Certain pharmaceutical drugs appear to be able to cause diabetes. It is also very clear that drugs can cause weight gain -- insulin is one well-known example.
Cancer immunotherapy drugs activate the immune system to attack cancer cells. One problem is that they can also activate the immune system to attack other cells, like the insulin-producing beta cells in the pancreas. A number of studies have documented cases of type 1 diabetes following or in conjunction with immunotherapy treatment:
Doctors are wondering if they can predict in advance who might be at risk of developing diabetes after immunotherapy. One lab did a genetic analysis on a patient who took ipilimumab and nivolumab and developed rapid-onset type 1 diabetes (ketoacidosis, positive autoantibodies, no detectable beta cell function). This patient did not have a genetic risk of type 1 diabetes, so genetic testing may not be useful (although larger studies would be helpful here) (Lowe et al. 2016).
A few studies have investigated whether light therapy, i.e., phototherapy, increases the risk of type 1 diabetes. Neonatal phototherapy is used to treat jaundice in newborns. A meta-analysis of 12 published studies found that newborns with jaundice had a slightly increased risk of later developing type 1 diabetes, especially if the jaundice required phototherapy (McNamee et al. 2012). However, a large study from California found no increased risk of type 1 diabetes from neonatal phototherapy (Newman et al. 2016).
A Danish study has found that numerous second-generation (atypical) antipsychotic medications were associated with diabetic ketoacidosis (DKA) and the development of type 1 diabetes (Polcwiartek et al. 2016).
One of these antipsychotic medications is olanzapine; a case study from Japan describes a 32 year old man who developed acute-onset, autoantibody-positive type 1 diabetes four months after beginning this drug, which was then followed by an extended honeymoon period (Iwaku et al. 2017).
According to a review, interferon therapy to treat hepatitis C increases the risk of developing rapid-onset type 1 diabetes 10-18 fold (Zornitzki et al. 2015).
A case study also showed a Japanese man developed type 1 while taking highly active antiretroviral therapy (HAART) for HIV. This appears to be partly due to a gene that is present in Japanese people but not Caucasians (Kamei et al. 2015).
I do not have the time nor inclination to review all the drugs that can cause weight gain here. There are a few lessons we can learn from some of them, however.
Diethylstilbestrol (DES), was a drug given to pregnant women decades ago to prevent miscarriage (it didn't work, but instead led to various health problems in these women's offspring, and now their grandchildren as well). As an estrogen, DES is thought to act similarly to endocrine disrupting chemicals. Fetuses are most vulnerable to its effects, and outcomes may not appear until adulthood. DES is strongly linked to vaginal cancer and adverse reproductive outcomes in offspring. Prenatal exposure to DES may also be linked to other health outcomes, including diabetes, cardiovascular disease, high blood pressure, and high cholesterol (the association with diabetes was not statistically significant, but the risk was higher) (Troisi et al. 2013). Prenatal DES exposure is also linked to slightly increased weight gain in adulthood (Hatch et al. 2015).
There is some limited evidence linking autoimmunity and DES in humans: women exposed to DES in utero seem to have a higher incidence of autoimmune disease, but only when various autoimmune diseases are grouped together (Ahmed et al. 1999). Yet a more recent study that followed these women over 25 years found that there was not an overall increase in autoimmune diseases in DES exposed daughters, although type 1 diabetes was not included in this study (only four autoimmune diseases were included). However, there was an increased risk of the autoimmune disease rheumatoid arthritis in women under 45, and a lower risk in those over 45 (Strohsnitter et al. 2010).
In animals, when female mice were exposed to a low dose of DES in the first five days of life, they gained more weight by six months of age than mice who were not exposed (Newbold et al. 2009). DES promotes the formation of fat cells in laboratory studies, and increases body weight in mice (Hao et al. 2012). DES also enhances autoantibody production in mice (Yurino et al. 2004).
Rosiglitazone, also known as Avandia, is a drug used to treat type 2 diabetes. It works by binding to PPAR receptors in fat cells and making the cells less insulin resistant. It also causes weight gain (and possibly heart attacks, and thus has been taken off the market in many countries). Activating PPAR receptors causes weight gain because these receptors play an important role in the development of fat cells and fat storage.
The interesting part is that some "obesogenic" environmental chemicals also bind to PPAR receptors, and therefore may also cause weight gain. Tributyltin, for example, binds the PPARγ receptor, and promotes fat cell development (Heindel et al. 2016). Phthalates also activate PPARγ receptors, and are linked to type 2 diabetes and insulin resistance (e.g., Lind et al. 2012; see more studies on the phthalates page).
The diabetes medication metformin is a common pollutant released from wastewater treatment plants, and can act as an endocrine disruptor to fish living in the water (Niemuth et al. 2015; Niemuth and Klaper 2015). Pharmaceuticals released from wastewater treatment plants are becoming more and more of a problem. Wastewater discharged from water treatment plants contains numerous endocrine disrupting compounds, and mice who drank this water gained more fat (Biasiotto et al. 2016).
Studies on antibiotics and diabetes/obesity are discussed on the Diet and the Gut page, as are studies on bariatric surgery. Studies on radiation for cancer are discussed on the Radiation page.
For these and other studies on pharmaceuticals and diabetes/obesity, see the PubMed collection, Pharmaceuticals and diabetes/obesity.