Kac Para Yarismasi

Arthritis Diet and Exercises

Grand Rounds_10.27.2016_Why We Get Sick And Fat_Dr. Benjamin Bikman

(crowd chatting) – All right, we’re gonna
get started, everybody. Thank you for coming today. It’s nice to see you all here. We have the pleasure of hearing from Dr. Benjamin Bikman today. I am going to just read
a little bit about him so he can be embarrassed by all of his accomplishments today. So, Dr. Bikman earned
his PhD in Bioenergetics and was a post-doctoral fellow with the Duke National
University of Singapore in Metabolic Disorders. Currently, his professional focus as a scientist and a professor, which he’s a professor at BYU, is to better understand
chronic modern day diseases with a special emphasis on the origins and consequences of obesity and diabetes. He frequently publishes his research in peer-reviewed journals and presents at international
science meetings. So, we’re very lucky to have him here to speak with us today. So, I’ll turn the panel over to him. (audience applauding) – Yes, I’m thrilled at the invitation. One of the problems being a scientist is we paid to ask questions
and to find answers to those questions, but sometimes it’s not
particularly gratifying when the only person who hears the answers are other scientists. So the opportunity to actually share some of these answers to
these important questions with people who actually have the ability to make a difference is very gratifying. I’m thrilled at the opportunity to present some of these
things that we’ve found and some of the questions
that I’ve been asking over the past several years. So I hope you’ll pardon the somewhat bold title here. What I hope to impress upon you is the fact that insulin resistance is not only remarkably prevalent and we’ll go over the details but also particularly relevant in the context of virtually
every chronic disease. I will give evidence
to support some of that and would be thrilled
to talk more about it at any other time you’d like. In fact, you’ll have a hard
time getting me to stop talking. (audience laughing) By way of an introduction, let’s sort of do a history lesson. I know it’s odd for a
hard science professor to talk history, it’s difficult, but I’ll do it anyway. Something terrible happened in 1977. It was a wonderful day
for Gary and Susie Bikman or a wonderful year in southern Alberta to bring another little
redheaded boy onto the earth. But it was terrible for how
we look at diet and disease. This is when, for the first time in the
history of the planet, so far as I know, a government decided to start
telling people what to eat. So this was the key aspect of what became the Food Guide Pyramid, particularly we need to
eat more carbohydrates than we were, we need to eat less fat
than we have been eating. That was the general change. When this happened, what
most people don’t know is that there was a great deal of outcry. Among the most vocal opponents of these dietary changes was the President of the
National Academy of Sciences in the U.S., Dr. Philip Handler. His quote was based on
the fact that there was no significant data to support
these dietary recommendations. So he was calling out the government saying what right do you have to conduct an experiment
with the population as the study subjects? We need to do studies before
you make these recommendations. The politician up for reelection needed some sign of productivity. This was his literal exact quote. “Senators don’t have the luxury “that a research scientist does “of waiting until every last
shred of evidence is in.” He wasn’t waiting for every
last shred of evidence, he wanted more evidence. But who won? Well, not the non-physician,
scientist won. The politician. And this was the beginning
of this significant departure from what had been very typical,
normal trends in the U.S. to a significant increase in carbohydrate, a significant reduction in fat, and then no change in protein overall. This will become relevant in a little bit. So this was the whetting your appetite. I promise we’ll come back to it. You might not care to. So why care about insulin resistance? Why devote my entire career to studying something that may seem as obscure as insulin resistance? The reality? It’s not obscure at all. So just some general statistics. Within the U.S., 30% of
the entire population is prediabetic, a.k.a. insulin resistant. Now when we look at just adults, half of all adults in
the U.S. are prediabetic. Again, that’s synonymous
with insulin resistant. This is the single most
prevalent health disorder in the country. Prediabetes, or insulin resistance. It’s not strictly within our own borders or even Canada where
it’s not quite as high, my beloved true north. But it’s close. However, when we go to
other developing countries like China and India, the reason they wanted
scientists like me in Singapore, where Duke Medical School
has a new little branch of its medical school, to study metabolic disorders was they were mindful of the
incredible increase in diabetes among two of the most predominant
ethnicities in Singapore, the Chinese and the Indian
ethnicities in particular. So this problem is even worse. It’s more than half of
the adults in China. More than half of the adults
in India are prediabetic. So you can see worldwide this is a problem that is unlikely to go away soon and indeed, within all of
our lifespan very likely, insulin resistance will even double. 30 years, we’ll have a doubling of this. So you can see this will
get far worse, likely, before it gets better. But maybe we can start making a change. So this is something that I don’t wanna take too much time on,
just for the sake of time, but I often will show this
just to help convey the idea that this is a far more
prevalent problem than you think. If you were to kind of
zip through this list and you’re answering
some yes’s and some no’s, some of these you may
think have nothing to do with insulin resistance. What does gout have to do
with insulin resistance? Water retention? In fact, a great deal and I’d be thrilled to talk about any of these
with you in more detail. The most common source
of female infertility? Yes, that’s fundamentally
an insulin problem, increasing androgen
production from the ovaries. There’s a lot to talk about. But the gist of it is, if you answer yes to two or more of these questions, you’re fitting within that category of very likely being prediabetic
or insulin resistant. Now, remarkably, almost
all of these people, there’s a range, depending on
the publication you look at. It’s about 50 to 90% of people with insulin resistance are undiagnosed. So I’m just using the
more sobering number here. But based on data, mind you, so they’re undiagnosed. They don’t know. They’re just going through their lives. Maybe they’re diagnosed with hypertension. Maybe they’re diagnosed with PCOS and they have no idea that likely the fundamental feature, the fundamental source of the ideology is in fact insulin and insulin resistance. So if they’re undiagnosed,
how do they look? How are they acting? How is it manifesting? Well, it can manifest with any of these. Heart disease is a manifestation
of insulin resistance. Even certain cancers, as we’ll talk about. Things like stroke or osteoarthritis which we look at now more
as a metabolic problem and less of the physical
wear and tear of the joint. We’re learning much, much more about it. Other things like muscle wasting. Migraines. Who’d a thunk? Are all related to insulin resistance. So in every instance here, insulin resistance is either
a fundamental component or at least part of the ideology or exacerbating the course of the disease. I would readily show you
evidence to support that if you’d like any time. Have me back next time. We’ll go into it in more detail. So what is insulin resistance? What is this villain that
