Cholesterol and statins — what you need to know

About this guide

Cholesterol is one of the most commonly discussed numbers in clinic — and one of the most misunderstood. Many of our patients have either been told “your cholesterol is a bit high, watch your diet” and not much else, or have been started on a statin and left to assume the story ends there. Neither is quite right.

Cholesterol management is really about reducing your lifetime risk of heart attack, stroke, and other cardiovascular events. Some of that is about food and movement; much of it is about targeted medication; and some of it is about looking carefully for reasons why cholesterol is high in the first place before committing to lifelong treatment.

This guide covers the essentials — what the numbers mean, who benefits most from statins, why targets have become stricter over the last decade, and why regular follow-up with your family doctor is the single biggest factor in how well this goes over the years ahead.

What is cholesterol?

Cholesterol is a waxy fat that every cell in your body needs to function. The liver makes most of what you use; a smaller amount comes from your diet. In the blood, cholesterol is carried inside packages called lipoproteins — essentially “cargo ships” made of fat and protein. The two that matter most clinically:

• Low-density lipoprotein (LDL) — often called “bad cholesterol.” LDL particles leave cholesterol behind in the walls of blood vessels, and over time these deposits harden into plaques. Lowering LDL is the single most evidence-based way to reduce cardiovascular risk.
• High-density lipoprotein (HDL) — often called “good cholesterol.” HDL carries cholesterol away from vessel walls back to the liver. Higher HDL is generally better.

You’ll also see two other numbers on a lipid panel:

• Triglycerides — a different fat in the blood. Very high levels increase the risk of inflammation of the pancreas (pancreatitis); moderately high levels often travel with insulin resistance and diabetes.
• Non-HDL cholesterol — total cholesterol minus HDL. This captures all the cholesterol-carrying particles that can cause atherosclerosis, and is increasingly used as a supplementary target.

Why it matters

The process that cholesterol drives is called atherosclerosis — the quiet build-up of plaque in artery walls over years, sometimes decades. For a long time it causes no symptoms. Then, if a plaque cracks and a blood clot forms on top, the artery can suddenly block — that’s a heart attack (in a coronary artery), a stroke (in a brain artery), or a blocked limb (peripheral artery disease).

The best research we have says that for every 1 mmol/L reduction in LDL cholesterol, cardiovascular events fall by about 20 to 25% — and the benefit is cumulative over years. It’s a big deal.

Your lipid panel — what the numbers mean

A standard lipid panel reports four numbers. In Singapore, a non-fasting lipid panel is often accepted as the initial screening test (since 2019), though fasting is preferred if your triglycerides are elevated or we’re making pharmacological decisions.

Your LDL-C is the main treatment target. We’ll talk about what number is right for you below.

Lp(a) — worth measuring once in your lifetime

Lipoprotein(a), often written as Lp(a) (pronounced “L-P-little-A”), is a cholesterol-carrying particle similar to LDL but with an extra attached protein. It’s strongly genetic — your level is largely set at birth and barely changes with diet, exercise, or statins. Elevated Lp(a) is an independent risk factor for heart attack, stroke, and calcific aortic valve disease, and affects roughly 1 in 5 adults worldwide.

Current consensus from the major lipid societies (2024 updates):

• Every adult should have Lp(a) measured at least once — a one-time test, not a recurring one, because the level doesn’t change
• Particularly important if you have a personal or family history of premature heart disease, familial hypercholesterolaemia, or an LDL that’s hard to control despite statin therapy
• Levels ≥ 50 mg/dL (≥ 125 nmol/L) are considered elevated and warrant more aggressive management of your other cardiovascular risk factors — LDL, blood pressure, smoking, diabetes

There is currently no widely-available medication that lowers Lp(a) with proven cardiovascular benefit, though several (pelacarsen, olpasiran) are in late-stage trials. For now, knowing that your Lp(a) is elevated strengthens the case for aggressive LDL-lowering and blood-pressure control.

If you’ve never had Lp(a) checked, please mention it at your next visit.

Other causes worth checking first

One thing that often gets missed: not everyone with high cholesterol needs lifelong medication. In a meaningful minority of patients, high cholesterol is driven by something else that is reversible or treatable in its own right — what we call secondary dyslipidaemia.

