The Cholesterol Paradox, Part 3 – LDL in Heart Disease & Pulmonary Hypertension

There is more to LDL than meets the eye… While it is true that LDL is an established marker of cardiovascular disease risk, we need to be clear just how and why exactly this is so. First things first. LDL is a means for delivering cholesterol to tissues that need it (and all cells need cholesterol to survive). Cholesterol (and thus LDL) is necessary for life: it is involved in hormone synthesis (including sex hormones), cell wall synthesis and maintenance, and the synthesis of vitamin D and bile acids. Additionally, it is involved in the process of repairing cellular injury. Now

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Can Diet Help Improve Pulmonary Hypertension? An Insight from Inflammatory Bowel Disease Research

While reading a recent paper titled “Endothelial dysfunction in inflammatory bowel diseases: Pathogenesis, assessment and implications” I experienced a feeling a remarkable familiarity… I felt as if I was reading a paper about endothelial dysfunction in Pulmonary Hypertension. It appears that endothelial cell (EC) dysfunction in both inflammatory bowel disease (IBD) and pulmonary hypertension (PH) are quite similar: the same mechanisms of dysfunction abound, the same proinflammatory molecules are released. There is proliferation, smooth muscle cell tone activation, platelet aggregation, hypoxia, eNOS downregulation, imbalance between vasodilators and vasoconstrictors, etc.  Even though this kind of makes sense (that pathology in a

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Lectins, Tissue Transglutaminase, & PH

As per this talk by Robb Wolf at UCSF (at ~1 hour in), non-Western Huntington’s disease carriers don’t seem to express the disease. Since Huntington’s Disease is a rare genetic neurodegenerative disease, this is intriguing and suggests that the expression of the disease may be epigenetic. As he points out a few minutes later, tissue transglutaminase has been implicated in Huntington’s Disease. What does this have to do with epigenetics and PH? Tissue transglutaminase is an enzyme that is responsible for modifying most of the body’s proteins. A key tenant of the “Paleo Diet” and similar metabolic/nutritional therapies is that consumption

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Dr. Rhonda Patrick On Cell Metabolism, Cancer, And More…

I recently listened to this podcast between Robb Wolf, author of The Paleo Solution and one of my favorite nutrition researchers, and Dr. Rhonda Patrick, founder of Found My Fitness and yet another one of my favorite researchers. It was a great discussion about a wide variety of topics mostly revolving around cell metabolism. I’ve included a summary of the key points discussed below. Summary & Key Points: For healthy cellular function and healthy aging in general, you need metabolic flexibility Once a cell acquires so much damage to the genome, it becomes glycolytic The act of becoming glycolytic does not cause

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Why “Starving Cancer” May Not Be So Bogus Of An Idea After All

It is well known that cancer cells switch their metabolism from a normal utilization of glucose and fats (glucose and fatty acid oxidation) to an abnormal, less efficient but more rapid, utilization of glucose. This abnormal utilization is referred to as glycolysis. When oxygen is not available, this is the pathway that is triggered.1 Glycolysis in itself doesn’t cause cancer per se, but it is a necessary consequence (i.e. necessary for cancer to develop). For example, our immune cells, red blood cells, cells lining the gut, and fast twitch muscle fibers, are all glycolytic, and they aren’t cancerous. They are

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The Cholesterol Paradox, Part I

Here is the quote from the above diagram from Metabolic Regulation: A Human Perspective by Keith N. Frayn, regarding cholesterol regulation (emphasis added): “The full length SREBP protein is located in the ER. It is associated with the SREBP cleavage activating protein (SCAP), which “senses” the level of cholesterol, or related sterols, within the membrane of the ER. When the cholesterol content is low, the SCAP-SREBP complex migrates to the Golgi complex, where specific proteases cleave SREBP to release the N-terminal portion, “mature” SREBP. Mature SREBP moves to the nucleus where it binds to sterol response elements in the promoter

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