Diet Doctor Podcast #12 — Dr. David Ludwig

Diet Doctor Podcast #12 — Dr. David Ludwig

Welcome to the DietDoctor podcast
with Dr. Bret Scher. Today is my pleasure to be joined
by Dr. David Ludwig. Dr. Ludwig is a pediatric endocrinologist
at Boston Children’s Hospital with affiliations at Harvard and he’s the director of the New Balance
Foundation Obesity Prevention Center. He’s also the author of “Always Hungry”. And Dr. Ludwig has great experience
both as a clinician taking care of children and seeing the epidemic of obesity
and type 2 diabetes affecting children and also he’s very involved in research and sort of helping us understand
the problems and complexity of nutritional research
and helping change the paradigm of how we can fund and design
nutritional research studies to make them more worthwhile so we’re not relying
on poor epidemiologic studies and we’re not relying
on industry funded studies as well. But trying to bridge that gap of industry
in the sense of food production but not biased industry
with a stake in the outcome combining with research to really help us
answer this question. The questions of, “Is a calorie a calorie?”
or the carbohydrate-insulin model. How does that affect us as individuals
in the free living world and how does that affect our health? And ultimately how can that affect
our policy to help us stem this epidemic of diabetes,
obesity, chronic health disease and help us reverse that course? Now David is a source of reason in today’s society with so much polarity,
with science being more like religion, with people so steeped in their own beliefs
that they’re not willing to see the other side, David tries to help bridge that gap and say,
we’re all fighting for the same thing, we all want to improve health. How can we foster this conversation so that
we can have a more reasonable debate, a more reasonable understanding
of the situation to find a solution? So I hope you get that from his message
and I hope you appreciate it as much as I do. Enjoy this interview with Dr. David Ludwig. Hi, everybody. Before we get to the interview
with Dr. David Ludwig I just wanted to give you a quick update. We filmed this interview
at the very first weekend of November and two weeks later
his study was published in BMJ. So when you’re a researcher
you’re not supposed to talk about your study until it’s been published. So unfortunately during the interview
we reference the study a few times, but can’t get into any details
because it hadn’t been published yet. But now that it’s been published I want
to give you some of the details about it so you have that in your brain
as you’re listening to this interview. Now in my mind this was one
of the best studies done to look at the quality of calories
and how it affects energy expenditure. What they did was they took 164 adults
with body mass index of 25 or greater and they had a two-week running period where they all had the same diet,
all lost the same amount of weight. Then he randomized them
to one of three groups, 20% carbohydrates,
40% carbohydrates, or 60% carbohydrates,
keeping the protein fixed, so the only variables were the fat
and the carbs, but here’s the best part; they supplied every single meal
to the participants over 100,000 meals and snacks
costing more than $12 million. And that’s what I think one of the biggest
strengths of the study, because it takes away one
of the largest variables in nutrition studies which is what do the subject actually eat? We can recommend whatever we want,
but what are they actually going to eat? With this study they supplied the food,
so we know exactly what they were eating. And it’s a great example of the way
nutrition studies should be done. Well, what did they find? They found that the group that ate
the lowest carbs, the 20% carbohydrates, compared to the highest, the 60%, the lowest carbs expended somewhere
between 200 – 260 cal more during the day, their energy expenditure went up without more exercise,
without more physical activity. Their energy expenditure went up. And if you look at the subset that had
the highest baseline insulin, they went up by over 300 cal per day. So the conclusion is pretty clear. The quality of calories do matter and it does
make a difference in your energy expenditure. Just 300 cal a day can make a tremendous
difference in overall weight loss. So in my opinion this was one of the best
and most well done studies to look at this question
with a pretty clear answer. Right now with those details we can go on
with the interview with Dr. David Ludwig. Dr. David Ludwig thank you so much
for joining me on the DietDoctor podcast today. Pleasure to be with you. Now as a pediatric endocrinologist you have had a front row seat
to this evolving tide of obesity and diabetes and as an adult doctor
I see it and it’s awful. But as a pediatrician
it must be heartbreaking to see this evolution of this disease
just take off in front of your eyes. Well. Indeed it is. This is a generation
that has excessive weight more of it from earlier in life
than ever before and the consequences to both body
and emotional well-being can be tragic. Right. Of course there has been lot of attention
to type 2 diabetes in adults, but children are now getting
type 2 diabetes. This is unprecedented. When I was training
as a pediatric endocrinologist type 1 diabetes was 90% and occasionally
I’d see a case or two of MODY, some of these rare genetic causes of
diabetes. But at least among adolescents type 2 diabetes is about a third
in minority populations. Type 2 diabetes can be half
or more new onsets. Yeah. You know think about it that it’s one
thing for an adult who’s gaining excessive weight
to develop type 2 diabetes at age 50 and then suffer heart attack, stroke
or kidney failure at age 60, and that’s bad enough. But if the clock starts ticking at age 10, we’re talking about
a profoundly different situation. Yeah. I read that the diagnosis
of diabetes at age 10 has a worse outcome
than the diagnosis of leukemia. I mean that kind of puts in to perspective
as to how serious this is. And I mean we can point to a number of
different reasons as to why this happened, but it seems like the primary one
