Erythritol: The Sugar Alcohol and the Blood Clot Findings

Table of Contents

1. What Erythritol Is
2. How Erythritol Is Made
3. Where Erythritol Occurs in Foods
4. How the Body Makes Erythritol Itself
5. How Erythritol Moves Through the Gut and Body
6. The 2023 Cohort Findings
7. The 2024 Platelet Study
8. The Limits of These Studies and the Published Dispute
9. Later Cohorts and Genetic Studies
10. The European Food Safety Authority Re-Evaluation
11. Erythritol's Status in the United States
12. Effects on Blood Sugar and Insulin
13. Gut Tolerance Data
14. What Is Not Known
15. Key Research Papers
16. Connections
17. Featured Videos

What Erythritol Is

Erythritol is a sugar alcohol, also called a polyol: a small carbon molecule that tastes sweet but is neither a sugar nor the alcohol in drinks. It has four carbons, which makes it smaller than sorbitol, xylitol or maltitol. It is about 70% as sweet as table sugar, according to the European Food Safety Authority (EFSA), and it is used in bulk, by the spoonful rather than by the speck, which sets it apart from the high-intensity sweeteners on the artificial sweeteners page.

Research papers often call it an "artificial sweetener", yet it occurs naturally in foods and is made in the human body. A 2023 review by Mazi and Stanhope writes that for nutrition labels it is assumed to carry 0 calories per gram, against 2.4 for other sugar alcohols. Two older human studies estimated its usable energy at no more than 0.4 kilocalories per gram (Noda 1994; Bornet 1996). It is also the filler in many tabletop stevia blends, a separate question covered on the stevia gut microbiome and safety page. Mahalak and colleagues note that stevia leaf extracts are often combined with it to add volume and reduce aftertaste.

Erythritol sits in the middle of an unresolved scientific argument. People with more of it in their blood have had more heart attacks, strokes and deaths in several cohorts. Short studies report that a large drink of it makes platelets, the blood cells that start a clot, respond more strongly in lab tests. Regulators in Europe found no demonstrated causal link, and set their intake limit on diarrhoea. The body makes erythritol from glucose, and that fact complicates all of these readings. This page reports each of these findings and what its authors or critics say about it.

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How Erythritol Is Made

Commercial erythritol comes from fermentation, not from extraction out of fruit. A microbe is fed glucose, turns part of it into erythritol, and the product is purified and crystallized. Witkowski and colleagues date large-scale industrial production to the 1990s, after microbial fermentation processes were found.

• In the European Union: the 2023 European Food Safety Authority opinion describes erythritol obtained by fermentation with two yeast-like fungi, Moniliella pollinis BC or Moniliella megachiliensis KW3-6, followed by purification and drying.
• In a 2026 United States notice: a U.S. Food and Drug Administration letter on a recent notice describes fermentation of glucose with a pure culture of the yeast Yarrowia lipolytica. The notifier's stated steps are filtration to remove the microbes, concentration, crystallization, decolorizing with activated carbon, ion exchange purification, a second crystallization, then drying and sieving. The stated purity specification is 99.5–100.5% on a dry basis.

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Where Erythritol Occurs in Foods

Small natural amounts occur in several foods. The European Food Safety Authority opinion lists mushrooms, some fruits (melons, watermelons, pears, grapes), wine, sake, and fermented products such as soya sauce and miso, at levels from 22 to 1,550 mg per kilogram of food. The panel estimated that these foods would probably add 1–2% to its exposure estimates. It also notes methods for measuring naturally formed erythritol in ripened cheese.

Added erythritol reaches far higher levels. Witkowski and colleagues write that processed foods typically carry about 1,000 times natural levels, up to 60% of food weight in some creams and pastry products. A 2025 survey of 110 processed products in Korea measured 47.50 to 81,688.95 mg per kilogram, with the highest value in an ice milk mix (Kim 2025). The U.S. Food and Drug Administration's 2026 letter lists maximum use levels in one notice, including 3.5% in reduced- and low-calorie drinks, 10% in regular and soft serve ice cream, 25% in cakes and 75% in chewing gum.

