How Knowledge is Power in Nutrition | Dr. Wendy Pogozelski | TEDxSUNYGeneseo

How Knowledge is Power in Nutrition | Dr. Wendy Pogozelski | TEDxSUNYGeneseo


Translator: Rhonda Jacobs
Reviewer: Ellen Maloney Good evening. It’s a privilege to be here. I would like to thank the organizers
for doing a great job. And I’m very happy to begin
sharing with you some of my experiences, and I really want to emphasize the point
that knowledge is power. So when I came to Geneseo,
I had to teach a course in metabolism. And this is metabolism. So talk about needing
some memory techniques. If you’re learning
all these reaction pathways, the students really had to pull out
some memory links. But also, as a teacher, I felt that
I was being deathly dull in teaching this. So I knew that I had to find some ways to make this interesting
and memorable for the students. So I thought, well, everybody eats, right? The obvious thing would be to link
biochemistry with nutrition. You’d think that the biochemistry
textbooks would do this, but they don’t do it. So I said, let’s look at some of these
controversial diets that are out there, and maybe I can compare these diets
and bring this information into class, and make it a little more exciting
for the students to learn. I especially began focusing
on some of these low-carb diets, there are even ones in Russia and France,
Australia and across the United States. And these diets were very useful
because they illuminated many of the things about metabolism
and about insulin in particular. The approach was very good in my classes. The students really liked the approach
of linking biochemistry with nutrition. And since I’d read
a couple billion papers, I thought, why don’t I just
write this up in a paper and save some other
biochemistry professors the trouble? But I never expected all of this work
to actually benefit me personally. But then in February of 2007, I began
experiencing some strange symptoms. I had raging thirst, debilitating fatigue,
and I’m not being overly melodramatic, this is really the case, blurry vision, I couldn’t even distinguish
the people in the front row of my freshman chemistry class. And then crazy, overnight weight loss,
which for all my life had been impossible, but was suddenly possible. So I had this diagnosis,
“You have type 1 diabetes.” And I was very surprised by this,
and devastated, of course. But it was unusual because I was age 40, and usually type 1 diabetes
is the autoimmune attack on the pancreatic beta cells
that make insulin, and usually that affects people
in adolescence. That’s why it’s usually
called juvenile diabetes. But in fact, about ten percent
of the newly diagnosed type 1 diabetics are in adulthood. Since I had spent three of four years
studying the metabolic effects of various diets,
I thought I knew just what to do. So I, of course, began taking insulin, but I also began reducing
the carbohydrates in my diet, and I did that partly because I knew that carbohydrate is the biggest
dietary contributor to high glucose. And I also know that it’s difficult
to estimate the amount of carbohydrate and then match that with estimating
the amount of insulin needed. So you just minimize your errors
with a low carbohydrate approach. And I had very nice,
flat, normal blood sugars. My doctor said that I had the blood sugars
of a non-diabetic, basically, on this approach, and that I was his best patient ever. And being an academic,
I’m addicted to gold stars, and so I was very pleased with that. So, then my endocrinologist
insisted that I visit a dietician, and the dietician did not give me
a gold star, not at all. She was, in fact, appalled by my diet. And what she told me is that you have to eat a minimum
of 130 grams of carbohydrates a day. I was eating, maybe 30-50 grams per day. So I tried to protest. She said, “No, the brain needs
130 grams of glucose.” And of course,
as a biochemistry professor, and someone who had been teaching
about metabolism for a long time, I said, “Well, what about
gluconeogenesis?” Gluconeogenesis is the body’s
making its own sugar. Usually the brain survives
quite nicely on that. Well, she said, “The American
Diabetes Association, the ADA, gives me these guidelines, so I have to
give these guidelines to you.” And again I still
tried to fight a little bit. And what she did was she got
the rest of the health team to enforce her position, and one of the nurse practitioners said, “I want you to eat chocolate;
I want you to live.” Now who can resist medical
advice to eat chocolate, right? And, I kind of do understand the link
between chocolate and living, but, in any case, I was in a quandary
as to whether I should accept this or not. So here is the American
Diabetes Association diet. In the guidelines
that are published by the ADA, the authors, of course, say
that carbohydrates turn to glucose. The more carbs you eat,
the higher your blood glucose goes. But then they bring up the food pyramid,
the USDA food pyramid, and say, at the bottom of the food pyramid
is bread, cereal, rice and pasta, and you need six-eight servings
of these per day. So it’s pretty much a very similar diet
to the actual food pyramid. And then, of course, those carbohydrates
will then need to be covered with insulin or with drugs. So, I was in this quandary.
