It is clear that obesity increases the risk of developing type 2 diabetes. A large U.S. study has found that of adults with diabetes, 80% were overweight, and 49% were obese. While the dataset used in this study does not distinguish between type 1 and type 2, many other studies have also found clear associations between overweight/obesity and type 2 diabetes. It is interesting to note that 20% of the adults with diabetes in this study were not overweight (Nguyen et al. 2011). While important, overweight and obesity cannot explain all cases of type 2 diabetes (although some of these adults may have had type 1).
A large, multiethnic U.S. study looked at children with diabetes and body mass index (BMI). It found that 80% of children with type 2 diabetes were obese, and another 10% were overweight. In comparison, 13% of the children with type 1 diabetes were obese, and 22% overweight. Among U.S. youth without diabetes, 17% were obese, and 16% overweight. So, the obesity rate was lower among children with type 1 than the general population, although the opposite held for those overweight (Liu et al. 2010).
Obesity likely increases the risk of type 2 diabetes by increasing insulin resistance. But how? Adipose tissue (fat tissue) produces hormones, such as leptin and adiponectin. Leptin is pro-inflammatory, while adiponectin is anti-inflammatory. In people with severe coronary artery disease, obesity is associated with high leptin levels and low adiponectin levels. These hormones have opposite effects on insulin resistance as well; leptin promotes it and adiponectin reduces it (López-Jaramillo et al. 2014). Adiponectin levels tend to be lower in obese people. Low adiponectin levels increase insulin resistance. Obesity also often entails low-grade inflammation in fatty tissue, which can lead to oxidative stress and damage organs throughout the body, in turn leading to diabetes as well as other diseases (Matsuda and Shimomura, 2014).
Taller height has long been recognized as associated with type 1 diabetes; in the 1920s, Dr. Elliot Joslin, a pioneer in diabetes treatment said, "overheight was more frequent a precursor of diabetes in children than was overweight in adults" (quoted in Gale 2005b).
We all know that type 1 diabetes is an autoimmune disease, and not affected by body weight, right? Well, not everyone agrees.
Some researchers propose that increased weight gain is also responsible for the increased incidence of type 1 diabetes (see "The Accelerator Hypothesis" on the why is diabetes increasing? page; Wilkin 2001; Wilkin 2008). Since Wilkin proposed this hypothesis, researchers from around the world have been testing it. It is important to note that even moderately increased growth rates, not necessarily to the level of obesity, could be associated with an increased risk of type 1 diabetes (Dahlquist 2006).
A number of studies have in fact found evidence that a higher BMI or weight gain, may affect the development of type 1 diabetes. For example:
And yet, a number of other studies have found that higher weight gain or BMI did not increase the risk of type 1 diabetes:
In his Accelerator Hypothesis, Wilkin (2001) proposes that weight gain causes an increase in insulin resistance. Beta cells stressed by insulin resistance are more of a target to the immune system, and insulin resistance thus accelerates beta cell death and the appearance of type 1 diabetes. Weight gain and physical inactivity, Wilkin proposes, account for the rising incidence in both type 1 and type 2 diabetes in developed countries. However, there is conflicting evidence, and the data do not necessarily support this hypothesis.
An extensive literature search shows that obesity may contribute not only to type 1 diabetes but to the development and progression of other autoimmune diseases as well, especially rheumatoid arthritis, multiple sclerosis, and psoriasis (Versini et al. 2014).
Some studies have found that increased growth rates early in life may increase the risk of type 1 diabetes:
In a longitudinal study from Australia that followed people over time, weight gain (but not taller height) early in life has been found to increase the risk of type 1 diabetes-related autoimmunity in children who have an increased genetic risk of type 1 diabetes (Couper et al. 2009). In a U.S. longitudinal study of genetically at-risk children, however, taller height was found to increase the risk of autoimmunity and type 1 diabetes. Weight gain, however, did not show an increased risk (Lamb et al. 2009). These authors suggest that the differences in their findings may be due to the different ages of the children, or because of differing genetic risk. A Swedish study, meanwhile, did find that the risk of type 1 diabetes in relation to BMI did depend on genes. They found that being overweight may contribute to an increased risk of type 1 diabetes in children with certain genes (Carlsson et al. 2012). An Australian study found that in adults just diagnosed with type 1, those with higher body weight were less likely to have the high risk genes than those with lower body weight (Fourlanos et al. 2014). A large-scale prospective study of children at genetic risk for type 1 from around the world found that in general, the average BMI did not change among those with various type 1-associated genes at any age. Yet one gene was associated with a higher risk of obesity at age 4 (Yang et al. 2014).
