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Bravo Doc! :)

At 57:40 minute of the video Dr Lustig proudly presents his part he played in the project for reduction of sugar intake down to 6 teaspoons for women and 9 teaspoons for men.

I have no problem with reducing sugar intake in anyone. I have done it myself. But, except that many nutrition professionals consider this amount as unrealistic in this current sugar loaded society and market, it was interesting to find out the story behind these amounts of newly recommended limits on sugar consumption. I found it just by chance and I believe that you will find it as interesting as I did.

The background was discussed by another nutrition educated man called Alan Aragon, which also questioned the fructose story of Dr Lustig back in 2012. Have a look at 31 minute of this video, the explanation only lasts 5 minutes.

For those who cannot watch the video here is a short extract: It came out that these amounts of sugar, corresponding to 100 kcal for women (6 teaspoons) and 150 kcal for men (9 teaspoons) were just made up as half of the discretionary calories recommended by the U.S. government as a percentage of average total energy intake. These discretionary calories are those that people can 'fill' with unhealthy and non-nutritious food items or fluids for a pure hedonistic experience. The team, including Dr Lustig, just halved these amounts and allowed SEDENTARY people to consume this amount calories in a form of sugar, because they assume that the remaining calories will be filled with added fat intake. Exercising people can consume more, of course, but this was not mentioned. From percentages we have suddenly came to the absolute amounts - the same amounts for everybody, regardless of their actual energy needs or expenditure.

So, after knowing this, the following piece of information, cropped from the slide presented at 59:53 minute, comes intriguing:

Two points I would like to make here:

That new amounts (limit of 9 and 6 teaspoons of sugar per day) were therefore not based on any study, they were just made up. Dr Lustig & co. basically created these amounts and based on these amounts he judges the general population about the amounts of sugar they are consuming today; exercising or not, obese or not, guilty as charged.

These amounts still reflect the relative body size and muscle mass of two sexes (men and women). But they do not reflect to the actual size and capacity of the liver to metabolize the fructose. From these new thresholds it still appears like if men could safely handle 30% more fructose than women, which does not have a support in the studies.

Is it in the liver or pancreas after all?

I am getting confused now. Where does the fructose cause diabetes then?

Dr Lustig explained the mechanism of oxidation stress and how this affects the binding of proteins inside the cell compartments at 55:20 of the video. It was illustrated with a picture:

I agree with most of what he said, but then what caught my attention, he was suddenly speaking not about the liver cells but about the pancreatic cells. This pointed at how bad fructose is for pancreas. Well, did he not say some while ago, that fructose can, after consumption of excess sugar, occur in the blood at 5 micromoles concentration, which is 1000 times lower than of normal glucose concentration?

My question is: if little fructose is good for the liver (certainly at higher concentration than 5 micromoles), but this small concentration in the systemic regulation can damage pancreas to such extend it can lead to diabetes and insulin resistance, where glucose comes into this picture? Pancreas responds primarily to glucose levels in the blood... glucose, albeit 7-times slower in browning reaction, has a more capacity for this damage as it appears in the blood in 1000 times higher concentrations than fructose.

What was Dr Lustig talking about?

More doubts about the relevance of the data

At 43:09 minute of the video you could see Dr Lustig presenting a slide where he discussed how fructose increased the liver lipid content by 38%.

He said that the adults were normal, therefore I assume that means healthy and not obese and they were randomly assigned for four weeks to either high fructose diet or high complex carbohydrates diet in an isocaloric manner. With this Dr Lustig wanted to demonstrate that a calorie is not a calorie.

Learning from my research that many studies provided their participants with very high doses of fructose I wanted to check this study myself. Just because something is reported as isocaloric it does not automatically mean it refers to the energy balanced settings. Vast majority of the negative fructose effect on human metabolism was achieved by too high doses of fructose either within or on top of the daily energy requirements of the participants.

However, I could not manage to find this particular study. Maybe I am a bad database searcher or something, but when I typed the name Noworlowski into the Pubmed, it did not find anyone of this name and the Google mostly offered materials of Dr Lustig or others referring to them, apparently just copying the reference without actually seeing the study itself. I then listened to the video again and noticed Dr Lustig mentioning a friend Dr Jean Marc Schwarz. I have done little online search and sent an e-mail to the research team with a request for the study, according to the slide from the Dr Lustig presentation. Fingers crossed. One must be a detective to find the truth here.

For now I just want to tell you that even without the data of the whole study, the comparison of fructose against the complex carbohydrates is not too good design and that was why I decided to dedicate a little of my attention to this slide.

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 and many of them contain my disbelief that obesity is not a problem, in contrast with claims of Dr Lustig. 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 pretty 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 from people of truly normal weight.

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, instead of accepting claims of one MD without a critical thinking. Just type key words 'healthy obese' what will come 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 summarises 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 and while he does not believe in common sense, he believes in data - selectively picked by him to keep the sugar agenda going and selling his books, at least. Sorry doc.

Obesity, diabetes, insulin resistance, fatty liver ... getting confused?

I continue watching the video of Dr Lustig how he reveals new information that he did not say in his older lectures. I will come to these later. Firstly let me recap one slide that you might have seen before:

This slide is very likely misleading, whether intentionally or not.

