High fructose corn syrup (HFCS) is hard to avoid if you eat processed foods — it’s used to sweeten soft drinks, candy bars, bread, salad dressings, fruit drinks and thousands of other items. But it’s worth the effort to read labels and avoid the stuff. The reason? Research has mounted over the past couple of years that HFCS may be just plain dangerous to health.
For example, researchers from Loyola University Health System have found women who drink at least two cans of HFCS-sweetened soda pop daily are twice as likely to show signs of kidney disease as those who don’t drink that many sodas (http://www.naturalnews.com/025582_s…). And although HFCS has been linked previously to the widespread rise in obesity, a new study has produced evidence showing exactly why fructose could be making people fatter than ever, starting in childhood.
It turns out that when the sugary stuff is present as children’s fat cells mature, fructose turns more of these cells into belly fat. Defined by a large waistline often dubbed a “spare tire”, abdominal obesity ups the risk of both heart disease and type 2 diabetes. What’s more, cells in both belly fat (visceral fat) and subcutaneous fat located below the skin were found to be less able to respond to insulin if they had been exposed to fructose. That means fructose could up the risk for metabolic syndrome, a precursor of type 2 diabetes, while spurring weight gain.
This research was just presented by lead author Georgina Coade, a PhD student at the University of Bristol in the United Kingdom, at the Endocrine Society’s 92nd Annual Meeting held in San Diego. “Our results suggest that high levels of fructose, which may result from eating a diet high in fructose, throughout childhood may lead to an increase in visceral (abdominal) obesity, which is associated with increased cardiometabolic risk,” Coade said in a statement to the media.
Coade and her research team studied biopsy specimens of both subcutaneous and visceral fat from 32 healthy-weight children who had not gone through puberty yet. Then they took preadipocytes (precursors to fat cells that have the potential to differentiate, or mature, into fat-containing cells called adipocytes) from the specimens and allowed these precursor cells to mature for 14 days in culture media containing normal glucose (the main sugar found in the bloodstream), high glucose or high fructose.
Next the investigators measured the activity of an enzyme dubbed GPDH and the abundance of the adipocyte fatty acid binding protein — both of which are found only in mature fat cells. The results showed that fructose caused fat cells to form more mature, visceral fat cells. In addition, the cells that matured in the fructose solution all showed a decrease in insulin sensitivity (the ability to successfully take up glucose from the bloodstream into fat and muscles) — and decreased insulin sensitivity is a characteristic of type 2 diabetes.
“Fructose alters the behavior of human fat cells if it is present as the fat cells mature,” Coade concluded. “We can maybe compare this (timing) to periods in children when they are making their fat.”