Does fructose make you fat?

Here we go again. I have watched the first lecture of Dr Lustig about the bitter truth about sugar from 2009 maybe 5 times. As I said elsewhere, this lecture gave me an idea for the topic for my final year project at the university: Fructose and Metabolic Syndrome. I have read a lot about this topic and while I studied for my degree I have also gained a great insight into the complexity of factors contributing to obesity of the population. Because I would like to complete my 'mission' to debunk some claims about the sole role of fructose in obesity and some other metabolic issues, and to offer my own view about the mechanisms, I have returned to the very beginning of my journey. By doing so I would like to focus on several other points from the 2009 lecture of Dr Lustig, which were not covered in much detail or not covered at all in my previous almost 60 articles of this blog.

Here is the summary of the 2009 lecture of Dr Lustig: 

I have discussed some parts of it in my previous articles so I will not elaborate too much on each of these summary points. In this article I will focus on the supposed weight gain promoting properties of fructose which were presented to you by a qualified clinician and professor, expert in endocrinology, admired and praised by perhaps millions of people today. Before proceeding I would like to say that I have no idea where Dr Lustig got it from that fructose interferes with obesity intervention. I have a different information based on a scientific data and I have decided to share it with you. 

Energy balance - does fructose promote weight gain?

There are several aspects to this question and I will try to cover them in separate paragraphs, reflecting on the content of Dr Lustig's presentation from 2009.

You could see this simple scales diagram showing the traditional view of the causes of obesity: eating more energy that can be burned leads to weight gain - just to learn from Dr Lustig that this scheme is flawed. He explained to you that it is not the amount of food you eat - it is the composition of the food you eat. He aimed at a specific compound in the processed food that makes you storing energy instead of burning it, disrupting the healthy energy balance.  

You could that things which make you spend energy make you feel good, such as coffee or exercise. In contrast, things that make you gain weight make you feel less energetic and sluggish, whether it is overeating or starving. I can agree with that. Eat too much and you feel like having a nap. Do not cover your energy needs and the body will make you slow down, conserving the energy for its survival. It was suggested that the compound disrupting healthy energy balance was sugar. But we eat combined sugar named sucrose. This sucrose is a molecule consisting of glucose and fructose which are metabolized differently to some extent.

Which sugar makes you storing energy rather than burning it?

Then you could hear an impressive story about how insulin promotes weight gain. This mechanism was explained as working by promoting storage of the food energy instead of burning it. When you eat too much sugar, the insulin rises and clears up the sugar and fat from the blood stream, because the blood sugar has to be controlled and kept within narrow limits. And then, when the energy (here: sugar) is stored, the sugar concentration in the blood drops fast, which leads to fatigue, hunger and further eating. So, as Dr Lustig presented it on an example, even if you require 2000 kcal per day and you have eaten 2000 kcal, you end up with 1500 kcal available for metabolism because those 500 kcal were stored (presumably as fat, but that is not that simple). Then you end up eating further 500 kcal to feel balanced, but by then you have overeaten those 500 kcal and you are gaining weight. Here, it was not made clear to you, that it is mainly the glucose part in sugar that is responsible for this. But read further, it is getting interesting.

How does FRUCTOSE variable come into the equation?

Just a reminder: Dr Lustig announced at several occasions that 'glucose is a good guy' while fructose is the bad guy. He demonstrated it on comparison of Atkins and Japanese diet and blaming fructose for the increased prevalence of obesity and gastric surgeries in Japan today. Or China, or Australia, after they adopted the westernized diet and lifestyle. Remember?

Do you think the countries suffering from an obesity boom today adopted only fructose consumption and nothing else??? 

Is it fructose that dominates the processed food industry and fast food???

I tell you something. That diagram above is an outstanding example of flawed logic and perhaps of a direct manipulation of the minds of people who do not have a deeper insight into the topic. This concept of the fructose as a common factor is just fundamentally wrong. We should not ask what the Atkins and Japanese diet have in common. We have to ask why they work?! 

The fact is that Atkins diet eliminates ALL CARBOHYDRATES, while traditional Japanese diet was LOW IN FAT (read more). They are quite an opposite of each other and fructose had little to do with that. It is the merging of the two factors these diets lack that leads to obesity: consuming excess of the insulin promoting carbohydrate with the excess of fat. Remember, that insulin also helps storing fat, not just glucose. One without the other result in a trim body like in case of Japanese or Atkins dieters. 

Back to basics: A recap what promotes energy storage in the body.

Now you know it is the glucose part in sugar that makes pancreas producing insulin significantly more than the little portion of fructose you can find in the blood stream. While in the past Dr Lustig said that fructose does not lead to insulin secretion, in a more recent lecture he said that even the tiny concentrations of fructose in the blood can make pancreas producing insulin. He basically contradicts himself. I cannot help myself but seeing it this way: blaming fructose for increased insulin then sounds like not seeing the forest because a single tree is obscuring our vision.

