Misreporting in the scientific literature.

When I was reading the American Heart Association Scientific Statement (AHA Statement) published in 2009, in which Dr Lustig also participated and which I mentioned in my previous article, I have come across interesting reporting of findings of two studies. 

In the section titled Dietary Sugars and Obesity on page 1014 I found this passage: 

The highlighted references were these: 

Something did not quite seem right to me so I checked the two studies myself. Unfortunately I no longer have a free access to the full content of the studies which were not made available in full, so I rely on their abstracts now. Nonetheless, the abstracts seemed to be a sufficient source of information for this purpose, therefore hear what I found so interesting that made me write this article. 

According to the AHA Statement, the reference 69, Rolls et al. (2006) suggests that when people had offered a larger sugar sweetened beverage (SSB), they also ate more solid food as a consequence of that and therefore the SSBs make people eating more so they gain weight. However, the aim of the study was: 

"We tested the effect on energy intake of increasing the portion size of all foods and beverages served over 2 consecutive days."

Therefore they did not examine how increased portion size of soft drink increased food intake at all. 

Their findings: 

"There was a significant effect of portion size on energy intake in both men and women (P<0.0001). Increasing portions by 50% increased daily energy intake by 16% (women: 335 kcal/day; men: 504 kcal/day), and increasing portions by 100% increased intake by 26% (women: 530 kcal/day; men: 812 kcal/day). Energy intake did not differ between the 2 days of each week. Daily ratings of fullness were lowest in the 100% portion condition (P=0.0004), but did not differ significantly in the 150% and 200% conditions."

So, what the study reported was that people ate more when they were offered more, whether it was a drink or food and that extra energy in drink consumed did not lead to naturally decreased portion of the food eaten, therefore the body does not recognize the excess of consumed calories. What's more, people did not compensate on the second day for the overeating during the first day. They received palatable food, they were given larger portions and they ate more of it. That is it. Nothing was reported about the stimulating effect of SSB on food intake and the study did not aim to examine this effect either. There was a difference, however. As you can see, the increased portion by 50% or 100% did not lead to increased energy intake by 50% or 100%, it was less. I assume people were limited by the size of their stomachs, but should they continue eating like this, they would manage to eat it all over time as obese people easily shovel in larger quantities of food and drink than slim people. There is also a psychological mechanism in us: we tend to eat more from a bigger portion than from a smaller portion, and the scientists confirmed this by the study.  

Their conclusion was: 

"Increasing the portion size of all foods resulted in a significant increase in energy intake that was sustained over 2 days. These data support suggestions that large portions are associated with excess energy intake that could contribute to increased body weight."

See? Nothing about the effect of drink on the consumed size of meal. What were they talking about in the Scientific Statement of the American Heart Association? 

Regarding the reference 70 corresponding to Flood et al. 2006, the Statement gives the same impression: the increased size of SSB led to an increase in consumed portion of food. 

What was the aim of the study? 

"This study examined the impact of increasing beverage portion size on beverage and food intake."

Well, this could suggest what was claimed in the AHA Statement. However, it could as well mean that they also studied whether the participants consume more of the drink when they are offered more, and whether this increased portion makes them to compensate with lower food intake, as I have mentioned in my comment to the first study above.

What were the actual findings of this second study? 

"Increasing beverage portion size significantly increased the weight of beverage consumed, regardless of the type of beverage served (P<0.05). As a consequence, for the caloric beverage, energy intake from the beverage increased by 10% for women and 26% for men when there was a 50% increase in the portion served (P<0.01). Food intake did not differ between conditions, so when the energy from the caloric beverage was added to the energy from food, total energy intake at lunch was increased significantly (P<0.001) compared with noncaloric beverages."

I am sure you understand what was written in there, but let me just clarify: 

• The study reports that when they increased a portion of the drink offered to the participants, they consumed more of it. 
• Diet cola and water did not make difference in the consumed volume of drink when compared with sugary drink. It is still a fluid and the sweetness, whether from the sugar or artificial sweetener did not make difference from pure water. 
• Obviously, when you offer a caloric drink at the lunch and this drink is consumed, the energy value of the ingested content (food and drink together), will increase. Would you expect something different when compared to the drink of the same volume but with little or no calories?
• Food intake did not differ - yet the Statement from 2009 suggests that this study reported increased food intake after consuming SSB. I have no words for commenting this. 

But let's check the conclusion: 

"Serving a larger portion of beverage resulted in increased beverage consumption, and increased energy intake from the beverage when a caloric beverage was served. Serving a caloric beverage resulted in an overall increase in total energy consumed at lunch. Therefore, replacing caloric beverages with low-calorie or noncaloric beverages can be an effective strategy for decreasing energy intake."

Now compare the underlined parts of the test with the text in the AHA 'Scientific' Statement: 

"When the size of a regular cola was increased ... energy intake from food increased..." 

