It actually happened: off statins!

[RENjutsu]

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

 

[Calm Logic]

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

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):

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.

 

[rixsternaz]

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.

 

[Zydeceltico]

Regarding calcium CT scoring for intermediate risk:

Risk calculators:



Related guidelines:

My CAC score was 790. 🙂

 

[lessthanhalf]

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

 

[lessthanhalf]

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

 

[Calm Logic]

Percentiles for calcium scoring, categorized by sex and age:

Checking your browser - reCAPTCHA

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:]

 

[Neptide]

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!

 

[tubby]

(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.

 

[tubby]

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?

 

[Calm Logic]

Redneck doctoring: Women generally age slower than men cardiovascularly, so men might as well consider statins (even at low doses) for at least a small competitive boost for anti-aging or healthspan (in addition to everything else, including GLPs, diet, and exercise):

Concept​	Mechanism & Study Reference​	The "Competitive Boost" Logic​
The Gap	JACC (2020): Women show slower progression of vascular aging across the lifespan compared to men.	Men use statins to "offset" the biological 10-year head start women have in arterial plaque accumulation.
ApoB & LDL-Years	JAMA (2019): Long-term exposure to lower LDL-C/ApoB levels is associated with a 54% lower risk of CHD per mmol/L.	Low-dose statins early in life mimic the "low-exposure" environment women naturally have pre-menopause.
Plaque Stability	PARADIGM Study: Statins promote plaque calcification and reduce high-risk "soft" (non-calcified) plaque volume.	Protects men from the "vulnerable" plaque ruptures that typically cause premature male cardiac events.
Inflammation	JUPITER Trial: Statins significantly reduce hsCRP, even in individuals with "normal" cholesterol but high inflammation.	Counteracts "inflammaging," a key driver of rapid biological aging in the male vascular system.
Endothelial Function	Circulation Research: Statins increase eNOS (Nitric Oxide) activity, improving vessel dilation and health.	Maintains "younger" vessel responsiveness, directly targeting the primary site of male cardiovascular decline.
The "Side Effect" Gap	Cleveland Clinic (2023): Women are significantly more likely to report statin-associated muscle symptoms (SAMS).	Because men tolerate the "boost" better, they face fewer trade-offs in muscle performance and "thrive" factors.

​

 

[aRareUnicorn]

GLP had zero effects on my lipids profile with the exception of trigs (stooped eating sugar and overall fewer calories intake = lowered trigs).
I have super high LP(a) and inflammation (Reta did not impact my inflammation levels, either!).
Had lipids NMR done and always terrible. Decided against CAC score, instead, simply assumed it is very high based on other tests. No need to add stress to my life with a confirmation of what is a given based on everything else, lol…
I refused statins but instead started Repatha and it got my ldl to 90. Added now zetia. And plan on staying on both long term, hoping it will minimize the risks for me!

 

[tubby]

GLP had zero effects on my lipids profile with the exception of trigs

At the risk of sounding like a broken record here, a decrease in triglycerides (particularly the triglyceride to HDL ratio) is far more impactful on correlating with reduced heart disease risk than LDL. If GLPs brought your triglycerides down that is a very significant outcome:

https://pmc.ncbi.nlm.nih.gov/articles/PMC2664115

 

[lessthanhalf]

The evidence for lowering LDL looks pretty solid to me. This is a very large scale meta analysis.
doi: 10.1016/S0140-6736(10)61350-5. from the lancet Cited by 6102 - this is the number of scientific papers that referenced this study , a strong indicator of relevance and importance.

Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials

main findings
Across all 26 trials, all-cause mortality was reduced by 10% per 1·0 mmol/L LDL reduction (RR 0·90, 95% CI 0·87-0·93; p<0·0001), largely reflecting significant reductions in deaths due to coronary heart disease (RR 0·80, 99% CI 0·74-0·87; p<0·0001) and other cardiac causes (RR 0·89, 99% CI 0·81-0·98; p=0·002), with no significant effect on deaths due to stroke (RR 0·96, 95% CI 0·84-1·09; p=0·5) or other vascular causes (RR 0·98, 99% CI 0·81-1·18; p=0·8). No significant effects were observed on deaths due to cancer or other non-vascular causes (RR 0·97, 95% CI 0·92-1·03; p=0·3) or on cancer incidence (RR 1·00, 95% CI 0·96-1·04; p=0·9), even at low LDL cholesterol concentrations.

CAC screening is complicated, there is not a lot of evidence that screening unselected populations is beneficial. Using it to decide on therapy or not for those with some risk factors but borderline 10 year risk is generally regarded as a good idea.

I cannot find a lot of supporting evidence , but I wonder if it is worth doing in a lot of people with severe obesity in those over 40 or 50, especially in the context of improved lipids and other risk factors after large weight losses from GLP's, where the numbers no longer look definitive for needing preventive therapies, but the odds of pre existing significant coronary artery disease is high. Both I and another person in this thread discovered very high ccs numbers, requiring secondary prevention level treatment. The science on obesity and cardiovascular risk is complicated and the standard risk equations do not include it.

