Selenium is an essential trace element, but it can also be toxic at high doses. Most Americans have high levels of selenium intake as compared to people in some other countries, due to the higher levels of selenium in U.S. soils as well as the use of dietary supplements containing selenium (Laclaustra et al. 2009). High levels of selenium have been found in streams subject to mountaintop mining and valley fills in central Appalachia. In some streams, selenium has bioaccumulated to four times the toxic level in the food chain, a level that can cause harm in fish and birds. Groundwater wells are also affected, and state advisories are in effect for consumption of fish due to high selenium levels (Palmer et al. 2010). There is a high prevalence of diabetes in many counties in central Appalachia (Centers for Disease Control and Prevention 2009).
The strongest evidence for the ability for environmental exposures to contribute to the development of diabetes comes from longitudinal studies. These are studies that take place over a period of time, where the exposure is measured before the disease develops.
One prospective study from France found that elderly men with higher selenium levels had a lower risk of later developing type 2 diabetes or impaired fasting glucose (there was no association in women) (Akbaraly et al. 2010). A long-term study found that higher toenail levels of selenium were associated with a lower risk of type 2 diabetes in U.S. adults, at dietary levels of intake (Park et al. 2012). However, a study of elderly Swedish men found no association between selenium levels and the development of type 2 diabetes, beta cell function, or insulin resistance 20 years later (Gao et al. 2014). Neither did an Italian study-- it found no association between toenail selenium levels in women and risk of type 2 diabetes 16 years later (Vinceti et al. 2014).
Cross-sectional studies are studies that measure exposure and disease at one point in time. These provide weaker evidence than longitudinal studies, since the disease may potentially affect the exposure, and not vice versa.
Laclaustra et al. (2009) found that in U.S. adults exposed to background selenium levels, the prevalence of diabetes increased with increasing levels of selenium. Fasting glucose levels and hemoglobin A1C levels (a measure of long-term glucose control) increased with increasing selenium levels as well. Another study using the same dataset but from an earlier time period also found selenium levels to be associated with diabetes (Bleys et al. 2007). A study of elderly Taiwanese found that higher selenium levels were associated with higher fasting glucose (as well as higher triglycerides and cholesterol) (Yang et al. 2010). Another study from Taiwan found high selenium levels were associated with diabetes, independent of obesity and insulin resistance (Lu et al. 2016). In Chinese adults, dietary selenium intake was associated with type 2 diabetes (Wei et al. 2015). Also in Chinese adults, blood levels of selenium were associated with metabolic syndrome and higher fasting blood sugar levels (Yuan et al. 2015).
In countries with lower selenium levels, including Singapore and France, studies have generally not found associations between selenium and diabetes or glucose levels (Laclaustra et al. 2009).
A study of older adults in China found that higher selenium levels were associated with higher triglycerides, LDL (the "bad" cholesterol), fasting blood glucose, post-meal blood glucose, higher average blood glucose levels (HbA1c), higher insulin resistance, as well as NAFLD (non-alcoholic fatty liver disease) (Yang et al. 2016).
Since selenium is an essential element, it is sometimes found in dietary supplements. Interestingly, two trials of selenium supplementation suggest that selenium may increase the risk of type 2 diabetes. A randomized, double-blind, placebo-controlled study from the Eastern U.S. found that selenium supplementation may increase the risk of developing type 2 diabetes (Stranges et al. 2007). Another large, randomized, double-blind, placebo-controlled study, aimed to determine whether selenium (and/or vitamin E) supplements could prevent prostate and other cancers. It found instead that those who took selenium supplements alone had higher rates of type 2 diabetes (although the increased risk was not significant). The study was discontinued early. It was conducted in the U.S., Canada, and Puerto Rico (Lippman et al. 2009). Another trial, also for cancer, also found that selenium supplements did not prevent cancer and did increase the risk of type 2 diabetes (Thompson et al. 2016).
On the other hand, randomized, double-blind, placebo-controlled trials, from the western U.S., did not find any increase in diabetes risk or glucose levels with selenium supplementation in men at risk of or with prostate cancer (Algotar et al. 2013; Algotar et al. 2010).