Have you noticed the misreporting of the information? The study did not suggest the increased consumption of food at all! I am speechless. Who wrote that stupid paragraph? 

All what the study reported was that people again did not compensate for the sugar in the drink, or even to the volume of the drink with reduced food intake to balance the calories. The fact is that in both studies there was nothing reported about the increased food intake as a direct consequence of consuming SSB. 

Just check the AHA Statement paragraph again, so that you do not have to scroll up and down: 

And that is not all, I have found some more of such 'scientific' writing. And that was only from the materials I have checked or with which I was familiar from my own research. I did not inspect every single reference they used. 

In one of my following articles will make you see the cherry picking reporting in this particular statement. 

What happened to the food dollars and what it means?

At the minute 55:39 of the video you could hear Dr Lustig summarizing how the spending for different food items has changed over the past 30 years. There you could see and hear that the spending for meat has decreased (-9.8%) as did for dairy products (-2.6%). All remaining categories saw increased spending of dollar on them, although the diagram below suggests otherwise. The spending on fruits and vegetables increased by +0.1%, grains and baked products + 1.2%, beverages +0.1% and the processed foods and sweets by +11.4%. The data came from Bureau of Labor Statistics, just in case somebody was interested. 

This graph followed a short speech about how the processed food has been spiked with sugar, that sugar is in everything and it makes people to buy more of these products. I do not object against this argument but there is more into the picture you could see. Have you noticed almost no change in beverages? Large portion of these on the market are occupied by sugar sweetened beverages (SSB) which contribute to the sugar intake the most, sweets are the negligible part of sugar intake on the population level and it was rather the SSBs that were studied the most in relation to obesity and metabolic diseases. 

In light of what you have just read, how it match the diagram, Dr Lustig repeatedly presented to you all the time?

I have already discussed the true trend of sugar sweetened beverages over a longer term period than is in this second diagram and how flawed were the argument of Dr Lustig in this respect:

"... between NHANES 1999-2000 and 2007-2008, the total consumption of added sugars decreased by mean 23.4 grams per day, representing a decrease 3.5% by which added sugars contributed to the total energy intake... two thirds of the decreased added sugar consumption was due to the decrease in soda intake, corresponding to net mean reduction by 14.6 g/d." 

Moreover, the first diagram says nothing about the increased consumption of sugar as such, which, as we know now, has been decreasing since 2000 in the U.S. This graph simply illustrates how the spending of the population has changed over 30 years, dollar per dollar, not capturing the changes of prices for different commodities and the dietary changes of the population - the lower expenditure on meat does not necessarily mean that people purchase less meat. It may as well mean that the cost of meat has declined due to the rise of intensive livestock farming. Or it also could mean that there are more vegetarians nowadays so that the sale of meat has plummeted - also due to the increase of food processing, offering meat substitute alternatives such as soy mycoprotein based, my favorite Quorn. However, the category Meats most likely only referred to the meat bought as such whereas the Processed Foods category may also contained processed meats and meat products. This was not said. 

All Dr Lustig actually presented was that people pay more for the processed food and some sweets within, but nothing about the actual consumption of sugar and fructose. And I do not quite understand why sweets have been put together into one category with processed foods, but the beverages were listed differently. The sweets are more related to the beverages (mostly sugar sweetened) than to processed foods, are they not?

It is true that the processed food market has seen its boom over the past decades but this category is too large for us to be able to draw a final conclusion which nutrient in this category has increased the most, whether in terms of consumption or increased spending. Processed foods refer to anything from those sweets (a minor contributor to sugar intake), through pastries for the microwaves to ready-made pizzas or peanut butter. My peanut butter contains only about 2g of sugar per over 200g of product. Can we say that this extra two grams of sugar and about one gram of fructose within can contribute significantly to the consumers health issues if the consumer drunk a tin of coke afterwards? Meanwhile, we do not consume the whole pack of peanut butter at once... I taste it more salty than sweet, anyway. How about added salt in most of the processed food products and hypertension in salt sensitive part of the population? People love salt as much as they love sugar. And the most fattening foods, those chips and crisps are rather salty than sweet... Sugar came as third, remember?

At 56:04 you could hear Dr Lustig saying, in relation to the category of Grains and Baked goods that carbohydrates went up but not much (1%). 

Excuse me? 

Was it only this category that contained carbohydrates? There is a lot of carbohydrates in the category of Processed foods, too! 

The analysis of how much the non-sugar carbohydrates has increased over about 30 years can be found here. What the graph actually means, is, that the dollar spent for this particular food group has grown only by 1%, not that the consumption of the particular commodity has increased that little. It has increased much more over the 30 years. 

