Erythritol and Cardiovascular Health: What the Research Actually Shows

In February 2023, a study in Nature Medicine found that people with higher levels of erythritol in their blood experienced more cardiovascular events over the following three years. We published our analysis at the time: Erythritol and Cardiovascular Health, March 2023. Below, you’ll find our update on what the research has shown since.

In This Article

• Why blood erythritol and dietary erythritol aren’t the same thing
• What cardiovascular studies published since 2023 have found
• What research suggests about erythritol, blood clotting, and cardiovascular risk
• What the FDA and EFSA currently say about erythritol safety
• How much erythritol was previously used in NOVOS Core
• Why NOVOS ultimately removed erythritol from the formula

What Recent Research Says About Erythritol and Heart Health

Three years of further research have changed the picture in both directions. The association has been looked for in larger groups of people, with mixed results depending on the outcome measured ^{[5, 7, 8]}. Research has also drawn more attention to an important distinction: erythritol in the blood doesn’t come only from food. The body also produces it from glucose. That makes it difficult to know whether higher blood levels are contributing to cardiovascular risk or are a marker of underlying metabolic processes ^{[9, 10,11]}.

Two regulators have now examined the question. After a full re-evaluation, the European Food Safety Authority concluded that “a causal relationship between dietary exposure to erythritol and cardiovascular disease risk has not been demonstrated by the available studies,” while adding that “further studies might be helpful to clarify the nature of the association” ^[2]. The U.S. Food and Drug Administration determined that the observational studies “did not establish a causal link between consuming erythritol and the observed effects”^[3]. NOVOS Core no longer contains erythritol. Later in this article, we explain why we removed it and how that decision relates to the evidence.

Blood Erythritol Isn’t the Same as Dietary Erythritol

Erythritol can enter your bloodstream in two ways: from the foods you eat, and from your body’s own production. The body naturally produces erythritol from glucose through a metabolic route called the pentose phosphate pathway ^[2]. That distinction matters. When a study measures erythritol in the blood, it is measuring a combination of what a person consumed and what their body produced, not dietary erythritol alone.

Figure 1. Two routes to the same measurement. Erythritol in the blood is partly what a person ate and partly what their body produced from glucose. Almost every study linking erythritol to cardiovascular events measured the blood level and could not distinguish the two.

Almost every study reporting a link between erythritol and cardiovascular events measured the amount circulating in blood, not the amount people ate ^{[1, 5, 7, 8]}. One measured it in urine ^[18]. Very few studies have estimated dietary intake, and fewer still have given people a known quantity and watched what happened.

That matters because of what has been learned about the endogenous side since 2023:

• In male mice, sugar intake rather than a high-fat diet drove erythritol production. Removing either of the two enzymes thought to be responsible did not change erythritol levels ^[9]. (Animal studies are not relied upon to support any representations of health benefit in humans.)
• In cell studies, a muscle cell line raised its internal erythritol under both high glucose and oxidative stress, while human kidney cells did not respond to oxidative stress in the same way ^[10].
• Across 218 fasting plasma samples from lean young adults, lean adults, and adults with obesity, the significant predictors of fasting erythritol were age and circulating erythronate. Body mass index, glucose, and insulin were not predictors at all. The authors note the age effect was driven largely by the comparison of young adults with adults ^[11].
• In a secondary analysis of a weight-loss trial (802 participants at baseline, 664 at six months), people whose plasma erythritol fell the most also showed the largest improvements in insulin resistance and blood sugar markers. The authors note that circulating erythritol reflects both what the body makes and what a person eats, and their analysis could not separate the two ^[12].

These findings raise another possibility: higher levels of erythritol in the blood may be a marker of underlying metabolic strain, rather than a cause of it

A 2023 perspective in Clinical Chemistry raised the same question: is the potential risk coming from erythritol we consume, or from erythritol already circulating in the body? The authors concluded that the relationship between habitual erythritol intake, blood levels, and cardiovascular risk remains inconclusive ^[13].

The regulator that examined this most closely reached the same point independently. Reviewing the 2023 cohorts, EFSA noted: “No information was available on dietary intake. No distinction between endogenous and exogenous erythritol can be made; therefore the source of the measured levels could not be identified. The low circulating levels suggest that the main source for most participants was endogenic formation” ^[2].

