What is the difference between LDL and HDL cholesterol?

LDL-C (low-density lipoprotein cholesterol) is the main driver of atherosclerosis — it deposits in arterial walls and narrows them over decades. HDL-C carries cholesterol away from arteries, so higher levels are generally protective. Triglycerides are another blood fat that rises with excess alcohol, refined carbohydrates, weight gain, and insulin resistance. Total cholesterol alone is a poor predictor of risk; Australian guidelines use the full lipid panel — LDL-C, non-HDL-C, HDL-C, and triglycerides — interpreted within the context of your absolute five-year cardiovascular risk.

Do I need medication if my cholesterol is only slightly elevated?

Not automatically. Whether treatment is recommended depends on your absolute cardiovascular risk over five years — a calculation that factors in age, blood pressure, smoking, family history, diabetes, and kidney function alongside the cholesterol number. The 2023 Heart Foundation guideline recommends lipid-lowering medication for high risk (≥10% five-year risk), established cardiovascular disease, familial hypercholesterolaemia, and certain high-risk conditions. For lower-risk people with mildly elevated cholesterol, lifestyle measures — Mediterranean-style diet, physical activity, weight management, and stopping smoking — are the priority.

Are statins safe for long-term use?

For most people, yes. Statins are among the most studied medications in history, with consistent trial data showing cardiovascular benefit. The most common concern is muscle aches; however, the SAMSON trial found about 90% of muscle symptoms attributed to statins are a nocebo effect — participants reported the same rate of symptoms on blinded placebo. True statin myopathy is uncommon and rhabdomyolysis is rare. Statins modestly increase new-onset type 2 diabetes risk, but this is substantially outweighed by cardiovascular benefit in high-risk individuals. A baseline blood test before starting is standard; further monitoring only if symptoms develop.

What lifestyle changes actually lower cholesterol?

Several lifestyle measures have solid evidence. A Mediterranean-style or DASH diet — high in olive oil, nuts, fish, vegetables, legumes, and wholegrains — independently reduces cardiovascular risk and lowers LDL-C by 10–15%. Soluble fibre from oats, psyllium, and legumes (5–10 g daily) cuts LDL-C a further 3–7%. Plant sterols or stanols at 2 g daily in fortified foods add a further 7–10% reduction. Regular physical activity at least 150 minutes per week improves the full lipid panel. Weight reduction, smoking cessation, and limiting alcohol further improve triglycerides and HDL-C.

What is familial hypercholesterolaemia and why does it matter?

Familial hypercholesterolaemia (FH) is an inherited genetic condition affecting about 1 in 250 Australians, causing markedly elevated LDL-C from birth and accelerated atherosclerosis. Without treatment, men commonly experience heart attacks in their 40s and women in their 50s. FH is suspected when untreated LDL-C is ≥5.0 mmol/L, when there is a family history of premature cardiovascular disease, or when physical signs such as tendon xanthomas or corneal arcus before age 45 are present. About 90% of affected Australians remain undiagnosed. Identifying one case triggers cascade testing of all first-degree relatives.

Dyslipidaemia

Dyslipidaemia and cardiovascular risk: the AU general practice approach

By Dr HB Lo, FACRRM Reviewed 22 May 2026 10 min read

About 63% of Australian adults have abnormal blood lipids, with only 38% achieving LDL-C targets. The 2023 Heart Foundation guideline shifts focus to absolute cardiovascular risk — the overall probability of heart attack or stroke within five years.

Statins are the cornerstone of lipid-lowering therapy. Every 1 mmol/L LDL-C reduction over five years reduces major vascular events by approximately 22%. Ezetimibe, PCSK9 inhibitors, and inclisiran provide further reduction when a statin alone is insufficient.

Lifestyle underpins all treatment: Mediterranean-style diet, physical activity, smoking cessation, and weight management each reduce cardiovascular risk and amplify medication benefit.

Cholesterol is one of the most common reasons Australians visit their GP, and dyslipidaemia — abnormal blood lipid levels — is among the most modifiable contributors to cardiovascular disease. According to AIHW data on high cholesterol in Australia, about 63% of Australian adults have abnormal blood lipids, yet only around 38% are achieving their LDL-C goals. The treatment gap is real and consequential: cardiovascular disease remains the leading cause of death in Australia.

The modern approach, codified in the 2023 Heart Foundation Australian guideline for assessing and managing cardiovascular disease risk, treats cholesterol not as a standalone number but as one component of absolute cardiovascular risk — the probability of a heart attack or stroke over the next five years. This risk-based framework changes who gets treated, how intensively, and with what.

