Thank you Jack CT 6 is amazing!!!! I just finished reading the monk who sold his Ferrari, good book. My question is I CT with cold water covering all my legs and half. Paleo Diet (Paleolithic, Primal, Caveman, Stone Age, Hunter- Gatherer Diet). How statin drugs really lower cholesterol & kill you one cell at a time – Zo. Suffice to say your body makes cholesterol because it is so utterly vital, the body cannot leave it to chance that you would consume it. You would die instantly without cholesterol – it is a fundamental part of every cell in your body. This book should be read by every person BEFORE they either prescribe or take statins. I would be interested to know if any person could prescribe or take statins AFTER reading it. The book takes one drug company, Merck, and the American Food & Drug Administration (FDA) and a number of other related bodies (e. And it is a scandal. Let us look at the three main findings that the Yosephs have given us: 1) How statin drugs really lower cholesterol. Every cell needs sustenance. The cell says “I’m hungry” and makes a protein called “reductase.” Reductase activates something called the mevalonate pathway. Mevalonate is cell food just as glucose is brain food. Mevalonate is utterly vital for the life of every cell in the human body. The Yoseph’s put it this way: “Mevalonate is the essence of cell renewal. In all cells, mevalonate travels down the mevalonate pathway to make cholesterol and isoprenoids (five- carbon molecules). Both stimulate the cell to grow, replicate its DNA and divide into two cells. This is the . This is life.”Cell renewal is continuous throughout the body – cells lining the gut are turned over every 1. Without the cholesterol and isoprenoids made by the mevalonate pathway, none of this cell rejuvenation happens. Isoprenoids make our cells replicate and renew. Without mevalonate and without isoprenoids, cells age and die. They cannot be replaced. Co. Q1. 0 is an isoprenoid. Co. Q1. 0 is vital for cell energy. Heme- A is an isoprenoid. Heme- A is vital for cell energy and drug metabolism. Isopentenyl adenine is an isoprenoid. 244 thoughts on “ How statin drugs really lower cholesterol & kill you one cell at a time ” Comment navigation. Incerto 4-Book Bundle: Fooled by Randomness The Black Swan The Bed of Procrustes Antifragile - Kindle edition by Nassim Nicholas Taleb. Download it once and read it. Don’t worry about the names in all of this – just remember that Isopentenyl adenine is vital for DNA replication. DNA is the blueprint of every cell. Before a cell divides, it replicates its DNA and the new cell can be formed from the same blueprint. There are other vital isoprenoids – all are stopped from functioning by the disruption of the mevalonate pathway. In the simplified flow chart above, showing the cholesterol production pathway in the body, we can see why statins are called HMG- Co. A Reductase inhibitors – this is the part of the pathway that they disrupt. Statins disable reductase. Without reductase, the mevalonate pathway cannot function properly. Without the mevalonate pathway, cells cannot rejuvenate properly. It follows that the life of every cell in the human body is catastrophically impaired by statins. Per impostare come sfondo desktop: Cliccare sull'immagine con il tasto destro del mouse e seleziona "Imposta come sfondo". Sites by Individuals. The Paleo Diet Defined is my concise definition of the core paleo diet and the many variations of it. Life Expectancy in the Paleolithic by Ron.
How long does it take cells to be affected? That depends on the life cycle of the cell – 3. In chapter four of the Yoseph’s book there is one of the most incredible explanations about what statins actually do, which I have not seen elsewhere. The Yosephs describe the fact that statins are not just HMG- Co. A reductase inhibitors, they are also reductase stimulators. Because reductase is the . Reductase production increases to try to reopen the mevalonate pathway. It’s a terrific attempt by the body to fight back. However, the Yosephs sadly note: “So far, they have not figured out how to save statin- fed dying cells except by adding back mevalonate.”The book describes that there are two ways in which every cell of the body can get the cholesterol it so vitally needs: 1) it can make cholesterol and 2) it can take cholesterol from the blood stream. When someone takes statins, the cells are impaired from making cholesterol so they try to take the cholesterol from the blood stream. The LDL receptors on each cell go into overdrive and try to . This lowers the cholesterol in the blood stream. Similarly HDL stands for High Density Lipoprotein – it is not cholesterol, let alone good cholesterol). That’s how statins lower cholesterol and that’s how statins kill us one cell at a time. Familial Hypercholesterolemia (FH)It is time to mention Familial Hypercholesterolemia (FH) here. FH is a genetic condition caused by a gene defect on chromosome 1. The defect makes the body unable to remove LDL from the bloodstream, resulting in consistently high levels of LDL. Bearing in mind that FH is rare to start with – one in 5. FH the LDL receptors work to an extent (just not very well); in other cases the LDL receptors work barely at all. My logical consideration of FH suggests to me that the problem is that the LDL receptors don’t work properly and therefore the LDL (lipoproteins) cannot get into the body’s cells in the way that they are supposed