Estimates of how much people eat vary widely. Witkowski and colleagues cite United States survey data and filings to the U.S. Food and Drug Administration suggesting up to 30 g a day in some people. The Korean study estimated a mean of 13.84 mg per kilogram of body weight a day, or 2.77% of the European intake figure described below. The European panel's estimates were much higher and are described in the section on its opinion.

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How the Body Makes Erythritol Itself

Erythritol is not only a food ingredient. Hootman and colleagues showed in 2017, with labelled tracers in human blood samples and in volunteers, that human cells build erythritol from glucose through the pentose phosphate pathway, a side route of ordinary sugar metabolism. The same work showed conversion of erythritol to erythronate, a related acid.

• Young adults and waist size: in Hootman's 9-month study of 264 university freshmen, those who gained central body fat had 15-fold higher blood erythritol than those whose body fat stayed stable, in pooled plasma samples. Those with higher starting hemoglobin A1c (a measure of average blood sugar) had 21-fold higher levels. The authors state that production from glucose in the body may contribute to the link with obesity.
• Cell studies: in human lung carcinoma cells, erythritol inside the cell rose with the glucose in the culture medium and rose under oxidative stress (Ortiz 2022). This is a result in cells.
• Age: in 218 people, among them lean adolescents, lean adults and adults with obesity, age predicted fasting erythritol, while body mass index, glucose and insulin did not (Flad 2025). This differs from the earlier findings, and the authors state that the processes regulating production remain unclear.

A 2020 review by Ortiz and Field reports that elevated blood erythritol predicts central fat gain and type 2 diabetes in healthy adults, and that long-term dietary erythritol also needs evaluation. The practical research problem follows directly: one blood test cannot, on its own, say whether a person's erythritol came from a food or from their own glucose.

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How Erythritol Moves Through the Gut and Body

Most sugar alcohols stay in the gut, where they draw in water and feed bacteria. Erythritol behaves differently, because most of it is absorbed in the small intestine and leaves in urine.

• Absorption: the European Food Safety Authority reports that studies show 60% to 90% of ingested erythritol absorbed from the small intestine. In 17 lean volunteers given 10, 25 or 50 g, absorption was dose-dependent and saturable, meaning the gut's capacity to take it up has a ceiling (Bordier 2022).
• Urine: in 5 healthy men given 0.3 g per kilogram, urine recovery was 85.8% at 24 hours and 90.3% at 48 hours (Noda 1994). With a larger 1 g per kilogram dose, it was 78% after 24 hours, and the authors estimated that less than 20% stayed unabsorbed (Bornet 1996).
• Breakdown: early work reported no metabolism by the body (Hiele 1993). Later work reports dose-dependent conversion into erythronate (Bordier 2022). The European panel describes this as occurring to a small extent. Bordier and colleagues state that its health implications remain to be determined.
• Gut bacteria in lab tests: in fresh human stool samples, erythritol resisted fermentation for 24 hours, and only about 10% of a dose is described as entering the colon (Arrigoni 2005). In 6 volunteers, breath hydrogen did not rise after 25 g (Hiele 1993).
• Gut bacteria, other results: a 2020 study in a human gut microbial community in the lab and in capuchin monkeys found more butyric and pentanoic acid with erythritol and changes in the monkeys' microbial structure, and reported no negative impact (Mahalak 2020). In mice on a high-fat diet, 5% erythritol in water raised short-chain fatty acids and lowered body weight (Kawano 2021). In mice with chemically induced colitis, erythritol worsened the colitis and increased potentially harmful bacteria (Liu 2026). Mazi and Stanhope write that long-term studies of the human gut microbiota have not been done.
• The stomach and gut hormones: in 12 lean volunteers given 10, 25 or 50 g by nasogastric tube, erythritol raised the gut hormones cholecystokinin, glucagon-like peptide-1 and peptide YY with dose, and slowed stomach emptying (Wölnerhanssen 2021). In 20 healthy volunteers, 50 g before a test meal led to lower energy intake than sucrose, sucralose or water (Teysseire 2022). When erythritol partly replaced sucrose inside a meal in 10 lean and 10 obese volunteers, glucagon-like peptide-1, peptide YY and later food intake did not differ (Overduin 2016).

