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Episode 322: Drs. William Cromwell and Nick Norwitz

Episode 322: Drs. William Cromwell and Nick Norwitz

#Episode #Drs #William #Cromwell #Nick #Norwitz

“LowCarbMD Podcast”

Dr. William Cromwell is board-certified in Family Medicine and Clinical Lipidology with over 20 years of clinical research experience. Dr. Cromwell received his MD from Louisiana State University and completed his residency at the Trover Clinic Foundation in Madisonville, KY in 1990. Since…

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  1. What is liver-generated cholesterol used for if all nucleated cells make cholesterol? I was wondering if you guys could do a discussion on why is cholesterol synthesized and exported from the liver into circulation, being that most cells make their own cholesterol and are not dependent on systemic circulation. Few are dependent on circulating delivery, RBC's, adrenals and ovaries,. Which cells are dependent on LDL cholesterol? I'm wondering as to why there is liver cholesterol synthesis and export. Is it just for extrahepatic membrane maintenance? As far as the molecule of transport you're also looking at the importance/functions of phospholipids, and apoproteins. Apoprotein A's are synthesized first from intestines and liver via digestion signaling,, so maybe they are the important metrics rather than the cholesterol, . The apoproteins are many, and have specific functions. Maybe liver cholesterol export is just a way to have them have mobility and structure, some are ligands to receptors, some are cofactors, HDL is highly utilized in immunity, which makes sense given their site of synthesis intestine, and liver instigated by intestinal immune/food incoming alerts. LDL via VLDL liver, via chylomicron intake, breakdown and apob100 VLDLsynthesis, chylomicron is a mixed bag of 'lipids' and lymph first, so potentially immune-focused signaling, interactive with HDL, as are further liver VLDL/LDL's, I'm just a curious sorting out these fascinating interactions. 'Unneeded' cholesterol is being made into bile, bile is also probably used more for lipid digestion, the biggest intestinal pool of cholesterol is intestinal, with its' elimination via the poo, so with the LMHR I don't think is having huge amounts of bile, nor is high LDL cholesterol a burden, same common acetyl CoA, liver cholesterol in cytosol, ketones in mitochondria, so why would the LDL carrying cholesterol be high,?… Is that LDL carrying a lot of cholesterol? or trigs? i dont think so, i think the bulk of trigs is loaded off from the chylomicrons. Maybe there are some enzyme saturations in the acytlcoa synthesis in the mitochondrial ketone production, that shifts then to cholesterol production?? different lipoproteins have different halflives to consider,.
    Curious, if placing this cholesterol and triglycerides focus of lipoprotein synthesis only may be missing the mark of functions, I mean they provide for multi-function, one immune signaling and function, two fatty acids and glycerol transport, and the structures determine its function abilities, and they respond both to energies influx of foods, and immune stresses.
    i'm curious, a curious person, would like to hear about all this in discussions in the future. if possible, thanks

  2. One of the best interviews about this study Tro! It pays off that you were already involved with a similar study so you know your stuff. Something that was not discussed was that carbs and statins may not be the only options for reducing LDL in LMHRs thatvreally need to be in a strict keto or carnivore diet. Another option may be to slightly increase BMI by eating more calories, particularly fat. So you can have the comparison of Oreos vs Sticks of Butter intervention (it will obviously take longer to increase BMI but it may be worth it for people that need to be in those deeper states of ketosis)

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