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. 

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.

Exercise for weight loss does not work?

At 14:12 of Dr Lustig's lecture you can see the diagram of one meta-analysis which assessed whether there is the body of evidence that physical exercise helps to lose weight. Dr Lustig presented it in a very simple manner - not saying how long the exercise lasted, what the exercise actually was, how many calories equivalent it was to balance a daily energy intake, and so on. All these factors are important in evaluating why something like this works and why not. 

And that is exactly my point here. WHY exercise does not work to curb down the obesity levels? They say there was a small weight loss overall but it was presented as a negligible effect. Nothing was said about whether the people had also their diet altered or not and what their diet consisted of, in general.

Let me put it this way: when you are obese because you consume over 1000 kcal more per day than are your actual requirements for that body size and lifestyle, how long you have to exercise to burn this extra energy plus some more to achieve the weight-loss? 

Here is a brief overview where you can find that if a 68 kg weighing person performs light aerobics, within a half an hour they burn mere 120 kcal. That is not even half of a regular Mars bar in the UK! With the higher body weight the energy expenditure is higher, true, but is it that much? 120 kg heavy person burns around 200 kcal. Still not a regular Mars bar, which contains 260 kcal. How much was that burger? Over 1400 kcal.

How long DAILY can you expect an obese person to perform even light exercise? Not for 3.5 hours to burn off that extra burger calories, would you? And this is every day because they tend to overeat every day, some even double or triple the average energy requirements (extra 2000-4000 kcal) as I have seen in my favorite series Supersize vs. Superskinny. Watch it, it is eye-opening. Available on Youtube.

Any wonder why the exercise showed such a small result? And this is also why the first law of thermodynamics seems not to work here - because in such a high energy intake you cannot expect weight loss if the energy output is not exceeding it. Moreover, it needs a substantial amount of time to achieve significant results, which most of such studies do not have. They usually assess the participants over several weeks or a few months at their best. 

Therefore, the things have to be looked at from the whole perspective, not just looking at the data and dismiss this or that saying it is inefficient. The little success (half point of BMI as Dr Lustig said) actually has proven that the exercise works, but it has to be accompanied with dietary changes as well. It is generally easy to overeat when the food is so cheap, processed and palatable. Cheap processed food is very energy dense, which means that per 100 grams you can get more calories from the processed food than from the unprocessed, such as fruits and vegetables. And these calories are not always only sugar. Most of the time there is more fat calories than sugar calories. Add little salt and you have got a deadly trio that has the potential to make people addicted to this particular diet. 

Moreover, the exercise has been found to be very effective in decreasing the risk of metabolic diseases such as type 2 diabetes. In fact, the exercise alone was found to be even more effective than the dietary changes alone. Surprised? I am not. It has its rationale based on our physiology. It is very simple: when you over consume, you store the energy not only in the fat, but also in the muscles and liver. Especially muscles are responsible for the most of the insulin mediated glucose uptake in the body. When you overeat and have a sedentary lifestyle or remain bed bound for several days, they are kept in the 'full of energy' state during the day and cannot take in any more. In excess, the glucose, instead of refueling the muscles, keeps circulating in the body and the body keeps producing more insulin to fit it somewhere as it should not stay in the blood in high concentrations. And humans have quite a low capacity for the de-novo lipogenesis (DNL) as you could see elsewhere. There are other processes that happen in such a hypercaloric state but this is the main mechanism. Once the person starts exercising, the muscles burn the energy they have and start taking in more again which results in the drop of a high blood glucose and also blood lipids. That's it!

We as a species have evolved being physically active and that is the need of our physiology today, too. Stop being active and the consequences come. Plug the hole in the sink and it will soon overflow. As long as one or two days of being bed bound with excessive eating can lead to the changes in our biochemistry indicating a pre-diabetic state. Keep doing the exercise while overeating and you will just keep gaining weight while you will most likely remain metabolically healthy for a pretty long time. Just please do not take this as my approval to overeat, OK? Healthy weight also matters. 

