Transcript of the Video
Sugar: The Bitter Truth
Dr. Robert Lustig is a Neuroendocrinologist out of UCSF with a specialty in Childhood Obesity. By the end of this video, he hopes to debunk the last 30 years of nutrition information in America.
According to Dr. Lustig, the obese are getting obeser, but the BMI (Body Mass Index) curve is shifting. We all weigh 25 more pounds today than we did 30 years ago. All of us. Our genetic pool hasn’t changed in the last 30 years, but our environment most certainly has.
In order to talk about the environment, we need to talk about what is obesity. Of course, we’re all familiar with the concept of the first law of thermodynamics which states, in human terms, that “if you eat it, you better burn it, or you’re going to store it”. Calories in, calories out. Dr. Lustig used to believe that, but not anymore. He thinks it’s the biggest mistake. It’s this phenomenon that he will attempt to debunk because there’s another way to state the law, which is much more relevant and more to the point.
“Calories in calories out” means two behaviors, gluttony and sloth. If that were the case why are all these countries who have adopted our diet all suffering now from the same problem?
There’s another way to state this first law. If you’re going to store it, and you expect to burn it (normal energy expenditure for normal quality of life) then you’re going to have to eat it. Now all of a sudden, gluttony and sloth are actually secondary to a biochemical process which is primary. It’s a different way to think about the process and it also alleviates the obese person from being the perpetrator but being the victim. Which is how obese people really feel because no one chooses to be obese. In fact, we have an epidemic of obese 6 month olds. If you want to say it’s all about diet and exercise, then you have to explain this! So any hypothesis proffered to explain the obesity epidemic must all explain this too. And it’s not just in America, but around the world now. More on this later.
So what’s the real story?
Let’s talk about calorie intake. Sure enough, we are eating more now than 20 years ago. Teens now eat 275 calories more, males eat 187 more calories and women eat a whopping 335 more calories per day. No question, we’re all eating more. The question is “why”? We’re all eating more because our leptin isn’t working properly. Leptin is a hormone that comes from our fat cells and tells our brain “I’ve had enough. I don’t need to eat anymore and I can burn energy properly”. Something is wrong with our energy balance. If we’re eating more calories now than we were 30 years ago, our leptin isn’t working. It makes no difference whether or not the food is there. There’s something wrong with our biochemical negative feedback system that normally controls energy balance and we have to figure out what caused it and how to reverse it.
So where are all the extra calories from? It’s all in the carbohydrate. We eat more carbs now, especially since we’ve been told since 1982 to reduce our fat consumption from 40 to 30 percent. So what happened? We did it. We reduced our fat consumption from 40% to 30% and look what’s happened to obesity, Metabolic Syndrome, non-alcoholic fatty liver disease, Cardiovascular Disease and stroke prevalence? They’ve all skyrocketed as our fat consumption has gone down.
It’s not the fat, it’s the carbohydrate. Which carbohydrate? Our beverage intake has increased. There has been a 41% increase in soft drinks and a 35% increase in fruit drinks. Just remember that one soda per day added to your diet calculates to a 15.5 lb/yr weight gain.
This is nothing new, but the question is how come we can’t stay energy stable? How come leptin doesn’t work?
Dr. Lustig calls this The Coca Cola Conspiracy. Caffeine is the main ingredient in Coke. It’s also a mild stimulant and diuretic, which makes you pee. There are 55 milligrams of sodium added per can of coke, which makes you thirstier. So why is there so much sugar in Coke? To hide the salt. Anyone remember New Coke in 1985? More salt, more caffeine. They knew what they were doing. That’s the smoking gun. They know. That’s why it’s called the Coca Cola Conspiracy.
Are soft drinks the cause of obesity? It depends on who you ask. If you ask scientists from the National Soft Drink Association, they’ll say no. However, Dr. David Ludwig did a prospective study which found that each additional sugared drink increase over a 19 month follow up period in kids increased their odds risk ratio for obesity by 60%. If you look at Meta Analyses (conglomeration of numerous studies subjected to rigorous statistical analysis) 88 studies all showed significant associations.