Figure 2. What was published, and when. Read down the left column, then the right. Blue marks a study, orange a regulator, green a NOVOS action. Reference numbers correspond to the list at the end.

What We’ve Learned Since 2023

Our original article covers the 2023 study in detail, including how it was designed, who participated, and what it measured. Read our analysis of the 2023 study on erythritol and cardiovascular health.

Since then, several new studies have added to the evidence.

The mechanistic finding was repeated with a control group

In 2024, researchers gave 10 people 30 grams of erythritol and another 10 people 30 grams of glucose. Platelet reactivity increased in the erythritol group, but not in the glucose group ^[6].

Circulating erythritol has since been measured in four more groups of people, with results that vary by outcome

In the ARIC study, 4,006 adults free of cardiovascular disease were followed for a median of 8.4 years. Erythritol tracked heart failure and mortality, but showed no association with coronary heart disease or ischaemic stroke. The authors’ own conclusion describes what they measured as “markers of cardiometabolic health and cardiovascular outcomes” ^[7]. In the Nurses’ Health Study, 762 women who developed coronary heart disease were compared with 762 matched controls. Women in the top quartile had a relative risk of 1.55 (95% CI 1.13 to 2.14), which fell to 1.21 (95% CI 0.86 to 1.70) and lost statistical significance once diabetes was accounted for ^[5]. In the ATBC study, 4,468 men were followed for an average of 19.1 years ^[8]. A fourth examined pregnancy outcomes, gestational diabetes and large-for-gestational-age infants, rather than cardiovascular ones ^[14].

Genetic studies have not settled the question, and two of them do not favour erythritol

Mendelian randomisation uses inherited genetic variation to test whether an exposure causes an outcome. Four such studies have now been published and they disagree.

One found no supportive evidence that increased erythritol raises coronary artery disease risk ^[15]. A second reported positive associations for coronary heart disease (odds ratio 1.0020), myocardial infarction (1.0015) and stroke (1.0463), which the authors describe as suggestive. The first two are statistically detectable and biologically very small; the stroke estimate is larger but only marginally significant ^[16]. A third reported substantially larger associations, with odds ratios of 1.077 for coronary heart disease and 1.157 for ischaemic stroke, consistent across sensitivity analyses and with no evidence of pleiotropy for those two outcomes, although its venous clotting results were inconsistent across methods ^[17]. A fourth, examining liver fat, concluded that “an active role for erythritol per se was excluded by MR analysis,” and suggested erythritol may instead serve as a urinary marker of activity in the pentose phosphate pathway ^[18].

The authors of the study reporting the smaller positive association name the limitation this article opened with: “current genetic instruments cannot distinguish between endogenous and exogenous erythritol, nor can they reflect metabolic differences across tissues or microbial communities, potentially leading to underestimation of true causal associations” ^[16]. That last clause matters and cuts against the reading offered here: those authors think the blur would hide a real effect rather than manufacture one. Three of the four research teams name a version of this limitation. The fourth ran specific analyses to separate dietary erythritol and considered it excluded ^[18].

A published critique literature now exists

A 2023 review pointed out that people born with metabolic conditions that keep erythritol permanently high do not show increased platelet activation or clotting risk, which is difficult to reconcile with erythritol as a direct cause ^[20]. A second study asked directly whether there are enough data to conclude that dietary erythritol intake is associated with cardiovascular risk, and examined endogenous synthesis alongside the cohort findings ^[21]. A 2025 review in Cardiovascular Research summarised the position as: pilot trials suggest these sweeteners might temporarily alter platelet aggregation, while studies in intensive care patients given large intravenous doses, along with the genetic studies, do not link sugar alcohols to significant cardiovascular risks ^[22].

Two newer areas are at an early stage

Human brain blood vessel cells exposed to erythritol in a dish showed reduced nitric oxide production and increased markers of stress ^[23]. A letter to the same journal cautioned against reading too much into it, noting that “sustained exposure at constant high concentrations for many hours does not reflect physiological kinetics,” since in the body erythritol peaks and then clears with a plasma half-life of about four hours ^[24]. Separately, an eight-year Brazilian study of 12,772 people associated estimated intake of several low-calorie sweeteners, erythritol among them, with faster cognitive decline in participants under 60. The amounts were small: its highest intake group spanned 102 to 857 milligrams per day for all seven sweeteners combined ^[25]. Neither finding establishes cause and effect, and both need testing in people.

