Fructose: the sweet truth

Very few nutrients have received as much attention as fructose. Especially since Robert Lustig drew parallels^[1] between the consumption of fructose and alcohol in 2010, there has been a barrage of recommendations from both mainstream and integrative health professionals claiming that excessive fructose intake has serious health consequences. More specifically, fructose has been blamed for many of the chronic diseases faced by the developing world today, such as obesity, type-2 diabetes, cardiovascular disease, and non-alcoholic fatty liver disease (NAFLD), in what has been termed “the fructose hypothesis^[2].”

There is a tremendous amount of research showing detrimental effects of fructose consumption on numerous cardiometabolic health parameters. However, the majority of this research suffers from some combination of three critical limitations:

1. The fructose was provided in isolation

2. The dose provided was unrealistically high, and

3. The study was conducted on animals.

As an example, the average and 95th percentile levels of fructose intake are 9.1% and 14.6% of total energy intake, respectively, in the U.S. population. However, as Figure 1 illustrates, very little research is actually conducted at these intake levels.

In fact, most experimental doses exceed even the 95th percentile for human fructose intake. Few Americans consume the levels of fructose being tested, and fewer still consume these levels in the absence of glucose. Extreme dosing protocols drastically alter glucose-to-fructose (G:F) ratios and may promote a somewhat distorted view of fructose metabolism, especially if each of these trial results are extrapolated into public health impacts, rather than being seen as part of mechanistic and exploratory studies.

Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3649105/figure/fig7/

More recently, there has been a growing interest in the potential effects of fructose consumption on the brain. Several recent rat studies report that the consumption of fructose may contribute to cognitive impairment by reducing the formation of brain cells^[3] and increasing neuroinflammation^[4]. However, just as with trials evaluating metabolic outcomes, the fructose dose is an important limitation when drawing conclusions. Additionally, many trials evaluating fructose are short, lasting only a couple of weeks. The study under review was an attempt to examine the long-term impact of fructose consumption in relation to glucose consumption on body composition and cognitive performance in mice, at doses that represent the top fructose consumers in the U.S. population (18% calories).

The majority of research on fructose uses doses that are well above what could reasonably be expected to be consumed by an individual living in the United States. This study examined the impact of fructose on body composition and cognitive performance in mice at more reasonable (but still high, 18% of total calories) doses.