It actually happened: off statins!

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@tubby

I am seriously interested in your take on my numbers.

I had my CAC on 10/8 and my PCP started me on rosuvastatin on 10/9.

My stent was placed on 12/9.

Again -seriously curious about your take. thx

I should add that I started tirzepatide on June 6, 2025.

SW: 242 lbs, GW 187 lbs reached 11/1/25 and have maintained since.

[Imported image pending local asset: attachments-zyd-bloodwork-webp.18787]
 
Zydeceltico said:
@tubby

I am seriously interested in your take on my numbers.

I had my CAC on 10/8 and my PCP started me on rosuvastatin on 10/9.

My stent was placed on 12/9.

Again -seriously curious about your take. thx

I should add that I started tirzepatide on June 6, 2025.

SW: 242 lbs, GW 187 lbs reached 11/1/25 and have maintained since.

View attachment 18787
Let me preface this by saying that I'm not a doctor and you shouldn't listen to anything resembling medical advice that I might say. It's not medical advice and I'm not qualified to provide that.

I'd start by ignoring the LDL-C numbers entirely. On a basic lipid panel they don't actually measure LDL, they estimate it using something called the Friedewald Equation (Google that if interested in learning more). In addition, even if LDL-P (a proper measure of LDL that is actually a direct measure of it rather than a crude guess) was done, since you're going through a period of weight loss, that can bias your LDL result significantly, making it less reliable than it would be if you were at a stable weight prior to having the lab done.

However, looking at the numbers on your lipid panel that actually are strongly correlated with cardiovascular risk as well as directly measured rather than estimated (triglycerides and HDL), I do see some cause for concern there. At present, the best estimator of cardiovascular risk is the triglyceride to HDL ratio, which is much more strongly correlated with it than LDL-C. And honestly, that's not looking great. 140/34 = 4.1 is bad, but then that was before you started taking a GLP-1 and you don't need me to tell me that you were in bad shape before the GLP-1.

Jumping ahead to 9/17/25, your trig/HDL ratio is now 96/30 = 3.2. That's still bad, but a significant improvement over where you were before the GLP-1 and honestly a pretty positive change over a 3 month period. And honestly with such a rapid weight change in such a short period of time, I'd probably want to see things "settle" for a bit before making any sort of judgement call there.

Now jumping to your January numbers, 44/35 is looking a lot better at 1.3. Of course, getting to that ratio via a statin is very different than getting to that ratio via lifestyle changes. Just as holding a bunch of helium balloons as you step on the scale isn't going to lead to any of the health improvements that actually losing weight would come with, I don't know that examining statin-mediated numbers is really going to tell us anything useful there. Also, you probably have many years at which your cardiovascular system was under strain and built up plaque, which has to be factored in too.

The traditional school of thought with that is that by taking a statin you'll increase the amount of calcified plaque in your arteries. Normally that's a bad thing, since more calcified plaque means more cardiovascular risk. Of course, cardiologists being the dogmatic people that they are, upon discovering that rationalized it as actually being a good thing since it meant plaque was more stable and less likely to break off from a deposit (which could potentially be fatal). I can't say I disagree with them on that point to be honest, but just throw the dogmatic dig in there because, while likely true, it's also the kind of rationalization one would invent in trying to justify their own past actions and practices, and such things are probably worth considering when evaluating recommendations. They also have a long history of giving bad advice based on very limited evidence, but I digress...

Another school of thought (that hasn't been studied extensively) is to seek out other ways of reducing plaque deposits (natto kinase shows some promise there) rather than calcifying them, but I don't think that's well enough understood for a responsible recommendation to be made there, since one could argue that's just as easy to lead to catastrophe for you as improvement, based on things I don't know the answer to. But you kind of have to pick a lane there: Either stabilize/calcify the plaque via the traditional/statin route or attempt to actively reduce it somehow.

I guess my main takeaways going forward if I were you would be that your low HDL is hurting your trig/HDL ratio (if not for that, your triglycerides are at a really nice level right now). At the same time, you can't really trust your lipid panel numbers to tell you anything useful in the future, as they're biased by the statin that you're taking, making them suspect at best when applied to risk models that may conflate statin and statin-free numbers. I might consider seeking out an "LDL skeptical" doctor and pay for a consult with them. In the end there's a good chance they will also recommend staying on the statin that you're on, but they're going to have less blind spots than I will and be in a position to actually give you a proper recommendation.
 
