DEBUNKING DR LUSTIG

I have typed this title in capitals, because I think it deserves it. I have written about 45 articles in this blog so far as a response to some points in his lectures he delivered worldwide and many of them contain my disbelief that obesity is not a problem as Dr Lustig claims. Before that he used to say that fructose consumption causes obesity, but he stopped saying this because the body of evidence disproved his claims from 2009 and suddenly sugar is not THE cause of obesity anymore:

Dr Lustig has changed his focus and says that the obesity actually does not matter.

Instead it is only the metabolic syndrome that is the problem, plus the type 2 diabetes and other metabolic disorders:

He kept supporting his argument by one diagram, saying that 20% of obese people are metabolically healthy and that the people of 'normal weight' contribute to the pool of metabolic diseases by 40 percents: 

He had even put it in numbers: 

I have highlighted several times throughout this blog that this group of 'normal weight' did not distinguish between slim and overweight people and I suspected that most of these 40% would apply to the overweight subgroup. Therefore, in my opinion, the prevalence of metabolic diseases closely relates to the prevalence of excess adiposity among the population, where the overweight and obese people form a distinct group from people of truly normal weight. My suspicion was proven correct, as the linked article shows at its end, based on earlier published content of Dr Lustig himself. In the light of this information, now his sudden turn looks suspicious. 

Dr Lustig has been saying again and again that anybody can get metabolic syndrome and that the obesity is irrelevant. Well, I have different information, which contradict this thesis. One of such information can be easily found online if one puts a little effort in it. Just type key words 'healthy obese' and see what comes up.

One of several studies I have found, published in 2012, concluded:  

"...metabolically healthy obese individuals are at higher risk to develop hypertension, type 2 diabetes and the metabolic syndrome than their non-obese counterparts. Our data provide further evidence that opposes the notion of metabolically healthy obese as harmless conditions."

The study also stated: 

" ...there is no evidence that these subjects are permanently protected from the risk of obesity-related co-morbidities."

This was a prospective cohort study on Taiwanese population and they applied the cut-off points typical for Asians: BMI 23 for overweight and BMI 25 for obese Class I, and for Class II the BMI cut-off point was 27. All participants with any feature of metabolic syndrome were excluded, except the waist circumference, which is larger in obese people anyway. 

Here you have another article which summarizes the current research on what is the truth about the healthy obese people. Here you can also read, that: 

"We have an enormous challenge at a public health and individual level in dealing with obesity-related disorders. Being obese doesn't just affect the heart. Being obese means you're more likely to have joint disease, psychiatric disorders and cancers," Puri said.

He added that, over the next couple of decades, obesity and its consequences will be driving health care costs."

So, where does the money go, Dr Lustig? And what do people actually die from? I have discussed my concerns, before I actually looked at these data, in another article here. 

I think this was enough to make you see that Dr Lustig is ready to ignore objective facts, announcing that he does not believe in common sense, because he believes in data - selectively picked by him and presented so it fits his agenda, I add.

In fact, as I have realized some time ago, Dr Lustig even negates his own work from 2005, where he published together with E. Isganaitis that obesity is central to the development of insulin resistance - which was in opposite to his newer claims that liver is the primary target to insulin (which it is not as you will read later) and that people get obese because they firstly develop a hepatic insulin resistance, as another article of mine discusses. Below you see the snapshot of the 2005 work of Dr Lustig which, despite it was emerging from the new evidence back then, does not seem to be true anymore - according to the new information presented by Dr Lustig. 

The 2005 article further discusses the role of increased concentration of free fatty acids in the peripheral insulin resistance and I will come to this point later as well. The scientific community is accepting this mechanism, but Dr Lustig seems to go against the flow with his fructose induced hepatic insulin resistance as a primary cause of the peripheral insulin resistance in 'normal weight' people and that the insulin resistance causes obesity, not vice versa.  

In addition, at the end of the snapshot you can read how the evidence shows that reducing of body weight leads to improvement of insulin sensitivity. Yet Dr Lustig claimed quite recently that reducing obesity does not lead to improved metabolic health. Come on! All this twist just to rise the argument about how excess fructose causes all the metabolic issues in people indulging on fast food rich in both sugars and processed fats, being of high glycemic index, consuming larger portions of highly palatable food and not exercising enough, as he published in the 2005 article as well???

Obesity does not cause metabolic syndrome; insulin resistance causes obesity. True?

