Cholesterol and statins — what you need to know
In this article
In brief
- Treating cholesterol is about lowering your lifetime risk of heart attack and stroke, and LDL (“bad”) cholesterol is the main target.
- Your LDL target depends on your risk, from below 3.4 mmol/L at lower risk to below 1.4 mmol/L after a heart attack.
- We check for treatable causes, such as an underactive thyroid, before starting lifelong medication.
- Statins are the mainstay and most people tolerate them well; if you get muscle aches, tell us rather than stopping.
- Seek same-day care for severe muscle pain or weakness, or dark, cola-coloured urine.
We assess cardiovascular risk and review cholesterol treatment at our Punggol clinic. See our chronic disease care.
What is cholesterol?
Cholesterol is a waxy fat that every cell needs. The liver makes most of it; the rest comes from your diet. In the blood, it travels in packages of fat and protein called lipoproteins. Two matter most:
- Low-density lipoprotein (LDL), or “bad cholesterol”, leaves cholesterol in blood vessel walls, where it hardens into plaque over time. Lowering LDL is the most evidence-based way to reduce cardiovascular risk.
- High-density lipoprotein (HDL), or “good cholesterol”, carries cholesterol from vessel walls back to the liver. Higher HDL is generally better.
A lipid panel also shows:
- Triglycerides, a different blood fat. Very high levels raise the risk of pancreatitis (inflammation of the pancreas). Moderately high levels often go with insulin resistance and diabetes.
- Non-HDL cholesterol: total cholesterol minus HDL. It captures all the particles that can cause atherosclerosis, and is increasingly used as an extra target.
Why it matters
Cholesterol drives atherosclerosis: plaque building up quietly in artery walls over years, with no symptoms. Then a plaque can crack, a clot forms, and the artery blocks suddenly. In a heart artery this is a heart attack; in a brain artery, a stroke; in a limb, peripheral artery disease.
Every 1 mmol/L reduction in LDL cholesterol cuts cardiovascular events by about 20 to 25%, and the benefit builds over years.
Your lipid panel — what the numbers mean
A standard panel reports four numbers. In Singapore, a non-fasting panel has often been accepted as the initial screening test since 2019. Fasting is preferred if your triglycerides are raised or we are deciding on medication.
| Test | What it measures | General interpretation |
|---|---|---|
| LDL-C | Your “bad cholesterol” | Target depends on your cardiovascular risk (see below) |
| HDL-C | Your “good cholesterol” | Higher is better. Low HDL (<1.0 mmol/L in men, <1.3 in women) raises risk |
| Triglycerides | Other blood fats | <1.7 mmol/L is desirable; ≥4.5 mmol/L needs attention because of pancreatitis risk |
| Total cholesterol | All cholesterol particles | Useful as part of the picture, not a target on its own |
Lp(a) — worth measuring once in your lifetime
Lipoprotein(a), or Lp(a) (“L-P-little-A”), is a particle similar to LDL with an extra protein attached. It is strongly genetic: your level is largely set at birth and barely changes with diet, exercise or statins. A high Lp(a) is an independent risk factor for heart attack, stroke and calcific aortic valve disease. It affects roughly 1 in 5 adults worldwide.
The major lipid societies’ 2024 consensus:
- Every adult should have Lp(a) measured at least once. It is a one-time test, because the level doesn’t change.
- It matters most if you have a personal or family history of premature heart disease, familial hypercholesterolaemia, or an LDL that is hard to control on a statin.
- Levels of ≥ 50 mg/dL (≥ 125 nmol/L) are elevated. They call for more aggressive management of your other risk factors: LDL, blood pressure, smoking and diabetes.
No medicine has yet been shown to prevent heart attacks or strokes by lowering Lp(a). The first large outcome trial, of pelacarsen, reported in September 2026 that it lowered Lp(a) but did not reduce cardiovascular events; trials of other Lp(a)-lowering medicines, such as olpasiran, are still running. For now, a high Lp(a) strengthens the case for aggressive LDL and blood pressure control. If you’ve never had it checked, ask at your next visit.
Other causes worth checking first
Not everyone with high cholesterol needs lifelong medication. In a meaningful minority, another treatable condition drives it (secondary dyslipidaemia). Before long-term statin therapy, we usually look for:
- Hypothyroidism (an underactive thyroid): the most common secondary cause of raised LDL. A TSH blood test picks it up, and correcting the thyroid often normalises the cholesterol. Finding it early matters, because starting a statin before correcting thyroid function can increase the risk of muscle side effects.