Regarding calcium CT scoring for intermediate risk:

Risk calculators:

quoted said:
The American Heart Association PREVENT™ Online Calculator

Welcome to the American Heart Association Predicting Risk of cardiovascular disease EVENTs.

professional.heart.org

The PREVENT equations estimate absolute 10–year risk for total CVD (PREVENT-CVD), ASCVD (PREVENT-ASCVD) and HF (PREVENT-HF) for adults aged 30–79 years and 30-year risk for total CVD among adults aged 30–59 years. In addition to absolute risk estimates, the calculator provides complementary risk information, including PREVENT–Age and age- and sex-specific 30-year risk percentiles, to help contextualize predicted risk and support clinician–patient discussions.

CVD Risk Estimator Plus - American College of Cardiology

Combining traditional ASCVD risk modeling with modern cardiovascular kidney metabolic (CKM)–inclusive risk equations, CVD Risk Estimator Plus provides clinicians with a comprehensive, personalized cardiovascular disease (CVD) risk assessment.

www.acc.org

CVD Risk Estimator Plus computes risk estimates using:

2013 ASCVD Pooled Cohort Equations (PCE) , which calculate 10‑year and lifetime risk of atherosclerotic cardiovascular disease using age, sex, race, blood pressure, cholesterol profile, diabetes status, and smoking status.

2023 PREVENT™ Equations , which estimate 10‑ and 30‑year risk for total CVD, ASCVD, and heart failure (HF), incorporating kidney and metabolic health measures such as BMI and estimated glomerular filtration rate (eGFR), and supporting optional predictors including urine albumin‑creatinine ratio (UACR), hemoglobin A1c (HbA1c), and social deprivation index (SDI).

Framingham Risk Score for Hard Coronary Heart Disease Calculator

The Framingham Coronary Heart Disease Risk Score estimates risk of heart attack in 10 years.

www.mdcalc.com

MDCalc uses the 'Hard' coronary Framingham outcomes model, which is intended for use in non-diabetic patients age 30-79 years with no prior history of coronary heart disease or intermittent claudication. This version was selected because it is the most widely applicable to patients without previous cardiac events.

See the official Framingham website for additional Framingham risk models.

Related guidelines:

quoted said:
https://www.jacc.org/guidelines/dyslipidemia

(2026)

In adults at intermediate risk and select adults at borderline risk with no prior ASCVD, if the decision regarding LLT [lipid-lowering therapy] remains uncertain, a CAC score should be used for further risk stratification and to guide the decision to withhold, postpone, or initiate therapy.

Major Global Coronary Artery Calcium Guidelines (2022)

The figure elucidates an algorithm for suggested CAC scoring and assessing ASCVD risk. CAC = 0 suggests withholding statin therapy, while CAC = 1 to 100 favors lifestyle improvement. CAC = 101 to 400 indicates treatment for individuals >75th percentile, and CAC >400 requires initiation of statin therapy.
 
And for those curious about what diet can achieve, these are my pre to post-diabetes lipid and A1c results (achieved through diet). I don't have any labs with GLP results yet so not sure how those will impact me. Ignore the weird trend-line from the left on my A1c plot as there was about a 5 year gap between results so it's just connecting those dots.

Also note that I engaged in no significant exercise during that period other than walking around the neighborhood a bit. All diet.
 
Calm Logic said:
Regarding calcium CT scoring for intermediate risk:

Risk calculators:

Related guidelines:
Can't speak to those specific links, but I'd take anything the AHA says with a huge grain of salt. They have a history of making claims that seem to benefit industry (pharma and big food) and are scientifically dubious at best and then digging into their positions even after it's clear that claims they've made are flawed (e.g. their long-standing positions on saturated fat and low-carb diets). At a minimum I would check to see if there's a Cochran review article on the same topic and if Cochran supports the AHA position and guidelines or comes to a different conclusion.