Which pathway should I trust? I’d already had some good effects
with a low carbohydrate diet, but here was the medical establishment
giving me some opposition. So what would you do? Well, I was actually trained
to respond well to authority, and any anti-authoritative impulses
were kind of squelched. Also, I’m not somebody
who distrusts the medical establishment. I’m not someone who tells cancer patients
that they should just use essential oils, or that kale smoothies
are going to cure everything. So I really believe
in knowledge and training. So my tendency was to really
trust the medical establishment, to assume that they knew more than I did. But I also had my own training. And so as a bench chemist,
I feel that I’d really been trained in recognizing a good experiment, and I felt that I was trained
in understanding the basis for some of these recommendations. And so that’s what I am going to do here. I’m going to try to give you
a feel for how knowledge is power, and for understanding
a little bit about how diabetes can make you much more
confident about your choices. We haven’t had any graphs yet, right?
So let’s look at some graphs. So here’s blood glucose concentration. And these would be hours after
the start of a meal, here on the Y-axis. So we’re starting
at the beginning of a meal. And the green here is a non-diabetic. So normal blood glucose
is about 85 milligrams per deciliter. A type 2 diabetic, for example, might be starting at a much higher
blood glucose to begin with. And then as the meal progresses, as the glucose is absorbed by the body,
of course, blood sugar rises, and it rises much greater
in the type 2 diabetic. And then, of course, insulin begins
helping the cells take that back in, and the blood sugar decreases. And within about two hours,
in a non-diabetic, blood sugar is back to normal. In a [diabetic],
it takes much longer to decrease, and in this case, never returns to normal. And these are very typical results. So the thing to realize here is that carbohydrate is really
made of glucose molecules, by and large, I’m simplifying a lot. But of course, these glucose molecules
are released from the carbohydrate, and they contribute
a great deal to blood glucose. But that glucose has to be
metabolized to give energy, so that glucose has to enter cells. The glucose can’t just cross a membrane,
it needs a special transporter. And so there are proteins
in cell membranes that are very specific for glucose that will enable
the glucose to enter cells. Some cells, like red blood cells,
for example, have a transporter that’s pretty much always open
and the glucose can just slide in. Other cells, like muscle and fat,
have to have insulin. And so insulin can be thought of
as the key that unlocks the gate for that glucose transporter
to let in glucose. And I’ll show you how that works
in muscle and fat cells. Our components here are insulin, our insulin receptor in the membrane, and then in muscle and fat, the glucose receptor
is actually sequestered inside the cell. And only when insulin
binds to the receptor are there a series of signalling reactions that then activate this glucose receptor
to move to the membrane. Let’s look at that: there’s insulin
binding to the receptor, there’s the glucose receptor
moving to the membrane, and then this lets glucose
into those cells. So the point is that you really need
insulin for that process to work. Now in type 2 diabetes,
insulin is present, but the downstream reactions
are affected in some way. We call this insulin resistance. Insulin is made, but
the cells no longer respond. So the big difference between
type 1 and type 2 diabetes would be either the presence of insulin
or the absence of insulin, by and large; we’ll talk more about that. But we know that insulin
is a very, very powerful hormone. This is a three-year-old boy,
referred to as JL in the original Journal of the American
Medical Association paper. He was one of the first children
actually treated with insulin back in 1922. This is a very disturbing picture
of him in his mother’s arms. He weighed 19 pounds at this stage. And this is him three months later,
after being injected with insulin. So you can see that this
is a very powerful hormone. Okay, so the type 1 versus the type 2: In type 1, we really have
too little insulin, so it’s not getting into cells. And then the other thing
to realize about insulin is that insulin puts the brakes
on the body’s ability to make glucose – that process I mentioned
called gluconeogenesis. Without insulin,
gluconeogenesis occurs greatly. In type 2 diabetes, cells
become insensitive to insulin, and because a lot of biology
is all about feedback, what happens initially is that the body
actually turns out more insulin, and then eventually,
there can be insulin insufficiency, but at first, individuals
with type 2 diabetes are hyperinsulinemic – they actually
have a lot of extra insulin – and insulin is a fat storage hormone. So in type 2 diabetes,
the extra insulin is driving obesity as well as obesity probably
