1/6 What’s really going on when you take a Statin drug ? Do any of you who take them really know or even care ? Have you ever questioned it ? Statin drugs effectively reduce plasma cholesterol levels, by inhibiting the chemical transformation HMG-CoA to Mevalonate, which is an
2/6 early and rate-limiting step in the biosynthesis of cholesterol. The Mevalonate pathway is blocked which induces cells to increase LDL receptors. Increased LDL receptors forces more cholesterol into cells (bear in mind that excess cholesterol in cells is TOXIC)
3/6 However, no worry. Serum cholesterol is lowered. Take Statins, choke off the life cycle of liver cells into mass producing cholesterol receptors that soak up the supposedly 'BAD' blood cholesterol, most of which is normally made by the liver via the Mevalonate pathway
4/6 in the first place. Get blood tested and WOWSER, just like MAGIC - LDL is lower.😱 You and your Cardiologist are ecstatic - It’s marvellous. Serum cholesterol has been shoved into organ/muscle cells causing cell death, your cholesterol results look great (on paper), 😉
5/6 Like the magic trick with the disappearing Dove, lowering LDL cholesterol with a Statin comes with a death sentence. The bird didn't disappear. As the cage was crushed, it was shoved into a secret box at the bottom of the cage.
6/6 It happened so fast and you were so distracted, you didn't hear the dove cry, the bones crunch or see the blood splatter.

What a wonderful drug eh ?

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More from @holmanm

24 May
1/6 "This is the latest hype everyone is so eager to debunk but actually the obesity insulin model hasn't been debunked it's just become more nuanced.
Here's what we know for sure. Wherever you find obesity you find high carbohydrate consumption. Every single time.
2/6 You find high insulin. You find high blood glucose.
So carbohydrates themselves do not cause obesity but you will not find obesity without carbohydrates.
And if you throw in low protein you really up the possibilities of metabolic dysfunction.
3/6 and if you throw high fat on top of the high carb, then you're really off to the races and your fatty liver disease and insulin resistance will start accelerating. Especially if that fat is not natural saturated fat but instead soybean oil or some kind of seed oil/trans fat
Read 6 tweets
24 May
1/4 The Guideline Development Group advise that there is no evidence of benefit from adding supplements of CoQ10 to reduce muscle related adverse events. They ignored the fact that Statins block the endogenous production of CoQ10. Tiredness, or muscle pain,
2/4 become an inevitable side effect for many people due to this fundamental interference with mitochondrial energy production.
CoQ10 is the most important acceptor and donor of electrons in the Krebs citric acid cycle (oxidative phosphorylation).
3/4 Biochemist Dr John McLaren-Howard’s ATP profile test measures the rate of oxidative phosphorylation which controls the rate of ADP (adenosine diphosphate) to ATP (adenosine triphosphate) conversion. His clinical co-author, Dr Sarah Myhill, writes that Statins invariably
Read 4 tweets
24 May
1/5 Statins and other cholesterol lowering meds undoubtedly have pleiotropic effects that may largely account for the minuscule clinical benefits observed. However you have to balance those against the very unfavourable consequences of taking this type of drug.
2/5 It is my opinion that the epidemic of heart failure and atherosclerosis we are seeing right now is aggravated by the pervasive use of cholesterol lowering drugs. In the case of statins they inhibit the synthesis of vitamin K2, the cofactor for matrix Gla-protein activation,
3/5 which in turn protects arteries from calcification. Statins also inhibit the biosynthesis of selenium containing proteins, one of which is glutathione peroxidase serving to suppress peroxidative stress. Statin treatment also leads to decreased insulin secretion in the
Read 5 tweets
5 May
1/6 I visit FB forums to see what's going on: Read this and do some SERIOUS thinking.

Sleepless night: I, with HIGH cholesterol (notably LDL), and NOT on a Statin - just passed a Coronary calcium score with a flying colors mark of ZERO.
2/6 (Yes, I know this doesn’t show soft plaque, and that I shouldn’t assume that I have dodged all bullets).
Contrast that with my husband, who is on a Statin, and has “BETTER” LDL cholesterol numbers than I do - has just had a heart attack and catheterization this late night
3/6 and more issues to address. I will find out the extent of things once I get back to the hospital in a few hours.
Just heard he has 100% blockage in the LAD and will need a bypass. WOW.
Read 6 tweets
26 Apr
1/5 It is very, very hard to explain how utterly disreputable the lipid hypothesis is. All of this angst about increased LDL-C and/or apoB counts on LC diets is based on the assumption that somewhere, somehow, cholesterol is the cause of heart disease. How LDL-C invades"
2/5 (by active and controlled transcytosis!) the sub-endothelial space, disappears from there and then suddenly appears at over 200 micrometres deeper, with none showing in the intervening zone requires a belief tenet which bears no resemblance to reality...
3/5 No one would reasonably doubt that the lipid deep down at the intima/media junction level comes from lipoproteins (though there are other plausible explanations). No one would doubt that loading the lipoproteins with with Linoleic acid is likely to be a Bad thing.
Read 5 tweets
25 Apr
1/5 It appears we are still comparing FH (defective LDL receptors) with Keto/LMHR and the Low carb community
2/5 If we look at a population stratified by all 3 standard lipid markers, (TG), HDL, and LDL, the Framingham Offspring Cohort, we can see that there is no increased risk of CVD associated with higher LDL levels in persons with high HDL and low TG
3/5 Elevations in LDL due to eating saturated fat are more usually accompanied by increases in HDL and decreases in Triglycerides than not, especially when total fat replaces carbohydrates.
Read 5 tweets

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