You could have heard the doctor saying in other videos that although sucrose or HFCS contain about the equal amount of glucose and fructose, most of fructose (claimed 100%) is directly metabolized by the liver and only a tiny fraction is released into the blood stream. He presented calculations about how many calories from glucose and fructose are metabolized in the liver and how fructose is the alcohol without the buzz. Hence, the actual amount of fructose in the circulation can be lower by the magnitude of thousand of that of glucose. We measure glucose concentration in blood in milligrams, but fructose can be found there in micrograms concentrations. Even if such small concentration of fructose in the bloodstream was able to stimulate pancreas producing some more insulin, this effect would be dwarfed by the capacity of glucose doing the same. After all, that property of glucose is the basis of the modern low-carb or Atkins dieting, is it not? They do not cut down on sugar or fruits only, they exclude most sources of carbohydrates, including starches which are polymers of glucose. Got it?

Because fructose does not lead to noticeable insulin secretion, it does not cause drops in blood sugar levels, therefore it cannot contribute to the disrupted energy balance as you were made to believe (read more).

It was claimed that fructose is not a sugar, it is a fat (as it ends up as fat after all). You may remember the claim of sugar being the only compound being a carbohydrate and fat at once. However, that is not quite true. Only a small fraction of fructose is converted to fatty acids in humans. We are not rodents who have a significantly higher potential to convert sugars into fat in the process called de-novo-lipogenesis (DNL). Regardless, even when a small portion of fructose is converted into fat, how does this little amount compare to the amount of ever increasing fats and oils consumption by the Americans and other nations worldwide, so that one could say that fructose is the sole responsible factor for obesity epidemics? This just does not make sense. You might have already learned about the trends in macronutrients consumption among the Americans, where it is apparent that the sugar consumption was decreasing since year 2000 (and fructose within) while the fat and oils intake continued rising, along constantly rising obesity levels in the country. Put it together and see another fundamentally wrong argument. Or, just read more here.

Could it be due to different appetite inhibitory mechanisms?

It was not a long time ago when the scientific papers (one, two), and Dr Lustig himself, kept explaining to you that fructose leads to a higher food consumption because it does not function in the body like glucose does. The scientists explained this mechanism by appetite inhibiting action of glucose and insulin on the brain receptors, which was not observed with the fructose. Then there was ghrelin added to the equation with that the fructose did not reduce the production of this hunger hormone, but glucose did. Some leptin resistance in the brain was mentioned and for this fructose was blamed again.

What fructose, I am asking. That fructose which was mostly held by the liver and metabolized there?

1. The scientists supported this mechanism with the short term studies of which most lasted no longer than 24-48 hours. 
2. In addition to that, their participants were already overweight or obese with a disrupted metabolism (for whatever reason). That is not exactly what is discussed here: whether fructose can lead to overweight or obesity, is it?
3. The scientists compared mechanisms of overfeeding with fructose versus overfeeding with glucose in metabolically already affected people for the duration of one or two days. How this relates to the fact that people normally consume glucose and fructose combined??? Can you see the flaws?
4. With every gram of increased fructose intake, there is about the same increase of glucose intake. So, if glucose reduced appetite or hunger, it should do so and the fructose has nothing to do with that!

What really happens in free living conditions.

When I did my research on this topic, I came across one particular study which reported an opposite effect to what you have been told previously. People were recruited and asked to consume either glucose or fructose sweetened drinks in free living conditions and lead a normal life without any dietary restrictions. We call it ad libitum, or 'as much as they want'. Their diet was described as balanced (50% carbohydrates, 15% proteins and 35% fat), but that was before adding the drinks. The amount of either sugar they had to consume each day was 150 g (600 kcal), which is quite a lot. They did this for four weeks and they were assessed for the compliance. From the results of body weight changes it was apparent that it was the fructose group that reduced their calorie intake more because their body weight increased only slightly: by 0.2 kg over 4 weeks in comparison to 1.7 kg in glucose group on average. Both groups had reduced insulin sensitivity and it was in glucose group that expressed increased fasting insulin with the statistical significance. Just saying.
A note: the abstract in the link for this study did not mention changes in participants' body weight, which were not the core focus of the study. I have had the chance to read the full copy and there I found these details. If you are interested, I can scan the copy and post it to you so you can see yourself.

Although this study had some limitations, it still provides a great hint what this all is about and supports the current knowledge that glucose promotes weight gain more via its insulin action than fructose. I am very confident that if such a similar study was conducted again and it was designed to the standards, the body weight results would be the same. My belief is based on the fact that our food consumption fluctuates from day to day and it is the energy balance over a longer period of time that is responsible for weight gain or weight loss and the associated metabolic effects.

Some other effect of fructose on food intake.

Could it be its sweetness?

I remember Dr Lustig saying how fructose is the sweetest natural sugar we know and how sweet taste makes us to enjoy food and perhaps eating more than if the food was bland.

That is true.

Then he continued that glucose is not sweet enough to make us desire more.

That is not true.