- Uncontrolled diabetes: raises triglycerides and lowers HDL; lipids often improve once blood sugar is controlled.
- Chronic kidney disease: a mixed pattern, and one reason kidney function is part of the standard work-up.
- Nephrotic syndrome: heavy protein loss in the urine pushes LDL sharply up.
- Cholestatic liver disease: blocked bile flow raises cholesterol.
- Excess alcohol: mainly raises triglycerides.
- Medications: some diuretics, corticosteroids, oral oestrogens, non-selective beta-blockers, anabolic steroids, certain antiretrovirals and retinoids (such as oral acne medicines) can raise cholesterol or triglycerides.
- Pregnancy: normal lipid changes make assessment tricky, and statins are generally avoided in pregnancy anyway.
For a newly raised result, our standard work-up usually includes thyroid and kidney function, and a review of your medicines and alcohol intake. If we treat a reversible cause, we often recheck the lipid panel before starting a long-term statin. This occasionally saves patients from unnecessary lifelong medication.
Your LDL target depends on your risk
The benefit of lowering LDL is proportional to your baseline cardiovascular risk. Someone with established heart disease gains much more from a given LDL reduction than someone at low risk, so targets differ.
In Singapore, we use the Singapore-modified Framingham Risk Score 2023 (SG-FRS-2023) to estimate your 10-year cardiovascular risk. It is available at cvd.clinicaltools.mohtgroup.com. Certain conditions automatically place you in a “very high” or “high” risk category, whatever the calculator says.
| Your risk category | LDL-C target |
|---|---|
| Post-ACS / unstable angina / recent heart attack | Below 1.4 mmol/L |
| Established ASCVD (prior MI, stroke, TIA, stable IHD/CCS, PAD, AAA, post-CABG, post-PCI) | Below 1.8 mmol/L |
| Familial hypercholesterolaemia (FH) — adults with additional CV risk factors or over age 40 | Below 1.8 mmol/L |
| Diabetes with additional risk factors (CKD, microvascular complications, DM ≥10 years, persistently uncontrolled) | Below 1.8 mmol/L |
| Diabetes (without those additional factors) | Below 2.6 mmol/L |
| Chronic kidney disease (eGFR <60 or ACR ≥3 mg/mmol) | Below 2.6 mmol/L |
| SG-FRS >20% (high 10-year risk) | Below 1.8 mmol/L |
| SG-FRS 10–20% (intermediate risk) | Below 2.6 mmol/L |
| SG-FRS 5–<10% (borderline risk with risk enhancers) | Below 3.4 mmol/L |
| SG-FRS <5% (low risk) | Ideal below 3.4 mmol/L — lifestyle-led; a statin may be considered if LDL-C stays persistently above 4.1 mmol/L despite 3–6 months of diet and exercise |
Risk enhancers tip a borderline-risk patient towards treatment. They include a family history of premature heart disease, chronic inflammatory or autoimmune disease (such as rheumatoid arthritis, SLE, HIV), persistently high triglycerides, metabolic syndrome, premature menopause (before age 40), severe mental illness, an abnormal ankle-brachial index, and raised lipoprotein(a).
Why targets have become stricter
If you’ve had high cholesterol for more than a decade, you may have noticed the targets creeping down. In the early 2000s, an LDL “below 3 mmol/L” was often considered good enough. By the 2010s, the target for high-risk patients was below 2.6 mmol/L. Today, after ACS, we aim below 1.4 mmol/L. Two things drove this:
- Trials showed that “lower is better”, with no clear threshold below which benefit stops. IMPROVE-IT (ezetimibe added to a statin after ACS), FOURIER and ODYSSEY OUTCOMES (PCSK9 inhibitors added to a statin) all showed that pushing LDL lower kept reducing cardiovascular events, with no signal of harm at low levels.
- Newer medicines made low targets reachable. Even the strongest statin at maximum dose often couldn’t get LDL much below 1.8. High-intensity statins with ezetimibe, plus PCSK9 inhibitors for selected high-risk patients, now routinely reach 1.4 or lower.
So the bar has moved. If your LDL has been “around 2.5” for years and you thought that was fine, it’s worth a fresh conversation, especially if your risk has changed: new diabetes, ageing, menopause, or a relative with heart disease at a young age.
