A Nutrient Found in Red Meat Could Make Dangerous Inflammation Even Worse

A nutrient known for helping the body burn fat may also cause inflammation when the immune system is in overdrive.

Yale researchers found that L-carnitine, a nutrient abundant in red meat and widely used in exercise and weight-loss supplements, could worsen severe inflammation in mice. After a bacterial component triggered inflammation and sharply lowered blood levels of L-carnitine, restoring the nutrient made the animals sicker, suggesting the decline was protective.

The findings were published October 19 in Cell.

L-carnitine is best known for helping cells turn fat into energy. The body produces it naturally, and skeletal muscle contains particularly high concentrations.

“L-carnitine helps transport fats into mitochondria so they can be broken down for energy,” says Eric Elliott, MD, PhD, assistant professor of medicine (infectious diseases) at Yale School of Medicine (YSM) and the study’s first author. “In simpler terms, it has become synonymous with fat burning, which is why it has also gained prominence as an exercise and weight-loss supplement.”

The team was investigating metabolic changes during sepsis, a life-threatening condition in which the body’s response to infection damages its own tissues and organs. Much of that damage can come from uncontrolled inflammation rather than a failure to contain the infection.

“Sepsis is incredibly challenging,” Elliott says. “Patients with sepsis can become critically ill, and among patients with sepsis treated in intensive care units, some studies report mortality rates approaching 40%.”

To model the inflammation associated with sepsis, the researchers exposed mice to lipopolysaccharide (LPS), a bacterial component. When L-carnitine levels in the animals’ blood dropped sharply, the team tested whether restoring the nutrient would improve their outcomes.

Replacing the Nutrient Made Things Worse

“We predicted giving carnitine back to these animals might improve their outcomes, but they actually did much worse,” Elliott says. “That told us the reduction in carnitine was an adaptive response.”

To understand why, the researchers conducted experiments in mouse and human immune cells. They found that L-carnitine activated part of the cell’s internal alarm system called the pyrin inflammasome. This triggered an inflammatory response involving the immune signaling molecule IL-17 and increased deaths among the mice.

“What was particularly striking was how detrimental IL-17 was in this model,” Elliott says. The team now wants to investigate whether blocking IL-17 might eventually help a subset of patients with sepsis, although that possibility remains untested.

The findings offer a potential research direction in a field where treatment advances have been limited. “We have made frustratingly little progress in improving sepsis treatment beyond learning how to better deliver fluids, antibiotics, and medications that support blood pressure,” Elliott says.

Damaged Muscle May Fuel Inflammation

Because skeletal muscle contains high levels of L-carnitine, the researchers suspected that its release from damaged muscle could help drive inflammation. Senior author Andrew Wang, MD, PhD, associate professor of medicine (rheumatology, allergy & immunology) and of immunobiology at YSM, says the pathway may have implications beyond sepsis.

“There is tantalizing genetic evidence that the pathway we uncovered could be contributing to inflammation in a variety of diseases, particularly diseases in which muscle involvement has perhaps been thought to be a casualty of the disease rather than a potential driver,” Wang says.

The team found support for this idea in rhabdomyolysis, a condition in which skeletal muscle rapidly breaks down and releases its contents into the bloodstream, potentially causing acute kidney injury. In a mouse model, L-carnitine transport and pyrin inflammasome activation contributed to inflammation, suggesting that immune cells may interpret L-carnitine released from damaged muscle as a warning signal.

The pathway could also be relevant to cardiovascular disease, inflammatory bowel disease, and cancer. Further research is needed to determine whether it contributes to these chronic inflammatory conditions.

What the Findings Mean for Diet

People who eat meat get most of their L-carnitine from food. Vegetarians and vegans tend to make more of it within their bodies, but their overall levels remain lower. The study examined L-carnitine on its own, so the findings do not directly show how eating red meat or taking supplements affects inflammation.

“We did not study red meat as a whole, and carnitine by itself did not induce inflammation,” Elliott says. “A substantial background of inflammation was required, and we do not yet know what inflammatory context might produce this effect in people. We cannot say that carnitine supplementation or heavy red meat consumption is always harmful. It is probably safe most of the time, but there may be specific circumstances in which it becomes a problem.”

Understanding those circumstances is a priority for the team. The researchers want to learn how individual food components interact with a person’s underlying health and inflammatory state and why the same nutrient might have different effects under different conditions.

“Food science currently exists in the realm of phenomenology,” Wang says. “I think that a deep understanding of all the elements that make up food, akin to a periodic table, will be required to understand what makes a ‘good’ or ‘bad’ diet for a particular individual in a particular health state.”

Reference: “The pyrin inflammasome senses OCTN2-mediated uptake of extracellular ʟ-carnitine from muscle injury or ingestion” by Eric I. Elliott, Tomomi M. Yoshida, Susana C.B.R. Nakandakari, Scott Pope, Cuiling Zhang, Timothy Nottoli, Jae Jin Chae, Daniel L. Kastner, Richard A. Flavell, Vishwa Deep Dixit, Vijay A. Rathinam, Fayyaz S. Sutterwala and Andrew Wang, 19 October 2026, Cell.
DOI: 10.1016/j.cell.2026.09.015

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