Otherwise, I'd just assume that most positions promulgated by the AHA are primarily a means of influencing doctors (who themselves wouldn't knowingly behave unethically towards their patients) into giving bad advice that benefits industry. There isn't really a smoking gun that proves that's happening, but they've just been wrong so much historically that it would be naive to take them at face value.
 
tubby said:
...with such a rapid weight change in such a short period of time, I'd probably want to see things "settle" for a bit before making any sort of judgement call there....getting to that ratio via a statin is very different than getting to that ratio via lifestyle changes......you probably have many years at which your cardiovascular system was under strain....
Firstly, thank you for the thorough review. I know you're not a doctor nor would I be tempted to consider an anonymous post from a complete stranger as medical advice. That said (mostly as a caveat for others who may read this), I do appreciate your thoughts.

To the recognition of the short amount of time: yes - I am happy to report that I am apparently a super-responder. It should also be noted that due to the almost immediate balancing of blood sugar levels that I experienced, decades of what I used to believe was constant hypoglycemia has finally and completely subsided. Gone. With that, I was able to negate a vast quantity of daily food stuffs that I would intake simply to keep my energy, mental acuity, and emotions in precarious balance. For years I had desired to simply "eat clean" and had success a couple of times for several months at a time but not without the internal struggle of food noise. So it was relatively simple to instantly begin eating clean (no simple carbs, no sugar, no junk). I also immediately began strength and cardio training 5x/week and getting +2 more hours of sleep per night as my insomnia was also mitigated. So yes - lifestyle changes are a huge factor. I've been at GW since late October and eat without issue. Very happy and content with the -necessary for me - lifestyle changes.

Also pertinent: I had approx. 38% body fat last June. Now at 18% per DEXA in February. The great majority of my weight loss was VAT fwiw. According to a DEXA in Oct. and the second one in Feb., I have apparetly increased lean muscle mass by 6+ lbs in that amount of time, so it kinda feels like the plan is working as hoped.

Not certain where I stand on the statin question. I am not really concerned about it as I also have zero sides from the statin either and I feel better at 62 y.o. than I have in a decade.
 
Zydeceltico said:
Not certain where I stand on the statin question. I am not really concerned about it as I also have zero sides from the statin either and I feel better at 62 y.o. than I have in a decade.
Your situation is too complicated for me to have useful advice on, obviously.

One thing I will add is that there are a large number of studies out there that study the relationship between total cholesterol and all-cause mortality in very large populations (thanks to readily available public health data). A nice trait about all-cause mortality is that it's harder to fake/manipulate than an intermediate marker.

When a statin brings down cholesterol, it's impossible to know how that compares to bringing cholesterol down through other means or how much of a benefit it will actually lead to without studying it. Fortunately, this has been studied in large populations. Unfortunately, those who conducted the (expensive) research are mostly unwilling to share the raw data with groups that might be critical of their work so we're kind of stuck trusting that the pharma-friendly researchers have conducted a fair analysis of the data and haven't applied dubious correction factors or other tricks to skew the data towards a particular conclusion.

What we do know from population-level cholesterol data is that having too low of cholesterol and too high of cholesterol are both associated with significant increases in all-cause mortality. The curve varies by both age and sex. Here is an example of the first curve I could easily find on Google, but there are many studies and they all have somewhat similar results. Choose your favorite if you wish to read more.

[Imported image pending local asset: attachments-1775152177737-webp.18807]

Some of the low-end risk can be explained by cancer (in late-stage cancer your cholesterol does tend to drop), but that doesn't seem to explain all of it.

And that's why I suggest finding a physician who is skeptical of statin therapy (instead of listening to me) who can better flush out the other side of the equation, enabling you to make a proper objective comparison, since at that point you'll have heard both sides of the story.
 
tubby said:
Your situation is too complicated for me to have useful advice on, obviously.

One thing I will add is that there are a large number of studies out there that study the relationship between total cholesterol and all-cause mortality in very large populations (thanks to readily available public health data). A nice trait about all-cause mortality is that it's harder to fake/manipulate than an intermediate marker.

When a statin brings down cholesterol, it's impossible to know how that compares to bringing cholesterol down through other means or how much of a benefit it will actually lead to without studying it. Fortunately, this has been studied in large populations. Unfortunately, those who conducted the (expensive) research are mostly unwilling to share the raw data with groups that might be critical of their work so we're kind of stuck trusting that the pharma-friendly researchers have conducted a fair analysis of the data and haven't applied dubious correction factors or other tricks to skew the data towards a particular conclusion.