A meta-analysis of four randomized controlled trials found that selenium supplementation did not find a preventative effect (or any statistically significant effect); if anything, there was a slight increased risk (not significant). The authors state, "Our findings do not support the routine application of selenium supplementation for type 2 diabetes prevention in Caucasians" (Mao et al. 2014).
The fact that some trials have shown an increased risk of type 2 diabetes with selenium supplementation has raised concern about the use of supplements in people who are not selenium deficient. Selenium is often added to multivitamins, but "Based on current evidence, the indiscriminate use of selenium supplements in individuals and populations with adequate-to-high selenium status cannot be justified and may increase [type 2 diabetes] risk" (Rayman and Stranges, 2013).
A Iranian trial of selenium supplementation in people with diabetic nephropathy found that it had beneficial effects on insulin resistance, insulin levels, and beta cell function (Bahmani et al. 2015). Another Iranian trial of selenium supplementation in people with diabetes and coronary heart disease also found that it had beneficial effects in insulin resistance, insulin levels, and beta cell function (Farrokhian et al. 2016).
European women (without diabetes) who had higher levels of selenium in their blood were more likely to have metabolic syndrome than women with lower levels. There was no association in men (Arnaud et al. 2012).
Obese Korean adults with more insulin resistance had lower selenium levels in their hair than those with higher levels, perhaps indicating a mineral deficiency (Kim and Song, 2014). Obese children in Poland tended to have lower selenium levels in their blood, also perhaps indicating a mineral deficiency (Błażewicz et al. 2014); similarly, adults with low dietary intake of selenium had the highest body mass index (BMI) in another study (Wang et al. 2016).
Wang et al. 2014). A review of the laboratory evidence finds that while earlier studies found selenium to act like insulin and help prevent diabetes, recent studies (both animal and human) have shown that prolonged, high intake of selenium can cause insulin resistance and/or diabetes in mice, rats, and pigs (Zhou et al. 2013). Even fish, exposed to selenium in water, have higher glucose levels than unexposed fish (Kim and Kang, 2014). In mice, long-term selenium supplements reduced glucose levels at first, but then increased insulin levels and led to fatty liver disease and other harmful effects (Wang et al. 2014).
A mouse study suggests mechanisms by which high-dose selenium may affect the risk of diabetes. It found that selenium led to higher insulin resistance, higher insulin levels, and increased glucose tolerance via oxidative stress (Zhou et al. 2015). The effects of selenium related to insulin resistance also may vary by diet (Wang et al. 2016). A high-fructose diet in lab animal mothers, for example, affects the levels of selenium and induces metabolic disorders in offspring (Ojeda et al. 2016).
Female rats fed were fed a low-selenium or high-selenium diet while pregnant and lactating. A few months after birth, the offspring exposed to a high-selenium diet developed high insulin levels, insulin resistance, and glucose intolerance, as compared to the deficient rats (Zeng et al. 2012). The female lambs of pregnant sheep given selenium had higher birth weight, more fat storage and body weight later on, and selenium also affected their glucose tolerance (Vonnahme et al. 2010). These studies show the potential for selenium exposure to affect development of the offspring later in life.
In the same study as above, the female rats who were fed a high-selenium diet developed high insulin levels, insulin resistance, and glucose intolerance while pregnant (similar to gestational diabetes in humans), as compared to the deficient rats (Zeng et al. 2012). This is a somewhat surprising result, considering that some human studies have found lower selenium levels in women with gestational diabetes, and a higher risk of gestational diabetes in women with inadequate selenium intake (Kong et al. 2016; Mariath et al. 2011; Askari et al. 2014). Again, however, it may be that certain levels of selenium are protective against diabetes, while excess selenium can be harmful.
High levels of selenium may increase the risk of type 2 diabetes, while lack of sufficient selenium may also promote diabetes. A systematic review and meta-analysis of 5 studies found an association between selenium levels and type 2 diabetes in populations with both relatively low levels and high levels of selenium (Wang et al. 2016). Selenium supplements should be avoided unless deficient, especially in the U.S., or in people with adequate selenium levels. Supplementation of people who already have adequate intake with additional selenium might increase their risk of type 2 diabetes (Rayman, 2012). While selenium is an essential mineral, its toxic effects are now being found at lower levels than previously thought (Jablonska and Vinceti 2015).Selenium and diabetes/obesity in PubMed.