And finally: look at the diagram above again. The plot contains the results of different studies. Some worked, others did not, when examining the effectiveness of exercise on the weight management. It was only the overall figure of pooling all these together that Dr Lustig presented as the small and negligible difference. At least three studies (towards the left from the vertical line expressing that mean results) showed quite a success, did they not? I would have to look at each of them individually to give you a full report what made them show the effect and what not. But even from this you can see that it really depends on the circumstances whether the exercise does work or not. The first law of thermodynamics still applies here and the exercise DOES work when the energy output exceeds the energy input on a regular basis.  

One more thing I have noticed when listening the lecture further at the minute 18:55:

Look at the right column Activity. So, if the lowered level of activity has contributed to the obesity epidemics and associated metabolic diseases in children, why suddenly the physical activity does not seem to work, according to Dr Lustig? Yes, he did question this aspect and went for the usual toxic substance (fructose) in our diet after that but it is generally accepted in the scientific community that physical activity does play a role in the weight management and overall health of people and it is usually advised and promoted by the health authorities and implemented into the government policies, too. Dr Lustig provided no sufficient evidence that the physical activity is negligible or does not work in maintaining a healthy body weight, except of the meta-analysis study mentioned earlier. 

To be on a neutral side I must say that other studies also concluded that the exercise has little impact on weight loss and the change in the diet produces a higher effect, but this was only because of the insufficient balance of the calories I have discussed above. It is more effective not to eat that chocolate than trying to burn it off.

I know it from myself: I have been maintaining a lower body weight for some time now, with tiny fluctuations in one kilo up or down. And I know that when my physical activity suddenly increases for a couple of days while the diet remains the same and balanced, my body analyzing scales notice this and also estimate a lower percentage of body fat in my legs while increasing the percentage of water and muscles. I need no further evidence that the exercise works. I assess my body composition regularly. I maintain a record and do it at pretty constant conditions. The measurements were consistent, sometimes two or three days in a row produced identical results. 

And here I come to the last point of this article: there is a difference between maintaining a healthy body weight and reducing the body weight of obese people. These two premises are quite different, because when you are of a healthy weight, it requires less effort from you to exercise and you also need to exercise less to keep the energy in balance. For obese people this is particularly difficult to do on a regular basis and the drop-off rate is also very high, which contributes to the failure of such programs. What may be a light aerobic exercise for a fit person, for an obese person it can become quite a burden after 5 or 10 minutes. Now, imagine them doing this for an hour to merely burn the single Mars bar... 

But, as one large supermarket chains advertises: 'Every little helps'. The burned 120 or 200 kcal means they were not deposited in the fat stores and the muscles are now ready to take more glucose and more fat from the blood stream, reducing the risk of type 2 diabetes. Remember Dr Lustig saying that obesity is not a problem and that 20% of obese people are metabolically healthy? Well, 80% are not and physical activity has a huge potential in helping them out of this doom. He also admitted this in another video at 1:18:05 time that he has been struggling with his high body weight and the diet, but that the constant physical exercise helps him to reduce the abdominal fat deposits but his body weight does not change that much. He is simply replacing the fat with muscles. And if the studies do not examine the change in body composition of the participants but instead they only use BMI for the assessment, is it such a mystery they do not find significant changes? 

Fructose induced de-novo lipogenesis (DNL) - to what extent? Get ready for a surprise.

You have probably heard already that fructose is commonly portrayed as the fat sugar. Even Dr Lustig once said that 30% of fructose is converted to fat and the media keep repeating it. I would like to focus on this in this article because I believe the things are not so simple and we still do not exactly know enough about the lipogenic (fat forming) properties of fructose to make such statements. Make yourself comfortable, this will be long. 

Dr Lustig presented results of ONE study (Hudgins et al, 2011) that examined the de-novo lipogenesis (DNL) after fructose ingestion: 

I have done my own independent research on metabolic consequences of fructose intake given in various study settings for my final year project at the uni. And I know that the figures vary from study to study. Therefore - using only one study like this and demonstrate its results in figures that should be representative for everybody is not quite right. But there is far more to be criticized here. Get ready for an interesting surprise.

