Here is the full transcript of biochemistry professor Dr. Wendy Pogozelski’s TEDx Talk: How Knowledge is Power in Nutrition at TEDxSUNYGeneseo conference. This event happened on April 4, 2015 at Geneseo, New York.
Listen to the MP3 Audio: How Knowledge is Power in Nutrition by Dr. Wendy Pogozelski at TEDxSUNYGeneseo
Dr. Wendy Pogozelski – Professor of Biochemistry
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 iceberg 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. All right, 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.
All right, 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 thing 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.
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