An unusual form of diabetes may be caused by drinking arsenic-contaminated water

Like a careless criminal, even small amounts of toxic arsenic leave telltale fingerprints on victims’ bodies—although these fingerprints are different if the victim as Type 2 Diabetes, scientists report. And arsenic has many potential victims: more than 200 million people worldwide drink freshwater naturally contaminated with small amounts of arsenic. But for the first time, scientists have captured arsenic’s molecular fingerprint in the body fluids of people with and without diabetes from arsenic-contaminated Chihuahua, Mexico. By capturing these molecular fingerprints, the scientists have taken the first step towards reconstructing how arsenic may cause a little-understood form of Type 2 Diabetes.

While arsenic has many potential victims, Type 2 Diabetes has many confirmed ones. Roughly one out of fifteen adults—approximately 256 million people worldwide—has Type 2 Diabetes, and the excess glucose in their blood can damage their heart, kidneys, and nerves over time. But while people who drink arsenic-contaminated water are more likely to develop Type 2 Diabetes, scientists have observed that these arsenic-linked diabetics are different from most diabetics. Unlike most diabetics, their cells react normally to insulin, a hormone released by the pancreas that tells the cells to gobble up glucose from the blood. The problem—at least, the problem in arsenic-drinking lab rats which develop rat diabetes—is that the pancreas’s insulin-making cells seem to be poisoned by arsenic.

To figure out if this is true in humans, the scientists studied 176 people in Chihuaha, where the municipal water is contaminated with more than twice the WHO’s safety limit for arsenic. For each person with Type 2 Diabetes, the scientists matched them to another person the same gender, age, body-mass index, and the amount of arsenic in their tap water at home. The people with and without diabetes then donated their urine and blood plasma—body fluids which contain hundreds of known metabolites, the chemical residues of metabolism.

By examining the pattern of these metabolites, the scientists reconstructed how arsenic had changed people’s metabolism. When they looked at the metabolites unique to people who drank arsenic-contaminated water, they found that the people with diabetes had very different types of metabolites than people without diabetes. The diabetics’ different metabolites suggested that arsenic had changed how their bodies metabolize vitamins and amino acids, as well as how they get energy from food. Surprisingly, the metabolite pattern of the arsenic-linked diabetics was also very different from the metabolite patterns of most diabetics—providing the scientists with “a metabolic fingerprint” that hinted at molecular differences between these forms of diabetes.


Martin, E., Gonzalez-Horta, C., Rager, J., Bailey, K., Sanchez-Ramirez, B., Ballinas-Casarrubias, L., Ishida, M., Gutierrez-Torres, D., Hernandez Ceron, R., Viniegra Morales, D., Baeza Terrazas, F., Jesse Saunders, R., Drobna, Z., Mendez, M., Buse, J., Loomis, D., Jia, W., Garcia-Vargas, G., Del Razo, L., Styblo, M., & Fry, R. (2015). Metabolomic Characteristics of Arsenic-Associated Diabetes in a Prospective Cohort in Chihuahua, Mexico Toxicological Sciences, 144 (2), 338-346 DOI: 10.1093/toxsci/kfu318

Uterine fibroid growth increases with cadmium exposure, but not because cadmium acts like estrogen

Breathing or eating even small amounts of the toxic metal cadmium—a widespread contaminant of cigarettes and seafood—may increase a woman’s risk for developing uterine fibroids, but not in the way scientists previously thought. By the age of 50, at least seven out of ten American women will have developed these benign tumors that can cause infertility and miscarriage. Scientists have long suspected that cadmium encourages fibroid growth by mimicking the natural hormone estrogen. However, new research published this month in Environmental Health Perspectives indicates that cadmium may instead encourage fibroid growth through a molecular pathway involved in a third of all tumors. The North Carolina researchers suggest that treatments targeting this pathway may block cadmium’s dangerous effects, and help limit the growth and damage of uterine fibroids in women.

To figure out how cadmium encourages fibroid growth, the researchers added it to different types of uterus-like cells grown in Petri dishes. When they grew the cells with low concentrations of cadmium—concentrations similar to the cadmium blood levels of more than 70% of Americans—they found that the metal greatly increased the number of cells, similar to how estrogen increases the number of uterus cells. But the similarity stopped there: while estrogen increased cell growth by interacting with estrogen receptors—molecules on a cell’s surface which relay signals to its nucleus, thereby affecting which genes turn on and off—the cadmium did not interact with the estrogen receptors.

So how was cadmium increasing the uterus cells’ growth? The researchers figured out the answer when they looked at other molecules involved in cell signaling—specifically, the MAPK pathway, a series of signal molecules involved in both healthy cell growth and cancerous cell growth. When they exposed the uterus cells simultaneously to cadmium and to chemicals that interfere with the MAPK pathway, they found that cadmium couldn’t increase cell growth. While cadmium didn’t increase cell growth by interacting with estrogen receptors, the researchers suggested that it may act together with estrogen naturally present in a woman’s body (or estrogen-like molecules such as bisphenol A) to increase fibroid growth more than cadmium or estrogen alone could.

Gao X, Yu L, Moore AB, Kissling GE, Waalkes MP, & Dixon D (2015). Cadmium and Proliferation in Human Uterine Leiomyoma Cells: Evidence of a Role for EGFR/MAPK Pathways but Not Classical Estrogen Receptor Pathways. Environmental health perspectives, 123 (4), 331-6 PMID: 25343777