Before committing to long-term statin therapy, we’d usually look for:

• Hypothyroidism (an underactive thyroid) — the most common secondary cause of elevated LDL. A simple TSH blood test is enough to pick it up, and correcting the thyroid often normalises the cholesterol entirely. It’s worth identifying early because starting a statin before correcting thyroid function can increase the risk of muscle side effects.
• Uncontrolled diabetes — typically drives triglycerides up and HDL down; lipids often improve substantially once blood sugar is controlled.
• Chronic kidney disease — mixed pattern; part of why kidney function is part of the standard work-up.
• Nephrotic syndrome — high urinary protein loss pulls LDL sharply up.
• Cholestatic liver disease — obstructed bile flow raises cholesterol.
• Excess alcohol intake — primarily raises triglycerides.
• Medications — some diuretics, corticosteroids, oral oestrogens, non-selective beta-blockers, anabolic steroids, certain antiretrovirals, and retinoids (like oral acne medications) can all raise cholesterol or triglycerides.
• Pregnancy — physiological lipid changes make assessment tricky, and statins are generally avoided in pregnancy anyway.

Our standard work-up when we see a newly-elevated lipid result usually includes a thyroid function test and kidney function, and a careful review of your medication list and alcohol intake. In patients where a reversible cause is found and treated, we will often recheck the lipid panel before starting a long-term statin. It’s a small extra step that occasionally saves patients from unnecessary lifelong medication.

Your LDL target depends on your risk

The fundamental idea behind cholesterol management is that the benefit of lowering LDL is proportional to your baseline cardiovascular risk. Someone with established heart disease gets much more benefit from a given LDL reduction than someone at low overall risk. So the target isn’t the same for everyone.

In Singapore, we use the Singapore-modified Framingham Risk Score 2023 (SG-FRS-2023) to estimate your 10-year cardiovascular risk, available at cvd.clinicaltools.mohtgroup.com. Certain medical conditions automatically place you in a “very high” or “high” risk category, regardless of the calculator.

“Risk enhancers” — features that tip a borderline-risk patient toward needing treatment — 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 elevated lipoprotein(a).

Why targets have become stricter

If you’ve had high cholesterol for more than a decade, you may have noticed that the numbers we aim for have crept downward. There’s a reason for that: the evidence has moved.

In the early 2000s, an LDL of “below 3 mmol/L” was often considered good enough for most patients. 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 change:

1. Large trials showed that “lower is better” — with no clear threshold below which the benefit disappears. Trials like IMPROVE-IT (ezetimibe added to statin after ACS), FOURIER and ODYSSEY OUTCOMES (PCSK9 inhibitors added to statin) consistently showed that pushing LDL lower than previously thought possible continued to reduce cardiovascular events — without a signal of harm at low levels.
2. Newer medications made low targets achievable. Earlier, even with the strongest statin at maximum dose, LDL much below 1.8 was hard to reach in many patients. Now, with high-intensity statins combined with ezetimibe — and PCSK9 inhibitors for selected high-risk patients — targets of 1.4 or even lower are routinely reached.

So when you read an older reference, or remember what the target was when you first started treatment, be aware that the bar has moved. If your LDL has been “around 2.5” for years and you previously considered that acceptable, it’s worth a fresh conversation — especially if your overall risk has changed (a new diabetes diagnosis, ageing, menopause, or a family member diagnosed with heart disease at a young age).

Lifestyle that moves the dial

For all patients, lifestyle change is the foundation — and for some (particularly lower-risk patients with only modestly elevated cholesterol), it may be enough on its own.

The things that matter most:

• Cardioprotective eating — the Health Promotion Board’s My Healthy Plate is a useful starting point. Emphasise wholegrains, fruits and vegetables, healthy proteins (fish, tofu, lean meat, beans, nuts). Reduce refined sugar, saturated fat (especially in processed foods), and avoid trans fats. Replacing saturated fat with polyunsaturated fat and increasing soluble fibre specifically lower LDL.
• Physical activity — 150 to 300 minutes per week of moderate-intensity activity. Brisk walking counts. Movement matters even when it doesn’t produce weight loss.
• Healthy weight — 5 to 10% weight reduction improves lipid profile and lowers overall cardiovascular risk.
• Alcohol — no more than 2 standard drinks per day for men, 1 for women. If your triglycerides are above 4.5 mmol/L or you have a history of pancreatitis, abstinence is advised.
• Smoking cessation — smoking lowers HDL and multiplies cardiovascular risk. The I Quit national programme and medications (nicotine replacement, varenicline, bupropion) are available — ask us at your next visit.

If you’re starting from scratch, pick one realistic change per month rather than trying everything at once. A consistent 5% beats a heroic 50% that lasts two weeks.

