New research shows a startling prevalence of the disease among children younger than 5.
Cities has written before about the growing body of evidence connecting the shape of communities with the health of people who live there, particularly when it comes to explaining the rising epidemic of diabetes. Neighborhoods that enable more active lifestyles – i.e., walkable ones – have in some cases been linked to lower rates of the disease. But in that context we are typically talking about Type 2 diabetes, the kind that often results from lifestyle factors like poor diet and lack of exercise.
A new study out of Philadelphia further complicates this picture for urban public health officials. Researchers there have recorded a startling increase in Type 1 diabetes among children younger than 5. And in these cases, the built environment doesn’t readily appear to explain much at all. In the span of 20 years, from 1985 to 2004, the researchers found that the incidence of Type 1 diabetes had increased by 70 percent in these youngest children.
“I do not believe that this is a Philadelphia phenomenon,” says Terri Lipman, the lead investigator on the study, just published in the journal Diabetes Care, and a professor at the University of Pennsylvania School of Nursing. Philadelphia, however, happens to have one of our best data sources on the topic, an ongoing registry of local children with diabetes, derived from school and hospital records, that has been continuously maintained since 1985. Less comprehensive data sets in other cities and abroad have shown similar patterns. “If there were more registries and more ways to capture this,” Lipman says, “I believe we’d see this throughout the U.S. and certainly in major cities.”
So what’s behind this dramatic increase? This is a much trickier question to answer. Scientists don’t know what causes Type 1 diabetes in the first place, making it all the harder to explain changes in its prevalence. And it’s particularly perplexing that this is happening with such young children. Children typically aren’t at risk for developing autoimmune diseases (diabetes is classified as one because, with it, the body attacks cells – in this case those that produce insulin – as if they were foreign).
“We’ve always seen Type 1 before puberty, but we rarely saw it in children 0-5,” Lipman says. “Here, not only are we seeing it in children 0-5, but we’re seeing a sharp rise.”
And that rise hasn’t occurred steadily over the two-decade window of this registry, but in just the latest 5-year cohort of children diagnosed between 2000-2004. Lipman offered three theories for what may be going on. One, called the “accelerator hypothesis,” suggests that the body attacks insulin-producing cells at a much earlier age in children when they’re obese (although there was no indication in this data that these particular children were more obese than earlier cohorts).
The “hygiene hypothesis” suggests that children exposed to fewer environmental viruses and bacteria these days – thanks to our love of antibacterial handwash, for instance – may be less prepared to fight certain disorders. A third hypothesis says that the process of autoimmunity may be speeding up such that a disease that once took 10 years to develop may now do so in three.
“None of that has been proven,” Lipman says. “There are a number of hypotheses, and they’re all interesting. But there are no answers to why we’re seeing this large increase.”
We do know, though, that the public health infrastructure in Philadelphia and other cities will need to be prepared to care for all of these children, even if we can’t halt the disease. And we know that disparities exist particularly in the treatment and outcomes of black children with diabetes. For a long time, that demographic was by far the least likely to develop the disease. And now – as one other mystery in this story – that’s no longer the case.