#193

According to Thomas Dayspring there is no difference between the statins and crossing the BBB, so it’s a wash for side effects on potential increase in Alzheimer’s disease risk. From oversupression of synthesis in the brain.
And I thought I was so clever in taking Rosuvastatin over other statins…

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#194

But Dayspring is coming from the lipid perspective only, not the overall health perspective (I suspect). While I haven’t had time to dig into it, a statin that boosts SIRT6 might seem to have additional health benefits above and beyond the lipid lowering benefits…

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#195

My point is that there’s nothing stopping at least me from trying other statins now that’s out the way. I have to confirm again he said that and I didn’t dream about it…
I don’t know anything about boosting SIRT6, but isn’t there other things that can be used for that? If so why aren’t we doing it (supplement, etc)? Some googling suggest there could be SIRT6 boosting supplements.

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#196

For those with drastic glucose increases on other statins, I think I read fluvastatin relative to certain statins doesn’t raise it as much (like the one I’ve been taking - simvastatin) Effect of statins on fasting glucose in non-diabetic individuals: nationwide population-based health examination in Korea | Cardiovascular Diabetology | Full Text

Kachhela and another popular Indian supplier were out of fluvastatin when I asked about a month ago, hopefully one of these suppliers has it

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#197

I believe David Sinclair works on sirtuins as a health and lifespan regulators… they are linked to metabolic control, apoptosis, cell survival, development, inflammation, and healthy aging…

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#198

Maybe check the video I shared a while ago. It is very informative on the subject…

#199

It mostly important for us with APOE4 alleles, they are quite rare. I’ll continue to probably take statins until PCSK9 inhibitors are off patent unless I can’t get optimal apoB levels.

If I didn’t have APOE4 alleles I’d not care at all about “alzheimer’s - statins link”, I would have such much lower risk in the first place.

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#200

I don’t think they are that rare. The general frequency of the APOE4 allele ranges from 9% to 23% in diverse ethnic populations (23% in European descent population). It increases risk for Alzheimer’s disease and is also associated with an earlier Alzheimer’s onset. APOE 4 more than doubles chances of developing late-onset Alzheimer’s. Another 2% to 3% of people have two copies, which renders them 8 to 10 times more likely to get the disease. In addition to raising the chances of Alzheimer’s, the APOE4 variant increases a person’s risk of heart disease and stroke.

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#201

JUPITER trial counterpoint, and interesting perspective from a doctor how they think.

I will probably try atorvastatin 10 mg later on, when my supply of rosuvastatin is out. I don’t really prefer either drug that much. Atorvastatin for reduce diabetes risk, possibly decrease in parkinson, possibly better mood. Or Rosuvastatin that is more hepatoselective and might decrease brain desmosterol less.

For those with myalgia (muscle pain from statin), from Harvard:

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I would add trying a different statin.

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Check for gout, elevated uric acid before starting bempedoic acid.

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#202

Thx. for the video. Did you find the video endorsement for statins in primary prevention? I find it the opposite. It just confirms that statins for primary prevention in low risk (Jupiter was probably all median risk) individuals does not make any sense. There was a great reference in the video as well:

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#203

No it’s not an endorsement, it is a counterpoint like I said.
I don’t care about the JUPITER trial that much either way nor did I use it for my decision making. In fact I have not heard about it at all until recently.

It would only confirm as such if it’d be able to refute the mendelian randomization data which it cannot because of the duration of the study. And I don’t see a reason for why it would, hence it still makes sense to me.

#204

Good for you. I would still think twice. I don’t dispute that LDL-C is genetically linked with lifespan just that lowering it with drugs is more reasonable in genetic subtypes that promote higher LDL-C and especially in individuals who have additional risk factors.
At this moment I haven’t seen a convincing evidence that would support any of the lipid lowering medicine intervention that would allow saying with certainty that benefits outweighs any possible risk in low risk population. For a low risk individual trying to lower apoB burden only two medicines come to my mind as a possible interventions; Ezetimibe and fibrates. First as it does not influence cholesterol synthesis only reabsorption and the second cause they can favorably change lipid profile. Both mechanisms are safe enough IMO. Both are thus not strong in high risk population and almost useless for secondary prevention.
But saying the above, if you are medium/high risk and have unfavorable genetic burden and/or additional risk factors you should do anything to lower your LDL-C to extend your health and lifespan.

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#205

I don’t understand what you’re saying, feels like you’re talking in riddles, be clear what you mean.

How much would that lower apoB for someone around 70-80 mg/dl?

#206

This is worth reading : https://www.ahajournals.org/doi/10.1161/JAHA.118.009778

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#207

High LDL-C = lower lifespan
Medicine intervention makes sense if your genetic subtype favors LDL-C and if you have other risk factors (metabolic disorders, high BP, diabetes etc.)

Combination? I assume 15-25% (if your are cholesterol over absorber possibly little more).
Fibrates seem interesting as they don’t move that much lipids, but particle composition. Which might be IMO better for prevention. They lower TG and favor apoA-1 particles for lipid transport. Thus reducing apoB burden.

#208

I don’t think about risk, so I guess we’re different in that regard.

#209

Yes, most damage is done from your teens to middle age. If you start in middle age with advanced ASCVD the interventions must be very radical in order to prevent future events. Maybe @AnUser and others who are in their twenties must be far more hands on about it.

#210

Yes, I see you are trying to isolate LDL-C as an independent causal factor and I am trying to understand ASCVD as a far more complex degenerative disease.

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#211

No, I think about stopping atheroschlerosis from developing in the first place. Not any risk. Not risk calculators.

#212

But it doesn’t help you much if you choose an intervention that would reduce your lifespan by some other mechanism, does it?

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