Peter Attia has a blog entry about the weak xylitol-cardiovascular disease research. For Xylitol, see https://peterattiamd.com/xylitol-and-cvd/

  The problem with interpreting these results as a condemnation of 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. ...

  The rapid rate of xylitol excretion observed in healthy volunteers with return to near baseline (fasting) levels within hours following ingestion of a significant dietary exposure suggests that the plasma levels observed in our observational (validation) cohort represent variations in endogenous production/levels and not food intake.

Erythritol is commonly found in sugar-free or keto-friendly products like beverages, desserts, and snacks. A single serving of an erythritol-sweetened product (e.g., a sugar-free soda, keto ice cream, or protein bar) often contains 10–30 g of erythritol.

Studies, such as the 2023 Nature Medicine study, used a 30 g dose in intervention experiments to simulate typical consumption (e.g., one sweetened beverage or dessert). This dose raised plasma erythritol to 5–7 mM within 30 minutes, a level linked to increased platelet reactivity and clotting risk.