I’m talking so much about and have devoted my whole
career to better understanding? Insulin resistance in
short can best be told by looking at the cell. So here is a cell. Every cell in the body
has insulin receptors. Every single cell. I’ve never seen an exception
but I’m always looking. So an insulin binds to its receptor. There’s a series of biochemical events you’ve very all likely seen
from biochemistry classes with any receptor. We have all these second messengers. So just to make things simple, insulin binds to its receptor and then we have an
action, whatever it may be and there are hundreds or
thousands of consequences of insulin binding its receptor. We typically look at only one being that it will
allow glucose to come in if this were a muscle cell or a fat cell that would be true. But insulin does hundreds of other things. So insulin binds. We have an action. Over time, however, as a person
becomes insulin resistant, that same stimulus is
incapable of producing the same level of action as before. So the same stimulus as before is yielding a diminished
reaction or action. That’s insulin resistance in
its sort of cleanest sense. So what can the body do to
try to increase that action? What do you think? Am I allowed to make this
a little interactive? If one insulin molecule, let’s
just say, is insufficient, what does the body do? (crowd chattering) Yeah, the body will
become hyperinsulinemic in order to promote, to
return what was once, to get the action back
to where it once was. So there are two key features
of insulin resistance. One, some cells in the body are failing to respond fully to insulin and it’s not an all or nothing. You can have a cell like a
liver cell and a parasite where some aspects of insulin’s
effects are compromised and some are happily going on
their business per the norm. So one consequence, some
cells aren’t working well with regards to insulin. Another consequence is
that the body’s becoming more and more and more hyperinsulinemic so blood levels of insulin are heavy. They get higher and higher
in order to overcome the cell’s resistance to insulin. We’ll come back to that in a moment. But just to put it in a clinical context, if we had a patient come in, I’m just arbitrarily setting that sort of so-called normal levels. They have so-called normal
insulin, normal glucose, but in insulin resistance,
they have to have more insulin in order to keep the same
level of glucose in control. So higher insulin is
allowing a normal glycemia but the insulin’s working
harder to keep it there. Alright, so what are the causes? This is something that we could spend a great number of hours on. That indeed was my whole post doc and even now, we study this actively. Obesity is a cause of insulin resistance. Environmental toxins,
things like diesel exhaust, cigarette smoke, and
many, many other things that we could, in addition
in inhaling we can ingest. Like Bisphenol A, BPA,
and everybody has BPA-free water bottles now, right? You know what I’m talking about? BPA has been shown to
cause insulin resistance. So what these two have in common and what is on its own a
separate cause is inflammation. So these are three key
causes, undoubtedly important. Stress is another one,
physical or emotional stress as that increases cortisol which is the key component
of the stress response. Cortisol is a key insulin antagonist. So this is making us
more insulin resistant. Then the elephant in the room, it doesn’t seem like it would
be as relevant as it is, but indeed the single
most relevant variable is that insulin causes insulin resistance. Isn’t that odd? If it seems odd at first
it won’t be in second. I submit to you that it’s in fact a pretty logical series of events. It’ll make sense quite readily. So increased insulin leads
to insulin resistance. This is a fundamental feature, this paradox of insulin
and insulin sensitivity are inversely related. So in a person who’s living a lifestyle that is over time increasing
their insulin chronically, insulin sensitivity over
the same period of time is getting more and more diminished. So they’re becoming more
and more insulin resistant. This is a fundamental feature of biology and why I said that if you
actually think about it, it’s pretty intuitive. If you’re giving, a cell
is constantly exposed to a stimulus, it makes
sense that we will become desensitized to that same stimulus, right? It’s why we cycle antibiotics. We don’t want the
bacteria to become immune. So everything from bacteria to the most complex organisms, humans, if we can consider
ourselves the most complex. Every organism on the
planet will have a decay in its sensitivity to a chronic stimulus. The same thing’s happening here. Too much insulin is
causing insulin resistance. I actually took out, I had a slide here. I modified it and took it out. But if I wanted to bring you into the lab and make you insulin resistant, all we would do is give
you a steady infusion, a slightly hyperinsulinemic
infusion of insulin. You’d be insulin resistant
within about 48 to 96 hours. We would stop the insulin infusion and your insulin sensitivity
would go right back to normal. So anyone can become insulin resistant if their insulin is too high for too long. That’ll become relevant
when we start talking about what to do about it. So why are so many
people, I said 50 to 90% of people with insulin
resistance are undiagnosed. Why is it? Because we look at it wrong. If you were to have someone
come in to the clinic, these are all very familiar numbers. Any clinician would look at these. You could all nod your head and you could look at these cutoffs and within some very, very close range these are gonna be the
clinically acceptable cutoffs when you’re looking at a patient and their risk of insulin
resistance or diabetes as listed here. However, in the condition
of insulin resistance a.k.a prediabetes, what’s
conspicuously absent? Insulin. We’re not looking at insulin. So insulin has to be considered. By not looking at insulin as a diagnostic for insulin resistance, we are missing the relevant variable. We’re looking at all these other things and sure they’re descriptive, but they’re not the single
most important variable. So in this condition, to
take it to an extreme, based on the widely used
clinical diagnostic points with regards to diabetes
and insulin resistance if you had a patient come in the average blood test, let’s say here’s the normal patient arbitrarily setting insulin,
glucose just at normal although mind you, it’s never even close to actually being even,
just so that you know. I’m setting them both at normal. Someone comes into the clinic and they actually have higher
than normal levels of insulin but their glucose is normal. On most blood tests in most clinics would this be clinically relevant? It wouldn’t be because we wouldn’t have
measured the insulin. The same thing could be said
if the insulin were here. The same thing could
be said if the insulin were even, max, whatever that would be. Simply because most blood
tests on the average, I go every year for my birthday
to the BYU Health Center to get a blood test, insulin’s not even, it’s not even mentioned. There’s no option of
even getting it measured. It’s only ever glucose
and that’s unfortunate. This scenario can happen. This is the scenario on
some spectrum of insulin that typifies insulin resistance. This is frequent. Anyone with insulin resistance, this is what’s happening. They have more insulin in their body and that increased insulin is enough to keep all the other things in check. Now all of a sudden, what
happens when insulin is, we cannot produce enough? We are so resistant to insulin that no amount of our own insulin from our own pancreas is enough to keep glucose in check. Then glucose starts to come up. Now I have to ask would
