Height and Weight
Links Between Height and Weight and Diabetes
There is a clear link between higher body weight and and increased risk of type 2 diabetes or gestational diabetes. Interestingly, taller height is associated with type 1 diabetes. But does a higher body weight contribute to type 1 diabetes development as well? Most people think that it does not, but some studies have found that it might.
Environmental chemical exposures may contribute to increased weight gain, especially if exposure occurs during development. Chemicals linked to increased body weight are called obesogens.
Type 2 Diabetes
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). While the numbers vary by population, overall in the U.S., about of 10% people with type 2 diabetes are not overweight or obese, while in Africa and Asia, 24-66% of people with type 2 diabetes are not overweight or obese (Gujral et al. 2018).
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).
Type 1 Diabetes
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 2005).
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:
A longitudinal study from Finland (TRIGR) of children at genetic risk of type 1 diabetes found that annual growth measures were not associated with islet autoimmunity, but that being overweight at 2-10 years of life was associated with a twofold increase in the development of type 1 diabetes (Nucci et al. 2021).
In a large study of German and Austrian children, a higher BMI was associated with a younger age of type 1 diabetes onset (Knerr et al. 2005).
A very large, prospective study of Danish women found that obese women were at increased risk of type 1 diabetes (as well as other autoimmune diseases) (Harpsøe et al. 2014).
Another Danish study, of children, found that a higher BMI was associated with an increased risk of type 1 diabetes (but does not explain the increasing incidence of disease) (Antvorskov et al. 2018).
The TrialNet study cohort of autoantibody-positive relatives of people with type 1 diabetes found that a higher BMI in childhood was associated with an increased risk of developing type 1 diabetes, especially at younger ages and in females (Ferrara et al. 2017a).
TrialNet also found that in children under 9, BMI did not affect the progression of islet autoimmunity, but in children over 9, a higher BMI was linked to a faster progression from single autoantibody positivity to multiple autoantibody positivity, especially in children with lower genetic risk (Ferrara-Cook et al. 2020).
Another TrialNet study, this time of adults, found that in men over 35 and women under 35, sustained obesity increased risk for type 1 diabetes (Ferrara et al. 2017b).
A study from Kuwait found that the age of onset of type 1 diabetes was lower in heavier children (Channanath et al. 2017).
A meta-analysis that incorporated data from 9 separate studies found overall evidence for an association between increased BMI and increased risk for subsequent type 1 diabetes (Verbeeten et al. 2011).
And yet, a number of other studies have found that higher weight gain or BMI did not increase the risk of type 1 diabetes:
A German study found that there was no sign of excessive weight gain in children before type 1 diagnosis (Kuchlbauer et al. 2014).
Another German study found that overweight children did not develop autoantibodies or progress to diabetes faster than those who were not overweight (Winkler et al. 2012).
Weight gain did not increase the risk of autoimmunity and type 1 diabetes in U.S. children genetically at risk of type 1 diabetes (Lamb et al. 2009).
Another U.S. study found that the BMI of children newly diagnosed with type 1 diabetes was lower than that of the general population (Kaminski et al. 2013).
And another U.S. study found that there were no associations between obesity and type 1-related autoimmunity (Cedillo et al. 2015).
A UK study found that while increasing obesity increased the risk of type 2 diabetes in children and young adults, it did not increase the risk of type 1 (Abbasi et al. 2017).
A Polish study found that almost all children diagnosed with type 1 had a normal BMI, despite increasing type 1 incidence rates (Wasyl-Nawrot et al. 2020).
There is not much data from less developed countries, but one study from North India found that BMI was not associated with type 1 diabetes in children, despite a rapidly increasing numbers of children with type 1 (Dayal et al. 2016).
Other studies find some middle ground. For example, the TrialNet study (also mentioned above) found no increased risk of multiple type 1-related autoantibodies or type 1 diabetes with higher BMI or insulin resistance, in people who tested positive for one type 1-related autoantibody. However, among everyone (including those who were negative for autoantibodies), there was a slight increased risk of type 1 diabetes in those with a higher BMI, as well as a higher risk of type 1 in obese adolescents, and in adults with higher insulin resistance (Meah et al. 2016).