It is always going to be harder to get good evidence for primary prevention, generally the older and sicker the population being studied the more events are going to happen, so secondary prevention is going to show effects in much smaller populations, whereas you might need 10 times the number of patients to show similar effects in a healthier primary prevention population which makes the study 10 times as expensive to have the same statistical power . It is similar to GLP's where they are proven to reduce illness and death in high risk populations - those with heart disease or diabetes, but in unselected groups showing this effect is much more difficult and expensive, so there is no proof yet and may not be for many years.

 

[Zydeceltico]

CAC screening is complicated, there is not a lot of evidence that screening unselected populations is beneficial. Using it to decide on therapy or not for those with some risk factors but borderline 10 year risk is generally regarded as a good idea.

Ahhhh......I just realized that I have an important clarification to make: As Ihave mentioned, I self-selected to have a CAC run via self-pay. Insurance was not involved. That however is not the clarification. My clarification is that the CAC led my cardiologist to want to look closer at the issue and then I had to do a CT Angiogram, and that was blurry, so insurance OK-ed a closer look via catheter and my cariologist told me that, while he was looking, if he could re medy whatever he might find with a stent he would and he did. That is the actual and literal order of operations and logic.

 

[RadicalCrimson]

Percentiles for calcium scoring, categorized by sex and age:

Checking your browser - reCAPTCHA

Someone I know got a score waaay outside these tables.
I wonder what happened to him 😉
This calcium score test could turn out to be the best $99 he spent in his life, who knows.

 

[tubby]

It is always going to be harder to get good evidence for primary prevention, generally the older and sicker the population being studied the more events are going to happen, so secondary prevention is going to show effects in much smaller populations, whereas you might need 10 times the number of patients to show similar effects in a healthier primary prevention population which makes the study 10 times as expensive to have the same statistical power .

Of course primary prevention is where most of the money is when it comes to any prescription drug...

As a thought problem, let's pretend that every now and then pharma will exaggerate results, minimize side effects, or otherwise behave unethically if it financially benefits them. If that's a possibility, it would be wise to look for signs that might be happening. A major red flag for that would be a desire to closely guard the raw data from statin trials for primary prevention and ensure that only pharma-funded and very select groups of researchers are ever able to access that data.

Enter the CTT at Oxford University. They seems to do exactly what I just suggested would be a major red flag. They'll claim that their hands are tied due to confidentiality agreements with the researchers who gathered the data and that's likely true. But who are these "evil" researchers who refuse to release such important health data with such broad life-saving implications and will only let select groups of researchers access it to perform analysis on the benefits and side effects associated with statins? Weird, eh? I wonder what their rationale is for being willing to show their results to the world, but refusing to show their analysis work in getting from the raw data to the end result.

 

[aRareUnicorn]

At the risk of sounding like a broken record here, a decrease in triglycerides (particularly the triglyceride to HDL ratio) is far more impactful on correlating with reduced heart disease risk than LDL. If GLPs brought your triglycerides down that is a very significant outcome:

I would agree with you if… HDL was reasonably normal range. In my case it is at 30 mg/dl and the ratio remains high even with trigs lowered to 90 mg/dl… yes the ratio is now lower but by any means the risk has not improved…

 

[Calm Logic]

Using hs-CRP results as a consideration:

2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia

In adults without ASCVD with a borderline 10-year ASCVD risk estimate (3% to <5%) by the PREVENT-ASCVD equations, if high-sensitivity C-reactive protein (hsCRP) is measured and is ≥2 mg/L on 2 successive occasions with no identifiable underlying cause of hsCRP elevation, high-intensity statin therapy can be useful to reduce the risk of ASCVD events.

 

[Bellypearl]

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!!! It is so amazing when you reach a milestone you've been working so hard for.

 

[samIam]

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.

You should do some real research on this there is no real proof that high cholesterol causes heart attacks or heart disease. Statins are terrible for you.

 

[Foggy-Hollow]

only let select groups of researchers access it to perform analysis on the benefits and side effects associated with statins?

I hate this timeline.

Hiding is for cowards, science is based off of independent repeatability.

I’m reading up on the whole niacin thing and the obfuscation… sigh. I’ll go back to working with nuts.

Bolts and nuts.

 

[Calm Logic]

You should do some real research on this there is no real proof that high cholesterol causes heart attacks or heart disease. Statins are terrible for you.

Low-density lipoprotein cholesterol and lifespan

This genetic evidence supports that higher LDL-c levels reduce lifespan and longevity.