What the Regulators Concluded

Two independent authorities have looked at erythritol since the 2023 study. Neither works for a sweetener manufacturer, and neither works for us. The two exercises were not equivalent: EFSA carried out a full re-evaluation of erythritol as a food additive, while the FDA reviewed the 2023 paper and published a short position statement.

European Food Safety Authority, opinion adopted 25 October 2023

EFSA re-evaluated erythritol as a food additive and reached three conclusions worth reporting accurately, including one that does not favour the ingredient ^[2].

On cardiovascular risk

EFSA acknowledged the observational studies and then set out why it could not draw a causal conclusion from them: “it is highly uncertain whether this association is at all related to consumption of food containing erythritol (E 968). Overall, the Panel considered that a causal relationship between dietary exposure to erythritol (E 968) and cardiovascular disease risk has not been demonstrated by the available studies. Further studies might be helpful to clarify the nature of the association between plasma erythritol level and incidence of cardiovascular disease” ^[2].

There is some important context to EFSA’s conclusion. It described the cardiovascular findings as preliminary and the association as only “possible,” noting that the available evidence did not conclusively identify a health concern from erythritol as a food additive.

Cardiovascular disease was also not one of the health outcomes EFSA formally assessed in its re-evaluation. Its formal assessment focused on glucose regulation and gastrointestinal effects.

EFSA also examined the 2023 study directly and made the same observation this article opens with: “No information was available on dietary intake. No distinction between endogenous and exogenous erythritol can be made; therefore the source of the measured levels could not be identified. The low circulating levels suggest that the main source for most participants was endogenic formation” ^[2]. On the laboratory work, EFSA considered that “these studies provided insufficient basis to predict what may occur in humans.”

On genotoxicity

EFSA concluded that erythritol “does not raise a concern regarding genotoxicity”, and that the new studies it reviewed “did not alter the previous conclusion (SCF, 2003) that erythritol is not genotoxic”, meaning it does not damage DNA ^[2].

On intake, which is the finding that does not favour erythritol

EFSA set a numerical Acceptable Daily Intake of 0.5 grams per kilogram of body weight per day. This is the first time EFSA has derived an intake limit for a food additive from an immediate effect, in this case diarrhoea, and the figure is the lower bound of the range of no-effect levels reported across human studies. For a person weighing 70 kilograms it corresponds to 35 grams daily.

EFSA then found that “the 95th percentile exposure estimates for both acute and chronic exposure to erythritol (E 968) were at or above the ADI” in all population groups, and that average intake exceeded it in the highest-consuming surveys for toddlers and children. EFSA noted that its exposure modelling overestimates real consumption, and that the existing laxative warning on high-erythritol foods remains appropriate ^[2]. This is a digestive threshold rather than a cardiovascular one, and it applies to total intake across the diet rather than to any single product. It belongs in this article because leaving it out would repeat the omission we are correcting.

U.S. Food and Drug Administration

The FDA permits erythritol’s use as a sugar alcohol and has not changed that position since 2023. It states: “In 2023, the FDA reviewed a scientific paper about possible cardiovascular effects related to consuming erythritol and determined that the observational studies cited in the paper did not establish a causal link between consuming erythritol and the observed effects. The FDA will continue to monitor and review new information on erythritol, and other sweeteners, as it becomes available” ^[3].

In April 2026, the FDA also completed its evaluation of a manufacturer’s GRAS notification for erythritol and responded that it had “no questions at this time” regarding that conclusion. That letter concerns one company’s product and manufacturing process; the FDA states plainly that the letter “is not an affirmation that erythritol is GRAS under 21 CFR 170.35”, and it does not address cardiovascular research ^[4]. It shows the regulatory pathway remains open. It is not a new safety finding, and we are not going to present it as one.

Two national intake assessments

A Korean study measuring erythritol in 110 products estimated average daily intake at 2.77% of the EFSA limit ^[26]. A Dutch assessment found intakes generally below health-based guidance values, with the exception of toddlers under the most conservative modelling assumptions, which the authors noted likely overestimated real consumption ^[27].

