krsct
GLP-1 Apprentice
Been on GLP-1 for almost 3 years. Lost 1/4 of body weight in 8 months and maintenance since then. Took a while but my doctor stopped my statins today. Never thought it would happen. It took a while but another great NSV.
It actually happened: off statins!
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80s.diver
GLP-1 Apprentice
That is awesome, keep us posted to see if the cholesterol numbers creep back up.krsct said:
krsct
GLP-1 Apprentice
staffn1 said:
lessthanhalf
GLP-1 Specialist
Without knowing the full story it is hard to say if this is a good idea or a bad one. The purpose of statins is to reduce risk of cardiovascular disease either in the first place or after an event like heart attack or stroke has occurred. If the original assessment of absolute cardiovascular risk over 10 years was high, and statins were started for that reason, then unless that assessment is recalculated, then staying on them is the correct approach regardless of lipid levels. If they are being used for secondary protection then stopping them is always the wrong move.
If the loss of weight and improved blood pressure, lipids etc were enough to reduce risk to below 10% over the next 10 years then stopping might be correct, but it is definitely not as simple as better lipid numbers after weight loss. Looking at statin use based on absolute cardiovascular risk is the correct way to view it but it is not super simple or obvious. Anyone who has or had severe obesity is likely to have high absolute cardiovascular risk, and there is a fairly high chance of that still being the case if weight is lost especially if older. And there is a reasonable chance that damage has already occurred that will not be known about unless it is looked for.
I ended up diagnosed with early heart failure and coronary artery disease after losing a lot of weight and without symptoms, where treatment with statins and other medications reduce 10 year risk from about 25% to about 12%, but if it had not been looked into I would not have known until a heart attack years later, which might still happen , but being half as likely sounds good to me.
If the loss of weight and improved blood pressure, lipids etc were enough to reduce risk to below 10% over the next 10 years then stopping might be correct, but it is definitely not as simple as better lipid numbers after weight loss. Looking at statin use based on absolute cardiovascular risk is the correct way to view it but it is not super simple or obvious. Anyone who has or had severe obesity is likely to have high absolute cardiovascular risk, and there is a fairly high chance of that still being the case if weight is lost especially if older. And there is a reasonable chance that damage has already occurred that will not be known about unless it is looked for.
I ended up diagnosed with early heart failure and coronary artery disease after losing a lot of weight and without symptoms, where treatment with statins and other medications reduce 10 year risk from about 25% to about 12%, but if it had not been looked into I would not have known until a heart attack years later, which might still happen , but being half as likely sounds good to me.
Calm Logic
GLP-1 Specialist
It's like $100 here for a coronary CT calcium scan (CAC), if insurance doesn't pay.
It takes about three to five years for the plaque to calcify (enough to be detected on a scan). So a more expensive option is Cardiac CT Angiography (CCTA), which tells you both the past (calcified) and the present (soft plaque).
But most people who are paying out of pocket just do the calcium scan.
It takes about three to five years for the plaque to calcify (enough to be detected on a scan). So a more expensive option is Cardiac CT Angiography (CCTA), which tells you both the past (calcified) and the present (soft plaque).
But most people who are paying out of pocket just do the calcium scan.
skeptick
GLP-1 Enthusiast
FAREFFINOUTkrsct said:
lessthanhalf
GLP-1 Specialist
Agree with this, coronary calcium score is a very good way to determine if statins are needed or not, and is especially useful where calculated risk based on family history, blood pressure , lipids, blood sugar, smoking etc is intermediate, and it will still show changes if those numbers are improved by weight loss, and treatment is an extremely good idea if CCS is high even if the other numbers are much improved, as it shows very strong correlations with long term risk, possibly better than any other test including angiography. You could definitely argue than those over 40 or 50 who were or are obese and had evidence of metabolic syndrome should get this checked, even after weight loss. Not covered by medicare in Aus but costs $250 aud and gives very useful information and does not normally ever need to be repeated.Calm Logic said:
sheilarae74
GLP-1 Enthusiast
krsct said:
lessthanhalf
GLP-1 Specialist
Yes but that is the point. It is not practical or economic to treat every single person with statins. Treatment is decided by an estimate of absolute risk of MACE or major atherosclerotic cardiovascular events over the next 10 years. Biggest risk by far is age. Then the usual ones family history, smoking, diabetes, blood pressure and lipids. Calculations based on those risk factors are the standard method. Coronary calcium score is an alternate way of assessing risk and is very accurate at predicting future risk, which makes it an excellent tool for deciding if primary prevention is warranted or not.Habibibi said:
So it does also detect established coronary artery disease, in my case at 645 at 58 yo this equates to 97th percentile for risk for age or about a 25% 10 year MACE risk, which is treated more like secondary prevention. I am actually quite glad my doctor talked me into getting the test when I had thought it unnecessary.
