SKEWED STATISTICS: The Inclusion of People with Type 1 Diabetes (LADA) in the Statistics for Type 2 Diabetes

The advent of antibody testing[1] more than 40 years ago demonstrated that most Type 1 diabetes is autoimmune in nature. Another interesting outcome of the discovery of these antibodies was the finding that about 10% of people who had been diagnosed with Type 2 diabetes were antibody positive, were misdiagnosed, and in fact had Type 1 autoimmune diabetes (sometimes called latent autoimmune diabetes in adults, or LADA[2]). Although this population has Type 1 diabetes[3], and its presence is increasingly acknowledged, this population of Type 1 diabetics is still included in the statistics and information on Type 2 diabetes (a fundamentally different disease not only clinically but genetically). Here are some examples of skewed statistics and wrong information:

(1) Skewed Statistic: “Type 2 diabetes represents about 90-95% of the total diabetic population.” However, if people with LADA are removed from the Type 2 diabetes statistics and correctly included in the statistics for Type 1 diabetes, Type 2 diabetes represents about 75-85% of all diabetes and Type 1 represents about 15-25%. According to John Walsh, author of "Pumping Insulin", rapid onset Type 1 is about 5-10% and slow onset Type 1 is 10-15% of the total diabetic population.

(2) Skewed Statistic: “80% of Type 2 diabetics are overweight or obese.” If people with LADA are removed from this statistic, more than 90% of Type 2 diabetics are overweight or obese.

(3) Skewed Statistic: “40% of Type 2 diabetics eventually require insulin.” If people with LADA (autoimmune diabetes requiring exogenous insulin treatment) are removed from this statistic, about 25% of Type 2 diabetics eventually require insulin.

(4) Wrong Information: “Many women who have gestational diabetes go on to develop type 2 diabetes years later.” In fact, about 10% of Caucasian women with GDM have autoimmune gestational diabetes, and develop Type 1 diabetes[4].



[1] Glutamic acid decarboxylase antibodies (GADA), islet cell antibodies (ICA), and insulinoma-associated (IA-2) autoantibodies.

[2] More recently, diabetes researchers have discouraged the use of the term latent autoimmune diabetes in adults, because LADA is not a latent disease. In a recent article “LADA is Dead: Long Live Autoimmune Diabetes” researchers Rolandsson and Palmer suggest simply using the term autoimmune diabetes.

[3] According to the World Health Organization and the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus:“Type 1 diabetes results from a cellular-mediated autoimmune destruction of the beta-cells of the pancreas. In Type 1 diabetes, the rate of beta-cell destruction is quite variable, being rapid in some individuals (mainly infants and children) and slow in others (mainly adults)” and "Although the specific etiologies of Type 2 diabetes are not known, autoimmune destruction of beta-cells does not occur."

[4] In Europe, the literature on gestational diabetes mentions autoimmune gestational diabetes, but in North America the layperson literature doesn't mention it. However, the existence of autoimmune gestational diabetes is widely reported in North American scientific literature (for example, a July 2007 "Diabetes Care" article and also an April 2003 "Diabetes Care" article on GDM). The July 2007 issue of "Diabetes Care" indicated that autoimmune gestational diabetes (new onset Type 1 diabetes) accounts for about 10% of all Caucasian women diagnosed with gestational diabetes (Diabetes Care July 2007 vol. 30 no. Supplement 2 S105-S111 ). It says “A small minority (≤10% in most studies) of women with GDM have circulating antibodies to pancreatic islets (anti-islet cell antibodies) or to β-cell antigens such as GAD (anti-GAD antibodies)” and then notes, “They appear to have evolving type 1 diabetes that comes to clinical attention through routine glucose screening during pregnancy. Whether pregnancy can actually initiate or accelerate islet-directed autoimmunity is unknown.”