Lipid abnormalities range from mildly elevated LDL-cholesterol in an otherwise healthy person through to familial hypercholesterolaemia, severe hypertriglyceridaemia, and secondary dyslipidaemia from treatable underlying conditions. Each requires a distinct clinical approach.

A. Core clinical — the AU general-practice framework

Who to screen and when

The RACGP Red Book (10th edition) and Heart Foundation 2023 guideline recommend absolute cardiovascular risk assessment in:

All adults aged ≥45 years
Aboriginal and Torres Strait Islander adults aged ≥30 years
Adults with diabetes aged ≥35 years
Anyone with suspected familial hypercholesterolaemia at any age

A non-fasting lipid panel — total cholesterol, HDL-C, LDL-C, and triglycerides — is sufficient for most assessments. Fasting is only required when triglycerides are unexpectedly elevated above 4.5 mmol/L.

History

A thorough history underpins every dyslipidaemia consultation:

Personal cardiovascular history — prior myocardial infarction, angina, stroke, TIA, revascularisation, peripheral arterial disease, abdominal aortic aneurysm
Family history — premature cardiovascular disease in first-degree relatives (men under 55, women under 60); sudden cardiac death; known familial hypercholesterolaemia; tendon xanthomas in relatives
Lifestyle — diet (saturated fat intake, refined carbohydrates, alcohol), physical activity levels, smoking status, sleep
Drug history — corticosteroids, atypical antipsychotics (olanzapine, clozapine), antiretrovirals, oestrogen-containing preparations, ciclosporin, anabolic steroids
Comorbidities — type 2 diabetes, hypertension, chronic kidney disease, hypothyroidism, non-alcoholic fatty liver disease, polycystic ovary syndrome, autoimmune disease (rheumatoid arthritis, systemic lupus erythematosus, psoriasis — all independently elevate cardiovascular risk)

Examination

BMI and waist circumference — central adiposity threshold ≥94 cm in men, ≥80 cm in women (Caucasian reference; lower for South Asian and East Asian individuals)
Blood pressure — both arms at first presentation
FH stigmata — tendon xanthomas at Achilles tendons or finger extensors; tuberous xanthomas over extensor surfaces; xanthelasma; corneal arcus before age 45
Cardiovascular exam — peripheral pulses, carotid and femoral bruits, aortic palpation for aneurysm

Investigations

Per eTG cardiovascular guidelines and AMH:

Baseline workup:

Non-fasting lipid panel (total cholesterol, HDL-C, LDL-C, non-HDL-C, triglycerides)
HbA1c or fasting glucose
eGFR and urine albumin-to-creatinine ratio (UACR)
Liver function tests — ALT baseline before starting a statin
TSH — to exclude hypothyroidism as a secondary cause
Lipoprotein(a) — measure once in adult life, especially with premature cardiovascular family history

Absolute CVD risk calculation: The Australian CVD Risk Calculator is the AU tool for adults in the primary-prevention setting (no prior cardiovascular event, no diabetes-related kidney disease, no eGFR <45, no severe dyslipidaemia, no FH). Established cardiovascular disease, familial hypercholesterolaemia, diabetes with organ damage, and severe CKD are automatic high-risk categories — the calculator is not needed.

Reclassification: in intermediate-risk patients (5–<10% five-year risk), a coronary artery calcium (CAC) score can reclassify risk upward or downward. This test is not MBS-rebatable (out-of-pocket approximately $170–220) but provides clinically useful information to guide shared decision-making.

B. Evidence for treating to risk — the science of LDL reduction

The causality of LDL-C in cardiovascular disease is among the most robustly established in medicine. The Cholesterol Treatment Trialists (CTT) Collaboration (Lancet 2010) meta-analysed 26 randomised statin trials involving over 170,000 participants. The key finding: every 1 mmol/L reduction in LDL-C over five years produces approximately a 22% relative reduction in major vascular events — non-fatal myocardial infarction, coronary death, stroke, and coronary revascularisation. The benefit is proportional to the magnitude and duration of LDL lowering, supporting the principle of “lower for longer.”

Lifestyle evidence

The PREDIMED trial demonstrated that a Mediterranean diet supplemented with extra-virgin olive oil or nuts reduced major cardiovascular events by approximately 30% relative risk in high-risk participants over a median follow-up of nearly five years. This dietary pattern is recommended by the NHMRC Australian Dietary Guidelines and represents the highest-evidenced dietary intervention for cardiovascular risk.