Statins — the mainstay of medication

Statins are by far the best-studied class of lipid-lowering medications. They work in the liver to reduce cholesterol production and increase the liver’s ability to clear LDL from the blood. In large trials and decades of follow-up, they reduce heart attacks, strokes, and cardiovascular deaths reliably and cost-effectively.

SG-available statins, by intensity:

Which statin we choose depends on:

• How much LDL reduction you need (your target vs your current LDL)
• Drug interactions — simvastatin has the most clinically important interactions (it’s heavily metabolised by the liver enzyme CYP3A4, and common medications that inhibit CYP3A4 can dramatically raise simvastatin levels — including certain antibiotics like clarithromycin and erythromycin, amiodarone, diltiazem, verapamil, cyclosporine, and HIV protease inhibitors). Atorvastatin is also CYP3A4-metabolised but is much less affected than simvastatin. Rosuvastatin, pitavastatin, and pravastatin have the fewest CYP-related interactions
• Kidney and liver function
• Whether you’ve 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 status or plans to conceive (statins are generally avoided in pregnancy and breastfeeding)
• Baseline liver function — to exclude pre-existing liver disease that would be a contraindication (decompensated cirrhosis, acute liver failure), and to have a reference point if anything changes later
• Baseline kidney function — because some statins (e.g. rosuvastatin, simvastatin) need dose adjustment in significant renal impairment, and CKD itself influences your LDL target
• Your current medications for interactions
• Any history of unexplained muscle problems

What to expect on a statin

Most patients tolerate statins well, and the large body of trial and real-world evidence supports their safety over decades of use.

• Muscle aches (myalgia) — the most commonly reported concern. In placebo-controlled trials, most statin “muscle ache” is not actually caused by the statin (a nocebo effect where people who expect side effects report them even when they’re on placebo). If you do develop muscle aches after starting, please don’t stop on your own — let us know. Often a dose reduction, a switch to a different statin, or a brief trial off the medication to see if symptoms really do track with the statin will resolve the issue.
• Muscle damage (rhabdomyolysis) — severe and rare (roughly 1 in 10,000 patient-years), and is the main reason we avoid certain drug combinations. Signs: severe muscle pain or weakness, dark or cola-coloured urine. If this happens, please seek medical attention the same day.
• Blood sugar — statins slightly increase the risk of developing type 2 diabetes in predisposed people (about 1 additional case per 250 patients treated over 4 years in meta-analyses). The cardiovascular benefit in people at high risk far outweighs this.
• Pregnancy — statins are generally avoided in pregnancy. If you’re planning to conceive or might be pregnant, please tell us so we can adjust.
• Grapefruit juice — significantly raises the levels of atorvastatin, simvastatin, and lovastatin (but not pitavastatin, rosuvastatin, or pravastatin). Avoid grapefruit juice if you’re on one of the affected statins.

What we monitor — and why:

After starting or increasing a statin, we’ll usually check a lipid panel at 8 to 12 weeks to see whether you’re reaching your target. After that, routine lipid and kidney function checks are part of your 6-monthly chronic disease review.

The main purpose of monitoring is to make sure your treatment is still working for you — hitting target, adjusting dose, catching changes in your risk factors — rather than actively hunting for side effects. In practice, clinically significant new side effects after the first few months of stable treatment are uncommon, and routine liver function testing isn’t required in the absence of specific concerns.

When statins alone aren’t enough

For some patients — particularly those at very high risk — statins alone don’t hit target. The next steps are:

• Ezetimibe — an oral tablet taken once a day, added to your statin. Lowers LDL by a further 15 to 20%. Usually well tolerated. Evidence supports additional cardiovascular benefit when combined with a statin.
• PCSK9 inhibitors — a newer, more potent class. Includes evolocumab (Repatha) and alirocumab (Praluent) — both injected once every 2 or 4 weeks — and inclisiran (Leqvio), which is given only twice a year after the initial doses. LDL reduction of 45–60% when added to statin + ezetimibe. These are typically prescribed through a specialist (cardiologist or endocrinologist/lipid clinic), mainly for patients with established cardiovascular disease or familial hypercholesterolaemia who are on maximal statin + ezetimibe and still not at target, or for patients who genuinely cannot tolerate statins. If you’re in a high-risk category and your LDL isn’t where it should be despite best efforts, please raise it at your visit — we’ll arrange the appropriate referral.