What we do know from population-level cholesterol data is that having too low of cholesterol and too high of cholesterol are both associated with significant increases in all-cause mortality. The curve varies by both age and sex. Here is an example of the first curve I could easily find on Google, but there are many studies and they all have somewhat similar results. Choose your favorite if you wish to read more.

View attachment 18807

Some of the low-end risk can be explained by cancer (in late-stage cancer your cholesterol does tend to drop), but that doesn't seem to explain all of it.

And that's why I suggest finding a physician who is skeptical of statin therapy (instead of listening to me) who can better flush out the other side of the equation, enabling you to make a proper objective comparison, since at that point you'll have heard both sides of the story.
I highly recommend the book “Statin Nation” by Dr Malcolm Kendrick He has been a GP for over 25 years and has worked with the European Society of Cardiology.

Key Arguments:

Minimal Lifespan Increase: Kendrick cites data suggesting that even for high-risk individuals, taking statins for five years may only increase life expectancy by an average of four days.

Pleiotropic Effects: He argues that if statins do work, it is not because they lower cholesterol—which he views as an "unimportant bystander"—but because they increase nitric oxide synthesis. This helps dilate blood vessels and prevent clotting.

Hidden Side Effects: The book claims that side effects (such as muscle pain and cognitive issues) are often dismissed by researchers who have financial ties to the pharmaceutical industry.

The "Black Swan" Logic: Using Karl Popper's scientific method, Kendrick points out "black swans"—cases where people with high cholesterol live long lives—to argue that the "all-high-cholesterol-is-bad" theory is fundamentally flawed.

The also argues that the relative risk of death from heart disease is lower. The absolute risk of death is greater when taking statins. The book also examines the drug approval process and how the results are obtained by taking the best case scenario for the drug approval. Without taking into consideration the overall benefit.

My personal opinion on statins is that it increases insulin resistance and the side effects made running more difficult for me as I was combating my diabetes.

I gave this book to my Dr to enjoy while she’s on maternity leave. So she can understand my viewpoint on statins. ( this isn’t the first time I’ve given her a book assignment as her patient)
 
Turbo-Farmer said:
My personal opinion on statins is that it increases insulin resistance and the side effects made running more difficult for me as I was combating my diabetes.
I suspect there's at least some truth to the points you raised (or perhaps they're completely correct). There's enough of what I might call suspicious tells in regards to the history of statins to give me pause at the very least.

I will say that if someone is going to consider a statin, they'd likely be foolish to do so without assistance from a GLP due to the blood sugar issue/insulin resistance issue that you brought up. The GLP won't eliminate all of the risk associated with statins, but at least it should partially mitigate that particular one.

I still maintain that there are good reasons to believe that GLPs are going to prove to be more cardioprotective than statins as the data emerges where even if someone buys into the AHA guidelines for LDL many "borderline" people will drop below that simply from taking a GLP.
 
krsct said:
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.
That's really good, congrats! what statins were you on ? Mind sharing your blood work numbers ? Cholesterol over time
 
With @tubby mentioning the Cochrane Reviews, I am trying to find something more recent.

For CT calcium scoring for more people, the jury is still out:

https://bmjopen.bmj.com/content/15/7/e101472

quoted said:
The available evidence is insufficient to determine whether screening asymptomatic patients with CACS has an impact on all-cause mortality or CV events.

Repatha is available from India, but it is not cheap. It is popular among steroid users for damage control.

A popular poster on Meso (Ghoul) decided to go on a trinity of lipid-lower therapy ("Repatha / Eze / Statin") to get the numbers much lower (apparently LDL to 24):

quoted said:
The title of this document sums it up:

"LDL Cholesterol Management Simplified in Adults – Lower for Longer is Better: Guidance from the National Lipid Association"

Getting cholesterol as low as possible, for as long as possible.