Not all diabetes sufferers are obese. Many are just overweight. There are different BMI cut-off points for different ethnics and many of these may have slipped through, being overweight but already at a higher risk of metabolic diseases. For example, the BMI cut-off point for overweight for the South Asian is 23. What is more, overweight is just a transition state to obesity. And now you know how the positive energy balance can contribute to insulin resistance, mainly via the peripheral tissues such as muscles and fat.

Popkin et al reported in 2012 that while the sugar consumption in the developed world has increased by 74 kcal between 1960s and 2000s, the intake of total calories increased by 400 kcal. What contributed to the increased energy intake by those remaining over 300 kcal? Mostly oils and fats, of course. Developing countries continue to be a target market for American fast food chains and food industry, diverting them from the traditional diet to the diet based on processed and fattening food (rich in sugars, processed starches, salt and fat). Based on this trend we can only expect the prevalence of obesity and diabetes to rise worldwide.

Although Dr Lustig presented from the minute 37:15 of the video that the metabolic syndrome in adults and children was unrelated to weight, nothing was said about how the intake of fat and the positive energy balance affected the prevalence of metabolic syndrome:

Similarly for the Korean adult population:

Their T2DM was assessed against the total calories and obesity and Dr Lustig announced that their NAFLD was predicting the T2DM. Again, we have learned nothing about other dietary factors. I have tried to look for that particular study, based on the reference given at the bottom of the slide, but for some reason it did not appear in the journal, and when looking the key information on Pubmed (Sung+Kim+2011+Korean+adults+diabetes+NAFLD), only one different study came up. So I cannot say much more about the context and limitations of this interpretation. Even in that different study the obese ones had significantly higher NAFLD but some prevalence was reported in non-obese, too. However they again only distinguished obese and non-obese groups, nothing about overweight (BMI 25-29.9) vs. normal weight.

Moreover, the insulin resistance is not the same as type 2 diabetes. And since we do not agree on where the body insulin resistance develops first, there is not much I can add. But the title of this last slide does not negate the review from 2005 I mentioned earlier.

Dr Lustig further reported that the hepatic fat explained the metabolic perturbations better then visceral fat:

You could also hear him that they did not measure the effect of subcutaneous fat. Well, the truth is that all the participants were OBESE and most of them were in the Class II obesity:

Also the title of the study writes: Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity. So the obesity certainly represents risk for metabolic complications. The scientists only assessed which fat deposits were better correlating with the metabolic complications of obese participants. So, according to that study, even this diagram does not fully represents what is going on inside us:

Dr Lustig used the results of the study from the previous slide to skew the picture towards his fructose induced metabolic syndrome scenario via its action on the liver, ignoring the obvious patterns reporting by other scientists. In contrast, he called glucose as neutral, although it is the glucose that rises insulin, promotes storage of fat and together with fat CAUSES obesity. From my point of view and in the light of the presented evidence, the fact that glucose is not acting specifically on the liver, it does not make it innocent when consumed in excess in sugar.

Indeed, the study could not give an answer to what was the primary site of insulin resistance and whether the metabolic disruptions made people fat or whether fat people developed these disruptions. Just because liver produces more fats under certain circumstances it is not the proof that liver is the driving organ for the insulin resistance of the whole body in humans, regardless of what has been reported on genetically manipulated rats in the previously presented materials by Dr Lustig.

However, I have no problem to admit what is in the following snapshot:

I have also found the link between altered lipid metabolism in people consuming a lot of fructose in my independent review, but the effect of fructose on other metabolic outcomes was less clear and studies produced conflicting results.

And, I would just like to correct some bits in the two points above:

I would change the Metabolic Syndrome into the FEATURES of metabolic syndrome.

Adding to the green paragraph, that this is mostly relevant to the liver itself, not the systemic body circulation since fructose occurs in the systemic circulation in much smaller concentrations than glucose. It is glucose which causes damage in the extremities, kidneys or retina in diabetics and also the browning of the rib cartilage which you could see presented by Dr Lustig elsewhere.

The next post will critically look at some materials about how fructose selectively blamed for the metabolic issues.

The mechanism of insulin resistance development - which one is correct?

When discussing the causes or origin of metabolic syndrome, Dr Lustig highlighted few points:

Then he asks a question WHERE this insulin resistance happens?

He again presented quite an amount of biochemistry and recent advancements in research.

Firstly he refused the traditional adipocentric view of the metabolic syndrome development. This traditional view operates with a gradual accumulation of the excess adipose tissue leading to insulin resistance, which metabolically affects other organs and body systems:

The background of this Dr Lustig's refusal was that the obesity is not an issue, because 1 in 5 obese people are metabolically normal. Read more on my comments about this here and here.

