Haha. You never know. As long as they don’t charge me extra.
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Hi, I’m new to the site and love this thread. Thanks for all the info. I recently read Malcolm Kendricks book “The Clot Thickens”. I heartily recommend it to anybody believing in statins only. He has some great ideas. Also this:
http://orthomolecular.org/resources/omns/v06n20.shtml
I think Linus Pauling was the smartest guy to ever live. This is a great review of why to take vitamin C. Then I read some stuff from Chris Masterjohn about why to not take so much vitamin C. Lol.
Tough subject.
Thanks, that’s interesting Bicep.
Linus Pauling was an undeniable genius. When I was just an intern at the VA hospital, we fed some subjects a high fat meal and noticed significant arterial stiffening by cardiac cath shortly thereafter.
Interestingly, the stiffness completely reversed after administration of vitamin C. We didn’t know what to make of it and didn’t even publish it.
I’m a big believer in coronary calcium scores and its prognostic value. This study shows no benefits of statins if your score, like mine, is zero:
, Impact of Statins on Cardiovascular Outcomes Following Coronary Artery Calcium Scoring - PubMed
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This is a fascinating new mouse study that illustrates the interaction between LDL and inflammation in creating unstable coronary plaques, and a mechanism by which psychological stress amplifies the process:
Links connecting stress, depression and heart disease risk found in mouse model
American Heart Association Vascular Discovery Scientific Sessions 2022, Presentation 126
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We both probably agree that chronic inflammation underlies most modern illnesses and that stress plays a significant, though poorly understood, role.
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Ldl cholesterol inversely related to all cause mortality in the elderly.
The higher the ldl, the lower the total mortality risk. Hold the statins, maybe rapamycin is protective after all with its modest increases in ldl.
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The explanation I’ve heard for the U-shaped LDL mortality curve is that old/frail/sick patients have low LDL as a result of their illness and therefore die sooner. The low LDL didn’t cause it.
I have to admit, though, there has been accumulating evidence of increased mortality with low LDL levels in correlational research studies, and of course one of the primary goals of researchers in these correlational studies is to try to correct for confounding variables (other factors such as hypertension, obesity, diabetes, etc) which could explain the results.
What I haven’t seen, though, is any study showing that decreasing LDL with medication (statin or otherwise) causes any increase in mortality; in fact, we see either decreased mortality or at worst, no effect on all-cause mortality. If low LDL were responsible for increased mortality in the correlational studies, surely we’d see increased mortality in a prospective double blind placebo controlled study of a medication that lowers LDL well into the range marked as “dangerous” by the correlational studies(?)
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The studies I’ve seen claim 140 is optimal for all cause mortality. My heart doctor says they shoot for 70.
I use IR Niacin, 3 or 4 grams/day. NOT an easy supplement to take in that quantity. It took me months to work up to it. Chris Masterjohn again throws in a wrench. He doesn’t like high dose Niacin. He didn’t say why. I think he likes statins.
It is annoying that we don’t have a better handle on the health variables of the cohorts on seemingly conflicting studies of LDL levels. I am looking for a study where all of the participants were healthy with no underlying health issues. It looks like statins may be beneficial regardless of LDL levels.
Hypocholesterolaemia and mortality in patients with coronary artery disease
"suggesting that statins reduce the risk of mortality irrespective of cholesterol level."
https://onlinelibrary.wiley.com/doi/abs/10.1111/eci.13194
Statin Use Over 65 Years of Age and All-Cause Mortality: A 10-Year Follow-Up of 19 518 People
"All-cause mortality rates were 34% lower among those who had adhered to statin treatment, compared with those who had not"
Statin Use Over 65 Years of Age and All-Cause Mortality: A 10-Year Follow-Up of 19 518 People
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True. If the effect is so small and inconsistent that you need 20000 people to see a difference, it can’t be much.