is processed foods, sugars and just too much of it. Now, a lot of people focus
on the sugars themselves and some people focus more
on sort of the glycemic index. Now not to put you in a box, but you seem to be
more of the glycemic index camp. Is that true?
Or tell me a little more about it. But that would be
a bit too much out of the box. But stepping back a little bit more, there’s certainly no consensus
that sugars or processed carbohydrates, whichever side of that box one is in,
is in fact the cause. At least there’s no consensus
among the conventional nutrition community. The basic teaching is that all calories
are metabolically alike. The main problem is obesity and we just
have to get people eat less and move more, they’ll attain a healthy weight
and the problem will take care of itself. Now, that’s of course
disregarding much evidence that food independent of its calorie content
affects our hormones, metabolism and even the expression of our genes
in ways that would importantly influence not just the likelihood that we would succeed
with weight loss, avoid obesity, but also risks for type 2 diabetes,
cardio-vascular disease, even cancer at any given body weight. So for those of us
who are in this camp of understanding that it’s more than just eating less
and moving more it’s almost mind boggling that the sort of mainstream dietary
community does not embrace that. So that’s when we have
to look to the science, and say, “What does the science say?” And you and your group did a study
to show that calories do matter and so, you probably know
the details better than I do, but you had 21 overweight patients, and you had a running period
where they had a 10% weight loss, and then you had different iso-caloric
regimens that they were eating and you provided the food for them, and it was based on their
percentage of carbohydrates and you found
that the lowest percent of carbs had the highest increase in their resting
energy expenditure by 325 calories per day. That seems conclusive. The type of food you eat
affects your resting metabolic rate and it’s iso-caloric so it’s not simply
calories in, calories out. So why doesn’t a study like that
change the paradigm? Well first off, no single study
is conclusive and definitive, and we can talk about that in a moment. But let me provide the broader context. On the one hand obesity treatment
has focused on so-called calorie balance. Eat less, move more,
doesn’t matter how you do it and that is the primary focus
both for public health, as well as treatment in the clinic. An alternative paradigm which we’ve been
developing along with others is called the carbohydrate-insulin model. Now it focuses on carbohydrate and insulin,
because you need a name for something, but it’s not a single nutrient,
single hormone hypothesis. It proposes that we’ve had it backwards. That overeating doesn’t cause obesity
over the long term, that the process of getting fat
causes us to overeat. Now, that’s a little hard for the mind to hold,
but think about it, think about what happens in pregnancy. A woman typically eats a lot more. She’s hungry, she has food cravings,
she eats more, and the fetus is growing. But which is coming first?
Is the overeating causing the fetus to grow? Or, is the growing fetus
that’s taking up extra calories triggering the mother to be hungry
and to eat more? You know of course the latter,
we understand it. The same is true for an adolescent
in a growth spurt. You know, you and I
no matter how much we eat, aren’t going to force our bodies
to get any taller, unfortunately. It’s the process of getting taller
in that adolescent in a growth spurt that’s causing him or her to eat hundreds or sometimes thousands of calories more
than what otherwise would be the case. So that’s obvious in those situations. Why not consider the possibility that a
rapidly growing fat mass that’s been triggered to take in
too many calories could be the cause of excessive hunger
and the overeating that follows? That’s the carbohydrate-insulin model. We focus on carbohydrates because
they’ve flooded our diet in the last 40 years, during the low-fat years, carbohydrates especially the processed
kinds, sugar, but just as much or perhaps even more so,
the refined starches, raise insulin, and insulin, I call insulin
the miracle growth for your fat cells just not the sort of miracle
you want happening in your body. Fat cells don’t do much of anything
until they’re told what to do by hormones, and insulin is the most potent anabolic
hormone. Promotes fat cell store,
calorie storage at fat cells, it inhibits release of fat
from the fat cells. States of excess insulin action
consistently lead to weight gain, such as mutations,
that lead to overproduction of insulin or in type 2 diabetes where insulin
has started, weight gain consistently occurs. The opposite is also true, states of inadequate insulin action
such as type 1 diabetes. A child first coming to attention who because of an autoimmune attack on
the beta cells can’t make enough insulin, that child will have invariably lost weight
before treatment whether he or she is eating 3000,
5000 or 7000 calories a day. Now if you don’t have diabetes
the fastest way to change your insulin levels is with the amount and type
of carbohydrate you’re consuming. But beyond carbohydrate, protein,
the types of fats we’re eating, micronutrients, fiber,
the state of our gut microbiome and non-dietary factors like sleep deprivation,
stress and excessively sedentary life. All these things affect fat cell function and
determine whether the calories we’re eating are shunted a little bit more
towards storage rather than oxidation. All you have to do is store a few grams
of extra fat a day to mean the difference
between staying lean and having a substantial problem
with obesity after 10 years. So going back to the study, we brought
people’s weights down to stress out
their body adapted mechanisms. These were people who had
high body weight at baseline. Brought their weight down by at least 10%, and then we randomly assigned them
to either an Atkins type low-carb diet, a high-carb diet with 60% carbohydrate or something in the middle kind of
