You don’t need to worry: the association they found is for serum erythritol levels. They didn’t account for or consider how much erythritol was being consumed. So, serum erythritol correlates with CVD and stroke, but we can’t say whether dietary erythritol does. It’s similar to serum cholesterol vs dietary cholesterol.
This is an important distinction, because the body can make its own erythritol, and it’s actually known that the body will produce more under vascular damage and oxidative stress.
So, it’s quite likely that the results of this study are just a reverse causation. Dr Idz just posted a video about it, and Layne Norton will soon do the same.
That study was based on non-randomized association data of an 8 person sample. Plus, endogenous erythritol is a biomarker of weight gain, diabetes, and cardiovascular problems, which was not controlled for.
Like all things, your individual risk factors will dictate the actual danger. If you’re currently taking blood thinners, it’s probably best to completely avoid erythritol. The study included data from at risk individuals, elective observation individuals, and a small physiological trial to observe in vitro and in vivo effects of erythritol on otherwise healthy individuals (people not at risk or under observation for cardiovascular health). The mechanism discovered
>induced marked and sustained (>2 d) increases in plasma erythritol levels well above thresholds associated with heightened platelet reactivity and thrombosis potential in in vitro and in vivo studies
That said, 80-90% of erythritol is excreted via the kidneys (urine) within 24 hours of ingestion. Unabsorbed erythritol is excreted via feces. Erythritol appears to be resistant to gut flora fermentation over a 24 hour period.
Possible concerns from this would be if you have kidney dysfunction or low bowel motility.
I wouldn’t worry about the study. Erythitol can be endogenously produced via the pentose phosphate pathway.
Basically, some of the products of glycolysis (or the breakdown of glucose) can shoot into a separate pathway called the pentose phosphate pathway. This pathway is responsible for the production of NADPH which is required for the regeneration of the antioxidant glutathione. In essence, an increase in pentose phosphate pathway activation is associated with an increase in antioxidant production which occurs during periods of oxidative stress.
So people who have things like chronic inflammation and cardiovascular disease, have increases in endogenous erythitol as a consequence of increased inflammation. So this study is a case of reverse causation
Yes this was an interesting one. Seems to be gaining a TON of traction even though, as others have mentioned, single studies don’t mean much.
Important to note on this one, it was conducted on a population that was knowingly already at risk for CVD and many of whom, were diagnosed with díabetes. I would, for the most part, consider this study not applicable to most people.
Check out this video from Dr Idz he interprets research like this and explains why this study doesn’t change the general consensus: https://www.tiktok.com/@dr_idz/video/7205634133849115910?is_from_webapp=1&sender_device=mobile&sender_web_id=7205703025221043758
The media did not interpret this study properly.