Robert Lustig has called fructose the “alcohol without the buzz”, and when I first read the title of his article I was very intrigued. He presents a logical rationale behind this name-calling and needless to say, I felt that this was an argument worth sharing – although focusing on the fructose facts.
The increasingly popular low-carbohydrate (and high-fat) diet does in fact have a major similarity to the traditional high-carbohydrate (and low-fat) Japanese diet. They both strive to eliminate fructose. As they both lead to weight loss and provide health benefits, surely this common factor is relatively significant?
The metabolic syndrome (namely type 2 diabetes, hypertension, dyslipidemia, heart disease) is a health crisis, and most blame obesity as the common aggravator. Interestingly enough however, it has been shown that 20% of obese individuals have normal metabolic function, whilst as many as 40% of normal weight individuals may present with aspects of the metabolic syndrome. [1, 2, 3] Robert Lustig proposes that obesity be viewed as a marker for metabolic dysfunction rather than a cause.
So, if it isn’t necessarily our weight gain that is driving metabolic dysfunction, what is?
Across the globe, the monosaccharide fructose has increasing prevalence among foodstuffs, and has the capacity to promote chronic metabolic disease.  Fructose is made up of sucrose (beet or cane sugar) and 55% of high-fructose corn syrup (HFCS).  HFCS is found in a number of foods because it helps delay the expiration date whilst maintaining taste, and unfortunately for our health the tastier the food the more we tend to overeat it. Ominously, HFCS also has addictive properties, much like the sugar it is often replaced by.
HFCS is commonly found in:
- Breakfast cereals including e.g. Bran Flakes, Corn Flakes etc
- Sauces and condiments e.g. Tomato Sauce
- Snack bars and cookies e.g. Rice Krispies Treats, Cereal and Milk Bars etc
- Fizzy drinks e.g. Coke
- Sports drinks and gels
Fructose is completely unnecessary in the diet, based on the fact that there is no biochemical reaction in the body that requires dietary fructose. Humans do not nor have they ever produced fructose in the body, and are only used to consume dietary fructose when seasonal fruit were ripe. Fructose is somewhat the appendix of the diet world – a vestigial nutrient.
Side note: individuals with hereditary fructose intolerance (who cannot consume fructose without becoming hypoglycaemic) have fewer dental caries and are quite healthy as long as they avoid dietary fructose. [5, 6, 7]
There are three reasons presented by Robert Lustig as to why fructose is not healthy in the diet:
1. Fructose Metabolism in the Liver
Fructose is metabolized in the liver in a similar manner to alcohol, such that when consumed in excess it is converted directly into fat.  Both alcohol and fructose have the potential to generate free fatty acids in the liver, and drive inflammation and insulin resistance.  Ever heard of fatty liver disease as a result of excess alcohol? What if this could happen as a result of excess fructose? Case-control data has demonstrated that fructose consumption correlates with the development of fatty liver disease. [8, 9, 10] There is however one recent meta-analysis stating no connection between excess fructose and non-alcoholic fatty liver disease (although the authors concede the studies included are of poor quality).  The researchers state that the most likely cause of non-alcoholic fatty liver disease is the excess intake of calories (whether they come from fructose or carbohydrates), and so further studies are warranted.
Aside from all of this, the breakdown of fructose in the liver does lead to:
- elevated triglycerides
- increased LDL cholesterol
- promoted buildup of fat around organs (visceral fat)
- increased blood pressure
- tissue insulin-resistance, a precursor to diabetes
- increased production of free radicals (which can damage DNA and cells) – see point no.2
2. Aging and Oxidative Stress
Metabolism of various nutrients leads to the production of reactive oxygen species (ROS), which then need to be “neutralized” by our antioxidant systems. By comparison to consumption of glucose, excess fructose increases the production of ROS seven-fold! These excess ROS then can overwhelm our antioxidant systems in the liver and can result in liver damage. [12, 13, 14, 15, 16]
3. Effects on the Brain
We have, in our brains, a specific “reward” or “pleasure centre”. If these pleasure centers are triggered or stimulated by eating certain foods, our bodies will unconsciously increase food intake – driving weight gain! It has been shown that both sweet and high-fat foods lead to mobilization of opioids (feel-good neurotransmitters like endorphins) and dopamine, which establishes a pathway for cravings. [17, 18] Anecdotal evidence suggests sugar is also addictive based on withdrawal symptoms of “irritability”, “shakiness”, “nervousness” and “depression”. It has been pointed out however that sugar cravings may vary widely by age, time of day, and phase of menstrual cycle.  Overall whether the effects are as a result of pure “sugar addiction”, habituation or full-fledged dependence.
Fructose should not be considered just “empty calories” based on the evidence for negative effects presented in this article. Excess consumption can drive increased adiposity (“fatness”) and may impact liver function as well as the generation of excess ROS. Furthermore long-term fructose exposure has been associated with a paradigm of continuous food intake regardless of energy need, as well as symptoms of tolerance and withdrawal that are comparable to chronic alcohol abuse.
Lastly, here is the disease profile of chronic fructose consumption :
- Long-term fructose exposure
- Hypertension (high blood pressure)
- Myocardial infarction i.e. heart attack
- Dyslipidemia (abnormal lipid profile)
- Obesity (and insulin resistance)
- Malnutrition (poor vitamin and mineral status)
- Liver dysfunction
- Habituation (i.e. “addiction”)
Finally, perhaps it is time we place more emphasis on avoiding excess fructose in our diets.
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