The sweetness of glucose is lower than of fructose but it is sweet enough for us to sense it and to enjoy it. In fact, the standard oral glucose tolerance test (OGTT), containing 75 g of glucose in Rapilose drink (300ml) is still perceived by most people as unpleasantly sweet. That is half the concentration I was told they used to get before Rapilose was used in our Epidemiology Unit. That time some people had adverse reactions to the doubled concentration of glucose in the manually prepared drink for the OGTT test. They felt nauseous and generally unwell. I did the test myself with the Rapilose twice and I can tell you that it really tastes very sweet. So if we only fed people with glucose as a sweetener in their drinks and other confectionery, they would certainly experience a pleasure comparable to the combined sugars widely consumed today. The reason why the market is not using only glucose is perhaps the price and practicability. The natural sugar is a combination of glucose and fructose, and since fructose is sweeter than glucose, less sweetener is needed in the product to achieve a desirable sweetness, reducing the manufacturing cost.

Could it be epigenetics?

You could hear at some point how Dr Lustig announced that new research shows that the more sugar the mother consumes, more gets through the placenta and the child is developmentally programmed to like sweet taste – which was supposed to explain the obesity epidemics of 6 months old or even the increased body weight of a child at birth. 

Well, how does this preference to sweet taste relate to the already overweight embryo or a toothless infant still entirely milk fed or just being weaned? That sweet tooth refers more to its lager age. Even then, the individual can stay away from sugar but become obese just by eating processed carbohydrates and fats, like in pastry (starch and fat), for example. How can fructose be the villain here? 

Some metabolic outcomes you may not have been aware of

Here is a scientific paper from 1999 making it clear how human body adjusts its carbohydrate metabolism to the amount of carbohydrates consumed, rather sparing the consumed fat and storing it. It basically says that we have a very limited capacity for converting carbohydrates to fat. And that applies to fructose as well!

Other study confirmed that fructose consumption led to a higher metabolic rate than glucose, based on the recovered labelled carbon isotope in the exhaled carbon dioxide. That carbon isotopes were previously in either glucose or fructose the study volunteers consumed. 

These isotope labelled studies are an excellent way of how to distinguish between variable metabolic pathways of different sugars. Even more importantly, these studies allow us to see the level of contribution of glucose or fructose to their shared metabolic pathways, because it is known that they do share many metabolic pathways. Fructose is even converted to glucose and glycogen, did you know that? In fact, more fructose can be converted to liver glycogen than glucose! 

That brings me to the end of this particle with a conclusion that regardless of how I look at it, I cannot support the sole effect of fructose on the disrupted appetite control in people, especially when they are initially metabolic normal, which is the point of this article: Does fructose make you fat?

I welcome your comments and suggestions.

Another example of biased scientific reporting - does fructose consumption lead to weight gain?

As I have promised in my previous article: Misreporting in the scientific literature, I am going to show you another example of biased scientific reporting. 

In the previous article you could see how the American Heart Association Scientific Statement (AHA Statement) misreported the actual findings of two particular studies which in fact did not suggest at all that the sugary soft drinks led to increased food intake as a direct result of the drinks consumption. 

In this article I am going to distinguish between the effect of fructose and sugar sweetened beverages (SSB) on people's metabolism and body weight and to bring more light into reporting of the metabolic studies. 

Again, I have cropped the relevant pieces of the AHA Statement text and I am going to write my comments on it. 

Cross-sectional studies

The first sentence of the text above reports that people consuming energy dense beverages have a higher energy intake. I have already discussed this in my previous article as a logic consequence and why people ate more of anything that was put in front of them. I am not going to elaborate more on this.

That people in the Western world, habitually consuming processed foods, have poor nutrition is no news to me and most other people having a genuine interest in nutrition and health. 

It is the 'suggestions' made that related only the excessive FRUCTOSE consumption with various metabolic issues in humans which I have found intriguing. These suggestions seem to conclude that the excess of anything else is not a problem at all, despite this anything comes together with fructose at once. There were studies listed as reference. You can find these at the end of this article. 

Let's just repeat the obvious facts I have mentioned numerous times in my articles:

The USDA and NHANES data suggest that the trends in sugars intake almost copied the trends in fats intake, up to year 2000. In addition, it was the processed starch based carbohydrates the consumption of which had increased more prior year 2000 than the consumption of sugars or fat. Therefore the Americans have been eating more of EVERYTHING, not only of sugar or fructose. That is one fact. The another fact is that since 2000 it was mostly the processed cheap vegetable oils that shot up in consumption trends, while the carbohydrates remained stable and overall sugar (mainly the HFCS) consumption went down. So how could the cross-sectional studies suggest that it was only the excess fructose that played a role in the obesity, dyslipidemia, hypertension, insulin resistance and type 2 diabetes??? If they said it was sugar (the combination of glucose and fructose) I would partly agree, but at this point I cannot. This is because the population does not normally consume fructose alone. It is the combination of fructose and glucose and the two first references (25 and 26) listed the soft drinks as such (one comparing HFCS to aspartame), not fructose only sweetened drinks.

