Worldwide, the incidence of type 1 diabetes increased, on average, 3% per year between 1960 to 1996 in children under age 15 (Onkamo et al. 1999). Between 1990 and 1999, the worldwide average rate of incidence increase in children under 15 was 2.8%, reaching 3.4% during the 1995-1999 time period. Incidence increased in most continents, with a rise of 5.3% in North America , 4% in Asia, and 3.2% in Europe. This trend is especially troubling in the youngest children; from 1990-1999, for every hundred thousand children under age 5, 4% more were diagnosed every year, on average, worldwide (Diamond Project Group 2006). 

A study from Sweden provides some hope that the trend is leveling off: it found that incidence was increasing in children born through the year 2000, but after that the trend might be flattening. It is too early to say whether this is in fact the case, or just a blip in the data (Berhan et al. 2011). Data from Finland, however, show an opposite trend; type 1 incidence appears to be increasing even more rapidly since the mid-1990s than in earlier decades (Harjutsalo et al. 2008).

Essentially all researchers agree that changes of this magnitude cannot be explained by genetics alone. In fact, studies are finding that high risk susceptibility genes for type 1 diabetes are becoming less frequent over time in children, while more children with low to moderate risk genes are developing the disease more now than in years past (Vehik et al. 2008; Steck et al. 2011). An interesting study from Poland analyzed susceptibility genes from exhumed skeletons from the Middle Ages, and found that genetic predisposition to type 1 diabetes is lower today than it was 700 years ago (Witas et al. 2010).

The incidence of type 1 diabetes has been rising in children since about the mid-20th century in many European and North American countries (see figure A below) (Gale 2002b). What has changed during this time period? A number of things changed that may influence the development of type 1 diabetes, including: breastfeeding rates, diet, height and weight, vitamin D levels, infectious disease, vaccines, earlier puberty, factors relating to gestation and birth, and more. A major change that has garnered less attention in studies of type 1 diabetes is environmental contamination. Yet perhaps we should pay attention: the historical patterns of contamination are consistent with historical patterns of type 1 diabetes incidence.

The rise in type 1 diabetes incidence is coincidental with the large-scale production and use of many industrial and agricultural chemicals. Like the rising incidence of type 1 diabetes, large-scale chemical production also began around the middle of the 20th century (Tanabe 2002). In 1975 about 60,000 chemicals were manufactured or processed in the U.S.; in 1997 there were over 75,000 (Endocrine Disruptor Screening and Testing Advisory Committee (1998) Final Report U.S. Environmental Protection Agency (EPA)). Chemical production increased during this time as well, and continues to rise (see figure B below).

Other pollutant levels have also increased, such as molecules called "reactive nitrogen." Reactive nitrogen levels in the U.S. doubled between 1961 and 1997 due to human activity. The largest increase was in the use of nitrogen fertilizer, but air emissions from the combustion of fossil fuels also increased significantly (Howarth et al. 2002) (see figure C below, and the nitrate/nitrite page for information about type 1 diabetes and nitrogen-containing compounds). Reactive nitrogen molecules can increase air pollution levels (see the air pollution page for information on type 1 and these pollutants), and increase water acidity (Galloway and Cowling 2002) (see the nitrate/nitrite page for information on more acidic drinking water as a risk factor for type 1 diabetes).

 

 

Figure Sources:

A. Type 1 diabetes incidence rates in children per 100,000 per year in selected North American and European countries with high incidence of type 1 diabetes. Data redrawn from Onkamo et al. 1999; DIAMOND Project Group 2006; Gale 2002b; Vehik et al. 2007. Data with dotted lines were originally fitted and represented logarithmically but are shown here linearly for simplification.

C. Reactive nitrogen inputs from nitrogen (N) fertilizer and NO_x emissions, U.S. 1 Tg = 1 million metric tons. Data redrawn from Howarth et al. 2002.