this be clinically relevant? It is because this is a diagnostic that we’re very comfortable using and we have very acceptable ranges for it and it’s just easy to test. Much easier than insulin which up until recently required radioactive approval. It was a very complicated asset. Glucose measurement, not complicated. So it’s somewhat forgivable that we’ve ignored this
other half of the equation, if you will. So the assumption with
this diagnostic method is that glucose is the key variable but I’ll show you in just a moment that it is in fact insulin. So what I would humbly add to this, again, not being the clinician, being the person whose whole job is to just sit back and ask questions. You can imagine we get paid accordingly. (audience laughing) So in this case, what I would add you try to find clinical
cutoffs for insulin you’ll find different numbers whereas these quantities
are very widely accepted. With insulin, to the
cleanest, most pure data that I can find, these are the best
cutoffs I can come up with without any ulterior motives. This will seem low to some. However, what’s relevant, just a couple years ago a study from the Med School
at the University of Arizona found that in women, the difference between having
insulin at six micro units per mil verses eight micro units per mil, both of them below a
typical number of around 10. So often you’ll see 10 as
sort of a normal number. But just going from six to eight, the women with eight micro
units a mil of fasting insulin had a doubling of their
risk of type two diabetes. So this is a relevant transition. Just staying under 10, I believe
is not descriptive enough. So I’m going with a little
more rigorous numbers, again based purely on data. So these numbers really fit better with what we’re actually
seeing in primary literature. Thus, to me, when someone’s asking me about their blood numbers, I’m looking at their insulin and their risk of insulin resistance or whether they are insulin resistant. Typically six and below is
going to be a great number. Now just to prove that I’m not a heretic and I’m not just making these things up, this was a study, a 25
year follow up study. Down here I’ve highlighted the development of type two diabetes is preceded by and predicted by defects in both insulin dependent and insulin independent glucose uptakes. The defects are detectable when the patients are normal glycemic in the most cases more than a decade before the diagnosis of disease. So they’re saying that 10
years before we actually detect a problem in glucose,
they’re manifesting problems with insulin resistance. Another study is indicating
that the only marker of insulin resistance should be insulin. Not glucose. Because as I’ve already shown you, it’s possible and indeed often the case that that hyperinsulinemia is sufficient to keep the patient in normal glycemia and thus often undetected. So measuring glucose is not enough. Insulin must be measured. Now let’s get down to brass tacks. Let’s talk some specifics. So here are just kind of the biggest ones that I figured were worth bringing up and among all this group what we can find in each instance is that each of them is either or both. It’s a consequence of too much insulin and or a consequence of
insulin not acting well. In other words, insulin resistance. So how can we lower insulin? If we had more time, I would
talk about drugs and exercises. Well, we don’t. So we’re just gonna talk about diet ’cause this is the one that
I have the most to bring although I have strong
feelings about various drugs and would be thrilled to talk
about that more another time. But with diet. This is where it gets
a little controversial only because someone wouldn’t be familiar with the incredible data supported. So there are four pillars, if you will, to cut it down to its simplest concepts. Someone who wants to mitigate their risk of insulin resistance or
indeed reverse the course needs to do the following. Reducing sugar. Reducing starch. I will put this in context. That’s of course a very
broad class of nutrient. Increasing their dietary fat consumption and engaging in intermittent fasting. Now let’s go to each of these. So firstly with sugar. This is kind of an obvious villain and it’s not gonna really upset anyone that I’m implicating sugar in the context of causing
insulin resistance. Sugar will increase a person’s insulin almost higher than anything. So we need to have it on our radar. What’s important about
it is that we actually, this is obvious. We need to determine how much the patient or we, how much we’d be eating. But we also need to recognize it in all of its many, many sources because it is remarkably prevalent. Try to find a peanut butter without sugar. You can’t. Try to find a ketchup. Try to find mayonnaise. Try to find salad dressing or bread. Whatever else we wanna go through. It is not easy. Sugar has pervaded our food system. You have to try and you can and I submit it’s worth it to find products that don’t have sugar. Who wants sugar in their ketchup anyway? I don’t want it. We like the ketchup
’cause it’s a little tart. We don’t want it sweet. But it’s everywhere. Indeed, trying to find
a ketchup without sugar is profoundly difficult. But we didn’t always think sugar was bad and again I can very readily
defend any of these things with science if called upon. Look at this. This was in 1955. This lady standing on a
scale hoping to lose weight. What? Eat candy and reduce? Reduce being the earlier
term for weight loss. Yes, says the doctor. Here’s why. Why is it hard to believe this doctor and his book of liquid sugar? (man mumbles) Yeah, we used to think
smoking was good, too. (audience laughing) So it’s not surprising that we
once thought sugar was good. We’re learning new things all the time and this one’s a little more sobering. A wonderful decade. Good for music, bad for fashion. If sugar is so fattening, how
come so many kids are thin? Boy. Imagine an advertisement
like that nowadays. You couldn’t do it. But it just goes to show
how far we’re coming in understanding where
the real villains are. Now I add this. Artificial sweeteners. You want something sweet. Everybody wants something
sweet from time to time and if you are beginning to appreciate how insulin-spiking sugar is,
what are the alternatives? There are some alternatives and this is kind of a
tricky topic in a way ’cause it’s a bit muddy water. But the three sweeteners that I’ve found in any research that have
no increase on insulin whether on their own or
with a meal are these ones. Xylitol, Erythritol, Stevia because something like aspartame actually the patient alone taking
aspartame, there’s mixed results. It may increase insulin, it may not. But add that aspartame to a meal, in other words, that
diet soda being consumed with whatever that mixed
macronutrient meal is, you are increasing the insulin effect of whatever that meal had been. So again, it’s muddy water. These are the three that
consistently come up okay as having no insulin effect and again, I make no
money by promoting that. (audience laughing) I’m not affiliated with them at all. Now what do insulin mean by less starch? I’m not making a blanket
accusation against carbohydrates which is what fits in, of
course, the family of starches. I’m not saying that. But I’m saying we have spent decades talking good and bad fats when in reality, we maybe should have been at least adding to the conversation, if not replacing entirely, by talking good and bad carbohydrates. This is a phenomenally
broad class of nutrients and you can acknowledge that
we’ve had our hand in it. We have been mucking
