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Statins - are they helpful even for moderate levels of LDL? Does anyone take rosuvastatin?

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In EU there is an upcoming update 2023 on different recomendations, it is not available yet for non-members.

The one from 2021 describes how it works https://eas-society.org/publications/guidelines/

-> https://eas-society.org/pages/2021-european-guidelines-on-cvd-prevention-in-clinical-practice/

In short - it is risk-based and for those not passing the various filtering criteria the usage of drug will not be recommended.

I think an update will bring the lower criteria for the values but no chances in the coming years to get it like people joked "in the tap water", it is a drug and will be regulated for long time perhaps. I think it will take 2 decades to cover in practice those at risk at the planet scale, for profilactic usage it will probably be available only afterwards and in a limitied way.

In other developed countries the flow probably is similar.


From the data available on first heart attack and LDL levels in HeFH it seems the shift of the first heart event into 35-65 years diapason due to 2-3 times of higher to the "normal" LDL makes it plausible to assume that those with TC @150 like CR people often have makes their chances really low, probably it makes no sense to try drug to reduce the risk even more so that the HA will really hit after 120 years (unless people are really serious to meet this date in their bodies).




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Yeah, but I'm not CR'd. My neuroticism is already high enough as is. So my LDL is more like barely below 100 (it's not the worst value [ApoB levels are way more important than just LDL], and LDL doesn't increase core rate of aging. but rapamycin.news people rec'd it to me) [1]

Rapamycin also can increase blood lipids (esp TGs)

indiamart has statins for ridiculously cheap

[1] As of 2024 I'm starting semaglutide

Edited by InquilineKea
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From my observation when a person is trying to be as low on energy abundance as possible it actually happens a cat-and-mice play with hypothalamus that speeds up and slows down the metabolism trying to get more fat. So when daily spend is few percent close to the daily intake then there will be low TG (50-90 in my parlance, not 30))) and as close to the persons epi-/genetically possible TC and those should be on the low end unless other factors will play a role. The only unwanted thing - morning glucose could sometimes be in the upper range, often paired with -1h sleep cutoff (or subjectively worse sleep) when body "thinks" it is starved.

This is not CR regimen in hardcore defined way but from lipids perspective should be good enough for a healthy person.

But if in such a regimen there will be lipid anomaly visible - then it probably will pass the risk model filters (maybe not from the first doctor) and a drug could be prescribed.

Actually, a first sign that there is abundance of energy - TG coming to 100 or higher. Then LDL and TC will be higher. Then Insulin will be not on the lowest edge. Then there will be 10 years to change the things from lifestyle/diet perspective. Offcourse there needs to be several times done the bloodwork because sudden oscilations are expected. I do not know why some people here reported they have almost constant values, I can not imagine myself be soooo stable in the energy balance.

In more rare cases glucose anomalies (constant, not from one test and not for a person on tricky diet) could happen before the lipids but I don't know how to generalise them and they seems more rare.

That is all IMHO offcourse.





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I'll talk ApoB and not LDL since the latter is not always an accurate benchmark of atherosclerotic risk as we know.

As discussed in the other thread on Tom Dayspring and Peter Attia's outlive book, statins could be very helpful in making atherosclerotic risk equal to zero. Crestor/Rosuvastatin according to Dayspring decreases ApoB by 38% on average, and this on a baby dose (5mg per day). Zeroing the risk of course happens if ApoB is cut down at early ages, since the time horizon is about 30 years (for the deleterious effects of a high ApoB concentration to take place).

For those of us who are 60 or less, for example, and who surely want to reach 90 or more without significant plaques in the arteries, such a strategy could be very useful.

The benchmark is that an ApoB of 80 mg/dL is the 20% percentile of the population and, if no other risks are present, we should pose ourselves in this region (<= 80 mg/dL).

But staying around the 5th percentile (about 60 mg/dL if I remember well) would be still better.

I have read with interest the article on intermittent statins use, that would abate the already low risks of a baby dose and ensure some reduction in ApoB concentrations. Please note that the muscle pain observed in the group on statins were about the same as those in the control group, hence bespeaking of a nocebo effect.

So, the answer to the questions would be:

  1. Statins could definitely be helpful for moderate levels of LDL/ApoB, if we adhere to the zero-risk conceptualization
  2. I am tempted to take a baby dose of Crestor, but have been reluctant due to the possible side effects and even more to the possible occurrence of nocebo effect. I am probably between the 5th and 20th percentile of ApoB concentration, so not in immediate need of statins, but after reading the article on intermittent usage, might just do that. Or I may start using some supplement like red rice extract and see if it succeeds in abating an already moderate or modest ApoB.
  3. Question not posed, but, there are less potent alternatives like bempedoic acid and ezetimibe, which however are not without their possible side effect and whose price is probably higher than statins. Here, a 4 weeks supply of 5 mg Crestor is totally inexpensive, less than 10 US$ and the generic is even less.


Edited by mccoy
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  • 5 months later...


In a world in which cholesterol-lowering drugs are ubiquitous, it is interesting to mention that the attraction ofSCtoward
an SDF-1 gradient depends on the cholesterol content ofthe cell
membrane. Data reported by Kucia et al. suggests that depletion
of membrane cholesterol severely affects responsiveness of SC
to an SDF-1 gradient.”* Thus, drugs that contribute to lowering
cholesterol, such as statin drugs and polyene antibiotics (e.g.
amphotericin B, nystatin), could reduce the ability of SC to

migrate to tissues.””’”°



=> insulin resistance. I'm more decided on a no, esp b/c it's easier to decrease lipids via other ways (semaglutide...)

Edited by InquilineKea
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  • 3 weeks later...

statins also affect dolichol pathway..



We found that the cholesterol biosynthesis pathway also strongly impacted both mitochondrial superoxide and cytosolic ROS pools. Statins are drugs that inhibit cholesterol biosynthesis and are widely used to reduce morbidity and mortality from cardiovascular disease. Much work has been devoted to studying the antioxidant and ROS-lowering effects of statins (50); however, our data suggest that inhibiting cholesterol synthesis at the cellular level can elevate mitochondrial superoxide and cytosolic ROS. This is consistent with observations by Bouitbir et al., who showed that skeletal muscle from patients with statin-induced muscular myopathy had elevated ROS production and decreased antioxidant defense (51, 52). It is possible that the ROS-inducing effects of cholesterol biosynthesis inhibition may be caused by other important functions of cholesterol, including the regulation of membrane fluidity (53), which is known to regulate mitochondrial respiratory chain function (54) and increase mitochondrial ROS production and toxicity (55).


Edited by InquilineKea
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