“May choose”, is understating it, that should be the norm not the exception. Especially if the intervention is really safe.

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Of course it does. Already posted by @AnUser:

That’s already standard of care per the guidelines:

2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines | Circulation

The most important way to prevent atherosclerotic vascular disease, heart failure, and atrial fibrillation is to promote a healthy lifestyle throughout life.

A team-based care approach is an effective strategy for the prevention of cardiovascular disease. Clinicians should evaluate the social determinants of health that affect individuals to inform treatment decisions.

Adults who are 40 to 75 years of age and are being evaluated for cardiovascular disease prevention should undergo 10-year atherosclerotic cardiovascular disease (ASCVD) risk estimation and have a clinician–patient risk discussion before starting on pharmacological therapy, such as antihypertensive therapy, a statin, or aspirin. In addition, assessing for other risk-enhancing factors can help guide decisions about preventive interventions in select individuals, as can coronary artery calcium scanning.

All adults should consume a healthy diet that emphasizes the intake of vegetables, fruits, nuts, whole grains, lean vegetable or animal protein, and fish and minimizes the intake of trans fats, red meat and processed red meats, refined carbohydrates, and sweetened beverages. For adults with overweight and obesity, counseling and caloric restriction are recommended for achieving and maintaining weight loss.

Adults should engage in at least 150 minutes per week of accumulated moderate-intensity physical activity or 75 minutes per week of vigorous-intensity physical activity.

For adults with type 2 diabetes mellitus, lifestyle changes, such as improving dietary habits and achieving exercise recommendations, are crucial. If medication is indicated, metformin is first-line therapy, followed by consideration of a sodium-glucose cotransporter 2 inhibitor or a glucagon-like peptide-1 receptor agonist.

All adults should be assessed at every healthcare visit for tobacco use, and those who use tobacco should be assisted and strongly advised to quit.

Aspirin should be used infrequently in the routine primary prevention of ASCVD because of lack of net benefit.

Statin therapy is first-line treatment for primary prevention of ASCVD in patients with elevated low-density lipoprotein cholesterol levels (≥190 mg/dL), those with diabetes mellitus, who are 40 to 75 years of age, and those determined to be at sufficient ASCVD risk after a clinician–patient risk discussion.

Nonpharmacological interventions are recommended for all adults with elevated blood pressure or hypertension. For those requiring pharmacological therapy, the target blood pressure should generally be <130/80 mm Hg.

Your friend apparently won’t change his or her diet, doesn’t smoke, and isn’t diabetic. He or she either needs lipid-lowering medications, or a change in attitude about diet (supposing there are levers there, such as high saturated fat intake), or to quit rapamycin.

Because you’re hoping to live more than 10 years, and atherosclerosis is a chronic (compounding time-driven) disease.

Statins have been robustly demonstrated to lower risk of Alzheimer’s and all-cause dementia.

https://www.nature.com/articles/s41598-018-24248-8

… do not develop atherosclerosis without unphysiologic intervention by humans.

Medicines are what’s left if lifestyle changes are off the table (and often even with them, especially if one waits too long). We don’t have remotely the evidence of safety or efficacy (in terms of hard outcomes, not just lipid-lowering) for any supplement that we have for any approved lipid-lowering medication.

Niacin has repeatedly failed to impact hard outcomes in clinical trials; there are no hard outcomes for bergamot, and I don’t think there are even trials of more than 100 patients lasting more than one year.

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Below is the actual study.

They pooled three studies regarding lipids.

3.3. Effect of Brazil Nut Consumption on Serum Lipids Profile

Three studies [17,18,24] examined alteration of serum lipid profile as a consequence of Brazil nut intervention. All pooled results were nonsignificant, including results for total cholesterol (SMD = −0.22, 95% CI: −0.57; 0.14; Table 5, Supplementary Figure S5), HDL cholesterol (SMD = −0.04, 95% CI: −0.28; 0.19; Table 5, Supplementary Figure S6) and LDL cholesterol (SMD = −0.15; 95% CI: −0.43; 0.13, Table 5, Supplementary Figure S7). Alternative imputed missing correlations did not show any significant differences (Supplementary Table S4).

Two of the three studies involved hypertensive and dyslipidaemic subjects.

When considering the results of individual studies, in one trial [17], there were no significant inter-group differences at the start of the trial in any of laboratorial variables, but at the end of follow-up, lower values of total and LDL cholesterol as well as TG for the intervention group supplemented with Brazil nuts compared to the placebo group were observed. However, in studies examining hypertensive and dyslipidaemic patients, no significant differences in serum lipids between Brazil nut and control group were detected.

Unless you’re dyslipidaemic, it might work.

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I like Brazil nuts, cheap insurance!

“If you wait until you are ready, it is almost certainly too late.” ~Seth Godin

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Just key to not each too many though - without too much selenium build up (think Bryan Johnson now down to less than 0.5 nuts per day).

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In my post in another thread, I pointed to Dr. Greger’s article of four nuts a month.

And please. Do not mention Bryan Johnson to me. I am not a fan. I told DeStrider about this too.

