Dear Friends

Many of our young people are worrying about their body image and obesity. Most do not understand why they are becoming so obese in spite of their concerns over their weight and body image. In a recent interview, which was first aired on 9 July 2007 on the Australian Broadcasting Commission’s Radio National Morning News Program and again on 3 December 2007, we were given the basic reason for the problem. The interview was between science reporter Norman Swan and the US researcher Robert Lustig.

The interview deals with the problem that the reason for the obesity epidemic is more than the calories we eat and the lack of exercise. The real reason is a substance that the food manufacturers are widely using.

The audio is found at www.abc.net.au:
Listen Now - 03122007 |Download Audio - 03122007
Norman Swan began by referring to a theory with scientific evidence behind it as to why the obesity epidemic is perhaps worse than it should be. Norman Swan said that: “The food industry, especially in the United States, hates the message you're about to hear and while certain manufacturing practices mentioned don't happen in Australia, as you'll hear, some in fact do. The question is whether there's stuff in our food which makes us even fatter than our calorie excess would suggest. It's about how a carbohydrate may be behaving like a dietary fat.”
The person being interviewed was Dr. Robert Lustig, Professor of Pediatric Endocrinology at the University of California, San Francisco.

Dr. Lustig said: “I'm very interested in what's happened over the last 30 years that has fomented this obesity epidemic. And of course everyone says well, that's because you're eating too much, and you're exercising too little and of course that's true. But the question is: what about our physiology allows this to happen? We have some built-in negative feedback mechanisms that are supposed to stop us from gaining too much weight but clearly they are not working. The question I've been interested in now for the last ten years is what is actually blocking that signal to the brain to tell our bodies to eat less and exercise more? Clearly something is getting in its way.

Over the course of those ten years I've done numerous experiments in people and have come up with the notion that this is actually one of the main functions of the hormone insulin. Insulin's job is to store energy; insulin's job is to make you gain weight.”

Insulin’s job is to transport sugar from the blood into cells.

Robert Lustig said of insulin: “Let's take a diabetic off the street, blood sugar is 300 – in Australian terms that would probably be something in the order of 15. We give them a shot of insulin, the blood sugar goes down to 100 – that would be something like 4 or 5 – so the question is: where did the sugar go? It went to the fat for storage. That's insulin's job, insulin's job is to take sugar from the blood and put it into fat for storage – more insulin, more fat. Well all these kids who are walking around who are massively obese now have extraordinarily high insulins. The question is when your insulin is high and you're storing energy you make another hormone, and that hormone is called leptin, and leptin is supposed to go to your brain and tell your brain that you've eaten enough.”

Leptin is produced by fat cells and circulates in the bloodstream. It binds to specific receptors in the hypothalamus, the area of the brain that controls energy balance and it's supposed to turn eating off. In addition, it also raises the tone of an area of your brain called the sympathetic nervous system, which is designed to actually help you burn energy. So by reducing food intake and by increasing the burning of energy you're supposed to stay in balance. However, the children and adults of today are not in balance.

The question that was addressed in the interview therefore was: could insulin actually be interfering with that leptin signal? That issue was investigated by Robert Lustig and his team. It was shown by suppressing insulin with a drug.

Lustig took children who developed massive obesity after brain tumours. These children had a tumour in the area of the brain that controls energy balance, the most common of which is called cranial pharyngioma. Once the children were treated, that area of the brain was then dead, “it cannot see leptin”. When leptin cannot be distinguished the brain is starving. What it then does is increase your food intake because you need to eat more, in spite of the fact that there is plenty of leptin. It is as though it was not there. It also reduces your sympathetic nervous system. It makes you feel “lousy” and to burn less energy, according to Robert Lustig.

It was pointed out that energy expenditure, energy burning and quality of life are effectively the same thing. Therefore anything that raises your energy expenditure makes you feel good. Anything that reduces your energy expenditure, like for instance hypo-thyroidism as an example, makes you feel “lousy.” Therefore, when you can't see your leptin your brain thinks you're starving, you feel bad, and don't want to exercise and you will eat more.

The children with brain tumours were then used to see if the feedback cycle could be altered. The children were given a drug called Octreotide, which reduced their insulin levels. Spontaneously these kids stopped eating and started exercising.