around and changing things that were once very natural. For example, the wheat that we have now is indistinguishable from the wheat that prevailed 150 or 200 years ago. These are different plants and
it’s very well established, this isn’t controversial at all. What we have now we call
wheat is so different from what wheat used to be that we call that spelt
or an even older one which we call einkorn. So we’ve mucked around
when it comes to starches, just plant that seed. When people say the
natural plant-based diet, well, depends on what it is. Might not be so natural. So how would I, based on data, lump some of the most
prevalent carbohydrates? Sugar, of course, I’m solidly
putting on the bad side based on data. Fruit juice. Where would you think that’s gonna go? – [Audience] Bad side. – That’s absolutely bad. This is a profoundly unnatural thing. Pure fructose without any
fiber to come with it. Oh my goodness. We are doing our children and
ourselves such a disservice and indeed you can have people with full blown nonalcoholic
fatty liver disease and all you do is have
them stop drinking soda and fruit juice and the liver clears up. There’s less padded fat. Now what about a fruit smoothie? What’s the difference
between a fruit juice and a fruit smoothie? (audience chattering) Yeah the fruit smoothie
has kept the fiber in it. But we have just brutalized that fiber. If we were eating the
whole apple, for example, that’s profoundly different
from having sheered the fiber so sufficiently that we can now drink it without any work. We have changed the fiber. So a fruit smoothie is not
as good as we like to think. So when my kids, we’re
gonna go out for a treat, they want Jamba Juice. I’ll say alright, you
can have a Jamba Juice or you can have a milkshake
’cause it’s the same shite. Almost. (audience laughing) Can I not talk like that here? (audience laughing) I can talk like that at BYU. (audience laughing) Not really actually. Some of my former students in here they probably know. There’s good old Bikman
getting irreverent again and of course this is well-documented. (audience laughing) What about honey? Honey actually is really mixed. I’m not sure about honey yet. There’s evidence to
suggest it’s good and bad. In fact, the most consistent evidence is to show that raw and pasteurized honey is incredibly effective
as a topical ointment. Well documented. I never would have imagined this. You had people with
abrasions and test subjects. People with raw honey and people not and the raw honey, it will
increase the rate of healing by double, two fold. It’s just remarkable. But honey, I’m not sure. I’m really not. It’s nature’s only source
of natural sucrose in a way insofar as it’s pretty evenly split with fructose and glucose. But I don’t think it’s an accident in nature that early man, we’ve mitigated this process by having our little honey farms. But once upon a time, if we wanted honey for ourselves or our families, we would have had to be
prepared to undergo battle with these little (audience laughing) punks who are gonna do their best to prevent us from getting
their hard-earned honey. So we would have gotten a little honey and run like the dickens and it would have been months
before we tried that again. (audience laughing) So I say let’s treat
honey now like we used to with a great deal of respect for the little guys who made it. That’s a little bit of
an analogy, of course. Fruits and vegetables, eat ’em. Eat ’em. I’m not gonna get into
the fine points here. For the average type two diabetic, insulin resistant individual, you can, depending on how
severely diabetic they are, type two diabetic, you could, there’s some more scrutiny
that can go into this. In other words, the
starchiest of the fruits and vegetables should in
fact warrant some scrutiny. But just for the sake of time and ease we’ll leave them here. In the grains, boy this just depends. It depends on what the actual grain is, how refined they are,
how we’re eating them. Oatmeal is a wide spectrum. Are we eating oatmeal from a little pack that’s a bunch of powder? Or is it the big hardy steel cut oats that have to take 30 minutes to boil and then they’re finally ready? That’s the same plant but
they’re very different responses once we actually get it in our mouths. So this one’s delicate and I appreciate especially in Utah with the
predominantly LDS audience this smacks of a heretic who’s challenging the world of wisdom. If you are feeling that, let’s talk later and I believe there’s not
quite as much to reconcile as you may think. Alright, so the general conclusion with the patient hoping
to mitigate their risk of prediabetes or reverse the prediabetes, just be mindful of the
starchiest of the starches, these most common. Bread, pasta, white rice, potato. Now I add this. Get fermented. By that I mean I think
there’s something to be said for eating foods the way we used to before refrigeration
practices are what they are. Once upon a time if you
wanted your bread to rise you would allow the natural
yeast within that bread to ferment to chew through the starches and create gas or CO2
and that would result in the rising of the bread. We bypass that with quick-acting yeast but the same thing would be said of dairy. Before refrigeration, the
dairy would have fermented and it would have been kefir or sour milk. When you have let a beneficial bacteria chew through some of the natural starches you are improving the insulin sensitivity. So this is something as obvious
as eating sour dough bread. Yes, calorie for calorie, sour dough bread will have less of an insulin
response than normal bread. Same thing with milk verses sour milk. The same thing with adding other sources of these kind of versions
of fermented foods like raw apple cider vinegar
which the data support. A tablespoon in the morning with water, a tablespoon in the evening with water improves insulin sensitivity. It’s such an easy thing to do. Now, increasing fat. Am I going way too fast or is this okay? – [Woman] No. – [Man] It’s good. – Okay. Alright now more fat. Let me defend this. – [Man] You didn’t have
on your last slide. Where does chocolate go? (audience laughing) – So if it’s like the, nowadays thank heavens, with
all these gourmet chocolates we can really get to the good range. No question. If it’s like an 80% dark chocolate and it’s sweetened with something
like Stevia or Erythritol, you know what? You can really enjoy
that fairly frequently. You can’t go banana balls with it. But it’ll be on the green side. – [Man] What about nuts? – Absolutely good. No question. The fattiest of the nuts, the better. But remember peanuts aren’t nuts. Where are my former dietitians? Right? Peanuts are lentils or something else. They’re not nuts technically. So when we talk nuts, any
study you’ve ever seen that talks about nuts, they’re
talking about the walnuts, the pistachios, almonds,
whatever, cashews. – [Man] Brazil nuts. – Those are fatty. I don’t know. Seeds. Yes many seeds are good too. Anyway, those would be good. They’re very fatty. So that’s actually in this range. So now increasing fat. Again, don’t crucify me. Let me defend this before you get upset because I appreciate that this challenges the most fundamental paradigms. Even still, the American
Diabetes Association of which I am a member implicates to insulin resistance. I would love to talk more
about that another time. It’s just a matter of how we’re actually looking at the data, I believe. So more fat. Now what’s the relevance of fat? What happens? Let’s look at what happens
when we give a human strictly individually
the three macronutrients. If you give a human pure protein in case it’s just one type we could have used whey here
or any other pure proteins. This is the insulin response where at around 90 minutes
you have what may be an increase of about three