a 40% fat, 40% carb Mediterranean diet. And everybody got each of these diets
for a month and we measured energy expenditure
both resting and total energy expenditure by a method called doubly labeled water. We found that despite the weight loss, on the low-carb diet there was no decline
in the total energy expenditure at all. We know that typically your body
adapts to weight loss by becoming more efficient,
that makes losing weight harder and harder. But there was none of that adaptation
on the low-carb diet, a potentially tremendous advantage
to losing weight. On a high carb diet, energy expenditure
plummeted by more than 400 calories a day. That difference of 325 calories would translate
into 35 pounds perhaps of weight loss without any change in calorie intake. So that’s the difference between
being lean and being obese, right there. Potentially, a big part
of the difference. And if you get changes in hunger, if you get lower hunger
and fewer food cravings on a low-carb diet has been reported in other studies
the effects could be potentially even larger. So, this was a study that
was published in JAMA, certainly got considerable attention. You know itself has limitations it’s just one
study that needs to be reproduced and then a group from the NIH
published a sort of rebuttal, a counter attack, on this hypothesis
and on this study, reviewing other studies of diet composition
and energy expenditure, claiming that there was no effect. And this meta analysis by the NIH group was used to claim
that they had literally– the term they used was “falsified”
the carbohydrate-insulin model. Now if you look at the studies
that were included in this meta analysis, virtually all of them
with just maybe three exceptions, 20 or more studies
were two weeks or less. So the folks in the low-carb movement
are immediately going to understand that when you cut back carbohydrate
especially into the ketogenic range and some of these studies did, you need to allow the body to undergo
an adaptive process. You’ve cut off carbohydrates which is
the main source of fuel for the brain, but yet ketones have not yet
reached a steady state. The classic starvation studies by Cahill
and all and others show that ketones with complete fasting
was starvation. Don’t reach steady state
until about two to three weeks afterwards. And how long was your study? -Ours was a month.
-A month, alright. Ours was long enough
to see these adaptive changes. But almost all of the other studies
published didn’t. And so if you’ve cut off carbohydrate but
you’re not yet adapted to that high fat diet, what’s going to happen?
You’re going to feel tired. You know physically tired,
mentally a little sluggy, we have a name for this,
it’s called the keto flu. Very well described, there are dozens of
papers showing that it takes several weeks, and if you conduct your study during
that short period of time of adaptation, you know of course you’re not going to see
the full benefits of a low-carbohydrate diet, in fact you might see some adverse effects. But I would make the comparison
to a scientist wanting to study the effects of intense
physical training on a sedentary population. You take a group of 45-year-old men who are overweight,
sit around all day watching TV, and suddenly you’re giving them 6 hours
a day of physical activity boot camp. You know they’re running track,
they’re doing calisthenics, they’re engaged in contact sports
6 hours a day. And then you measure them three days later.
What’re you going to say? They’re going to feel awful. They’re going to feel tired,
their muscles are going to be sore, they’re going to have
decreased physical abilities. If you concluded at that point
that physical training worsened fitness you would be doing the same thing that these very short-trimmed
low-carb diet states are doing, that they’re missing the boat. So we need longer studies… our study and the only 2 or 3 others to date that are of a month duration
show benefit to the low-carb diet. I say we need longer studies
and we’ve just completed one. We’ll be presenting the first public… we’ll be unveiling the results
of the study to the public at the obesity society meetings
in November, we’ll be doing so in November 14th. And, this is a study
that actually cost 12 million dollars, it was done with philanthropy. NIH, unfortunately doesn’t typically fund
nutrition studies of this size. And the after weight loss same design
as an initial weight loss phase, in this case we studied
three diets parallel, so you just got into one diet either 20%,
40%, or 60% carb controlling protein and the test phase was 20 weeks. So four times as long as our JAMA study
and ten times or more, as long as most of the studies
that were in that NIH meta analysis. So this study will be
of sufficient power and duration to put the carbohydrate-insulin model
to a definitive test. That sounds fascinating. We look forward
to showing those results very soon. You’re just teasing me now,
I can’t wait to hear those results. And they’ll also be in press,
they’ll also be published soon as well. Good.
Yeah that’s always a problem too. When a study is presented at a conference
but we don’t have all the details and then the media starts publicizing it
about these amazing results but the devil sometimes
is in details. And I like that it will be published
shortly after. We’re actually hoping
that they’ll be simultaneously published. You said a few things in there
that I wanted to touch on. One it is funded by philanthropy. Now that’s a big problem because, not a
problem that it was funded by philanthropy, but a problem that it needs to be funded
by philanthropy, because if you have a drug trial
no problem getting funded. Even some studies probably
showing calorie in calorie out, or trying to show that that’s the paradigm
could be funded by industry, because Coca-Cola said just exercise more
and drink your coke and you’ll be fine. But funding first studies like this is
got to be hard to get, and that’s part of why
they’re not being done because it’s such a challenge
and expensive to do it correctly. So was that one of your bigger challenges? Getting the right funding