From my research I have learned that there are many methodologies of the assessment of DNL. All these have their strengths and limitations. I am not going to bore you with details, but I would like to say that most of these (including the one presented here) rely on isotope traced acetate and/or palmitate, as an indirect method when the effect of fructose intake on DNL is assessed. Other studies followed the metabolic pathway of the examined sugar as such: when examining the metabolic fate of fructose, they also labelled the fructose with an isotope and then assessed to which extent the fructose contributed to the DNL. The reason why I have brought these two examples to your attention was the comparison of the findings of two such studies of fructose effect on DNL within as similar conditions as possible. 

Dr Lustig presented the results of the study mentioned above (Hudgins et al) and said that in a fasting state fructose increased DNL by 5%. I have read that study myself. For achieving this result they fed their overweight to obese participants with 0.5 g of fructose per kg of body weight, corresponding to about 35 g of fructose for a 70 kg man. Heavier participants received proportionally more, of course. FIY: one 330 ml tin of Coca Cola has exactly 35 g of sugar, of which it is around half fructose, the other half is glucose. 

In comparison, Chong et al (2007) also performed similar assessment on fasting participants with similar amount of people, similar profile of people but tracing also the labelled fructose as such, which the previous study did not. They fed the participants with 0.75 g of fructose per kg of body weight, which would be 52.5 g of fructose for a 70 kg man, therefore more than the previous study. What they have found was that fructose contributed only with 0.4% to the DNL. The remaining increased appearance of lipoproteins and triglycerides above this amount was explained as re-esterification of free fatty acids already present in the system (their concentration is always reported to decrease in this kind of studies) and by reduced lipids clearance into the fat cells because fructose does not trigger such high insulin response as glucose does. Now, do you not think that the 33% higher dose of fructose resulting in 12.5 times lower DNL outcome is interesting? 

If you were shocked by the substantially increased effect of fructose in a fed state that Dr Lustig discussed later (those 25% increase), let me tell you what amounts of fructose/sugar it was based on. The team of Hudgins et al fed the participants with the following amounts of sugars:  

• 35/35 g of fructose and glucose = 70g of sugar = 280 kcal for a 70 kg heavy man (0.5/0.5 g of fructose and glucose per kg of body weight)
• 70/70 g fructose and glucose = 140g of sugar per 70 kg man = 560 kcal. If the overweight or obese person weighing 100 kg (they did not include people of healthy weight in this second protocol) consumed the adequate proportion of sugar for their weight, it would be 200g of sugar = 800 kcal, because this group received 1 g of fructose and 1 g of glucose per body weight.  

Any wonder why the results were so bad after all? Dr Lustig did not give you these numbers, he only shocked you with the results. 800 kcal of sugar given in the morning in a form of drink - do you think it is real for most of us? This amount would correspond to the consumption of mere 3% of the US population. 

Putting this in numbers, Mariott et al 2010 reported that the 97th centile of the U.S. population consumed 35% of total energy intake in a form of sugar between years 2003-2006. I have calculated that this corresponds to about 14% of daily calories from fructose or 350 kcal for a person consuming 2500 kcal. In normal diet the approximate ratio of fructose to glucose is 0.8, not half on half as it is for sucrose. Even the top 10% of highest sugar consumers (90th centile) had 25% of total calories from sugars (10% from fructose), meaning that 90% of the U.S. population had lower sugar intake. And these amounts are consumed during the whole day in a liquid and solid form, not only in a drink within 15 minutes on an empty stomach as the study participants had to. This is the reality check. And remember that since year 2000 the sugar consumption has been decreasing.

If this study had examined the effect of sugar on DNL using the method of Chong et al (isotope labelled fructose as well) are we sure we would achieve the same results? You could already see how different the results were when compared the two similar settings with different methodology earlier. 

Moreover, the high sugar effect (those 25% increase from the diagram) was found in people already overweight and obese, suggesting they already might have had their metabolism affected, not only by the high sugar feeding but also by their body weight. This was not told to you either.