It became evident that insulin was having an influence on the brain itself. By getting the insulin down, instead of the energy that they were eating being forced to fat, the energy that they were eating could now be burned by muscle and by the rest of the body. It made them feel better.

Lustig stated that, to date, all the studies giving leptin to obese people have basically been failures, because of what is termed leptin resistance. Basically the body can’t see its leptin. If it could recognise the leptin the person would not be fat. It was stated that: “Leptin resistance and obesity are actually the same thing.” So the question was, therefore, “What causes the leptin resistance; what causes you to not be able to see your leptin?” With the brain-tumour children it was because that area of the brain was dead. Lustig then asked the obvious: “The question is, what's wrong with the rest of us? “

The next step was to drop insulin in otherwise normal, healthy, obese adult people, using the same mechanism. The answer was the same. The team was able to get them to stop eating. They stopped eating carbohydrate immediately. They reportedly went from 900 calories a day in carbohydrate intake to 350 calories a day in carbohydrate intake, they stopped snacking between meals, and they stopped drinking soft drinks.

The interview said that: “They were not told to do this, they just did it, they didn't need to do it. Their insulin went down, they felt better, they started exercising and they lost weight and continued and kept losing weight.”

It was emphasised by Robert Lustig that of all of the drugs that are out on the market today, all cause some weight loss, and then at the four-month time point you can't lose any more, you hit the negative plateau and you can't go any further. And the reason that you hit this negative plateau is because your leptin has finally gotten down to a point where your brain is now starving.

According to Lustig, the key breakthrough appeared to be: “When we got the insulin down, not only did the leptin keep going down but it kept going down even further. They kept losing more weight, they kept feeling better, they kept exercising and we were able to not have a negative plateau. We lost even more weight over the course of the year.”

Norman Swan then asked a key question: “So how come anti-diabetic drugs which effectively do that, they reduce insulin resistance, get your insulin levels down – how come they don't universally cause weight loss, in fact some of them can cause weight gain? “

Robert Lustig explained: ‘It depends on which one. In fact, Metformin is an insulin sensitiser. It does get insulin levels down and we've shown that it's actually a very good promoter of weight loss, especially in insulin-resistant children. If you look at the adult data it's a relatively mediocre response. The question is why does it work in some patients to cause weight loss and not in others? And that's a very complicated answer. I think it has to do with how insulin resistant you are when you take the medicine.

There are some new generation anti-diabetic drugs that cause you to gain weight. They are called the glitazones. One is called rosiglitazone or piaglitazone. “

Dr Lustig said: “The reason they cause weight gain is because they actually cause pre-adipocytes, that is fibroblasts that are not adipocytes themselves yet...”

Robert Lustig said that they became almost adipocyte stem cells, and they “actually cause them to differentiate into adipocytes, giving you a larger tank to store energy, and when you do that you actually can clear energy better and that makes you insulin-sensitive for a time. But only at the expense of increasing the size of the tank.”

Norman Swan then raised the issue of why people are still searching for weight-loss drugs if all you need to do is to depress insulin and the technology exists to do that.

Dr Lustig answered: “Well, it's not that easy. It's actually quite difficult. Not everybody has a disorder that's amenable to an insulin antagonist. Only about 20% of adults have the disorder called insulin hyper-secretion that is responsive to this drug called Octreotide. 80% are insulin-resistant and Octreotide does not work in them at all. Metformin will work in them but only to a certain point because it's not the perfect drug either and it has other side effects.”

Norman Swan pointed out that there was a non-drug that does it which is exercise, particularly resistance exercise in building up your muscles.

Robert Lustig agreed and said exercise is the best treatment. “The question is why does exercise work in obesity? Because it burns calories? That's ridiculous. Twenty minutes of jogging is one chocolate-chip cookie. I mean, you can't do it. One Big Mac requires three hours of vigorous exercise to work that off. That's not the reason that exercise is important. Exercise is important for three reasons exclusive of the fact that it burns calories.

The first is it increases skeletal muscle insulin sensitivity, in other words it makes your muscle more insulin sensitive, therefore your pancreas can make less, therefore your levels can drop, therefore there's less insulin in your blood to shunt sugar to fat. That's probably the main reason that exercise is important.” Lustig said he was totally for it.