Lifestyle that moves the dial
Lifestyle is the foundation for everyone. For some lower-risk patients with modestly raised cholesterol, it may be enough on its own. What matters most:
- Cardioprotective eating: the Health Promotion Board’s My Healthy Plate is a useful start. Choose wholegrains, fruit and vegetables, and healthy proteins (fish, tofu, lean meat, beans, nuts). Cut refined sugar and saturated fat (especially in processed foods), and avoid trans fats. Replacing saturated fat with polyunsaturated fat, and eating more soluble fibre, specifically lower LDL.
- Physical activity: 150 to 300 minutes a week of moderate-intensity activity. Brisk walking counts. Movement helps even when it doesn’t bring weight loss.
- Healthy weight: losing 5 to 10% of body weight improves your lipid profile and lowers overall cardiovascular risk.
- Alcohol: no more than 2 standard drinks a day for men, 1 for women. Avoid alcohol completely if your triglycerides are above 4.5 mmol/L or you have had pancreatitis.
- Stopping smoking: smoking lowers HDL and multiplies cardiovascular risk. The national I Quit programme and medicines (nicotine replacement, varenicline, bupropion) can help; ask us at your next visit.
If you’re starting from scratch, pick one realistic change a month. A consistent 5% beats a heroic 50% that lasts two weeks.
Statins — the mainstay of medication
Statins are the best-studied class of cholesterol-lowering medicines. They reduce cholesterol production in the liver and help it clear LDL from the blood. Large trials and decades of follow-up show they reliably and cost-effectively reduce heart attacks, strokes and cardiovascular deaths.
Statins available in Singapore, by intensity:
| Statin | Moderate intensity (30–49% LDL reduction) | High intensity (≥50% LDL reduction) |
|---|---|---|
| Atorvastatin (Lipitor) | 10–20 mg | 40–80 mg |
| Rosuvastatin (Crestor) | 5–10 mg | 20–40 mg |
| Pitavastatin (Livazo) | 1–4 mg | — |
| Simvastatin (Zocor) | 20–40 mg | — (80 mg is generally avoided because of myopathy risk) |
| Pravastatin | 40–80 mg | — |
| Lovastatin | 40–80 mg | — |
Which statin we choose depends on:
- How much LDL reduction you need (your target versus your current LDL)
- Drug interactions. Simvastatin has the most important ones. Medicines that block the liver enzyme CYP3A4 can sharply raise its levels, including the antibiotics clarithromycin and erythromycin, amiodarone, diltiazem, verapamil, cyclosporine and HIV protease inhibitors. Atorvastatin also uses CYP3A4 but is much less affected. Rosuvastatin, pitavastatin and pravastatin have the fewest CYP-related interactions.
- Kidney and liver function
- Whether you have tolerated a particular statin before
- Cost and availability: most statins are on the HSG Chronic Tier list and subsidised
Before starting a statin, we check:
- Pregnancy or plans to conceive (statins are generally avoided in pregnancy and breastfeeding)
- Baseline liver function, to exclude liver disease that rules statins out (decompensated cirrhosis, acute liver failure) and as a reference point
- Baseline kidney function, because some statins (such as rosuvastatin and simvastatin) need dose adjustment in significant kidney impairment, and CKD affects your LDL target
- Your current medicines, for interactions
- Any history of unexplained muscle problems
What to expect on a statin
Most people tolerate statins well, and decades of trial and real-world evidence support their safety.
- Muscle aches (myalgia): the most commonly reported concern. In placebo-controlled trials, most statin “muscle ache” is not caused by the statin; people who expect side effects report them even on placebo (the nocebo effect). If you do get aches, don’t stop on your own; let us know. A lower dose, a different statin, or a short break to see whether symptoms track the statin usually resolves it.
- Muscle damage (rhabdomyolysis): severe and rare, roughly 1 in 10,000 patient-years, and the main reason we avoid certain drug combinations. Seek medical attention the same day for severe muscle pain or weakness, or dark or cola-coloured urine.
- Blood sugar: statins slightly increase the risk of type 2 diabetes in predisposed people, by about 1 extra case per 250 people treated over 4 years. In people at high risk, the cardiovascular benefit far outweighs this.
- Pregnancy: statins are generally avoided. Tell us if you are planning to conceive or might be pregnant.