Additional lifestyle components with meaningful lipid effects:

Saturated fat reduction — replacing saturated with polyunsaturated fat reduces LDL-C and cardiovascular risk
Soluble fibre (5–10 g daily from oats, psyllium, legumes) — LDL-C reduction of 3–7%
Plant sterols and stanols (2 g daily via fortified foods) — LDL-C reduction of 7–10%
Physical activity — ≥150 minutes moderate-intensity exercise per week improves the full lipid panel and independently reduces cardiovascular risk
Weight reduction — each 4.5 kg lost reduces LDL-C by approximately 3–8%

Statin pharmacotherapy

Statins are the most important lipid-lowering pharmacotherapy. NPS MedicineWise and eTG both recommend:

High-intensity statin (atorvastatin 40–80 mg, rosuvastatin 20–40 mg) — ≥50% LDL-C reduction — for established atherosclerotic cardiovascular disease (ASCVD), familial hypercholesterolaemia, and very high absolute risk
Moderate-intensity statin (atorvastatin 10–20 mg, rosuvastatin 5–10 mg, simvastatin 20–40 mg, pravastatin 40 mg) — 30–49% LDL-C reduction — for high absolute-risk primary prevention

Drug interactions: rosuvastatin and pravastatin have minimal CYP2C9/3A4 interaction; atorvastatin and simvastatin are CYP3A4 substrates (caution with macrolides, azole antifungals, diltiazem, amiodarone, ciclosporin, and grapefruit).

The statin intolerance challenge

The SAMSON trial (NEJM 2020) administered matched statin and placebo tablets in a blinded crossover design to patients who had previously stopped statins due to muscle symptoms. Approximately 90% of muscle symptoms attributed to statin were also reported on blinded placebo — a nocebo effect. The clinical implication is that most apparent statin intolerance can be overcome with structured rechallenge: offer a different statin at the lowest available dose with explicit reassurance about the nocebo finding. CK measurement is indicated only when muscle symptoms are present, not routinely.

Add-on therapy evidence

Ezetimibe 10 mg daily provides approximately 15–20% additional LDL-C reduction on top of statin and is the standard second-line agent. The IMPROVE-IT trial confirmed that further LDL-C reduction below what statin achieves provides additional cardiovascular benefit.

PCSK9 inhibitors (evolocumab, alirocumab) reduce LDL-C by 50–60% on top of maximally tolerated statin plus ezetimibe. FOURIER (evolocumab) and ODYSSEY OUTCOMES (alirocumab) both demonstrated approximately 15% relative reduction in major cardiovascular events in established high-risk ASCVD populations.

Inclisiran — a small interfering RNA targeting PCSK9 mRNA — is PBS-listed since 2023. Administered subcutaneously twice yearly after initial doses, it achieves similar LDL-C reductions to PCSK9 monoclonal antibodies with a different mechanism and dosing schedule.

C. Familial hypercholesterolaemia, hypertriglyceridaemia, and monitoring

Familial hypercholesterolaemia

The FH Australasia Network estimates that FH affects approximately 1 in 250 Australians — around 100,000 people — of whom an estimated 90% are currently undiagnosed. The condition results from mutations in the LDL receptor, apolipoprotein B, or PCSK9 genes, causing lifetime accumulation of LDL-C from birth and markedly accelerated atherosclerosis.

Suspect FH when:

Untreated LDL-C is ≥5.0 mmol/L (high probability at ≥6.5 mmol/L)
Personal or first-degree family history of premature cardiovascular disease (men before 55, women before 60)
Dutch Lipid Clinic Network score is ≥6 (combining LDL-C level, clinical features, family history, and genetic testing)
Physical signs: Achilles or extensor tendon xanthomas, corneal arcus before age 45

Management: Start a high-intensity statin as soon as FH is confirmed — typically in early adulthood, or childhood in homozygous FH. LDL-C targets are lower than for primary prevention (LDL-C <2.5 mmol/L for heterozygous FH without ASCVD; <1.8 mmol/L if established ASCVD). Ezetimibe and PCSK9 inhibitors or inclisiran are frequently required. Identify and test all first-degree relatives through the FH Australasia Network cascade testing pathway.

