oh yeah that's a
good point I kind of forgot about that
you know so the idea that society
there's research showing it's a satiety
hormone but that doesn't negate what you
want to do is negate the research
showing that it's a fat storage hormone
as well so it could be both in our a
part story I mean by the homeostatic
feedback mechanisms I want one that does
one thing in one place is like them
likely to do an opposite thing you know
they have a negative feedback loop to
which you know is a great great design
like this whoever designed that should
get credit for it but to consider what
it does in the brain to negate what it
does in the body is just sort of weirdly
naive and is indicative of this kind of
drunk in the streetlight approach to
research where you pay attention just to
that one thing you're doing research on
and then you forget that there are these
other people for example the brain and
you forget that there's a body and the
problem is in the body and you know so
moving on to another common objection
not only carbs secrete insulin in the
body right it's also if you have protein
for example whey protein milk protein is
is very incidental genic meaning it
releases insulin to the bone there
there's one study that everyone cites
with the Jenny Brand Miller study from
the late 90s where the protein sources
they use were extremely low fat so
trying to I assume they were trying to
you know to detect the effect from
protein and they yeah they got
significant insulin secretion but even
at one group when they publish an
article looking at mixed meals
and insulin a decade later shall look at
see ya the protein effect basically
washes out and that's the the presence
of fat that suppresses insulin as much
or that that tracks with low insulin
secretion as much as the presence of
carbs determine science and secretion a
more important question could be what
causes insulin resistance it's not just
the insulin secretion that's a problem
it's the relative insulin sensitivity of
the lean tissue to the fat tissue it's
the sort of different enzymes the LPL
distribution on there's a lot of
variables involved in this you know
insulin like when I talk about it
simplistically it's insulin insulin
insulin just like when we talk about
type 2 diabetes there's a whole host of
factors involved I mean you could argue
a virtually infinite number of
relationships between enzymes and
receptors and pancreatic beta-cells and
the nutrients ultimately it's an insulin
signaling disorder and we're happy with
that we can treat it knowing it's an
insulin signaling disorder leptin it's
obviously involved right but we don't
really care that much and type-2
diabetes although if we got left and
involved and we understood it maybe we
could craft drugs that would do a better
job of treating the disease but
fundamentally it's insulin and type 2
diabetes in obesity are so tightly
linked that people consider them two
sides of the same disease like diabetes
insulin and the other is what leptin
resistance some eating too much you know
it's just no hypothesis I mean right now
what are we going to believe until you
mentioned leptin which is also a common
objection people saying that insulin has
nothing to do with obesity because
obesity is simply a matter of leptin I
don't think they say insulin has nothing
to do with it but they do say because
leptin is obviously involved that
somehow seems to negate the influence of
insulin
and it seems weird because no one's
disputing that cortisol for example
stress hormones so connected to obesity
or thyroid hormone but when it comes to
insulin
some people don't you know it's a
difficult again it's hard to talk about
this without singling out individual
research there's a lot of people the
ideas come from a few sources and the
few sort you know the problem with
insulin is if you talk about let's just
look at let's take a Kate let's say we
have a growing child and that child is
getting taller and getting fatter it
will make it a girl so she's getting
fatter but she's also developing
sexually so fat is going specific places
on her body and here's my fundamental
issue with leptin is you know as a
hormone that's regulating energy intake
or suppressing you know hunger we know
that that this child is taking more
calories and she expends because she's
getting bigger and she's getting bigger
in some places altom utley one way the
other the something has to be
determining where the calories go and
how they're used are they used for
energy are they go to fat they go to the
breasts which are developing or the gut
that's getting fatter are they going to
the bones and the muscles in the lean
tissue that's growing and extending
something has to decide how the fuel is
used just the idea that the body has
some preset number so it knows how much
to spend on this growth issue and the
sexual development issues and what's
left over get to the fat seems to me
kind of naive at some level the tissues
themselves have to be taking what they
need it's not as simple as looking at
calories in and calories out no because
it's because the calories can go to
different uses the example I just gave
you happen to be someone where they're
going to multiple you know different fat
depots different amounts of fat
different lean tissue bones your all the
things that are growing plus all the fat
tissue that's expanding through things
regulated on the it's got to be locally
regulated as well I mean they're
obviously systemic you know arguments on
that case even the sex hormones wouldn't
be secreted by the brain while the brain
might have some role in stimulating the
sex hormones to secrete them but they're
not coming from the brain they're coming
from other areas of the body you know I
used to say you can cut this after I say
it but one of the effects is men get
