Why do some people with crazy high LDL-C and ApoB develop no plaque in their arteries, while others – including those with far lower LDL and lower ApoB – do develop plaque? 🫀- featuring Thomas Dayspring So, let’s tackle one possible explanation centered around the following term: “Transcytosis.” ✋Quick... Definition & Analogy Transcytosis is the process whereby a cell – in this case, the endothelial cells lining your arteries – sucks up something from outside (here, an LDL particle containing cholesterol), passes that something through its interior, and then out the other side. By way of analogy, think of your artery wall like an exclusive nightclub. Some particles get waved in VIP-style. Others get stuck outside. But what if LDL wasn’t just passively slipping through a hole in the wall, but was actually being escorted through by a bouncer? That is - more or less - transcytosis. #LDL #ApoB #heartdisease #cholesterol #LEM #LMHR #HDL #hearthealth #insulinresistance #metabolichealth #cholesterolcode #staycurious Dave Feldman Adrian Soto-Mota LipoFan Austin Dudzinski, PharmD, BCACPshow more

In today’s full video we walk through transcytosis in more detail, discussing mechanisms and the relevance of Metabolic Health in Cardiovascular disease.  Video 🫀🫶 Here: 

𝑾𝒉𝒚 𝑷𝒆𝒐𝒑𝒍𝒆 𝑺𝒚𝒎𝒑𝒂𝒕𝒉𝒊𝒛𝒆 𝑾𝒊𝒕𝒉 𝑳𝒖𝒊𝒈𝒊 𝑴𝒂𝒏𝒈𝒊𝒐𝒏𝒆 𝒂𝒏𝒅 𝑵𝒐𝒕 𝑷𝒓𝒊𝒗𝒂𝒕𝒆 𝑯𝒆𝒂𝒍𝒕𝒉 𝑰𝒏𝒔𝒖𝒓𝒂𝒏𝒄𝒆 We, the working class, are realizing that political struggle is not left versus right, it's rich versus poor. ★ NEW ARTICLE ⬇️

This just gets worse. It doesn't matter at this point if its magic BBs, the clot thickens, open arterial scabs, even all 3 and more. They been targeting the wrong thing for decades. Blocking an essential metabolic pathway and lipids trying to fix the damage from the food were told to eat to prevent it in the first place. 🤡🌍

@Drlipid I'll help: because neither LDL-C nor ApoB cause atherosclerosis. There you go.

Hi Nick, Great video—super thought-provoking! I’ve got a question about a LMHR and plaque progression in the context of transcytosis 🙏 Imagine someone who was metabolically unhealthy, developed a CAC of 100, and then became a metabolically healthy LMHR (low insulin, high HDL) with LDL-C of 250 mg/dL. If that same person had the same metabolic health improvements and CAC but an LDL-C of 80 mg/dL, would their plaque progress faster at 250 mg/dL? Does high LDL-C pose an independent risk of up regulating transcytosis once “plaque begats plaque,” or is transcytosis rate not influenced by LDL-C levels on its own without underlying poor metabolic health? Thank you!

@Drlipid Keto => (low inflammation && high HDL && insulin sensitivity) => reduced transcytosis => lower cardiovascular risk Got it, Doc. Who wants to live forever anyway?

@Drlipid Kind suggestion to read Dr Malcolm Kendrick’s work.

@Drlipid inflammation, seed oils/initiation, insulin resistance (see inflammation), homocystine, hypercalcemia. tada.

@Drlipid Or.. Normal physiological trancytosis can’t change to said pathological trancytosis when eNOS function and nitric oxide is high

@Drlipid I don't know. I've tuned out. What I'm hearing is- Lean mass hyper responders are doing great, and everyone else is fekked, lol. Perfect.. :P

@Drlipid Great video! More discussion is needed about the role of insulin resistance in cardiovascular disease as well as its effects on the glycocalyx. @BenBikmanPhD