Diabetes 2 epidemic from pollution?
Maybe. Phyllida Brown writes in New Scientist:
ON 10 July 1976, a reactor at a chemical plant near the small town of Seveso in northern Italy exploded, sending a toxic cloud drifting into the summer sky. Around 18 square kilometres of land was contaminated with TCDD, a member of the notorious class of industrial chemicals known as dioxins.
The immediate after-effects were relatively mild: 15 children landed in hospital with skin inflammation and around 3300 small animals were killed. Today, however, the accident casts a long shadow over the people of Seveso, who are suffering increased numbers of premature deaths from cancer, cardiovascular disease and, perhaps surprisingly, diabetes (American Journal of Epidemiology, vol 167, p 847).
To some diabetes researchers, Seveso serves as a warning to us all. Ask why diabetes is epidemic in the 21st century and most people will point the finger at bad diet, laziness and obesity. According to a small but growing group of scientists, though, the real culprit is a family of toxic chemicals known as persistent organic pollutants, or POPs. If these researchers are right, POPs – which include some of the most reviled chemicals ever created, including dioxins, DDT and PCBs – may be key players in the web of events that lead people to develop the disease.
The claim has yet to attract widespread attention from mainstream diabetes research. Even its champions were initially surprised by it. “I had never even heard of POPs until 2005,” says Duk-Hee Lee, an epidemiologist at Kyungpook National University in Daegu, Korea, who led the work. Lee and her co-workers are now convinced, albeit reluctantly, that they are onto something. “The hypothesis is one that I wish were not true,” says her colleague David Jacobs of the University of Minnesota, Minneapolis.
Diabetes, and particularly its commonest form, type 2 (see “Diabetes basics”), is practically everyone’s business. The World Health Organization estimates that it already affects 180 million people worldwide, with the number predicted to more than double by 2030. Last year the epidemic cost $174 billion in the US alone, according to the American Diabetes Association.
The standard explanation for type 2 diabetes is that it is a “lifestyle disease” caused by laziness and gluttony. For at least a decade, however, epidemiologists have known that people briefly exposed to high concentrations of POPs face a modest increase in their risk of developing diabetes later in life. Those affected include the people of Seveso and US veterans who were exposed to dioxin-contaminated Agent Orange during the Vietnam war.
Two years ago, Lee, Jacobs and others decided to see whether everyday exposure to POPs is also linked to diabetes. To their surprise and horror, they found that it is.
For most people, POPs are inescapable: meat, fish and dairy products all contain them. They enter the food chain from sources such as pesticides, chemical manufacturing and incinerated waste, and accumulate in animals higher up in the chain. Once in the body they take up residence in fat.
POPs have long been recognised as nasty substances: their effects include birth defects, cancer, immune dysfunction and endocrine disruption. Since the 1970s, various measures have been put in place to phase them out – 12 of the worst POPs, known as the “dirty dozen”, (see table) were banned in 2004 – but despite these efforts, POPs remain a significant presence in the environment and food chain, partly because many are still in use in the developing world, and partly because these chemicals can take decades to break down.
Role of fat
Prior to her 2005 introduction to POPs, Lee was working on a humble enzyme called gamma-glutamyltransferase (GGT), which is essential for maintaining antioxidant levels in the liver. She was puzzled to find that obesity combined with an elevated level of GGT is a strong predictor of diabetes, but obesity alone isn’t. “I searched the literature and finally got an idea,” she says.
As it turns out, GGT has an essential role to play in removing some pollutants, including POPs, from inside cells (Diabetologia, vol 51, p 402). Could increased GGT activity simply be a marker of exposure to POPs?
To find out, Lee and her colleagues analysed data from more than 2000 people in the US National Health and Nutrition Examination Survey (NHANES), which measured both diabetes status and bloodstream levels of POPs, among other things. They discovered that people with high levels of six different POPs in their bloodstream were much more likely to have diabetes, regardless of obesity (see diagram). The six POPs were chosen because they were detectable in at least 80 per cent of the participants.
Taking into account factors such as weight, age, waist circumference and ethnic group, Lee calculated that in people with the highest combined levels of all six POPs the rate of diabetes was a massive 38 times greater than in those with the lowest levels (Diabetes Care, vol 29, p 1638). “The people who disagree with us will say it’s all noise,” says Jacobs, “but it’s pretty hard to get odds ratios of 38 with noise.”
To her even greater surprise, Lee found that in people with undetectable levels of POPs the expected link between diabetes and body weight melted away – those who were obese were no more likely to have diabetes than their lean counterparts. “This suggests that POPs may be a more fundamental factor in the risk of diabetes than obesity,” says Lee. “The absolute risk of diabetes was extremely low among subjects with very low concentrations of POPs.” …
The full article, along with several diagrams, graphs, and charts, is found here, but you must subscribe to New Scientist to read it. (On-line only subscription is $39 for a year.)