Here he provides a different scenario:

In order to go deeper into this problem he firstly presented how the scientists bred animals lacking insulin receptors in eight various tissues and examining how their metabolism was affected:

Dr Lustig pointed ad the PODIRKO mouse, which was insulin resistant in its kidneys, although the blood glucose were normal. In this breed the insulin caused severe damage to the animal kidneys, similar to those of poorly managed diabetics. Dr Lustig concluded that it was not the glucose causing the tissue damage, it was insulin. Of course it was insulin, because their blood glucose was NORMAL. In diabetic patients the blood glucose is elevated, often together with insulin - can we say that in these it is again only the insulin that causes kidney (and other organs) damage? Dr Lustig said nothing about that but you could repeatedly hear how fructose is a browning agent and damages the cells and tissues. Except the fact that the fructose concentrations in blood are 10-100 times lower than the concentrations of glucose. In one video Dr Lustig even announced that 6 micromoles of fructose concentrations can occur in blood, which is 1000 times less than a physiological concentration of glucose measured in millimoles.

Now please look at the MIRKO mouse, which is of interest for me. These animals were insulin resistant in their muscles, but protected from obesity. I am fine with that, except the fact, as I have mentioned elsewhere, a lack of physical activity while overeating can result in the signs of prediabetes within 1 or 2 days. So, does the focus on the liver and brain insulin resistance, when associated with obesity, matter that much? What is more: does not the insulin resistance induced by non-exercising muscles affect the brain, which then fails to read the leptin? I guess it does. Although the study reports that MIRKO mice were not sufficiently affected in terms of glucose homeostasis (which drives insulin higher for some time), it also stated that:

" muscle...communicates with and regulates insulin sensitivity in other tissues."

The study also mentioned in their conclusion, that: "...primary insulin resistance in muscle may lead to increased adiposity and development of obesity." This seems to be in contrast with the content mentioned by Dr Lustig in the slide. Moreover, the group of 6 traits was only presented as immune against obesity, but nothing was indicated how prone they were to the metabolic syndrome.

Overall, the slide above does not disprove my point that a person can become insulin resistant when overeating and not being physically active; and this can emerge from the diet lacking fructose. Please bear this in mind as you will read further, because Dr Lustig will try to convince you that it is the fructose that is the absolute villain in the development of hepatic insulin resistance and as such it drives the metabolic syndrome development or even type 2 diabetes.

Secondly, you could see a brief overview of how the body functions under different conditions in relation to insulin sensitivity or resistance:

When the liver is functional and insulin sensitive, in the presence of insulin it stops producing glucose and at the same time it produces fat (triglycerides) which are released into the blood. This happens primarily after glucose consumption, no fructose was mentioned here. Fructose has very little insulin stimulating activity because it almost does not occur in the blood. This fat stimulating effect can easily happen in fructose-free diet, based on processed starches of a high glycaemic index.

Dr Lustig also said at 17:55 minute that the produced VLDL from the hepatic DNL can "CAUSE atherogenesis as a direct effect". The fact is that the presence of VLDL is only a risk factor, not a direct cause of atherosclerosis. Other factors must be present, such as hypertension, damaging the delicate epithelium of the arteries, being oxidized by elevated glucose concentrations and other processes such as inflammation. The circulating lipoproteins on their own are not as bad, it is what acts upon them that makes them a time bomb.

A similar diagram, illustrating the LIRCO (liver insulin resistant mouse), shows how the liver is blind to the insulin stimulated triglycerides production and the inhibition of gluconeogenesis is not stimulated either, so the animal has a high blood glucose, but allegedly not the metabolic syndrome. Well, since for the metabolic syndrome at least the three of five main features of the clinical definition must be present, while this scenario does not support it, I must agree. But is the elevated glucose harmless? Hardly so.

Then Dr Lustig moves to a third scenario. where there is a selective insulin resistance because although the glucose is high, also the triglycerides are high.

In this case a metabolic syndrome, along obesity, were the result while in the previous case there was only the obesity without the metabolic syndrome (albeit the hepatic insulin resistance was present), on which Dr Lustig has probably built his own new theory: obesity is not enough and insulin resistance is also not enough. Well, for me and also for the diabetics it is enough to have a high blood glucose to go blind or have a leg amputated. But Dr Lustig apparently pushes the boat towards the more complex condition - metabolic syndrome so that he can make fructose a king of the story.

One thing I would like to highlight here: these mechanisms were studied on mice which were bred to lack the insulin receptors at specific tissues while other insulin receptors remained functional. Is this representative for the general population? I do not think so.

I have already outlined my concerns about how the inactive muscles are not able to take in any more glucose or fats for energy and this can lead to prediabetic condition within a couple of days in humans. These have elevated glucose and also can have elevated lipids, upon which the glucose will act and make them atherogenic. Do you think that the insulin resistance due to a positive energy balance develops in isolation on specific organs in normal free-living humans? I mean those without a genetic predisposition, because those with some genetic trait would be similar to the selectively bred mice in their risks. The study I mentioned earlier suggested that the metabolism in normal organisms is interconnected and the insulin resistance of one organ can affect the metabolism of other organs and the whole glucose homeostasis. According to Dr Lustig, the scenario is the opposite: a dietary fructose overload makes liver to store fat and AFTER THAT it becomes insulin resistant while still producing extra triglycerides - leading to metabolic syndrome and affecting the rest of the body.