The second reason that exercise is important is because it's the single best treatment to get your cortisol down. Cortisol is your stress hormone. It's the hormone that goes up when you are mega-stressed. It's the hormone that basically causes visceral fat deposition, which is the bad fat, and it has been tied to the metabolic syndrome. So by getting your cortisol down you're actually reducing the amount of fat deposited, and it also reduces food intake. People think that somehow exercise increases food intake. It does not – it reduces food intake.

Robert Lustig then made an important point. He said: “The third reason that exercise is important, which is somewhat not well known, but I'm trying to evaluate this at the present time, is that it actually helps detoxify the sugar fructose. Fructose actually is a hepato-toxin. Now fructose is fruit sugar but we were never designed to take in so much fructose. Our consumption of fructose has gone from less than half a pound per year in 1970 to 56 pounds per year in 2003“ (emphasis added).

This was the point where the interview switched to identify the real cause of the obesity epidemic and that was the hepato-toxin fructose. It is now in everything and in the US you cannot avoid getting it placed in everything from hamburger buns to a vast array of foods that were never designed to be eaten with such sweeteners. As we will see, it is deliberate and deadly.

Norman Swan pointed out as an example that it was the dominant sugar in these so-called sugar-free jams, these so-called “natural fruit jams”.

Dr Lustig agreed. He said that, “Originally it was used because, since it's not regulated by insulin, it was thought to be the perfect sugar for diabetics and so it got introduced as that. Then of course high-fructose corn syrup came on the market after it was invented in Japan in 1966, and started finding its way into American foods in 1975. In 1980 the soft drink companies started introducing it into soft drinks, and you can actually trace the prevalence of childhood obesity, and the rise, to 1980 when this change was made.”

It was identified that the problem was not the calories but the fact that the only organ in the body that can take up fructose is the liver – and remember, Dr Lustig identified it as an hepato-toxin or liver toxin.

Robert Lustig said: “Glucose, the standard sugar, can be taken up by every organ in the body. Only 20% of glucose load ends up at your liver. So let's take 120 calories of glucose, that's two slices of white bread, as an example: only 24 of those 120 calories will be metabolised by the liver, the rest of it will be metabolised by your muscles, by your brain, by your kidneys, by your heart etc. directly, with no interference. Now let's take 120 calories of orange juice. Same 120 calories, but now 60 of those calories are going to be fructose because fructose is half of sucrose and sucrose is what's in orange juice. So it's going to be all the fructose, that's 60 calories, plus 20% of the glucose, so that's another 12 out of 60 – in other words, 72 out of the 120 calories will hit the liver, three times the substrate as when it was just glucose alone.

That bolus of extra substrate to your liver does some very bad things to it.”

Norman highlighted the importance of the Health Report special on ABC Radio National as being, “How food manufacturers, by adding fructose to our foods, either from corn syrup as in the United States or added sucrose as in Australia, may actually be making the obesity epidemic even worse, starting with damage to our liver cells, the hepatocytes.”

Dr Lustig then pointed out how fructose in its cycle actually increases uric acid. Uric acid causes gout. Thus children are exposed to highly increased levels of uric acid and thus are prone to gout later in life and bone damage during exercise by storing this uric acid.

Robert Lustig said: “The first thing it does is it increases the phosphate depletion of the hepatocyte which ultimately causes an increase in uric acid. Uric acid is an inhibitor of nitric oxide. Nitric oxide is your naturally occurring blood-pressure lowerer. And so fructose is famous for causing hypertension.”

Norman Swan then explained: Hypertension is high blood pressure, so once the liver gets depleted of the phosphate the downstream reaction [of hypertension] occurs.

Robert Lustig agreed and said: “When you have excess uric acid you're going to end up with increased blood pressure and we actually have data from the NHANES study in America – the National Health and Nutritional Examination Survey in America – which actually shows that the most obese hypertensive kids are making more uric acid and have an increased percentage of their calories coming from fructose.”

They will ultimately suffer from serious gout.