It may also be more complicated (of course)... data from two large German cohorts found that in children whose mothers did not have diabetes, islet autoimmunity was associated with a rapid growth in BMI until age 3, and above-average height. High height at birth that lessened to average height at age 3 was associated with a lower risk of autoimmunity. But no associations were found in children of mothers with diabetes (Yassouridis et al. 2017).
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.
It seems pretty clear now though that non-immune processes like insulin resistance or obesity can stress beta cells, as well as amplify autoimmunity and contribute to type 1 diabetes (Redondo et al. 2019). A review finds that "Emerging evidence suggests that obesity contributes to insulin resistance, dyslipidemia, and cardiometabolic complications in type 1 diabetes" and that there is a gap in knowledge of the role of obesity in the development of type 1 diabetes (Corbin et al. 2018).
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."
For those with type 1 diabetes, excessive weight is a common problem (especially in the U.S.), and is associated with higher blood glucose levels (HbA1c) and more frequent severe hypoglycemia (DuBose et al. 2015). In some places, people with type 1 diabetes have been found to have a higher BMI than the general population, including for example in Austria (Fellinger et al. 2019). Rates of obesity and overweight in people with type 1 diabetes are also higher in minority groups (Minges et al. 2017). A review of the literature on type 1 diabetes and obesity finds that while overweight and obesity are common among people with type 1 diabetes, levels may have reached a plateau in some parts of the world. Overall, obesity increases the risk for type 1 diabetes development. It also increases the risk of complications and metabolic syndrome in people with type 1 (Polsky and Ellis 2015). (Note however that taking insulin does cause weight gain, so that may affect these findings as well).
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). Fatty tissue releases inflammatory molecules into the body, which may contribute to the development of chronic inflammation and eventually autoimmune disease (Hutcheson 2015). One of these molecules, adiponectin, increases dramatically when people newly diagnosed begin taking insulin. A study from Pittsburgh found that adiponectin levels were highest in the newly diagnosed who had the most autoantibodies (Hecht Baldauff et al. 2016).
Interestingly, people who are obese-- with or without type 2 diabetes-- test positive for type 1-related autoimmune antibodies than controls. This finding implies that obesity itself is associated with autoimmunity (Tiberti et al. 2018). A review looks at the mechanisms by which obesity and autoimmunity may be related (Tsigalou et al. 2020).
Birth Weight and Early Growth
Some studies have found that increased growth rates early in life may increase the risk of type 1 diabetes:
The TEDDY study of genetically at-risk children in Finland, Germany, Sweden and the U.S. found that greater weight in the first year of life was associated with an increased risk of development of islet autoimmunity (Elding Larsson et al. 2016). A more recent publication from the TEDDY study also noted a higher rate of weight gain in infancy was associated with increased autoimmunity risk. It also found that a height growth pattern with a lower rate in infancy, higher rate in early childhood, and younger age at autoantibody appearance was associated with increased risk of progression from autoimmunity to type 1 diabetes. And, that a higher rate of weight gain in early childhood was associated with increased risk of progression from autoimmunity to type 1 diabetes, but only in children where the first-appearing autoantibody was the GAD antibody (Liu et al. 2020). So, it seems complicated!
The international Trial to Reduce IDDM in the Genetically at Risk (TRIGR) found that increased height velocity during the first two years of life was linked to a higher risk of developing multiple autoantibodies (Pacaud et al. 2020).
An analysis of data from multiple studies found that increased weight gain during the first year of life were associated with an increased risk of type 1 diabetes (Harder et al. 2009).
A study based on two large population-based datasets from Scandinavia found that babies who gained the most weight during their first year of life had an increased risk of type 1 diabetes during childhood. The effect was highest in the first 6 months of life. Height gain was not associated (Magnus et al. 2015).