times over fasting insulin. So the change 300%. So about a three-fold increase. So proteins will increase insulin. That’s not bad. That’s probably a good thing insofar as the protein you’ve consumed increasing insulin will help with the anabolic reactions
anywhere, including muscle, so it’s not a bad thing. But too much protein
needs to be scrutinized. There was just a study
published in a very good journal just over the past few weeks
looking at putting people on a high protein calorie-restricted diet and they lost weight but
their insulin resistance didn’t improve as much as the other people who lost a similar amount of weight. So protein is something
that we can’t go crazy with and indeed we should never
be taking as protein powders. There is just no reason for that. If you’re a body builder
and you wanna get swole, you just need to eat more real food. Skip the powders. Don’t drink shakes. Protein shakes. Not worth it. Alright, now what happens
if you give someone a pure carbohydrate? Of course the response
is much more dramatic where you can get upwards over a 10 time increase in your insulin. Now, appreciate again there’s a tremendous spectrum of starches. If we were to put sugar
or bread on here or potato it would be even higher. If we were to put broccoli that’s gonna be much, much lower. So when it comes to carbs, not
all carbs are created equal. Of course they’ll be a very
different insulin response. But the average carbohydrate
like pure glucose we’re gonna be around
10 to 15 times increase. Now what happens if you
gave a person pure lard which mind you, we always look at lard as just this horrific thing. There’s as much unsaturated fat in lard as there is saturated. If that pig especially
has been pasture-raised and allowed to eat something
other than corn and wheat which the pig wouldn’t
normally eat anyway, allow it to eat what it would normally eat it has much more unsaturated fats in its fat than saturated or than normal. So if you give someone pure lard, what’s gonna happen to their insulin? You can’t even see it barely. There’s no effect whatsoever. Dietary fat has no effect on insulin. Now I appreciate how
somewhat artificial that is. You could eat a pure
carbohydrate in nature. You couldn’t eat a pure
protein in so far as I know. Erin, am I right or wrong? I think I’m right. You wouldn’t eat pure fat in most cases. Typically in nature, you’re gonna get fat and protein together. So I appreciate that
by strictly eliminating the protein aspect, we’re
kind of creating something that’s a little artificial but can still in our day
be taken advantage of. When you’re eating more pure fat, you can feed the body
while keeping insulin low and that has several
benefits as we’ll get into. So fruit and animal fats
should be primary sources of dietary fat for the patient who wants to mitigate the risk of insulin resistance or reverse the trend. What I don’t have on here, vegetables oils which we can talk more about. – [Woman] What’s a fruit fat? – A fruit fat. There are the three fatty fruits. (audience chatting) Avocados, olives, coconuts. Those are fruits that are meant, early man, all we would have done, we would have squished it
and we would have gotten the oil out of it. But get oil from canola or soy beans? Oh, no, no. The chemical process, the pressure, the heat that you have to have to get oil from a vegetable, that’s
a new kid on the block and there’s just not
enough data out there yet for me to just blanket,
throw that into the mix. We’ve been eating these for a millennia. Early man, we cut our
teeth on these things. We can handle them. Okay, this isn’t as
controversial as you think. Lest some of you are still
thinking of me as a heretic. I, even as a boy, remember this vividly on my grandparents’ coffee table. What unfortunately has not
gotten nearly as much press was this Time cover. Eat butter. Scientists label fat the enemy. Why they were wrong. This is really going mainstream. The idea that fat isn’t the villain and in fact probably never has been is really becoming accepted more and more. So again, I’m not quite
as crazy as it may seem. Indeed, the most recent dietary
recommendations in the U.S. no longer restrict fat or cholesterol. They do place a limit on sugar. They still place a limit on saturated fat which I won’t get into now but you’ll notice that
even though they’re not saying a limit of fat like they used to, no more than 30% of calories or something, they’re still kind of going
along same old party lines. Eating low fat or no fat. My goal in my home is
for when my kids someday leave my home and go to college, I want them to be in a
place with their roommates, open up their fridge and
say what is low fat yogurt? What is skim milk? No. In my home, we eat things
the way God intended them to be eaten. Who am I to take fat out of milk if God put it there? (audience laughing) And so on and so forth. So we eat real food and real
food has fat and that’s okay. Alright so that’s the end of the fat one and again, we’ll defend, we’ll
put some of these in context when we look at some
disorders if we have time. Intermittent fasting. Just for the sake of time. I emphasize the intermittent nature. This is not the same
as calorie restriction. It is not the same as every
meal you leave the meal hungry. I just don’t think
that’s a sustainable idea to constantly be hungry. You are fighting fundamental
urges in the body to eat and so constantly telling a patient who has insulin resistance
oh you need to lose weight. How do I lose weight doctor? You need to eat less and exercise more. That doesn’t work. It just doesn’t work. If it worked, the problem would have ended right when it began if
it were that simple. It’s not sustainable. So here’s just one piece of evidence looking at it made an
attempt to put people at a 25% calorie restriction either as a constant part
of every meal of every day for the study period, six months, or allowing them to eat
liberally for five days and then restricting calories for two days to get them to the same general
25% of calorie restriction week over week for six months. Now mind you, in the end, this group actually ate
more than this group. So the calories consumed in the intermittent
fasting group was higher. Now let’s just look at
these key variables. Body weight was comparable. No statistically significant difference. So we can’t say there was a difference. Body fat over the six months was not statistically different either. Now when you get to waist circumference, we’re getting really close. In fact, this one is even closer. We’re getting to the .05. So we’re starting to see
that there is a trend for statistical difference that the intermittent fasting
group, the light blue, had a greater reduction in
their waist circumference. Then the last thing we look at, changes in insulin sensitivity, now we have a significant departure. In fact, it’s quite dramatic. Despite these error bars, it’s still highly
statistically significant in as little as three months and then much more
noticeable at six months. So this group, by even
eating more calories, by having a period of time that they were making sure their glucose came down to fasting and stayed fasting for a significant period of time, allowing insulin to come down
to basal levels and stay low, that resulted in a significant improvement in their insulin sensitivity. So intermittent fasting is
the context of prediabetes and insulin resistance
is a relevant aspect and should at least be
considered in the therapy insofar as the patient can perhaps eventually get to that point, especially as they wean themselves off of a high carbohydrate diet. – [Man] Describe intermittent fasting. We think of fasting for 24 hours. – Yeah we do. So the way I interpret this. I’ll talk about that. I’ll have some