Hypertriglyceridaemia

Mild to moderate (2.0–9.9 mmol/L): Address lifestyle causes first — alcohol reduction, weight loss, reduced refined carbohydrate intake. Statin therapy incidentally reduces triglycerides by 10–25%. Fenofibrate 145 mg daily can be added when lifestyle and statin alone are insufficient. Avoid combining gemfibrozil with statin (rhabdomyolysis risk).
Severe (≥10 mmol/L): Acute pancreatitis risk — urgent specialist referral, consider fenofibrate plus omega-3, insulin if hyperglycaemia is contributing, and cease oestrogens and alcohol

Per eTG, icosapent ethyl (a purified EPA omega-3) at 2 × 2 g daily has demonstrated cardiovascular outcome benefit in high-risk patients with elevated triglycerides on statin (REDUCE-IT), though it is not currently PBS-listed in Australia.

Monitoring lipid-lowering therapy

Per eTG and AMH:

After initiating or changing statin dose — recheck lipids, LFTs, and eGFR at 4–12 weeks; aim for ≥50% LDL-C reduction or LDL-C <1.8 mmol/L in established ASCVD
Stable on therapy — annual lipid panel, annual eGFR; LFTs only if symptomatic
CK — only if muscle symptoms present; not a routine monitoring test
Re-stratify absolute risk — every 5 years for low risk, every 2 years for intermediate, annually for high risk

D. Australian operations

MBS-rebatable pathways

The Heart Health Check (MBS item 699, telehealth item 177) provides a rebatable framework for absolute CVD risk assessment in eligible adults aged 45–79 (Aboriginal and Torres Strait Islander adults from age 18). It includes the lipid panel, blood pressure measurement, lifestyle assessment, absolute risk calculation, and management planning. Available once per 12 months.

The GP Chronic Condition Management Plan (GPCCMP) (items 965 and 967) supports ongoing management when dyslipidaemia is part of a chronic-disease framework. This replaced the legacy GPMP/TCA items (721/723/732) from 1 July 2025. Established cardiovascular disease, type 2 diabetes, familial hypercholesterolaemia, and CKD are natural GPCCMP candidates. Allied health referrals — dietitian, exercise physiologist — are accessible via GPCCMP, up to 5 visits per year (10 for Aboriginal and Torres Strait Islander patients).

Pathology MBS items: lipid studies (66536), HbA1c (66551), eGFR/creatinine (66500), UACR (66659), LFTs (66512), TSH (66716), Lp(a) (66523).

PBS

On the PBS:

Statins (atorvastatin, rosuvastatin, simvastatin, pravastatin, fluvastatin) — General Schedule, no Authority required
Ezetimibe monotherapy and fixed-dose combinations — Authority Required (Streamlined): LDL-C inadequately controlled on maximum tolerated statin, or statin contraindicated or not tolerated
Evolocumab and alirocumab (PCSK9 inhibitors) — Authority Required: specialist initial application; GP repeats via streamlined; criteria are symptomatic ASCVD or FH with LDL-C above threshold on maximum tolerated statin plus ezetimibe
Inclisiran — Authority Required with similar criteria to PCSK9 inhibitors; listed since 2023
Fenofibrate — General Schedule

Telehealth

The existing-relationship 12-month rule applies to Heart Health Check telehealth (item 177) and GPCCMP telehealth equivalents.

E. Special populations

Older adults (≥75 years). Continue statins in people with established cardiovascular disease — the evidence for secondary prevention is clear and consistent. Primary-prevention initiation in adults aged ≥75 requires individual shared decision-making: meta-analyses suggest the relative risk reduction is preserved, but frailty, polypharmacy, drug interactions, and falls risk must be considered. Lower starting doses are appropriate in frail older adults.

Pregnancy. Statins are traditionally avoided in pregnancy because of theoretical teratogenicity. Emerging TGA and international guidance permits continuation in selected very high-risk women — particularly those with homozygous FH or prior ASCVD — with specialist input and detailed informed consent. Most women with heterozygous FH can pause statin safely during pregnancy and breastfeeding.

Aboriginal and Torres Strait Islander Australians. Cardiovascular disease presents at younger ages. The Australian CVD Risk Calculator begins risk assessment at age 30 for First Nations people. The ATSI Health Assessment (MBS item 715) should include lipid assessment and cardiovascular risk calculation at every eligible visit. Equity in lipid management access is a documented gap.

Type 2 diabetes and CKD. Both conditions are automatic high-risk categories — no risk calculator needed. High-intensity statin is appropriate even without established ASCVD when eGFR is <45 or UACR is elevated. Statin dose adjustment may be needed in severe renal impairment; per eTG, rosuvastatin dose is capped at 10 mg in eGFR <30.