I have already discussed my concerns about whether obesity is a disease or not and here we have another attempt of Dr Lustig to make the obesity irrelevant, pronouncing it as only an associated factor with the metabolic syndrome (MetS). He believes that not obesity causes insulin resistance but that insulin resistance causes obesity. He also believes that it is only the abdominal fat (inside the abdomen) that is a factor for the insulin resistance development whereas the subcutaneous fat is not the cause of anything.  

I agree that fat deposits in different body parts represent a different risk of metabolic diseases. However, does that make the excess subcutaneous fat irrelevant, so that we could ignore the obesity and focus only on the MetS features? I doubt so. 

Just a recap: 80% of obese people still suffer metabolic diseases (that is 4 out of 5) and as Dr Lustig said, so does the 40% of those having a 'normal weight'. However, about 50% of these 'normal weight' are actually overweight. So, is the obesity and excess adiposity under the skin really irrelevant? What percentage of these overweight would actually suffer metabolic issues in contrast to those really of a normal weight? 

Dr Lustig insists that firstly there is an insulin resistance, leading to leptin resistance, which leads to obesity and when this insulin issue is fixed, then the leptin issue is fixed, and then the obesity will be fixed as well: 

Because:

You know what? I AGREE with that. Partly. People tend to develop metabolic issues as they are becoming overweight and obese. In this mechanism it is really difficult to distinguish to what extent it is a marker (due to wrong diet and lifestyle) and to what extent it is a cause. Meanwhile, it is individual for each person WHEN and at what level of excess adiposity they will qualify for the diagnosis of MetS.

Just think: if people were not constantly in a positive energy balance for weeks and months - would they develop metabolic disturbances? Would they get high cholesterol, high blood pressure, would they become insulin resistant, because the muscles cannot take any more energy molecules in? I bet that most of them would not and as you may be aware, in many people, who reduce their body weight, their metabolic markers also improve. Slim people do not tend to suffer metabolic syndrome at such a large scale as obese and overweight people do. 

Should we therefore dismiss the link between obesity and metabolic diseases just because some thin people become ill and 1 in 5 obese does not?

Dr Lustig made it clear: people develop metabolic diseases irrespectively of the excess of subcutaneous body fat and he did it via this slide: 

He said that insulin resistance is what the obesity and lipodystropy have in common. However, you might have already read my objections against using this lipodystrophy case. It was because these people are genetically predisposed for insulin resistance which makes them too different from the rest of us. In addition, these familial partial dystrophy cases are rare. In the nutshell, the lipodystrophy means abnormal distribution of body fatness and represents a group of various diagnoses that are characteristic with lipodystropny. People are either genetically predisposed or they acquire this condition as a consequence of other condition such as being HIV positive and treated with various medication of having a history of autoimmune disease. 

The lipodystrophy is a specific condition and is rather rare in comparison to the prevalent overweight and obesity cases which mostly occur due to simply overeating and having low levels of physical activity. People suffering from lipodystrophy are often overeating due to leptin deficiency, while overweight and obese people become leptin resistant due to constantly positive energy balance, often leading to insulin resistance, too. What they have in common is that both cases: lipodystrophic and obese people have disturbed metabolism of energy. However, there is difference: 

• lipodystrophic people are unable to store fat in some body parts (under the skin in limbs), but  they can store it in other body parts (neck, face, around the organs), which makes them to look slim, but in fact they are metabolically ill and obese inside. The inability to store fat under the skin and excess adiposity in other places affects the whole endocrine system, sometimes also leading to overeating, which further worsens the condition. This is what Dr Lustig has been describing. Nonetheless, the whole condition is caused by some other condition, as mentioned above. Overeating is a consequence of reduced subcutaneous fat tissue and low leptin levels and the insulin resistance develops as a consequence of this.
• obese people, on the other hand, usually develop metabolic disturbances as a consequence of simply consuming too much energy, (or unhealthy diet as such, this is a broader topic) while they were initially healthy and metabolically normal. They become insulin resistant and as such, because the elevated insulin interferes with leptin receptors of hypothalamus, they also become leptin resistant as a consequence. And so they continue eating like they did from the time when they were slim, because they love food, it is cheap, plenty of it and unaware of its energy content. And the leptin resistance does not make them stop even if they have increased leptin concentrations in blood. Therefore the mechanism is the opposite than in people suffering various forms of lipodystrophy. 