What if you take the soft drinks away? There’s a Fizzy Drink study from Christchurch, England where they went into schools and took out the soda machines for a year. Prevalence of obesity stayed constant over the year whereas the prevalence of obesity in the control schools (where nothing changed) continued to rise over the year.
What about soft drinks and diabetes? Dr. Lustig explains 2 different studies that say “yes”.
So what’s in soft drinks? High Fructose Corn Syrup (HFCS). We were never exposed to HFCS before 1975. Today it’s in everything. We are exposed to 63 lbs of HFCS per person per year in America.
So what is HFCS? One reason we use it is because it’s sweeter. HFCS is sweeter than table sugar (120 Index in sweetness vs 100). Pure fructose (lab fructose) is 173. You should be able to use less? Right? Wrong! We use just as much, in fact, we use more. Even lab (crystalline) fructose is being added to soft drinks (without cutting back on it) and they’re advertising it as a good thing. We use HFCS because it’s sweeter but also because it’s cheaper.
HFCS is one glucose and one fructose. Glucose and fructose are NOT the same. HFCS contains 42-55% fructose and sucrose contains 50% fructose. Sucrose and HFCS ARE the same. There is no difference between them. They are equally bad. They are both dangerous. They are both poison. It’s not about the calories. Fructose is a poison by itself.
Before food processing, we used to get our fructose from fruits and vegetables, which would be about 15 grams/day of fructose. Not sugar. It would be double (30 grams). More and more of our caloric intake is being accounted for by sugar every year so it’s not just that we’re eating more, we’re eating more sugar!
For adolescents today, we’re up to almost 75 grams (12% of total caloric intake). Twenty five percent of adolescents consume at least 15% of their calories from fructose alone. Compared to the 16-24 gr/day pre-WWII, this is a disaster. The fat’s going down, the sugar’s going up and we’re all getting sick.
How did this happen? Why did this happen? This is where the politics comes in. There was a perfect storm, created from three political winds swirling around at the same time.
First, Nixon, in 1972, took food off the political table in an effort at re-election, making food cheap.
Second, HFCS came on the American market in 1975, making it a cheap form of sweetener (half the price of sugar) and creating stability in the sweetener market. HFCS is evil because it’s economically evil. Because it’s so cheap, it has found its way into everything, including hamburger buns, pretzels, condiments, almost everything. We are being poisoned by process foods.
HFCS refiners like to say that it’s just been a substitution. As HFCS has gone up, sugar consumption has gone down, gram for gram. Not exactly. Compare 73 lbs of sugar/year in 1973 up to 95 lbs by 2000. What’s also missing is juice, since juice is sucrose. Now the most recent data shows that we are eating up to 141 lbs of sugar/year/person now.
Third, dietary fat reduction was issued in 1982 to stop heart disease. Did we stop heart disease? No, it’s worked the opposite. We created more!How did this come to be? In the early ’70s, we discovered LDLs. In the mid ’70s, we learned that dietary fat raised your LDLs. In late ’70s, we learned that LDL correlated to CVD (Cardiovascular Disease). The thought process was that dietary fats led to heart disease, but this premise is incorrect. The logic is faulty.
This was a battle back in the ’70s. There were people lined up on both sides of the fence. “Pure, White & Deadly” was written by John Yudkin, a British Physiologist, Endocrinologist & Nutritionist, in 1972. Everything he wrote back then is the truth. It’s a true prophecy because everything he said has come to pass.