Before I end this post I would like you to look at the adipocentric picture at the beginning of the post again. There you can see that it was published in 2005. In my other article you could also read, that in the same year a scientific paper supported the peripheral insulin resistance as a more likely reason for developing fatty liver condition than the insulin resistance of the liver itself, as Dr Lustig advocates. They basically said that the NAFLD was a consequence of the peripheral insulin resistance and not the other way round, according to the available evidence. But Dr Lustig does not seem to accept this in 2014 and focuses on hepatic insulin resistance only, supporting his theory by the research on the genetically manipulated animals and persistently blaming the fructose in the diet as an ubiquitous factor that explains all the following aspects:

What followed after this slide I have discussed in another article.

To conclude and answer the question in the title: I do not have the answer. You could see how complicated the issue is, but from my point of view I tend to contradict Dr Lustig, at least in part, because the metabolism is really complicated and things do not tend to happen on isolated tissues or organs at once unless there is a genetic condition that makes it happen on a single tissue or organ. Maybe both of these opinions are partly true and the mechanism of insulin resistance can have different scenario in different people, depending on their genetic traits, lifestyle, exposure to different factors, etc.

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, as you could read elsewhere. So, does the obesity and excess adiposity under the skin really not matter? 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. Most people develop metabolic issues as they are getting 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 their 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 has nothing to do with their adiposity whatsoever and which makes them too different from the rest of us. In my opinion, this example should not have been used to disprove the link between the body fatness and metabolic diseases in the population not affected by this genetic trait.

The Reframing the debate slide ended with this:

Does this disprove the close link between excess body 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.

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 sensitive 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.

The next post will look closer on the different premises for the insulin resistance development. Before you proceed to that one, you may like to read one of the older posts with a similar topic: Why are we all hyperinsulinemic today? Another surprise is awaiting you.

Nobody can fix the obesity?

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

I know from my own experience how my extra kilograms secretly kept piling up over a few years but I have never been insulin or leptin resistant. My blood tests and fasting sugar were perfectly normal. And then I have managed to come from the BMI 27+ to my current 23.5 and counting. The weight gain period was simply a result of having an abundance of palatable and fattening food, which, however, was not too sugar rich, and I did not have to walk miles every day. After I have had enough of myself being overweight, I started to watch my diet and walk more. One summer I even did some regular jogging in my area. Should I not have halted my slow and creepy weight gain, I could end up like some members of my family - obese and sick. I have managed all this without a help of a doctor or some private consultations.

However, I understand that the individual case is different than the task for the government to tackle the obesity on the population level.

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

That was the time the UK government started to apply robust intervention campaigns against childhood obesity. These campaigns involved dietary changes, behavioral consultations and also increased physical activity. It is still not perfect and more can be done, but tell me again that nobody can fix the obesity.

In this short article you can see that the American adult obesity has also started to level off in 2012. I will wait for the statistics to see whether this had some effect on metabolic health of the population, too.

Fixing obesity does not improve metabolic health?

Everybody knows that when they gain weight, they are at a higher risk of metabolic diseases and many were lucky enough to reduce their medication for blood pressure or to lower their blood glucose levels when losing some weight.

Yet Dr Lustig calls this connection a dogma:

He also said that they have been trying this for 30 years and it did not work, because the number of obese children has tripled since 2001.

So, what does not work Dr Lustig? Reduction of obesity or reduction of metabolic diseases with the reduced body weight? I am getting confused.

Then the slide adds two more lines:

He gave an equal sign between the obesity and leptin resistance. He said that within 12 hours in an attempt to lose weight the levels of leptin are 25% lower, which he called leptin deficiency and claimed it makes things worse because on top of the leptin resistance, there is also this leptin deficiency and the brain sees it as starvation. How flawed this very simplistic picture is you can realize after reading a short article here.

Then two more lines were added to the slide:

Dr Lustig said that if leptin was working people would not be obese. Really? Is it the only reason for obesity? Not the palatable and caloric food that makes people eat more than they normally would? It was well documented by behavioral research that people feel the satiety later when eating palatable and well presented food or when they eat while they are socializing. Is that not an issue anymore, Dr Lustig?

I accept that in many diseased people the fixing the metabolic dysfunction will improve their obesity. However, does this apply to everybody? Take an individual who has just started to live a comfortable life with abundance of palatable food, which will inevitably lead to increased body weight. Is his metabolism dysfunctional already or not? Yes, there are people who have very strong homeostatic mechanism for maintaining stable body weight, but others do not seem to have it as strong. Is that a metabolic dysfunction? We have evolved on laying the fat deposits when the food was abundant because it was not the case for the whole year and there were hungry periods when the stored energy was a life saver. The problem is we do not experience a true hunger anymore. But the physiology needs more time to change.

The doctor once used to say that it is the trick of the food industry to create palatable foods so that people will eat more, bringing more profit to the industry. Does this apply on those who have not yet developed insulin and leptin resistance, or these were not included in the model?

For now we have the official statements of many health bodies that reducing body weight of obese people cuts their risks of disease or even death. In fact, I have just found this study, which compared the metabolically healthy obese and diseased obese people. You know what? They both were at a higher risk of death whether of all causes or due to the cardiovascular disease, in contrast to overweight. How completely different from what Dr Lustig has been presenting to you, is it not?

