🐊ZK For Tre🐊 Profile picture
UF MD/PhD. PhD Neuroscience. Neurobio/Neuroimmuno/Metabolism/Stress Biology. Artist formerly known as Dr. Love/Pre-Med Guy. 🤟
Feb 28, 2023 16 tweets 6 min read
Erythritol paper getting lots of legs, which is too bad because there are many better papers in NM everyday.

Linked is a great thread for a synopsis of key takeaways, but I am still seeing people and media make spurious claims, so let's look at the relevant biochem/metabolism 🧵 1. The paper used plasma polyol (erythritol) levels for all their metrics. This is a problem, because erythritol is made endogenously as a normal part of metabolism. Glucose is metabolized through glycolysis (left), but can also be shuttled into the PP pathway (right)
Oct 17, 2020 21 tweets 7 min read
So, this is indeed an interesting finding (though the linked does not provide access to the entire manuscript, which was hard to find), but it should be taken alongside the entirety of the LDL/Cancer relationship data.

An extended thread: A bit of background first-- LDL levels in the context of chronic disease are a bit tricky. (Chronic) Inflammatory conditions decrease LDL levels (via IL-6, TNFa, other cytokines), making it essential to consider the role of reverse causation in these types of analysis.
Oct 17, 2020 8 tweets 2 min read
I’d like to use this to highlight why defining terms matters, and refusing to do so severely reduces the utility of such conversations.

LDL risk stratification are best predicted by AUC. Point/cross-sectional sampling is only weakly predictive.... Therefore, proposing this as a hypothetical without specification of age, first and foremost, limits the ability to extrapolate conclusions extensively. Is the person 70 with no history of events? Likely very mild difference? 30, with family history of ischemic events?