On the other side was Ancel Keys, a Minnesota Epidemiologist. Keys performed the very first multi-variate regression analysis without computers. He was interested in CVD so he did this study called the Seven Countries Study. He studies percentage of calories from fat on the x axis and CVD death rate on the y axis. It looks obvious that fat correlates to CVD. However, there’s a problem. The fat migrated with the sugar and Keys didn’t hold fat and sugar constant. Wherever there was fat, there was sucrose too. When you do a multi variate linear regression analysis, you have to do it both ways. You have to hold fat constant showing sucrose doesn’t work and then you have to hold sucrose constant and show that fat STILL works. He didn’t do it! This was done before computers so we can’t check the work. Ancel Keys died in 2004 so we can’t ask him. We’re left with a conundrum because we based 30 years of nutritional education, information and policy on this study. However, now there’s a big hole left in this theory.
Now to further complicate things, there is not really one LDL. There are two types of LDL.
- Pattern A LDL are large and buoyant (VLDL) – this one does not correlate with CVD. They are light and buoyant and they float. Because they are so large they cannot form plaque.
- Pattern B LDL are small and dense. They don’t float and are responsible for starting plaque formation. It’s been shown by numerous investigators that it’s the small, dense LDL that is the bad guy.
When you measure LDL in a lipid profile, you measure them together. So when you get an LDL, you get both of them, the good one and the bad one. So how do you tell which LDL is the neutral one and which one is the bad one? You look at your triglyceride level in association with it. For pattern A LDL, typically your triglycerides will be low and HDL will be high. Pattern B will show high triglycerides and low HDL. So determining the good from the bad is done through testing your triglyceride levels. Your triglyceride:HDL ratio predicts CVD way better than LDL ever did.
Dietary fats raises your large buoyant Pattern A LDL (VLDL) and carbs raise small, dense Pattern B LDL.
So in 1982, we all went on a high carb diet because low fat processed food needs sugar to make it palatable. When we find a mistake, we admit the mistake and right the ship. We haven’t done that. We’ve had our food supply adulterated, contaminated, poisoned, tainted – on purpose – and we’ve let it through the addition of fructose for palatability and also as a browning agent, which has its own issues. Why it browns so well with the sugar in it is what’s going on in your arteries because it causes protein glycation and cross-linking, which is actually contributing to atherosclerosis.
Fifty thousand years ago, we consumed 100-300 grams of fiber per day. Now we consume 12 grams. Why? We took the fiber out because fiber takes too long to cook, it takes too long to eat and it decreases shell life. The definition of fast food is fiber-less food.
Then we had the substitution of trans fats, which were clearly a disaster, but we’ve gotten rid of most trans fats. Not completely, but most.
This pretty much sums up the past 30 years.
Now to the Biochemistry. I will show you the following:
- Fructose is NOT glucose, that what the liver does to fructose is really unique.
- Fructose is 7 times more likely than glucose to do that browning reaction, the advanced glycosylation end products.
- Fructose does not suppress the hunger hormone from your stomach, called Grehlin.
- Acute fructose ingestion does not stimulate insulin because there is no receptor for fructose on the beta cell that makes insulin so the insulin doesn’t go up. If insulin doesn’t go up, then leptin doesn’t go up and if leptin doesn’t go up, your brain doesn’t see that you ate something. Therefore, you eat more.
- Liver Hepatic fructose metabolism is completely different between fructose and glucose. They are NOT the same. I am going to show you that chronic fructose alone causes Metabolic Syndrome (cluster of obesity, Type 2 Diabetes, lipid problems, hypertension and CVD).
Dr. Lustig goes on to explain glucose, ethanol and fructose and how they are each metabolized. If you can watch the video, I highly encourage it. To make things easier, it’s located about 45 min into the video. I can not do his summary justice because he uses charts to explain each process. You don’t need to be a Biochemist to understand this!
Let’s consume 120 calories of glucose, which is equivalent to 2 slices of white bread. What happens to that 120 calories? Ninety-six calories, or 80%, will be used by all the organs in the body. Every cell, bacteria, every living thing on the face of the earth can use glucose because glucose is the energy of life. That’s what we were supposed to eat.
