I Am Now a Bionic Woman

written by Sarah Howard
Coordinator of the Diabetes-Obesity Spectrum Working Group

Just in time for World Diabetes Day (#WDD, November 14th), I have started wearing an artificial pancreas to help manage my type 1 diabetes. Normally I wear an insulin pump along with a continuous glucose monitor (cgm), but the two gadgets do not actually talk to each other. That means I still have to manage my diabetes manually 24/7, like everyone else with diabetes. While manufactured artificial pancreases are being developed and are now performing well in clinical trials, they are not yet available to the public.

Your Health the Week of June 15th

written by Nancy Hepp, MS Research and Communications Specialist

Green Space and Cognitive Development

An article in Pacific Standard this week reported on a study finding that green space at school, at home and on the commute is associated with greater working memory and attentiveness in school-age children. This finding is similar to one from last October showing that the amount of greenery around a school relates to higher math and English test scores. In both studies, detailed maps were used to assess green space—neither study looked at whether children actually get outdoors into the greenery.

An Environmental Perspective of the American Diabetes Association’s 75th Scientific Sessions

written by Sarah Howard
Coordinator of the Diabetes-Obesity Spectrum Working Group

Over 18,000 people from around the globe gathered in Boston June 5-9, 2015, for the American Diabetes Association’s premier annual scientific conference. Thanks to CHE, I was able to attend, and here summarize information I found on the development of diabetes—including environmental factors (especially chemicals), developmental origins, and the natural history of the disease.

Environmental chemicals

While there were not any sessions on environmental chemicals per se, I did find ten posters on this topic (see below for links to abstracts and online e-posters). The one that struck me most was by Su Hyun Park, who found an association between levels of persistent organic pollutants (POPs) and beta cell dysfunction in 7-9 year old Korean children. Exposure to POPs, as well as to other chemicals, have been associated with beta cell dysfunction in other studies before, but there are few studies in humans, even fewer in children, and few at exposure levels found in the general population. (I told her I thought that hers was the most important poster of all 2373 of them and she laughed, but I stand by my opinion).

Are There Environmental Causes for Type 1 Diabetes?

This is an excerpt of an article by Sarah Howard, Coordinator of CHE’s Diabetes-Obesity Spectrum Working Group. More information on this topic will be presented during CHE’s November 12th teleconference call: Type 1 Diabetes and the Environment, which is free and open to the public. After the call, a recording will be posted.

Type 1 researchers generally agree that the increasing incidence in Type 1 diabetes must be due to environmental factors. What those factors are, however, remains an area of active debate and research. Some of the top contenders include: viruses (either too many or too few), vitamin D deficiency, the gut microbiota, diet/nutrition (including cow’s milk or gluten), being overweight or obese, and environmental chemicals. It very well could be a combination of factors to blame, with different factors playing different roles in each person, depending on genetic make-up, and thus making it difficult to identify any root causes of the problem.

Read the full article on the Insulin Nation website.

Type 1 Diabetes Incidence Skyrocketing in China

written by Sarah Howard
Coordinator, Diabetes-Obesity Spectrum Working Group

You may have seen the news, published in JAMA, that type 1 diabetes prevalence in US children increased by 21.1% between 2001 and 2009 (Dabelea et al. 2014).

You may not have seen the news from the other side of the world, that type 1 diabetes incidence increased by 14.2% per year in Shanghai’s children. At this rate, the incidence of type 1 will double in just four years in Shanghai (between 2016 and 2020), and prevalence will sextuple by 2025 (Zhao et al 2014).

What might explain an increasing incidence that is this rapid and this large? The first thing that comes to my mind is pollution. Indeed, air pollution exposure has been linked to type 1 diabetes incidence in children from Los Angeles (Hathout et al. 2006). However, most environmental chemical exposures have not been well studied in type 1 diabetes—or even studied at all (Howard and Lee 2012). The extremely rapid increase of type 1 diabetes incidence in China—in an area where type 1 has traditionally been rare—deserves our full attention. Pollution as a potential cause or contributor to this increase should not be ignored.

Critically High Blood Sugar, Critical Science

In recognition of CHE’s 10th anniversary, colleagues who have been particularly instrumental to shaping CHE this past decade will be invited to write an introduction. This month’s introduction is by Sarah Howard, who serves as the national coordinator for CHE’s Diabetes-Obesity Spectrum Working Group.

“It’s critically high,” the ER nurse informed me, describing my toddler’s blood sugar level. She had just pricked his tiny finger, but it wasn’t enough; she needed a blood draw to see how just how high it really was. Two nurses held down my son, while I tried to comfort him, while he screamed, while they prodded and poked, failing to hit a vein. The pediatric team was called in, and eventually he slept while I heard the result: 798, a number seared in my memory forever, a dangerously high blood sugar level. My 23-month-old little boy had diabetes.

That was five years ago, almost 10,000 needles ago. After the shock of his diagnosis wore off, I started reading more about type 1 diabetes. I found out that type 1 incidence was increasing in children—in 58 different countries around the world. That the increasing type 1 incidence was due to some environmental factors, that genetics alone could not explain it. That the increase was most rapid in the youngest children, the children who, like my son, developed diabetes before their fifth birthday party. This much was clear. What was not clear was why.