What we know about plastic and your liver

Your liver has an important job. Almost everything you eat, drink, or swallow passes through it before it ever reaches the rest of you. That design is what keeps you safe from most of what shows up on your plate.

It also means that if something slips past the wall of your gut, the liver is the very next stop.

Why the liver sees everything first

Blood leaving your intestines does not go straight back to your heart. It first travels through a large vessel called the portal vein, which delivers about three-quarters of the liver's blood supply. From there it fans out into a dense network of tiny, leaky capillaries lined with cleanup cells called Kupffer cells.

Think of it as a customs checkpoint. Nutrients pass through and get distributed. Anything the body wants to break down, store, or flag gets pulled aside. It is a beautiful piece of plumbing when the cargo is food.

It is less beautiful when the cargo includes particles the body never evolved to handle.

In April 2026, researchers at the University of Plymouth published a review in Nature Reviews Gastroenterology & Hepatology laying out what is known, and what is not, about how tiny plastic particles interact with the liver ^[1]. They floated a working idea they call “plastic-induced liver injury.” It is not a diagnosis. It is a question being tested.

What has actually been found in human livers

Two studies anchor the human side of this story.

In 2022, a team led by Horvatits examined liver tissue from a small group of patients. They found six different kinds of plastic in the tissue of people with cirrhosis, and none in the livers of people without underlying liver disease ^[2]. That was the first direct look at plastic sitting in a human liver.

It is also a small study, and the direction of cause and effect is genuinely open — did a damaged liver simply let more plastic through, or did plastic help injure it? The data cannot say.

A larger 2025 study from Nihart and colleagues, mostly focused on the brain, also looked at liver tissue ^[3]. They reported a meaningful amount of polymer material per gram of liver, with polyethylene as the most common type. Samples collected in 2024 carried more plastic than samples archived in 2016.

Both studies show that plastic, or at least a plastic-like signal, reaches the human liver. Neither shows that it causes disease there.

For a longer look at the measurement science behind these numbers, and their limitations, see The challenge of measuring plastics in humans.

What the animal work is starting to show

Where the picture gets a bit sharper is in mice.

In several studies, adding tiny plastic particles to a high-fat diet made liver injury worse than the high-fat diet alone ^[4-5]. The particles did not appear to cause disease from scratch. They amplified damage that another factor had already started — what researchers call a “second-hit” effect.

A 2025 study pushed this further using very low doses of plastic, closer to what a person might actually encounter, and still found the animals became more vulnerable to fatty liver disease ^[6]. The pathway ran through the gut first, then to the liver. Our companion piece on the gut and microplastics covers that gut side in more depth.

Most of this work has used polystyrene, but researchers have now seen similar patterns with PET, the plastic used in most single-use bottles ^[7].

Why fatty liver disease keeps coming up

Fatty liver disease is now the most common chronic liver condition in much of the world. It has plenty of well-established causes — weight, insulin resistance, diet, genetics, alcohol — none of which have anything to do with plastic.

But the mouse work suggests plastic may act as an amplifier on top of those causes rather than a stand-alone driver. That is a very different claim from “plastic causes fatty liver disease in people.” On the current evidence, that stronger claim is not supported.

What we still do not know

The list of open questions is long, and worth being honest about.

• No study has followed a group of people over time and connected plastic in their liver to whether they later developed liver disease.
• Current techniques cannot always tell whether particles are truly lodged in liver tissue or simply passing through.
• Doses used in animal studies are often much higher than what a person encounters day to day.
• Plastics carry other chemicals (such as plasticizers, additives, PFAS) and it is not yet clear how much of the observed harm comes from the particles themselves versus what they carry.

None of that makes the signal go away. It just means the honest step from “seen in mice” to “matters in people” has not been made yet.

Notes on the science

One important caveat to the human numbers: the main technique used to weigh plastic in tissue works by burning the sample and reading the resulting fragments. In fatty tissue like liver, some of the body's own lipids can produce fragments that look very similar to the ones used to identify plastics, which can inflate the estimate ^[8]. The Nihart paper is the subject of an active back-and-forth in Nature Medicine on this exact point ^[9-10] The measurement is real; the exact numbers should be read with room to move.

Where Winnow fits in

The liver is one of many reasons people are paying closer attention to what plastic is doing in the body. That concern is reasonable, and the science supporting it is moving quickly.

Winnow’s work sits upstream, within the gut lumen — before anything reaches the portal vein or the liver at all. Our probiotic strains have been shown in laboratory testing to bind micro- and nanoplastics within the gut lumen, with the aim of reducing what the digestive system has to handle in the first place.

A probiotic cannot address plastic that is already in tissue, and we would not suggest otherwise. But the everyday work of supporting your gut is a reasonable place to start.