older their brains move slowly above
their waist moves north the older you
get um you know but these are the issues
so at some level ultimately the tissue
itself and the hormonal signals on that
tissue have to be working together to
decide whether or not that cell like a
mammary cell versus a you know abdominal
fat cell are going to take up the excess
nutrients that are always in the
bloodstream anyway there's got to be
some thing ultimately there and the
problem is if you want to put obesity in
the brain and this is one of the
fundamental arguments I have against you
know these ideas is then you have to
still figure why is it why do the
calories go into the fat tissue now
we've established we've created positive
energy balance we got more calories in
the body than we need but now they have
to end up in the fat tissue maybe there
are like no no it's good they are they
are there are nervous system impulses
that will do so the central nervous
system does play a role in fat
accumulation the thoth of these other
hormones so the tendency is to ignore
refute the other hormones you don't have
to pay attention to that so we can put
everything in the brain and then it
becomes this focus there's a lot of a
lot of beliefs in the field that played
very useful roles to refute quacky with
the establishment research considered
krakozhia ideas like the idea calorie is
a calorie was very effective in refuting
the notion that particular diets have a
unique ability to reduce weight because
that's what the diet doctors were
pushing you know if he ate a low-fat
diet fats particularly fat
carbohydrates are particularly fattening
so we don't like quack diet doctors we
think they're quacks so if we argue that
every calorie is identical we can use
that as an argument but then they get in
this trouble or even the research
community tends to think sugar is pretty
bad but now they've already set up this
argument that a calorie is a calorie
another stock so now what do we say
about sugar because we have a definitive
we know it's metabolized differently
than pure glucose or fat or protein
they're all metabolized differently but
we've established that the only effect
they could have on obesity is through
the energy they carry in a calorie is a
calorie so we're trapped in our sort of
argument and now we have to figure out a
different way to implicate sugar that
doesn't actually involve the biological
effects of these compounds when they get
into your body like how your body
metabolize them and how it responds to
them which is crazy if you think about
it at all it's often said that the
liquid calories are sort of processed
differently like if you're doing sugar
so don't for example it's not that it's
not that the calories are different it's
just that it's in liquid form and that
makes it sort of and this is one of the
interesting things is why shouldn't the
speed of delivery have an effect on the
body's response you know if I lean on
you I could probably apply 50 pounds of
pressure by you know holding my hand up
against you gently for relatively gently
for an hour and the accumulative
pressure will be 50 pounds of pressure
or I could apply 50 pounds of pressure
in a second by punching you one's
damaging the other is not I don't know
if I have the unit's right there by the
way of you know in your argument I get
it but that's a thing so it's sort of it
makes prey it seems perfectly natural to
assume that the speed of delivery speed
of which these things hit your
bloodstream your liver your pancreas are
going to have an effect even the blood
sugar on your lean tissue on your muscle
cells how quickly it's delivered or I'm
going to have an effect on how the body
the organs the cells themselves
to respond and you know I'm actually
beginning to think maybe a huge amount
of the problem is that the calories and
sugars are coming in liquid form and not
over fest and so very fast you can
digest it quickly you know you think
about the difference between drinking
beer and eating the equivalent amount of
you know barley if you may in a malt but
again it's so anyone just denying that
out of hand seems kind of naive and
biologically naive and why shouldn't
make a difference part of what science
is examining all all alternative
hypotheses and ask yourself you know it
doesn't make sense does it pass this
sort of forget what the term the
physicists used to use you know like the
idiot test and if it makes sense how do
we test it right you know how do we try
and determine whether you know it has an
effect that I'm curious about some of
the recent randomized control trials of
sugar they compare for instance sugar
sweetened beverages to glucose sweetened
beverages but normally evolutionarily we
would never have drank glucose any more
than we would have drank fructose or
sucrose or high fructose corn syrup so
maybe even the putting the glucose in
liquid form changes the way our bodies
respond to it and these you know they
did researchers hate when you say this
because you've just made their life more
complicated like it's complicated enough
this is science so it's getting really
complicated yeah I want to ask you a
very simple question which is also a
common objection to this whole
carbohydrate insulin obesity theory
what about Asians like Japanese Chinese
people eating a lot of rice or other
cultures eating a lot of high carb diets
basically without obesity well this is
and you know it's an obvious question
because you have in my book my lectures
I present evidence here you know poor
populations sort of third-world
populations with high levels of obese
our poor populations with very low
levels of obesity and the ones with the
bee city have a lot of diabetes and the
ones without obesity or very little
diabetes so the question is um how do
they differ and there are two things in