Metabolic studies

Then, in the text, there is a small metabolic study mentioned. This study was of Stanhope et al (2009). I have reviewed the results of this study (among other 28 studies of various designs) and this is what the authors reported:  

• The participants were fed in various settings, during which they received glucose or fructose sweetened drinks after each main meal.
• The participants were aged 40-72 years, just to give you an idea. They were not very young and fit, only having their body weight stable in terms not gaining or attempting to lose, or doing so for several months prior the study. 
• They were sedentary, i.e. not exercising more than 3.5 hours per week and at no higher intensity than fast walking. 
• The participants were either overweight or obese. I have written a separate paragraph below to address my concerns about this detail. 
• Both sugar groups had increased body weight at the end of the study: fructose fed by 1.4% from the baseline and glucose fed by 1.8%. Therefore this study produced results which were is in contrary with the past beliefs that fructose was responsible for the population weight gain while glucose was OK. I have also elaborated more on this later in this article.
• Fructose group had increased visceral (in the abdomen, risky) adiposity while the glucose group had increased subcutaneous (under the skin, 'healthy') adiposity, also around the waist.
• Blood pressure did not change among any of the two groups - in contrary to many who believe that fructose leads to hypertension. 
• Fructose group had (surprisingly?) increased HDL - the good (Happy) cholesterol. 
• The team reported increased DNL in fructose group. This also needs more discussion, see below this bullet points paragraph.
• Fructose group had increased lipoproteins and 23-h curve triglycerides, fasting glucose and fasting insulin while having reduced insulin sensitivity index (data for the glucose homeostasis metabolism). 
• However, the glucose group had increased fasting triglycerides and mean 24-h free fatty acids concentrations in blood plasma while fructose had not. It was commonly reported that fructose feeding led to drop in FFA and increase of triglycerides, on the synthesis of which those FFAs were used.
• Interestingly, men were more affected in their blood lipids (increased) whereas women were more affected in their insulin sensitivity (reduced).

Regarding the DNL levels mentioned above, these were differed between glucose and fructose settings, depending on whether they were postprandial (after eating a meal) or fasting. Have a look: 

In a fasted state the glucose group had continued producing new lipids, while the fructose group reduced their production in comparison to the baseline levels, but after eating and drinking the sugary drink straight after, the liver was overwhelmed so it produced more new lipids than those consuming glucose. In addition, I have already challenged the different methodologies of DNL measurement and how these can vastly differ as a result of different methodology used.

Interestingly, the fasting HDL in glucose group was decreased (-2.4%) and I have already mentioned that in the fructose group it increased (+3.5%) from the baseline. Fasting HDL is one of the five metabolic syndrome features for the clinical settings assessment. Fasting triglycerides (TG) are another one in the assessment of dyslipidemia. The increase of fasting TG was more than twice as high in the glucose group (+9.7%) than in the fructose group (+3.9%), in comparison to the baseline. However, some scientists suggest that postprandial TG are more relevant to the cardiovascular disease risk than the fasting TG. It was the postprandial TG levels that shot up and kept the overall 24-h levels of TG markedly increased in the fructose group when compared to the glucose group. This was also partly due to the reduced clearance of the lipids to the adipose tissue (mediated by lower insulin excursions after fructose intake) - which actually aids in the control of the body weight. So, although in contrast with the current definition of metabolic syndrome, the lipids metabolism results of this study were used as a proof of dyslipidemia caused by excess fructose consumption.

Have you found the information above overwhelming? And that was just an overview of the most relevant details. And, by the way: 

1. Glucose or fructose sweetened drink were given at 25% of total energy intake (TEI) - that is beyond the usual intake by the average American population. Can you imagine a quarter of your daily calories coming from sugar? Sure, there are some individuals who can manage that and they do. However, when stratified the population into the levels of sugar consumption, those consuming combined sugar at > 25% TEI formed only 13% of the population (as per data between NHANES 2003-2006, sugar consumption continued to decrease after that) and the majority of these were adolescents, especially male, not people in middle age or elderly. On top of that, fructose contributes less than half to this amount of added sugar. Doubling the fructose intake so much beyond the usual or habitual intake as it was in this particular study is considered toxic. You would have to consume over half of your daily calories in sugar to cover this amount of fructose intake - which is ridiculous. Such high doses of fructose are often given in the metabolism challenge studies. These are designed to study the mechanism of action and they should not be interpreted as an every-day situation typical for the general population.
2. The fructose or glucose drinks were tested for 8 weeks in ad libitum free-living settings and then for 2 weeks of energy balanced settings. The ad libitum means that people could eat anything and any amount of food they normally consume, plus consuming these drinks at each of three main daily meals. Positive energy balance was reported and this variable has constantly been a confounding the outcomes of similar studies. Blood samples were taken at 0, 2, 8 and 10 weeks of the study duration. 