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The 2023 Cohort Findings

The study that brought erythritol to public attention appeared in Nature Medicine in February 2023 (Witkowski 2023). The work began with a broad screen of many small molecules in the blood of 1,157 patients undergoing cardiac risk assessment, looking for what predicted major adverse cardiovascular events over 3 years, defined as death, non-fatal heart attack or non-fatal stroke. Levels of several sugar alcohols, especially erythritol, stood out.

They then measured erythritol with a targeted test in two separate groups of stable patients having an elective cardiac evaluation. A hazard ratio compares the rate of events between two groups, so 1.80 means about 1.8 times the rate.

• United States cohort (2,149 patients): the highest quarter of blood erythritol against the lowest had an adjusted hazard ratio of 1.80 (95% confidence interval 1.18–2.77).
• European cohort (833 patients): the same comparison gave an adjusted hazard ratio of 2.21 (95% confidence interval 1.20–4.07).

The paper went beyond association in three further steps:

• In the lab: at levels seen in fasting blood, erythritol made human platelets respond more strongly to clotting triggers in a dish.
• In animals: the paper reports more clot formation, and Mazi and Stanhope's later review describes this as faster clotting in mice injected with erythritol, a route that differs from eating it.
• In people: 8 healthy volunteers drank 30 g of erythritol in 300 mL of water. Median plasma erythritol went from 3.84 micromoles per litre to 5.85 millimoles per litre at 30 minutes, which the authors describe as about 1,000-fold higher. Levels stayed raised for more than 2 days, and stayed above the thresholds linked to heightened platelet reactivity in the lab and animal work.

The authors conclude that erythritol is both associated with these events and fosters enhanced clotting, and that studies of its long-term safety are warranted.

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The 2024 Platelet Study

The same research group followed with a human experiment (Witkowski 2024, Arteriosclerosis, Thrombosis, and Vascular Biology). Twenty healthy non-smoking adults, with a mean age of about 30, took 30 g of erythritol or 30 g of glucose in water, 10 people in each group. Blood was drawn after an overnight fast and again 30 minutes after the drink, and platelets were tested in the lab with clotting triggers.

• Blood level: erythritol reached a median of 6,480 micromoles per litre in the erythritol group, against 3.75 in the glucose group, more than 1,000-fold higher.
• Platelet clumping: the response increased in all subjects, with all triggers and doses tested.
• Release of platelet contents: release of serotonin increased (P<0.0001 with one trigger, P=0.004 with the other), and so did release of the protein CXCL4 (P<0.0001 with one trigger; P=0.06 with the other, which is not conventionally significant).
• The comparison: glucose produced no significant rise in either marker.

The authors write that the findings raise concern that erythritol may enhance clotting potential, and that discussion of re-evaluating its "generally recognized as safe" designation is warranted. The study did not measure any actual clot, heart attack or stroke in a person.

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The Limits of These Studies and the Published Dispute

The authors of both papers name limits of their own work:

• One measurement: in the 2023 cohorts, erythritol was measured once, as a fasting level at enrolment.
• Who was studied: the 2023 patients were recruited at specialist referral centres, with a high prevalence of heart disease and risk factors, and the authors state that whether the results apply to the general population needs to be determined. They add that the signal also appeared in lower-risk subgroups.
• Association only: they state that the cohort design can show association, not causation, and that unmeasured factors such as diet may have affected the results.
• Source of the erythritol: the authors speculate that levels reflect both eating and production in the body. They write that fasting samples in the United States cohort, whose enrolment largely came before erythritol spread through processed foods, likely reflect production in the body.
• Small and short: the 2024 authors state that their study was small, that replication is needed, and that they did not test long-term changes in platelet function.

