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.