Plaque stabilization also makes lifestyle/supplements NOT a replacement of medications for those that are indicated them by their cardiologist.

They are in use because they work for certain type of patient that has high LDL-C (apoB) and is at high risk for ASCVD. If you are at hight risk of getting MI it makes more than enough sense to take them.
But there is also discrepancy in all statin studies between the reduction in LDL-C and reduction in mortality which don’t correlate. Simple or more complex logic tells you that it is plausible beyond reasonable doubt even if they do reduce LDL-C they introduce some unknown factor(s) that offset benefit of reduced LDL-C (and there are studies that give an insight into this mechanisms and are not done only by rouge doctors… even “blogger” Peter Attia states that in certain groups of patients there need to be caution with statins). And I am not at all denying that LDL-C is causal in ASCVD. Of course you can argue that damage is cumulative and that if you start intervention too late there is only so much you can do, but also saying that taking statins for primary prevention of ASCVD in low risk individuals would reduce their risk to zero as @AnUser would like often make us believe is based on data is in fact highly speculative. I am not against people using it off label in that sense, I am just saying that in my case ATM statins don’t make sense as a primary prevention. And I am just showing that if someone would like to go down that route that there are some factors and risks to consider. Up until now I picked up some definite points that I would recommend someone wanting to use satins for primary prevention to consider carefully:

  1. if you are APOE4 carrier watch your desmosterol levels and maybe consider PCSK9 inhibitors
  2. if you are predisposed or pre-diabetic watch sugar closely and again consider PCSK9 inhibitors or add metformin
  3. watch your Lp(a) carefully while on statins (again if elevated consider PCSK9 inhibitors or add niacin)

My risk is low and I can spare some time to see where further research may lead the ASCVD and consider later if I would do any other intervention besides lifestyle. There are some new drugs coming, some already available but without enough data ATM.

Why do you think it’s highly speculative?

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Other’s more qualified than yourself, have a different view.

And people even smarter than those three Chinese scientists prove that there is no such association between statin use and risk of dementia.
Sex and Race Differences in the Association Between Statin Use and the Incidence of Alzheimer Disease - PMC (nih.gov)
Do statins impair cognition? A systematic review and meta-analysis of randomized controlled trials - PubMed (nih.gov)

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In my view

Brad Stanfield is not that smart, as of July, 22, 2023 he has never published a peer reviewed paper.

He is a YouTube schnorrer.

The $400,000 rapamycin study that will produce Bupkis.

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Association between Use of Statin and Risk of Dementia: A Meta-Analysis of Observational Studies | Neuroepidemiology | Karger Publishers.

A meta analysis of 30 studies suggested that statin use is associated with a 17% reduction in dementia.

It’s surprising since people taking statins will live longer and hence have a higher likelihood of getting dementia from old age.

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From the paper post above;

Conclusion: …“This study suggests that the use of statin is significantly associated with a decreased risk of dementia. Future studies measuring such outcomes would provide useful information to patients, clinicians, and policymakers. Until further evidence is established, clinicians need to make sure that statin use should remain restricted to the treatment of cardiovascular disease”…

Certainly, they’re emphasizing that this analysis only suggests a lower incidence in the context of cardiovascular disease but it may not treat dementia directly, ie they’re not suggesting based on this analysis that it is an all-cause dementia treatment.

‘The study design was supervised by professor Matt Kaeberlein.’

And everybody knows what an unpublished profiteering hack he is. (/sarc apparently needed)

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I stand by my statement, this “study” will produce Bupkis.

In the future{if this study is ever complete] we will see who is correct.

“The trial will produce very little results, if any of scientific value. With a reported cost of $400,000, the one positive result, the trial will be quite profitable to some individuals.”

Carnac the Magnificent

Carnac was a “mystic from the East” who could psychically “divine” unknown answers to unseen questions.

Speculation is an opinion or conclusion formed on the basis of incomplete information rather than knowledge.

I while I agree that LDL-C exposure is main drive of ASCVD use of statins in low risk population based on knowledge we have today about statin therapy might be that statins only marginally add to cumulative effects of lifestyle and because of possible adverse effects I would think twice before recommending them to anyone in this situation.