Therefore, in my opinion, this example of lipodystrophy should not have been used to disprove the link between the body fatness and metabolic diseases in the population not affected by the lipodystrophy.

The Reframing the debate slide ended with this: 

Does this disprove the close link between excess body weight (or the process of gaining weight) and various features of metabolic syndrome? I do not think so. I see this initiative as messing around because at the end, there will again be FRUCTOSE. 

Going back to The Reality image, I have already highlighted that the metabolic dysfunction cannot be the cause of obesity for people who are metabolically normal and start to gain weight because of the obesogenic environment. And you could see that I gained weight without the symptoms of the metabolic disturbances just because I enjoyed the palatable and fattening foods too much and did not bother to move to burn the extra energy. I halted this trend when I reached BMI 27+ but if I did not do so I would most likely follow the fate of my close family who suffer a whole spectrum of metabolic dysfunctions, including obesity, hypertension, high cholesterol, cardiovascular diseases, fatty liver, type 2 diabetes, etc. I currently suffer none of these as a result of my lifestyle, I never did and I hope I will successfully avoid such conditions in the future. 

What Dr Lustig was talking about were his obese patients who struggled to lose weight because of having their biochemistry already affected for various reasons: hypothalamic trauma, specific genetic condition, being obese for some time already, unhealthy lifestyle, etc.

What I am saying is that although for many people the insulin resistance makes them to fail losing weight, but for them to gain weight firstly the insulin resistance is not a necessary factor. It tends to work the other way around: as people are gaining weight, they become insulin resistant in the process of gaining weight or when they finally become obese, because having this extra amount of fat in the body is not healthy at all. 

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. 

The more fat the better?

You could hear at about 20:12 minute of another video of Dr Lustig that the more subcutaneous fat - the better. Really? 

He supported this claim by a single image: 

Of course, the intra-abdominal fat is far worse than the subcutaneous one (under the skin). No question about that. But is it really true that the more subcutaneous fat - the better? Is it better to be obese than slim? Not at all. 

I know that researchers reported that people with BMI in the overweight category (BMI 25-29.9) lived longer than those below BMI 18.5. But was it because they had more fat or because of something else? This article summarized the research quite well. Among other things there you can read that many of those overweight people received a preventative treatment with statins to cut down the risk of cardiovascular conditions which are associated with increased body weight and elevated cholesterol. It also said nothing about the quality of life of those people or the other diseases they suffered. It only summarized that overweight people had a lower chance of death in comparison to healthy weight and other weight categories. Those obese had a higher rate of mortality and those underweight even higher - also probably because of already having some disease that made them underweight. 

Therefore we can conclude that the mortality has little to do with the quality of life. This is also supported by the statistics: people die later in developed countries, but the amount of healthy years has decreased. We pay for living longer by increased healthcare costs and the increased medical treatments, the lack of which meant early death in the past. 

It was Dr Lustig that repeated at each video of how much money is being spent on the few major metabolic diseases and that the healthcare will collapse within two decades. You also may have heard in the media that this young generation is the first that has the change to be outlived by their parents - because of the youth obesity and associated ill health. Then you could see in one of my previous articles and in Dr Lustig's presentations: that while 80% of 30% of the population (obese) suffers ill health, it is the 40% of remaining 70% of the population that also suffers the same diseases. I brought more light into this manipulative picture and made it clear to you that about half of those 'normal weight' are actually overweight. So while they may die later, their quality of life is unlikely to be better than of those of really normal weight. The advanced medicine nowadays can keep an ill person alive for a pretty long time. 

One thing I would agree with, though: more subcutaneous fat (up to a certain, healthy, level) means sufficient amounts of estrogen in women. That means stronger bones for them and also a higher protection from metabolic disruption which are more prevalent in men (such as gout). Women after the menopause often start suffering the diseases typical for men, too. That is a fact. But saying that the more fat under the skin the better is a heresy, especially when it is not specified that this fat should rater be stored around hips and thighs, not in the abdomen, albeit under the skin. Excess fat tissue promotes inflammation and that is by no means healthy. Obese people have difficulties to move around, the fat mass weights on their lungs and heart during sleep and the excess weight also leads to early wear-off of the knee cartilage causing further health problems due to reduced mobility.

Meanwhile, high estrogen levels promotes various forms of cancers, of which the breast cancer is probably the best studied in women - the extra body weight has been linked with the increased incidence of breast cancer. 