driving the insulin resistance, to a certain extent. Okay, but in both cases,
there’s high blood glucose. And what’s wrong with that? Why is that dangerous? Well, glucose is very reactive, and one of the things
it reacts with is proteins, and it gums up proteins, basically,
it makes them very sticky. And one of the proteins
that’s largely affected is hemoglobin. That is the protein that carries oxygen
from the lungs to the cells. Now, where is oxygen delivery the worst? Well, in the extremities. So by the time hemoglobin
gets to your toes, it’s really not working so well. But now gum that up with glucose, and now your hemoglobin delivery of oxygen
is even more compromised. So one of the big risks
of high blood sugar is having inadequate oxygen delivery
to the cells in the extremities and those cells begin to die. One of the reasons why untreated diabetics
or insufficiently treated diabetics will often have to have toes amputated
or even feet amputated. Kidney cells are also greatly affected. There’s an osmotic effect; the presence of lots
of molecules of glucose means that lots of water rushes in
to try to dilute the glucose, and so that’s the reason for the increased
thirst with high blood sugar. And then, of course,
there are all kinds of diseases associated with hyperinsulinemia, but with blood sugar itself,
there’s damage to blood vessels, and increased risk
of cardiovascular events. Now, if you ask the average
person on the street, they’re going to say that diabetics
shouldn’t eat things that are sweet, but they tend to think that bread
or crackers or rice or potatoes are going to be fine. Well, in fact, both of these have very,
very similar effects on blood sugar. Now, I mentioned that hemoglobin
gets gummed up with glucose. So there’s actually a measure of this,
it’s called the hemoglobin A1c, and you might have seen this
on some lab sheets or you may have had
this test done yourself. So this is a measure
of how much of your hemoglobin actually has a glucose molecule
sticking to it. And most people have a fair amount – four to five percent of their hemoglobin
glycosylated at any time. So a non-diabetic would have
about four to five percent hemoglobin A1c. An untreated diabetic might actually
have as much as 14 percent. And usually targets
are below seven percent for treating diabetics. Well, here’s a study of the effect
of a low-carb diet vs. a high-carb diet. In some type 2 diabetics who started out
with glycosylated hemoglobin between nine and ten percent. One group was treated
with a high-carb diet and the other group was treated
with a low-carb diet. And after five weeks,
so just a little over a month, the hemoglobin A1c
in the low-carb group had decreased. Okay, now this is just
the very tip of the iceburg for me explaining
the molecular basis of nutrition and how we can use knowledge
and clinical studies. But the ultimate power
is your own experience, right? So I did the N=1 experiment. So N meaning just one subject, right? Me. Alright, so fortunately,
some new sensor technology can monitor your blood sugar all the time. And the red here is my blood sugars
on a higher carbohydrate diet, not even 130 grams,
probably more like 75 or 80 grams. And this is a lower-carb diet,
more about 50 grams per day. So you can see that there were
much greater excursions, even though I was trying to be smart
about dosing my insulin and timing things correctly. Now, the average blood sugar here
was just about the same. But, these peaks and these valleys
made it much more dangerous. So I definitely, you can see,
came to the conclusion that a low-carbohydrate diet, in my case,
as a type 1 diabetic, is better. Of course that means going against
some of the nutritional establishment, although I do have quite a bit
of support for this position. Alright, so you guys are kind of saying, “Well, wait, I don’t have diabetes,
what can I get out of this?!” Well, chances are you probably
do know someone with diabetes, right? Not counting me. But about twenty percent of the population
right now in the United States is either diabetic or pre-diabetic, meaning their blood sugars are elevated but not quite at the range
considered to be diabetic. The other things
is that even for a non-diabetic, it’s useful to think about
this concept of overall glycemic load. And while most people can tolerate
a fair amount of carbohydrate, there might be a certain amount
which people cannot tolerate. And then also, I really want to emphasize,
it’s a great idea to learn some science and then base your decisions on them. And as you’re learning things,
really go after the ‘why’s,’ okay? Not just a bunch of facts. We can’t always rely on authorities. And I really want you to be inspired
to know that knowledge really is power. And my philosophy, and the one that I try
to encourage my students to have, and my whole goal in my teaching,
is to empower my students. So I have the philosophy
that I attribute to Dr. Gerald Reaven, who came up with the term
‘metabolic syndrome,’ and he says, basically, what we need
is more information and less advice. Thank you very much. (Applause)