Anonymous35
Member
Yes but rosuvastatin with bad kidney like mine can accumulate and then as a result rhabdo
MESO-Rx
Anabolic Steroids
Who here is on a statin?
- Thread starter Juicedhead
- Start date
OldGHGuy
Member
Never knew. Thanks
Ghoul
Member
Yeah I see that's the "default" for severe chronic kidney disease, although Rosuvastatin is considered safe up to 10mg with CKD, even in dialysis patients,
FYI Pitavastatin has lower risk of muscle related sides in chronic kidney disease than Atorvastatin. Unlike Pitavastatin, Atorvastatin is metabolized by CYP3A4, and so are AAS, potentially causing a buildup of levels leading to muscle pain and rhabdo with simultaneous use of steroids.
Also Atorvastatin raises the risk of new onset diabetes higher than Rosu, and much higher than Pita, which actually improves rather than worsens insulin sensitivity.
Anonymous35
Member
yes in france pita doesn’t exist. I have pravastatin so its good.
Yeah but most people on dialysis doesn’t workout lmao
So those safe doses are probably not safe for bodybuilders athletes with chronic kidney disease
Do you have a link to the FDA study looking at various ezetimibe dosages, I can't seem to find it?
*Edit found it https://doi.org/10.1016/S1520-765X(01)90107-5
16% reduction at 5mg vs 19% reduction at 20mg. Hard to believe how effective even 0.25mg is. For example, with an LDL of 100, there is only a ~3 point reduction between 5 and 10mg of ezetimibe. I don't have a prescription and don't want any cholesterol drugs on my medical history right now, so I will stick with 5mg per day.
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Ghoul
Member
I've highlighted the LDL drop in 5 to 10mg doses found in the confirmatory protocol trial. Each square represents the doses used .25mg, 1mg, 2.5mg, 5mg, 10mg, 20mg (max). After 10mg you see it flattens out as it goes to 20mg with no further significant LDL reduction, but 5 to 10 shows a meaningful drop.
From this, the confidential drug approval response from the FDA. Some data is considered proprietary and redacted, but it's easy to extrapolate from the trial linked below.
(from clinical pharmacology review Part 1)
FDA Zetia Approval Docs
Here's the underlying trial used for the FDA application. I have a subscription that gives me access to (and can't see of its blocked to public view). If you can't read it lmk and I'll upload a copy here for you.
*It's worth noting a lot of "underpowered" papers came out chopping ezetimibe into smaller doses, as low as 2.5mg and concluding it was as effective as a full 10mg dose. Keep in mind this is when each tablet cost $50(!!!) so trying to get 4 for 1 made sense. Now that the price is 15¢, there's far less incentive to stray from the dose that's clinically proven to provide max benefit for the largest group of people.
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You give great information, and then just completely embellish this part. This is the reality:
At 5000 at 50, you'd only have a 1% cumulative risk of a heart attack. If you extend the line out, mean age of heart attack would be around 75.
That's not to say you shouldn't get it under control now. The risk increases exponentially after 5000. But hitting 5000 is certainly not the death sentence it's being made out to be.
Ghoul
Member
Speaking of embellishment, I'm pretty sure I didn't say "death sentence" lol.
I'm curious where you found that chart.
The "5000mg" cumulative exposure is a great way to make it easy for people to grasp the concept of, as you pointed out, the way the threat is slow slow slow then starts to take off like a rocket,
A few updates regarding the cumulative risk numbers in the chart:
In the near decade since it was released, newer studies looking at larger pools of data along with the results of advanced imaging and autopsy results, reveal that the risk is substantially underestimated—2–3× higher for most adults, finding that nearly 60% of adults below the 5,000 mg·years threshold already have early atherosclerosis. As young as in their 20s.
Also, that chart uses an "average" level of risk factors. Anabolic steroid users have well above average risk factors, some obvious, ie, higher BP, others not completely understood, like the changes in heart tissue found in autopsies of young bodybuilders.
Anyway, it's great to see so many people interested in getting started earlier than the current reactive standard of dealing with lipids only once they've laid down a base of plaque for 40 years, and who see the obvious benefit of being proactive and stopping accumulation before it becomes an imminent threat. Those of us who started this later in life can only do a limited amount to reduce risk because of the accumulated damage.
carbmaster
New Member
Yo Ghoul, what is a good maximum daily amount of saturated fat to reduce LDL. Is the AHA recommendation of less then 6% of total calories from saturated fat reasonable for AAS users, or should we strive for even less?
Ghoul
Member
That AHA recommendation is really most appropriate at high LDL levels.
If your LDL is low, below 60, up to 10% (the recommendation most other health orgs use) is fine. If your LDL is above that, no more than 6% is sensible so you don't bump your LDL even higher because it'll go up disproportionately.
For example, the same amount of saturated fat in the diet that would raise 160 LDL by 30 points, would raise 40 LDL by 5 points, which is insignificant.
Another good reason to get your LDL down. It gives you some dietary flexibility without raising risk.
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I guess people don't die of heart attacks.
On this internets thing I have on my computer.
Ghoul
Member
I guess it was absurd to suggest a lifetime of high LDL may lead to a heart attack.
Got it, Reddit.
I've been on Lipitor for two decades. I'm currently off of Lipitor because it appears that Lipitor, after all these years, has started to injure my liver. That is a possible side effect. I'm actually generally for statins. (I'm not expert.) You shouldn't rely on my anecdotal experience as a reason for not taking a statin. Also, although the liver doctor thinks the statin is the most likely cause of my high liver enzymes (my ALT is 10 times the upper limit of normal), the cause still has not been determined. It's extremely rare for a person to have liver problems develop after many years on a statin not preceded by a dose increase. I want the cause to be the statin because then my liver would likely be fine so long as I don't take Lipitor. Whether I'd take another statin is another matter; my risk profile may have changed due to my weight loss and and the possibly greater risk of liver problems if I take another statin. My liver doctor said to stop taking reta (although he said it's probably not the cause) but to continue taking tirz. From what I've read, of the medicines I take, the second most likely to cause injury is the tirzepatide. (I should say third because reta hasn't been tried enough to obtain good data on the rate of liver injuries. Liver injury data tends to come after approval of drugs.)
Ghoul
Member
Thanks for sharing this. It is very unusual. They used to require liver enzyme tests while on lipitor, though that's been dropped. .
Not to keep beating this drum like I'm selling the stuff, but if you decide to go back on a statin, Pitavastatin is the least hepatoxic since it isn't metabolized like other statins. In fact it's excreted essentially unchanged, so it doesn't increase ALT/AST.
Lower is better, true! In my country we have guidelines. But every cardiologist I know personally, even young ones with “normal” LDL, are self prescribing statins, to get low low, real low. Just saying.
Thanks for the reply, that is the same paper I was able to find and they had it on Sci-hub. The FDA approval page you linked was exactly what I was searching for, I hate how bad the search is on the FDA site.
Ghoul
Member
I wish there was a rule that all the redacted "trade secret" portions of the documents was released after the patent expires. Lots of useful info in there we can't see.
Agreed, what you said in that post was absurd.
Sorry chatgpt couldn't find it for you. It's ok, your fragile ego will be ok. Take a deep breath.
