The first longitudinal (long-term) study of stress and type 1 diabetes found that experiencing a stressful event during childhood was associated with an increased risk of developing type 1 diabetes later in life (Nygren et al. 2015). A large study from Denmark found that if a child experienced the death of an immediate family member after age 11, they were more likely to develop type 1 diabetes (Virk et al. 2015).
Sepa and Ludvigsson (2006) reviewed earlier studies concerning psychological stress and type 1 diabetes. They found that 9 of 10 studies found associations between stress and type 1 diabetes. Additionally, one large study found an association between stress and type 1-related autoimmunity at early ages in life in the general population. They conclude that psychological stress can accelerate the appearance of type 1 diabetes, and may also contribute to the induction or progression of type 1 diabetes-associated autoimmunity, but more research is needed. The mechanisms for these effects are not known, but may involve stressing the insulin-producing beta cells, or direct influence on the immune system; psychological stress can also increase insulin resistance. Psychological stress in children is linked to changes in the immune system, as well as effects on beta cells (Carlsson et al. 2014).
Major life events have also been associated with the onset of type 1 diabetes, possibly due to increased levels of stress hormones, which are also increased in conditions involving inflammation (such as type 1 diabetes) (Dahlquist 2006).
A study from Israel found that that trauma of war was associated with an increased risk of type 1 diabetes. Children living in regions that were attacked during the Second Lebanon War had a higher risk of type 1 in the four years after the war, as compared to those living in areas that were not attacked. The associations were strongest in boys (Zung et al. 2012). In Croatia, two of 77 children during the siege and war in the city of Vukovar developed type 1 diabetes (Habek et al. 2016)-- but I am not entirely sure if this rate is higher than normal or not, and is a pretty small sample size.
During the week following the 1994 earthquake in Los Angeles, six new type 1 diabetes diagnoses occurred at the Children's Hospital of Los Angeles. During the 5 years prior, on average, 0-1 children are diagnosed with type 1 at that hospital in a week. The authors noted that the increased incidence of type 1 diabetes in the week following the earthquake may be related to the emotional trauma of the quake (Kaufman and Devgan, 1995).
The "Beta Cell Stress Hypothesis" suggests that any phenomenon that induces insulin resistance, and thereby extra pressure on the beta cells, should be regarded as a risk factor for type 1 diabetes (Ludvigsson 2006; Sepa and Ludvigsson 2006). In the "Overload Hypothesis," Dahlquist (2006) also points out that various environmental factors, including physical or psychological stress, could overload beta cells, thus hastening the appearance of type 1 diabetes (see the why is diabetes increasing? page for more on these hypotheses).
There is growing evidence that environmental exposures early in life can affect the risk of disease later in life. An interesting study analyzed a large number of people in Denmark, and found that if mothers experienced severe bereavement during pregnancy, their offspring were more likely to develop type 1 diabetes. The link was strongest for traumatic death of a sibling or the father, not for non-traumatic death or deaths of grandparents. And, the effect was strongest in girls (Virk et al. 2010). A different study on stress, however, did not find that exposure to stressful life events in the first year of life was associated with later type 1 diabetes (Nygren et al. 2013). Another study found no association between stress in mothers during pregnancy and fasting glucose levels in offspring at 5-6 years of age (van Dijk et al. 2014). Perhaps the different results are due to the different timing of stress experiences (fetal vs. first year of life), or some other difference in the populations.
Stress has also been linked to type 2 diabetes. In a large German study, people who suffer from post-traumatic stress disorder (PTSD) are more likely to have type 2 diabetes than those who do not (Lukaschek et al. 2013). Survivors of the 9/11 World Trade Center attacks who suffer from PTSD have a high risk of diabetes development as well (Miller-Archie et al. 2014). Adult European Jews who were born during the Holocaust in countries under Nazi rule have higher risk of diabetes and higher BMI (as well as numerous other conditions), as compared to Jews born in Israel (Berkovich et al. 2014). And Finnish children who were separated from their parents during World War 2 had a higher risk of type 2 diabetes later in life than those were were not separated (Alastalo et al. 2009).
Chronic stress is also linked to diabetes. Chinese men who work over 55 hours per week have a higher risk of diabetes than those who work fewer than 45 hours per week (Tayama et al. 2014). A German study found that high job strain was associated with a 45% increase in type 2 diabetes after 14 years (Huth et al. 2014). A large, prospective pan-European study found that job stress is a risk factor for type 2 diabetes in both men and women, and in those with healthy and unhealthy lifestyles (Nyberg et al. 2014).
A large study of adolescents from 10 European cities found that cortisol levels (a marker of stress) were associated with levels of insulin and insulin resistance, as well as with glucose levels in boys (Huybrechts et al. 2014). A meta-analysis and systematic review of 39 prospective studies found that there seems to be a association between chronic stress and the development of metabolic syndrome (including weight gain and diabetes) (Bergmann et al. 2014).
A systematic review from Europe found that long working hours were associated with type 2 diabetes, but only in people of a lower socioeconomic status Kivimäki et al. 2014).