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Ok, just didn’t want anyone to overdo it as it would so easy to eg just start eating 5-10 or 15 nuts a day or something.

(My selenium levels were way too high a few years ago and it took a while to understand that the mixed nuts I was eating was enough to give too many Brazil nuts).

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Certainly statins may not be warranted: no one, including Attia, is suggesting treating them the way some people treat multivitamins. If your apoB is 50 and all your other risk factors are under control, there’s no reason to take a lipid-lowering therapy. We’re talking, of course, about what to do if your apoB is high or you have other substantial risk factors and lifestyle alone has been insufficient. That’s exactly what makes a statin (or a blood pressure med for BP or an antidiabetic for elevated blood sugar or insulin) warranted.

All else equal, sure — but the point, again, is that people reading this want to live longer than ten years, and atherosclerosis is a progressive compounding disease. Waiting until disease is established before removing a causal risk factor (apoB or smoking) is the analogy.

CAC being present at all in a person under 70 is a calamity; having it progress is compounding neglect with failure.

Granted how little is known about either the safety or the hard-outcome efficacy of CB, taking it instead of a known lifesaving drug such as a statin would reflect a distortion in the weighing of risks and benefits.

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It’s often not as simple as you suggest. We frequently see people with no risk factors other than borderline lipid levels. If it’s the lower the better, then virtually everyone will be on statins for life. .So when do we go to statins? In this case, CAC can be very helpful and can guide our decisions.

This would be easier if statins were benign, but they’re not. I’ve posted several times a mendelian randomization study showing an increased risk of cognitive decline. This matches what many of us have seen in clinical practice with people complaining of difficulty in focus and word retrieval as well as memory. Many people have muscle aches and constipation. Many of them stop the meds.

Bergamot, pantethine, amla and metamucil have multiple trials exhibiting both efficacy and safety.

I understand your preference for meds over supplements, but all medications have side effects and sometimes it takes years for them to manifest. Sulfonylureas have been around for decades and we never suspected them of leading to cognitive decline, but recent studies show them to be a significant cognitive risk. Who knew?

It’s always about the benefit risk ratio.

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I tried Red Yeast Rice for a bit and I think it did have some impact on recall so I dropped it.

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FWIW

As long as the Red Yeast Rice active ingredient Monacolin K (lovastatin) is not removed.

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Yes, that terrible cognitive decline of 0.067 ms increase in reaction time per 38.7 mg/dL decrease in LDL from HMGCR inhibition.

The standard decline for each year between 18-65 is 2.8 ms.

So you’re aging about 1 month cognitively, while going back to an age of 5 when it comes to LDL.
That is also from lifelong LDL reduction and gene variation that affects the brain as far as I can tell.

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Lovastatin is an older drug it is also lipophilic meaning it can cross the blood brain barrier easily.
Rosuvastatin is hydrophilic meaning it has a harder time crossing the BBB.

If you also knew about the cognitive side effects before taking it, you could’ve been primed for a nocebo effect.

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Your statement is inaccurate and incorrect.

Have you reviewed the published work by William B. Parsons Jr. MD?

If you are that interested in Niacin.

Locate a copy of

Management of the hypercholesterolemic patient

W B PARSONS Jr. Ill Med J. 1959 Mar page’s 120 -127

It’s interesting when it comes to cognitive issues. If you just ask a patient something general you’ll get a different response than if you ask specifics like, “ how’s your focus, word retrieval, memory, and sharpness”.

Many people swear to Mendelian randomized studies on this site, unless those same studies show cognitive impairments from statins.

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Monacolin K{ which is Lovastatin] is one of the active natural compounds in Red Yeast Rice{RYR].

In the US the FDA required the removed on. Monacolin K from RYR “supplements”.

RYR only been use in Chinese Medicine for a few thousands years.

In my view grow/ferment your own RYR.

You can keep the statins.

It’s a statin drug as it’s a HMG-CoA reductase inhibitor, it’s the first statin drug to get to the market as far as I can tell.

The size of the effect matters… like the apoB-lifespan effect or apoB-ASCVD effect, which are massive.
You will probably never find a large effect on cognition in mendelian randomization since it is highly polygenic. Meaning each gene have very small effect.

You did prove there is a mechanism, but not the size of the effect. And many of us are taking precautions by using hydrophilic statins. Simply saying statins are bad for cognition when there is hydrophilic statins seems like it is lacking nuance.

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Statin use decreases the chances of dementia and Alzheimers. Statin use increasing cognitive impairment has been discredited many times. I don’t know why this is even mentioned anymore.
Here is one example of a recent meta-analysis:

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I am in the UK and I bought an Italian version which definitely had the active statin in the RYR.

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There is quite a lot of debate about HMG-CoA reductase inhibition. I have not personally tried to get to a final conclusion about the arguments, but as cholesterol is a key part of cellular metabolism it would not be surprising if there were all sorts of effects from inhibiting it. On a purely personal basis I remember having specific problems recalling certain information when I was taking RYR.

I am OK with my cholesterol figures anyway. Hence I would not say I have a massively strongly held viewpoint on this.

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