Fructose consumption is associated with metabolic risk factors for cardiovascular disease.
Fructose consumption has increased in recent decades as soft drinks have been more widely marketed. In the United States soft drinks tend to be sweetened with high fructose corn syrup, but in Europe sugar is used. Between 1977 and 2004, United States fructose consumption increased 32 % across all age groups, and this increase mirrored increases in the use of high fructose corn syrup to sweeten beverages. Fructose consumption is detrimental because animal experiments and human studies show that high intakes can cause insulin resistance, which can over time cause metabolic syndrome. Fructose consumption has therefore been linked to increases in blood sugar disorders such as diabetes. Because soft drinks are the main reason that fructose consumption has increased, it stand to reason that the age group most likely to consume such beverages may be most affected by such changes. In this regard adolescents may be at increased risk of metabolic syndrome compared to previous generations not exposed to such quantities of fructose.
The fructose consumption of adolescents has been investigated and related to the presence of cardiometabolic risk factors. For example, one study1 assessed the fructose consumption of 559 adolescents between the ages of 14 and 18 years using 24 hour diet recall, and then measured their adiponectin, glucose, insulin and C-reactive protein levels in plasma. The results showed that fructose consumption was associated with the degree of visceral adipose tissue in the subjects, but not with subcutaneous adipose tissue. As fructose consumption increased there were trends for increased blood pressure, increased fasting glucose, increased C-reactive protein and increased insulin resistance (as measured by homeostatic model assessment insulin resistance : HOMA-IR). In addition, significant downward trends with increasing fructose consumption were measured for high density lipoprotein (HDL) and adiponectin. Adding visceral adipose tissue as a covariate attenuated all of these trends, suggesting that visceral adipose tissue was the causative factor.
This study confirms the results from intervention studies that show that fructose consumption is able to cause metabolic dysfunctions such as insulin resistance and this can lead to the rapid development of visceral adipose tissue. Collectively then, fructose consumption is a likely causative factor in the aetiology of metabolic syndrome, development of which is known to increase the risk of type 2 diabetes and cardiovascular disease significantly. The higher concentrations of C-reactive protein and lower concentrations of adiponectin seen with fructose consumption support the viewpoint that accumulation of abdominal adipose tissue is associated with systemic inflammation. This inflammation is likely caused by the influx of macrophages to abdominal tissue which is characteristic of metabolic syndrome. In this study, both free fructose and the fructose moiety of sugar were measured This is an improved method design from some studies that have measured only fructose in their analysis.
