THE PURPLE PILL INCREASES THE RISK OF HEART ATTACKS[1]
As surprising as this may be it makes perfect sense when you consider the problems that have been associated with the use of over the counter drugs like the purple pill and others like Nexium. They are referred as PPI drugs. We were warned about them in Medical School when they came out in the early 80s (yes, I am old…) We were then told they should be used only in the most dire cases of GI bleeding from ulcers and colitis, and only when Zantac and Tagamet failed. The latter suppress stomach acid only partially. PPI drugs shut off acid 100%. Our professors were leery of the consequences of doing so; eliminating an essential function of our physiology-proper digestion, did not seem right back then…
But, over the years PPI drugs slowly expanded their marketing. Most patients are now prescribed these drugs for practically any digestion-related problem, from simple reflux, to ulcers, and colitis. Interestingly, TV commercials tell you exactly what the problem is: “Is your favorite food fighting you?” In other words, improving one’s diet takes care of the problems in the vast majority of people.
So, what have we learned through three plus decades of using PPIs? Blocking the proper digestion of food has been associated with many obvious problems. The best documented are poor absorption of nutrients like B vitamins, and minerals. PPI drugs also alter the pH of the gut downstream; it becomes less acidic, which has been shown to alter the health and balance of the microbiome therein. These are the main reasons why these drugs increase the risk of heart attacks.
B vitamins are essential for methylation and “arginine-dressing” of proteins.[2] All, proteins, including those that line our arteries (endothelium) are not finished products until they get micronutrients added to them. A deficiency of B vitamins and the amino acid Arginine have been associated with cardiovascular problems. Specifically, they raise the levels of Homocysteine and Asymmetric DiMethylArginine (ADMA,) both of which signal oxidation and inflammation of the endothelium. Poor balance of minerals also impacts negatively the health of our arteries, to say nothing of osteoporosis problems associated with PPI drugs.
Then, there is the matter of altering our gut flora: the proper digestion and absorption of nutrients to maintain the integrity of our arteries is thus compromised. Think of them as getting oxidized and inflamed. Here is the evidence:
“L-Carnitine Consumption, Its Metabolism by Intestinal Microbiota, and Cardiovascular Health,” J. Mayo Clinic Proceedings 2013;88:786
“Intestinal microbiota metabolism of L-Carnitine, a nutrient in red meat, promotes atherosclerosis,” J. Nature Medicine Epub April 7 2013. Red meat and high energy drinks induce gut flora to metabolize TMAO (trimethylamine-N-oxide) which leads to enhanced capacity to deposit cholesterol on arterial walls. They recommend a test to look for TMAO.
“Effect of probiotics on blood pressure: a systematic review and meta analysis of randomized, controlled trials,” J. Hypertension DOI:10.161/hypertensionaha.114.03469. Abstract. Miso, sauerkraut, yogurt: 3.3 reduction in systolic and 2.4 in diastolic. Mortality down 22%
“Oxidized phospholipids are found in the vasculature of animal models of atherosclerosis, in human atherosclerotic lesions, and in other inflammatory diseases,” J. Arterioscler Thromb Vasc Biol. 2012;32:2553 Oxidized phospholipids cause vascular and nonvascular cells to initiate an inflammatory reaction. Metabolites of arachidonic acid, such as 12-hydroxyeicosatetraenoic acid, can mimic some of the inflammatory properties of oxidized phospholipids. In vitro and in vivo normal high-density lipoprotein (HDL), normal apolipoprotein A-I, and apolipoprotein A-I mimetic peptides, each likely acting in a different manner, prevent the inflammatory reaction characteristic of atherosclerosis, and this is associated with decreased levels of oxidized lipids in tissues and cells. HDL from animal models of atherosclerosis or from humans with atherosclerosis or from humans or animals with other chronic inflammatory diseases does not prevent the inflammatory reaction characteristic of atherosclerosis and may even enhance the inflammatory reaction. In mice and perhaps humans, ≈30% of the steady-state plasma HDL-cholesterol pool is derived from the small intestine. The metabolism of phospholipids by gut bacteria has been recently implicated in atherosclerosis in both mice and humans.
Do you still think that it is ok to pop the purple pill so that you can eat your greasy, sugary foods?
They are fighting you for a reason, you know…