which they do first like the Asian
populations eating high for instance a
lot of rice high carb diets have been
doing it for thousands of years so maybe
they had time to adapt maybe they had
their obesity and diabetes epidemics
2,000 years ago hence buddha was not a
particularly lean individual you know um
and then there's a sugar content these
are two most obvious things and the
sugar content of the diet so Southeast
Asians have very low sugar consumption
Caribbean Islanders for instance have
higher sugar consumption they're working
you know a lot of them have been
imported as slaves or indentured
servants to work on sugar plantations so
maybe that's the difference
and what would sugar do well we know
that the fructose component is
metabolized in the liver and there's
evidence that fructose causes insulin
resistance at least when consumed in
sugar sweetened beverages and once your
insulin resistant then you're going to
secrete more insulin to all the other
carbs in the diet so maybe it's the
presence of sugar that turns a healthy
low-carb diet into an unhealthy low-carb
diet but does it refute the role of
insulin now it's kind of like saying
here are populations that have no lung
cancer and don't smoke cigarettes
therefore cigarettes can't be the cause
of lung cancer wait we didn't smoke
cigarettes
um actually that's a lousy metaphor
because a cigarette you'd still need the
sugar to trigger it and we don't have
something like that for cigarettes and
less sugar causes cancer as well in
which case it would be interested TV you
have the Japanese I do believe have like
the highest smoking rate in the world I
wonder what their lung cancer rates are
like actually one of the interesting
findings I did while researching good
calories bad calories is that the French
women in the late 1990s had the fourth
lowest rate of
lung cancer of any population in which
was measured and that's pretty amazing
because I lived in Paris in the 80s on
the late 90s and there was on smoking or
home there's a lot of cigarette smoking
going on matter of fact if I ever get to
move back to Paris I'll probably take up
smoking again but how could they have
such low rates of lung cancer when I
suggest ask that to lung cancer research
or is it like the American Cancer
Society their attitude Belle was who
knows you know it could be anything my
attitude it's in the anomalous evident
data that you find that you can expand
your theories and find out if your
theories are right so when you find
something that doesn't fit with what you
believe to be true finding out why is
very important to judging the worth of
your theory you know when the reason we
believe that smoking causes lung cancer
is because we can find populations with
high levels of lung cancer that don't
smoke cigarettes don't use tobacco I
mean I don't know about its bestest
workers and asbestos factories but if we
could find populations with high levels
of obesity and diabetes that didn't
consume sugar that would be interesting
now you've started a few of the theory I
personally don't population know but
they they could be out there that's a
refutation that's a black swan let's see
what I see if you can't find it well
again I said okay are you with me I
haven't looked hard enough because I'm
too much in love with my theory um of
course finally last one last objection
some people are saying today that
obesity is all about food reward it all
happens in the brain the some foods have
high reward values I mean meaning that
we can't basically stop eating them
and we too much while other foods is
that with food reward means I'm not too
sure I understand what food reward means
but I think the people who think they
understand would argue that that's tell
me what one of the things food reward
does but food one of the things you have
to
to explain is obesity in populations
that are food deprived the importance
with a lot of malnutrition some
starvation and yet for instance obese
mothers so they you can argue that they
could not have been eating too much of a
food they didn't have enough food
available so and a lot of obese people
don't aren't out there at McDonald's
sucking down 32 ounce sodas because they
can't stop themselves they can stop
themselves but there's still obese so
you need a theory of obesity doesn't
require having excess rewarding food
around to me and you need a theory of
obesity that doesn't require that we
define a food is rewarding by the
presence of obesity in that population
seeing one of the things we all hear is
people who go on paleo diets or low very
low carb diets you know I I find
porterhouse steak slathered in butter
very rewarding and I could eat enormous
quantities of them and I won't get fat I
just I don't believe I'll get fat so why
isn't that rewarding and say the
equivalent amount of ice cream is and if
it's because and then let's say I will
get fat on the ice cream I'm going to
assume I will they don't need it anymore
so I don't know but I used to and I used
to be fatter so what's the difference
between the two is it their effect in
the brain that that ice cream is
rewarding and it's sealing my
hypothalamus there's a lot of rewarding
food out there so expand my fat stores
which is possible but then we have to
know why the fat stores are expanding
like what is the hypothalamus doing is
it central nervous system connections it
doesn't have to use any hormones way
through the sub-point some people
sitting okay so it's raising the
setpoint how is it doing it I'm of
course it causing insulin with is it
causing insulin levels to go up because
I pyth Alamos is hardwired to the
pancreas to the vagus nerve so it can
stimulate insulin secretion and
resistance could be increasing leptin
resistance which would build I think
it's a leptin resistance again it gets
complicated
but the problem is what is let's say