The crunch came in the interview when Norman Swan said: “So what you're saying in fact is that whilst we are clearly eating too much, we're passively eating too much of the wrong thing, that the food-manufacturing industry is putting stuff in which is fuelling the epidemic? “

Robert Lustig answered: “Absolutely! We're being poisoned to death. That's a very strong statement but I think we can back it up with very clear scientific evidence.”

They both agreed that there was clear scientific evidence on this fructose pathway in the liver.

Robert Lustig said: “There's clear scientific evidence on the fructose doing three things that are particularly bad in the liver. The first is this uric acid pathway that I just mentioned. The second is that fructose initiates what's known as de novo lipogenesis.... which is excess fat production and so VLDL, very low-density lipoproteins, end up being manufactured when you consume this large bolus of fructose in a way that glucose does not, and so that leads to dyslipidaemia” (the bad form of cholesterol).

The last thing that fructose does in the liver is it initiates an enzyme called Junk one. According to Robert Lustig, investigators at Harvard Medical School have shown Junk one to be the inflammation pathway. When Junk one is initiated the insulin receptor in your liver stops working. He said: “It's phosphorylated in a way that basically inactivates it. Serum phosphorylation it's called, and when your insulin receptor doesn't work in your liver that means your insulin levels all over your body have to rise. And when that happens basically you're going to interfere with normal brain metabolism of the insulin signal, which is part of this leptin phenomenon I mentioned before. It's also going to increase the amount of insulin at the adipocyte, storing more energy. And you put all of this together and basically you've got a feed-forward system of increased insulin, increased liver fat, liver deposition of fat, increased inflammation – you end up with non-alcoholic, fatty-liver disease. You end up with your inability to see your leptin and so you consume more fructose, and you've now got a vicious cycle out of control.“

Robert Lustig made a very important point in saying that fructose, because of the way it's metabolised, is actually damaging your liver the same way alcohol is. In fact it's the exact same pathway. He said fructose is alcohol without the buzz.

Norman Swan then put it: “So this is the obesity-related, fatty-liver disease that people talk about?” To which Robert Lustig agreed, and Norman said: “Some people say, ‘I've heard obesity experts say it's surprising that with all the ready availability of food that we're not fatter’. In other words, that we are actually controlling our appetite pretty well given that we've probably been evolutionary designed to eat anything that goes, and there's anything that goes all around us, so why aren't we actually fatter? It's not so much why is there an obesity epidemic, why isn't it worse, is what people say and therefore you don't need to postulate fructose, it's just the fact that we've evolved in the Savannah to eat in times of plenty.“

Robert Lustig replied: “I've heard those same concerns you know, why, if we have so many calories, aren't we fatter? Well there are a few reasons why that might be. I do want to mention that the American food industry produces 3,900 calories per capita per day. We can only eat 1,800 calories per capita per day. In other words the American food industry makes double the amount of food that we can actually use. Who eats the rest? We do, through this mechanism. They actually know that by putting fructose into the foods that we eat, for instance pretzels. Why do you need fructose in pretzels, why do we need fructose in hamburger buns? “

Norman Swan then asked the big question: “Are you postulating here a fructose conspiracy, the way the tobacco industry had a nicotine conspiracy? “

Robert Lustig answered: “Well I can't call it a conspiracy per se. I certainly know, and they certainly know, that they sell more of it when they add the fructose to it. That's why it's in there, otherwise why would it be in there? Do they know that this is actually harmful? That's what I don't know. There's no smoking gun. Ultimately we found the smoking gun for smoking; you know, we found the documents. I'm not prepared to say that about the food companies. I do not know that they know that they are hurting us. However, they definitely know they sell more, and it temporarily coincides with the advent of fructose being added to our diet.”

Norman Swan pointed out that: “And of course you could argue that it's going up because they are responding to the market and they've got sugar-free, fat-free etc.”; to which Dr. Lustig replied: “Well in fact fat-free doesn't help. If anything, as the fat content of our foods has gone down – and it has gone down, it has gone from 40% to 30%, – in fact our obesity prevalence has gone way up. So that's not the answer. “

The problem was then identified.

Norman Swan said: “This is because they're adding carbohydrates and sugars to it to replace the fat”.