And, please, Dr Lustig, how come you had no idea that the sweet BBQ sauce had added sugar in there, until you were told or checked the ingredients list? Tomato sauce often contains sugar, not only because it appeals on the taste buds of the consumers, but also because it is a processed food that aims to survive a long shelf-life without being prematurely spoiled. And: how much sugar is in there actually and what the natural sugar found in tomatoes anyway? 

I have grown my own tomatoes and they were exceptionally sweet - unlike those in the shop. Mine grew in a compost rich soil, too, with all the nutrients available that the plants scrappings had in them, not just a few artificial minerals in the fertilizers which are used to grow beautiful but tasteless and of lower nutrition value tomatoes available in the supermarket. Were these sweet and full of flavor and nutrients rich home grown tomatoes harmful to my health just because some laboratory would be able to extract the extra sugars (also fructose, tomatoes are botanically a fruit) from my tomatoes and put the same sugar back? I doubt so. 

And the final point: Sugar not only makes food palatable so people tend to buy more. The increased purchase of processed foods simply reflects on the busier than ever population that likes quick fixes and convenience. And within these there you can find the occasional candy or chocolate bar, but also potato crisps and other savory snacks, in which you also can find a a tiny gram of sugar for flavoring or moisture. 

I hope you now have an idea about the complexity of the issue with the changed purchases for various food items. Adding sweets to the processed food is a very unfortunate move and only misleads the audience, again. It is for sure that the sugar consumption has decreased but the purchase of processed food, mainly fast food and ready-made meals and snacks has increased, as did their portion size. This increased portion size is also a reason for increased spending because people want a value and buy a double portion of a ready meal. But instead of sharing it with a partner they often manage to shovel it in alone, usually in front of the TV or a computer.   

Take it that it is the increased purchase and the consumption of processed food that has been behind the increased obesity and metabolic issues trends because even the increased addition of sugar into these foods has not managed to reverse the sugar consumption trends in the available data.  

Thinking outside the box and seeing the whole picture

When watching the video of Dr Lustig against sugar/fructose I was amazed by his attempts to manipulate the game towards his agenda. 

At 10:27 minute he shows a slide:

What he says was already picked up by others and made fun of it because at other time Dr Lustig even said:

"There is no foodstuff on the planet that has both fat and carbohydrate at the same time. It is one or the other..."

He used a few examples, such as coconut, avocado or olives that have fat but no carbohydrate. Well, a quick check on Wikipedia and you can see that 100g of avocado contains 14.7 g of fat and 8.5 g of carbohydrate (of which sugars are 0.7 g). Similarly for olives: 15.3 g of fat in 100 g of fruit, and some 3.8 g of carbohydrates. Sugars again form only mere 0.5 g. The rest of the carbohydrate is listed as fiber, but this does not mean that it is THE fiber, which we cannot digest. This includes all sorts of carbohydrates, including resistant starches. So the nature DOES put carbohydrate and fat together, although in different ratio and one of them usually dominates over the other. In most of fruits there is little fat but mostly carbohydrates. But saying that no food stuff on the planet has them both at the same time is a pure nonsense. 

Besides that, Dr Lustig further talks that it is the sugar that has fat and carbohydrate at the same time - now it becomes clearer - he considers a glucose as carbohydrate and fructose as fat. I am not surprised after what I have heard from him over the past five years. And this alleged properties of sugar should make it so dangerous for people. 

Only the blue sentence at the bottom of the screenshot suggests that Dr Lustig knows and admits that fructose is converted to fat under certain conditions and until these conditions are met, fructose is not converted into fat - I suppose. Or not at such a large scale to be considered dangerous. And that is exactly the real mechanism.

However, humans do not have such capacity for the de-novo lipogenesis (DNL) as some scientists promote. The lipogenic properties of fructose are much lower in humans, especially in healthy humans. So saying that fructose is fat while glucose is a carbohydrate is wrong, because glucose also can be converted to fat when consumed in large amounts, i.e. beyond the capacity of the cells to convert it to energy directly. 

Here I would like to point out at a wider picture instead of focusing on one dietary compound. That larger picture is the DIET rich in both: carbohydrates and fats as it is typical for the Western diet. You could have seen elsewhere what were the trends in the intake of sugars, fats and non-sugar carbohydrates among the U.S. population. You could also see that the sugar consumption decreased since 2000 and the consumption of fat has increased while the consumption of flours and starches leveled off. Here you have a perfect example of the both: non-sugar (glucose based) carbohydrates and fats dominating the general American diet since 2000 while the sugar consumption went down. This was all in kcal per capita, no need to convert the grams into energy. People have been consuming more energy while the technological advancements made them less and less physically active over time - in general. I know there are many people who exercise regularly. 

