Update on statins

[Sampei]

I feel great on 5mg/10, but I have a feeling it's the Ezetimibe doing the majority of this, especially given that 2.5mg Crestor did 0...

Kinda worried that the lowering effect might be too much, lol.

try youu can always go back to 5

 

[FuriousAngus]

try youu can always go back to 5

True, will try and report

 

[egruberman]

I’m going to have to disagree.

Lower is better. There’s no well-established floor for LDL-C and the benefits are inversely correlated with diminishing LDL.

 

[Vanargandar]

try youu can always go back to 5

Maybe just 5/5 respectively?

 

[Sampei]

Maybe just 5/5 respectively?

No side effect wise I would prefer to take 10mg ezetemibe instead of 5mg rosuvastatin.

I would take rosu 5mg EOD and ezetemibe 10mg ED and see if the numbers don't change much.

It's always best to get good numbers with the least quantity of meds

 

[frenske]

I’m going to have to disagree.

Lower is better. There’s no well-established floor for LDL-C and the benefits are inversely correlated with diminishing LDL.

I've spent the last day looking into this extensively. I'll share interesting quotes I found

How low is safe? The frontier of very low (<30 mg/dL) LDL cholesterol

Sub-studies focused on patients achieving very low LDL-C have demonstrated a statistically significant reduction in the composite of cardiovascular death, myocardial infarction, ischaemic stroke, coronary revascularization, and unstable angina compared to patients with LDL-C values >30 mg/dL ... whether achieved by any combination of a statin, ezetimibe, and PCSK9 inhibitor.

Evidence supports that cardiovascular clinical benefit increases monotonically in association with lowering LDL-C, without reaching any plateau even for LDL-C as low as 10 mg/dL. However, there is concern with the limited data regarding long-term safety of exposure to LDL- C < 15 mg/dL in RCTs (Table 1). Thus far, it remains unclear if the incremental benefit of reducing LDL-C below 30 mg/dL is significantly advantageous to warrant the potential for in

Safety and efficacy of very low LDL-cholesterol intensive lowering: a meta-analysis and meta-regression of randomized trials

The present study-level meta-analysis on > 109 000 patients found that very low LDL-C levels (<40mg/dl) obtained with intensive lipid-lowering treatments are not associated with any adverse event and maintain a persistent reduction of cardiovascular events; however, data on the safety over the long term of therapeutically-achieved very low LDL-C values are lacking.

Our results are supportive of the most recent international guidelines recommending a further lowering of LDL-C target up to at least 55 mg/dL in patients with very high cardiovascular risk and up to at least 40 mg/dL in those at prohibitive risk with recurrent events.

There appears to be no significant effect on cholesterol based hormone levels or function in patients achieving very low LDL-C

Interesting to note is that the above review found some studies showing that lowering of LDC-C in certain ethnicities might not exhibit protective effects. However, further analysis of those studies showed this was not the cause. There is a need for higher quality research in this regard

Available studies on the topic included in large majority white patients and to date there is no specific analysis evaluating the safety of very low LDL-C levels across different ethnicities.

A study found an inverse correlation between cholesterol levels on statins and occurrence of haemorrhagic stroke;23 this relationship was more consistent in Asian population..... Our findings on a larger population confirm the lack of association.

In summary, I'd say that getting lower than >30mg/dl LDL-C through pharmacological means is beneficial, but outright crushing it to >15mg/dl doesn't have as much data. Though I believe very few could get to that low unless you are staking all the currently available Lipid lowering medications (statin + ezetimibe + bempoic acid + PCSK9 Inhibitor).

I can't express how it is insane that we can even float the idea of crushing our LDC-C to nothing now. It’s a testament to the ingenuity of modern medicine.

 

[egruberman]

In summary, I'd say that getting lower than >30mg/dl LDL-C through pharmacological means is beneficial, but outright crushing it to >15mg/dl doesn't have as much data. Though I believe very few could get to that low unless you are staking all the currently available Lipid lowering medications (statin + ezetimibe + bempoic acid + PCSK9 Inhibitor).

