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Dr. Colin Champ – Dietary Recommendations for Cancer/Warburg Metabolism

– All right, thank you very much. Thanks everyone for having me. As she told you, I’m a clinician at the
University of Pittsburgh. I’m a clinician researcher so no animal or mouse research for me. The animal mouse research which is vital, my job is to bring that into the clinics. So for all the physicians in the room, my research, my goal is to figure out what were supposed to
actually tell patients. And so my talk today, Ken read me the riot
act, or not Ken, sorry. Jeff read me the riot act and told me I had to be quick here so, I’m gonna basically
touch on the high points. My pictures and everything
was made as brief as possible, just to get, again, some of the high points across. And I’ve given lots of talks
in the past that are online, so I’m gonna try not to
repeat a lot of our data that we’ve presented in the past. My talk is Dieteric Clinicians for Cancer, Warburg metabolism, clinical applications. Again, thanks everyone for having me. I was here last month. I always love to come to Ohio. It’s like, basically Pennsylvania, just everyone drives 40 miles
per hour in the passing lane, and in Pennsylvania our
professional sports teams know how to win championships, so. (audience laughing) All right, we’re off to a good start here. How do I flick? (audience member yelling) How do I change this to the next? Is there a. (audience laughing and yelling) What’s, I don’t have a remote. Is there a, next slide please. (audience murmuring) Okay, so my financial conflicts, I receive compensation for
diet and lifestyle books, I founded and run the
Cancer Prevention Project. So a lot of my talks, the money I make goes to that non profit. So I don’t benefit from it personally. My dietary conflicts, we all have them, mine are that I eat a real food diet. Just, thank you. I never count calories and I believe the food pyramid was the largest public history
mistake in US history and that will certainly effect everything I’m telling you today. So, Warburg metabolism is
basically a PhD topic in itself. So, we’re gonna go through this
here in 17 and 1/2 minutes. No, in all seriousness, I’m just gonna boil it down
to one very simple picture, so depending on how you look
at the Warburg metabolism. About 70 years ago, Warburg found that cancer
cells rely on sugar and that’s basically the end
of the Warburg hypothesis at that point. But realistically, if you dig deeper, there’s a couple reasons why. So they have faulty mitochondria, that may be the cause as to
why they use a lot of sugar for both energy metabolism
and biomass production. It’s a chicken or the egg. It may be the opposite, but anyway you look at it, they rely on, there’s a bottle of wine there, fermentation, glycolysis,
anaerobic metabolism of glucose for energy, even though using a mitochondria would be much more efficient. Is it because they have
faulty mitochondria? Is it because of something else? It depends on who you talk to. It’s a very contentious topic, but any way you look at it, if there’s glucose around, cancer cells tend to do better
at growing and being fatal. Realistically, from a
clinical point of view, in terms of what do I say to patients from Warburg metabolism? This is still way, way, way oversimplified but some of these pathways, which a lot of the presenters, yesterday, especially
yesterday morning, discussed. These are kind of the key pathways when I distill down all these millions of metabolic pathways
in terms of how is diet gonna effect this cancer patient, of glucose and insulin combined
at the insulin receptor, that can up regulate many,
many, many molecular pathways. On here I have AKT and mTOR, these are survival and growth
pathways in cancer cells. IGF receptors, one we know less about, but that can be promoted through IGF, also insulin protein in the diet. And that can also increase
cancer pathways, so. Realistically, we wanna
decrease both of these pathways, and through drugs, we are trying to decrease
both of these pathways but we can also do that through diet. We can also increase these
pathways through diet, which many people talked about yesterday, so I won’t dwell too much on it, ’cause I think at this point, it’s becoming very obvious. So the glucose connection in cancer cells, again, Warburg brought
this up 70 years ago, and frankly, it’s been
shown again and again. One of the first studies
it stood out in my field was a study from Johns Hopkins looking
at blood glucose levels in patients with glioblastoma multiforme, higher blood glucose was correlating with poor overall survival. We’ve seen this in our clinic as well. On the left here, these are over 300 local, regionally advanced
pancreatic cancer patients. A lot of them were
unresectable at diagnosis, which is nearly a fatal diagnosis. So they were treated with high dose ablative
stereotactic radiation therapy. They got chemotherapy. Some of them got amino therapy, and then some of them got surgery. When we looked at all
their blood glucose values on the left, those patients experiencing
a single blood glucose value over 200 had a significant
detriment in their survival. And again, that’s nothing new. We’ve seen this in a bunch
of different cancer sites but what we’re trying to do is
