The truth about fructose and metabolic syndrome: Part 1 – Introduction

By Dagmar
In Opposing
Apr 1st, 2014

It seems that the ‘fructose is a poison’ hysteria is slowly calming down, but I have decided to write my first series of articles about it. ‘Fructose and metabolic syndrome’ was the topic for my BSc dissertation and I spent about two years researching it.
At the beginning was a random click on the YouTube video of Dr Robert Lustig, MD: Sugar: The Bitter Truth (Lustig, 2009). It was just before the start of the semester in which we had to choose a topic for our final year project. I had no topic at that time, but during the lecture of Project Preparation module I recalled seeing this video and that it was very interesting and relevant. Dr Lustig appeared to be qualified and things he presented in the video made sense. Initially, I knew little about how difficult this topic actually was and that there was so much research already done, mostly favoring the thesis that fructose plays a significant (or even causal) role in various metabolic diseases grouped into one term: the metabolic syndrome. When I started to research the subject I thought it was going to be easy as the evidence already was there, but when I looked deeper into the studies and other data, my conclusion contradicted some aspects highlighted by Dr. Lustig and other researchers. Therefore, I have decided to write about this topic and actually to debunk the debunkers’ claims about how bad the fructose is and that it drives the epidemic of obesity and related metabolic diseases among the westernized population. Because this topic is very complex and exhausting, I will split its content into several articles so that the readers can digest it in steps.

First things first: the definitions. 

Fructose is a simple sugar that can be found in fruits and in some vegetables in smaller amount. You can find it in honey or agave nectar, too. It forms half of the table sugar (sucrose), of which the other half is glucose, the sugar we essentially need for the function of our brain and the red blood cells. In fact, sucrose[1]almost the whole body prefers glucose as a primary fuel for the metabolism. These two simple sugars are identical in composition, but one single difference in their structure, i.e. how the atoms are attached to each other, makes these sugars quite different chemically and metabolically. Due to this single detail the two sugars gain a different 3D shape, which influences what enzymes will act upon them and therefore how our body handles them. Even their sweetness is different – fructose is the sweetest natural simple sugar we know. I have borrowed this diagram from another website and it illustrates a sucrose molecule.

A few decades ago fructose was praised as a good substitute for sucrose for diabetics because it does not require insulin to enter the tissues and to serve as a metabolic fuel. It was also sought by dieters because of its intense sweetness. This property of fructose allowed for reducing its amount in the product by up to one third, resulting in a lower calorie content. Such products were labelled light, in addition to those containing artificial sweeteners such as saccharin or aspartame.

High-fructose corn syrup (HFCS) has been mentioned in the media a lot recently. It is an equivalent to sucrose by taste, but cheaper. The technology of enzymatic conversion of some glucose (dextrose) portion in the corn syrup to fructose had been developing over decades in the past century.  The corn is largely subsidized in the U.S. so this sweetener is cheaper and preferred in most of the processed food products. When people hear: “high fructose” they assume this sweetener contains a lot of fructose, more than the sucrose does, but this is not quite true. The market offers three main forms of this sweetener: HFCS-42, HFCS-55 and to a small extend the HFCS either 90 or 95 (a crystalline form). The number indicates the percentage of fructose content and the remaining is free glucose or glucose polymers. So, if HFCS-42 has 42% fructose, the glucose moiety is 58%. Similarly, in HFCS-55 there is only 45% glucose, but 55% fructose. These are the two main corn sweeteners used in American production. Europe calls it glucose-fructose syrup, but it is not as widely used in the EU as it is in the U.S. So, when you recall that your traditional table sugar contains 50% glucose and 50% fructose, does the HFCS look so scary? Obviously not. Moreover, the studies have shown that there is no significant difference in how we absorb and metabolize these two sweeteners, therefore they are usually taken as equal in the research.

metsyn1Metabolic syndrome refers to a group of adverse metabolic conditions of which different combination can be present in different individuals, hence the name SYNDROME. Its definition has not been unified across different countries or health organisations, but, to my knowledge, the latest interim statement of Alberti et al. published in 2009 defines the metabolic syndrome for the clinical use as the three or more of the following conditions which are present or already treated: increased fasting blood glucose (fasting hyperglycaemia), increased triglycerides (hypertriglyceridaemia), increased waist circumference (this also varies across different countries and the risk cutoff points are different for some ethnics), increased blood pressure (hypertension) and lowered high-density lipoproteins (HDL, the good ‘cholesterol’). The threshold values can be found in the Statement of Alberti et al. There are other biomarkers or indicators of the metabolic disturbances used in the research. These were listed in the International Diabetes Federation (IDF, 2006) on page 13, although other sources mention more. As the research continues, we can expect other factors emerging from time to time.