from the right people? That’s terribly short-sided and as you point out not that any drugs
study will get funded, but if you are a big drug company and you have a new agent that you think that is going to be useful
for just one obesity related complication, you can routinely get funding
in the many hundreds millions of dollars to take it to phase three clinical trial. You know you can count on one hand
the number of nutrition studies addressing a specific dietary hypothesis
over a hundred billion dollars. And it’s terribly short-sided because
we’re investing a fraction of a cent for every dollar of diet related disease
that the United States and the, you know,
the rest of the world suffers. You know, we do want the funding
infrastructure to be skeptical of new ideas, that’s the scientific method. Very few new ideas
will ultimately prove valuable, because the state of science
is an accumulation of many years of study and so the next study statistically
isn’t going to change the paradigm. So we want some skepticism,
we just don’t want to suppress new ideas, and that’s the problem because
we clearly need new ideas in obesity and diet related disease, where based on the latest evidence seeing prevalence rates
that are continuing upward the current mind set of eat less move more
has failed. And yet there is an attempt,
it seems like an attempt by folks who are
in the leadership of the nutrition community to really prematurely falsify,
dismiss new ideas, such as the carbohydrate-insulin model with data that are
plainly not up just enough. I mean if the folks on this side of the debate
were to publish studies of that quality we would be shut down immediately and yet these poor quality studies
are being used to falsify the model. So that’s not in anybody’s interest. We don’t want to claim victory
or insist upon defeat prematurely, in fact this is a little too binary. We want a more nuanced discussion, recognizing that we have a public health crisis
that the current mind set has not solved, and whether the carbohydrate-insulin
model is 90% right or 10% right, we need to understand
what we can learn from it and not attempt to dismiss
these new ideas so fastly. And that’s why nutrition science starts
to look more like religion than science, and that’s a problem. Well that can be true
on both sides to be fair. On social media, just like the calorie in
calorie out folks can be close minded. The low-carb community has its own dogma,
its own accepted ways of dialoging. I think both sides
should really tone down the rhetoric and not to make this ad hominem. On Twitter it’s just all too common
to accuse our opponents of being intentionally pigheaded, and I don’t think they are,
I think they may be wrong but by promoting ad hominem attack and I’ve been on the receiving end
of ad hominem attack. Ad hominem attack
is always a distraction from the science. Let’s stay focused on the science,
the public health issues, deal with your frustrations. Yeah, people aren’t always
going to understand. I mean look at the history of science; some correct ideas have taken decades
or centuries to finally be proven. You know,
let’s have a little maturity here just because you may be right
and the world might not recognize it, but that’s not going to help the cause
to attack the other side. You’re definitely a voice of reason
in a world that likes polarity, because polarity sells,
it gets clicks, it gets views. You know, there’s nothing wrong
with polarity. Actually we need more vigorous debates
that clarify the polarity. One of my other problems with the
conventional paradigm is it keeps morphing. You know, every time a new finding
comes up it morphs in a way that tries to account
for that finding without having to reassess the basic principle,
the basic assumptions of that. So yes we need to shine a bright light. Let’s have debates that really clarify
the polarity but let’s not make it personal. Right, now, I like something else
you said, that maybe the carbohydrate-insulin model
is 90% right or 80% right. Or 10%, right. Right, like it doesn’t have to be
in all or none and some people still put it
into that camp that, well, if it’s the carbohydrates
and insulin, then calories don’t matter. Well, calories do still matter, if you have 10000 calories on a low-fat diet
you’re still probably not going to lose weight, you’re going to overeat. Whereas if you have 800 calories
on a low-carb diet you’re still probably going to affect
your resting energy expenditure and your metabolic rate. So I have a personal problem saying
it has to be one way or the other. But yet some people who are very
prominent in this field still think it’s one way or the other. How do we address that and explain
that it is not so black and white? We have remind ourselves
that science shouldn’t be religion. You’re talking about one of the most complex,
multifactorial clinical challenges we have, which is body weight regulation,
we know that it is affected by genes, but also by diet, physical activities, stress,
sleep, family dynamics, community, the food supply,
political and policy decisions. We can all look at one little piece
of the elephant and delude ourselves into thinking
that we have the full picture. Some humility is in order here,
and as you say it’s not that carbohydrate-insulin model
acts in defiance of calorie balance. In fact I’ve tried to make that point in the recent review that we wrote
for JAMA internal medicine. It’s simply reinterpreting the first law
of thermodynamics in a way that’s more consistent
with the evidence around biology. I mean of course humans
aren’t toaster ovens. We respond dynamically to changes
in calorie balance, and unfortunately that has been
well demonstrated in the laboratory, it’s neglected in public health
and in the clinic. Right, and that gets into the issues
of how to design a study to measure this. Is it real world, free living people? Is it in a metabolic chamber?
Is it only measuring doubly labeled water? It’s all of it. Right, we need
a little bit of all that, right. Of course, we need to understand. Now the problem has been that we’ve jumped