Moreover, that particular study I mentioned above did not examine the difference between the intra-abdominal and subcutaneous fat. They only weighed the participants and assessed their BMI. The fact is, though, that you could hardly expect an obese person not having an excess fat wrapped around their internal organs. While there may be some significant difference in apparently normal weight individuals, in practice with every kilo of extra fat under the skin, more fat is allocated inside the abdomen too. 

Therefore I appeal on everybody to be careful about such one-sided statements that the more fat is better and I mean that regardless of where it is stored. It is doing no good service to anyone and people may wrongly assume that if they carry extra fat on their hips or the body in general then their inside is as slim as of a a poor African suffering famine right now. 

One-sided push towards the fructose again - what was left out?

At 43:12 minute of the video you could see the selection of prevalence across the USA in terms of the obesity, diabetes, perceived happiness, 'laziness', heart diseases and finally the soda consumption: 

The aim was to point at the soda and sugar consumption that was behind all these variables. You know what? I will add one more: 

Here you see how the metabolic diseases, obesity and sugar consumption correlate with the poverty. One can argue: yes, but that is the point! Poor people cannot eat healthily and they stick to soda! I agree. But look at this:

The description says that it represents the visualization by the distance to the nearest McDonald's. And what is McDonald's typical for? FRIES and other fried food, among others. But fries and the burger are the icon of this fast food chain. It does also sell sweet stuff, including sodas, but the diet sodas have gained more popularity in the recent years, despite the worries about aspartame among health-conscious individuals. Fast food outlets now offer diet soft drink and the customers are buying it.

In this slide, from another video at 12:08 minute, which presented the obesity issue in more complex view (which is more correct than looking only at the sugar and addiction) you will understand that it is mainly the poverty that makes people going for cheaper and nutrient depleted food. They often do not have a choice. 

Now look at the picture below and read the comment under it. I have copied it from the Mirror website: 

I also recommend you to read the Mirror article based on the statements of the scientists. It basically says what I have been saying all the time: obesity DOES matter as with obesity there go various diseases, especially the fatty liver. Obesity is not only a marker, it is a direct factor contributing to the fatty liver prevalence. Something made people obese and that something contributes to their fatty liver, too. Or change the order: something contributes to the fatty liver while making that person fat at the same time. And this does not have to relate to only obese people with BMI over 30. Positive energy balance is the factor and that starts way before people reach BMI 30, got it? Meanwhile, people kept gaining weight and the fatty liver disease prevalence kept rising in times when the sugar consumption went down, also in the UK. Do you think it is the fructose fault? 

The following map only confirms the trend, taking the fast food in general, not only one brand:

Let's continue. Soon after the presentation of the six maps on the top, Dr Lustig continues with another map, showing the USA as one of the highest consumers of sugar in the world: 

Are you impressed? 

How about this? 

This fat intake diagram is an equivalent to the sugar intake diagram above it. The darker the color, the higher the consumption of substance in question. Any similarities? 

Make your own mind and listen to your intelligence. Do not let anybody fool you in their chosen direction. 

After watching another video of Dr Lustig, where he presented the same 6 maps, he said at 45:25: 

"The question is - is it that unhappy people with diabetes and heart disease drink soda, or is it that soda causes diabetes, heart disease and unhappiness..."

Why should drinking soda be so markedly correlated with unhappiness? Cannot people be unhappy because they are poor and live in a region with the high prevalence of crime, which is also just a result of poverty? We can guess what was the purpose of using the map with the level of happiness and not this one instead because it is well documented that the high sugar intake (also fat, alcohol and cigarettes smoking) is more prevalent among the lower socio-economic class. The poorer you are, the less healthy lifestyle you have and of course that does not make you happy. And this additional stress has also been found to contribute to the metabolic diseases, especially the cardiovascular events. 

While I agree that this is just a correlation, not a causation, and I appreciate that Dr Lustig and his team made an effort to perform statistical analysis in terms of causal medical inference, after I have seen how he constantly distorted the information and presented selectively chosen and outdated data, I have concerns about the accuracy and correctness of their analysis, too. Even the best tool can be used inappropriately when people have a specific interest in mind. And here it was sugar and specifically fructose within. Just an example: the soft drinks consumption data from 1990s repeatedly presented by Dr Lustig until today is out of date because since then the consumption of soft drinks decreased markedly in the U.S. and there is data for that, too.