- Grapefruit juice: significantly raises levels of atorvastatin, simvastatin and lovastatin (but not pitavastatin, rosuvastatin or pravastatin). Avoid it if you take an affected statin.
What we monitor, and why
After starting or increasing a statin, we usually check a lipid panel at 8 to 12 weeks to see whether you have reached target. After that, lipids and kidney function are checked at your 6-monthly chronic disease review.
Monitoring is mainly to make sure your treatment is still working for you: hitting target, adjusting the dose, and catching changes in your risk factors, rather than hunting for side effects. Significant new side effects after the first few months of stable treatment are uncommon, and routine liver tests aren’t needed without a specific concern.
When statins alone aren’t enough
For some patients, particularly those at very high risk, statins alone don’t reach target. The next steps are:
- Ezetimibe: a once-daily tablet added to your statin. It lowers LDL by about a further 20 to 25% and is usually well tolerated. Evidence supports added cardiovascular benefit when combined with a statin.
- PCSK9-targeting medicines: newer and more potent. PCSK9 is a protein that reduces the liver’s ability to clear LDL. Evolocumab (Repatha) and alirocumab (Praluent) are antibodies that block it, injected once every 2 or 4 weeks. Inclisiran (Leqvio) works differently: it is a small interfering RNA (siRNA) that stops the liver making PCSK9, and is given only twice a year after the initial doses. Added to a statin plus ezetimibe, they lower LDL by 45–60%.
- They are typically prescribed through a specialist (cardiologist, or endocrinologist/lipid clinic).
- They are mainly for people with established cardiovascular disease or familial hypercholesterolaemia who are not at target on maximal statin plus ezetimibe, or who genuinely cannot tolerate statins.
- If you are high-risk and not at target despite best efforts, ask us and we’ll arrange referral.
A note on familial hypercholesterolaemia (FH)
Familial hypercholesterolaemia (FH) is an inherited condition that causes very high LDL from birth. Untreated, it raises the risk of early heart disease about 20-fold. It often runs in families with premature heart attacks (before age 55 in men, 60 in women). It is more common than most people realise: roughly 1 in 250 to 1 in 500 people.
We may suspect FH if:
- your LDL is very high (for example, ≥ 5.5 mmol/L untreated) without an obvious secondary cause
- a first-degree relative (parent, sibling, child) has been diagnosed with FH or had heart disease young
- you or family members have cholesterol deposits in the tendons (tendon xanthomas), around the eyes (xanthelasmas), or in the cornea (corneal arcus before age 45)
Singapore launched a National Familial Hypercholesterolaemia Genetic Testing Programme in 2025. Singapore Citizens and Permanent Residents with LDL-C ≥ 5.5 mmol/L can be referred to the Genomic Assessment Centre (GAC) at SingHealth, located at National Heart Centre Singapore. It offers genetic testing, genetic counselling, and subsidised cascade screening for first-degree relatives, so that children and siblings can start preventive treatment young. Subsidies are up to 70% (means-tested) for eligible Citizens and PRs.
If you or a family member have very high LDL, or a family history of early heart disease, please tell us. FH is one of the clearest cases where referral meaningfully changes outcomes.
Triglycerides — a short note
Triglycerides deserve their own attention. The approach is staged: lifestyle first, then statin, then fibrate where needed.
- Mildly raised (1.7–4.5 mmol/L): usually lifestyle-driven (excess calories, refined sugar, alcohol, weight, sometimes poorly controlled diabetes). Treatment is mainly lifestyle, plus any secondary cause.
- Moderately raised (4.5–10 mmol/L): lifestyle is essential, and a statin is usually added. Statins lower both LDL and triglycerides, so in most people they address both at once.
- Very high (>10 mmol/L): the main concern becomes acute pancreatitis, and treatment is more urgent. A fibrate (usually fenofibrate) is often added to lower triglycerides further, alongside the statin for cardiovascular risk. Reversible causes (uncontrolled diabetes, heavy drinking, certain medicines) are corrected urgently. Prescription omega-3 fatty acids (icosapent ethyl) may also be considered in specific situations.
A few practical points
- Feeling fine is the point. High cholesterol has no symptoms. Feeling well on a statin means it is working, not that you can stop.
- If the regimen isn’t working for you, tell us rather than quietly skipping doses. Missed doses erode the benefit, and we can almost always adjust the plan to fit your life.