But it also often detects a CCS of 0 which translates to a low 10 year risk, which would usually mean primary prevention medications are not needed, unless calculations based on the usual risk factors were bad, but if you were going to use that to decide then doing the CCS test was pointless. So it is often used when the traditional risk factors give a borderline result as to whether primary prevention is needed or not. And it is sometimes used for more broad screening , but the science on whether this is justified is not well established.
Almost all adults on a western diet have some degree of atherosclerosis, especially after the age of 40 or so, the point is to determine those at highest risk, to decide who to treat or not , as treating everyone is not cost effective or practical and exposes a lot of people to side effects. Anti platelet agents like low dose aspirin are going out of fashion now, but they carry risks of bleeding as well, and are more typically used in secondary prevention only but this is fairly recent.
As far as I know as I have not read it in detail yet, the new US guidelines on lipid management are suggesting testing at younger ages but not recommending treatment unless absolute risk is significant, but are recommending lower LDL targets.
Prior to starting tirzepatide, my pcp put me on a low dose statin. My numbers weren’t crazy, but definitely elevated. Fast forward a year later, and now I have too low cholesterol. I think that that is adversely affecting some hormone production (mainly testosterone), and that is affecting other aspects of my life. Anyhoo, my pcp doesn’t want to take me off the statin until I talk with a cardiologist. I’m like WTF, but the more I research there are other health benefits of statins beyond lowering cholesterol, so I lowered my dose and will see cardio at some point. My pcp doesn’t think that I can split my medication, but that’s clearly not the case. So, I didn’t tell her. Lately, my numbers are more in the normal range, but I continue on the statin.
Zydeceltico
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Exactly. It was a self-chosen, self-pay CT calcium scan last August that revealed an 80% occlusion of my LCX and a stent in December that decreased that 80% to 0%. I sent the CAC results to my PCP and she put me on rosuvastatin the same day. LDL went from 141 to 54 between August and December. It was discovered that occlusion is the result of atheriosclerosis.lessthanhalf said:
To your point re: secondary intentions: I am to stay on the statin due to it slowing the progression of further calcification and hardening which apparently is another function it performs.
If I had not decided on my own out of curiosity to get that CAC on my own, I would have been surprised at some point by a heart attack.
Statins have always been an odd decision, since they work in such a roundabout way and so strongly impact a substance (cholesterol) that your body has systems in place specifically to avoid ever getting too low and will ramp up production if it's not getting enough from your diet.
The current thinking is that the things (LDL) that transport fats, cholesterol, and other fat-soluble nutrients through your bloodstream are a key step in arterial plaque growth. The data here is rather inconclusive. We know SOME of the LDL will readily deposit in that manner and cause real problems, but we haven't nailed down exactly what it is that determines whether an individual LDL particle will do so. On average, higher LDL blood levels correlate with cardiovascular disease, but it's a fairly weak correlation (with other risk factors linking much more strongly to cardiovascular disease than LDL itself).
So instead of making an effort to explore why sometimes LDL tends to deposit in arterial walls and sometimes it does not, it's just assumed that all LDL must be bad and we should seek to reduce blood levels of this essential transporter.
So how does pharma tackle the problem? By directly going after LDL (the rationale of which is already on somewhat shaky ground)? Naw, they eventually got to doing that with PCSK9-inhibitors many years later, but instead came up with statins, which are quite the roundabout solution.
Instead of going after LDL itself, statins go after one of the essential substances that LDL shuttles around your body (cholesterol), such that your body stops making as much of it. To cope with this shortage your liver starts recalling the cholesterol transporters (LDL) more rapidly, pulling them out of your bloodstream sooner, as if it were trying to recall the cholesterol still remaining in them sooner. That succeeds in keeping the amount of LDL particles floating around in your blood lower, but also means that your body is coping with a supply shortage of cholesterol, which isn't entirely without consequence itself.