Towards the end of this article I would like to bring to your attention Dr Lustig's struggle with his body weight for years announced in the video at 1:18:05 time when answering the questions of the audience. He said that he regularly exercises and that helps him to reduce the abdominal fat deposits while his body weight does not change. With no sugar and fruit drinks in the house, Dr Lustig? He said that he stays away from refined carbohydrates and sugar mostly and how it is difficult for him to have a healthy diet, that he has half a bagel with cheese for breakfast... let me remind you that the bagel is mostly starch, not sugar and that cheese is probably not of the low-fat range. What is preventing his body fat loss if he does not consume sugar/fructose at the average population levels? That is the question. 

Was the causal effect between the sugar consumption and diabetes prevalence confirmed?

Please make yourself comfortable, this also will be long.

This particular article aims to comment on the effort of Dr Lustig to convince the audience that he has proven the causative link between the diabetes incidence and sugar/fructose consumption. It is not aimed to contradict the found link.

Dr Lustig proudly presented the study in which he participated and its design at 31:34 minute: 

He explained why it is so great and what they have examined. It looks good so far. They even mentioned the oils in the food supply, which is a surprise after the previous attempts based on the EPIC InterActive analysis that failed to mention this at all. 

He also announced they estimated that sugar explained 25% diabetes cases worldwide:

Similarly, he said that 29% of diabetic prevalence in the U.S. is explained by sugar and sugar alone, irrespectively of its calories and irrespective of its effect on weight. My critical mind is asking: what about the remaining 75 or 71%? This was not explained. 

After reading the original study I can tell you that they did a hell lot of analysis and statistical tests. I am not going into depth of the details. What I would like to say is that there were so many limitations, mainly about the quality of the data from all named sources, that even the team ended their discussion with this: 

...any of the findings we observe here are meant to be exploratory in nature, helping us to detect broad population patterns that deserve further testing through prospective longitudinal cohort studies in international settings, which are only now coming underway.

Therefore, although they found statistical significance in the link between the sugar AVAILABILITY (not consumption) and the prevalence of diabetes, independently from the BMI or total calories availability, even when adjusted for other potential confounders (including fat), this was just an extensive statistical analysis of the data of a limited quality, despite allegedly being the best they had at that time. 

Moreover, the basic rule, which is taught in the first epidemiology lecture, is that the causation effect cannot be obtained from the observational data and based on the associations as this particular study was. So what causation effect was Dr Lustig talking about? 

Oh yes, the Medical Causation Inference, or causation inference in short. What do they say about it? 

Causal inference is the process of drawing a conclusion about a causal connection based on the conditions of the occurrence of an effect. The main difference between causal inference and inference of association is that the former analyzes the response of the effect variable when the cause is changed. The science of why things occur is called etiology: the study of causation, or origination.

From this it emerges that all he did (and he also said it) was that he expanded on the single snapshot of the EPIC study correlations with the 10 years long temporal relationship (still based on associations) that the changes of diabetes prevalence followed the previous changes in the availability of sugar and not the other way round. Nothing else. This may have captured the causative effect or it may have not. 

Here is more information about what the inference actually is. So even if they statistically found a seemingly causative effect, it came with the discussed limitations and the nature of the data (observational) and therefore it is not a solid proof about the true causative effect. And, as they said: this is only the beginning and the hypothesis outlined here needs further testing by longitudinal prospective cohort studies. 

Although I said I was not going into the details of the study, I would like to highlight one point of the announced Bradford Hill Criteria, which was not included in the four points Dr Lustig mentioned. The strength. Look at the diagram:  

Despite the link between the sugar availability and the prevalence of diabetes among all these countries was found to be statistically significant, the strength of the correlation coefficient looks quite low. The direction of the scatter plot seems to have very small angle against the x-axis, but this was calculated by the computer, so let’s accept it. The low strength here does not mean the causation is non-existent, but the higher coefficient means that the causation is more likely, according to the Bradford Hill criteria on the Wikipedia. This was just to highlight another weak point in the conclusion for the causal effect of sugar consumption on the prevalence of diabetes. 

Many scientists often stick to the statistical significance and push this finding through, despite the correlation coefficient is often found small. And, just for the comparison: try to recall the critique of Dr Lustig towards the scatter plot of Ancel Keys. He had an apparently stronger association between the fat intake and coronary heart disease mortality, did he not? Yet that much stronger coefficient was named as VERY MINOR by Dr Lustig. How would you then evaluate the one above? Moreover, Dr Lustig criticized few outliers in the Ancel Keys study, but here you can also find a few.  