Twenty four of those calories (20%) will hit the liver so let’s watch what happens to those 24 calories.
Glucose 6 phosphate (G6P) is created, which can’t get out of the liver without hormones, glucagon or epinephrine. Now the glucose is fixed in the cell, but it’s not very much, just 24 calories worth.
Almost all of the G6P is going to end up going to glycogen. Glycogen is a storage form of glucose in the liver. Glycogen is easy to fish the glucose out with glucagon and epinephrine. The liver can store an unlimited amount of glycogen, which means that glycogen is a non-toxic storage form of glucose in the liver. So the whole goal of glucose is to replete your glycogen. This is good.
A little of the glucose will go through de novo lipogenesis, turning sugar into fat. You then end up with a small amount turned into VLDL. Maybe 1/2 calorie will end up as VLDL. That serves as a substrate for adipose deposition into your fat cell here; triglyceride.
In addition, because the insulin went up in response to the glucose, your brain sees that signal. And it knows that that is supposed to shut off further eating. It’s a nice negative feedback loop between glucose consumption, the liver, the pancreas and the brain to keep you in normal energy balance. This is good.
Ethanol is a carbohydrate and a toxin. We know that ethanol is not good for us.
The brain doesn’t metabolize fructose, but since ethanol affects the brain, it is an acute toxin. Therefore, it is controlled and taxed to limit consumption of ethanol…. because it’s a toxin and we know it.
So let’s consume 120 calories of ethanol. Of 120 calories, 24 calories right off the top go to stomach, intestine, kidney, muscle and brain.
So 96 calories hits the liver (vs 24 calories from glucose). So four times the substrate will hit the liver and there’s the rub. This is a volume issue.
There’s no receptor, no transporter for it. First thing that happens is the ethanol is converted to aldehyde in the liver, which is obviously bad. They cause cancer and cross-link proteins. If you cross-link enough proteins in your liver, you get Cirrhosis.
You have 96 calories to metabolize so it will get metabolized to lots of VLDL, which is the dyslipodemia of alcoholism. Your liver tries to export the VLDL out of the liver so you don’t get sick because when fat builds up in the liver, it’s not good. Some will exit as free fatty acids, which will take up residence in the muscle. This causes muscle insulin resistance. Some won’t make it out and you get a lipid droplet, which is alcoholic steototic hepatitis, liver disease.
Let’s consume 120 calories from sucrose, equivalent to a glass of orange juice. Of those 120 calories, 60 calories are from glucose whereby 12 calories goes to the liver and 48 calories goes to the body. The all of the other 60 calories from fructose are metabolized by the liver. Why? Because only the liver CAN metabolize fructose.
So what do you call it when you take in a compound that’s foreign to your body and only the liver can metabolize it and in the process it creates various problems? We call that a poison. So let me show you how it’s a poison.
Fructose comes in without stimulating insulin. Before, with glucose, we had 24 calories to be phosphorolated, now we have 72 calories. We have 3 times the substrate. It’s a volume issue. We’re going to lose a lot of phosphate. From this process, uric acid is produced as a waste product, which causes gout or hypertension. Consequently, fructose consumption increases your risk for gout. We have a hypertension epidemic in this country. Here it is; it’s the sugar.
As a side note, sports drinks have a place for elite athletes because HFCS helps replace glycogen faster. But who’s drinking the sports drinks? Fat kids.
Fructose activates de novo lipogenesis, creating large amounts of VLDL, which is the dyslipodemia of obesity.
A study of normal medical students found that when taking in a glucose load, almost none of it ends up as fat. However, taking in a fructose load with the same number of calories, 30% of it ends up as fat. So when you are consuming fructose, you aren’t consuming a carbohydrate, you’re consuming FAT! A high sugar diet is a high FAT diet. That’s the point.
Another study with acute administration of fructose shows that it raises triglycerides.