In my previous articles you could see that even Dr Lustig admitted that the foods causing obesity were french fries and potato crisps. Other times you could hear him saying a word DONUT, although by this example he meant something different than it actually was (sugar and fat vs. fat and starch plus some sugar). And in another article of mine you could see how the U.S. not only has a high consumption of sugars but also the fats. Dr Lustig kept showing the sugar map, I have found the fat map for you to see the whole reality, not just the cherry-picked information on which this agenda was based. 

I always prefer to see the problem in its complexity instead of fiddling with one dietary compound in the corner and trying to push the single macronutrient agenda across the whole room, ignoring the complexity of the problem. 

The same measure for everyone?

Over the years Dr Lustig has repeatedly been presenting the following material: 

I agree that this epidemic of obesity among 6-months old should be explained. Or even the supposed 'obesity' in newborns, because they are born in general 200 grams heavier (in comparison to usual 3000 g body weight). However, Dr Lustig brought this up in the midst of his speech about the personal responsibility (22:25), not about the proximate cause of this epidemics. I agree that the baby is not responsible for its fat deposits.

Now I wonder whether Dr Lustig had in his mind that the reason for the obesity of 6-months old was the extra fat deposits at its birth or the sugar sweetened milk formula when the mother cannot ordoes not want to breastfeed for some reason. Or both? Can be. I do not argue. 

However, do you think that you could use the same argument for an obese person that was born of a healthy weight. grew up with a healthy weight and suddenly started to gain weight just because of wrong dietary choices or the changes of lifestyle in general? Could we use the same mechanism for all people, regardless of their antenatal or early postnatal environment? You now know that the sugar consumption as per capita has been decreasing and this was confirmed by both USDA and NHANES data. And within this sugar the same happened for fructose. 

FYI, the increased risk for metabolic diseases has not only been found on the babies born heavy but also among those who were born underweight. Check out the Barker hypothesis for more details. Such individuals are at a higher risk of obesity, hypertension, cardiovascular diseases and perhaps even diabetes.

So what could explain the increased body weight and metabolic issues among the population more than the reduced intake of sugar? Those who read my other articles in this blog already know the answer. 

Nobody can fix the obesity?

You could hear Dr Lustig saying at about 14 minutes of the video that NOBODY can fix the obesity as such, but then he offered a solution: fixing the leptin resistance by fixing the insulin resistance, the obesity will be fixed also. But he did not believe in lifestyle changes, such as exercise, because in his eyes (selectively supported by some research) it does not work. 

I know from my own experience how my extra kilograms secretly kept piling up over a few years but, to my knowledge, I have never been insulin or leptin resistant. My blood tests and fasting sugar were perfectly normal, although they did not test the leptin and insulin levels. And then I have managed to come from the BMI 27+ to my current 24 and counting. The weight gain period was simply a result of having an abundance of palatable and fattening food, which, however, was not too sugar rich, and I did not have to walk miles every day. Partly it was due to the shift pattern job, which stimulates appetite and makes people gain weight. But at that time I have already been avoiding sugary drinks and used sucralose to sweeten my tea or coffee. After I have had enough of myself being overweight, I started to watch my diet and walk more. One summer I even did some regular jogging. Should I not have halted my slow and creepy weight gain, I could end up like some members of my family - obese and sick. I have managed all this without a help of a doctor or some private consultations and more importantly - without any medications!

However, I understand that the individual cases are different from the task for the government to tackle the obesity on the population level. 

Here is the trend of childhood obesity and overweight in England. Can you see the drop after 2004?

That was the time the UK government started to apply robust intervention campaigns against childhood obesity. These campaigns involved dietary changes, behavioral consultations and also increased physical activity. I guess that only few children were receiving some medicines to manage their extra weight. The achieved results are still not perfect and more can be done, but tell me again that nobody can fix the obesity.

Similarly for the U.S. I have already written a brief article with data about the trends in obesity int he U.S. for the adults and that the same is predicted for children. The article clearly shows that while sugar consumption was decreasing after 2000, the obesity has been still increasing, until it started to level off from 2010. What in the American diet has caused this change? 

I will wait for the statistics to see whether this had some effect on metabolic health of the population, too.

What causes obesity? Finally - he said it.

I was pleased to hear, when watching another of the repeated lectures of Dr Lustig in the video at 38:07, that sugar does contribute to the obesity but it is not THE cause of obesity. 

What it was then?

As I kept saying: french fries and potato chips are the most obesogenic food stuffs. In other words: glucose based carbohydrates accompanied with a load of fat/oil, usually cheap processed oil. 

Added sugar is just one part of the whole problem and if people have stopped eating sugar and kept eating other processed food, which is also palatable enough, they would keep gaining weight. Depletion of beneficial nutrients and consuming excess of wrong nutrients (such as omega-6) would further contribute to the metabolic issues, even without the sugar present. These metabolic issues probably would not be as prevalent as they are now but we would hardly see their complete disappearance when sugar would disappear from the diet of these people. 