figure out which cancer sites do we see that. In our lung cancer, lungs are very, lung cancers
are very metabolically active. They light up on PET scans. We did not find that glucose
mattered in those cancer cells. We don’t know exactly why that’s the case, but these are the studies we need to do to figure out before we
start enrolling patients on clinical trials to see
how we can effect this. And on the right here, as you see, with each stepwise increase of blood sugar levels over diabetes, there was a detriment in
two year overall survival, from 130 milligrams per
deciliter to 150 to 175. By 200 your survival at two years goes from a little under 50% to 26.5%. So this is a big deal. That’s a big difference. And backing up, this is our study, I’ve presented this before. So back, this was in
2014, so back in 2012, when the initial data came
out from Johns Hopkins and some other places, we said, well if blood glucose is bad, why don’t we put these
patients on a ketogenic diet and see if we can lower it? You can’t always lower blood glucose below a normal threshold on a ketogenic diet, but you can bring it back down to normal, in those patients that have a higher than normal blood glucose. So we did this, just a very basic study, but again, in 2014, a ketogenic diet study in cancer patients was met
with quite a lot of opposition, to a, to put it lightly. On the left here, these were all of our patients. There’s about 55 total patients, before surgery they were diagnosed with what looked like glioblastoma multiformes. They came to the ER. They were put on steroids, they’re blood sugar shot
up to about 135, 140. We know that anything over about 120, 130, based on some of these other studies, portends the worst survival. So, they’re already at that point. They get surgery on the blue here, second to the left, they get put on more steroids. They’re blood sugar goes up. It’s almost 150 now. So they’re rolling right in diabetes. They come in for radiation
with a blood glucose of 150, which we know will associate
with the worst survival. All patients in red there in the middle, this was all of our group of
patients during radiation. We checked blood glucoses
quite frequently. They’re getting Temodar chemotherapy, and their blood glucose is right at the diabetes level. So, in the pink there, was our six patients that
we put on a ketogenic diet, just to see, just to see if we could lower their blood glucose, and it was certainly successful. So they’re average blood glucose was 84. 1/2 of them were on high dose Decadron, which shoots your blood
glucose through the roof, and it stayed totally normal. And this guy on the
right here, in the gray, this is one of our
patient’s who was awesome, he was a chef and he just
had a giant binge day that day of his blood
glucose and it was still 90. So it, very simple study but some of the other docs
are finally saying whoa, there’s actually something to this. So realistically, that last slide I showed with these mechanisms is very simplistic, and this is a whole nother, whole nother talk for a whole nother day. But when I give my
patients recommendations on what they should be eating or doing, I incorporate all the. This is basically my lifestyle pathway. So on the left here, we discussed at length
this whole conference, how we can impact those
metabolic pathways, insulin glucose, IGF, AMP-kinase is another one. It regulates when cells
are in feast versus famine, and when they’re in famine
from things like exercise, lifting weights, fasting,
calorie restriction, or ketogenic diet, it is activated. It turns off all those growth pathways that cancers love. It also turns on our mitochondria, again, mitochondria up, glucose down, is bad for cancer cells. It also creates quite a
a bunch of free radicals in our normal cells, and then our normal cells
create antioxidants to offset these free radicals. You do things like live longer, have better metabolic function, and hopefully fight cancer better. Pamela Goodman told us about 20 years ago, now that breast cancer patients
with higher fasting insulin have a poor outcome. She published this in the Journal of Clinical Oncology. This is at five years for women with stage one and two breast cancers. This is very curable. And they’re survival on the left there is about 95 plus percent and that’s what it should be. These women should be
cured of their disease, however, as you move
stepwise to the right, women with higher insulin, this is a growth hormone, it tells things to grow, it tells cancer cells to grow. As you move far to the right, you see their survival there
drops quite significantly, almost by 25%. So again, we wanna lower
insulin through the diet. And a lot, these are
association studies so there’s limitations for sure. And then this is another study, which was very intriguing, 2014, and unfortunately we haven’t
heard much about it since. There’s a nurses health study, and several other studies, where they spent 100’s
of millions of dollars, with 10’s of thousands of women looking at different risk factors for cancer. They looked at some dietary changes that didn’t pan out so well, but that same group, this is the group at Harvard
that was really trying to link fat and breast cancer. They found that women who
ate a high carbohydrate diet after diagnosis and had