The best lipid lowering protocol is the one that you’re willing to adhere to. It’s “time on target” that’s as important as absolute reduction. Because once you get it low enough to stop progression of plaque, the next goal is to minimize the damage already done. Low enough LDL will regress plaque. Literally pulling it back out of your arteries. But that’s only possible with the “freshest” plaque. Once that’s gone, the next benefit of very low LDL is to “suck” the inflammatory goo out of the plaque that’s not removable. That transforms the remaining plaque from unstable (likely to break off causing a heart attack), to dry, “mummified”, hardened plaque that’s still there but poses little risk.

We know from the huge, ongoing, long term Repatha studies, the first capable of achieving ultra low LDL, that there’s no “floor” level of these benefits, down to single digits. It’s also put to rest the theories of potential harms from ultra low LDL. Theres no indication whatsoever they exist.

The lower you get LDL the better off you’ll be. The limits are cost and what meds you can use without side effects becoming an issue.

Ideally, Repatha / Eze / Statin is the best stack, with the best results. But 2, or even 1 of any of them is significantly better than none.

On all three I’m down from 140 to 24.

Repatha and Eze are a potent combo, and great particularly for those fearful of statins who would otherwise let their high cholesterol go untreated. The only caveat is that inflammation is a major CVD (and general health) risk factor (makes “pimples” grow under plaque, which can make a piece more likely to break off and cause a heart attack). Statins have uniquely potent anti-inflammatory effects, 50% reduction of systemic inflammation, that other classes of lipid drugs don’t offer.
 
Grogu said:
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.
Most cardiologists/pcp's will prescribe a low dose statin, usually Rouvastatin (5-10mg), for lowering inflammation in the arteries and not necessarily to lower your cholesterol. This is to minimize plaque build up. At least, this is what my cardiologist told me when I asked since my cholesterol was in normal range.
 
In large and complex fields in medicine you are going to find people , even doctors and researchers with varying opinions, but some opinions have more solid science behind them than others. I think the science behind statins to reduce secondary and primary cardiovascular disease is solid, is supported by every national and international cardiovascular guideline in existence.

Avoiding statins on the basis of low quality science is a bad idea and supporting it could lead to unnecessary heart attacks, strokes or deaths. Statin therapy is not a contested field in medicine it is established and proven doctrine, finding dissenting opinions does not change that.

Statins act to stabilise existing plaques, making them less likely to rupture, it is when they rupture and a clot forms in a coronary artery that a heart attack occurs. They also reduce the build up of new plaque.

People who are at high cardiovascular risk can substantially reduce that risk with statin (+/- others ) and sometimes antiplatelet therapy, stopping them without medical advice is really not a good idea.

To give a good overview of the science supporting statin therapy would require days of research, so here is a simple prompted chatgpt summary of the main studies showing they work.

Here are the main trials that established statins reduce major adverse cardiovascular events (MACE) and, in some cases, mortality. I’ll keep it focused and practical.

Secondary prevention (people who already have cardiovascular disease)

These show the clearest mortality benefit.

Scandinavian Simvastatin Survival Study (4S)

Patients: prior MI or angina

Statin: simvastatin

Result:

~30% reduction in all-cause mortality

Large drop in coronary deaths and MACE

This was the first big “proof” trial

Heart Protection Study (HPS)

Patients: high-risk (many with prior vascular disease or diabetes)

Statin: simvastatin

Result:

~25% reduction in major vascular events

Significant reduction in mortality

Showed benefit even when LDL wasn’t very high

PROVE-IT TIMI 22

Patients: recent acute coronary syndrome

Compared: intensive vs moderate statin

Result:

More intensive therapy → lower MACE

Key idea: lower LDL is better
 
continued

Primary prevention (no prior events)

Benefits are still real, but mortality effects are smaller.

West of Scotland Coronary Prevention Study (WOSCOPS)

Patients: middle-aged men, high LDL, no prior MI

Statin: pravastatin

Result:

Reduced MI and coronary death

Long-term follow-up showed mortality benefit

JUPITER trial

Patients: normal LDL but high CRP

Statin: rosuvastatin

Result:

~44% reduction in major cardiovascular events

Some reduction in mortality

Showed benefit beyond just high cholesterol groups

ASCOT-LLA

Patients: hypertensive, moderate risk

Statin: atorvastatin

Result:

Reduced MACE

Trial stopped early due to benefit

Meta-analysis (arguably most important)

Cholesterol Treatment Trialists' Collaboration

Pooled data from many statin trials

Key finding:

For every ~1 mmol/L LDL reduction:

~20 - 25% reduction in major vascular events

~10% reduction in all-cause mortality

This is the clearest “big picture” result.