to. This means that cells don’t get the vital LDL, carrying the vital protein, lipids and cholesterol needed for the cell’s health. LDL in the blood stream is high because the LDL has stayed in the bloodstream and has not been able to get into the cells – where it is supposed to go. Hence high LDL blood levels are the sign that someone has FH. The high LDL levels are, however, a symptom and not a cause or a problem per se. The problem is that the health of every cell is compromised by LDL not getting to the cell. This includes heart, brain and muscle cells – all cells. An FH sufferer can therefore have heart problems – because of too little LDL reaching the heart cells – not because of too much LDL! How differently things can be seen when one is not blinded by thinking that cholesterol or lipoproteins are bad. This also explains why high HDL would be seen as good. HDL is the lipoprotein that carries used lipids and cholesterol back to the liver for recycling. If the LDL were not able to get to the cells to do its job then there is little for HDL to carry back to recycle. Hence HDL would be low and this would be seen as bad with impaired understanding as to why. Ironically, the most serious form of Familial Hypercholesterolemia would receive no benefit from statins anyway. As the extreme form of FH is characterised by LDL receptors working barely at all, even the body going into crisis mode, and trying to take LDL from the blood stream with increased LDL receptor activity, will not work if the LDL receptors are not working well enough in the first place. Hence the LDL will stay in the blood stream with an extreme sufferer of FH and yet the statin has reduced what little chance the FH sufferer’s body had of making cholesterol within the cell. The FH sufferer should ideally be given medication (if anything existed) to stimulate cholesterol production within the cell, so that the cell would at least get the vital cholesterol it needs, even when it couldn’t get it from the blood stream. What was known by whom and when as statins were pushed through to approval? We need to introduce some key players here: – Brown & Goldstein were awarded a Nobel Prize for their work with lipoproteins. We will see what they knew along the way and their involvement with statin approval.– Akira Endo was a Japanese biochemist who graduated from Tohoku University in 1. Sankyo Pharmaceuticals in Tokyo. Endo is the guy who discovered the poison that statins are made of. In 1. 97. 1 he began his search for a fungal mycotoxin that would lower cholesterol. He discovered that citrinin lowered blood cholesterol and published a report on this. In the same year he abandoned his work with citrinin because it was too toxic. He extracted another mycotoxin from Penicillium Citrinum called “ML- 2. B”, which was less toxic but still lowered cholesterol. ML- 2. 36. B became Endo’s first experimental statin. Merck shafted Sankyo and Endo was wrongly seen as the betrayer and was ostracised by Sankyo). Endo was then . The book states “Statins – secondary fungal metabolites – are anti- life or anti- bios. Statins are antibiotics. Because antibiotics are anti- bios and kill . Statins, on the other hand, are often prescribed for life. Most antibiotics also have specific action on specific microbes. Not so with statins. Statins indiscriminately kill any cell including human cells.” (Their emphasis). This could explain the warnings about gut health on statin patient leaflets.)In 1. Watson and Crick discovered the structure of DNA. In 1. 97. 9 Marvin Siperstein discovered that DNA replication (cell rejuvenation) required isoprenoids from mevalonate (specifically the isoprenoid called isopentenyl adenine). These articles were sadly ignored.)In 1. Beecham Labs in the UK (what became Smtih. Kline Beecham and then Glaxo Smith. Kline) had discovered a statin named “compactin”. Sankyo Pharmaceuticals had discovered the same compound in parallel in Japan. They called it Mevastatin. So they knew exactly what they were stopping when they named this drug. Within an hour of adding compactin to cholesterol- rich cells, the cell reproduction cycle was completely stopped. Within minutes of adding back a small amount of mevalonate, DNA replication and cell cycles were completely restored. This bit is key – because the cells were given ample cholesterol before the experiment (they were “cholesterol- rich cells”), it was clear that the problem was not cholesterol deprivation but isopentenyl adenine deprivation (that isoprenoid that enables DNA replication). The absence of this isoprenoid prevented DNA replication and the entire cell cycle. As the Yosephs state “Cells are poisoned by statins because statins block the making of isoprenoids from mevalonate. If cells cannot replicate, they inevitably die.”In 1. Yoseph book), Endo, Brown and Goldstein published a paper documenting that statins caused an increase in reductase. It was therefore known back this far that statins should not necessarily be called reductase inhibitors, but reductase stimulators. They didn’t detect the increase in LDL receptor activity at this time. In 1. 97. 8 Merck developed their own statin. In 1. 97. 9 Endo patented another statin and sold it to Sankyo to try to restore his honour. On p. 14. 3 of the book, The Yosephs present an image of a paper written by Brown and Goldstein in The Journal of Biological Chemistry (1.
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