Other factors may also affect the risk as well. A six-center U.S. study found increased BMI was associated with a younger age of type 1 diabetes diagnosis only among children with reduced beta cell function (Dabelea et al. 2006). A U.S. study from Washington State found an increased risk of type 1 diabetes in children of mothers with a high BMI (D'Angeli et al. 2010, although other studies have not confirmed this finding (Robertson and Harrild 2010).
Interestingly, obesity is sometimes associated with vitamin D deficiency, probably because vitamin D can be deposited in fat stores which decreases availability to the rest of the body (Holick 2004). Vitamin D appears to be protective against the development of type 1 diabetes (see the vitamin D page).
Looking at weight gain and diabetes without considering the role of environmental chemicals may not be sufficient. A provocative study found that adults who were obese did not have an increased prevalence of diabetes (mostly type 2, some probably type 1) if they also had very low concentrations of persistent organic pollutants (POPs). Only in people with certain POP levels was obesity associated with diabetes. This study is discussed further on the POP page (Lee et al. 2006). There have not yet been any other studies large enough to further examine this finding, although it certainly merits further research.
Environmental chemicals may also affect other growth rates, such as height, but the evidence here is not very strong or consistent. In humans, prenatal exposure to DDE has been associated with increased height (and weight) in boys at puberty (Gladen et al. 2000), and lower height earlier in life (Ribas-Fitó et.al. 2006). The effects of chemicals appear to depend on gender, as well as the type of chemical. PCBs, for example, have usually been associated with lower growth rates in animals and humans, but sometimes various PCB types have been associated with increased height in boys (Lamb et al. 2006) or girls (Hertz-Picciotto et al. 2005).
Growth rates, especially body weight, may also be influenced directly by environmental chemical exposures. In 2002, Baillie-Hamilton (2002) proposed the hypothesis that environmental chemical exposure could help to explain the modern obesity epidemic. She pointed out that numerous widely-used chemicals could actually produce weight gain in animals, including a number of POPs, pesticides, organophosphates, heavy metals, solvents, phthalates, and bisphenol A. Subsequent research has largely supported this hypothesis, and identified additional chemicals that may also promote weight gain, including PFCs and organotins (reviewed in Kelishadi et al. 2013). The mechanisms likely involve the ability of these chemicals to interfere with PPAR receptors, which control metabolism (Casals-Casas et al. 2008).
In fact, the obesity epidemic is not limited to human beings. Other species have also gained weight over the past decades, including feral rats (both urban and rural), laboratory animals (kept in controlled conditions), and domestic dogs and cats. It would be hard to explain all of these trends if diet and exercise were the only factors influencing obesity (Klimentidis et al. 2011). Exposure to environmental chemicals, however, could easily be an explanation.
The term "obesogen," coined by Dr. Grun and Dr. Blumberg in 2006, is now used to refer to chemicals than promote weight gain. The Collaborative on Health and the Environment provides a fact sheet on obesogens. Environmental Health Perspectives also has an informative article, Obesogens: An Environmental Link to Obesity (Holtcamp 2012).
Please see the pages on specific chemicals that describe studies on obesity-related outcomes and environmental chemicals.
In the opinion of Gale (2007), the former editor of the journal Diabetologia, "Children destined to develop type 1 diabetes grow faster and fatter in early life, but this could be a consequence rather than a cause of their predisposition to diabetes. Childhood obesity may have contributed to the linear rise of childhood type 1 diabetes over the past 50 years, but does not explain it."
Environmental chemical exposures may contribute to increased weight gain, especially if exposure occurs during development. Increased weight gain is associated with type 2 diabetes. But, weight gain may also be able to accelerate the appearance of type 1 diabetes and may contribute to the increasing incidence of type 1 diabetes, as well as type 2. The possibility that weight gain can increase the risk of type 2 diabetes only in people exposed to certain levels of chemicals deserves further study.
To see or download a list of references cited on this page, as well as other environmental factors linked to obesity or body size, see the collection Obesity and metabolic syndrome in Pubmed.