1/9 Apoptosis (the process of programmed cell death), is an essential component of the maintenance process of our bodies. It is a highly regulated and organised technique for removing unwanted cells from any organ by the process of induced metabolic suicide.
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2/9 Interfering with this process is a catastrophic game where that good old law of unintended consequences has a field day.
Statins promote apoptosis. They do it in diseased tissues, including cancer cells; three cheers for Statins.
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3/9 Unfortunately they also do it in normal tissues too; boo for Statins.
Statins promote apoptosis in Heart muscle cells. Imagine what having heart muscle cells commit suicide does for your pumping ability, not to mention the risk of heart failure
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4/9 Statins promote apoptosis in the Vascular epithelium. Again you have to wonder what the death of smooth muscle cells lining the vascular wall does for your circulation. Loss of vascular smooth muscle cells via initiation of cell death leads to fibrous cap thinning
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5/9 and promotes necrotic core formation and CALCIFICATION.
The current thinking, as I'm sure everyone knows, is that excess LDL-C in the blood causes atherosclerosis. Ergo, lowering the level will reduce the burden. If this model is correct then, as LDL-C levels go down, /6
6/9 this should lower the risk of Atherosclerosis and therefore we should see less calcium in the arteries.
However – as I have known for some time – this is not what we see. If you take Statins you will increase the amount of calcium in the arteries.
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7/9 CLEVELAND, OH – "The results of a new study suggest that there is a paradoxical relationship between calcification of the coronary artery and atheroma volume among individuals treated with Statin therapy.
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8/9 In the analysis, statins, specifically high-intensity statin therapy, actually promoted coronary calcification"
Statins also promote apoptosis in brain cells, inducing growth suppression and/or apoptosis in neuronal cells, which helps explain the /9
9/9 central nervous system “side effects” associated with Statin ’therapy’.
THINK ! While you still have sufficient brain cells to do so
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1/8 Circulating Oxidised LDL is associated with increased risk of Coronary Heart Disease. Small dense LDL is more Atherogenic or more toxic to the endothelium, and can trigger the atherosclerotic process. Statins Do Not Decrease Small, Dense Low-Density Lipoproteins. /2
2/8 Because the presence of coronary artery disease can be associated with the proportion of small dense LDL, we analyzed the effect of Statins on small dense LDL subfractions in persons without CAD. Unexpectedly, in that analysis, the proportion of small, dense LDL was /3
3/8 significantly HIGHER in patients who were treated with Statins. Moreover, there were no differences in CRP, plasma fibrinogen, HOMA–IR, body mass index, or metabolic syndrome between the Statin and control groups and therefore, we concluded that /4
1/4 Why focus on driving down Lp(a) count when damage to the Intima is what mobilizes Lp(a) to the injured site in the first place ?
We also know from intervention studies (DELTA) that a simple change of 7% of calories in the Standard American diet from Saturated Fat to
/2
2/4 CARBOHYDRATE INCREASED Lp(a) levels by 20%. Another study by Faghihnia et al. found a significant 2.2 mg/dl mean INCREASE in Lp(a) levels following an 8% reduction in Saturated Fat REPLACED with CARBS in healthy participants
What does this tell you ?
@andrewnjiraini
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1/4 While it said that Statins reduce or block cholesterol. The fact is that Statins block the Mevalonate Pathway and by doing so cause the transfer of cholesterol from the bloodstream into organ and muscle cells. The blood cholesterol lowers. /2
2/4 Cells eventually die because Mevalonate, blocked by Statins, is essential to cell life and cell replication. Excess cholesterol forced into cells damages organ/muscle cells throughout the body. Excess cholesterol (minus Mevalonate) is toxic to cells. /3
3/4 Slow cell death begins. On PAPER your lipid profile may look better, but you haven't done anything to reduce your risk of Cardiovascular disease. You've just increased your chances of falling prey to very serious /4
1/6 Newer agents to lower LDL-C levels, such as the PCSK9 inhibitor (Repatha), can reduce LDL-C to extremely low levels.
LDL-C binds toxic bacterial products such as LPS and has other immunologic effects that prevent or ameliorate many of the manifestations of sepsis.
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2/6 Low LDL-C levels were associated with increased risk of death in patients with pneumonia and with increased risk of sepsis in hospitalized patients.
Lately the recommended target LDL level in very high risk patients was reduced to <70 mg/dl, raising the
/3
3/6 question of what the price of such a LOW level will be. To elucidate this concern, we investigated the associations of low serum LDL-C levels (≤ 70 mg/dl) and the incidences of fever, sepsis, and malignancy. Retrospective analysis of 203 patients’ charts was carried
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1/6 Failure to disclose known drug risks by the FDA & MHRA must be prosecuted. Failure to provide raw data from Statin trials should be illegal.
(what are they hiding ?) Studies on safety and efficacy of Statin drugs must be done by truly INDEPENDENT entities without ties to /2
2/6 the pharma industry. With clear evidence of a totally corrupt process being so patently clear, nobody should sit on an FDA approval committee who has vested interest in the outcome. All approval-related meetings, & papers,should be completely transparent and free /3
3/6 from conflict of interest. The medical system is now reminiscent of 2 snakes wrapped around a pole sitting on a pile of dung, and hissing at us, daring us to require it to change. We NEED to snatch its twin tails, break its back and return it to the dung heap. /4
1/11 This post comes right from the heart.
Back in 2007 I knew nothing about Statin drugs.
That changed in 2008 when my Father was prescribed 40mg Atorvastatin, post a minor stroke. The stroke didn’t harm him, but Statins decimated his health. /2
2/11 My Father suffered muscle pain, brain fog, dizziness & memory loss. I recall a day when we both hurriedly crossed a road. He said “Marion, I feel like I’ve torn a tendon, I can hardly walk”. After further investigation it transpired he had indeed ruptured a tendon.
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3/11 I wanted to know why. I spoke to his Consultant and expressed my concern that Atorvastatin may be causing all these issues. His response was to de-prescribe Atorvastatin and put my Father on Ezetimibe (Ezetrol). Within weeks my Father was admitted to hospital with
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