A Danish study found that children who developed type 1 diabetes were taller and had a higher BMI at age 1 than those who did not (but that changes in growth rates did not explain the increasing type 1 incidence overall) (Svensson et al. 2007).
A Finnish study found that those who developed type 1 diabetes as young adults had a higher BMI gain in infancy than those who did not. Those who developed type 2 diabetes as young adults had a higher BMI gain during childhood (Lammi et al. 2009).
German babies with a BMI peak at earlier ages had a higher risk of islet autoimmunity (Beyerlein et al. 2014).
A study from five European countries found that rapid growth in the first two years of age (growth in height, weight, or BMI) was associated with an increased the risk of type 1 diabetes (EURODIAB Substudy 2 Study Group 2002).
A study of Swedish children found that rapid growth before age 7 and increased BMI increased the risk of developing type 1 diabetes (Ljungkrantz et al. 2008).
Do Other Factors Affect the Association Between Growth and 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).
Exercise is also related to weight, and in men, the type 1 "honeymoon" period (of partial remission after diagnosis) is five times longer in those who exercise (Chetan et al. 2018).
After diagnosis, weight may also affect the rate of beta cell decline. A Korean study found, interestingly, that people with a lower BMI had a faster rate of beta cell decline (Hwang et al. 2017).
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).
It is clear that excess weight increases the risk of gestational diabetes. Adipokines-- those molecules like leptin and adiponectin mentioned above that adipose tissue releases-- also may influence the risk of gestational diabetes. A meta-analysis found that in early pregnancy, adiponectin levels are lower and leptin levels are higher in women who go on to develop gestational diabetes (Bao et al. 2015).
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, heavy metals, solvents, phthalates, and BPA. Subsequent research has largely supported this hypothesis, and identified additional chemicals that may also promote weight gain, including PFASs and organotins (reviewed in Kelishadi et al. 2013). One mechanism may 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). Aquatic animals are also affected by obesogens (Capitão et al. 2017). Other studies find that diet and exercise are not the only factors in human obesity. For example, comparing the diet and exercise levels of people in 1988 vs 2006 shows that in 2006 people are heavier if they eat/exercise at the same levels as they did in 1988 (Brown et al. 2016). Exposure to environmental chemicals could be an explanation of these trends.
The term "obesogen," coined by Dr. Grun and Dr. Blumberg in 2006, is now used to refer to chemicals than promote weight gain. Environmental Health Perspectives has an informative article, Obesogens: An Environmental Link to Obesity (Holtcamp 2012). For a history of the obesogen research field, see Heindel 2019.
Early Life Exposure to Environmental Chemicals Can Cause Obesity in Animals
Exposure to environmental chemicals can cause obesity in laboratory animals.
A number of researchers are working to screen chemicals for obesogenic potential; simply identifying obesogens is not easy (e.g., Foley et al. 2017; Wang et al. 2017; Janesick et al. 2016), with the Janesick article receiving subsequent debate (Houck et al. 2017; Janesick et al. 2017). For example, some authors point out that the source of cells as well as the way they were differentiated (developed) in studies has a significant impact on the potency and effects that they have (Kassotis et al. 2017). Chamorro-Garcia and Veiga-Lopes (2021) and Chamorro-Garcia and Blumberg (2019) review research approaches and challenges in the obesogen field.
The list of chemicals linked to obesity is growing rapidly. Please see the pages on specific chemicals to see the studies on obesity-related outcomes. One free full text review provides a nice summary of the evidence and includes a number of older and more recently identified potential obesogens. The older chemicals include tributyltin, BPA, phthalates, PFAS, POPs, and more. The newly identified obesogens include things like dibutyltin, BPS and BPF and other BPA substitutes, acrylamide, surfactants, food additives, and pesticides (Egusquiza and Blumberg 2020).
