We’ve gotten sadly accustomed by now to warnings about obesity and its effect on health: joint damage, heart disease, stroke, diabetes and its complications such as blindness and amputation. We almost take for granted that as obesity increases worldwide, diabetes will also, and it is. That is, type 2 diabetes — the kind that is linked to obesity and used to be called adult-onset diabetes — is rising as obesity does.
But here’s a puzzle: Type 1 diabetes — the autoimmune disease that begins in childhood and used to be called juvenile-onset diabetes — is rising too, around the globe, at 3 percent to 5 percent per year. And at this point, no one can quite say why.
I have a column in the February Scientific American, on newsstands now and live on the web, exploring this conundrum. There is a raft of researchers exploring the issue, but so far there is only one thing they can say for sure: The increase, which began in the 1950s and accelerated in about the 1980s, is happening too fast to be due solely to genetic change. Something in the environment is driving the increase. But what?
The challenge for explaining the rising trend in type 1 diabetes is that if the increases are occurring worldwide, the causes must also be. So investigators have had to look for influences that stretch globally and consider the possibility that different factors may be more important in some regions than in others.
The list of possible culprits is long. Researchers have, for example, suggested that gluten, the protein in wheat, may play a role because type 1 patients seem to be at higher risk for celiac disease and the amount of gluten most people consume (in highly processed foods) has grown over the decades. Scientists have also inquired into how soon infants are fed root vegetables. Stored tubers can be contaminated with microscopic fungi that seem to promote the development of diabetes in mice.
None of those lines of research, though, have returned results that are solid enough to motivate other scientists to stake their careers on studying them. So far, in fact, the search for a culprit resembles the next-to-last scene in an Agatha Christie mystery — the one in which the detective explains which of the many suspects could not possibly have committed the crime.
One of the best-elaborated hypotheses suggests that lack of exposure to infections in childhood keeps the various components of the immune system from learning how to hold themselves in balance. If this sounds familiar, it’s because it’s a version of the “hygiene hypothesis” (past posts here, here and here), which says that a too-clean childhood can lead to allergies later in life.
The diabetes version of this hypothesis explores whether conditions that are a proxy for exposure to infections — not having older siblings in the house, not attending day care, being born by Caesarean — can have an effect on the occurrence of diabetes. No clear culprit has been found yet.
Some researchers say it is possible that obesity may play a role. In type 2 diabetes, tissues in the body that receive the hormone insulin, which regulates blood sugar, become insensitive to it. In type 1, the body destroys the insulin-producing cells. But an “overload” hypothesis is now suggesting that if a child is obese to begin with, that could prime the insulin-producing cells for failure, with the autoimmune attack pushing them over the edge.
If obesity is an explanation, it’s not a comforting one. As the CDC’s National Center for Health Statistics noted today, a whopping percentage of United States adults — 36 percent — are obese. And the trend is not reversing. By 2048, according to Johns Hopkins researchers whose work is discussed in my story, every adult in America will be at least overweight if the current trend continues.
That’s a lot of potential diabetes cases: a lot of glucose monitors, syringe jabs and inevitable blood sugar swings, if you care for it well, and a lot of kidney disease, heart disease, amputations and blindness if you don’t. (Not to mention effects like this image of insulin lipohypertrophy published in the New England Journal of Medicine this week, from years of administering insulin injections.) Let’s hope we find, if not a cure, at least a cause for rising type 1, before the trend gets out of control.
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