Even more: while our bodies can vary enormously in their size due to the fat or muscle content, our liver size does not. And since you know that fructose is primarily metabolized by the liver, do you not think that such immense overload of sugar will show up with negative consequences after all? Whether the person is 70 kg or 120 kg, their liver capacity for metabolism of fructose does not vary that much, but the second person receives almost double the dose of the first one. Bear this in mind. 

Something I found fascinating in the study (among few other things). Look at the bit I copied for you: 

Have you noticed something? Fifteen mild to moderately overweight participants, of which the BMI ranged from 25.8 to 35.6. For those who are familiar with the grades of BMI this must be a bad dream. Those moderately overweight were not only obese, but beyond BMI 34.9 it is even Class II or severe obesity. Even the mean BMI was in the range of obesity (31.0). It took me a while to realize that their term 'overweight' was probably just a politically correct one since I remember a suggestion by someone to avoid using a word 'obese' because it could traumatize the obese person. Take it as a curiosity.

The truth is that no person had a weight below 80 kg in the second protocol, including women, so my reference man weighing 70 kg (once a true reference man for the Europe, 60 kg for women) was a different league. They intentionally tested these high doses of sugars on people with already altered energy metabolism. Moreover, while consuming the mega doses of sugars they were only allowed to remain passive, such as reading or watching the TV. In contrast, most of us move around daily. We take care of ourselves, we go to work, chase the bus, some walk the dog regularly or pick up children from school and do not normally consume such amounts of sugar anyway.

I have also found one part of the study discussion a bit manipulating. They compared the highest dose of sugars they gave to the obese participants (if weighing 100 kg -> 200g = 800 kcal) to the "amount of sugar in a commercial "supersize" soft drink consumed by 60 kg person". I tried to find out how big this supersize soft drink was but I could not find a specific figure for this term. Instead I calculated the amount of sugar the 60 kg person would consume in this study and it came out that it would be 120g of sugar or 480 kcal. That is far more than a 500 ml coke (53 g sugar, 210 kcal) or 16 ounces, above which the sale of soft drink volume was banned by the major of New York. While I agree that some extra large people may gulp down the 1300 ml of mega size soft drink in one sitting, I have doubts that an average 60 kg person would manage it.  

To make you more amazed, I will continue with debunking the blame put on fructose when combined sugars were consumed. To make the diagram from above more legible, I will copy it from the actual study:

I want you to focus on the two bars in the middle, the F and F:G ones. From the description you see that the first group received 0.5 g of fructose per kg of body weight and the second one received the same plus the same amount of glucose. The figures above them (0.49 and 1.50) refer to the magnitude of change from the baseline. The rationale of added glucose to he fructose was to mimic the consumption of sugar or HFCS because we rarely consume fructose alone and also that the fructose has poor absorption rate on its own whereas it has the highest absorption rate when accompanied with the same amount of glucose. 

How much more fructose do you think we absorb in the presence of glucose so it could increase the DNL three times as much? Do you guess it TRIPLED? WRONG. The same study reported the increased blood concentration of fructose in the presence of glucose from the mean 57 micrograms per mililitre (fructose alone) to only 72 micrograms (when fructose and glucose consumed together in the same amounts). The difference was not 2x57, but only mere 15. Even if one would argue that this was the systemic blood circulation level, whereas the liver captures most of the ingested fructose and may not release the extra in the proportional manner to the influx, this high jump is unlikely to be only due to the fructose alone. So the two-fold rise from the first test you can see above could have been largely accountable to the glucose, not fructose, since the dose of fructose has not changed and even at its highest absorption rate it is not 100% absorbed. 

Yet the scientists still focused on fructose as the main villain, similarly as Dr Lustig has been all the time. And nobody should now have doubts about the flawed argument that when the glucose tolerance test alone caused the reduction of the blood lipids (the very first column marked OGTT) that the enormous rise of new palmitate after added glucose to fructose was only due to the fructose alone. The truth is that glucose not only enhances absorption of fructose, but the body also alters the metabolism of both sugars when they are in the system both at once. Unless the labelled fructose AND glucose are traced and only fructose detected in the newly formed palmitate while the glucose is not, we cannot be 100% confident about the findings. The metabolism of glucose and fructose is very much inter-connected and that is why these specific tracer studies came into place: to distinguish between the resultant effects of these two sugars.