When to escalate

Refer to a lipid clinic, cardiologist, or endocrinologist for:

Suspected familial hypercholesterolaemia — for specialist management and cascade testing of relatives
LDL-C remaining above target on maximum tolerated statin plus ezetimibe — to assess eligibility for PCSK9 inhibitor or inclisiran
Statin intolerance persisting after structured rechallenge with at least two different statins at the lowest available doses
Severe hypertriglyceridaemia ≥10 mmol/L — pancreatitis risk; urgent specialist referral
Very elevated Lp(a) (≥1.0 g/L) with strong family history of premature cardiovascular disease
Suspected homozygous FH (LDL-C ≥13 mmol/L untreated, childhood xanthomas) — urgent; may require LDL apheresis

Send with the referral: untreated and on-treatment lipid profiles, all statins tried with doses and adverse effects reported, three-generation family pedigree, any genetic testing results, CAC score if performed, all current medications.

What this article is and is not

This is general health information drawn from current Australian general practice evidence — the 2023 Heart Foundation CVD risk guideline, Therapeutic Guidelines, AMH, NPS MedicineWise, and FH Australasia Network resources. It does not constitute personal medical advice and does not create a doctor–patient relationship. Decisions about which lipid-lowering medication to use, at what dose, and for how long, are made between you and your own GP and treating specialists who have access to your complete clinical picture.

For reliable consumer information: HealthDirect — High cholesterol, Heart Foundation — Cholesterol, Better Health Channel — Cholesterol.

Sources cited

Frequently asked questions

What is the difference between LDL and HDL cholesterol?

LDL-C (low-density lipoprotein cholesterol) is the main driver of atherosclerosis — it deposits in arterial walls and narrows them over decades. HDL-C carries cholesterol away from arteries, so higher levels are generally protective. Triglycerides are another blood fat that rises with excess alcohol, refined carbohydrates, weight gain, and insulin resistance. Total cholesterol alone is a poor predictor of risk; Australian guidelines use the full lipid panel — LDL-C, non-HDL-C, HDL-C, and triglycerides — interpreted within the context of your absolute five-year cardiovascular risk.
Do I need medication if my cholesterol is only slightly elevated?

Not automatically. Whether treatment is recommended depends on your absolute cardiovascular risk over five years — a calculation that factors in age, blood pressure, smoking, family history, diabetes, and kidney function alongside the cholesterol number. The 2023 Heart Foundation guideline recommends lipid-lowering medication for high risk (≥10% five-year risk), established cardiovascular disease, familial hypercholesterolaemia, and certain high-risk conditions. For lower-risk people with mildly elevated cholesterol, lifestyle measures — Mediterranean-style diet, physical activity, weight management, and stopping smoking — are the priority.
Are statins safe for long-term use?

For most people, yes. Statins are among the most studied medications in history, with consistent trial data showing cardiovascular benefit. The most common concern is muscle aches; however, the SAMSON trial found about 90% of muscle symptoms attributed to statins are a nocebo effect — participants reported the same rate of symptoms on blinded placebo. True statin myopathy is uncommon and rhabdomyolysis is rare. Statins modestly increase new-onset type 2 diabetes risk, but this is substantially outweighed by cardiovascular benefit in high-risk individuals. A baseline blood test before starting is standard; further monitoring only if symptoms develop.
What lifestyle changes actually lower cholesterol?

Several lifestyle measures have solid evidence. A Mediterranean-style or DASH diet — high in olive oil, nuts, fish, vegetables, legumes, and wholegrains — independently reduces cardiovascular risk and lowers LDL-C by 10–15%. Soluble fibre from oats, psyllium, and legumes (5–10 g daily) cuts LDL-C a further 3–7%. Plant sterols or stanols at 2 g daily in fortified foods add a further 7–10% reduction. Regular physical activity at least 150 minutes per week improves the full lipid panel. Weight reduction, smoking cessation, and limiting alcohol further improve triglycerides and HDL-C.
What is familial hypercholesterolaemia and why does it matter?

Familial hypercholesterolaemia (FH) is an inherited genetic condition affecting about 1 in 250 Australians, causing markedly elevated LDL-C from birth and accelerated atherosclerosis. Without treatment, men commonly experience heart attacks in their 40s and women in their 50s. FH is suspected when untreated LDL-C is ≥5.0 mmol/L, when there is a family history of premature cardiovascular disease, or when physical signs such as tendon xanthomas or corneal arcus before age 45 are present. About 90% of affected Australians remain undiagnosed. Identifying one case triggers cascade testing of all first-degree relatives.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.