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You probably don’t notice it when you pick up a “sugar-free” protein bar or reach for a low‑calorie soda. It tastes familiar, like sugar. It won’t spike your blood sugar. It’s marketed as harmless. But new laboratory work raises a worrying question: might erythritol, the sugar alcohol found in thousands of packaged foods, chip away at the brain’s natural defenses?
Researchers at the University of Colorado exposed cultured cells that form the blood‑brain barrier to concentrations of erythritol comparable to those measured after drinking a sweetened soft drink. The result was more than a shrug from stressed cells. What scientists observed reads like a chain reaction: an onrush of oxidative stress, loss of antioxidant protection, impaired cell function and, in some cases, cell death. Short phrase: the barrier weakened.
How a sweetener could unsettle brain protection
The blood‑brain barrier acts like selective security at an airport: it lets nutrients and essential molecules through, and blocks toxins and pathogens. Endothelial cells and supporting structures do the heavy lifting. When those cells suffer oxidative stress — a biochemical mismatch that floods them with reactive molecules known as free radicals — their ability to regulate permeability and vessel tone falters.
In the Colorado study, erythritol tipped that balance. Cells produced fewer antioxidant defenses and more markers of damage. At the same time, the sweetener interfered with two central regulators of blood‑vessel behavior: nitric oxide, which relaxes vessels, and endothelin‑1, which constricts them. With nitric oxide suppressed and endothelin‑1 elevated, blood vessels may remain constricted when they should dilate. That mismatch can reduce oxygen and nutrient delivery to brain tissue — conditions that favor ischaemic stroke, the kind caused when a clot blocks blood flow.
There was another troubling finding. When blood clots form, the body normally mobilizes tissue plasminogen activator (tPA), an enzyme that helps break down clots before they cause lasting damage. Erythritol appeared to blunt this response in the cultured cells, potentially allowing clots to persist longer and increase stroke risk.
These mechanistic clues line up with patterns seen in epidemiology. Several observational studies have reported higher rates of cardiovascular events among people with elevated blood levels of erythritol. One large cohort found that participants in the highest quartile of erythritol exposure had about twice the risk of major cardiac events compared with those in the lowest quartile.
Context, caveats and why more testing matters
There are important limits to keep in mind. The new work used isolated cells in petri dishes. Cells out of their native environment may be more sensitive to stressors than those embedded in intact vessels or whole organisms. Whole blood flow, immune interactions, and organ‑level feedback loops are missing from such setups. That’s why scientists recommend follow‑up studies using more sophisticated models — for example, microfluidic “blood vessel on a chip” systems that reproduce flow and tissue architecture better than static cell cultures, and ultimately controlled animal and human studies.
Still, the mechanisms observed — oxidative stress, altered nitric oxide and endothelin‑1 balance, and impaired clot resolution — are well‑established contributors to vascular disease. Seeing them triggered by erythritol in a lab setting is clinically meaningful, not merely anecdotal.
Erythritol occupies a special place among sugar substitutes. It’s a sugar alcohol produced naturally in small amounts by the body and found in some fruits, which helped it sidestep recent World Health Organization guidance that cautioned against many artificial sweeteners. It tastes like sugar — about 70–80% as sweet — and behaves like sugar in recipes, so food makers favor it. That utility explains its ubiquity: protein bars, energy drinks, “keto” snacks and thousands of processed foods now list erythritol on the ingredient panel.
Regulators such as the European Food Safety Authority and the U.S. Food and Drug Administration currently recognize erythritol as safe based on available data. What this new research does is nudge the conversation toward nuance: safety assessments built on short‑term toxicity may miss subtle, chronic effects on vascular and brain health that accrue over months or years of repeated exposure.
Expert Insight
“We shouldn’t panic,” says Dr. Laura Mendes, a vascular physiologist and science communicator. “But we should pay attention. When a compound interferes with nitric oxide signaling and clot‑dissolving pathways in model systems, it raises a red flag. The appropriate next steps are targeted animal studies and well‑designed human trials that measure vascular function, clotting biomarkers and cognitive outcomes over time.”
Dr. Mendes adds: “For clinicians and consumers, the practical takeaway is simple: treat erythritol like any additive — useful in moderation, questionable in excess. If you’re relying on multiple ‘sugar‑free’ products every day, reconsider the habit.”
The broader lesson touches nutritional science at large. New food additives can be rapidly adopted by industry and consumers before long‑term physiology is fully understood. That gap creates a trade‑off: immediate benefits, like fewer calories and better glucose control, weighed against possible chronic costs to cardiovascular or brain health.
Until more definitive human data arrive, people who use erythritol heavily — daily sodas, bars, or chains of low‑calorie snacks — may want to reassess. Choose whole foods more often. Ask manufacturers for transparency. And support research that moves beyond cells in dishes to models and trials that reflect how our bodies really operate.
Source: sciencealert
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