A separate issue is how much statins help. If cardiovascular risk factors are less, the benefits of statins will be less obvious for primary prevention:

The Hierarchy of Heart Health: Ranked Cardiovascular Risk Factors (2026)​

Based on the 2026 Heart Disease and Stroke Statistics Update from the American Heart Association (AHA) and the latest CDC clinical data, risk factors are prioritized by their statistical impact on mortality and their "population attributable fraction."

The primary ranking is now centered on Life’s Essential 8, a framework that splits risk into health behaviors and health factors.

---

Master Risk Table: Impact and Prevalence

Rank	Risk Factor	Impact Category	Key Statistic / Clinical Threshold	Primary Source
1	High Blood Pressure	Health Factor	>130/80 mmHg; linked to ~50% of CVD deaths.	AHA 2026 Statistics Update
2	Tobacco & Nicotine	Health Behavior	Leading preventable cause; 2–4x higher risk.	CDC / AHA Expanded Chapter
3	High Cholesterol	Health Factor	Focus on Non-HDL and ApoB levels.	AHA 2026 (Life’s Essential 8)
4	Blood Sugar / Diabetes	Health Factor	HbA1c > 6.5%; 2x risk of heart attack.	CDC NHIS 2026 Trends
5	Obesity (High BMI)	Health Factor	BMI > 30; drives 90% of CKM syndrome.	AHA CKM Syndrome Chapter
6	Physical Inactivity	Health Behavior	<150 min/week moderate activity.	AHA Preventive Science
7	Poor Diet	Health Behavior	High sodium/ultra-processed food intake.	2026 Dietary Guidance (AHA)
8	Inadequate Sleep	Health Behavior	<7 hours; increases inflammation/cortisol.	AHA Life's Essential 8

 

[ltjltj]

You should do some real research on this there is no real proof that high cholesterol causes heart attacks or heart disease. Statins are terrible for you.

This is abject nonsense and anyone doing some "real research" and looking at the mind boggling amount of data supporting them will come to the same conclusion.

They don't work for everyone, and some people have unacceptable side effects, but that applies essentially to all medicine, whether peptide or other pharmaceutical.

 

[tendency]

Total cholesterol: 314
Triglycerides: 93
HDL: 66
VLDL Chol Calc: 19
LDL Chol Calc (NIH): 229

And this is after 3.5mg reta/week. Triglycerides and HDL both decently improved on reta no change for LDL.

Been like this for 25 years .. personally, don't have any risk factor of CVD on both sides of family. Doc wants me on a statin.

 

[Calm Logic]

On the positive side, per Google Gemini:



OTOH: "Most clinical guidelines still treat an LDL above 190 as a high-risk "threshold" regardless of how good the other numbers look" (Google Gemini).

 

[lessthanhalf]

Total cholesterol: 314
Triglycerides: 93
HDL: 66
VLDL Chol Calc: 19
LDL Chol Calc (NIH): 229

And this is after 3.5mg reta/week. Triglycerides and HDL both decently improved on reta no change for LDL.

Been like this for 25 years .. personally, don't have any risk factor of CVD on both sides of family. Doc wants me on a statin.

If your doctor wants you on a statin , it is most likely there is a reason. Family history is only one of many risk factors, the largest one by far is age, but also blood pressure, blood glucose, lipids , smoking , obesity. It is not hard to make an estimate of absolute cardiovascular risk from that information, and if high then statins and or other lipid lowering drugs are useful and reduce risk. No idea of the other risks but if you are taking reta then presumably weight is an issue, and the ldl numbers are pretty high. If lipids have been like that for 25 years then there has been lots of time to grow atherosclerotic lesions where you really do not want them to be, in coronary and cerebral arteries.

 

[Calm Logic]

A possibile, additional cardiovascular risk factor:

I've always (well, last 25 years at least) had borderline high calcium measured via bloods, like, say 10.0, 10.1 (reference 8.7-10.2).

In any case, the chronically high LDL seems to be begging for a statin. Some docs do EOD dosing with Crestor (or Monday, Wed, Friday dosing) to prevent sides, which are apparently low in incidence anyway, much less frequent than believed.

As discussed earlier in this thread, a CT calcium score could help if you are on the fence, or could inform how low to get LDL.

 

[lessthanhalf]

Really hard to know without age, but if he has test results from 25 years ago then likely to be at least 45, which is old enough for risks to start being a real issue rather than some far away concern. And coronary calcium score is the ideal test to use if uncertain about starting statins or not , it classifies long term risk more accurately than standard risk factors in that situation.
Most people do not get any side effects from statins. Apart from rare muscle damage issues which are not hard to diagnose, the most common complaint by far is vague muscle soreness, but in large studies the odds of it on statins are more or less the same as for placebo.

 

[Calm Logic]

Family history is only one of many risk factors, the largest one by far is age

From a marketing perspective, statins would have more traction if they were seen as anti-aging supplements (which is arguably what they are, in addition to being reactive treatments). Especially for men, since they age cardiovascularly about 9 years faster (on average).