Bottom line

Secondary prevention: strong evidence for both

↓ MACE

↓ mortality

Primary prevention:

Clear ↓ MACE

Mortality benefit is smaller but present in some groups

Overall:

The benefit scales with baseline risk and LDL reduction
 
Percentiles for calcium scoring, categorized by sex and age:

Checking your browser - reCAPTCHA

quoted said:
Men usually develop CV diseases approximately 9–10 years earlier than women. The CAC consortium study showed that a 75% prevalence of a non-zero CAC score was observed nine years earlier in men than in women. As expected, the present study shows that the percentage of patients with zero CAC score decreases significantly with age and that the decrease is more noticeable in men than in women.

[Percentile of non-zero scores:]
 
krsct said:
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.
Congratulations!!! That’s awesome!
 
Calm Logic said:
(Quoting a study) The available evidence is insufficient to determine whether screening asymptomatic patients with CACS has an impact on all-cause mortality or CV events.
This may seem like a dissatisfying answer, but to provide some additional context, critical/skeptical positions like this are important because if medicine finds a new test they can roll out at the population level tied to a new treatment modality it can lead to real harm if not justified. The most obvious harm would be the financial cost of testing a large number of people who don't need it or don't need it yet. The slightly less obvious harm would be if performing the test leads to a significant number of "false positives" receiving treatments that they don't actually benefit from. By false positives I mean both those who don't actually have a condition and those who have a condition but at such a minor level where premature treatment would be of minimal benefit. That's why it's so important to say something is inconclusive when it is inconclusive.

Taking this back to CACs, I personally think at the individual value there could be value in getting one done since the cost (at least in the US) is low. They're not as reliable of predictors as many would like (since plenty of plaque is NOT calcified yet and the test is for calcified plaque), which is to say that a high result is probably a bad thing, but a low result doesn't guarantee an absence of plaque and could provide a false sense of security.
 
lessthanhalf said:
continued

Primary prevention (no prior events)

Benefits are still real, but mortality effects are smaller.

West of Scotland Coronary Prevention Study (WOSCOPS)

Patients: middle-aged men, high LDL, no prior MI

Statin: pravastatin

Result:

Reduced MI and coronary death

Long-term follow-up showed mortality benefit

JUPITER trial

Patients: normal LDL but high CRP

Statin: rosuvastatin

Result:

~44% reduction in major cardiovascular events

Some reduction in mortality

Showed benefit beyond just high cholesterol groups

ASCOT-LLA

Patients: hypertensive, moderate risk

Statin: atorvastatin

Result:

Reduced MACE

Trial stopped early due to benefit

Meta-analysis (arguably most important)

Cholesterol Treatment Trialists' Collaboration

Pooled data from many statin trials

Key finding:

For every ~1 mmol/L LDL reduction:

~20 - 25% reduction in major vascular events

~10% reduction in all-cause mortality

This is the clearest “big picture” result.

Bottom line

Secondary prevention: strong evidence for both

↓ MACE

↓ mortality

Primary prevention:

Clear ↓ MACE

Mortality benefit is smaller but present in some groups

Overall:

The benefit scales with baseline risk and LDL reduction
Those reading carefully will see that my position didn't really differ from lessthanhalf's chatbot's position that much. We both agree that statins could be a useful tool for secondary prevention. The main difference seems to be that lessthanhalf's chatbot frames statins as being generally appropriate, while my position is that they may or may not be part of an overall strategy employed at that point. That is to say that I'm not opposed to their use, but don't assume their use either.

When it comes to primary prevention, it's always going to come down to which studies you cherry pick and how you weight side effects and second order risks from statins against their potential benefit. Where we seem to differ is that I believe the result to be somewhat ambiguous, while lessthanhalf seems to conflate medical consensus with certainty, which history has taught us can be a risky assumption to make. It is a sadly common technique to try to settle results differing from study to study with "but every doctor agrees"-type arguments, which are circular. One should ask why it is that every doctor agrees? If they're basing their agreement off of studies and the studies are ambiguous, then what is the source of their agreement exactly?
 
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