Reviews on Obesogens
There are a number of reviews of obesogenic chemicals (e.g., Amato et al. 2021; González-Casanova et al. 2020; Griffin et al. 2020; Muscogiuri et al. 2017; Yang et al. 2018; Zoeller and Heindel 2017). Here are a few of them and their overall findings:
"Prenatal exposure to environmental obesogens can produce lasting effects on the exposed animals and their offspring to at least the F4 [fourth] generation." (Lee and Blumberg, 2019).
"Accumulated evidences show positive associations between pollutants and obesity in humans." (Wang et al. 2016).
"There is now considerable evidence that other environmental factors may contribute to the rapid increase in the incidence of ... metabolic diseases." (Heindel et al. 2017).
A review of human studies on maternal exposure to chemicals and effects on the offspring finds that the strongest evidence exists for DDE, a persistent organic pollutant. Many studies are inconsistent, perhaps due to small sample sizes and other issues (Liu and Peterson, 2015).
A review of the literature by staff of the National Institute of Environmental Health Sciences finds that, "A substantial body of evidence suggests that a subclass of endocrine-disrupting chemicals (EDCs), which interfere with endocrine signalling, can disrupt hormonally regulated metabolic processes, especially if exposure occurs during early development. These chemicals, so-called 'obesogens' might predispose some individuals to gain weight despite their efforts to limit caloric intake and increase levels of physical activity" (Heindel et al. 2015).
"... besides excessive individual energy intake and inadequate lifestyle, other broadly diffused and modifiable factors (mainly ingestion of toxic chemicals with food) seem to have a critical role in the rapid epidemiological growing of obesity, also considering trans-generational transmission of risk and later development of obesity due to exposure during early life" (Di Ciaula and Portincasa 2017).
While not many studies have looked at total food intake, there is evidence that early life exposure to obesogenic chemicals may influence the amount of food eaten (Walley and Roepke, 2018).
Oil Dispersant Chemical Linked to Obesity
A chemical component of the oil dispersant used in the Deepwater Horizon oil spill, DOSS, is shown here to increase the growth of fat cells. Rosi stands for rosiglitazone, a pharmaceutical drug known to cause weight gain. PGM is "before," and MIM is the control solution.
Source: Temkin et al. 2016, EHP.
According to the Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals, "Both cellular and animal models demonstrate a role for EDCs [endocrine disrupting chemicals] in the etiology of obesity and T2D [type 2 diabetes]. For obesity, animal studies show that EDC-induced weight gain depends on the timing of exposure and the age of the animals. Exposures during the perinatal period trigger obesity later in life." (Gore et al. 2015).
The Uppsala Consensus Statement on Environmental Contaminants and the Global Obesity Epidemic is available for free online (Lind et al. 2016). It concludes, "Since there are now numerous animal and epidemiological studies indicating that environmental pollutants could contribute to the global obesity epidemic, there is an urgent need to reduce the burden of environmental contaminants so that obesity does not become the normal outlook in the future. The workshop attendees concluded that public health efforts should focus on the importance of early obesity prevention by means of reducing chemical exposures, rather than only treating the established disease. Just as a bad start can last a lifetime and beyond, a good start can last a lifetime as well."
The Parma Consensus Statement on Metabolic Disruptors developed an "overarching hypothesis for the role of environmental chemicals in the current worldwide epidemics of obesity, diabetes and related metabolic diseases." (Heindel et al. 2015).
More on Obesogens
Listen to Dr. Juliette Legler, VU University, discuss Prenatal Exposure to Endocrine Disrupting Compounds and Obesity: Combining Toxicology and Epidemiology, sponsored by the Collaborative on Health and the Environment (2014).
Listen to Dr. Bruce Blumberg, UC Irvine, discuss Obesity and the Environment, on a podcast sponsored by NIEHS (2014) and What Do We Know about Obesogens? on a podcast sponsored by Environmental Health Perspectives (2012).
To see or download a list of references cited on this page, additional references on obesogens, as well as references on other environmental factors linked to obesity, body size, or metabolic syndrome, see the collection Obesity and metabolic syndrome in PubMed.