This 2009 study was a parallel-arm study to another similar one of Stanhope et al (2011). In the 2011 study the fasting insulin in the fructose group was NOT increased in comparison to glucose group, which was in contrast with the results of 2009 study. The participants were the same and they consumed the same amounts of sugars over the same weeks pattern. Also the plasma glycated albumin was lower in fructose than in glucose group which is in contrast with Dr Lustig's claims that fructose is 7-times faster in browning reactions in the body, hence causing irreversible damage to the arteries. On top of that, the fructosamine levels did not differ between fructose and glucose groups.

Although this 2011 study was not included in the AHA Statement from 2009 (obviously), I would like to elaborate a little on the difference between these two parallel studies. 

Below is an overview of some variables assessed by the 2011 study:

From the table you can see that the differences were small, albeit statistically significant. However, were they clinically relevant? That is the question. 

The scientists have found slightly increased fasting glucose, but the fasting insulin levels were not significantly different between fructose and glucose groups. Although the fasting insulin levels were initially higher at the 2 weeks of ad libitum settings, at the end of 8 weeks it was lower in fructose than in glucose group. This may have been due to the metabolic adaptation or an effect of different diets of the free-living participants. I have seen conflicting results on glucose homeostasis among similar studies many times and it is not easy to come to a final conclusion whether fructose does lead to insulin resistance or not. Therefore, if the insulin sensitivity was slightly reduced in the fructose group at the end of the study that is true for this study only and others have produced different results. On top of that, this was after the final 2 weeks of energy balanced settings, nothing was reported after the first 2 weeks and at the the 8 weeks of ad libitum settings. All other variables had the parameters reported for both time points during the ad libitum settings. I wonder why this parameter was missing here. 

It is also worth to mention that the female participants were post-menopausal which could also contribute to the adverse metabolic outcomes. It is well established that women after the menopause start to catch up with men in several metabolic variables, mainly the lipid metabolism. 

It is also important to note that it is the teenage boys that consume most sugar from the whole population and as the population ages, the consumption of sugar decreases. Therefore, if we wanted to assess the effect of some dietary compounds on the population, it should be studied in amounts relevant to that population instead of feeding toxic amounts of an individual sugar (fructose) to middle-aged and elderly sedentary participants. To match the composition of the sugar to the real life situation, the population would need to consume over 50% of their daily calories in sugar or HFCS, which is a non-sense. 

Meanwhile, do you recall that it was conducted on overweight and obese people? I have already debunked one particular claim of Dr Lustig based on one such study. And you may recall my other article The matter of relativity and relevance, which outlined that 80% of obese people have metabolic issues in comparison to 40% of those with BMI below 30. Yet, just because 20% of obese appear as metabolically normal at a given time and the scientists put the overweight, normal weight and underweight into the other category (those 40%), this led some researchers and other individuals to the conclusion that excess body fatness is not a problem. 

Now you see what everything has to be taken into consideration before you interpret and use the results in the argumentation. It is not as simple as the articles often print. 

Discrepancies in the reporting

Moving to the last part of the selected content: the reduced SSB led to decreased body weight among children. That takes us back to the beginning: when removing some sugar calories from the diet would you not expect the weight go down in case you have not replaced the sugar calories with some other?

However, what I wanted to point at, and that is very important, is that in the selected text  from the AHA Statement, the sugar (HFCS) was used interchangeably with the sole effect of fructose as if the glucose was without the effect. You could see in the discussion of the metabolic studies above that glucose also has some metabolic effect and it led to a higher weight gain than fructose. On top of that, the text I have placed here was published under a subheading FRUCTOSE. Now you might appreciate the level of misreporting in the AHA Statement. They really believed (or wanted us to believe) that fructose makes people obese.

Back in 2009 and even before that, as per Elliott et al. 2002 listed as a reference for the AHA Statement at the end of this chapter, it was common among the scientific community to present fructose as THE sugar that promotes weight gain. The mechanism was explained this way: because it does not lead to the insulin release typical for glucose, it does not sufficiently stimulate the hypothalamus which should otherwise responds with the satiety signals and make us stop eating. One of the listed references, Havel (2005) said:

"Fructose does not increase insulin and leptin or suppress ghrelin, which suggests an endocrine mechanism by which it induces a positive energy balance."

This mechanism, as a leading factor to hyperphagia (increased feeding) due to sugar (HFCS) consumption, is no longer true. However, people still believe this mechanism is the main contributing factor in the weight gain of people consuming added sugars. I have written a short article about why I think the children ate more food in a restaurant after they consumed a soft drink. It was just my idea as the studies uniformly pointed at fructose or discussed sugar as such, without taking into account the possible effects of glucose in it. As I mentioned previously, about half of the usually consumed sugars consist of glucose. Would you not expect this glucose to do some job on the hypothalamus, making it stop requiring more food when sugar or HFCS sweetened drinks and food items were consumed? Yet the 'professionals' tried to convince us that the brain or even pancreas perhaps do not see that glucose either, like if there was no insulin release when glucose was consumed along fructose in the sodas. In fact, the hypothalamus also responds to glucose as such by reducing the appetite. So it is both: glucose and insulin that trigger satiety signals and even if the half fructose in the sugar did not have such effect, the other half of the sugar comprised of glucose should do something. And it certainly does. 