Why NOVOS Removed Erythritol From NOVOS Core

The previous NOVOS Core formula contained 1.85 grams of erythritol per serving, where it was used as part of the flavour system. By comparison, the Nature Medicine platelet experiment gave participants a single 30-gram dose ^[1]. That means a serving of NOVOS Core contained about 6% of the amount used in that study. It was also about 5% of EFSA’s Acceptable Daily Intake for a 70-kilogram adult ^[2].

Figure 3. Every amount of erythritol ever tested in people, and the amount NOVOS Core used to contain. The shaded band marks the range below 2.7 g, the smallest amount given to a person in any published study we found. The five-week trial (36 g/day, reference 20) and the two platelet experiments (30 g, references 1 and 6) are the only human studies that tested erythritol against a cardiovascular or blood vessel endpoint. The 35 g figure is the EFSA Acceptable Daily Intake for a 70 kg adult (reference 2), based on the threshold for diarrhoea rather than on cardiovascular risk.

Here is the comparison that matters most, because it is the one about hearts rather than percentages. Every human study we identified that tested erythritol against a cardiovascular or blood vessel endpoint used 24 grams or more: 30 grams in the two platelet experiments ^{[1, 6]}, 36 grams daily in the five-week randomised trial ^[19], and 36 grams daily plus a single 24 gram dose in an earlier four-week pilot in type 2 diabetes ^[31]. The amount in a serving of NOVOS Core was a fraction of all of them.

Beyond cardiovascular endpoints

Going wider than cardiovascular endpoints, we searched the published human literature for the smallest amount of erythritol ever given to people for any purpose. The lowest we found was a 2002 Finnish dental study in 98 people, most of them with an intellectual disability, cared for in nursing homes or at home. They chewed tablets containing a one-to-one mixture of erythritol with either xylitol or sorbitol: about 1.35 grams of erythritol daily for the first week, then 2.7 grams daily for the remaining 57 days ^[28]. We put it that way rather than claiming no lower dose exists anywhere, because a literature search establishes what we found, not what is absent.

The evidence at lower doses is much more limited. The only human exposure we found near this range was one week of a dental study, which measured saliva and oral bacteria—not cardiovascular outcomes.

So, while we can compare the amount previously used in NOVOS Core with doses that have been studied, we can’t say what effect 1.85 grams has on cardiovascular measures. No published study has tested that dose for those outcomes.

The gap is not for want of anyone trying. In July 2013 Boston University registered a trial titled “Dose-Dependent Effects of Erythritol on Endothelial Function in Type 2 Diabetes Mellitus.” It was an open-label pilot in twenty-four people with type 2 diabetes, giving escalating drinks of 6, 12 and 18 grams of erythritol and measuring blood vessel function after each. Its stated purpose was to plan a randomised, placebo-controlled study. The registry records it as completed, and states “No Study Results Posted on ClinicalTrials.gov for this Study” ^[29]. We found no publication reporting it, which is the outcome of our search rather than proof that none exists.

Why did we reformulate?

Customers asked for an erythritol-free version of NOVOS Core. We found we could remove it without changing the active ingredients or their intended role in the formula, so we did.

These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

We did not remove erythritol because we concluded the previous formula was unsafe. We continuously review new research on every ingredient we use, and the evidence available did not indicate that the amount previously used in NOVOS Core posed a cardiovascular concern. No published study has tested erythritol at that amount, so the research neither establishes nor rules out an effect there. Both regulators declined to accept a causal link between dietary erythritol and cardiovascular disease ^{[2, 3]}. Neither made any finding about the amount used in NOVOS Core.

Revision History

Date	Change
March 1, 2023	Original article published, the same month the Nature Medicine study appeared
August 2026	Fully revised. Every reference read in full text and checked against the sentence that cites it. Added the EFSA re-evaluation adopted in October 2023, the FDA’s position, and research published between 2023 and 2026.

References

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These statements have not been evaluated by the Food and Drug Administration. This product/information is not intended to diagnose, treat, cure, or prevent any disease.

This article is for general information and is not medical advice. Speak with your physician about your own circumstances.