Now if someone had a prior cardiac history or was at significant risk, such a bargain might be very reasonable. Instead, it's just routine for your doctor to push statins on you as soon as your LDL hits a slightly elevated number on a couple of lab tests, as if it were as benign of a decision as taking a vitamin supplement.
The current thinking is that the things (LDL) that transport fats, cholesterol, and other fat-soluble nutrients through your bloodstream are a key step in arterial plaque growth. The data here is rather inconclusive. We know SOME of the LDL will readily deposit in that manner and cause real problems, but we haven't nailed down exactly what it is that determines whether an individual LDL particle will do so. On average, higher LDL blood levels correlate with cardiovascular disease, but it's a fairly weak correlation (with other risk factors linking much more strongly to cardiovascular disease than LDL itself).
So instead of making an effort to explore why sometimes LDL tends to deposit in arterial walls and sometimes it does not, it's just assumed that all LDL must be bad and we should seek to reduce blood levels of this essential transporter.
So how does pharma tackle the problem? By directly going after LDL (the rationale of which is already on somewhat shaky ground)? Naw, they eventually got to doing that with PCSK9-inhibitors many years later, but instead came up with statins, which are quite the roundabout solution.
Instead of going after LDL itself, statins go after one of the essential substances that LDL shuttles around your body (cholesterol), such that your body stops making as much of it. To cope with this shortage your liver starts recalling the cholesterol transporters (LDL) more rapidly, pulling them out of your bloodstream sooner, as if it were trying to recall the cholesterol still remaining in them sooner. That succeeds in keeping the amount of LDL particles floating around in your blood lower, but also means that your body is coping with a supply shortage of cholesterol, which isn't entirely without consequence itself.
Now if someone had a prior cardiac history or was at significant risk, such a bargain might be very reasonable. Instead, it's just routine for your doctor to push statins on you as soon as your LDL hits a slightly elevated number on a couple of lab tests, as if it were as benign of a decision as taking a vitamin supplement.
tendency
GLP-1 Enthusiast
TL;dR re: LDL. The latest research shows, to my understanding, that if you have significant CVD risk factors then you should be paying attention to your LDL numbers. If you don't have CVD risk factors then LDL numbers are probably not that important.
latviantower
GLP-1 Enthusiast
Excellent point. I recently had my calcium CT and guess what? Despite being on a statin for 20 years and keeping my my cholesterol well below even borderline, my calcium score is off the charts. So now I have a cardiologist! Good news? The calcium is in my arterial walls, stabilizing the whole thing. No narrowing. Aced stress test. Hit the gym every day. Only have to see the cardiologist once a year. My LDL is 40 (yes still on a statin, different one at higher strength), total cholesterol <100.Habibibi said:
A high calcium score is not a death sentence - it can be a wake up call. The key is to have to scan earlier in life - for example, my trainer (37) had a scan showing very mild calcification (horrible family CVD history), but they are being aggressive NOW to slow the process before it gets critical.
Jfrick11
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I think what’s missing here is that LDL alone doesn’t define cardiovascular risk.
The more complete question is: what is this person’s actual risk right now?
That usually involves ApoB, Lp(a), inflammation (hs-CRP), and sometimes CAC.... not just LDL.
So LDL of 90 and stopping statins could be reasonable… or premature.
It depends on factors we’re not seeing discussed: ApoB, LDL-P, Lp(a), inflammation, family history, insulin resistance, CAC, etc.
Without that, it feels like an incomplete picture
The more complete question is: what is this person’s actual risk right now?
That usually involves ApoB, Lp(a), inflammation (hs-CRP), and sometimes CAC.... not just LDL.
So LDL of 90 and stopping statins could be reasonable… or premature.
It depends on factors we’re not seeing discussed: ApoB, LDL-P, Lp(a), inflammation, family history, insulin resistance, CAC, etc.
Without that, it feels like an incomplete picture
Completely agree with this, but there is a greater implication here too. It's very likely OP was put on a statin without evaluating these factors to begin with and purely based on one or two LDL-C (estimated) values from a basic lipid panel alone, as is commonly done in the US and a rather disappointing state of affairs.Jfrick11 said:
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