In addition, you are probably familiar with the glycaemic and insulinaemic effect of dietary glucose (also in white bread or other processed starch products) and how it promotes lipid storage and blunts the lipid oxidation - leading to easier weight gain when lots of fats are consumed along starch or sugar. It is glucose and its effect on insulin that promotes weight gain more than fructose and the modern low-carb enthusiasts bet exactly on that. This fructose caused weight gain myth was also disproved by other study of Swarbrick et al (2008). 

This study was published before the AHA Statement was published in 2009. In this study, the post-menopausal women reduced their body weight after 10 weeks of energy balanced diet by 1.5% on average (representative of 1 kg for 70 kg heavy lady). They also consumed 25% of their energy in fructose but they did not over-eat. This is nearly a proof that it is rather due to overeating that people gain weight, not because of fructose. Those consuming fructose in this study, similarly to those in Stanhope et al 2009, did not consume glucose along as the normal population does. Yet the fructose led to reduced body weight in energy balanced settings (proving Havel 2005 wrong) and in lower weight gain in comparison to the same amounts of added glucose consumed in the Stanhope et al (2009). Yet in 2009 the AHA 'Scientific' Statement announced that fructose plays a role in obesity. How big role and in what context?

Conclusion

Fructose is a known lipogenic agent, whether by enhanced DNL when consumed in high amounts or as a re-esterifying agent which brings together the glycerol and FFAs for the formation of triglycerides or the lipoproteins (the blood 'cholesterol'). And, although fructose has been repeatedly presented as contributing to the very low density lipoproteins (VLDL), now you know that it has been found to increase HDL as well and producing lower levels of glycated proteins in the blood plasma - in comparison to glucose. To my understanding, it is the increased oxidation of various blood components and other tissues that is responsible for the atherosclerosis more than the presence of lipids and lipoproteins. And, because fructose occurs in blood in much smaller concentrations than glucose, it is unlikely that fructose would be a leading factor in the atherosclerosis development, leading to the biggest killer in the world: cardiovascular diseases. However, it does contribute to oxidized VLDL - released from the liver, which metabolises majority of the ingested fructose. Regarding the insulin sensitivity or resistance, I have seen during the research for my dissertation that the scientific papers produced conflicting results for the risk factors of type 2 diabetes. Hypertension as a result of excess fructose feeding was also not confirmed here.
Things are rarely only black or white and a deep knowledge is needed to see through the flaws even of the peer-reviewed scientific papers. Therefore, I would rather think about the combined effect of glucose and fructose in the sugar as we consume it, along the positive energy balance (over-eating and under-exercising) and perhaps other components of the diet (processed vegetable fats), than blaming fructose alone for most of current metabolic issues.

Indeed, as Stanhope et al (2011) wrote:

"a limitation of the current study was that it did not address the possibility that there is a synergistic relation between increased glucose and insulin excursions and unregulated hepatic fructose metabolism, which occurs when fructose and glucose are consumed in combination."

And, regarding the obesity due to fructose consumption, I think it does not need any further comment except that the opposite was found to be true. 

Below are the references I mentioned earlier and I am looking forward to read your comments. 

Coca-Cola conspiracy by Dr Lustig - how true is it?

I have already touched this topic in one of my previous articles, but there I focused on sugar content. This article is about the sodium content in the Coke.

In his oldest video from 2009, at 33.40 minute, Dr Lustig said that there is 55mg of sodium per can of Coca-Cola and that it is like drinking pizza. Did Dr Lustig want to say to us that we get thirsty from 55 mg of sodium in a can (0.330ml) of a soft drink? 

Well, let’s look at how much sodium does one isotonic drink contain per 100ml: it is 28 mg. To compare it to 330ml can of coke it makes 92.4 mg which is almost twice as much than in the same volume of Coke. And you an also taste it in the isotonic drink. The isotonic drinks are designed to contain similar tonicity to our blood so that they hydrate us well during spots activities. These drinks are not designed to make us thirsty or drink more. So what Dr Lustig meant by the Coca-Cola conspiracy based on 55mg of sodium? 

I have found no mention of salt in the nutrition facts of Coca-Cola for the UK market up to the 500ml drink size. Of course, it does not mean that no sodium is present. It means that according to the food and drink labeling rules the amounts are so negligible that they can be claimed as 0. What Coca-Cola actually says about it?

“The level of sodium in the most of our products (except for tomato and vegetable juice cocktail) is minimal and is mostly related to sodium in municipal water sources. Most of our beverages can be classified as "low sodium" or "very low sodium" as defined by FDA's labeling regulations. In the U.S. and many other countries, we declare sodium content on the product label.”

