The investigators did not collect any data on xylitol intake from their human cohort, so we have no way of correlating consumption with MACE risk because we have no way of knowing which participants were regularly consuming xylitol-containing foods. And although xylitol is currently a very common sweetening additive, Witkowski et al. note that the majority of their study participants were enrolled prior to xylitol’s widespread use, suggesting that circulating levels measured in their observational cohort may not be attributable to dietary intake.

Summary from your article:

> xylitol consumption is that diet isn’t the only source of circulating xylitol. This compound is also produced by our own bodies through a process known as the glucuronate pathway, one of the pathways by which we metabolize glucose. So how did the authors ensure they were investigating the relationship between dietary xylitol intake and MACE risk? They didn’t.

> This research group followed the same flawed design and ended up with the same flawed conclusions. SSDD – same [study], different day.

> At best, this work shows that endogenous xylitol correlates with – but doesn’t necessarily contribute to – cardiovascular risk. Far from condemning xylitol as an ingredient in foods and beverages, these data provide no insight whatsoever on potential negative effects of dietary xylitol intake [...] xylitol may even offer advantages for health.

> So in summary, this work should ring a few bells – but there’s no need for it to ring any alarms.