Thinking inside the box again

I remember Dr Lustig elaborating in 2009 about how fructose leads to obesity because brain does not read it as a source of energy. The mechanism was explained and supported by some studies, that fructose is not a glucose and it does not rise insulin levels to the same level as glucose. According to this scenario the hypothalamus does not see the calories and therefore it does not stop the person eating more. We now know that is not true, but Dr Lustig had put a lot of effort in his presentation to convince you that he was right. I have not heard him saying that anymore. Instead of obesity he now focuses on fructose effect on metabolic diseases and again exacerbates things quite often.

You could hear him elaborating with a similar passion in the video at 13:23 where he was explaining the mechanism of insulin and leptin resistance in obese people like if there were only these two hormones regulating appetite or hunger and the energy metabolism. He talked about how every attempt to cut down the energy intake for losing weight leads to decreased leptin concentration down to only 25% within 12 hours so now the poor obese folks not only are leptin resistant, but they no longer have enough leptin to stimulate those few responsive receptors in their brains and this is supposed to drive the hyperphagia (excessive eating) or yo-yo dieting further. The body supposedly thinks it is starving.

Except one thing: the levels of released hormones in the body are not always constant and the leptin is rather a hormone of a long-term energy regulation than acting in a short-term manner. Our endocrine system is very complex and inter-dependent. Leptin levels can decrease even when the fat cells have not been affected in the acute settings. Or course they could not, who loses fat within 12 hours? There are other functions for leptin in the body, not all are fully known and its levels are affected by other factors, too.

I remember my professor of endocrinology saying that we have more anorexigenic hormones (make us to stop eating) but those orexigenic (the opposite) are more powerful, such as ghrelin, which acts in a short-term manner in response to the actual food consumption. Do not eat for many hours and you will get hungry, regardless of the leptin and insulin concentrations in blood.

Switch your brain on and put it together in your head. And learn more about leptin before you will be fooled again.

This is just a very unfortunate practice by many who are seeking sensations: taking things out of context and elaborating on them so much that it will become a topic of the week. People then do not understand or see the whole context and are disappointed that the media publish one thing one day and the complete opposite the next day. Does that sound familiar to you?

I am not saying that Dr Lustig is completely wrong. I am saying that he again focused too much on one mechanism, which is not as important in isolation because our endocrine system is too complicated for that. After all, he is the endocrinologist, not me.

What is the metabolic syndrome?

You could hear from the minute 8:45 onwards about the disagreement of six different metabolic syndrome (MetS) definitions and what variables should be assessed in order to classify someone as suffering the MetS.

Dr Lustig dismissed the classic diagnostic criteria for MetS as phenomenological (via the cut-offs of various factors such as waist circumference, blood pressure, etc) and suggested that the mechanistical approach should be used instead:

He further pointed at two aspects of this mechanistical approach:

where is the subcellular dysfunction

where is the insulin resistance.

This was presented as a widely agreed and accepted mechanism of manifestation of MetS. I have no problem with that, but I also do not see a big problem with the previous system. It is a syndrome and its features appear in different combinations and severity in different people. Disease has a specifically defined points that also have to be met for a person to be classified as suffering that particular disease. And, from my point of view, the MetS is an equivalent of a disease once present in an individual.

Going back to the second picture and looking at the final question: Where is the insulin resistance? makes me puzzled. Insulin resistance syndrome or Syndrome X was were older names for the metabolic syndrome and some sources are still using the first one.

Dr Lustig mentioned six different definitions by six different health bodies in the first image. One of these was the IDF 2005 which stands for International Diabetes Federation. Where is the insulin resistance? Well, If you look at their Table 3 you will find it thee. It is one of the additional criteria of metabolic syndrome for research. These criteria are more biochemical than physiological, which are used in the clinical definition of MetS and are present in various combinations among those six definitions discussed earlier. IDF also reported on the definition of MetS in children and adolescents.

For now we have the most recent definition of metabolic syndrome for adults, published in 2009 in the Circulation journal, titled Joint Scientific Statement by Alberti et al. Why this definition did not appear among those six presented in this video of Dr Lustig uploaded in 2014, I do not know.

Overall, the usual five main symptoms of MetS are called the clinical criteria, the additional ones are used for research. But once these main clinical criteria were called together as an insulin resistance syndrome and when in doubts the insulin resistance can also be assessed on demand by the laboratories.

Now I would like to ask a question: does the person have to be insulin resistant in its own definition to be diagnosed clinically as having a metabolic syndrome? Cannot there just be a hypertension, dyslipidemia (which covers two separate features) and increased waist circumference? I recall hearing Dr Lustig saying in another video that when a person develops insulin resistance, it is already very bad. So? Does he want people to be diagnosed with metabolic syndrome only when they become very sick or would it be better for them and the society if they were diagnosed a bit earlier when not all of them have to express this serious damage? They do not need to have elevated blood glucose, as a hint for a possible insulin resistance, to be metabolic abnormal and heading towards cardiovascular disease.

So Dr Lustig called for the insulin resistance as the mechanistic approach instead of those cut-off points he criticized. WHY? Even for the insulin resistance, there are some numerical criteria serving the purpose of cut-off points used to assess whether the person does suffer from insulin resistance or not. There is no other way to assess this condition than to set up certain threshold which will distinguish two individuals as one having this feature and other not having it.