Two more limits come from the numbers themselves. The volunteers took a single 30 g dose, dissolved in 300 mL, which works out to about 10% by weight. The authors describe this as comparable to a can of sweetened drink or a pint of keto ice cream. The most recent United States notice above lists a maximum of 3.5% for reduced- and low-calorie drinks. The study also reports what happens in the 30 minutes after one large dose; it does not report what happens with smaller amounts spread through a day.

Published critics go further. Mazi and Stanhope (2023) argue that erythritol may be a harmless marker of a disturbed pentose phosphate pathway caused by poor blood sugar control, not a cause of disease. Their review makes three points:

• People with inherited errors of this pathway, who have chronically high erythritol, do not show higher platelet activation or clotting risk.
• Most long-term animal feeding studies do not support a role in platelet activation and clot formation.
• Clinical data on long-term intake are limited, so it cannot yet be concluded that dietary erythritol promotes clotting.

Other work sits alongside this dispute. A 4-week pilot in 24 people with type 2 diabetes, given 36 g a day, reported better small-vessel function after a single dose and lower central pulse pressure (47 to 41 mmHg) after 4 weeks (Flint 2014). It measured artery function, not platelets or clots. A 1998 safety review reported no evidence of toxicity in animal and short human studies (Munro 1998). A 2025 review describes the recent platelet trials as suggesting that sugar alcohols might temporarily alter platelet aggregation (Wölnerhanssen 2025).

Competing interests appear on both sides of the published literature. The 2023 paper's statement lists patents and consulting relating to cardiovascular diagnostics and therapeutics among its authors. The statement in Mazi and Stanhope's January 2023 review says a company approved its submission, and had no input on the scientific content beyond a general list of topics.

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Later Cohorts and Genetic Studies

Studies since 2023 have reported similar associations in other populations, along with signs that point toward production in the body:

• Older adults without heart disease: in 4,006 older adults followed for a median of 8.41 years, higher erythritol and erythronate were associated with heart failure hospitalization, cardiovascular death and death from any cause after adjustment. Erythronate alone was reported as additionally associated with coronary heart disease (hazard ratio 1.30, 95% confidence interval 1.04–1.61) and stroke (1.40, 1.08–1.83). Those with the highest levels were older and more likely to have diabetes, high blood pressure or high cholesterol. The authors describe both substances as markers (Abushamat 2025).
• A long follow-up in men: in 4,468 men, with 3,377 deaths over an average of 19.1 years, higher serum erythritol was associated with death from any cause (hazard ratio 1.50, 1.17–1.92), cardiovascular death (1.86, 1.18–2.94) and cancer death (1.54, 1.09–2.19). The abstract gives the study's years as 1985–1993 and dates sweetener use from the 1990s. The authors call for work separating body-made from dietary erythritol (Lim 2024).
• Weight-loss diets: in a 2-year randomized weight-loss trial, 664 adults had erythritol measured at the start and at 6 months. Greater declines went with lower estimated cardiovascular risk (Heianza, American Journal of Clinical Nutrition, 2026) and with lower insulin resistance, fasting glucose and hemoglobin A1c at 2 years (Heianza, International Journal of Obesity, 2026). The authors describe an observational analysis; these were diets for weight loss, not trials of removing erythritol from food.
• Liver fat: in 1,494 adults, 24-hour urine erythritol was associated with more liver fat, but genetic analysis found no significant link, and the authors write that an active role for erythritol itself was excluded (Buziau 2026).