to effectiveness studies prematurely where you put large numbers of people
on different diets, you give them some typically
very low intensity nutritional counseling, and then tell them to go follow it. And if you’re lucky they will change their diet
moderately for a few weeks or few months but almost invariably by a year
all groups are eating pretty much the same. Not surprisingly their weight and their other
health outcomes are pretty much the same, but can you conclude then
that diets don’t matter, and it’s just a question of compliance? No, that’s very sloppy thinking. We would never do that in any other area,
biomedical research. Imagine you had a promising new drug
for cancer it could potentially wipe out
acute leukemia in children. You gave one group the drug,
prescribe on group the drug and you gave the other group placebo. But it turned out that the kids
in the treatment group never got the drug at the right dose at the right time. They may be have gotten
the wrong instructions, or maybe many of the families couldn’t afford
the drug or there were some mild,
transient side effects that good counseling
could’ve gotten them through, but didn’t. So it turned out, that you know,
that the drug wasn’t taken as intended, and there wasn’t a statistically significant
difference in cancer outcomes. Would you conclude that the drug was
ineffective, or that the study was a failure? We need a better quality study
to ask these basic questions. We make that mistake in nutrition. We’ve skipped over mechanisms,
and especially efficacy. What happens under ideal circumstances? Prematurely gone to effectiveness,
what happens in the real world, especially when this real world
antagonizes healthy behaviors? If we find out that a lower carb diet
is going to be really optimal for a third or half of the population,
or two thirds of the population, then that knowledge will help us design
behavioral interventions and environmental interventions
that will help them become more effective. It’s not like, you know,
you have to understand that smoking cause lung cancer before you could go beyond just telling
people not to smoke to developing environmental policy, environmental base policy actions
that actually helped people not smoke. Right, proving that first
in an ideal trial then figuring out how to move that
to a real world scenario. Those are separate questions,
separate scientific facts that get confounded all the time. So one of the things in your study
that you did was that you actually provided food
rather than saying go eat. Is that what you did
in your upcoming study as well? Yes, the recently completed study which
is called the Framingham State Food study, we did it in collaboration
with the Framingham state University where we could recruit students, staff
and faculty and local community members and feed them through the college kitchen, the commercial food service. So we took advantage of the synergies that the food service knew
how to make tasty foods financially efficient and in large volume. We controlled the quality of those foods and so we were able to test
a mechanistically oriented hypothesis. If people actually eat different ways,
do you get a difference in metabolism? Yeah, that shows sort of a new way
of doing these studies… not a new way but a way
that should be done, and I remember you wrote something
about that on Twitter about a sort of a new paradigm on how
to incorporate research and industry, bring them together to help find
the answers and that takes money. Right, although we’re in this case
bringing industry and not with a risk
for conflicts of interests. It’s very different to pair up
with the food service provider who has no vested interest
in one particular diet, but can serve high quality foods much tastier
than a metabolic kitchen in a hospital. That’s one thing to pair up with them. It’s another to pair up with Coca-Cola
to do a study as to whether sugary beverages are a good
way of preventing dehydration in children. -Yet that happens all the time. Those types of partnerships
and funding and you know… Yeah, so we do the– NIH has really I think dropped the ball in terms of adequately funding
high quality nutrition research of a sufficient scale on power to definitively address questions
that have bedeviled us for centuries. So it’s really been up to philanthropy
to step in and fill that gap. And I think that
if there are any other billionaires out there please come find us at Harvard
and we will do our best to give definitive answers
to some of these long term challenges. Well so along those lines
there was a philanthropy funded study run by– well not run
but sort of spearheaded by Gary Taubes, a very publicly anticipated study with– -NuSI.
-With NuSI. Okay so we were funded by NuSI. This is one of their three
initial major studies. There was a study, a pilot study, it was
actually a non-randomized pilot study done through the NIH
and several collaborators that was published in AJCN and despite some spin it actually showed
an advantage to the ketogenic diet… See, that’s what I wanted to talk about. …by both doubly labelled water
and metabolic chamber, the ketogenic diet
had a metabolic advantage. It wasn’t huge but it was statistically
significant in a pilot study that’s not powered
to get a precise estimate and it was non-randomized in a way
that biased against the low-carb diet. Why? Because everybody got
the standard diet first for a month and then they were all in a non-randomized
way put on to the ketogenic diet, but the experimenters
miscalculated energy. They wanted it to do it
a weight stability, they miscalculated and the participants
were at substantial negative energy balance. They were at about 300
or more calories a day, they were losing weight systematically. So this is why you randomize;
to cover mistakes like that. In this case without the randomization
on a conventional diet their average weight was substantially higher
than their weight was on the ketogenic diet, and so of course that’s going to bias you
in terms of total energy expenditure. Despite that, and despite other biases the low-carb diet still came out
