At Karolinska Institutet, scientists have uncovered a quiet but consequential partnership between the food we eat and the bacteria that inhabit us: microbes in the gut transform iron and nitrate from leafy vegetables into protective molecules that appear to guard the heart and metabolism. Published in Cell, the discovery does not simply confirm that vegetables are good for us — it begins to explain the hidden chemistry by which they become so. The finding invites a deeper question about individuality: if our microbiota shapes how we extract benefit from food, then two people eating the same me
Gut bacteria transform spinach and beets into heart-protective compounds
Gut bacteria unlock protective compounds from vegetables we eat
So the bacteria in our gut are essentially processing vegetables into something our body can use to protect itself?
Exactly. They're taking nitrate and iron from the plants and converting them into these molecules—DNICs—that then get absorbed and travel to organs like the liver and kidneys. It's a partnership.
But we should be clear: this is all demonstrated in mice and cell cultures so far. The human relevance is still theoretical.
Right. That's why the researchers are explicit about that. They're saying the mechanism exists and it works in their models, but they need to measure it in actual humans before we know if it matters clinically.
What would it mean if it does work in humans the same way?
It would mean that eating vegetables isn't just about getting vitamins and fiber. It's about feeding your microbiota so they can make these protective compounds for you.
And it would also mean that if someone's microbiota is disrupted—say, by antibiotics—they might lose this benefit even if they're still eating the same vegetables.
That's a really important point. The bacteria have to be there and functioning.
So the next step is figuring out how to measure this in people and whether we can actually boost it?
Yes. They want to see if diet changes or even targeted microbiota interventions could raise DNIC levels enough to prevent disease.
Which is still years away from any clinical application. But it's a solid foundation for that work.
El Pulso
- A class of molecules called DNICs — previously undetected in this context — has been found circulating through the organs of animals fed plant-based nutrients, produced entirely by gut bacteria.
- The complete absence of these molecules in germ-free mice created a striking alarm: without a microbiome, the protective conversion simply does not occur, no matter how many vegetables are consumed.
- In diseased animal models, raising DNIC levels brought measurable relief — lower blood pressure, steadier blood sugar, less liver fat — suggesting a mechanism potent enough to matter clinically.
- The gap between animal model and living human remains wide, and researchers are now racing to build the measurement tools needed to detect DNICs in people before any therapeutic claims can be made.
- The deeper disruption may be conceptual: nutrition science may need to account not just for what we eat, but for which bacteria we carry to unlock what we eat.
At Karolinska Institutet, scientists have uncovered a quiet but consequential partnership between the food we eat and the bacteria that inhabit us: microbes in the gut transform iron and nitrate from leafy vegetables into protective molecules that appear to guard the heart and metabolism. Published in Cell, the discovery does not simply confirm that vegetables are good for us — it begins to explain the hidden chemistry by which they become so. The finding invites a deeper question about individuality: if our microbiota shapes how we extract benefit from food, then two people eating the same meal may not be receiving the same medicine.
Scientists at Karolinska Institutet have identified a hidden step between eating vegetables and benefiting from them: gut bacteria. The research, published in Cell, shows that microbes in the intestine convert dietary nitrate and plant-based iron — found in spinach, beets, beans, and dark leafy greens — into molecules called dinitrosyl iron complexes, or DNICs, which then travel through the body and appear to protect cardiovascular and metabolic health.
The team traced this process using mouse experiments, cell cultures, bacterial samples, and human tissue, employing advanced analytical methods to detect DNICs across multiple organs. The decisive observation came from germ-free mice: animals raised without any microbiota showed no DNICs at all. The bacteria, it turned out, are not incidental — they are the mechanism.
When DNIC levels were elevated in animal models of disease — through dietary supplements or synthetic versions of the molecules — the results were consistent and encouraging. Blood pressure fell, vascular function improved, blood sugar stabilized, and liver fat decreased. Professor Mattias Carlström noted that this helps explain why vegetable-rich diets correlate with lower rates of heart disease: the benefit is not simply nutritional, it is microbial. First author Andrei Kleschyov framed it plainly — gut bacteria convert food components into biologically active molecules that shape how the body functions.
The researchers are deliberate about what remains unproven. The work was conducted primarily in animals and isolated human samples, and the path to human validation is neither short nor guaranteed. Their next steps include developing reliable methods to measure DNICs in living people, mapping how the molecules move through the body, and determining whether diet or microbiota adjustments can raise DNIC levels meaningfully enough to prevent disease. They also want to understand whether certain bacterial strains perform the conversion more efficiently — and whether differences in individual microbiomes explain why some people extract more benefit from the same plant-based meal than others.
Scientists at Karolinska Institutet have identified a previously hidden mechanism by which vegetables protect the heart and metabolism: gut bacteria transform compounds found in spinach, beets, and leafy greens into molecules that circulate through the body and strengthen cardiovascular function. The discovery, published in Cell, reveals that the microbiota in our intestines acts as a chemical factory, converting dietary nitrate and nonheme iron—the form of iron present in plant foods like beans, whole grains, and dark leafy vegetables—into compounds called dinitrosyl iron complexes, or DNICs.
The research team used a combination of mouse experiments, cell cultures, bacterial samples, and human tissue to trace this transformation. They employed advanced analytical methods to detect DNICs in various organs and made a striking observation: the molecules were completely absent in germ-free mice, animals raised without any microbiota. This finding established that gut bacteria are essential to the process. Without them, the conversion simply does not happen.
When the researchers increased DNIC levels in animal models of cardiovascular and metabolic disease—either by adding dietary supplements containing nitrate and iron, or by administering synthetically produced DNICs—measurable improvements followed. Blood pressure dropped. Blood vessel function improved. Blood sugar control became more stable. Fat accumulation in the liver decreased. These results, Mattias Carlström, a professor of cardiorenal physiology at the institute, noted, help explain why populations that eat diets rich in vegetables have lower rates of heart disease and metabolic disorders. The mechanism is not simply that vegetables contain nutrients; it is that the body's own bacteria unlock protective compounds from those nutrients.
Andrei Kleschyov, the study's first author, emphasized the broader implication: "Our results show that gut bacteria can convert components in food into biologically active molecules that influence important bodily functions." The finding points to a new layer of interaction between diet, the microbiota, and human health—one that had not been clearly mapped before.
Yet the researchers are careful to mark the boundary between what they have shown and what remains unknown. The experiments were conducted primarily in animal models and isolated human samples. The leap from mouse to human physiology is not automatic. The team has outlined the next phase of investigation: developing methods to measure DNICs reliably in living humans, understanding how these molecules move through the body, and determining whether dietary changes or deliberate shifts in the microbiota composition can raise DNIC levels enough to prevent disease. They also want to know whether certain bacterial strains are more efficient at this conversion than others, and whether individual differences in microbiota composition explain why some people benefit more from a vegetable-rich diet than others. The collaboration included researchers from medical centers in Hamburg and Mainz, Germany, and the work now awaits the slower, more complex process of human validation.
Citas Notables
Gut bacteria can convert components in food into biologically active molecules that influence important bodily functions— Andrei L. Kleschyov, senior researcher, Karolinska Institutet
The results help explain why a diet rich in vegetables is linked to a lower risk of several diseases— Mattias Carlström, professor of cardiorenal physiology, Karolinska Institutet