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.