Robert Lustig replied: “Absolutely. In fact, fat does not raise your insulin but certainly sugar does. And fructose has been bandied about...because after all it doesn't raise your insulin directly because there's no fructose receptor on your beta cell in your pancreas. So people say, well it doesn't raise your insulin, but in fact it does because it's a chronic effect, not an acute effect. This has nothing to do with one fructose meal. This has to do with a year's worth of fructose meals, or a lifetime's worth of fructose meals, because as you become insulin resistant – which fructose clearly does and has been shown by many investigators not just me – that interferes with that leptin signal which causes you to eat more. “

The interview pointed out that insulin resistance increases your insulin levels because your pancreas pumps out more to get the insulin working, especially since your liver is not responding to it because of the effect on the serum phosphorylation of the insulin receptor. So that causes you to make a whole lot more insulin, which interferes with your leptin, which makes you eat more – and the cycle keeps going out of control.

No experiments have as yet been done on a fructose free diet but Dr. Lustig said he is trying to do that in conjunction with the Atkins Foundation in America in order to answer the question directly.

The ingredient to avoid is identified as high-fructose corn syrup. Truth in labelling is important to this issue. Soft drinks (sodas) in Australia have sucrose which is half fructose.

High-fructose corn syrup is either 42% or 55% fructose, the rest is glucose. Well, sucrose is 50% fructose and the rest is glucose. In fact high-fructose corn syrup and sucrose are equally problematic according to Robert Lustig.

Norman Swan said that it was basically table sugar. Robert Lustig agreed and said we were not designed to eat all of this sugar. We're supposed to be eating our carbohydrate, particularly our fructose, with high fibre. Well the fact is we have 100-pound bags of sugar that go into the cakes, and the donuts.

Norman Swan said: “So we don't need to get obsessed on fruit sugars. It's sugar itself, sucrose.”

Robert Lustig agreed: “Absolutely, it's sugar in general. So people say, 'Oh does that mean I can't eat fruit?' No, let's take an orange. An orange has 20 calories, 10 of which are fructose, and has high fibre. A glass of orange juice has 120 calories. It takes 6 oranges to make that glass of orange juice and there's no fibre. You tell me which is better for you? So by all means eat the fruit, just don't drink the juice. Juice is part of the problem and there's plenty of data, not just mine. Miles Faith had an article in Pediatrics, December 2006 showing that in toddlers in inner-city Harlem in New York, the number of juice servings correlated with the degree of BMI increase.”

The interview then turned to the discussion of the glycaemic index. The University of Sydney pioneered the glycaemic index, which is based on the idea that there are some foods that actually boost your blood sugar very quickly and some that are slow. They think that it doesn't actually matter terribly much what kind of sugar it is, it just depends on how fast your insulin is going to go up.

What we see here is that the glycaemic index is half the story; the other half of the story is fibre.

Dr Lustig explained the problem in relation to carrots. “Carrots are very high glycaemic index. What is the definition of glycaemic index? It's how high your blood sugar goes if you eat 50 grams of carbohydrate in that food, that's what glycaemic index is. So if you eat 50 grams of carbohydrate in carrots your blood sugar goes up very high and so that would be a high glycaemic index food. Fructose is a low glycaemic index food because fructose does not stimulate insulin; it's all of these calories but it doesn't stimulate insulin. So in fact a soda has a glycaemic index of 53, which is low. So you'd say, 'Oh, wait a second, carrots are bad for you and a soda is good for you?' Because glycaemic index is not the whole story, in fact what you really want to talk about is a related concept called glycaemic load.”

He then went on to explain glycaemic load.

“Glycaemic load is glycaemic index times the amount of food you'd actually have to eat to get the 50 grams of carbohydrate, so in carrots you'd have to eat the entire truck in order to get that. Well you can't do that, you wouldn't do that, so in fact carrots, even though they are high glycaemic index are actually low glycaemic load. Carrots are fine, there's nothing wrong with carrots. On the other hand fructose, I mean a soda, there's a lot wrong with it but you wouldn't see it in just looking at glycaemic index.”