One thing came to my mind: the links between other factors (dietary, lifestyle, economic) with the diabetes were found either statistically insignificant or non-existent. For those that showed some link, albeit insignificant (there is a difference between the statistical significance and clinical relevance), I would be curious to find out whether some of these also would come out positive in the causation inference test. This was not done.

And finally: at the 36th minute you could hear Dr Lustig saying that "this is proximate cause". And here you can learn the difference between the proximate and ultimate cause. The proximate cause that the ship is sinking is the hole in its body below the waterline, but the ultimate cause was that it hit a rock that made the hole. And, as Wikipedia says:

"Separating proximate from ultimate causation frequently leads to better understandings of the events and systems concerned."

So we now have to find the ultimate causation, since we already have the proximate one (or we think we have it). How? 

We now know that their statistical analysis found other individual factors (dietary, lifestyle, economic) as insignificant or non determining in the relationship with the diabetes prevalence. Maybe those 71 and 75 unexplained percents are needed to be explained? What factors do they refer to? Maybe a cluster of various factors that are naturally present with the actual sugar consumption (not average availability per capita). Examining each of these other factors separately might not give the objective result, because in reality we consume composite foods within a certain lifestyle and they interact in the etiology of the disease. Where some may not come up significant on their own, they may help other factor becoming significant, or these coupled together in real living conditions, especially when they commonly occur together in the society with increasing prevalence of diabetes, or any other metabolic disease. And now even Dr Lustig knows that a 'donut diet' (sugar and fat) coupled with the lack of physical activity and positive energy balance is detrimental to our health. Yet their analysis points only at the sugar and sugar alone, but only within about the quarter of the diabetes cases prevalence.

Finally, later during the lecture, at 56:20 you could hear: 

"90% of what we know in medicine today is causal medical inference. Only 10% is scientific proof."

Well, I did not know that, but OK. As I said at the beginning, this article was written to comment on the claim that we have a proof about the causal influence of sugar only on the diabetes prevalence, independently of the factors that were already discussed. I have no problem with accepting it if it was correct but there is still a space for doubt and that was my point. Unless we will do a proper scientific study (which we will not do in this case for obvious reasons also outlined by Dr Lustig), we can only say: this is the best we have and it looks solid. Not that it IS a definitive evidence. I still have a sort of feeling that dietary fats consumed along sugars in excess do have a significant impact on the development of insulin resistance and also other metabolic disruptions. 

Remember that liver is the major organ for energy metabolism and it not only metabolizes fructose but the dietary fats as well. 

Now I would like to cite my own work based on similar analysis of dietary patterns worldwide, performed by Popkin et al  2012: 

"...the worldwide trends, the increase in obesity, MetS, CVD and other metabolic illnesses between the years 1962 and 2000 came along increased estimated per capita availability of calories from sweeteners by 74 kcal/d but the TEI rose by 403 kcal/d, indicating that the consumption of other energy rich nutrient had also increased."

And the study presented by Dr Lustig also said: 

"The impact of sugar on diabetes was independent of sedentary behavior and alcohol use, and the effect was modified but not confounded by obesity or overweight."

Leaving behind the questionable quality of the data mentioned earlier, these two quotations need an explanation in a specific context. The Popkin et al study was related to the developing countries. However, as you could see in one of my other articles, in the US the trend of sugar consumption also did not particularly correlate with the ever increasing rise of metabolic diseases for the past 14 years. There certainly was other dietary factor or factors that made this trends worse and it not only could have modified these trends but actually contribute to them. Just because one study did not find a statistical significance it does not mean that a different study performed by different scientists and maybe based on better quality data would not find it. It is quite common that studies do not always come to the same conclusion or they even report the opposite results. 

And that was my point. I did not disprove the findings of this study because I do not see behind all of it. They might have found a true cause-effect relationship, or may not. We cannot be sure for sure because of the limitations associated with it. But my 'feeling' does not let me to leave out the substantially increased fats and oils consumption along the sugar in the world, and the actual drop of sugar consumption in the U.S. while the metabolic diseases, including diabetes, have been increasing. I agree though, that there are groups of people who consume way too much sugar and these are far more likely to develop diabetes. However, their diet is not only rich in sugar but also rich in processed fats and poor in essential nutrients and as Dr Lustig said, this also was not examined in their study. 