A large, nation-wide, long-term study of military conscripts from Sweden found that those with low resilience to stress had a higher risk of developing type 2 diabetes. The conscripts were followed until up to 62 years of age, and they included 98-99% of the young men in that country between 1969 and 1997 (Crump et al. 2016).
In US Hispanics who do not have diabetes, chronic stress is associated with higher fasting blood glucose levels, higher long-term glucose control (higher HbA1c), and higher post-meal glucose levels (McCurley et al. 2015).
Disruption of the circadian clock (e.g., sleep disruption, shift work) is linked to metabolic syndrome (Gamble et al. 2014), type 2 diabetes, and obesity (Kalsbeek et al. 2014). For example, a meta-analysis found that shift work is associated with an increased risk of type 2 diabetes (Gan et al. 2014). African-American women who work the night shift have a higher risk of type 2 diabetes-- the more years they work the night shirt, the higher the risk (Vimalananda et al. 2015). Circadian clock disruption may also contribute to beta cell destruction in people with type 2 diabetes (Rakshit et al. 2014).
A review of the literature on shift work and endocrine disorders finds that levels of melatonin, cortisol, ghrelin, and leptin are all affected by shift work. These hormones are involved in insulin resistance and metabolic control, perhaps affecting the risk for diabetes (Ulhôa et al. 2015). Epigenetic changes may also be involved; staying awake just one night affected gene expression and increased blood sugar levels in men (Cedernaes et al. 2015). Sleep restriction also affects fatty acid levels in men, along with increased insulin resistance (Broussard et al. 2015). In U.S. women, sleep difficulties (e.g., sleep apnea, snoring, inadequate sleep) are associated with the development of type 2 diabetes-- especially if there are multiple sleep difficulties combined (Li et al. 2016). For a review of sleep disorders and type 2 diabetes, and the multiple mechanisms involved, see Briançon-Marjollet et al. 2015).
Pregnant mice who experienced disrupted sleep had male offspring with a sort of metabolic syndrome as adults (accompanied by epigenetic changes) (Khalyfa et al. 2014).
Interestingly, there may be interaction between some environmental chemicals and the circadian clock, specifically dioxin. For more info on that topic, see Wang et al. 2014.
Psychological tress is also linked to obesity, even in children (Koch et al. 2008). Anyone who has eaten an entire pint of ice cream when stressed can probably attest to this.... yet the mechanisms go beyond ice cream. If a mother is stressed while pregnant, her offspring have an increased risk of overweight/obesity as adults (these authors have previously found an increased risk of overweight/obesity in the children at age 10-13 as well) (Hohwü et al. 2014).
We know that diabetes and depression are linked; depression is more common in people with diabetes. Yet depression might also precede diabetes, increasing the risk of type 2 diabetes development as well (Tabák et al. 2014). We do not know if depression can also lead to type 1 diabetes.
Animal studies show that stress may increase the risk of type 1 diabetes. When exposed to chronic stress (for 14 weeks), rats genetically prone to insulin-dependent diabetes had a higher rate of diabetes development that unstressed control rats. (Interestingly, the stressed female rats developed diabetes at a later age than female controls, although the overall rate with higher) (Lehman et al. 1991).Chronic exposure to stress also makes mice more susceptible to autoimmunity (Harpaz et al. 2013).
Animal studies also show that stress may increase the risk of type 2 diabetes. Mice exposed to chronic stress in combination with a high fat diet showed impaired glucose tolerance (Castañeda et a. 2011). And mice genetically at risk of obesity and diabetes and exposed to chronic stress developed high blood sugar and glucose intolerance (Razzoli et al. 2015).
Mice whose mothers experienced stress while pregnant where more susceptible to metabolic disease later in life (Brunton et al. 2013).
Even worse, these effects can be passed down to multiple generations. When a rat is exposed to stress during pregnancy, her offspring and even their offspring have increased blood glucose levels (Yao et al. 2014).
In humans, stress may have a modest risk on the development of gestational diabetes (László et al. 2015).
In animals, pregnant ewes exposed to the stress hormone cortisol developed higher blood glucose levels similar to gestational diabetes. Cortisol also increased fetal death (Keller-Wood et al. 2014).
Meanwhile, gestational diabetes can affect the stress response in the offspring as well. Children whose mothers had gestational diabetes had higher cardiovascular responses to stress as teenagers than those whose mothers did not have gestational diabetes (Krishnaveni et al. 2014).
Environmental chemicals can exacerbate the effects of stress. For example, stress and air pollution can act synergistically, exacerbating respiratory disease (Clougherty and Kubzansky 2009). A combination of stress and chemicals may also affect offspring when parents are exposed. In one study, exposing rat mothers to either stress or the heavy metal lead altered the response to stress in their offspring, and the effects were greater when combined (Virgolini et al. 2006). Thus exposures to chemicals may be important when studying the effects of stress on diabetes development.
It will come as no surprise to people with diabetes that stress can also affect blood glucose management and control. For example, a small study of 20 adolescents with type 1 diabetes found that higher stress levels were associated with higher blood glucose levels (HbA1c levels) (Oritz and Myers, 2014).
To download or see the references cited on this page, as well as other articles on stress and diabetes, see the collection Stress and diabetes/obesity in Pubmed.