However, Dr Lustig only said that sugar is not the main cause of obesity and continued with his focus on the metabolic diseases as separate issues from obesity. According his and other scientists' views, if 20% of obese people do not suffer metabolic diseases right now, obesity is not a problem, because 40% of 'normal weight' people also suffer the same metabolic issues. And you could read in another of my articles that nothing was said about the proportion of overweight within the 'normal weight' group and the the prevalence of these metabolic issues among the overweight and the truly of normal weight (up to the BMI 25). But we know today that about half of those of 'normal weight' group are actually overweight.

To keep this post short and the topic intact, I will talk more about the obesity and its consequences in the next article. But before that you may want to refer to my older article where Dr Lustig tried to dismiss the fact the obesity has been pronounced as a disease on its own by the American Medical Association. 

Sugar or fructose? Or something else?

When watching the TEDx talk of Dr Lustig, where he just repeated what he used to say elsewhere and other times, he finally showed this list of added sugars to the food (15:40 minute), saying that 80% of food on the supermarket shelves is spiked with sugar. 

Do you remember saying that it is just fructose that is a poison and that glucose is fine? Well, dextrose, dextran, glucose, glucose solids, malt syrup, maltose, diastatic malt, barley malt, are all glucoses or polymers of glucose. Lactose and galactose also contain no fructose. Regarding the rice syrup I have only managed to find a brown rice syrup, which is again only glucose or glucose polymers. Similarly the corn syrup is not the same as high-fructose corn syrup and it again only contains glucose molecules. Ethyl maltol or maltol are not sugars as such and are related to maltose, so again, no fructose I am afraid. Caramel is rather a food coloring, not a form of sugar - to my knowledge. According to diatase (second column) I have found nothing in the Google of this name, but instead there was a diastase, which is an enzyme, not a sugar. After all, refer back to the diastatic malt above. 

This  impressive list of 56 names of sugar is suddenly shorter by 15 items which are not fructose related. 

Moreover, as I discussed elsewhere, saying that 80% of foods on the market contain added sugar also sounds impressive, but it says nothing about the amount of consumed sugar. Adding a gram or two of some sweet flavor enhancer into a 100g of final product is something different than a pure candy or a soft drink, especially if the sweet taste is not readily detectable. Claiming that this sugar contributes to the rise in insulin and weight loss, while ignoring the remaining 98g of mainly starch is a nonsense. Yet many tend to repeat this 80% figure like a mantra, not understanding the whole concept.

It would be more practical to provide a stratified chart about the amount of foods containing different amounts of added sugars so that we could actually see how bad it is.

For now I am confident to announce that the sugar consumption in the U.S. has been on the decline since 2000 and this included all the major caloric sweeteners, not just the items called either sugar or high-fructose corn syrup. The following diagram illustrates the trends of per capita availability for various caloric sweeteners in the U.S., based on the USDA data. 

Dr Lustig tried to dismiss these trends as not reliable and referred to the NHANES data instead. However, the NHANES data also support these trends in consumption of sugars. The amounts of consumed sugars vary between these two sources but they both agreed on the trends. And you know that the metabolic health does not get better in the U.S. population with the decreasing sugar consumption, does it? So is it sugar or fructose or something else contributing to ill health of America and possibly other countries worldwide?

He does not even get the biochemistry right

This is a strong announcement, is it not? Who am I to question such a famous and experienced doctor who has based his fame on fighting against sugar and delivering the lectures about fructose metabolism over and over again for the past years? 

Well, the data says something in contrary to his claims and this data has been available before 2013 when he delivered the speech I am focusing on right now. In fact, the sentence I have used as a title for this article was said by a Masters student of human nutrition in a private correspondence to me. She examined the link between fruit juices and health and I had a chance to read her dissertation work. It was an enriching experience, building up on my knowledge gathered until then. 

At about 38 minute of the video you could hear him discussing the liver metabolism of fructose, when he said: 

"Only the liver has the fructose transporter. Only the liver has the GLUT5 transporter that lets fructose to enter the cell."

I remember questioning this statement in my e-mails to Dr Lustig back in 2012 when I commenced my own research on the topic of fructose and metabolic syndrome. His famous video Sugar: The bitter truth was the trigger so I actually am thankful to him for that. What an irony. In my e-mail to him I highlighted that studies have shown the activity of gene for fructose transporter (GLUT5) in other tissues, including brain. His response that time was: 

"Other organs can "transport" fructose across their apical membranes, because they have the Glut5 transporter, such as the kidney and intestine. But they do not metabolize fructose for energy, because they do not possess the enzyme fructokinase, which is necessary to phosphorylate fructose to fructose-1 phosphate for production of energy."

So, in 2012 other organs had the fructose specific transporter and in 2013 it suddenly did not? How strange. 