FYI, there is a general converting factor to see how much salt contains how much sodium. The molecular weight of sodium is lower than of chloride, to which it is ionically bound, forming our usual salt. Therefore, if you want to find out how much sodium is in 1g of salt, you have to multiply it by 0.4, so you get 400mg. The other way round, multiply amount of sodium by 2.5 to get the amount of salt needed to get this amount of sodium. So, in the 330ml of coke, if it contains 55mg of sodium, that equals to 137.5 mg of salt, which is virtually nothing in comparison to the daily limit of 4-6 grams of salt for an average person. Now take one 28.4g bag of salted crisps and you will consume 136 mg of sodium or 340 mg of salt. 

Finally, how about pizza? According to NHS, some takeaway pizzas are saltier than Atlantic Ocean, containing about 10g of salt. The Guardian reported that the supermarket pizzas generally contain half of that amount of salt, which is still about the whole daily allowance of salt. Of course, the content of salt will depend on the ingredients used, not all pizzas are the same. When you search the content of salt in pizza, the Wikipedia will offer you a figure 598mg sodium pre 100g, which translates to 1495 mg of salt, or 1.5 g, about a third of our daily allowance. 

So, again, Dr Lustig has been pushing too hard and a quick check of the facts made me and you see the flaws in his claims once again. It is not the salt that will make us drinking more Coke, it will be its sugar content and perhaps the salt in the food or the delicious and secret formula of the Coca-Cola syrup, which is known to only two men on the globe. For us to be thirsty for more fluid, the Coke would have to contain significantly more salt and we would need to taste it, despite a high content of sugar in it. Period.

Obesity does not cause the loss of productivity. Is that true?

In the current pandemic of obesity and obesity related metabolic diseases, when the governments of countries are looking for a quick solution to prevent the collapse of health care, some people seem to believe that obesity is not a problem. 

I have discussed this topic in several of my articles, of which one can be found here. In that article I pointed at several aspects of obesity, independently of the metabolic disorders, that directly affect people's health and wellbeing and one does not have to be a scholar to understand that it also can cost the society a lot of money. 

However, Dr Lustig believes that obesity is not a problem. He said so in a panel talk at 31 minute of the video and also that it is diabetes where the money goes. He specifically said that 

"Obesity does not cause the loss of productivity." 

Really? 

I remember reading a story in the papers a couple of years ago. It was about a woman who was on benefits, because she was too fat to be able to work. And her daughter was the same! Check the Mail Online article about the cost of the obesity to the society. On Youtube you can also find plenty of videos of extremely obese people how they need a constant care because they are bed bound or immobile, they are often in a constant pain due to excess body weight and all they can do is remain at home and get support. 

Now tell me that the obesity does not lead to absenteeism or the loss of productivity, whether on the side of the affected individual, or the employer or the whole society. Just because there is more money going into research of diabetes or cancer, and not to the research of obesity, it does not mean that obesity does not cause a loss of productivity or that it is not a burden to the society. 

Of course the obesity causes the loss of productivity, in addition to the tremendous health care costs! 

If you do not believe my description, check the official figures: 

"The cost to the UK economy of overweight and obesity was estimated at £15.8 billion per year in 2007, including £4.2 billion in costs to the NHS."

Too little? Well, in 2014 it was £47 billion, according to The Guardian, referring to the McKinsey Global Institute. The NHS costs have also jumped up to £9 billion a year, which means it more than doubled since 2007, which was not that long ago, what do you think? 

And these were just in the UK. I can predict that the U.S. will have even worse figures. In fact, read this: 

"About 37% of the obese population in the U.S. is in the two highest grades of obesity -- a body mass index (BMI) of 35 to 39 and a BMI of 40 or more. But these two groups are responsible for 61% of the costs resulting from excess weight, Finkelstein and colleagues calculate."

Or another source:

"Loss of productivity due to obesity costs as much as medical expenditures for the condition, according to a new study that pegs the cost of obesity among full-time workers in the United States at $73.1 billion per year.

Obesity's hidden costs, the researchers said, stem from the fact that obese people tend to be less productive than normal-weight people while at work — simply accounting for the extra sick days they take misses a big part of the picture. “

The following diagram shows the trends in the rise of bariatric surgeries - the quick-fix of the stubborn obesity among people who could not lose weight the natural way. Why would they be doing it if it had no impact on their life? 

For comparison, below is the table illustrating the cost of both types of diabetes to the NHS in 2012: 

There you see that only little more money was spent for treatment of the type 2 diabetes  than those £9 billion for the obesity mentioned earlier, can you see? Yet Dr Lustig claims that it is diabetes where all the money goes and that the obesity means nothing because people do not die from it:

In addition, the newer version of the 'good old' video: Sugar: The bitter truth from 2011, starts with Dr Lustig saying how the "obesity is chewing through our healthcare dollars like nothing ever before..." Has he changed his opinion in three years? It seem he did because back then he presented this information to the audience: 

There you have it: $65 billion reduction in work productivity... In addition, he also explicitly said, when quoting another professional at 1:07:29 of the 2011 video that "if they recoup that $150 billion they would resolve the healthcare problem".