recommendations in just a sec. This is a study that showed
that severe calorie restriction or starvation diets
causes insulin resistance. So the patient who has
anorexia, for example, will have profound insulin resistance. But I won’t get into that. So at its simplest, I at least recommend the
12 hour fast every night. So you eat dinner at six. You don’t eat anything again
until six that next morning. There’s some fascinating studies looking at neurological function and they do this to the patients and it’s just remarkable how they improve these early stage Alzheimer patients. Then a couple times a
week, skip breakfast. But again, you’re eating full
meals at every other meal. You’re not going hog wild. You’re eating until full
and then you’re done. Controlling the starch, avoiding the starchiest of the starches and being more liberal with fat and thus calorie number has
become far less important than calorie type. Then every so often, one
of two times a month, a 24 hour food and again,
these are just food fasts. Food fast, food fast. Not liquid, not water. So with these four pillars I wanna just look at some data that’s looking at the effects
of controlling starches and being more liberal with fat. So in short, in essence, we’re taking the trends
that were once initiated by a government that maybe shouldn’t have and we’re just reversing them. We’re starting to flip them on their head and we’ll see what happens. So we’ll look at four conditions
insofar as time allows. We really don’t have much. So too much body fat is a problem. Body fat is a problem of too much insulin. This isn’t a new idea whatsoever. The idea that various foods,
particularly these starches, increase body fat more than other foods has been very well-documented. In fact, type one diabetes
is an excellent example. This is a woman. Type one diabetes. This is her thighs, her crotch, her knees are down here. What on earth is happening here? – [Man] Injection sites. – Injection sites. She’s a type one diabetic. These are not tumors. She’s simply not good
rotating her injection sites. This is a pretty dramatic
example and it’s old. This one is more dramatic and not as old. This was published just last year in JAMA. This they called it in
UK belly bottom syndrome. (audience laughing) He wasn’t rotating his injection sites. So this is just proof of just
how lipogenic insulin is. Indeed it is impossible. I know of no single
circumstance in human history where a patient can
gain fat or become obese without insulin driving it. It’s a thyroid problem, cortisol problem, or any other steroid, nonfunctioning steroid, whether
it’s a brain damage problem or genetic origin, it always
comes back to insulin. I actively try to find the exception. In 10 years, I’ve still not found one. It always comes back to insulin. Here’s the first type one diabetic patient in the U.S. to get insulin. Six months later, the
profound difference of course is that she, in addition
to having a monthly hair do now has gained some weight. So two things happen typically when a type one diabetic
begins treatment with insulin. They start eating less. They have better appetite control and they start gaining fat. This condition of a type one diabetic avoiding insulin shots to stay thin is very much a real eating disorder referred to as diabulemia. About 15% of all type
one diabetics have it. What about type two diabetes? When you take a type two diabetic and in month zero, the beginning
of their insulin therapy, let’s look what happens. So you’ll see at month zero
from one to three to six, what’s happening in their
overall required dose of insulin to maintain normal glycemia? – [Woman] Increasing.
– It’s increasing. That’s not surprising, right? You can appreciate now that insulin causes insulin resistance. What’s happening to body weight over the same period of time? From month zero in kilograms to month six they’ve gained about 20 to
25 kilograms of pure fat. That’s actually quite common
in a type two diabetic. They start insulin therapy, they will gain a significant amount of fat in fairly little time. What’s perhaps the most relevant now is what happens to how much they’re eating over the same period of time. You look at their daily consumption, they’re eating roughly
300 calories fewer per day at six months and yet
they’re 25 pounds heavier. So every day that goes by
they’re trying to fight this weight gain but because
the more and more insulin’s creating more and more insulin resistance, and the insulin is promoting
the growth of the fat cell, this isn’t making a difference. It’s not enough. So patients with cancer,
what typically happens to body weight in a cancer patient? Typically they lose weight, right? That syndrome of wasting,
known as cachexia. Now this isn’t the universal trend but it’s common enough in
insulin-secreting tumors of the pancreas,
insulinomas, this study found that almost three quarters
of them were gaining weight throughout the course of their cancer. Again, not a typical
response when it comes to the cancer in the body. So with body fat what happens
if we make these changes? Here is a study. A randomized trial, of
course the goal standard. They put people on a low carb
calorie-unrestricted diet. So low carb, high fat,
unrestricted access to calories, verses a calorie-restricted low fat. So it’s kind of the typical dogma when it comes to losing weight. The 24 weeks, which is fairly short term, there are longer studies
that we could go into, we see that the fat
liberals starch-controlled, not the quiet exit she hoped for, (audience laughing) (background noise drowns out speaker) So several kilograms
difference in body weight even though this group
is eating more calories than this group. So the calorie number was very different but of course the calorie type was too. – [Man] What qualifies as low carb? – That’s a great question. There’s a tremendous range. It could be simply putting
it below the 50%, 60% norm which many would say, even other sort of scientists, especially in the nutrition realm, would balk that I would be even talking about lowering carbs below 50%. I am a big advocate at a minimum of going back to where we were
before the food guidelines. At a minimum, which was a 40, 40, 20. That should be, in the
case of insulin resistance, or someone who wants to avoid
it and its consequences, a minimum macronutrient ratio. 40% fat, 40% carbs, 20% protein. But even in people who
are more carb intolerant, you can really swing that ever further where it gets to a 60% fat, a 60, 20, 20 or even a little further and then you have profound benefits. More studies looking at reduction in body fat but altering. More studies looking at a
low carb or a low fat diet, body mass going down more, abdominal fat going
down significantly more than with carb restriction as
opposed to fat restriction. Now diabetes, sorry that I’m rushing now. In fact, let’s just kinda skip this one. Type two diabetes is a
problem of insulin resistance. If you remove the insulin resistance there is no type two diabetes. That is a fundamental
cause of the disease. So with type two diabetes,
I’ll just show this study. Due to the potent effect
of carbohydrate restriction and decreasing blood glucose levels, we must reduce the insulin
by 50% on the first day of dietary carbohydrates restriction to avoid hypoglycemia. As the weeks pass, most patients achieve normal
glycemia without medication. Obese patients lose weight
and patients save money because of the lack of
need for medications. So this is increasingly accepted. More data dogma. The carb restriction needs to be a part of the dietary protocol for someone hoping to reduce the risk
of insulin resistance or reverse it. Sulfonylureas, which are
insulin-secreting drugs, they were reduced or
eliminated all together. The patients who couldn’t
