Regardless of the undertaking, I admire thoroughness and excellence.
The Corn Refiners Association has demonstrated both. That's why it has my admiration as well as my postal and e-mail addresses.
And that's why I'm expecting a letter from them. No later than Monday.
On Saturday, May 23, 2009, I wrote a column that expressed no surprise that 20 percent of U.S. 4-year-olds were now obese. One reason why is because too many kids ingest too much sugar a higher and higher percentage of which comes in the form of high-fructose corn syrup (HFCS), what I called "the worst form [of sugar] possible."
By Sunday, I received an e-mail. By Monday, I received a large envelope that included a letter from the president of the CRA stating that "the suggestion that high-fructose corn syrup is a unique contributor to obesity and is metabolized differently than other caloric sweeteners is misleading."
Also included in that large envelope, 20 pages of information attesting to that fact.
In it, Consumer Science in the Public Interest calls blaming HFCS for the obesity epidemic "an urban myth" and writes that "there isn't a shred of evidence that HFCS is any more harmful (or healthier) than sugar." James M. Rippe, M.D., a cardiologist and biomedical professor at the University of Central Florida, echoes that sentiment in a New York Times article, saying, "There is no difference in how the human body handles HFCS and sugar. The two sweeteners are equivalent metabolically."
Additionally, all of the research included in the CRA super packet was legitimate.
In short, the excellent and thorough defense of HFCS made me write in a subsequent column that I regretted calling it the "worst" sugar because there were such conflicting studies. I ended that column by echoing the American Medical Association's call for "further independent research."
Well, the independent research recently performed by researchers at the University of Southern California and the University of Oxford in England suggests that maybe I did not need to write a retraction three years ago. They found what Medical News Today calls "the global epidemic of type 2 diabetes" to be directly linked to the use of HFCS.
Furthermore, the research revealed the link between the two to be independent of total sugar ingestion and level of obesity, a discovery that suggests HFCS to be not a contributor but a cause. It also uncovered that countries with a higher use of HFCS had a 20 percent higher rate of type 2 diabetes, leading Professor Stanley Ulijaszek, director of the Institute of Social and Cultural Anthropology at Oxford to say, "Our metabolism has not evolved sufficiently to be able to process the fructose from the high fructose corn syrup in quantities that some people are consuming it."
Many of those people, it appears, live in the U.S. We have the highest per capita consumption rate of HFCS at 55 pounds per year.
Not surprisingly, the U.S. has undergone what the Centers for Disease Control and Prevention (CDC) calls a "dramatic" rise in diagnosed diabetes cases in the last 15 years. In 1995, for instance, there were only three states where the diagnosed diabetes rate exceeded 6 percent.
Fifteen years later, all 50 states exceeded that rate, with six states topping 10 percent. Furthermore, in those 15 years, six states recorded individual increases between 135 and 226 percent.
To what degree is HFCS responsible for this increase? According to Ulijaszek, "There is evidence that the body struggles to metabolize large amounts of fructose that does not come from fruit, [which] creates a risk for type 2 diabetes, a risk that could occur because "fructose and sucrose are not metabolically equivalent."
Ulijaszek's final comment, curiously enough, directly contradicts Rippe's, the doctor prominently quoted in CRA literature.
So who's right? Who knows?
What I do know is that fructose is processed in the body differently than other sugars. Glucose, for instance, can go immediately into the bloodstream without the need for digestion, which is why certain sugars have the reputation for providing quick energy.
But fructose is shuttled to the liver where two things can happen: it can be used to replenish liver glycogen, what the brain prefers for fuel and the body uses to keep blood sugar levels steady, or it can be converted to fat. Unfortunately, the liver can only store a small amount of glycogen.
Since the brain does not require anywhere near the amount of energy as the muscles, the muscles do not have the ability to use fructose for energy, and the consumption of fructose is increasing primarily through the increased use of HFCS it doesn't seem to be a stretch to cite the increased use of HFCS as a culprit in the obesity epidemic.
But now I know something else: that the USC/Oxford research linked the use of HFCS to type 2 diabetes independent of obesity.
While this is only one study, and such results would need to be replicated to really give them validity, this study suggests that phrase I retracted three and a half years ago was on target.