A study of medical students after 6 days of a high fructose feeding, their triglycerides doubled, de novo lipogenesis was 5 times higher and free fatty acids (which cause insulin resistance) doubled. So this is the dyslipodemia of fructose consumption.
But we’re not finished. Some of the fat won’t make it out of the liver just like with ethanol so you have a lipid droplet. Now you have non-alcoholic steototic hepatitis, liver disease.
Another study analyzed sugar consumption against the liver enzyme marker, ALT, which tells you about fatty liver. Sure enough, ALT rises with fructose consumption.
So there’s the lipid droplet of non-alcoholic steototic hepatitis. Some will come out as free fatty acids and populate the muscle, which will tell the insulin to go up higher.
Now insulin can’t do it’s job in the liver so now you have liver insulin resistance as well. That’s going to make the pancreas work that much harder, generating higher insulin levels, which raise your blood pressure even further, causing further fat making, causing more energy to go into your fat cells (there’s your obesity) and finally the higher your insulin, the less your brain can see its leptin. From there, you have continued consumption because your brain thinks it’s starving. And it’s been shown that fructose consumption changes the way your brain recognizes energy, all in a negative way. You basically think you’re starving even though your fat cells are sending a signal that they are full.
You also get an increased reward signal. Continues appetite, continues more fructose, more carbohydrate, generating more insulin resistance. You can see you generate a vicious cycle of consumption and disease:
- hepatic insulin resistance
- muscle insulin resistance
- continued consumption
“Looks like Metabolic Syndrome to me.”
In comparing chronic ethanol exposure to chronic fructose consumption, they share 8 out of 12 phenomenon. Why? Because they do the same thing. They are metabolized the same way. They ARE the same because they come from the same place. Alcohol is made by fermenting sugar. They have all the same properties because it’s taken care of by the liver in exactly the same way and for the same reason because sugar and ethanol ARE the same.
Dr. Lustig explains their clinical intervention. It’s very simple.
- Get rid of all sugared liquids, including juice (there is no such thing as a good sugared beverage) – only water and milk allowed
- Eat your carbs with fiber. Fiber is an essential
nutrient even though the government doesn’t want it to be. Otherwise, they couldn’t sell food abroad.
- Wait 20 min for 2nd portions for satiety signals to take effect
- Buy your screen time minute for minute with physical activity. This is the hardest one to do.
Does it work? Yes.
We were interested in what made it work and what made it not work so we did a Multi-variate Linear Regression Analysis. The thing that made it not work was sugared beverage consumption. The more sugared beverages the subjects drank at baseline, the less well the lifestyle intervention worked.
So why is exercise so important in obesity? Because it burns calories? Come on! Twenty minutes of jogging is one chocolate chip cookie. “Are you jokin’ me?” So why is exercise important?
- Exercise is important because it improves skeletal muscle insulin sensitivity because the insulin actually works better at your muscle, which brings your insulin levels down, which is good for you.
- Exercise is also your endogenous stress reducer. It’s the single thing that actually stress. The resulting cortisol release decreases appetite.
- Exercise makes the TCA cycle run faster and detoxifies fructose, which improves hepatic insulin sensitivity. Exercise allows you to burn the fructose off before you make the fat. That means a higher metabolism, but it has nothing to do with burning calories. You simply can’t burn off all the calories you consume through exercise. You’d need to bike for 10 hours to burn off a Big Mac.
So why is fiber important in obesity? This is my motto. “When God made the poison, he packaged it with the antidote”. Fructose is a poison, but whenever there’s fructose in nature, there’s way more fiber. Sugar cane is a perfect example. It’s a stick! Consequently, you need to eat carbs with fiber.
That’s why fruit’s okay because first, it limits the amount of fructose you’re going to take in and second, it gives you an essential nutrient, which you needed in the first place. And you get some micro-nutrients along with it so that your liver works healthier.
Here’s what fiber does:
- Fiber reduces the rate of intestinal carb absorption, reducing insulin response.
