Low-level cadmium toxicity and fatty liver disease

A recent study concluded that it’s more difficult for adults today to maintain the same weight as those a few decades ago, even with the same levels of food intake and exercise. On one level, this news is comforting to anyone in middle age, who may have been athletic as a teenager in the 1980s but isn’t anymore. It’s just harder nowadays!

However, the study authors also suggested, in an interview with The Atlantic’s Olga Khazan, an array of factors that might be contributing to the rise in obesity: exposure to chemicals such as pesticides and flame retardants, prescription drugs such as antidepressants, and altered microbiomes linked with antibiotic use in livestock.

The heavy metal cadmium may belong on that list of chemicals, not primarily as a booster of obesity, but instead in connection with the increase in prevalence in NAFLD (non-alcoholic fatty liver disease) over the last few decades.

Researchers led by Young-Mi Go and Dean Jones exposed mice to low levels of cadmium, so that the amounts of cadmium in their livers were comparable to those present in average middle age Americans, without tobacco or occupational exposure. They observed that cadmium-treated mice had more fat accumulation in the liver and elevated liver enzymes in their blood, compared with control mice with 10 times less cadmium.

Cadmium accumulates in the body over time. Tobacco smoke and the industrial workplace can be routes for cadmium exposure, but food is the major source for most non-smokers. Until the 1990s, most batteries were made with cadmium, and much cadmium production still goes into batteries. It is also found in paint and in corrosion-resistant steel.

Jones notes that population-based cadmium exposure continues to decrease, because fewer people are smoking. “The key change is that now that smoking contribution is getting low, it is easier to recognize the effect of Cd in non-smokers,” he emails.

It was already known that high levels of cadmium exposure can lead to weakened bones and kidney failure, such as in “itai-itai disease” in Japan, and cadmium is a known carcinogen. But the effects of lower levels of cadmium, which many people are exposed to, are still unclear.

Usually researchers tend to blame sugar, whether it’s fructose or sucrose, for the increase in NAFLD in recent decades. But this finding suggests that cadmium toxicity may be contributing to liver disease as well.

A 2013 study from Johns Hopkins, drawing upon NHANES data, found that people in the top quartile for levels of cadmium in their urine were more than three times more likely to die of liver disease. Still, in many cases, NAFLD would not be expected to be lethal, even if it does contribute to diabetes and cardiovascular disease.

The top quartile of exposure also had more NAFLD (measured via liver enzymes/ultrasound), but not three times more. Men showed stronger effects than women.

Perhaps the main issue is not so much causing fatty liver, but in promoting progression of fatty liver from simple steatosis to NASH, a condition with inflammation and fibrosis that can lead eventually to liver failure. “My concern is that a 20- to 30-year disease course from fatty liver to NASH could be shortened to 15-20 years with considerable health and economic consequences,” Jones emails.

Note for Emory readers: Jones and Go are hosting a workshop Wednesday, November 4, with guests from the Karolinska Institute and other US universities, on cadmium and selenium.

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Quinn Eastman

Science Writer, Research Communications qeastma@emory.edu 404-727-7829 Office

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