Overall, untreated metabolic syndrome can easily lead to the diabetes type 2 or cardiovascular diseases, or both. The meta-analysis of Motillo et al. (2010) revealed that the metabolic syndrome was linked to the all cause deaths, predominantly the cardiovascular disease mortality. These diseases, obesity and type 2 diabetes are not separated conditions. They share most of the risk factors and the diseases often occur together. For example, an insulin resistance or a full blown type 2 diabetes is a risk factor of cardiovascular diseases. What is more, the atherosclerotic changes were found in children who suffered obesity and hypertension. This was found when these children were followed in a longitudinal Framingham Heart Study from early childhood for years and some of them died in accidents. Their bodies were examined and the atherosclerotic plaques were found already forming in their arteries. As you can see these damaging processes can start very early and because it does not hurt, the affected people are not aware of it. 


The diagram on the right was based on the data from the Health Survey for England published in 2011. The (A) refers to adults and (C) to children aged between 2-16 years. It illustrates how some health conditions associated with metabolic syndrome have been changing in England during the past decades. The trends have been similar between the UK and the U.S. You can see that while the hypertension was relatively stable and the obesity among children has gone under control to some extent since 2004 due to the government policies and interventions, the diabetes and waist circumference (WC) kept rising steadily. The graph basically indicates that more than one in 20 people had diabetes in 2010 and the trend is increasing. However, this only covers the cases that were diagnosed, which is just a tip of an iceberg. More people have disrupted sugar metabolism, a so-called pre-diabetic stage, which is already doing the harm to the arteries and other organs. In addition, almost half of the English adult population stores excess abdominal fat, one of the key predicting features of type 2 diabetes (IDF, 2006). What is more, other sources report that although the cardiovascular mortality has decreased in the western world due to an improved treatment (has your GP prescribed the statins to you already?), the risk factors of the diseases were on the rise.

It is therefore very important to find what enhances the development of metabolic syndrome in the first place so that we can address the prevention and the treatment accordingly. Metabolic syndrome is no longer an exclusive ailment of developed and wealthy countries. In fact, there is an interesting paradox: in developed countries such as the U.S. or Europe, the metabolic diseases are more prevalent among the socially disadvantaged people, whereas in the developing or transition countries with the improving economy, those financially better off are affected more. Why is that? What role does fructose play in this?

The second part of this Fructose and metabolic syndrome series is dedicated to disproving the claims of Dr Lustig about the trends in sugar and fat consumption.


Alberti, K.G.M.M., Eckel, R.H., Grundy, S.M., Zimmet, P.Z., Cleeman J.I., Donato, K.A., Fruchart, J-C., James, W.P.T., Loria, C.M., Smith, S.C.Jr.  (2009) Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation 120 pp: 1640-1645.

Framingham Heart Study [Online]. Available at: (Accessed: 25.3.2014)

Health Survey for England (2011) [Online]. Available at: (Accessed: 13 March 2014)

IDF (2006) The IDF consensus worldwide definition of the metabolic syndrome [Online]. Available at: (Accessed: 13 March 2014)

Lustig (2009) Sugar: The bitter truth [Online]. Available at: (Accessed: 25.3.2014)

Mottillo, S., Filion, K.B., Genest, J., Joseph, L., Pilote, L., Poirier, P., Rinfret, S., Schiffrin, E.L., Eisenberg, M.J. (2010) The metabolic syndrome and cardiovascular risk: A systematic review and meta-analysis. Journal of American College of Cardiology, 56, pp: 1113-1132.

About "" Has 48 Posts

Graduated at London Metropolitan University: BSc (Hons) Human Nutrition in 2014. Working as a research assistant at the MRC, The University of Cambridge.

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