This is beautiful.
A previously undruggable target was finally properly drugged, doubling the survival time for a very deadly form of pancreatic cancer.
The profession gave it the standing ovation it deserved.
Miller Lite is a bad beer but an incredible beverage, @Tyler_A_Harper argues: “It is neither complicated nor offensive, and it derives its magic from this bland alchemy, this delicate equipoise of fizzy nothingness.” https://t.co/1bsBtA7uzV
@foundmyfitness Does it not impact hypertrophy the same way a cold plunge would? Or does timing matter? I’m super ignorant on the data and mechanisms, would love to hear your opinion.
@foundmyfitness@foundmyfitness I’ve known about the anti-inflammatory effects of curcumin for a while, but have hesitated to take in case it blunts the pro-inflammatory effects that’s needed for hypertrophy to occur. Similar to how cold plunge impacts muscle building too close to weightlifting
The totality of evidence does not support the conclusion that dietary erythritol drives cardiovascular harm.
The paper referenced claims erythritol “adversely affects brain microvascular endothelial cell function,” but it’s an in VITRO study bathing isolated cells in erythritol for 3 hours. People are using epidemiology data to frame the results of that mechanistic, in vitro study as confirming cardiovascular risk from erythritol consumption. The referenced study is interesting and possibly defensible from a mechanistic perspective, but using it to make conclusive claims about the dangers of erythritol consumption is a different story.
Erythritol-harm supporters largely ignore that humans produce erythritol endogenously.
It’s a byproduct of the pentose phosphate pathway, and that pathway is upregulated in states of hyperglycemia, oxidative stress, and pre-existing cardiovascular disease.
The landmark paper from Nature Medicine (2023), often referenced by many who are concerned about erythritol’s safety, never controlled for this. The ARIC metabolomics study from the late 80s (before erythritol entered the food supply) already showed the erythritol-CVD association. If the signal predates dietary exposure, elevated circulating erythritol is almost certainly a biomarker of metabolic dysfunction, not necessarily the cause of it.
People with diabetes and insulin resistance endogenously overproduce erythritol and might preferentially consume erythritol-sweetened products. That’s a major confounding factor, making it essentially impossible to untangle in observational data.
The strongest causal evidence we have, Mendelian randomization, doesn’t support the conclusions many are making about the safety of erythritol consumption. Most MR analyses find no causal link between genetically-predicted erythritol levels and coronary artery disease, diabetes, or chronic kidney disease.
A 2025 MR did find associations with CVD and stroke, but the effect sizes were negligible. It’s also worth emphasizing that MR analyses can’t distinguish endogenous from exogenous erythritol. Actual human clinical trials show erythritol improved endothelial function and reduced aortic stiffness in T2D patients over 4 weeks.
Introducing Project Glasswing: an urgent initiative to help secure the world’s most critical software.
It’s powered by our newest frontier model, Claude Mythos Preview, which can find software vulnerabilities better than all but the most skilled humans.
https://t.co/NQ7IfEtYk7