I can't express how it is insane that we can even float the idea of crushing our LDC-C to nothing now. It’s a testament to the ingenuity of modern medicine.

1. Who are you? Welcome to the discourse.
2. Thanks for digging into that at that level of detail. You saved me the effort.
3. Mine was 17mg/dL last I checked. I'm taking all the things. 10mg Rosuvastatin, ezetimibe, bempedoic acid, and Repatha. No adverse effects to speak of.
4. Yes, the fact that we're having that conversation is amazing. Unfortunately, there's still a lot of myth around cholesterol and the great statin conspiracy.

Finally, there's a little bit of data around folks with abetalipoproteinemia. It's not very meaningful and suggests potential vitamin deficiencies at levels below 25mg/dL. There's the potential impact on hormones as well, which we all typically mitigate with exogenous testosterone.

 

[frenske]

1. Who are you? Welcome to the discourse.
2. Thanks for digging into that at that level of detail. You saved me the effort.
3. Mine was 17mg/dL last I checked. I'm taking all the things. 10mg Rosuvastatin, ezetimibe, bempedoic acid, and Repatha. No adverse effects to speak of.
4. Yes, the fact that we're having that conversation is amazing. Unfortunately, there's still a lot of myth around cholesterol and the great statin conspiracy.
Finally, there's a little bit of data around folks with abetalipoproteinemia. It's not very meaningful and suggests potential vitamin deficiencies at levels below 25mg/dL. There's the potential impact on hormones as well, which we all typically mitigate with exogenous testosterone.

I'm just a chill guy who likes to read about biology in his freetime

I think at some point where you achieve an LDL of >30mg/dl the focus should move to other parts of your lipid profile. In fact from my cursory glance at the research it appears that most people are moving away from total cholesterol, LDL and HDL as the only measurements to be looked and more and more are looking at triglycerides and ApoB.

In fact PCSK9 inhibitors are the only currently approved medications that can lower Lp(a) which might have further beneficial effects.

 

[egruberman]

it appears that most people are moving away from total cholesterol, LDL and HDL as the only measurements to be looked and more and more are looking at triglycerides and ApoB.

In fact PCSK9 inhibitors are the only currently approved medications that can lower Lp(a) which might have further beneficial effects.

If you took a look at my post history, you’d see me preaching about ApoB and Lp(a).

LDL can vary in size and isn’t a representation of the quantity of atherogenic particles. ApoB is a direct measurement and correlates linearly with risk.

 

[Photon]

1. Who are you? Welcome to the discourse.
2. Thanks for digging into that at that level of detail. You saved me the effort.
3. Mine was 17mg/dL last I checked. I'm taking all the things. 10mg Rosuvastatin, ezetimibe, bempedoic acid, and Repatha. No adverse effects to speak of.
4. Yes, the fact that we're having that conversation is amazing. Unfortunately, there's still a lot of myth around cholesterol and the great statin conspiracy.

Finally, there's a little bit of data around folks with abetalipoproteinemia. It's not very meaningful and suggests potential vitamin deficiencies at levels below 25mg/dL. There's the potential impact on hormones as well, which we all typically mitigate with exogenous testosterone.

What are your trigs at? I'm more concerned about crashing that than crashing my LDL.

I'm at single digit LDL with repatha + rosu. Interestingly my trigs have remained around 20 with or without repatha.

 

[egruberman]

What are your trigs at? I'm more concerned about crashing that than crashing my LDL.

46mg/dL

 

[dick_starbuck]

I'm just a chill guy who likes to read about biology in his freetime

I think at some point where you achieve an LDL of >30mg/dl the focus should move to other parts of your lipid profile. In fact from my cursory glance at the research it appears that most people are moving away from total cholesterol, LDL and HDL as the only measurements to be looked and more and more are looking at triglycerides and ApoB.

In fact PCSK9 inhibitors are the only currently approved medications that can lower Lp(a) which might have further beneficial effects.

I have watched some interesting content on Lp(a) and baby asprin supplementation.

From anecdotal experience berberine hcl 1000mg daily reduces my sky high Lp(a) to a borderline high number.