Mendelian randomization studies use inherited gene variants as a natural experiment, on the reasoning that genes are not changed by diet or illness. Their results on erythritol disagree or are read differently:

• A 2025 analysis reported that genetically higher erythritol was associated with coronary heart disease (odds ratio 1.077, 1.060–1.090) and ischemic stroke (1.157, 1.135–1.179), with weaker and inconsistent results for clots in veins (Sun 2025).
• A 2026 analysis reported an association with stroke (odds ratio 1.246, 1.101–1.410), and its authors state that this exposure is not direct evidence that dietary erythritol causes stroke (Zhong 2026).
• A 2025 review in Cardiovascular Research states that Mendelian randomization trials and studies of critically ill patients given large intravenous doses do not link sugar alcohols to significant cardiovascular risks (Wölnerhanssen 2025).

A cell study adds a separate strand. Human brain blood-vessel cells exposed to 6 millimoles per litre of erythritol for 3 hours showed more reactive oxygen species (204% against 105%), less nitric oxide (5.8 against 7.3 micromoles per litre), and more endothelin-1 (34.6 against 26.9 pg/mL), and a blunted release of the clot-dissolving protein tissue-type plasminogen activator (Berry 2025). This is a result in cells. The site's xylitol news report covers related work on another sugar alcohol.

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The European Food Safety Authority Re-Evaluation

The European Food Safety Authority's panel on food additives published its re-evaluation of erythritol (E 968) in December 2023. It was also asked about a manufacturer's application to exempt erythritol from the European laxative warning. Foods with more than 10% added sugar alcohols carry the statement that "excessive consumption may produce laxative effects". The opinion states that erythritol is authorised in 66 food categories, representing 83 uses.

What the panel states:

• Intake figure: it set an acceptable daily intake of 0.5 g per kilogram of body weight per day. By simple arithmetic, that comes to 35 g a day for a 70 kg adult and 10 g a day for a 20 kg child. In 2000, the Joint Expert Committee on Food Additives of the Food and Agriculture Organization and the World Health Organization had assigned an intake "not specified".
• Why that figure: it is the low end of the range of no-effect levels for diarrhoea in human studies. The panel treated diarrhoea as adverse because of its possible link to electrolyte and water imbalance, and it notes this is the first time it has derived such a figure from an immediate effect of this kind. It applied no uncertainty factor, since the data came from people.
• Exposure: the highest chronic estimates, 742 mg per kilogram a day on average and 1,532 mg per kilogram a day at the 95th percentile, are above the intake figure. So is the highest single-meal estimate, 3,531 mg per kilogram for children at the 99th percentile. The panel calls these overestimates, but concludes that people with high intake may be at risk of adverse effects after single and repeated exposure. (The opinion's abstract attributes the chronic figures to children and adolescents; its summary and exposure section attribute them to toddlers and children.)
• Heart and clot findings: the panel reviewed Witkowski 2023 and states that the available evidence does not demonstrate a causal relationship between dietary erythritol as a food additive and increased cardiovascular risk, and that further studies might help clarify the association. It considered that the in vitro platelet studies provided an insufficient basis to predict what may occur in humans. It also notes that no cardiovascular adverse effects were seen in the animal studies evaluated in 2003.
• Warning label: the available data did not support the exemption, and the panel considered the existing warning appropriate.
• Genetic damage: the panel reports no concern regarding genotoxicity.

The opinion came out before the 2024 platelet study, the later cohorts and the genetic studies described on this page. The panel derived the acceptable daily intake from diarrhoea and effects secondary to it, not from a clotting endpoint. A 30 g dose, the amount in the Witkowski studies, falls below the figure for a 70 kg adult.

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Erythritol's Status in the United States

In the United States, erythritol reaches food through "generally recognized as safe" (GRAS) notices, not through the food additive approvals that six high-intensity sweeteners went through. In this route, a company concludes that its use is generally recognized as safe, and notifies the U.S. Food and Drug Administration. The agency's public inventory lists erythritol notices closed with the response "FDA has no questions" in 2001 (GRN 76), 2007 (GRN 208), 2011 (GRN 382), 2012 (GRN 401), 2019 (GRN 789) and on April 7, 2026 (GRN 1296).