I am not going to elaborate on the ability of other tissues or organs to metabolize fructose. Maybe there is some other mechanism in them to use fructose differently for energy or other purposes (absorption as in the intestine cells), and that needs to be studied yet, if it has not been already of which I am not aware. But the basic logic says: if the tissue has this transporter, it is likely the fructose inters the cells of this tissue and, if so, the cells must do something with the fructose after all. 

Another untrue statement of Dr Lustig at 39:04 time was that liver does not convert fructose into glycogen. He said:

"Let's follow what happens to that fructose. Can you see glycogen anywhere? Nope. No glycogen, it comes all the way here to the mitochondria, does the same as the alcohol does, makes that fat lipid droplet..."

And all that illustrated by a diagram that I remember seeing back in 2009: 

Of course, if the formation of glycogen from fructose was not painted into that diagram, it cannot be seen there, can it? 

In fact, a certain portion of fructose IS converted into glycogen by the liver, and this was proven by isotope tracer study when they labelled fructose molecules and followed their metabolic fate after its consumption by the participants. Some time after the fructose ingestion they received a glucagon which is a hormone for breaking down the glycogen and releasing glucose when its concentration in the blood drops. Guess what? The labelled glucose appeared in the blood stream. But the participants did not receive any labelled glucose. It was the fructose that was metabolized by the liver, converted to glucose, stored in glycogen and when the blood glucose dropped as in the fasting state, they sped the process of releasing the glycogen by administering extra glucagon and recovered the traced carbons in the blood again. And this was done in 2009, so Dr Lustig had enough time to get familiar with this detail after he firstly announced publicly the lack of glycogen formation from fructose in 2009 but before he said this again in 2013.

One point I would like to highlight here. All the simple mathematics he presented, such as the split of 120 kcal of glucose into the 80:20 for the liver and rest of the body metabolism, while 100% of fructose is metabolized in the liver only shows that Dr Lustig can count. All the rest is less certain regarding to how much glucose and fructose is converted to what when these two carbohydrates are consumed at the same time. The scientists have only an approximate idea and each study shows different figures. How the liver handles individual carbohydrates really depends on whether it was on an empty stomach or in a fed state, whether it was an athlete or a physically passive person, whether it was a man or a woman, etc. 

Let's say that these diagrams were only meant to illustrate a generally accepted approximate ratio of these two sugars metabolism by the liver, so they are fine. However, I cannot leave alone the previous two pieces of information that were far from the reality, but presented as facts with such a convincing authority. 

This is the final bit and the best one. The wine makers can confirm whether I spotted it right or not. Dr Lustig said that fructose and alcohol are THE SAME and that alcohol comes from fructose in fruits. Well, according to the Wikipedia, in wine making process it is the glucose that is fermented first and the different levels of fructose in the grapes will determine whether the wine will be more or less sweet, which means that not all fructose is converted to alcohol. It came out that not only Dr Lustig presented wrong information about the metabolism of fructose and the presence of fructose transport proteins in the body, but he again left out the glucose as the main alcohol producing sugar. So, are glucose and fructose so much different sugars?

You could see that fructose and alcohol are NOT the same, because although they share some metabolic pathways and they differ in their ability to be converted to glycogen (fructose) while ethanol is not, fructose also shares metabolic pathways with glucose and their metabolic intermediates are interconvertible. Especially fructose can be easily converted to glucose and other molecules such as lactate or glycogen. Yet the fructose has been presented here as COMPLETELY differently metabolized from glucose as I pointed at in my other article. 

So, based on this knowledge, the one-sided push of Dr Lustig, when he said that: 

Alcohol is metabolized through the fat pathway. Fructose is metabolized through the fat pathway. 

is not absolutely correct and this is regardless of how many articles Dr Lustig has written about this, as he said in at 1:01:10 in another video of this kind. There he again repeated that we get the alcohol from fermentation of fructose (nothing about the initial glucose fermentation in wine making process) and that people get fatty liver either from alcohol or from sugar, more specifically the fructose. All the time the same story all over again. 

NOTE:

It seems that Dr Lustig changes his facts over time. Only recently I watched a video from 2012 when he said more information about how the fructose is metabolized by the body and this time he made things a little bit clearer. However, this was not according to the facts and data - the body of evidence. He rather backed his claim sup with one study which has to be interpreted with caution. From the minute 45:25 onward he said this:

• he agreed that fructose receptors were found also in pancreatic beta-cells which also respond to glucose and release insulin. However, if fructose is bad because it makes pancreas producing insulin, why glucose is left out again? He also says that at 35 g of fructose load the blood concentration rises to 6 micromoles and that is enough to stimulate the beta cells to release the insulin. However, glucose appears in blood in millimoles, which is 1000 times higher concentration. So what is the deal? Can it really be a fructose action on pancreas that makes people sick and causes hyperinsulinemia with a subsequent insulin resistance? I doubt so. 
• he agreed that the extent of DNL in hypercaloric settings is higher in animals than humans, but he said that in humans it is still very significant. 
• He mentioned a study of Parks and Hellerstein (JSA 1998) that the DNL in humans, when fructose was given orally (they also test it intravenously), was just 3%. 
• However, he then continues that these were normal people, not calorically overloaded and they were fasting - so they were already glycogen depleted. Finally, we have heard Dr Lustig indirectly say that fructose does convert to glycogen, but he conditions this state as being on a fasted state. My question is - what happens with excess glucose in fed state? Is it COMPLETELY differently metabolized by the liver and body as he and his followers constantly repeat? 
• Then you hear, that it was pure fructose, which has a poor absorption rate on its own, so in real life situation we can expect that the absorption of fructose is higher and the liver is burdened more - which should eventually lead to more DNL.  
• As a contrasting scenario, Dr Lustig said that if this amount of fructose is given to obese, insulin resistant, fed people and give glucose and fructose at the same time (Hudgins and Hellers, 2011), the DNL increased to 25%, which was 6 times higher than in fasting state (I guess of the same obese and insulin resistant people). I have written a whole article about this issue and you will not like it if you are a follower of Dr Lustig.
• Dr Lustig ended this explanation with suggestions to take all these and to re-thing the whole argument of DNL. 

I have already mentioned earlier that it matters under which conditions and in what quantities the fructose is consumed (along glucose) in our diet and that it also depends what the diet actually is overall. But there are still some BUTs. Go back to the article I wrote elsewhere and you will find that fructose is oxidized (therefore not converted to fat) at a higher rate than glucose, when tested separately and we can expect that this is the case for the combined sugar - since fructose oxidation is less regulated by its by-products, which also leads to the metabolic issues with fructose overload. Higher supply of carbohydrates (fructose and/or glucose) also led to reduced oxidation of fats, which is probably the main problem in weight gain and failing weight loss, especially when refined sugars are consumed along fats, aka DONUT. 

You could also read the different findings with different methodologies used in the assessment of fructose induced DNL. That Hudgins and Hellers study from 2011 was probably the one I have already looked at and discussed here. Please check it out if you have not already read it. It is also an interesting reading. Just a recap: that 25% increased DNL was not assessed via isotope labelled fructose and the poor sick and obese participants, maintained at sedentary lifestyle, received 2g of sugar per body weight each. Take a person weighing 130 kg receiving 260 g of sugar (130 g of fructose) in a fluid that they had to consume within 15 minutes. Would you be surprised to find such alarming results? They also received their bolus on fasted state which means that although they had the glycogen depleted in the liver, at the same time the absence of food in the stomach made the fluid just flush through the intestines, being absorbed rapidly and overwhelming the liver. The reported the results were monitored over the following 24 hours when consuming normal food, so even this huge load of sugar was not administered at a fed state. Dr Lustig got it confused again. 

A really final word now: My dissertation work on the link between fructose and metabolic syndrome has focused on normal and metabolically healthy people because I have investigated what evidence we have that fructose alone (independently of the general diet rich in fats and being hypercaloric) makes people sick, not that it makes sick people even more sick with such horse doses.  

PEACE.

Every calorie counts but a calorie is not a calorie

In this video you could hear how Dr Lustig treated the patients after having a trauma on their hypothalamus by lowering the insulin levels using a drug. It certainly worked and my respects for that. It even worked in one lady who was not presented as being obese because of the trauma on her hypothalamus. She started to lose weight and also suddenly loved the exercise. But this was a treatment of the symptoms, not the causes. And Dr Lustig also started this lecture by intention to show how fixing the metabolic problem helps to lower the obesity instead of fixing the obesity in order to treat the metabolic issues. This fits his previous statement that the obesity is not a problem and it should not be called a disease. In principle I do not agree with that. 

I agree that if people have a defective tissue in their hypothalamus, the medication or other less natural invasion to their body is necessary to overcome the obstacle and to bring them a better health back. But is that necessary for other people who overate themselves to obesity and metabolic disturbances? 

In his attempts to make sugar responsible for this Dr Lustig pointed at the 'fiction' promoted by the sugar industry that Every calorie counts: 

This was an initiative of the beverages industry to promote artificially sweetened drinks in response to the current prevalence of obesity epidemics and because they were made to do it by the government and also to keep the customers who do not want to drink sugar anymore. The basic background is that regardless of what the beverages are sweetened with, the company wants to sell their drinks and earn profit. Simple as that. They acknowledged that their sugar helped to drive the current prevalence of obesity levels and they offered an alternative. They only said that all calories count and this was aimed at people who do not usually see the sweet beverages as source of energy because they only see calories in food. This statement had no intention, from my understanding, to suggest that all calories are equal as Dr Lustig also tried to imply in his TEDx talk at 10:51 and a couple times more in other lectures. 