- Supplements: please mention anything you take or are considering for cholesterol, such as “natural” cures, garlic capsules, plant sterols, red yeast rice, berberine or herbal mixes. The evidence for most is inconsistent at best. Some interact with statins or cause muscle problems themselves; red yeast rice contains low-dose monacolin K, essentially unregulated lovastatin. We’d rather discuss them openly than have you swap a prescribed medicine for something untested.
Why regular follow-up matters
Cholesterol is not “set and forget”. We ask you to come back regularly, even when all is well:
- Guidelines evolve. Your previous target may not match current evidence. “Well-controlled” in 2015 may be “needs intensification” in 2026.
- Your risk changes. New diabetes, a new high blood pressure reading, a relative diagnosed with heart disease, menopause, or simply ageing can shift your risk category and your target.
- Tolerance and adherence drift. Many people stop or cut back their statin without realising it matters. A routine review catches this.
- Side effects need a periodic look: liver function, kidney function, muscle symptoms, blood sugar, and interactions with any newly prescribed medicine.
- New options appear. Newer agents (inclisiran, for example) and changes to local subsidies can open options that weren’t there at your last review.
- Lifestyle support works better with accountability. Weight, activity, diet and smoking respond better to regular conversations than an annual pep talk.
We suggest a lipid review every 6 months as part of your chronic disease follow-up, and more often if you have just started or changed medication or your risk has changed. It needn’t be long. What matters is not letting 3–5 years pass on autopilot.
The Singapore context — programmes that support you
- Healthier SG Chronic Tier (from February 2024): enrolled patients can buy common chronic medicines, including statins and ezetimibe, at prices similar to polyclinic prices at their enrolled HSG GP clinic.
- Community Health Assist Scheme (CHAS): means-tested subsidies for consultations and selected medicines. Pioneer Generation, Merdeka Generation and CHAS Blue / Orange / Green tiers apply where eligible. Details at chas.sg.
- MediSave: usable for chronic disease consultations and selected medicines, up to annual withdrawal limits (currently $500 basic / $700 complex, rising to $700 / $1,000 in January 2027).
- Genomic Assessment Centre at SingHealth: for suspected FH referrals (LDL-C ≥ 5.5 mmol/L in SG Citizens or PRs).
Get in touch
Punggol — 658 Punggol East, #01-04, Singapore 820658 · Tel 6312 4589
Joo Chiat — 172 Joo Chiat Road, #01-01, Singapore 427443 · Tel 6920 1952
Email — admin@ktmc.sg
References
- Agency for Care Effectiveness (ACE). Lipid management — focus on cardiovascular risk. ACE Clinical Guideline, Ministry of Health, Singapore. December 2023, updated June 2025 (v1.1). ace-hta.gov.sg
- Singapore-modified Framingham Risk Score 2023 (SG-FRS-2023) — 10-year cardiovascular risk calculator. cvd.clinicaltools.mohtgroup.com
- National Familial Hypercholesterolaemia Genetic Testing Programme. Ministry of Health, Singapore. Launched 30 June 2025. moh.gov.sg
- SingHealth Duke-NUS Genomic Medicine Centre — Genomic Assessment Centre. singhealth.com.sg
- Health Promotion Board Singapore. My Healthy Plate dietary guidelines.
- Ministry of Health Singapore. Circular 08/2019 on use of HbA1c and non-fasting lipids for screening.
- Cannon CP, Blazing MA, Giugliano RP, et al. (IMPROVE-IT Investigators). Ezetimibe Added to Statin Therapy after Acute Coronary Syndromes. N Engl J Med. 2015;372:2387–2397.
- Ray KK, Wright RS, Kallend D, et al. (ORION-10 and ORION-11 Investigators). Two Phase 3 Trials of Inclisiran in Patients with Elevated LDL Cholesterol. N Engl J Med. 2020;382:1507–1519.
- Novartis. Novartis announces Lp(a)HORIZON Phase III topline results for pelacarsen in patients with elevated Lp(a) and established cardiovascular disease (CVD). Press release, 4 September 2026. sec.gov
- Amgen. Amgen reports second quarter 2026 financial results (pipeline update: OCEAN(a)-Outcomes trial of olpasiran ongoing). 2026. sec.gov
This information is for general education only and is not a substitute for medical advice. Lipid management must be individualised based on your overall cardiovascular risk, medications, and preferences — please speak with our team. v1.1 · October 2026 (v1.0 April 2026) · Review due April 2028.