The best for the last. Look at some information from the slide once more: 

What Dr Lustig said was that at fasted state the DNL after fructose was only 5% higher from the baseline whereas in fed, obese and insulin resistant state it was 25%. WRONG again. All these results from the diagram above were on the same people under the same conditions, only the composition and amounts of sugar changed. So all of them received the fructose in fasting state, just in different amounts and the diagram presents the effect of different doses of fructose, not the difference between fasting and fed state. All of these participants were overweight or obese (Protocol 2) and all of them were tested for the response to those three different doses of either fructose or fructose and glucose in the mentioned amounts. Do you understand? That 5% was of 0.5 g per kg of body weight of fructose alone, those 25% was of 1 g of fructose and 1 g of glucose together, for the same participants under the same conditions, just spaced in time because it was the cross-over study. I have found nothing in the study saying that this amount was given before eating and this was after eating or that they would come up with these different responses before or after eating.

The Protocol 1 was slightly different. Instead of giving the whole volume of drink at once to be consumed within 15 minutes, it gave the participants regular doses of fructose sweetened drink, which made total 1.4 g per kg of body weight within 6 hours. To give you an idea, this amount would represent 98 g of fructose for a 70 kg  man. 100kg person would receive 140g of fructose only. Too much of fructose, hardly representative of the general population. To match this amount of fructose with the glucose (as we normally consume them together), it would have to be mind blowing 280g of sugar = 1120 kcal consumed just within 6 hours and on empty stomach (if taking 50/50, not 0.8 fructose to glucose ratio). Luckily for the participants, the scientists did not bring this idea into practice. Note, this last protocol was not pictured in the diagrams above. 

Instead, the link illustrates how the measured concentrations of lipids shot up during the first 8 hours in the Protocol 1 and then steadily dropped towards the end of the 24-hour monitoring period when the participants consumed food, therefore were in a fed state. And when you look at the bottom picture, you will see that at the beginning of the curve the concentration of palmitate started to rise even before time zero, which means even before fructose was given! This is just normal because after the 12-h fasting there was not enough insulin secreted, which was a signal to the fat cells to release fat for energy metabolism because even the glycogen stores were at their minimum after so many hours without a food intake. The participants simply switched to the keto-metabolism. Once you eat carbohydrates again, insulin rises and opens the gates for the glucose to enter into the cells (and for fat into the fat cells, too) and the fat burning mode is reduced again. And because it was a 'fructose challenge', the same applies what was discussed in case of Chong et al: lower level of insulin secreted after fructose then after glucose, hence lower clearance of lipids into the adipose tissue and although fructose is converted to fats in high doses, it may not be as high as we think, especially in the fasting state as both Protocols administered it. 

Once again: nothing was mentioned in that study about fasted and fed state in terms of assessed biochemistry for the Protocol 2 and from the Protocol 1 you can see that the DNL steadily decreased after the participants no more received fructose and started receiving food (containing glucose and some fructose).

This slide presented by Dr Lustig was just a nonsense as were the claims related to it. 

However, I am not saying that consumed fats along sugars (as per fed state) do not worsen the situation when it is overdone. I am saying that this video was full of crap. 

Remember all these flaws and selectively presented information when you will listen to other Dr Lustig's horror conclusions about the sugar again. The studies like those two introduced here aim to assess the actual mechanism of the metabolism of the examined substrates. They usually do not aim to assess the real life situation of you or me. In fact, I consume very little added sugar, so I am not a good representative for this. Therefore I have no reason for trying to deny these results to curb the guilt or something. And I am definitely not sponsored by the sugar industry. These are the scientific findings that contradict each other to some extent, followed with my critical evaluation of how inappropriately these materials have been presented to you. And that was the point of this article, not to deny that fructose or sugar can be dangerous when consumed in excess.