You can’t watch the news today without hearing about the “obesity epidemic”.

In fact, recent research has shown that obesity is a bigger health threat than smoking.

But wait, it gets worse.

Now, we learn that our lifestyle has lead to an unprecedented increase in the rates of  Type 1 Diabetes.

According to medical journalist Dan Hurley, “the incidence of type 1 diabetes is now twice as high among children as it was in the 1980s, and 10 to 20 times more common than 100 years ago.”

While rising levels of type 2 diabetes are well known (and typically linked to increasing obesity), the corresponding rise in type 1, or “juvenile,” diabetes has rarely if ever been described in the news media, despite a substantial body of scientific evidence.

While widely accepted by leading diabetes researchers, the increase in type 1 has as yet received scant attention from leading diabetes advocacy organizations.

Scant attention???

I had no idea that the rates of Type 1 Diabetes had increased one iota.

Did you?

Hurley thinks that “the media has given so little coverage to the rise of type 1 because it simply doesn’t fit with the conventional wisdom that it’s supposed to be a super-rare disease caused by a genetic predisposition. Obviously, genes haven’t changed, so something in our environment or lifestyle has.”

Hmmmm, ye olde genetics vs epigentics debate.

And, once again, it looks like lifestyle is kicking some genetic butt.

But, what is it about our lifestyle that has caused this spike in Type 1 Diabetes?

In his new book, Diabetes Rising, Hurley examines five leading scientific hypotheses that offer an explanation:

• The “accelerator hypothesis,” which asserts that the rising weight and height of children over the past century has “accelerated” their tendency to develop type 1 by putting the insulin-producing beta cells in their pancreases under stress.
• The “sunshine hypothesis,” which holds that the increased time spent indoors is reducing children’s exposure to sunlight, which in turn reduces their level of vitamin D (the “sunshine vitamin”). Reduced levels of vitamin D, and reduced exposure to sunshine, have each been linked to an increased risk of type 1 diabetes.
• The “hygiene hypothesis,” which holds that lack of exposure to once-prevalent pathogens results in autoimmune hypersensitivity, leading to destruction of the body’s insulin-producing beta cells by rogue white blood cells.
• The “cow’s milk hypothesis,” which holds that exposure to cow’s milk in infant formula during the first six months of life wreaks havoc on the immune system and increases the risk to later develop type 1.
• The “POP hypothesis,” which holds that exposure to persistent organic pollutants increases the risk of both types of diabetes. “

The book cites recent studies which show that back in 1890, the reported annual death rate from diabetes for children under the age of 15 was 1.3 per 100,000 children in the United States. “Because any death due to diabetes in those days had to be caused by what we now call type 1, researchers consider the 1.3 per 100,000 figure to be a rough estimate of the yearly incidence of new cases at that time,” Hurley writes. “In Denmark, the rate was fairly similar, about 2 per 100,000 at the beginning of the 20th century. From that baseline, things took off.

By the mid-1980s, the yearly incidence of new cases of type 1 had jumped to 14.8 per 100,000 children in Colorado.

By the opening years of the 21st century, the incidence rate in six geographic areas of the United States, as measured in a new study run by the CDC, had climbed to 23.6 per 100,000 among non-Hispanic white children.

The rates were 68 percent higher than those reported in Colorado in the 1980s, and more than twice as high as reported in Philadelphia in the 1990s.”

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Well, that doesn’t sound very good.

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