Then you could hear Dr Lustig saying that it does not matter where the calorie comes from, that you can drink the sugary beverage or eat a carrot or a cheese cake and that the calorie is a calorie... ironically. He did not mean it. His many times repeated statement was the opposite: Calorie is not a calorie. I agree, different sources of energy trigger different metabolic processes to handle them. 

Here I would like to bring to your attention that there is a difference between the amount of consumed energy and the amount of absorbed energy, which is then available for the metabolism. The nutritionists know this very well. While you manage to absorb almost all sugar from the soft drink, from a food rich in fiber this is different. It is the fiber that prevents some portion of the energy molecules from being absorbed. And that is why people, when having a wholesome diet, they absorb less energy from a food than those who consumed the same amount of calories in the same food but more processed and depleted of fiber. This is just to highlight that every calorie matters - but every absorbed calorie, not every calorie in the food. And this is the point I would like to use against the results of the causal medical inference study Dr Lustig presented in this video and other videos as well. He reported 11-fold increased correlation between the prevalence of diabetes and 150 kcal from sugar in comparison to 150 kcal of total energy of whatever kind. Please remember this important fact when you will hear him repeating the results of their study again. 

So, if a calorie is not a calorie, what is their difference? 

You could hear Dr Lustig saying at 37:15 minute that

"we are all hyperinsulinemic now and that we all have higher insulin levels by two or three times than we used to." 

And I add, in agreement with Dr Lustig statements elsewhere: we are also heavier than out parents used to be. 

When answering the question why we all produce so much insulin today he played a video pointing at SUGAR. Then you already know that in this sugar it is the fructose moiety that is to be blamed for our insulin issues. I have a different answer and part of it has already been disclosed to you by Dr Lustig himself: 

Not only the alcohol contributes to the metabolic diseases and extra weight of people. Have you heard about the interesterified fat? These replaced the trans-fats and were also found to increase blood glucose (upon which the pancreas responds by producing more insulin). And you can see in another my article that not only the consumption of sugar is high in the U.S., but also the fast food, which is typical for the cheap vegetable oils, rich in omega-6 but low in omega-3.

Now, back to sugar. You could hear Dr Lustig dismissing the usual perception that it is the defect of energy balance that is the primary cause of obesity. I partly agree and that is because of the differences in metabolism of various energy molecules (fats, sugars, proteins). At some point all these molecules are absorbed and used or stored if in excess of the immediate use. There is a constant turnover of energy molecules in the body over the 24 hours. When we sleep the body reaches for the energy deposits, burning what we have temporarily stored in various energy compartments (liver, muscles, fat tissue). Unless a person over-eats and balances the inner energy scales over 24 hours, there will always be a balance and a stable body weight.

The problem is what makes us overeat during the day and why some people are hungrier than others? Is it because of the fructose in sugar?

In my other article I tried to explain to you why it is rather a result of consumption of glucose that makes people eating more after consuming a soft drink before going to the restaurant. And it is the glucose that is in starch and potatoes - fries. It is glucose that increases insulin far more than fructose or even fat and it is this insulin in response to consumed glucose that opens the fat cells for more fat to be taken in. 

Now I would like to remind you why I think the problem is somewhere else than in fructose (alone). I agree that too much fructose can also contribute to the insulin resistance, making people pre-diabetic. The basic problem is that obese people, or those that are yet to become obese, eat usually too much of everything: sugar, fat and also proteins. Please refer back to my simple explanation of positive energy balance while having a little energy expenditure, which makes the muscles unable to take any more of glucose and fats. This is also the cause of pre-diabetic condition. Since fructose is almost exclusively metabolized by the liver, it affects mainly the liver, not the muscles, which become insulin resistant because of too many calories consumed and too little burned off. Start exercising and the blood glucose and fat (also insulin) will go down, together with the insulin resistance.

So if Dr Lustig tried to treat the patient by interfering with the insulin response to GLUCOSE in the diet (not the fructose as he says that fructose causes insulin resistance) by cutting down on sugar, it would be more correct to say that people should stop over-eating in general. Cutting down sugar while munching on french fries and burgers will not do much change. Some weight will go away as many have reported dropping off some pounds, but if the positive energy persists and too much of processed carbohydrates will keep the high glycaemic LOAD (not index, these are different), the insulin problem will not be fixed completely. 

The solution for people without the previous hypothalamic trauma  is easy: start eating more wholesome diet and make an effort to keep your muscles working. With time it will be easier and easier and more enjoyable. Cutting down on sugar also helps but the amounts of consumed and absorbed calories will naturally also come down with a wholesome diet (my experience). Consider supplementation, especially with minerals.