After watching one of the older videos from 2012, Dr Lustig announced that there were some sensitive slides not to be published before the main work was published. These were not presented to the audience and were cut off the video. However, from the Q&A at the end of the video at 40:00 minute I have realized that this secret information was related to this econometric study. What I have learned from this video, Dr Lustig announced that they did not have the data available to evaluate the role of glycaemic index of the diet and its possible role in the diabetes development. He also said that the category of roots, pulses, nuts, etc, which have a low glycaemic load did not show a protective effect in the MODEL and that he was surprised, or rather shocked, as he said. Well, perhaps something was wrong with the data? Can we trust the final outcomes then? I leave it up to you. Only future will show the truth. 

At 41:44 minute you can hear the answer on my suggested question earlier in this article: the team had no answer for the remaining 71 or 75% of the causes for diabetes. They simply did not know. He mentioned the genetics... but nothing about dietary fat or the combination of fat with sugar as is for the DONUT or fast food outlets... The remaining three quarters of the 'causes' of type 2 diabetes remained a complete mystery and he tried to make the audience happy with those 25% as pretty good. Something smells here... 

The matter of relativity and relevance

You could hear Dr Lustig saying at 1:03:46 minute of the video that there are more non-obese people who are sick. This was in relation to the diagram he presented earlier: 

Taking that there are still more non-obese people in the U.S. than obese, it truly appears that more of the non-obese suffer metabolic diseases (0.4 x 70 vs. 0.8 x 30). 

Where are the overweight? 

We now know that of people older than 20 years in the U.S., 69% was NOT of a healthy weight, i.e up to the BMI 25, in 2011-2012. That meant that 31% of the U.S. population had the BMI up to 25. That includes underweight, which are also at health risk. But I accept that overweight has become a NORM in the U.S., so maybe that was one of the reasons why these were included in 'normal weight' blue diagram on the right. Nonetheless, Dr Lustig called this broad group comprising 70% of this non-obese U.S. population as THIN people, check the video at 58:27 minute. I was overweight with BMI 27 at my heaviest and I was far from being thin, I can tell you.

Let's continue: over a third (35.1%) of these adults from the 2011-2012 survey were obese (higher than 30% of the older data displayed on the diagram), leaving the 'only' overweight group at 33.9% of the adult population. The true healthy body weight was found only among 31% of the adult population. Quite a difference from those 70%, is it not? Now we suddenly have an opposite picture in mind: Healthy weight 31% and overweight+obese 69% of the population. I would be curious to find out the position of the oval referring to the prevalence of metabolic diseases... This data was not presented.

My question is: Do people start suffering metabolic issues only when they cross the magic BMI 30 point? I doubt so.

While we might have become accustomed to see overweight people as a norm, metabolically it is not healthy and for many being overweight is only a transition state to the obesity, while the obese tend to die prematurely, so the trend maintains itself. 

Put it together in your head and see what is happening. 

Adding up to this article I would like to bring to your attention more information why a positive energy balance, which leads to obesity, may be behind the insulin resistance more than the fructose consumption. This basically reflects the fact that the extra body weight has a negative impact on our metabolism, at least regarding the insulin resistance and hyperinsulinemia, with a possible causal link to the NAFLD (non-alcoholic fatty liver disease).

And after watching another video of Dr Lustig, you could hear him saying at 5:33 minute:

"Obesity is certainly associated with those diseases  but it is not the cause of those diseases (dementia, cancer, dyslipidemia, type 2 diabetes...). And when you do the math... obese or not, it is more than half of the U.S. population." 

I have trimmed the quotation - he basically said that it does not matter whether you are obese or of a normal weight, over a half of the U.S. population is metabolically sick.

Well, the same applies to the U.S. population in terms of being overweight and obese. Those 69% are also over a half of the U.S. population that is NOT of a healthy weight. 

To me it appears, that Dr Lustig has suddenly realized that fructose is not a leading factor in the development of human obesity as he used to say back in 2009 (it is glucose, what a secret), so now he left the obesity out and focuses on the link between the fructose and the metabolic diseases instead.

Update 9/12/2014: When reading an older work of Dr Lustig, which he published together with E. Isganaitis in 2005, I have found this:

This only confirms my point that splitting the population to obese with BMI > 30 and the remaining population, when discussing metabolic issues that are closely linked with excess body fat, calling the non-obese population of 'normal' weight and pronouncing that obesity is NOT a problem, is wrong.