1/6 Doctors, uninformed of how Statins really work, have clung on to the "pleiotropic effect" of Statins, rather than what Statins really are - Mitochondrial Toxins. For example, Statins suppress cell cycles of white blood cells. Patients with autoimmune disease sometimes /2
2/6 have immune "flare ups" with elevated white blood cell counts. Because Statins inhibit white blood cell turnover, people with autoimmune diseases appear to be doing better (on paper) because their white blood cell counts are down ! Drs WRONGLY conclude that Statins /3
3/6 have done some "GOOD". Similarly, acute infections often elevate white blood cells: Since statins can halt white blood cell cycles, Statins APPEAR to "decrease " infection. Because replication of any type of diseased cell is blocked/inhibited by Statins, the list of /4
4/6 so-called "pleiotropic effects" of Statins is growing. However, Statins eventually interrupt the cell cycle of EVERY cell in the body, and while there are benefits to be measured by blocking the life cycle of diseased cells, the cost is /5
5/6 doing HARM to EVERY HEALTHY CELL in the body. No matter how you look at it, the benefits-to-risk ratio of Statins is abysmal. In addition, Statin drugs have a number of negative effects on cardiomyocytes, in particular, increased oxidative stress, endoplasmic reticulum /6
6/6 stress, damage to both mitochondria and Intercalated discs, and inhibition of glucose transport into cardiomyocytes.
So please don't send me studies which claim that Statins are "anti-inflammatory" when the truth is that Statins increase ROS and oxidative stress !!
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1/14 The body manufactures cholesterol for a reason. Cholesterol is a primary constituent that provides cell membranes with support. It is a very important structural & functional molecule of the body. It has a job to do. It is both reparative and protective. So how does high /2
2/14 serum cholesterol cause Atherosclerosis ? It is said that more cholesterol in the blood causes more cholesterol to accumulate in the artery, & It is that cholesterol which becomes trapped and invades the arterial wall causing atherosclerosis. Hence, the lower the better /3
3/14 mantra which doesn’t make any sense. There have been numerous studies suggesting no relationship between the change in plaque volume & level of LDL. Isn’t it also true that atherosclerosis is more severe in areas of high arterial stress, which points to high BP being /4
1/11 Some people like liver. They eat it, but do not want anything eating theirs. A high percentage of Statin injuries are due to liver damage. A predicable direct effect of statins and not a "side effect" or adverse drug reaction. From the small intestines, Statins are /2
2/11 absorbed into the blood & pass through the liver. While all organs make cholesterol, the liver generates the most to make bile. Bile digests fat & is recycled to the liver. That makes the liver the “target organ” of Statins By blocking Reductase, liver cells are /3
3/11 'tricked' into thinking that Mevalonate levels are “LOW” & reflexively produce more reductase. Elevated reductase in cells is toxic and stimulates liver cells to make more LDL receptors that attract the LDL cholesterol from the dense blood tributaries that flow through /4
1/7 Andrew I'm sorry to hear this. As I recall we discussed Statin use some time ago when my old @holmanm account was active. Since Statins inhibit cholesterol synthesis in the liver more than in any other tissue, it is not surprising that elevations in the liver enzymes ALT
/2
2/7 and AST have been noted since the first clinical trials with Lovastatin. Statins can cause acute liver failure, hepatitis, cholestasis, and “transaminitis” (asymptomatic elevation of ALT and AST levels).
The 2 MOST clinically important adverse effects of Statins are
/3
3/7 hepatotoxicity, reflected by increased levels of alanine aminotransferase (ALT) and aspartate amino- transferase (AST), and myopathy, which includes a range of muscle symptoms and elevated serum markers of muscle injury such as creatine kinase (CK), AST, and Aldolase.
/4
1/4 New research published in the journal PLoS indicates that the use of statins is associated with an increased prevalence of microalbuminuria, a well-known marker of vascular dysfunction, affecting both cardiovascular and kidney disease risk.
/2
2/4 "Microalbuminuria is known to double the risk for a cardiovascular event in patients with type 2 diabetes mellitus and is a marker for endothelial function; endothelial dysfunction may, in fact, be far more significant than elevated blood lipids in determining /3
3/4 cardiovascular disease risk. (too right !)
This new finding therefore calls into question the justification for using statin drugs for prevention of cardiovascular disease, which is presently the standard of care in the drug-base conventional medical model"
/4
1/5 I've seen Warfarin prescribed alongside a Statin on many occasions. What a great way to calcify arteries. A long-term adverse effect of warfarin therapy is vascular calcification. The proven mechanism is warfarin’s near-shutdown of the body’s vitamin K recycling capacity. /2
2/5 As the availability of functional (that is, electronically reduced) vitamin K via the K cycle becomes limited, whether from warfarin therapy, from dietary inadequacies, or from other factors, the body progressively is deprived of vitamin K’s carboxylation capacity. /3
3/5 The Vit K dependent proteins OC and MGP are abundant in bone and vessel wall connective tissues, respectively, and are central to calcium homeostasis in these tissues. Vitamin K depletion impairs their physiological carboxylation, which translates into derangement /4
1/9 Nobel Prize winning Neuroscientist Eric Kandel says - "we are who we are because of what we learn and what we remember". Who am I, then, if my memory is
impaired🤔 ? People who take Statins very often complain about brain fog, inability to think clearly, memory loss, /2
2/9 depression. Even the FDA warns on Statin labelling that people have developed memory loss or confusion while taking Statins. Statins are - 'Thief of memory'
Here's how. The basic unit of communication in the nervous system is the nerve cell (neuron).
Each nerve cell /3
3/9 consists of the cell body, which includes the nucleus, a major branching fibre (axon) and numerous smaller branching fibers (dendrites). These circuits are highly dynamic with ongoing reconfiguration and refinement - characteristic of the structural plasticity for /4