get off their insulin were able to go down to 18 units per day which is a pretty profoundly low number in an insulin-dependent diabetic. More data looking at the
changes in glucose and insulin in an (mumbles). You’ll see that even isocaloric diets the high fat, low carb group,
look at their drop in insulin. They had a almost 50% drop in insulin as opposed to about a 15%
drop in the low fat group. Heart disease. This is the one that’s a
little, there’s a lot to it and when I appreciate
that when I’m encouraging the consumption of fat, one of the most common responses is well, then they’ll
die of heart disease. It’s just not that simple. So insulin resistance is a
key component to heart disease in any of its aspects
insofar as heart disease is quite an umbrella of
cardiovascular disorders and as you have the patients
start changing their diet, eating more fat,
controlling their starches, you’ll see that the
triglycerides drop by roughly 50% despite eating a high fat diet
compared to the low fat diet. HDL goes up by roughly 10%. Very importantly, the
triglyceride HDL ratio which is the poor man’s
method of determining the circumference and
density of LDL particles. LDL itself is not, it’s
a terrible predictor of heart disease. If you can look at the subclass of LDL, what the actual diameter is, is it more type B or more type A or pattern B or pattern A that becomes particularly relevant in the predictive setting. So anyway, beneficial lipid
changes in every condition when you’re in the
context of heart disease by eating more fat. More data on that. Cancer, of all the topics,
maybe this is the one, so the most common cancers are also prostate cancers
and breast cancers. So the average breast tumor
has six to seven times more insulin receptors on it
than normal mammary tissue. Prostate cancers as well have been found to have an increased expression
of insulin receptors. So they’re responding, this growth signal that insulin provides. The most insulin-sensitive men have the least risk of prostate cancer. The most insulin-sensitive women have the most reduced
risk of breast cancer. So insulin resistance is relevant. Part of this could be due to this thing called the Warburg Effect. Have you guys heard of this? Some of you. The Warburg Effect is the
phenomenon where we see that cancer cells love glucose. They don’t wanna use any other fuel to produce their ATP to fuel the growth if they don’t have to. So the problem with type two diabetes is that we have this perfect storm. We have too much insulin
which is an anabolic hormone telling the cancer cell to grow and we’re feeding that
growth by providing it with a hyperglycemic environment. That’s maybe why there’s such a connection between insulin resistance and diabetes and certain types of cancers. So here’s some interesting studies. When you give someone an
insulin-secreting drug like sulfonylureas or actual
insulin therapy itself they have up to a 50% increased risk of developing cancer. Another study looking
at sulfonylureas again, a drug that increases insulin
secretion in the pancreas, or just insulin itself, once again you have a 30 to 90% increase in the incidence of cancer
or the risk of cancer. So what happens if you do this? For the sake of time, I’ll just show this one study suggesting, ketogenic is a term I haven’t introduced. Just look at that as being synonymous with high fat, low carb. This is just indicating that this perhaps should be part of the therapy in addition to the well-established
chemo and radiation. I am in no way suggesting this is an effective replacement. I’m not that naive. But I am informed enough to believe that there should be some role
for it in clinical practice. We’ve got what, five
minutes for questions? Not a lot, I’m sorry. I’ll be thrilled to answer any questions in any time we have left. – [Woman] So you kind of
put insulin as an enemy but what do you suggest for people with type one diabetes? – Yeah. – [Woman] Get well.
– So a type one diabetic. The type one diabetic
would want to incorporate the same dietary changes
the type two diabetic would. There’s something, in
the end, the relevance is they just simply have
to then give themselves less insulin based on what they’re eating. The type one diabetic eats a doughnut, they theoretically need
the same amount of insulin that my pancreas would
make to handle that glucose but they’re injecting it. So the relevance of this
is highlighted in the fact that a type one diabetic can
develop type two diabetes. Did you guys know that? It’s a phenomenon referred
to double diabetes. If that type one diabetic
is giving themselves a lot of insulin to handle the incredible amount of
starches they’re eating, they will become insulin resistant and again, that’s double diabetes. So they have the worst of both worlds. What else? Anything else? Yeah. – [Man] Describe the glycemic index. We see that all the time. – Yeah, the glycemic
index is in fact terrible. (audience laughing) The glycemic load is very valuable. The difference between, I
hope I can explain it well. The glycemic index will
take the type of starch that is in that food and
assume a certain amount of it. Like it will take, assume
a hundred grams of starch from a watermelon and compare
that to a hundred grams of starch from a piece of bread. Both of them have very
high glycemic indexes. But the glycemic load actually accounts for how much starch is in that food. There’s actually very little
starch in that watermelon. So watermelon has a high glycemic index which gives it a sort of
falsely bad reputation because the actual amount
of glucose you’re getting from it is profoundly low. So it has a very low glycemic load whereas bread, for example, or sugar that has a high glycemic
index and glycemic load. So a low glycemic load diet, although I can appreciate
the utility of glycemic index simply because it’s so
much better documented. We have GI numbers for almost everything. We don’t quite have good
glycemic load numbers for everything but
insofar as a patient could and was able to let the glycemic
load dictate their diet, then they’d be in great
position, a great situation. But it gets a little complicated when you start mixing
your nutrients together. The glycemic load of a
hamburger patty is nothing but the glycemic load of
the bun is tremendous. When you put the two together, it’s gonna be somewhere in the middle. It just gets complicated. So just skip the bun
and wrap it in lettuce. – [Man] Plus the ketchup. – Plus the ketchup. (audience laughing) And the mayo. And whatever dressing they’re putting on. It’s loaded with sugar. – [Man] Any effect of caffeine (mumbles) things like that? – Yeah, so caffeine has no known effect on insulin resistance that’s direct. You can infuse humans and
animals with caffeine. They won’t become insulin resistant. I don’t think it’s that simple though. Caffeine increases the
sensitivity to cortisol so it enhances stress response and insofar as that is an
indicated, revealed phenomenon, it’s hard for me not to
think if cortisol’s up, insulin has to work harder. We haven’t seen that
connection yet, though. So I appreciate the
danger and the scientists making that leap. That is a leap. I’m admitting it. But caffeine is known to
increase the cortisol response. The same goes for cortisol is eliciting an exaggerated response in
the presence of caffeine. I am a huge opponent
of caffeine personally. I don’t think it should
be a part of our diet, as prevalent as it is. No question, it is an addictive drug and we should treat it like that. Anything else? Did I upset anyone by encouraging
the consumption of fat? I hope I didn’t. I didn’t mean to offend. (audience chatting) Simply inform. Okay, thank you guys, thanks. (audience applauding) Thank you. (audience chatting)