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I’m 61 and 2 years ago got a CAC of 285 out of the blue. I was eating a bag of chips every day or so. Went Keto and lost 25 lbs, nearly my ideal weight now. No more veg. oils of any kind. Started taking Rapamycin. Numbers went whacky when I got up to 6mg every 10 days. Backed off to 6 every 2 wks and all is well. I’ve gotten most of the side effects listed. Arthritis is gone and brain works better. I’m very happy with Rapa.
Last year CAC was 325. Disappointing, but I’ll do better this time. My goal is to back it up.
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No, 20,000 people show that there is little statistical aberration. A 34% reduction in all-cause mortality is a significant amount.
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This study references studies that show increased risk of infectious disease hospitalizations in those who had low cholesterol 15 years prior. They certainly weren’t driving their cholesterol levels lower when they were healthy 15 years prior.
It’s possible that the Highest LDL group was free of illnesses that could account for lower ldl levels, but shouldn’t the high ldl group be dying from cardiovascular disease and jacking up their mortality rates?
It’s certainly possible that the benefits seen in some statin studies are secondary to its anti inflammatory properties, and not to lipid lowering. In that case , I would still prefer more benign drugs but to each his own.
Back to my original point, it’s very conceivable that the lipid raising property of rapamycin isn’t harmful, and may indeed be beneficial. We just don’t know, and when you don’t know you need to proceed with caution negating any effects of a life extending drug.
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Bicep, your ultimate goal of course is preventing atherosclerosis so you should check out the human studies on pine bark( pycnogenol) plus Centella Asiatica.
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Yes, I do take pine bark and gotu cola, that’s the good news. The bad news is that I got them from bulk supplements, so may not be much active ingredients there. Can’t win. Tried to save a little $.
I’m also a believer in Nattokinase. It reduces fibrinogen (fibrin ?) anyway the stuff that makes clots. Since clots cause heart attack and stroke and according to Malcolm Kendrick they also are what plaque is made of. That’s the good part of Natto. The bad part is the mk7, which I’m told is not the right one. So I take 1000 mk4.
I take 500 mg pine bark from bulk supplements and even if it’s only the equivalent of 200 mg’s, that’s good enough.
I take 45,000 mcg of MK-4. Dose used in the Japanese study over 2 years to prevent osteoporosis.
Just stumbled upon this paper:
Several lines of evidence have demonstrated that rapamycin possess multiple protective effects against AS through various molecular mechanisms. Moreover, it has been used successfully as an anti-proliferation agent to prevent in-stent restenosis or vascular graft stenosis in patients with coronary artery disease. A thorough understanding of the biomedical regulatory mechanism of rapamycin in AS might reveal pathways for retarding AS. This review summarizes the current knowledge of biomedical mechanisms by which rapamycin retards AS through action on various cells (endothelial cells, macrophages, vascular smooth muscle cells, and T-cells) in early and advanced AS and describes clinical and potential clinical applications of the agent.
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One could just as easily state that if we don’t know, it’s worth playing it safe by lowering the lipids rather than not lowering them. I’m not saying a person with LDL 130, 0 calcium score and a decent quality diet and exercise program needs to be on a statin, but if there are plaques and risk factors it seems much more risky to not do something to lower the lipids.
Also another thought, I wish these studies would use something more accurate like ApoB (an easy cheap test which measures actual particle number of atherogenic lipoproteins) or directly measure LDL particle number/size/density rather than the amount of cholesterol carried on LDL, which is messy and indirect in its relationship to CVD.
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Great detective work RapAdmin finding that study. Couldn’t agree more.
Two points apropos to this discussion:
“Rapa can not only decrease the uptake of LDL by the VSMC, it can inhibit cellular cholesterol synthesis.
In addition, RAPA enhanced cholesterol efflux”.
Both inhibiting influx and enhancing efflux of LDL particles would result in less cellular, but higher plasma levels of LDL. In my mind, that’s not necessarily a side effect of rapamycin that needs to be addressed. Rapamycin would appear to prevent atherosclerosis through a multitude of mechanisms.
And that’s the bottom line after all.