A note on familial hypercholesterolaemia (FH)

Some people have an inherited condition called familial hypercholesterolaemia (FH) that causes very high LDL from birth. FH raises the risk of early heart disease by about 20-fold if untreated, and often runs in families with premature heart attacks (before age 55 in men, 60 in women). It’s more common than most people realise — roughly 1 in 250 to 1 in 500 in the general population.

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 at a young age
• You or family members have cholesterol deposits visible in the tendons (tendon xanthomas), around the eyes (xanthelasmas), or in the cornea (corneal arcus before age 45)

Singapore has a National Familial Hypercholesterolaemia Genetic Testing Programme launched 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. The programme includes genetic testing, genetic counselling, and subsidised cascade screening for first-degree relatives — because picking up the condition in children and siblings early allows preventive treatment from a young age. Subsidies are up to 70% (means-tested) for eligible Singapore 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 a referral meaningfully changes outcomes.

Triglycerides — a short note

Most patients focus on LDL, but triglycerides deserve their own attention.

In practice, 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, and sometimes poorly-controlled diabetes). Treatment is primarily lifestyle, alongside addressing any secondary cause.
• Moderately raised (4.5–10 mmol/L) — lifestyle is essential, but a statin is usually added at this stage. Statins lower both LDL and triglycerides, and in most patients this addresses both the cardiovascular risk and a meaningful part of the triglyceride elevation at the same time.
• Very high (>10 mmol/L) — the main concern shifts to the risk of acute pancreatitis, and treatment becomes more urgent. A fibrate (usually fenofibrate) is often added to lower triglycerides more aggressively, alongside the statin for cardiovascular risk. Any reversible cause (uncontrolled diabetes, heavy alcohol intake, certain medications) is corrected urgently. Prescription-grade omega-3 fatty acids (icosapent ethyl) may also be considered in specific situations.

A few practical points worth making

A few things that come up often at consultations:

• Feeling fine is the point. High cholesterol has no symptoms. If you’ve been on a statin for years and feel well, that’s the medication doing its job silently — not a reason to stop it.
• If the regimen isn’t working for you, tell us rather than quietly skipping doses. Missed doses erode the cardiovascular benefit, and we can almost always adjust the plan to something that fits your life better.
• On supplements — if you’re taking, or considering, any supplement marketed for cholesterol (“natural” cures, garlic capsules, plant sterols, red yeast rice, berberine, herbal mixes), please bring it up at your visit. The evidence for most of these is inconsistent at best, and some interact with statins or cause muscle problems on their own (red yeast rice, in particular, contains low-dose monacolin K — essentially unregulated lovastatin). We’d rather discuss them openly and build a plan that hits your target than have you stop a prescribed medication in favour of something untested.
• Targets may have moved since you started treatment. If your LDL target was set years ago, it’s worth a fresh conversation — especially if anything in your risk profile has changed.

Why regular follow-up matters

Cholesterol is not a “set and forget” condition. A few reasons we ask you to come back regularly — even when everything is going well:

• Guidelines evolve. The targets your previous doctor set may no longer match the current evidence base. What was “well-controlled” in 2015 may be “needs intensification” in 2026.
• Your cardiovascular risk changes over time. A new diagnosis of diabetes, a new hypertension reading, a family member newly diagnosed with heart disease, menopause, or just ageing — any of these can shift your risk category, and your target along with it.
• Medication tolerance and adherence drift. Many patients stop or reduce their statin at some point, sometimes without realising it matters. A routine review catches this.
• Side effects need monitoring. Liver function, kidney function, muscle symptoms, blood sugar, and interactions with any newly-prescribed medication all need a periodic look.
• New treatment options appear. The approval of newer agents (inclisiran, for example) and changes to what’s subsidised locally can open up options that weren’t there at your last review.
• Lifestyle support works better with accountability. Weight, activity, diet, and smoking all respond better to a regular conversation than an annual pep talk.

We suggest a lipid review every 6 months as part of your chronic disease follow-up — more often if you’ve just started or changed medication, or if your cardiovascular risk has changed meaningfully. It doesn’t have to be a long appointment. 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 medications (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 medications. Pioneer Generation, Merdeka Generation, and CHAS Blue / Orange / Green tiers all apply where eligible. Details at chas.sg.
• MediSave — usable for chronic disease consultations and selected medications, up to annual withdrawal limits (currently $500, 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

Joo Chiat — 172 Joo Chiat Road, #01-01, Singapore 427443 · Tel 6920 1952

Punggol — 658 Punggol East, #01-04, Singapore 820658 · Tel 6312 4589

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.

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. v1.0 · April 2026 · Review due April 2028.