just say we have this hypothesis that
some foods are uniquely fattening other
foods aren't so the foods that are are
fattening because they stimulate
metabolic and hormonal effects in your
body that work to store calories is fat
and we know that car bread sugar rich
foods do this in different ways
maybe those foods are make us crave them
ok because in if they're stimulating
storage they're not being available for
oxidation all right and we want to eat
to get energy in theory so if we're not
getting these fuels oxidized because
they're being locked away in storage
maybe we'd more of them to fill the void
so you can come up with a hypothesis
that says foods that simulate fat
accumulation our foods that our body
craves because they're foods that tend
to get diverted to a source other than
what we want to use them for so we don't
get the energy we need from them so we
have to eat more and now we have to
refute that hypothesis because that's to
me what science is and maybe it can be
done but like I said ultimately I want
to know why these calories go into the
fat tissue so even if the food's very
rewarding cool but you know why does it
end up in the fat tissue and we all know
we've all had this experience personally
that a food that's rewarding when we're
young like a coke when we're 20 won't
make us fat and that one we're 35 it
might so the rewarding properties
haven't changed but something's happened
in the 15 years that we've gone from
being 20 to 35 it's a common experience
with obese people that they can't eat
foods that used to be able to eat or
they can't eat the amount of food that
they used to be able to eat so what's
changed and is that changed in our brain
or is it changed in our body the
problems in our body so it would be the
first place I would look I mean the fat
is in the body um so what do you think
well I mean I obviously I think you know
is the
the body is where the primary effect is
that's where we find that I mean that's
where the probably where we'll find the
primary cause not that the brain isn't
involved but it's part of this sort of
complex homeostatic web of feedback
systems and you can break that web by
the way you can sever the hypothalamus
and have a defective left and you know
weed in system and you also have hyper
secretion of insulin when you do that
you know the interesting thing would be
if you infuse back enough leptin so that
lesion the hypothalamus is still sensing
the left then do you still does that
stop the hyper secretion of insulin does
that mean that leptin somehow primary
but when you do those kind of
interventions you're breaking the system
you know we break systems on you things
are going to find different yeah it's
very hard to you know you'll conclude
the causality based on your
preconceptions so then we go back to
null hypothesis like insulin regulates
fat accumulation or it's permissive of
fat accumulation whatever you want but
you raise insulin you're going to get
fat in your fat tissue and carbohydrates
stimulate insulin secretion low carb
diets work so where do we go from here
if that's the null hypothesis well again
one of our goals and this is where we
you know is to set up an organization to
test all this on I think their
experiments have been done and so I'm
going to talk about in my talk tonight
which can disassociate calories consumed
from fat accumulation you could do this
in animals effortlessly it's not
considered relevant so let's do it in
humans let's demonstrate for instance it
you could increase or you could keep
calorie intake constant and cause weight
loss by changing the mackinder GenCon to
the dye and doing it significantly
enough that you know you've changed
insulin signaling significantly and the
key is keeping calories high because
argument is that
it's not about how much you eats about
what your body does with what you eat so
we don't really have to we don't have to
lower the amount you eat we just have to
change the hormonal singling to your fat
tissue and if we keep the man you eat
what it always was we should be able to
show that macro nutrient composition has
a large effect on fat accumulation
independent of caloric intake that would
be an interesting study yeah and it's
not a hard study to do it's a hard study
I mean it's the setup is simple you have
to get people to follow the diet and you
have to prove that they ate everything
you gave them because when you write up
the paper and you say we fed this guy
3000 calories and they lost 30 pounds
reviewer is going to say that's
impossible right because I believe that
in order to lose 30 pounds you have to
lose weight you have to eat less so
obviously they need what you gave them
you have to be able to prove that they
3000 calories
another way to do it which is what this
fellow David Ludwig did recently is if
you measure energy expenditure they lose
30 pounds their energy expenditure has
to go up significantly so now in theory
you don't even have to measure intake
all that well you have to do a show that
they lost weight and increased energy
expenditure because that also
contradicts the current beliefs which is
that whenever you lose weight your
energy expenditure always goes down to
compensate so there are ways to do the
experiment that are very rigorous and
expensive in ways that require a little
less sort of monitoring in the subjects
to proving they did exactly what you
tell them to the way we do experiments
now like says we tell people to follow
different diets and we give them some
counseling and then we measure the
effect of telling them we don't actually
measure the effect of being on these
different diets and what we have to do
is measure the effect of being on the
diet because that's what we're
interesting that then tells us what
actually causes obesity to begin with so