In the UK, the constantly increasing prevalence of obesity and the threat that the NHS would collapse by 2020 because of it was also a reason why the public policies focused on obese people, not only on those that are metabolically sick. Only one campaign Change4Life which was run with the main aim to PREVENT obesity had a budget of £73 million over 3 years. Only one campaign and it was not even designed to reduce the obesity but to prevent it. It is well established that once the obesity develops, it is difficult to ged rid of and it comes with other diseases as well. The prevention is better than cure. 

So why the governments and other non-governmental organisations would focus on obesity if it was not a problem and if it did not lead to the loss of productivity? That is my question. 

Misreporting in the scientific literature.

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

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

The highlighted references were these: 

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

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

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

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

Their findings: 

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

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

Their conclusion was: 

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

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

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

What was the aim of the study? 

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

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

What were the actual findings of this second study? 

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

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

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

But let's check the conclusion: 

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

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

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

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

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

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

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

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

How did they come to the 6 and 9 teaspoons of sugar limit figures?

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

I have no problem with reducing sugar intake by anyone. I have done it myself. Aside from 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 new limits of sugar consumption. I found it just by chance and I believe that you will find it as interesting as I did. I admit I previously read the paper when I did my own research but I did not think hard about how they came to the figures because my focus was on the evidence of the negative health impact of fructose consumption. I have realized this interesting background only recently when I heard it discussed by Alan Aragon, who 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. 

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. These discretionary calories were set up as 10% of total energy intake, because it was understood that people were likely to cover their nutritional needs when nutritious food contributed with 90% to their total daily energy requirements. Hence they could expand on the hedonistic experience by consuming other food items, such as sweets, butter or alcohol, which made up no more than those 10% to fit into the balanced energy intake, i.e. not gaining or losing weight when eating this way. The team, including Dr Lustig, just halved these 10% into 5% and allowed people to consume this amount of calories in a form of sugar. Mr. Aragon hypothesized that the scientists assumed that the remaining calories will be filled with solid fat intake or also the alcohol. The AHA Scientific Statement (the one in the slide) says that when people consume alcohol, their added sugar and solid fat intake should be even lower to maintain those 10% of discretionary calories overall. Exercising people can consume more, of course, but this was not mentioned in the lecture and on the slide above. 

One thing should be noted: nobody can follow this guideline to the point on daily basis. The figures represent average value and should be met within overall daily consumption over several days as mean value. 

Now you might have realized that from percentages we have suddenly moved to the absolute amounts - the same amounts for every woman or man, regardless of their actual energy needs or expenditure. at least according to the slide mentioned earlier. 

However, the AHA Scientific Statement itself, albeit just briefly, included more information: 

Now I am asking: who is the average adult woman or adult man? 

They do not exist, it is just a reference point to give an approximate idea about the amounts. 

You have probably noticed that the figures in the Statement were slightly lower than those presented in the slide. This is because the figures on which the team made the recommendations refer to the past, when people had a lower body mass on average. You might already know that today we are heavier than our parents were, because we also eat more calories (or rather move less). The average woman energy intake today is 2000 kcal and for an average man it is 2500 kcal. You can find these figures on almost every processed food package, close to the Nutrition Facts table. Those old figures referred to an average woman, weighing about 60 kg, and it included young women as well as elderly. Those 60 kg is no longer real though. 

As I said previously, I do not object against the recommendations to eat less sugar. It was the method of coming to the specific numbers that amazed me. And the Statement also admitted that these numbers are not realistic: 

It seems that if you consumed more than the prescribed amount of teaspoons of sugar, your health would be affected badly, regardless of whether you drunk alcohol and/or ate the solid fat or not. Do you understand what I mean? They expect that everybody has the same diet as any other person and that everyone consumes half of their discretionary calories as sugar and half as solid fat. What if some people consume less solid fat? Will Dr Lustig tell them off for exceeding the new allowance for sugar, because they drunk one can of soda?

Finally, I have found the following piece of information, cropped from the slide presented at 59:53 minute, intriguing: 

Three points I would like to make here: 

1. These new amounts (limit of 9 and 6 teaspoons of sugar per day) were therefore not based on any study for a safe threshold of sugar consumption. The figures were just made up. Dr Lustig & co. basically created these amounts and he judges the general population about the amounts of sugar they are consuming today in respect to the newly created allowance limit; exercising or not, obese or not, guilty as charged. 
2. These new limits still reflect the relative body size and muscle mass of two sexes (men and women). But they do not correspond to the actual size and capacity of their livers 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 science.
3. In addition, what this basically means is that this argument still focuses on body weight, not on the metabolic health, especially of the liver. Although the Statement was published in 2009, Dr Lustig brought it to your attention again relatively recently; the video was published in March 2014. Therefore this is another discrepancy of the aims and efforts proposed by Dr Lustig. The obesity is not a problem anymore - he now says, it is the health of the liver. However, the metabolic risk for the liver was left out when using this argument. 

And that is it. You now know how some public health figures are made up. There was actually more I would like to comment on that paper. In the following article you will learn how some of such respected papers still can misreport the information which they refer to.