Today is the first day of the latest installment of the No Sugar Challenge, hosted my Skinny Ms. and the Gracious Pantry. Once again, I’ll be joining in, aiming to kick the old sugar habit that snuck up on me over the holidays. (Sound familiar? You should join in and be sure to follow along on Facebook for motivation and accountability).
Today’s blog post is timely and relevant and important to all of us seeking to understand the relationships between sugar intake, obesity and metabolic syndrome (diabetes, high blood pressure, heart disease to name just a few of the representative afflictions).
Sugar, in general, and high fructose corn syrup, in particular has recently come under fire in the media. While I’ve been working hard to get through and understand the latest scientific research, the cross-disciplinary nature of the work (as well as all the jargon!) has made my head spin. My hubby, good egg that he is, offered to summarize the research for me and even went as far as to write this post! Enjoy (and thanks, sweetie)!
(The following article was written by Bernard Crespi, Professor of Evolutionary Biology, Simon Fraser University, Burnaby, British Columbia, Canada. For more information about his research program, please visit his university website.)
Everyone loves a good mystery – unless we are the victim.
Our modern world harbors billions of victims, of obesity, adult-onset diabetes, high blood pressure, and resulting heart disease. The crime? Slow, early death.
Who, then, is the criminal? There is a host of usual suspects – most of them either personal (sloth, gluttony) or corporate (greed, envy, pride). But few solid clues.
Let us zero in, and deduce.
The ‘epidemic’ of obesity and metabolic disease is now about thirty or forty years old, and has been getting worse. Over that time, the USDA – who keeps general track of what Americans eat – reports that total calorie intake has very slowly increased, as have the proportions of food from fats, flour and sugar. But whether these increases in calorie count and composition can solve our mystery is unclear – bodies are normally reasonably good at keeping body weight within a narrow zone, and links of food intake alone with metabolic diseases remain weak. So the evidence for this obvious culprit remains circumstantial.
We need another clue.
What else has changed in the past 30-40 years? Until the 1970s, most all of our sugar intake came from sucrose – table sugar – which is made up of one glucose molecule stuck onto a molecule of fructose. Then clever chemists found a way to convert corn starches into a new compound – high-fructose corn syrup, comprised of 55% fructose, 42% glucose, and 3% other forms of sugar. Since then, high-fructose corn syrup has been steadily replacing sucrose in our diets, and creeping into myriad formerly-unsweetened foods, such as salad dressing, low-fat yogurt and barbeque sauce.
Sounds innocent, you say? One sugar (50% fructose and 50% glucose) just being superseded by another slightly-different one (55% fructose and 42% glucose)?
But a sugar by another name does not metabolize so sweet.
Glucose is the body and brain’s usual main fuel, for everyday activities like moving and thinking. It is trafficked into all our cells by insulin, using an elegant physiological system with built-in feedbacks to keep levels of blood and brain glucose just about right. This glucose-insulin system dovetails with our system for ‘feeling full’ – satiation – nicely avoiding the twin perils of slow starvation and runaway caloric excess.
Fructose does none of these things. It does not stimulate the insulin system to take sugars out of the blood. It does not serve as fuel for the brain, or the pancreas. It is preferentially converted by the liver into fats. It raises your blood pressure. Eating it does not make you feel full, as other foods do – instead, it may make you want to eat more. How can a simple sugar be so bad? By itself, in small amounts relative to other foods, and balanced with glucose, it is not. But up the amount and proportion, and your metabolism enters an altered state. Guilty, guilty, guilty? Not quite yet.
Our final clue comes from experiments in the lab, where rodents and monkeys fed diets relatively high in fructose develop obesity, diabetes, and high blood pressure – just the suite of inter-related ills that have been increasing in humans since high-fructose corn syrup came along. Is the increase in amount and percent fructose in our diet over the past 30-40 years master-minding the obesity and disease epidemic? Shadows of doubt will remain, until new studies provide additional clues. Until this mystery is solved, no one’s metabolism is safe.
Do you try to watch your sugar intake?
How many products do you have in your pantry that contain HFCS?