Abstract: The article by Vos and associates[1] in this issue of The Medscape Journal of Medicine focuses our attention once again on the amount of fructose that is consumed by the American public. Fructose in our diet comes from 3 main sources: sucrose (common table sugar), high-fructose corn syrup (HFCS) made from corn starch, and fruit. In fruit, fructose serves as a signal for sweetness and good nutrition. For our ancestors, foods with a sweet taste were likely to be “healthy” and to have other important nutrients in them. This quantity of fructose was small in comparison to today's intake. In contrast to the role of fructose in fruits, fructose in other foods serves as a source of sweetness, often without much, if anything, in the way of other nutrients.
All evidence suggests that fructose ingestion has been rising steadily for a long time[2,3] (Table), but analyses have been hampered in part by the lack of good data. Vos and her colleagues make an important step in remedying this lack of data. They obtained information from one of the recent surveys of the eating habits of Americans, called the Health and Nutrition Examination Survey, conducted from 1988 to 1994. It is clear from the analysis that Americans are getting a lot of fructose in their diet. Mean daily consumption of fructose was 54.7 g/d, with a range of 38.4 to 72.8 g/d, and accounted for 10.2% of total daily caloric intake. Consumption was highest among adolescents (12- to 18-year-olds), who consumed 72.8 g/d, or more than 12% of their total calories from fructose. One fourth of this group consumed at least 15% of calories from fructose. The largest source of fructose was sugar-sweetened beverages (30%), followed by grains (22%) and fruit/fruit juice (19%).
Table
World Sugar Consumption in Millions of Tons
So what difference does it make if children and adolescents get these large amounts of fructose? First, when fructose comes from sugar or HFCS-sweetened beverages (50% of sugar is fructose and 55% of HFCS is fructose), they get no other nutrients. This contrasts with the case when fructose is obtained from fruit with its supply of natural nutrients. Thus, our children and adolescents are being short-changed on nutrients when they drink calorically sweetened soft drinks and fruit drinks that have almost no fruit in them. In addition, the more soft drinks youngsters consume, the less milk they consume,[4] which shortchanges them again on the calcium and vitamin D that are so essential for making strong bones. Third, a substantial body of data suggests that calories in calorically sweetened beverages are not perceived by the body in the same way as those in solid food.[4,5] Calories in soft drinks appear to be “add-on” calories to the other foods in the diet rather than suppressing intake of other foods by the amount of calories in the soft drinks.
The current epidemic of obesity could be explained by the consumption of an extra 20-ounce soft drink each day. In addition to the calories these beverages contain, they are a major source of the fructose. A growing number of studies suggest that fructose intake, particularly when accompanied by fat, may be unhealthy. Sugar's attribution as “pure, white and deadly,” by Professor Yudkin in 1986, may be partly right. It is the fructose part of the sucrose (table sugar) molecule and the fructose from HFCS that best fit the title of his book. HFCS is a visible marker for highly refined foods – the kind of food I want to avoid in my diet. The conclusions I have reached here will not make the caloric sweetener industry happy. As Yudkin said 25 years ago,[2] “I suppose it is natural for the vast and powerful sugar interests to seek to protect themselves, since in the wealthier countries sugar makes a greater contribution to our diets, measured in calories, than does meat or bread or any other single commodity.” One needs to evaluate these financial interests in terms of their public health implications. This will not be an easy task.
Fructose consumption, either from beverages or food, may have an additional detrimental effect. In a study from Switzerland, dietary fructose was found to predict an increased level of low-density lipoprotein cholesterol in children.[6] Fructose, unlike other sugars, increases serum uric acid levels. Nakagawa and colleagues [7] proposed that this happens when fructose is metabolized in the liver, its major organ for metabolism. Adenosine triphosphate (ATP) is used by the enzyme phosphofructokinase to phosphorylate fructose to fructose-1-phosphate. The adenosine-5′-diphosphate that is thus formed can be further broken down to adenosine-5′-monophosphate, then to inosine 5′-phosphate, and finally to uric acid. Thus, the metabolism of fructose in the liver leads to the production of uric acid. These authors proposed that the high levels of uric acid could set the stage for advancing cardiovascular disease by reducing the availability of nitric oxide, which is crucial for maintaining normal blood pressure and for maintaining normal function of blood vessel walls (endothelium).[7] If this hypothesis is borne out, it will provide another reason that nature preferred glucose over fructose as a substrate for metabolism during the evolutionary process.
Soft drink consumption has been linked to development of cardiometabolic risk factors and the metabolic syndrome in participants in the Framingham Study.[8] Individuals consuming at least 1 soft drink/d had a higher prevalence of the metabolic syndrome (odds ratio, 1.48; 95% CI, 1.30–1.69) and an increased risk for the metabolic syndrome over 4 years of follow-up. The most recent relationship shows that fructose intake is directly related to risk for gout in men.[9]
It is amazing to me that many of our public schools have resorted to financial contracts with beverage companies to make calorie-containing soft drinks that have little nutritional value available on school premises. How we can put the children who are susceptible to obesity at risk by this strategy has perplexed me for years. Maybe it is time for the public to worry about what fructose may be doing to their children and themselves.
Publication Year: 2008
Publication Date: 2008-07-09
Language: en
Type: article
Indexed In: ['pubmed']
Access and Citation
Cited By Count: 9
AI Researcher Chatbot
Get quick answers to your questions about the article from our AI researcher chatbot