Sucrose or sugar has two components – glucose and fructose. Glucose is present in virtually all naturally-occurring sweet foods and also exists as starch (although in a different chemical form, so it doesn’t taste sweet). Fructose occurs naturally in fruit, honey and some vegetables. But the main sources of fructose in the typical western diet are processed foods and beverages that contain added sugar derived from sugar cane or sugar beet.
In some countries, notably the United States, a sweetener known as high-fructose corn syrup (HFCS) is used to sweeten many processed foods, but HFCS is not a common source of fructose in the Australian diet.
Ingested fructose is treated differently to glucose following digestion and absorption into the body. While glucose is readily transported around the body to where it’s needed as an energy source, fructose is metabolised almost exclusively in the liver.
Many studies have shown that feeding animals (such as rats and mice) high-fructose diets leads to increased body weight, higher levels of blood lipids and blood pressure, and other components of metabolic syndrome (a condition that pre-disposes to several diseases, including heart disease and type 2 diabetes).
There’s also good evidence that fructose is addictive in rats, perhaps in a similar way to cocaine. As a result, there’s speculation that the fructose component of sugar may be one of the major driving forces behind the current epidemics of obesity and type 2 diabetes in humans.
The proponent of this concept with the highest profile is a US professor of paediatrics, Dr Robert Lustig, who argues that fructose is “alcohol without the ‘buzz’”, that is, it’s addictive in people, toxic and equally harmful as alcohol.
Lustig hypothesises that consumption of added fructose (that is, other than that occurring in fruit) at virtually any level promotes metabolic syndrome, leading to obesity, type 2 diabetes and increased risk of heart disease. As a result, he argues, fructose consumption is the cause of the obesity epidemic, and 35 million deaths occur annually worldwide because of it.
But how strong is the evidence for this “fructose hypothesis”, and how much credence should we give to the claim that fructose is the sole cause of most of our health problems?
Although it would be wonderful if there were a simple solution (such as avoiding all sources of added fructose) to the epidemics of obesity and type 2 diabetes that are sweeping the world, the evidence implicating fructose as the sole cause is weak, to say the least.
There’s overwhelming support for the belief that high intakes of fructose are harmful to human health, but the evidence is, at best, equivocal that low or even moderate intakes of fructose are harmful, in either normal weight people or in those who are overweight or obese.
One of the problems with the fructose hypothesis is that much of the evidence comes from animal studies, especially those involving rats. But people are not rats, and it’s not appropriate to assume that similar effects will be seen in humans. Animal studies can only allow working hypotheses to be proposed, hypotheses that must then be subjected to rigorous testing.
In relation to the likelihood of sucrose (and therefore fructose) addiction occurring in humans, for instance, a review published in 2009 concluded there was “no support from the human literature for the hypothesis that sucrose may be physically addictive”, despite strong evidence for addiction in rats and mice.
Another effect that’s been claimed for fructose is that it’s less satiating than glucose, that is, fructose doesn’t make you feel as full, so you overeat. But, as applies to most of the claimed adverse effects of fructose on human health, the evidence for this is, at best, equivocal.
One 2009 review found that fructose was less satiating (so its consumption was associated with overeating), while another published in the same year concluded that “the case for fructose being less satiating than glucose … is not compelling.”
The most recent (2012) scientific review that addressed this issue concluded that “Fructose does not seem to cause weight gain when it is substituted for other carbohydrates in diets providing similar calories. Free fructose at high doses that provided excess calories modestly increased body weight, an effect that may be due to the extra calories rather than the fructose.” In short, if you overeat, you can expect to put on weight!
But there is evidence that, when taken in liquid form (such as soft drinks or fruit juices), consumption of fructose is associated with higher energy intake, increased body weight, and the onset of metabolic syndrome.
So what are we to make of all this? At this relatively early stage in our attempts to elucidate the role fructose may play in the epidemics of obesity and type 2 diabetes, it’s probably safe to conclude that very high fructose intake can have serious and adverse metabolic effects in humans. But there’s no convincing evidence to support the claim that fructose is the sole cause of these epidemics, or that fructose intake at moderate doses is harmful.