A recent study by Witkowski M., et al., has investigated correlations between various plasma “metabolomics,” including sugar alcohols, such as erythritol (ET), and cardiovascular disease (CVD) events.¹ Plasma ET may be derived from either endogenous production of ET (glucose or fructose) or exogenous intake of ET, some naturally occurring in fruits and some as a food sweeteners. Data included two cohorts, one in the U.S. (n = 2,149) and one in Europe (n = 833), and both were followed for three years; however, it did not include the intake of dietary ET or other carbohydrates, which is a severe limitation of the cohorts’ analyses.¹ Fasting blood ET levels were assessed only once at enrollment in the three-year-long cohort studies. The authors state that the time of enrollment largely preceded the proliferation of erythritol in processed foods, so they believe that the blood ET likely reflected endogenously produced ET. Thus, it is not clear how much of the blood ET was derived from ET intake and there is certainly a possibility most of it came from endogenous production.¹
The correlation analyses found that the highest quartile of blood ET levels had significantly more CVD events than the lowest quartile of blood ET levels.¹ It is well known that correlations do not always imply causation, as also stated by the authors. Most importantly, their analysis cannot be used to imply that the intake of ET raises CVD risk because ET intake was not assessed.¹ Various news outlets picked up the wording from the correlation results and spun this into the headline, “Erythritol sweetener may increase your risk of heart attacks and stroke.” Unfortunately, this alarming conclusion is very misleading, typical of media sensationalism and overzealous public relations departments at academic institutions attempting to create “buzz” for studies being published from their university.
It is also surprising that for a study of such magnitude, Witkowski M., et al., did not discuss the relevant issues related to the endogenous production of ET from glucose and fructose. A 2020 study by Ortiz SR, described the conversion pathways, as seen in Figure 1, where fructose seems to be a more direct precursor to ET.²