It is obvious from the discussion that the key is glycaemic index plus fibre. It is the fibre that turns any food into a low glycaemic-load food. The key solution is that we are supposed to eat our carbohydrate with fibre. Eat an orange, don’t juice it. Don’t eat processed food. For example, processed wheat is white. It is stripped of the natural bran, which is the fibre. That is the good part that we're supposed to be eating.

In discussing the problem of why Asians eat carbohydrates and are still thin, it is identified that the key problem is fructose, which is absent in Japanese and Asian diets generally. Fructose, which is really not a carbohydrate, causes fat production in the liver. It behaves like a fat in the liver. It does not stimulate insulin like a fat and causes de novo lipogenesis or fat production within the liver. Alcohol also behaves like a fat.

The discussion did not deal with the fact that alcohol in wine consumption is the reason that the French can eat twice as much fat as the Americans and not get obese, as wine helps maintain the body in equilibrium. Americans do not usually consume their alcohol as wine and so the results are distorted in American studies.

The alleged low-fat diets advanced within the US and increasingly the British and Australian systems are unpalatable and so they add fructose and it become a high-fat diet because of the way fructose operates.

Thus it is a fact that Asian diets where a lot of carbohydrates are combined with high fibre are good.

Having invented fructose in the 1966 and inflicted it on the Americans, recently the Japanese have added fructose to their diet and childhood obesity has doubled in Japan over the last ten years because of fructose and the fact they are now eating like Americans. The adult diet has not changed and their obesity rates are stable.

In 1978 the US Federal Trade Commission had an entire congressional hearing on marketing and advertising to children. The food companies actually lobbied congress to have that killed. Lustig says they knew why. They knew what they were doing then, and they will do it again because it's not in their best interest. Lustig says simply that they couldn't increase their profits by 5% a year if they didn't advertise and market to children.

The American Food Industry has to be driven by science and not by lobbying as it is at present. The tobacco industry proved one thing and that is that you cannot trust the US or the Australian corporate system to regulate its own policy based on science and concern for health. That also extended to the construction industry and the use of asbestos. It is a known fact that directors of asbestos corporations knew of the dangers and continued to make and use the product knowing it was highly carcinogenic. The Food and Drug Administration cannot be trusted to regulate based on science alone.

What is needed is legislation with teeth that can go after the directors of corporations that knowingly produce products that are hazardous to the health of the consumer. The International Obesity Task Force produced the Sydney Principles in October 2006 in the conference at Sydney. The objectives are to get rid of advertising and marketing to children. Some 52 health minsters of the European countries met in Istanbul under the World Health Organisation (WHO) in August 2006 and agreed that marketing to children has to stop, but that has been ignored in America and particularly the USA. The US people have to take action to force the legislature to enact responsible legislation to protect the health of the nation against its own corporate exploitation.

It is not happening in Australia either and the expectation of the Federal government to date has been naive in the extreme. Companies cannot be trusted to police themselves unless there is clear and punitive legislation against the estates of the leaders of the corporations and the corporations themselves.

It is the responsibility of parents to control the diets of their children. Advertising aimed at children must be stopped and the addition of fructose to foods must also be stopped. Who needs fructose or sugar of any sort in a hamburger bun or in a can of baked beans? I had to drive from Kansas City to Leavenworth to get a can of baked beans without sugar – imported from UK with other items from Australia at the store called the Queen’s Pantry – as there was not a supermarket in Kansas City that sold a sugar-free can of baked beans.

Get control of our diets and press to control these firms who kill by stealth.

Wade Cox
Coordinator General

The interview by Norman Swan with Dr Robert Lustig Professor of Pediatric Endocrinology at the University of California, San Francisco was based on the following references:

Robert H. Lustig, Childhood obesity: behavioral aberration or biochemical drive? Reinterpreting the First Law of Thermodynamics. Nature Clinical Practice, Endocrinology & Metabolism Review, August 2006; 2; 8:447-457
Robert H Lustig, MD, The 'Skinny' on Childhood Obesity: How Our Western Environment Starves Kids' Brains. Pediatric Annals, November 2006; 35; 12:899-907
Elvira Isganaitis, Robert H. Lustig, Fast Food, Central Nervous System Insulin Resistance, and Obesity. Arterioscler Thromb Vasc Biol. 2005; 25:2451-2462