At 10:09 minute Dr Lustig continues with the explanation of what he means by the mechanistic approach:

where is the cellular dysfunction

where is the insulin resistance.

Well, according to the Wikipedia summary of methodologies for the measurement of the insulin resistance, it truly appears as a mechanistic approach - but this test is more intrusive and restrictive on the tested person and now I hope you understand why this MetS criterion was rather included into the research than for the clinical assessment. I have no objections against the assessment of insulin resistance, but would that be necessary for the MetS diagnosis, practicable on a large scale (as an alternative to a simple fasting blood glucose test) and affordable for the healthcare system? I do not think so.

Oops, he did it again - presenting two different premises and using one as a proof for the other.

In the past you could see Dr Lustig turning the traditional perception of the obesity development upside down. It was not due to the behavior, when people reach for energy dense food and prefer to stay physically inactive because they can, but rather the sole role of biochemistry, after the exposure to something, that drove the behavior of people to over eat and gain weight. He even strengthened this premise by pointing at obese 6 months old, expecting that all cases of obesity will be explained by exactly the same mechanism.

Another supporting cases he used were his patients after suffering a hypothalamic trauma. These could not read the leptin which would stop them eating when full and being in a process of storing extra adipose tissue, leading to obesity. As a result of overeating they developed insulin resistance, which further drove the metabolic diseases, associated with obesity. As a proof that the obesity can only be fixed from the inside, he demonstrated how he managed to fix it by artificially reducing the release of insulin first and then watching how the patients started to lose weight and even enjoy the physical exercise. And, as a proof that this has the effect on people without the hypothalamic trauma, he demonstrated this on another patient - just being obese, proving himself right in his point. He also illustrated this mechanism on an example of two children receiving a cookie: a slim child became hyperactive but an obese child did not, because it was leptin resistant, most likely due to the insulin resistance and a subsequent hyperinsulinemia.

Well, how about the beginning of these cases? I mean the individuals without the hypothalamic trauma or leptin receptors deficiency, which are the majority of obesity and metabolic diseases cases. Before they developed insulin and leptin resistance they were perfectly metabolically healthy, but the wrong dietary and lifestyle choices made them gradually overweight, obese and metabolically sick. They did not express the gluttony and sloth before but they have developed these after a prolonged time of positive energy balance and wrong dietary choices. Dr Lustig never discussed this properly. Even when elaborating on how the food industry and the lack of effective policies promote these unhealthy choices, it was not about the unhealthy choices themselves in his argumentation. The blame was always put on somebody else, never on the individuals that actually made those choices. What is more, Dr Lustig always focuses on already diseased people and applies their conditions and ill metabolism on the healthy people as well. Why?

As you have noticed by now, Dr Lustig illustrated that it was not the behavior that drove obesity levels in his patients suffering a hypothalamic trauma. When thinking about the differences, I have realised that these patients were firstly resistant to the leptin present in their bodies and then they started to eat like crazy, storing excess fat and slowly developing insulin resistance. In other cases, without this trauma, it is either the regular spikes of insulin that makes the hypothalamus less responsive to leptin, or gradually developing the insulin resistance (most likely due to the constant positive energy balance), that makes them leptin blind. These are again - two different premises. However, Dr Lustig constantly pictures the later stages of obesity development or gradually developed insulin resistance as a cause of obesity or metabolic diseases. He uses a mechanism of consequence as a mechanism of cause in these people without the hypothalamic traumua. WHY? I know, you know.

In the video I am watching now, Dr Lustig uses the same tactic again. In order to dismiss the generally perceived and accepted adipocentric model of the metabolic syndrome development (and insulin resistance within), he used an extreme case such as familial partial lipodystrophy. This is a result of a serious genetic mutation and you can see on the patient that he is not quite like the rest of us:

The patient was genetically predisposed where he stored and did not store the extra fat, or rather from which body regions the affected people start losing the subcutaneous fat as they mature and age. Although we all have this differentiated fat storage places - we store extra fat on our hips, stomach, arms, but not too much on palms of hands, on our ear lobes or hair area - people like this patient are too different from the most of us due to having other metabolic problems ranging from ' inability to properly breakdown a simple sugar known as glucose (glucose intolerance), elevated levels of triglycerides (fat) in the blood (hypertriglyceridemia), and diabetes'.

What that means? The patients with this genetic condition do not develop metabolic diseases despite of not storing fat under their skin but because of their genetic susceptibility for them, in addition to the gradual loss of subcutaneous fat. So another inappropriately used supporting example by Dr Lustig proving NOTHING about the allegedly non-existent causal link between the excess subcutaneous adipose tissue and metabolic health of the average population.

Discrepancies and distortions of the reality - have we been screwed?

At 40:45 minute of the 2012 video of Dr Lustig you could hear that high glycaemic foods are not the same as insulin resistance. Based on the information I could hear from him so far I suggest that the insulin resistance develops due to fructose and its lipogenic properties, whereas glucose is good for us and as such the insulin secretion should not worry us.

However, at 42:22 minute Dr Lustig said:

"I am for getting insulin down, any way you can."