advantageously and yet I think it’s in a masterful display,
a spin that was dismissed. Right, the lead investigators said that it disproved the carbohydrate-insulin
model like you were saying. If you look at the registry, that study was
specified as an observational pilot study, a pilot study can never prove or disprove
a hypothesis, that’s the nature of it. It’s designed to assess study methods and to come up with broad effect estimates
that give you then definitely test. So that NuSI study was,
if you reinterpret it and we did, and we think that if you take into account
the biases then you get a benefit of the low-carb diet
in the 200, 250 calorie a day range. And that’s quite consistent
with what we got in our JAMA study and we’ll be able to compare that
to what we got in our new Framingham study. The third study that NuSI funded
was the diet fit study from Stanford published in the Journal of the American
Medical Association or JAMA recently. And that study found a non-significant,
non-statistically significant, very small non-significant advantage
to a low-carb as compared to a low-fat diet, but the low-fat diet, the people on that diet
were told to greatly reduce or eliminate all processed foods but specifically
refined grains and added sugars. As a result the glycemic load
that’s the best determinative of how your blood sugar and insulin
will actually change after a meal, that’s the product of glycemic index
and carbohydrate amount. That actually, went down as low as other clinical trials, low-carb
or low glycemic load group were. And so what this means I think is that
if you avoid processed carbohydrates you can do reasonably well on diets
with varying macronutrients, relatively more carbohydrate,
relatively more fat. It’s different if you have type 2 diabetes
but they weren’t included it in this study. But that’s again consistent
with the carbohydrate-insulin model. It’s focused
on the processed carbohydrates. It’s not saying your fruits, vegetables,
you know, traditional starchy tubers that might have been eaten
in the Okinawa diet are the problem. It’s focusing on the processed
carbohydrates that flooded our diet during the low-fat years
and that raise insulin too much. So I think that in a sense all– I don’t have the liberty
to give you the result of our study, but I think we’ll see that there are
consistencies among the results that the studies
funded by NuSI. And I like that you clarified
not considering type 2 diabetes patients because in those people,
the fruit, the tubers, that can be too much of a glucose load
and insulin response for them. But for the general more metabolically
healthy population then that’s not the evil
we’re talking about so far. Then clearly the world can’t give up
all carbohydrates, all grains, I mean with– Why not? We’re getting 10 billion, there just aren’t enough animals
for 10 billion humans to eat. So, you know, you need grains
to feed that many people. We’re not hunter gatherers anymore. The question is what are those grains? Are they minimally processed,
and can we also–? Because you know this traditional,
like the sourdough breads that were made
with less finely ground flours and that were fermented over a long time, so a lot of that rapidly available
carbohydrate got digested and turned into organic acids
which are very beneficial, that’s really different than wonder bread. And we can also be shifting to an agriculture
that produces more healthy fats, you know, avocado, nuts, dark chocolate. These are all delicious
and very nourishing, and can also help to feed
the world’s 10 billion people. So, with our current state of policy
with the farm bill, and who they supplement
and who they benefit, and with our current industry structure
and our current medical community how do we get there from here? It seems like there are so many roadblocks. And you’ve been involve with policy
and trying to affect things. What do you see as the necessary steps
we need to start taking to get there from here? First is what we’re doing, we have
to understand what the science tells us. About how the human body is designed
and how to care for it and feed it, so that it doesn’t all too often develop
these metabolic breakdowns. You know in our 50’s or 60’s or as we discussed
at the beginning of this session sometimes, you know, in a person’s teens. So we’ve got to understand the science
including whether there’s susceptibility, differences based on our genes
or other biological factors, we’re especially interested insulin secretions
but that’s another story. So what’s right for the general population, are there major subgroups
that need to be specially treated such as people with type 2 diabetes which is
highly prevalent. So it’s a public health issue. And then I think we begin to look
for collaborations of common interest. You know, one obvious place to look
is the insurance industry. They’re spending a fortune,
and increasingly a fortune. Unpreventable diseases; if the investment of $10 in good nutrition
or infrastructure change or policy could produce $100
of economic benefit, lower medical costs, but also then to employer’s greater worker
productivity, less days, lost in illness to diet related diseases, I think you’ve suddenly counterbalance
the power of Big Pharma and the food industry. So we need to begin to develop alliances. They’re going to help us create policies that
earn the greatest common good for society, not just the special interest that inordinately
have access to politicians and power. Right, very good point. So people have proposed factoring in the down
shame health cost of certain foods into the price of that food, I don’t know how’s that necessarily
practical but that’s the real mindset. That’s called the Pigovian tax,
and it’s well established capitalist principle. You know, you can’t just create a product,
that, let’s say it produces a lot of pollution let’s just make it very simple. You’ve got a pig farm that’s creating
massive lagoons of toxic waste; you can’t sell those products really cheaply
and then expect somebody else to deal with the environmental disaster
of that waste lagoon. Has this off to tax the case. So a Pigovian tax which is now used