IGF receptors present on their cancer cells
experienced a 5.5 times or 550% higher risk of occurrence, and women that were on a lower carb diet, they’re risk of occurrence
dropped by about 50%. This is with food
frequency questionnaires, so there’s certainly limitations but this is very intriguing. As we know we can effect
this through the diet and this study’s showing just that. And this is nothing new. Even Warburg’s hypothesis
at the time was nothing new. A lot of people in this room know that this data’s been
around, quoted Cahill. We quoted some of these
legends in the field. This is one of my favorite papers. This is the largest mouse study in low carbohydrate diets to date. And it’s from 1913 so
what’s that tell you, in the Journal of Medical Research. It’s by Eleanor Van
Ness Van Elsing in SPBB. And this came out of Cornell, where right now actually, some interesting similar
data’s coming out of Cornell with Louis Cantley’s lab. What they found in these mice is that, in their words, they’re seems to be no
reasonable ground for doubt in view of these experiments that a lack of carbohydrates in the diet produces such an influence upon the rats as to make them more
resistant to tumor growth. When the diet includes carbohydrate the tumors grow luxuriantly. And when the diet does
not include carbohydrate, the animals show a marked resistance. So this is nothing new, these guys knew over a
century ago what was going on. And so unfortunately, in humans
we don’t have a lot of data in terms of a ketogenic diet and outcomes for a lot of reasons. A lot of issues, it’s
tough to get funding, and it’s tough to get these
studies through IRV’s, so instead Rainer Clemen
and a group of us looked at all of the mouse data, formed a met analysis, certainly with limitations, but it’s the best we got and as you see, all those studies to the left of that dotted line at the one show a benefit of a ketogenic diet. And all those that cross show
no benefit, no detriment. What we found that
overall there’s a 45% risk in death in the mice that
were on a ketogenic diet. The key though that we also found was that the diet was effective
when it was started either before cancer was given to these mice, so we see it as a preventative measure. And if you look back through
the mechanistic support of a ketogenic diet, that’s very consistent. The other thing we found was that it was beneficial when the mice were undergoing treatment. So in Doctor Scheck’s study, which I’m sure she’ll bring up shortly, when they were getting radiation or when they were getting chemotherapy, the ketogenic diet made it work better. By itself, it did not work
as a cancer treatment. So that’s something we
need to keep in mind. It works synergistically with treatments. And we don’t know which
treatments those are but these are the things
we need to look at. And this is what Louis Cantley
and Siddharth Mukherjee has done recently, and this got a lot of publicity. I don’t know if anyone
out there’s seen this. This was in Nature. It was a very good study but apparently, when you have a Pulitzer
prize winner on your team, it gets a lot more publicity, so. They were giving mice
a PI3-kinase inhibitor, which basically blocks
insulin in its down regulation and that should work to
help fight cancer cells or kill cancer cells. The problem with it as you
see in the middle here, if you’re blocking insulin, you’re blocking its ability to pull the glucose from the blood. So these mice were getting hyperglycemic and this is a well known side effect of these PI3-kinase mTor other inhibitors. So what they do, they put the mice on a ketogenic diet. And it made the medication work better and it got rid of the
hyperglycemia so just like the GBM study that I showed you, you put mice and humans
on a ketogenic diet, and then put them on a medication that makes their blood glucose
shoot through the roof, it offsets that. So for that purpose alone, we need to start exploring the
ketogenic diet a little more. As you see to the left here, blood glucose shoots through the roof with a normal chow diet. This is their work. As you see to the right, C-peptide with a control
diet is quite high. Metformin did not work
so well in their study. SGLT, T2I did and a ketogenic diet did. And then as you see to the left, to the, see down they’re in the middle, a ketogenic diet and they’re testing
medication significantly, synergistically to decrease tumor volume. So these are the studies
we need to do more of. I have a patient right now with a glioblastoma who is on neratinib. Which is an EGFR inhibitor
and he’s on a ketogenic diet for a similar reason. It’s an N-of-1 so we’ll see what happens. These are more of the
studies we need to do. There’s a lot of other
metabolic interactions that we need to assess as well. We looked at statins in our patients and statins actually improved survival in local region advanced
pancreatic cancer patients as well. There’s a mevalonate pathway and multiple other metabolic pathways that are disrupted by statins. This had nothing to do with circulating cholesterol or anything, but those patients on and
actually did a lot better and they responded to the
radiation and chemotherapy better, so what we need to do is
keep insulting the metabolism of cancer cells and we can do that through other mechanisms as well. And what we found in our