This was initiated with the question of the audience about the reduced glycaemic index by accompanied fat in the meal saying that insulin is the problem and they have to get the insulin down. He further said that insulin is the bad guy because it makes fat cells to store fat and it also causes the cell proliferation - typical for cancers.

He then continues saying that there are two main approaches to bring the insulin down: to eat a low-carbohydrate diet, because glucose drives insulin up, or to reduce sugar intake to cut down the insulin resistance. I guess that this second part was again meant to be due to fructose moiety of the sugar. Nothing about fat, nothing about positive energy balance, nothing about full muscle cells, unable to take in any more glucose - making the pancreas producing more insulin to get rid of the glucose for any cost...

So, is the insulin good or bad? Is glucose good or bad? Sometimes you hear Dr Lustig saying that it is a good guy, other times less so. It is always about how it fits his momentary picture he wants to draw.

Another example.

Going back to whether obesity is a problem or not, in another video at 5:20 he said that because 20% of obese people are not metabolically ill, the obesity is associated with metabolic diseases but it is not a cause of them. This was supported by the diagram of 'normal' people who also get these problems such as hypertension, hyperinsulinemia, dementia, etc.

Pardon me?

You could have read my objections against this picture and that the overweight category was left out. Now I would like to know, where the statistics of Dr Lustig stands when he tried to convince the audience that if 25 or 29% of diabetes was statistically found to be CAUSED by sugar availability, how about those remaining 75 or 79%? That was not explained and he stated that also. They had no idea, they did not examine it. They just got happy with that little picture of the whole complex mosaic and they presented it proudly like something the world has been waiting for and it will stay as a fact til the end of the days.

On these two simple examples you can see that whatever fits the agenda, it is used the way it supports it, even if it is completely out of context and the facts are being skewed.

I am not happy with that.

Thinking outside the box and seeing the whole picture

I continue watching the video of Dr Lustig against sugar/fructose and I am still 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 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, he 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 take place, fructose is not converted into fat - I suppose. And that is exactly the real mechanism. However, humans do not have such capacity for the de-novo lipogenesis 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 at large amounts.

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.

In my previous articles you could see that even Dr Lustig admitted that the major dietary factor causing obesity were french fries and potato crisps. Other times you could hear him saying a 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 while ignoring the complexity of the problem.

Coming to an end

This will be one of the last articles of mine focusing on Dr Lustig's claims about sugar and metabolic diseases. I have watched most of the long videos on Youtube (randomly), many contained the same material with something else added or left out. I tried not to repeat myself too much but sometimes I felt the need to point at some things again, giving the content a context. I did not particularly focus on his very first video from 2009 but instead I looked at some newer ones. If somebody wanted me to write my comments on that one, I can. I have made about 30 sheets of notes on that video three years ago and I may like to put them together.

I also do not expect that Dr Lustig will disappear from the class and conference rooms after 2014 and sometimes I might come across of his newer content. If there will be something I will find worth to comment on, I will.

In the video (back from 2012), you could hear Dr Lustig at 3:38 minute to dismiss the well established causes of obesity, announcing it is wrong to say that:

we eat too much of everything and we exercise too little

we eat too much of everything.

He made it clear:

"We are not eating more of everything."

And then he displayed the notoriously familiar diagram of the increased soft drinks consumption among children and adolescents from years 1989-1996 - again, in 2012. I have written one of my first articles in this blog about this malpractice in the presentation of facts and the diagram can be found in another article here. We also know today (and knew it since 2011 when the study was published) that since then at least two thirds of reduced sugar consumption was in soft drinks, according to NHANES data from years 1999-2000 and 2007-2008.

So, at the beginning of that video Dr Lustig dismissed that 'we' are eating more of everything, but he still proved the empirical evidence that we DO eat more of everything: more calories, more fat and at that time it was also more of sugar. However, the American population increased the consumption of starch the most. Yet, Dr Lustig still tried to say that the fat did not matter, because of the secular trends of selected food items suggested otherwise and that it was the SUGAR we eat more of than of any other food compound:

The items on the bottom of the diagram are soft drinks, reduced fat milks, beer/ale, fruit drinks, coffee/tea, grain mixtures... mostly sugar, no flour and starchy processed food. Something does not match here with the actual data presented by the NHANES and USDA.

How does this come together with his later admission published in 2014 that it is not sugar which was THE cause of obesity? It was suddenly french fries and potato crisps and Dr Lustig said that we knew it. I KNEW IT, and other opponents did know it as well, but he kept saying all the time that sugar drove the obesity and then the metabolic diseases, even in this video from 2012. Now he said that sugar came as a distant third in the 2014 video at 38:36 minute. I have pointed at this turn-around in my previous article, too.

This post was just a recap of Dr Lustig's manipulative tactics to trick you into thinking that we ate more sugar in relation to a recent point in time (not back to year 1820) when the data suggested otherwise. So if nothing else was right in my blog here, this proves the pure nonsense and lies presented to the audience by a renowned doctor and health professional, calling himself a scientist. Because of what? Sugar agenda.

He also said he 'did not believe in common sense, he believed in data'. This statement in this light is just a grotesque.