across the country with cigarettes says we need to have some
of the long-term costs of that product such as taking care of people’s emphysema
or lung cancer included in the price so it doesn’t fall back on the population. That’s a capitalist idea of, you know,
market responsibilities as you can get. But we do need more of that. Yeah, and I agree. But when it’s well done
and the caveat out there is that there is so much epidemiology
and observational studies that this type of tax I think
would be based on and so many studies say
increasing meat intake will increase your risk of heart disease
and cancer. And those are frequently promoted
by the school of public health at Harvard. That doesn’t factor
in sort of the reduced quality of the science. The studies we’ve been talking about so far
are controlled studies, prospective studies, not these retrospective studies looking
at societies with healthy user bias
and confounding variables and with entirely too small hazard ratios that then make
this broad sweeping conclusion. So my concern is if we do go in that route
we’re going to be facing a meat tax because of what
this poor epidemiologic studies shows. So I think you’ve just conflated
two important issues. One issue is what the evidence based
suggests, and you know, do taxes or subsidies that fairly balance the long-term costs
on the prices on the product are those an appropriate policy measure
when the science indicates? And I think that the answer is yes and
it sounded like we might agree on that. I agree on that. A second question is why do you need
to get an adequate knowledge base for action? So that is a whole another debate. And there are issues
with observational research but there’s also problems
with clinical trials. Did you know that there was never
a clinical trial to this day that shows reduction of lung cancer
from cigarette from smoking cessation interventions? There’s never been one. Yet we all agree
that it’s a true cause and effect and it’s a huge cause and effect. So why, despite attempts to find it,
why has no clinical trial ever seen it? Those are the limitations
of a clinical trial. You didn’t get complete compliance. You got washed in and washed out, and you were looking at effects that take
decades in some cases to emerge. So just because a clinical trial
doesn’t show it or alternatively if it shows it,
doesn’t mean it’s true, there are limitations in both sides, and I think it’s become fashionable
among the low-carb community to focus exclusively on the limitation
of observational research and not those of interventional research. Both have a place. You know, there are many questions
that will never be answered by a clinical trial. You just have to understand
good ATBI from bad ATBI. Just as we understand good clinical trials
from bad clinical trials as we were discussing earlier. Right, so smoking
is considered good ATBI because the hazard ratio
is above three, three and a half. As one of the reasons why
and there’s a dose response effect and you know
this Bradford hill criteria that it meets. Whereas saturated fats, red meat,
a lot of the nutritional ones don’t even come close
to that level of ATBI, yet the Harvard school of public health
reports these studies over and over again probably overstating what they can prove. Does that bother you? Well, I’m in favor of appropriate
interpretation of all data. I also want to say that there’s no monolithic
Harvard school of public health. Good point. There are investigators
who have a diversity of opinions including those who’ve published, explicitly stating that the prior
recommendations on saturated fat were overblown and that saturated fat,
in the context of conventional diet, doesn’t increase cardiovascular disease risk. You know I’ve got a secondary appointment
at the school of public health and I’m on record in saying in the comparison
between white bread and butter, butter is the healthier component. Even if you say that leads to many topics
that’ll be beyond our capacity today, but I do think that saturated fat in a context
of high carbohydrate diet is a big problem. I think the ATBI consistently shows that,
and I think those are true associations. That doesn’t mean that saturated fat on
a low-carb diet is going to do the same thing, and in fact, I think likely,
you have to be eating more sat– you can vary the amount of saturated fat
you eat on a low-carb diet, but it’s inevitably going to be higher, but when you’re not eating a lot
of carbohydrate, that saturated fat has, Steve Phinney says,
to use his metaphor, “goes to the front line of oxidation”,
and it doesn’t stay around as long. And you get compensatory changes
in triglycerides and HDL and chronic inflammation. So I think we do a disservice
of both directions including among the low-carb community of totally dismissing any adverse effects
of saturated fat in a conventional high carbohydrate diet. I think that’s a mistake. Well, as usual I really appreciate
your perspective and you really have a great way
of seeing both sides of the coin and trying to bring them together
to make a reasonable decision and trying to further the science in a way
that will help answer these questions, not that it has to be one way or the other
but that we need true answer to help our patients and help us understand
the complexity of this. So thank you very much for that. Great, you know I just want to say it’s wonderful that you as cardiologist
are taking a deep dive on these issues. I think you’ll be able to do so
with a perspective and credibility that’s oftentimes lacking
and so congratulations on your work. Thank you. I appreciate that very much. So where can people go
to learn more about you and hear more about what your thoughts? Well if you are, I don’t know
when is this coming out, but you can come to the obesity society
meetings in Ashville in mid-November. We’d love to see you there
for presentation of our data. Otherwise follow me on social media
Twitter, Facebook. I’m @davidludwigmd and you can also find
all of my links on my website which is,
that’s Well, Dr. David Ludwig, thank you so
much for joining me today, it was a pleasure.

