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.
4/6 Reply: Same here. Dr kept telling me my LDL was high and was pushing statins like a bitch. But I kept refusing. CAC scan was zero.
Husband had low LDL and had a heart attack and catheterisation with more problems.
5/6 He died 10 months after his first heart attack, from a second heart attack
6/6 How many more people are going to die because the medical profession continue with their "lower the better syndrome"? I can't tell you how sad this makes me feel. How the hell did anyone buy into this ?

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More from @holmanm

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
24 Apr
1/ Ever heard of a KETO/LMHR motherfucker with a Triglyceride level of 1,109 ??? (no I haven't). That's what we are talking about here. Maybe he didn't read the study 😂
2/ To vilify saturated fat is to assume that, over the span of our evolution, our bodies have developed a predilection for a deleterious energy source that contributes to Cardiovascular Disease. Maybe Darwin got it wrong with the whole natural selection thing. 🤪
3/ I think we can agree that exceptionally high levels of serum Triglycerides/uncontrolled diabetes can lead to eruptive xanthoma, and that the clinical features of hypertriglyceridemia, including eruptive xanthomata, typically resolve after the correction of triglyceride levels
Read 5 tweets
6 Apr
1/ VACCINE: Definition "A product that stimulates a person's immune system to produce immunity to a specific disease, protecting the person from that disease. Remind me, how does that work with the Covid Vaccine ? It doesn't provide immunity, nor does it prevent the /2
2/ spread, so why are we touting it as a vaccine ? Given that the antibody response to the spike protein is so focused, could mutations in these restricted sequences lead to a less efficacious vaccine, if the human immune response is specific to the vaccine sequence?
/3
3/ These mutations might be driven by antigenic drift, or by selection, either during natural infection or due to the VACCINE itself. When a virus is grown under the selective pressure of a single monoclonal antibody that targets a single epitope on a viral protein,
Read 5 tweets
5 Apr
1/ The pharma industry would have you believe that Statins are most beneficial in the early stages of Covid-19, so I guess they’re not going to fund any studies which contradict this theory. They would be shooting themselves in the foot. /2
2/ We know that Pandemic influenza infection causes increased oxidative stress, and that low levels of CoQ10 cause immune dysfunction. Statins interfere with the production of mevalonic acid, which is a precursor in the synthesis of Coenzyme Q10.
3/ Statins also act through the reversible block of the HMG-CoA reducing cholesterol synthesis and vitamin D production. Interventional and observational epidemiological studies show that vitamin D DEFICIENCY may confer INCREASED risk of influenza and respiratory tract infection
Read 6 tweets
24 Mar
1/6 Remember Professor Rory Collins, Clinical Trial Service Unit, University of Oxford, UK ?? The person who VILIFIED LDL cholesterol, because the Oxford CTSU was receiving MASSIVE donations from Astra AstraZeneca ?
2/6 He, as you probably know, thinks STATINS are wonder drugs that should be prescribed to almost everyone. Actually, that is not entirely true. He doesn’t believe they should be prescribed to almost everyone. He believes that they should be prescribed to EVERYONE.
3/6 He thinks STATINS have no adverse effects at all. In fact, they actually make people feel better when they take them. He viciously attacks anyone who might dare to suggest otherwise, and has accused them of killing people 😂
Read 6 tweets

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