Erythritol

Erythritol is the sugar alcohol that solved the two problems the others have. It barely raises blood glucose, and unlike Sorbitol it is absorbed in the small intestine and excreted largely unchanged, so it mostly avoids the digestive trouble the family is known for.

For several years it was the uncomplicated one. Then 2023 happened, and this is now the only page in this family with an open question on it.

What the studies found

A 2023 paper reported that higher blood erythritol was associated with major adverse cardiovascular events in two independent patient cohorts, and that erythritol enhanced platelet reactivity and clot formation in the laboratory.

A follow-up in 2024 tested it directly in people. Ten healthy volunteers were given 30 grams of erythritol and ten were given glucose. After erythritol, “postprandial circulating erythritol levels were increased >1000-fold compared to baseline”, and platelet activity rose measurably. After glucose, nothing changed.

That is a real result and it should not be waved away. It is also, as the authors themselves record, a study where “the study size was small and replication of results with different cohorts is needed”, and where they “did not test long-term changes in platelet function”.

Why the causal reading is contested

Here is the part most coverage leaves out, and it is the part that decides what the finding means.

Your body makes erythritol. It is produced endogenously from erythrose-4-phosphate, an intermediate in the pentose phosphate pathway, and production goes up when glucose handling is impaired.

So a review of the question puts the alternative explanation plainly: erythritol “may be merely a marker of dysregulation in the Pentose Phosphate Pathway caused by impaired glycemia” rather than a cause of anything, and it is “too early to conclude that platelet activation and enhanced thrombosis is the underlying mechanism”.

The arithmetic supports taking that seriously. The same review notes that global per capita erythritol consumption has been estimated at around 0.023 grams a day, against the 30 grams used in the intervention study. If most circulating erythritol in most people is made rather than eaten, then finding high levels in people who later have cardiac events may be telling you about their metabolism rather than about their sweetener.

This is the same shape as the Parabens story: something found in people with a disease is not thereby a cause of it. The difference is that the paraben question has been worked through and this one has not.

What that leaves you with

An honest position rather than a comfortable one.

The association is real and it was found in two cohorts.

The mechanism is plausible and was demonstrated in a small human study at a large dose.

The causal direction is not established, there is a specific competing explanation, and the doses people actually consume are far below the tested one, except in the case of someone using erythritol-sweetened products heavily and daily.

If you have existing cardiovascular risk, that last exception is the part worth taking to your doctor rather than resolving here. If you use it occasionally, the evidence does not currently support alarm.

Reading the label

Erythritol is rarely alone. It has about seventy percent of the sweetness of sugar, so it is usually blended with a high-intensity sweetener, most often stevia or monk fruit, to make the rest up. A product listing erythritol first and stevia last is mostly erythritol by weight.

The amount is frequently absent. Sugar alcohols may be declared voluntarily under the US rule, so a product built on erythritol need not tell you how many grams it contains, which is the general problem set out on the page for reading labels when you are watching blood sugar.

In Europe it carries the number E968.