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, only confirm this. 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. Excess fat tissues produces cytokines, an inflammation promoting compounds 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 research 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 Somali national.

He does not believe in common sense, he believes in data. I believe in both.

Dr Lustig said repeatedly that he does not believe in common sense but he believes in data. You could hear it in several of his lectures of which one was in this video, when he said it at 18:00 minute. The background behind this statement was the obvious conclusion we make that when people are less physically active, it is their responsibility while his alternative explanation was that it was their physiology that made them sloths and therefore not their fault as such.

Dr Lustig presented a common sense as a dogma which was in opposite to research, saying that that if we knew everything already we would not need to do the research. Is this really the common sense? What wikipedia says about this term?

"Common sense is a basic ability to perceive, understand, and judge things..."

I consider myself a scientist, too, but I believe in common sense and also in data - but only when they are presented in the whole context, not cherry-picking those that favor my agenda while leaving the rest out and muting the common sense so that one is not able to spot the flaws in the INTERPRETATION of the data. A common sense should be a sort of assessment whether the sense we make from the data actually fits the real world. And because I have been doing this all the time, I have decided to write this blog to debunk the selectively presented data of Dr Lustig after a careful judgement of the perceived and understood content of what he has been presenting to people over the past 5 years.

Dr Lustig has also earned the critiques elsewhere so I am not alone but I am probably the only one that tried to debunk his claims at such a wide scale as you could see. You could read my attempts to debunk his numerous claims in the previous 32 articles of this blog and on my very own website.

To cut this short I would like to relate this post back to the example outlined at the beginning: that it is the physiology that makes people sloths and gluttonous, not their initial actions - hence they are not responsible for how sick and unhappy they are. The data he has presented strongly suggest this mechanism, but me and my common sense reach further to the past and says this:

In the past, our ancestors were simply forced to expend the energy in search for food or earning the living. They also often went hungry, so they also experienced the lack of energy due to the physiology - but there was no other way to survive than to overcome this and go and seek the food. Today the technological advancements allow us to earn living and spend our free time without the need of expending extra energy. The technological advancement and food almost waiting for us at our doorstep actually encourages us to be physically passive. We are encouraged to focus on our mental stimuli and reward, forgetting about our bodies, which simply sit or lay down for hours each day. It is only when this continues for a long period of time that the metabolism is changed and the physiology is harmed by the excess calories in and almost no extra calories out except of what we need to burn to stay alive. Only then we can see how people develop insulin resistance and fail to read leptin which further exaggerates the problem. Only at this point I can join the argumentation of Dr Lustig that it is not the peoples fault and that their biochemistry is taking control over them.

But until then it was our own choices to sit and play a video game and to reach for fat and sugar laden processed food instead of going for a walk and biting into an apple or some other nutritiously superior food item. When I go to the supermarket, in every single one of them I am welcomed by the fresh produce - in England, I do not know how it is in the U.S. I firstly start putting the fresh produce into my basket or trolley. There are isolated places at the entrance with the promotional products that offer the processed food stuff or laundry detergents or nappies, but in principle we are all welcomed in our supermarkets by the fruits, vegetables and salads based on various sorts of lettuce. The same is on the streets in front of many local shops: there are boards with a number of bowls full of fruits or vegetables for £1. You have to go inside the shop to get the chocolate, beer or a bag of crisps. Now tell me that most of us do not have a healthy choice?

I agree that there are food deserts and many people do not have a drinking water running from their tap, but these are the minority in the developed countries. I sympathize with the poorer countries in which the drink industry rather sales (and their governments allow this) the Coca-Cola instead of plain water. They are really not responsible for their choice. But for the most of us int he U.S. or the UK this is not the case.

Another such case of wrongly presented information (not just data) is the suggestive conclusion put into the mouth of the beverage industry that the industry has never actually said - that all calories are the same and therefore a calorie is a calorie - as Dr Lustig repeatedly said in other lectures:

I have written a post about this already but I would like to bring it up again here for you to see that the common sense really matters in terms of the perception, understanding and judgement. The Coca Cola company admitted in their statement, that ALL OF US (including them) have to take an action to beat the obesity and that All calories count, regardless of their origin. There was said nothing about the quality of the calories and how they behave in the body. They simply admitted that the sugar calories in the drink also matter, as do the sugar or other calories from food, because people often ignored the calories in the drinks and only focused on the calories in their food. Coca Cola made it clear that their sugary drinks also contribute to the obesity and therefore they provided an alternative - artificially sweetened drinks.

Therefore, the claim of Dr Lustig that the food industry said that the calories are all equal from the perspective of metabolic pathways is unwarranted and wrong. The drink industry only admitted that their calories also count and that they play their part in the current trends of ill health of the nation. Nothing less and nothing more. Meanwhile, I am not sponsored by any food or drink company, just to dismiss possible worries of my readers. I also have NO disclosures. I just want to be objective and factual as much as I possibly can.

And this is the end of my discussion on the data and common sense. Any computer will read and evaluate the data, but only humans (for now) have the common sense to give it the actual meaning - or to distort it towards their own interests.

I will keep using the common sense when listening to the presentation of data by the biased presenters and so should you.

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