1. Nuttall, Frank Q. PhD, MD

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Complements to the authors for an excellent review of what high fructose corn syrups (HFCSs) are, how and why they currently are being used by the food industry in the United States, the metabolic response to their ingestion, and the putative untoward health issues of HFCSs raised by some reports in the literature.


I am particularly impressed with the straightforward scientific nature of this report.


The concept that HFCSs are particularly high in fructose content is widely assumed by the general population, and even by scientific writers who should know better. The authors clearly point out that the composition is similar to sucrose (table sugar). HFCSs are widely used because they are cheaper than refined sucrose.


The use of sucrose and its surrogate HFCS-40 and HFCS-55 in the diet often has been and continues to be presented in an emotionally laden fashion which often extends beyond our current knowledge base. Most likely, this is due to the hedonic attributes of these food items, just as with sucrose. In the past, sucrose was implicated in the development of coronary heart disease and dental caries and to represent "empty calories." The latter is a pejorative term implying that dietary sucrose crowds out more "nutritious" food items in the diet. None of these concerns have proven to be major public health issues.


Continuing this assault has been efforts by authors to implicate the use of HFCS in the so-called obesity epidemic, even though an increase in obesity is occurring in many industrialized and industrializing countries where HFCS are not used in significant amounts. Indeed, the rate of development of obesity in Australia apparently is similar to that in the United States, even though use of HFCS is insignificant. In addition, as pointed out in this review, a cause and effect relationship between HFCS consumption and obesity has not been demonstrated. Data to date indicate only an association between the two. Indeed, one could speculate that a cause and effect relationship, if present, is the opposite of that proposed. For example, obese children and young adults are likely to ingest an amount of food energy which extinguishes their drive to seek energy-yielding foods (hunger), just as occurs in their nonobese cohorts. Because they are severely criticized by their peers and other members of society for being obese, and thus, for eating too much, they can covertly ingest their required calories by drinking HFCS-containing beverages. By so doing, they could eat less at times of shared meals, and thus, escape criticism. It seems that carrying around a bottle of water or a beverage has become not only acceptable, but a national obsession.


In addition, if HFCS in beverages is implicated in the genesis of obesity, then, following this logic, fruits and fruit juices should be implicated as well. The content and concentration of sugars in fruit juices generally is very similar to that of HFCS in beverages. Of considerable interest a recent study from the University of Texas Health Service Center in San Antonio found that teen-agers who drank diet soda everyday were more likely to gain weight than those who drank regular soda (quote in Diabetics Forecast, page 46, Nov 2005).


As pointed out in the review, the concept that a major increase in fructose ingestion has occurred in recent years also is not supported by available data.


The metabolic consequences of the use of fructose is the culprit in the "obesity epidemic" because it does not stimulate insulin secretion, and thus, leptin levels also lacks scientific proof,1 as does the concept that fructose metabolism is not regulated.2 Fructose metabolism, as with all energy-yielding substrates, is highly regulated. It also has not been shown that low-carbohydrate, high-fat diets, with or without fructose, that is, diets expected to be associated with a low integrated insulin concentration and leptin concentration, result in extraordinary weight gain in a free living environment.3-5 Body weight and body fat mass, in particular, are highly regulated in humans, regardless of diet composition.


The role of obesity as currently defined (BMI of 30 or greater) in the development of diabetes needs to be better defined. Not all obese people develop type 2 diabetes and many who develop diabetes are not obese. Type 2 diabetes is largely genetically determined. Its expression is dependent on both aging and truncal obesity and not merely on an increased BMI per se.


Also contrary to popular belief, sucrose (and presumably HFCS-40 or HFCS-55) raises the blood glucose less than do refined cereal starches.6,7 It is the glucose content of foods that is largely responsible for the postprandial rise in blood glucose.


In summary, as indicated in the present review, much more and better data are required in humans before accepting the concept that HFCS (or sucrose), in the range currently being ingested in the US population (up to 25% of food energy), poses a risk to health. Certainly, the information currently available is an insufficient basis for beginning a national campaign to remove HFCSs from foods or for implementation of a national policy to limit the use of HFCSs. Parenthetically, this issue may become moot if Congress removes the barriers to importation of sucrose (table sugar) in the United States. In the world markets, sucrose is considerably cheaper than HFCSs.




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