26 thoughts on “Grand Rounds_10.27.2016_Why We Get Sick And Fat_Dr. Benjamin Bikman

  1. The future and outcome of nutrition's effect on health lies in the work of young men and women such as our Dr.Bitman.

  2. if the cortisol is causing insulin resistance, why elevate it with a low carb protocol which will elevate stress hormones on a continual basis?

    if insulin resistance is made worse by elevated fatty acids, why not remove them from the diet?

  3. Probably the worst and most disrepectuful bunch of morons sitting in this audience… everybody makes noises… watching this is a pain in the ass…

  4. I never saw a person to bring lunch to a meeting like this. But, let's applaud the guy brought a salad and not a bunch of donuts!!

  5. the audience are Hospital Staff
    Doctors , Nurses, Dietitians, Physiotherapists etc……
    they are eating because their lunch break
    is the time this talk was given…..
    they were fortunate to be able
    to attend in their busy shifts…
    the healthy food may have been provided as part of the talk…
    Fabulous Dr Bikman

  6. So according to this presentation fat in the cell is not the one cause of insulin resistance? Then why does it clear up with body fat loss?

  7. Should have moved the mic location and asked everyone to settle prior to the introduction. Or better yet, don't record again in a hospital.

  8. Everyone needs to familiarize themselves with carbohydrate density. That clears up the muddy waters of glycemic index and glycemic load.

  9. What a shame that no directional mic was setup. Don't use camera audio, else you get this awful sound. Hopefully a lesson learned other than the great info from Dr Bikman

  10. What are the 3 artificial sweeteners that he recommends? They are listed on the slide, but he never says what they are.

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