16 thoughts on “Diet Doctor Podcast #12 — Dr. David Ludwig

  1. Great to see the paradigm shift starting to take place.

    While I’m optimistic future generations will not have to suffer from the diseases due to refined sugar, as low carb will just exist across the greater general population, I would expect that the benefits of low carb will mostly pass at least the baby boomers due to entrenched habitual compliance with prior dogma.

    However, similar to automotive seat-belts, they too didn’t save as many lives when they were first becoming available. A full paradigm shift to mass compliance will go through many phases (development, mass production, legislation, enforcement, compliance).

    Keep up all the great work Dr’s!!!

  2. I think the work you do is invaluable to how we see our food and even though research is highly underfunded hopefully the ripple it causes will have an effect on the general mindset of society . I am morbidly obese and studies like these opens my mind to choices other than what has been recommended to me in the past.

  3. I love you Dr. Ludwig! You rock! I love your voice of reason and calm with debate. Where can I follow you?

  4. (my doc is poo pooing all natural remedies(ie activepk which im gonna try anyways vs pills)I just got in from a diabetic clinic appt. Ive lost 20 lbs (in the past few months)since being diagnosed (TYPEII)3 yrs ago. Ive really struggled …doc tells me im doing great on Janumet(for the past 6mos). And wants to put me on cholesterol pills now. (as i am told that i am in a high risk group and need statins to bring it down) until i can get the right diet going. Glad to be watching this now so i can sort out what more i need to modify in my current dietary intake. My question is by going keto …will that reduce my cholesterol levels naturally as well??? please advise if anyone knows thx ( ps I just have about 20lbs left to drop to feel healthy again) and i truly dont want to take meds the rest of my life if i dont really have to ..told the doc this too) SINCERELY , from ANOTHER diabetic in CANADA

  5. Thanks Doc's … good new term "Carbohydrate Insulin Model". We subscribe to the model as presented in LCHF communities.
    #CitizenScientist – References to "The Saccharine Disease" started in 1956 (Cleave) and go back as far as 1869 Tanner MD, 1824-1871. We knew how the cure Diabetes Mellitus in 1921 outlined in The Principles and Practice of Medicine – Sir William Osler, MD
    and –

  6. Excellent presentation I agree with everything doctor ludwig said
    Especially the need to avoid making diet religion and keeping a scientific open to mind
    For myself I think it is patently ridiculous to think that everyone on the planet should eat the same way

    As a practicing obesity medicine specialist for the patient who has obesity type 2 diabetes or hyperinsulinemia Currently I do use the Ketogenic diet below 20 total grams. I am willing to entertain alternatives but in the clinic I have to offer what I see as the best I can offer for my patients now. ObesityDocATL

  7. I really found this interview helpful to my understanding of how nutritional science is so necessary to helping us understand the interrelationships between dietary choices and health outcomes. Things are not just black and white out there, though when we are in the passionate throes of experiencing benefits from choosing a LCHF, ketogenic, fasting protocol, it is easy to become blinded by our own enthusiasms. Thank you Dr Ludwig! I shall listen to some more of your talks on youtube. Thank you Dr Sher, for the great interview!

Leave a Reply

Your email address will not be published. Required fields are marked *