The 2026 letter shows how the process is worded. The agency states it has "no questions at this time" regarding the notifier's conclusion, and that the letter "is not an affirmation" that erythritol is generally recognized as safe under 21 CFR 170.35. It adds that manufacturers and producers are responsible for ensuring marketed products are safe. The letter records the notifier's statement that a literature search through May 2025 revealed no new data contradicting safe use, and it excludes infant formula. The letter does not discuss the Witkowski studies by name. The inventory entries and this letter give no acceptable daily intake figure.

Mazi and Stanhope write that the agency has not officially defined the word "natural" and that it considers erythritol produced by microbes to be a natural sweetener. The 2026 closure came after the 2023 and 2024 papers.

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Effects on Blood Sugar and Insulin

Studies consistently report that eating erythritol does not raise blood sugar or insulin in the short term. Most of them are small.

• Healthy adults: no rise in glucose or insulin after 0.3 g per kilogram in 5 men (Noda 1994), after 1 g per kilogram (Bornet 1996), after 0.4 or 0.8 g per kilogram in a snack (Bornet 1996, second study), or after 10 to 50 g by nasogastric tube in 12 volunteers (Wölnerhanssen 2021).
• Lean and obese volunteers: 75 g given to 10 lean and 10 obese volunteers did not affect glucose or insulin (Wölnerhanssen 2016). In 18 healthy subjects, 50 g did not affect them either, with no effect on blood lipids, uric acid or high-sensitivity C-reactive protein, and an exploratory drop in the appetite hormone ghrelin (Teysseire 2023).
• In place of sugar in a meal: glucose and insulin rose less after erythritol meals than after a sucrose meal (Overduin 2016).
• People with diabetes: in 5 patients, 20 g produced no change until a meal 3 hours later. In a separate 14-day study of 11 patients given 20 g a day, mean glucose and hemoglobin A1c decreased; the abstract describes no control group (Ishikawa 1996).
• People with glucose intolerance: after 2 weeks, erythritol and the stevia compound rebaudioside A did not differ in fructosamine or other glucose markers (Shin 2016). The comparison was between the two sweeteners.
• People with obesity: in 46 participants, 12 g of erythritol or 8 g of xylitol three times a day for 5 to 7 weeks, against no substance, did not change how much glucose the gut absorbed (Bordier 2021).

This is the reverse side of the cohort data. Eating erythritol has not been shown to raise blood sugar in these studies, while in several studies higher blood sugar markers go with higher erythritol in the blood (Hootman 2017; Heianza 2026), though not in all (Flad 2025). Both findings can be true at once, and they are why researchers separate dietary erythritol from body-made erythritol. Mazi and Stanhope note that long-term controlled trials on blood sugar and body weight are almost completely lacking.

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Gut Tolerance Data

Because little reaches the colon, erythritol is reported as better tolerated than other sugar alcohols at comparable doses, but tolerance has a limit and it depends on how the dose is taken.

• Young adults, one drink: in a randomized double-blind study completed by 64 people, 20 g and 35 g did not significantly increase digestive symptoms. At 50 g, significantly more people reported nausea and rumbling of the gut. Xylitol produced significantly more watery stools at all levels tested (Storey 2007).
• Spread through a day: in 12 men, a dose rising to 1 g per kilogram a day over a 7-day period, split across five portions in foods, brought no signs of digestive intolerance. Urine calcium rose slightly, and some urinary proteins rose slightly while staying within the normal range (Tetzloff 1996).
• In a snack: doses up to 0.8 g per kilogram gave responses comparable to sucrose and did not change electrolyte balance, in three groups of six (Bornet 1996, second study).
• Young children: in 184 children aged 4 to 6 given a single drink, 20 g and 25 g caused significantly more diarrhoea or severe digestive symptoms than placebo, while 5 g and 15 g did not. The no-effect level was 15 g, or 0.73 g per kilogram. Children appeared no more sensitive than adults per kilogram (Jacqz-Aigrain 2015).
• With fructose: in 37 healthy adults, 33.3 g of erythritol taken with 50 g of fructose doubled the breath hydrogen seen with fructose alone and worsened digestive symptoms and watery stools, which the authors read as increased malabsorption (Kim 2011).
• Tube-fed doses: 10 to 50 g caused no abdominal pain, nausea or vomiting in 12 volunteers (Wölnerhanssen 2021).