- It increases the speed of transit of intestinal contents to the ileum to raise PYY and induce satiety, which means you get your satiety signals sooner.
- Fiber inhibits absorption of some free fatty acids to the colon, which are metabolized by colonic bacteria to short chain fatty acids (SCFA), which suppresses insulin.
If you ate a Paleolithic Diet, eating everything as it came out of the ground, raw, with no cooking, you would cure Type 2 Diabetes on a dime. Takes about a week. Because you’re getting that 100-300 grams of fiber daily.
Remember where we started? With an epidemic of obese 6 month olds? Could formula be the reason? For example, formula contains 43.2% corn syrup solids and 10.3% sugar (sucrose). It’s a baby milkshake! Soda is 10.5% sucrose compared to the 10.3% sucrose found in formula. Any difference?
And there’s a huge literature coming of age that shows that the earlier you expose your kids to sweet, the more they will crave it later. Furthermore, there’s new literature that shows the more sugar a pregnant woman eats or drinks during pregnancy, the more it gets through the placenta and actually causes what is termed developmental programming, changing the child’s adiposity even before he is born. And driving this whole epidemic even further.
So, what’s the difference between soda and beer? There are 150 calories each. When you actually compute the number of calories hitting the liver, there’s no difference between the two. You wouldn’t give your kid a beer, but wouldn’t think twice about a Coke. But they’re the same. Fructose is ethanol without the Buzz!
Fructose is a carbohydrate but it is metabolized like a fat. Thirty percent (30%) ends up as fat so when people talk about high fat diets doing bad things, they’re talking about high FRUCTOSE diets doing bad things. That’s what Ancel Keys was looking at. In America, and any other country who has adopted our diet, a low fat diet isn’t really a low fat diet because the fructose/sucrose doubles as fat. It’s a high FAT diet and that’s why our diets don’t work. And fructose, just like ethanol, for the same reason, through the same mechanism, is also a toxin.
So what can we do about it? How about the FDA? Fructose has GRAS (Generally Recognized as Safe) status. It came from the notion that fructose is natural. It’s in fruit, it must be okay. Well, tobacco’s natural and it’s not. Ethanol is natural, but it’s not.
The FDA will only regulate acute toxins, not chronic toxins. Fructose is a chronic toxin as the liver doesn’t get sick until after 1000 fructose meals. So the FDA isn’t touching this. The USDA isn’t touching this. That would be an admission to the world that our food is a problem. There are 3 things in this country that we can sell overseas. They are weapons, entertainment and food. So who runs the food pyramid? The USDA. In other words, the fox is in charge of the hen house because it’s their job to sell food.
- Fructose consumption has increased in the past 30 years, coinciding with the obesity epidemic.
- A calorie is NOT a calorie and fructose is NOT glucose. The more you think a calorie is a calorie, then the more you think that if you eat less and exercise more, it would work. It doesn’t. Because a calorie is NOT a calorie and fructose is not glucose. There’s good fats and bad fats, good proteins and bad proteins, good carbs and bad carbs. Glucose is the energy of life. Fructose is poison.
- You are not what you eat; you are what you do with what you eat. And what you do with fructose is dangerous.
- Hepatic fructose metabolism leads to all the manifestations of Metabolic Syndrome:
- de novo lipogenesis, dyslipodemia and hepatic steatosis inflammation
- hepatic insulin resistance
- CNS leptin resistance, promoting continuous consumption
- Fructose ingestion interferes with obesity intervention – the more soft drinks consumed, the the less diet and exercise worked
- Fructose is a chronic hepatoxin. It’s alcohol without the buzz. Alcohol is metabolized by the brain so you get alcohol effects whereas fructose is not metabolized by the brain so you don’t see alcohol effects. However, everything else it does is the same. But the FDA won’t regulate it. It’s up to us.
I’m standing here today to recruit you in the war against bad food.