Until recently, it was called “nonalcoholic fatty liver disease.” Now, notes a research team in a recent issue of the peer-vetted journal Environmental Research, it’s referred to as metabolic-dysfunction-associated steatotic liver disease.”

This naming shift may help underscore that it’s not only individuals of drinking age who are vulnerable to the diagnosis. In fact, in their study, a team of 22 U.S. researchers specializing in fields like public health and pediatrics, investigated what they called the “growing” phenomenon of this type of fatty liver disease among young people—specifically, 284 individuals ranging in age from 8 to 23.

“The study aimed to evaluate associations between [per- and polyfluoroalkyl substances] and MASLD risk and the modifying role of age, lifestyle factors, and genetic risk,” state the authors in the abstract. Eight types of PFAS—the “forever chemicals” formally called per- and polyfluoroalkyl substances—were also measured within the blood.

Data from these young people was collected and tracked for between four- and 12-year spans. The youngest participants had been part of the Study of Latino Adolescents at Risk of Type 2 Diabetes, while the elder group were part of the Metabolic and Asthma Incidence Research. This type of fatty liver disease had been diagnosed if MRI imaging showed greater than 5.5% “hepatic fat fraction,” while values such as body mass index, fasting glucose, cholesterol, and blood pressure were also taken into account.

The researchers concluded: “Our findings support that PFAS may increase the risk of [metabolic-dysfunction-associated steatotic liver disease] in youth.”

In adolescents, higher blood levels of PFOA (a common PFAS) were associated with roughly 2.7 times higher odds of developing fatty liver disease, with each doubling of exposure. That risk grew as adolescents got older, suggesting a cumulative effect—one reason for the nickname “forever chemicals.”

Older kids who also carried a risk variant of a gene that regulates liver fat saw even greater risk, possibly highlighting an interplay between genetic predisposition and habits.

Among smokers, several PFAS were associated with meaningfully higher fatty liver risk. Overall, age, smoking, and a specific genetic variant all appeared to increase susceptibility.

The study doesn’t assert that PFAS cause fatty liver disease, per se. There’s a good chance eating the type of foods that carry the most “forever chemicals” also contribute to the breakdown of good metabolic health.

Other factors that can contribute to PFAS consumption are drinking water, food packaging, some types of cookware, and even using cooking utensils made of synthetic materials (as an example, one expert told us using a wooden cutting board, instead of a plastic one, is a way to cut down consumption). Black plastic containers, like those used for takeout, may also heighten exposure.

Because PFAS have also been associated with processed foods and their packaging, the research serves as a reminder eat fresh and natural, whenever you can.

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