This isn’t your usual story about the evils of high-fructose corn syrup (HFCS).
Many observers have blamed America’s epidemic of diabetes and obesity on the rise in use of HFCS as a sweetener.
This sweetener-shift was driven by the rising cost of cane sugar (pure sucrose) to American manufacturers in recent decades, and the falling cost of heavily subsidized corn and corn byproducts like HFCS.
But there have always been under-reported problems with the HFCS hypothesis of obesity and diabetes.
|
Key Points
-
Persuasive hypothesis assigns major blame to fructose for rising obesity and diabetes rates.
-
Problem seen as stemming from excess intake of either corn syrup or cane sugar.
-
Corn syrup and cane sugar share equal amounts of fructose, and may share equal blame for obesity and diabetes. |
For one thing, we’re seeing the same sorts of increases in diabetes and obesity in countries where the price of cane sugar is not artificially high, and manufacturers of sweets and sodas never switched from cane sugar to HFCS.
If HFCS is the villain, then people overseas who eat sucrose-sweetened candy and soda shouldn’t be getting fat and diabetic as fast as Americans are.
Two years ago, a University of Florida team proposed an intriguing hypothesis to explain why fructose is the most unhealthful form of sugar.
And there is just as much fructose in cane sugar as in HFCS, so this would explain why people who eat too much sugar in either form – HFCS or cane sugar (sucrose) – would become more prone to obesity and diabetes at about the same rate.
Both HFCS and cane sugar are one-half glucose and one-half fructose.
- Cane sugar is pure sucrose: a compound consisting of one molecule each of glucose and fructose.
- Most HFCS is 45-55 percent fructose, with the remainder being glucose.
One difference is that sucrose occurs naturally in cane syrup and most fruits, while the various forms of HFCS are synthetic combinations of fructose and glucose, none of which occur in nature.
Some argue that there is something about the structure of HFCS that makes its fructose worse than the fructose in sucrose, but so far, that hypothesis lacks evidence.
The Florida team proposes that sweets and sodas of all kinds are unhealthful because they contain high levels of either HFCS or cane sugar, hence equally large amounts of fructose.
Here’s the scoop on the evidence they presented, which should make us all leery of enjoying sweets or sweetened foods and drinks in more than very small amounts.
Florida team presents strong circumstantial case against fructose
Our story starts in 2006, with publication of an article by the University of Florida researchers.
The Florida group noted that the rise in rates of obesity and metabolic syndrome over the past two decades coincided with a marked increase in American’s fructose intake (Johnson RJ et al. 2007).
While suggestive, this correlation cannot prove cause and effect. But then a group led by kidney specialist Richard Johnson, M.D., built a persuasive case consisting of three logical steps (Heinig M, Johnson RJ 2006):
- Unlike other sugars, fructose causes blood levels of uric acid to rise rapidly.
- Uric acid in the blood reduces levels of nitric oxide (NO), especially in the endothelial lining of our arteries … so-called “endothelial NO”.
- NO enhances the efficiency of insulin, increases blood flow to muscle, and enhances glucose uptake.
- Animals that lack endothelial NO develop insulin resistance and other features of metabolic syndrome: a cluster of symptoms linked to increased risk of diabetes and cardiovascular disease.
So, the Floridians proposed that the current epidemic of metabolic syndrome is due in part to fructose-induced rises in people’s blood levels of uric acid, which reduce endothelial NO levels and induce insulin resistance.
Their hypothesis is supported by the fact that, as they wrote, “… changes in average uric acid levels correlate with the increasing prevalence of metabolic syndrome in the US and developing countries.”
Researchers propose ranking foods on a “fructose index”
We’d not heard of the Florida team’s persuasive prosecution of fructose until we caught wind of their recent proposal to replace the popular glycemic index with a “fructose index”.
As you probably know, the glycemic index is used by diabetics to rank foods by the amount by which they raise blood sugar levels. (The words glycemic and glucose both come from the Greek word glukus, meaning “sweet”.)
The glycemic index (GI) is a scale used to rank carbohydrates based on their ability to raise blood glucose levels.
And the GI index has been popularized in bestsellers as a way for selecting foods to reduce the risk for obesity, diabetes, and cardiovascular disease, all of which are linked to chronic high blood sugar and its evil result: the near-diabetic metabolic disorder known as “insulin resistance”, which is an increasing failure of our cells to react to the signals sent by insulin.
Diabetes is always preceded by insulin resistance, which is the failure of our cells to be sensitive to insulin, and therefore fail to absorb glucose from the blood as they should, thus worsening blood sugar control.
The Florida team noted that the GI scale is better at identifying foods that stimulate release of insulin (by spiking blood glucose levels) than it is at pinpointing foods that stimulate insulin resistance (Segal MS et al. 2007).
And interestingly, low-glycemic diets have not proven particularly good at promoting weight loss, which suggests that they may not be as helpful at preventing diabetes as has been generally presumed.
The Floridians noted that the correlations observed between high GI diets on one hand and diabetes and cardiovascular disease on the other are related to high consumption of cane sugar or HFCS, because while both are one-half fructose, both also have high GI rankings due to their high glucose content.
Dr. Johnson’s research suggests that, compared with glucose content, the fructose contained in sugary foods is much more responsible for promoting diabetes and heart disease. (To be sure, excessive glucose consumption is not good, either.)
Last fall, their hypothesis led them to propose the use of a fructose index to categorize foods and to propose studies to determine the effectiveness of low fructose diets for reducing the risk of obesity, diabetes, and cardiovascular disease.
These matters are complex, and time will tell, but the folks in Florida make a pretty good case.
Sources
- Segal MS, Gollub E, Johnson RJ. Is the fructose index more relevant with regards to cardiovascular disease than the glycemic index? Eur J Nutr. 2007 Oct;46(7):406-17. Epub 2007 Sep 1.
- Johnson RJ, Segal MS, Sautin Y, Nakagawa T, Feig DI, Kang DH, Gersch MS, Benner S, Sánchez-Lozada LG. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr. 2007 Oct;86(4):899-906. Review.
- Heinig M, Johnson RJ. Role of uric acid in hypertension, renal disease, and metabolic syndrome. Cleve Clin J Med. 2006 Dec;73(12):1059-64. Review.