The European panel's review adds dose-finding studies with higher diarrhoea rates. In one, cited there, about half of participants had diarrhoea at about 1.1 g per kilogram in women and 1.6 g per kilogram in men, and the authors placed the threshold near 0.8 g per kilogram in women and 0.7 g per kilogram in men. The panel chose 0.5 g per kilogram as the low end of the range across studies.

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What Is Not Known

• Cause or marker: whether blood erythritol contributes to heart attacks and strokes, or only reflects disturbed glucose metabolism, has not been settled by the cohorts.
• Long-term eating: no long-term controlled trial of dietary erythritol with heart attack, stroke or death as the outcome appears in the papers read for this page. Witkowski 2024 states that clinical trials of long-term cardiovascular risk are absent, and Mazi and Stanhope call for them.
• Amount and pattern: the platelet findings come from one 30 g dose tested at 30 minutes. How smaller doses, repeated doses or doses taken with meals affect platelets is not reported in these abstracts.
• From lab response to clot: whether a stronger platelet response in a lab test translates into more clots in people has not been shown in a human study.
• Erythronate: its role is unclear. Abushamat 2025 links it to more outcomes than erythritol, and Bordier 2022 states that its implications remain to be determined.
• Gut bacteria: animal and lab results point in different directions, and long-term human data are missing.
• What controls production in the body: Flad 2025 states that the processes regulating it remain unclear.

Decisions about sweeteners and an individual's health belong with a clinician.