let's hope those experiments get done
gets done on the
and the mayor we can stop people from
getting fatter
well this is the argument ten years from
now let's not about it let's not have
anything to argue about you know I think
to some extent that's possible to some
extent people argue about diet
regardless of the evidence so it's like
religion you know presence or absence of
evidence doesn't really affect people's
beliefs to a large extent but people
stopped smoking from the 1950s until now
most people did anyway yeah no they did
and that's what we hope that we can
convince enough that if we're right
these experiments will confirm them and
then with the experiments with enough
sort of public advocacy political you
know getting people to really pay
attention to this data why these
experiments were done what the purpose
was get them to understand the
experiments prior to the experiments
being done getting them to give us their
feedback so we can say his experiment
you predict this will happen you know as
I'm talking to a leading obesity
researcher you think this will happen
and we think this will happen let's
assume we get this how are you going to
talk yourself out of it what are you
going to say we didn't do right here's
the experimental details here's what
we're going to measure here's what we're
going to feed them here's how we're
going to monitor them you know this is
what we're going to be able to provide
you as evidence and now we're going to
give you something that's equivalent of
telling an atheist that God showing
proving to an atheist that God exists or
to a god-fearing person that he or she
doesn't yeah how he has you doing what's
your response going to be because if we
can figure out what's what you're going
to criticize about the experiment in
advance which could be a correct
criticism could be a valid morning can
we build that into the experiment so
that at least we know that that point
has been addressed as best we could you
know let's build these things in an
advance I know my own complaints about
how these experiments are done and it's
very difficult when you're using real
humans you can but to account
away from it right if you go and improve
what happens in humans this is tested on
humans you know what I learned in my
history you know the advantage I had
being a science journalist covering
these non-existent phenomenon my two
books are about non-existent phenomena
so I'm dealing with excellent
experimental physicists nuclear
physicists nuclear engineers chemists if
an experiment is an ironclad you don't
know if you foot you don't know how to
interpret it you know you don't know if
you are preferred interpretation of the
evidence it's a correct one you can
suspect it but you just don't know if
it's true and so the keys expand you
can't do ironclad experiments with
humans in the world won't let that
happen
and even if you could do it it would you
know treat them like geese that you're
making foie gras out of then you're
creating an artificial situation because
you're you know constraining them so
they can't be physically active so the
question is how do you do it well we do
the very best job we can so far the jobs
people haven't cared it's like they have
a different they really are concerned
about this issue like if we tell
somebody to follow this diet will that
be beneficial you know they not they
don't think that there's an issue about
what causes obesity is a calories is it
that's not what they're interested in so
we got to get them to think differently
as well and to do that we have to engage
with them on a level where you know we
can sort of get them to understand the
points that we've been making so this is
a complicated business so we're going to
be discussing this for a long time I'm
sure yeah you know at least think we got
a decade at least although the funny
thing is like I think sugar I can
actually see the sugar situation tipping
I mean the power of the sugars the
beverage industry and the sugar industry
is so strong that it's hard to imagine
the government's really getting behind
it but the idea that sugars just bad for
you you shouldn't consume and your kids
shouldn't consume it that's that's going
to that I think that's going to tip I
think it is tipping like tobacco like
tobacco
it's not like we can buy cigarettes at
every convenience store
we just don't buy them right um I was
talking to a law professor at Berkeley
who's been involved in the regulation
tobacco regulation for a long time and
he said you don't we can get like nine
ten percent of smokers it's the best you
like the smoking levels down to nine ten
percent that's like the best you're ever
going to do you're never going to reach
those last ten percent for whatever
reason they're just until we can get
sugar consumption down but from the
smoking that means they cut smoking by a
third or so maybe even you know eighty
percent since the 1960's if we can get
sugar down by that level that would be a
major I think it would be a major public
health breakthrough I think so too
yeah let's let's hope for it well let's
see what happens you have to do the
research thank you so much for the
interview
well thank you Andre

Why do we get fat -- and what should we do about it? Conventional wisdom says eat less, move more. The problem is that this advice rarely works very well. Science writer Gary Taubes has spent the last decade finding a better answer. His book Good Calories Bad Calories has been very influential, changing the minds of many. Here Taubes discusses his controversial theories as well as the criticism of them. Why do we get fat? The blog of Gary Taubes: http://garytaubes.com More for your health: http://www.dietdoctor.com More similar videos: http://www.youtube.com/playlist?list=PL9E35F689C3F67D03

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