There is an epidemic of pre-diabetes and diabetes in the United States. Fifty years ago, diabetes was a relatively uncommon disease. Today, the latest estimates are that 50% of Americans are now diabetic or pre-diabetic.
There are some obvious reasons to explain why this epidemic has developed: excess weight, inactivity, the proliferation of fructose in our diets. It is also my firm belief that the diets advocated by official agencies, like the USDA, the American Heart Association, the American Dietetic Association, and the American Diabetes Association, have also contributed with their advice to eat more "healthy whole grains."
I know that, when I was a kid, I ate Lucky Charms® or Cocoa Puffs® for breakfast, carried Hoho's® and Scooter Pies® in my lunchbox along with a peanut butter sandwich on white bread. We ate many TV dinners, biscuits, instant mashed potatoes for dinner. Back then, it was a matter of novelty, convenience, and, yes, taste. Many of the processed foods of the 1960s and 70s were indeed tasty.
Did such foods, consumed over many years, lead to diabetes? Did our eating habits as children and young adults contribute to the conditions that create diabetes many years later? Could sugary breakfast cereals, snacks, and candy that many of us ate in virtually unlimited quantities have impaired our pancreas' ability to produce insulin, leading to pre-diabetes and diabetes many years later?
There is a phenomenon called "glucose toxicity" that underlies the development of diabetes and pre-diabetes. Glucose toxicity refers to the damaging effect that high blood sugars (glucose) have on the delicate beta cells of the pancreas, the cells responsible for producing insulin. This damage is irreversible: once it occurs, it cannot be undone, and the beta cells stop producing insulin and die. The destructive effect of high glucose levels on pancreatic beta cells likely occurs through oxidative damage, with oxidative injury from toxic oxidative compounds like superoxide anion and peroxide. For unclear reasons, the pancreas is ill-equipped to resist oxidative injury, lacking little more than rudimentary anti-oxidative protection mechanisms.
Glucose toxicity that occurs over many years eventually leaves you with a pancreas that retains only 50% of its original insulin producing capacity. That's when diabetes enters the picture, the situation that develops when insulin production from the pancreas can no longer keep up with the demands put on it.
(Interesting but unanswered question: If oxidative injury leads to beta cell dysfunction and destruction, can antioxidants prevent such injury? Studies in cell preparations and animals suggest that anti-oxidative agents, such as astaxanthin and acetylcysteine, may block beta cell oxidative injury. However, no human studies have yet been performed. This may prove to be a really fascinating area for future.)
Now that 50% of American have diabetes or pre-diabetes, how much should we blame on eating habits when we were younger? I would wager that eating habits of youth play a large part in determining potential for diabetes or pre-diabetes as an adult.