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Key Research Papers

1. Witkowski M, Nemet I, Alamri H, Wilcox J, Gupta N, Nimer N, Haghikia A, Li XS, Wu Y, Saha PP, Demuth I, König M, Steinhagen-Thiessen E, Cajka T, Fiehn O, Landmesser U, Tang WHW, Hazen SL. The artificial sweetener erythritol and cardiovascular event risk. Nat Med. 2023;29(3):710-718. PubMed PMID: 36849732
2. Witkowski M, Wilcox J, Province V, Wang Z, Nemet I, Tang WHW, Hazen SL. Ingestion of the Non-Nutritive Sweetener Erythritol, but Not Glucose, Enhances Platelet Reactivity and Thrombosis Potential in Healthy Volunteers-Brief Report. Arterioscler Thromb Vasc Biol. 2024;44(9):2136-2141. PubMed PMID: 39114916
3. Mazi TA, Stanhope KL. Elevated Erythritol: A Marker of Metabolic Dysregulation or Contributor to the Pathogenesis of Cardiometabolic Disease?. Nutrients. 2023;15(18):4011. PubMed PMID: 37764794
4. Mazi TA, Stanhope KL. Erythritol: An In-Depth Discussion of Its Potential to Be a Beneficial Dietary Component. Nutrients. 2023;15(1):204. PubMed PMID: 36615861
5. EFSA Panel on Food Additives and Flavourings (FAF), Younes M, Aquilina G, Castle L, et al. Re-evaluation of erythritol (E 968) as a food additive. EFSA J. 2023;21(12):e8430. PubMed PMID: 38125972
6. Hootman KC, Trezzi JP, Kraemer L, Burwell LS, Dong X, Guertin KA, Jaeger C, Stover PJ, Hiller K, Cassano PA. Erythritol is a pentose-phosphate pathway metabolite and associated with adiposity gain in young adults. Proc Natl Acad Sci U S A. 2017;114(21):E4233-E4240. PubMed PMID: 28484010
7. Ortiz SR, Heinz A, Hiller K, Field MS. Erythritol synthesis is elevated in response to oxidative stress and regulated by the non-oxidative pentose phosphate pathway in A549 cells. Front Nutr. 2022;9:953056. PubMed PMID: 36276829
8. Ortiz SR, Field MS. Mammalian metabolism of erythritol: a predictive biomarker of metabolic dysfunction. Curr Opin Clin Nutr Metab Care. 2020;23(5):296-301. PubMed PMID: 32412980
9. Flad E, Altstädt A, Drewe J, Gaugler S, Beglinger C, Peterli R, Wölnerhanssen BK, Meyer-Gerspach AC. Predictors of Fasting Endogenous Erythritol and Erythronate Concentrations in Humans: Cross-Sectional and Post-Bariatric Surgery Analyses. Int J Mol Sci. 2025;26(19):9763. PubMed PMID: 41097029
10. Bordier V, Teysseire F, Senner F, Schlotterbeck G, Drewe J, Beglinger C, Wölnerhanssen BK, Meyer-Gerspach AC. Absorption and Metabolism of the Natural Sweeteners Erythritol and Xylitol in Humans: A Dose-Ranging Study. Int J Mol Sci. 2022;23(17):9867. PubMed PMID: 36077269
11. Noda K, Nakayama K, Oku T. Serum glucose and insulin levels and erythritol balance after oral administration of erythritol in healthy subjects. Eur J Clin Nutr. 1994;48(4):286-92. PubMed PMID: 8039489
12. Bornet FR, Blayo A, Dauchy F, Slama G. Plasma and urine kinetics of erythritol after oral ingestion by healthy humans. Regul Toxicol Pharmacol. 1996;24(2 Pt 2):S280-5. PubMed PMID: 8933644
13. Bornet FR, Blayo A, Dauchy F, Slama G. Gastrointestinal response and plasma and urine determinations in human subjects given erythritol. Regul Toxicol Pharmacol. 1996;24(2 Pt 2):S296-302. PubMed PMID: 8933646
14. Hiele M, Ghoos Y, Rutgeerts P, Vantrappen G. Metabolism of erythritol in humans: comparison with glucose and lactitol. Br J Nutr. 1993;69(1):169-76. PubMed PMID: 8457525
15. Arrigoni E, Brouns F, Amadò R. Human gut microbiota does not ferment erythritol. Br J Nutr. 2005;94(5):643-6. PubMed PMID: 16277764
16. Mahalak KK, Firrman J, Tomasula PM, Nuñez A, Lee JJ, Bittinger K, Rinaldi W, Liu LS. Impact of Steviol Glycosides and Erythritol on the Human and Cebus apella Gut Microbiome. J Agric Food Chem. 2020;68(46):13093-13101. PubMed PMID: 31869223
17. Kawano R, Okamura T, Hashimoto Y, Majima S, Senmaru T, Ushigome E, Asano M, Yamazaki M, Takakuwa H, Sasano R, Nakanishi N, Hamaguchi M, Fukui M. Erythritol Ameliorates Small Intestinal Inflammation Induced by High-Fat Diets and Improves Glucose Tolerance. Int J Mol Sci. 2021;22(11):5558. PubMed PMID: 34074061
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Regulatory Documents

1. U.S. Food and Drug Administration. GRAS Notice Inventory, search results for erythritol. FDA GRAS Notice Inventory
2. U.S. Food and Drug Administration. Response letter, GRAS Notice No. GRN 001296, erythritol produced through fermentation of glucose by Yarrowia lipolytica. 2026. FDA letter GRN 001296

PubMed Topic Searches

1. Erythritol and cardiovascular events
2. Erythritol and platelets
3. Erythritol and the pentose phosphate pathway
4. Erythritol gut tolerance
5. Erythritol, blood sugar and insulin

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Connections

• Artificial Sweeteners
• Stevia, the Gut Microbiome and Safety
• Sucralose
• Aspartame
• Acesulfame Potassium
• The Xylitol Paradox
• Platelet Function
• How Blood Clots
• Stroke

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