lung cancer patients, the numbers were limited so it really just was a trend but it was quite close to significant. Those patients that we
were ablating their tumors with stereotactic radiation, those patients in the green here, had blood glucose levels
in the diabetic amounts, and we actually had worse local control with the radiation. So simply having more
blood glucose around makes the radiation work much less effectively and this was one of the first study’s to show that in humans. The other thing that we found is that simply having
excess adipose tissue, and this is a, this is the
first study of this kind, simply having excess adipose tissue makes radiation work worse. So we’re treating your pancreatic cancer with high dose radiation, and the risk of it coming back, the risk of it coming back doubles goes from, at 10 months it returns, versus over 20 months. Unfortunately a lot of
these tumors do return, ’cause they’re quite hard to treat. And as you see on the right here, freedom from regional recurrence, those curves start
separating with patients with BMI’s of 25 to 29.9. So simply having excess body
tissue secretes hormones, increases insulin, does all these, this metabolic derangement that actually makes our
radiation not work better. So to me that is, we can effect this, and we can effect this quite instantly and we can hopefully
effect this before people are even diagnosed with cancer. So as a clinician we need to
look at population studies, and remember there’s some
statistical issues with those. We need to look at mechanistic support so the next couple of studies coming out, or the next couple of
researchers coming after me, pay attention to the important studies that they’re presenting, animal studies we have quite a bit. We don’t have a lot of randomized. Well, we don’t have any
human randomized studies on cancer patients with ketogenic diet or some of these other things. But if you look back at that data, right, the overarching picture here is insulin, glucose,
excess adipose tissue. We know in randomized studies in humans that we can effect those. So, as last time I checked, a low carbohydrate,
calorically unrestricted diet has won over a low fat calorically
restricted diet, 28 times. They’ve tied 29 times, and a low fat diet, which is often recommended
to cancer patients, if you add up the simple championships of the Bengals and the Browns, you get the number of times a low fat diet’s been successful, so. (audience laughing) But as a clinician, this is data that I can
show to my other physicians when they say what the heck
are you doing putting patients on a low fat diet or on
a low carbohydrate diet? I say I’m just supporting the data here. That’s all I’m doing. (audience laughing) And again, there’s a lot more to this. There’s a lot of other metabolic pathways that we’re gonna have to effect and we’re gonna have to research, so. The recommendations I make
really do not sway at all from a paper that we published, what is it now, six and 1/2 years ago, for breast cancer patients. The same thing, we wanna decrease adipose tissue. We wanna decrease glucose. We wanna decrease insulin. So you’re probably thinking
if that was published in 2012, why haven’t things changed? So my research group, I have some savvy med students, they actually filled out a Freedom of Information Act request, and if you fill this
out with the government, they have to tell you what they’re doing at their hospitals, and this is what they’re
doing at they’re hospitals. This is what is mandated. Mandated by Coke to be out
into their vending machines. 50% of the drinks on this
list directly are against what the government’s saying. Right, you only can have 10%
of your daily calories in sugar throughout the entire day. 50% of these supply that
in a single serving. This is the other mandated items. Candy bar, it’s mostly candy
bars, pretzels, potato chips. How the heck are we supposed to do anything in this research field if we’re telling patients not to eat the same foods that they’re
selling in our hospitals? This irks me to no end, and we should, we need to stand up and fight this. It should not be at any hospitals. We need to riot. Tip these over. (audience applauding) Last but not least with
my 20 seconds here, I got married two months ago and that’s my beautiful wife, and, this was our wedding in Italy. We had a seven course meal, we had. She’s Indian, we had vegetarians, we had my derelict friends, alcoholics. We ate a seven course ketogenic diet meal and everyone loved it, and no one noticed anything. So these are foods that
culturally support our patients and patients will enjoy, thank you.

11 thoughts on “Dr. Colin Champ – Dietary Recommendations for Cancer/Warburg Metabolism

  1. Thanks Colin, even my doctors now understand Keto – Doctors are finally identifying with CHO restrictions and the Warburg "Otto Warburg" effect … my "GoTo's" Dr. Colin Champ, Dr. Jocelyn Tan (Keto Oncologist), Dr. Eugene Fine, along with Prof Thomas Seyfried … Cancer as a Metabolic Disease, and Dominic D'Agostino and Travis Christofferson ….

  2. 5:30 Lung cancer does not light up in scans because in liver, Glutamine used as main source of energy for cancer cells.

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