  1. LDL-C is not the only cause of ASCVD
  2. there is enough evidence that while on statins other risk factors might become elevated (e.g. while reducing apoB concentration there might be increase in number of (other) atherogenic particles)
  3. data from statin studies show decrease in ASCVD events but decrease is smaller than decrease in LDL-C levels
  4. there are no studies on primary prevention in low risk population with decent duration that would allow unambiguous conclusions
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Yes, Cochrane review confirm this.

Authors’ conclusions

There is good evidence that statins given in late life to people at risk of vascular disease do not prevent cognitive decline or dementia. Biologically, it seems feasible that statins could prevent dementia due to their role in cholesterol reduction and initial evidence from observational studies was very promising. However, indication bias may have been a factor in these studies and the evidence from subsequent RCTs has been negative. There were limitations in the included studies involving the cognitive assessments used and the inclusion of participants at moderate to high vascular risk only.

https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD003160.pub3/full?highlightAbstract=dementia|dementi|statin|statins

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Did you conveniently ignore the two studies I posted above the video (which Dr. Stanfield references)?

Do not take this the wrong way.

I do not waste my time* {the most valuable asset any person has] on a YouTube schnorrer.

Who’s comments and interpretation on papers are minimal a best.

If he{Brad Stanfield] would have a debate with any of the people who were the authors of the papers, the authors would chew him up and spit him out.

  • "Time is our most valuable asset, yet we tend to waste it, kill it and spend it rather than invest it.*
    ~ Jim Rohn

Every single study shows that reducing LDL (and better yet ApoB) results in a reduction of cardiovascular events and mortality. And people like me that have relatively low LDL and high ApoB are at a greater risk than than people with high LDL and low ApoB.

Recent studies demonstrate that you keep gaining benefits by continuing to lower LDL and ApoB even below normal levels.

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No particular reason to continue the statin debate. No minds are going to be changed at this point.

When my first cardiologist suggested a statin and was addressing my misgivings, I had no misgivings about statins but drugs in general, he said that was some evidence that statin use might also lower the incidence of dementia.

There is no definitive proof that statins prevent dementia. There is even less proof that statins increase dementia.

The risk of taking a statin is minimal. The risk of not taking a statin if you need to is much greater than not taking one.

“Compared with no statins use, statins use was associated with dementia risk decrement (relevant risk [RR]: 0.85; 95% confidence interval [CI], 0.80–0.89; P < 0.01) (Table ​(Table3).3). Furthermore, statins use was significantly associated with dementia risk decrement in female (RR: 0.89; 95% CI, 0.80–0.98; P < 0.01) (Table ​(Table3)3) and male (RR: 0.88; 95% CI, 0.83–0.93; P < 0.01) (Table ​(Table3).3). In addition, statins use was significantly associated with dementia risk decrement in Caucasia (RR: 0.89; 95% CI, 0.83–0.96; P < 0.01) (Table ​(Table3)3) and male (RR: 0.92; 95% CI, 0.84–0.97; P < 0.01) (Table ​(Table33).”

“Results from Egger’s tests indicated no evidence of publication bias among these studies”

“To sum up, statins use was associated with dementia risk decrement, and it is expected to become an important auxiliary means of dementia treatment. Due to the limitation of the quality and quantity of the inclusion study, more high-quality, large sample, and multicenter RCT are needed to verify the conclusions of this study in the future.”

Statins use and risk of dementia - PMC

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Yes the association studies are mixed for/against statins. For dementia decrease. Or increase in some studies. And liver cancer a large decrease. Kidney disease small increase. The “ground truth” is the randomized controlled trials they were based on - the benefits and side effects on those trials are probably the closest thing to real, and most side effects are <10% probability and reversible.

I totally agree with this! If you need statins TAKE THEM!

But the study on dementia is probably one of these fake Chinese ones. One author has published over 15.000 articles, the other 9.000… to put it in perspective, Blagosklonny published 275 articles, Sinclair 264…