Cholesterol Ratios Explained
Why total cholesterol is a poor risk marker on its own — and the four ratios (plus ApoB) that actually matter.
The Quick Answer
Total cholesterol on its own is a poor predictor of cardiovascular risk. The same TC of 6.0 mmol/L can mean very different risk depending on the underlying balance of atherogenic particles (LDL, VLDL, lipoprotein(a)) versus protective HDL.
The four ratios that matter capture this balance: TC/HDL (overall), LDL/HDL (atherogenic focus), Triglyceride/HDL (insulin resistance marker), and Non-HDL (every atherogenic particle in one number). Adding ApoB as a particle count and Lp(a) as a genetic check gives a complete cardiovascular risk picture — far better than total cholesterol alone.
How Lipoproteins Cause — And Prevent — Heart Disease
Cholesterol does not travel in blood as cholesterol. It moves around in protein-coated spheres called lipoproteins. The two families that matter most are the atherogenic particles (LDL, VLDL, IDL, lipoprotein(a)) which carry cholesterol into artery walls, and the protective particles (HDL) which carry it back out.
Every atherogenic particle carries one molecule of ApoB on its surface. So ApoBcounts the number of atherogenic particles directly. Each particle that lodges in an artery wall and gets oxidised becomes the seed of a plaque. The more particles in circulation, the more plaque builds — regardless of how much cholesterol each particle is carrying.
HDL is the cleanup vehicle. It removes cholesterol from arterial macrophages and brings it back to the liver for disposal. Higher HDL is generally protective — though beyond 2.0 mmol/L the benefit plateaus, and very high HDL (above 2.5 in women, above 2.0 in men) in some genetic forms is not protective.
Small dense LDL is the worst sub-type — small particles slip more easily into artery walls, oxidise faster, and are missed when you measure LDL cholesterol mass alone. People with insulin resistance, high triglycerides and low HDL have a preponderance of small dense LDL. This is why ApoB and the TG/HDL ratio matter more than LDL alone in that group.
The Four Ratios — Plus ApoB
Each ratio captures a different aspect of cardiovascular risk. None of them on its own is perfect, but together they tell a story that total cholesterol simply cannot.
TC / HDL ratio
The single most useful cholesterol ratio. Combines the burden of all artery-damaging particles (TC) with the protective HDL. A ratio above 5 doubles cardiovascular risk compared to below 3.5. Improving HDL by exercise, fish and quitting smoking lowers this even when TC barely changes.
LDL / HDL ratio
A more focused atherogenic ratio. LDL is the main carrier of artery-damaging cholesterol, HDL the cleanup vehicle. Ratio above 3.5 is high risk; above 5 is very high. Drops fast with statin or ezetimibe treatment.
Triglyceride / HDL ratio
The most sensitive single marker of insulin resistance and metabolic syndrome. Above 2.0 predicts small dense LDL, fatty liver and rising HbA1c. Drops quickly with weight loss, low-GI diet and reduced alcohol. Often the most modifiable of all the ratios.
Non-HDL cholesterol
The American Heart Association and updated Australian guidelines now prefer non-HDL over LDL alone. Captures every atherogenic particle, including the lipoproteins missed by a standard LDL calculation. Particularly accurate when triglycerides are high (above 4.5 mmol/L).
ApoB / ApoA1 ratio
The most direct measure of atherogenic particle number versus protective particle number. ApoB above 1.2 g/L is very high cardiovascular risk regardless of other markers. Useful when LDL underestimates risk in diabetes, fatty liver, or familial high lipoprotein(a).
Australian Targets By Risk Group
The Heart Foundation 2024 guidelines use the AusCVDRisk calculator to estimate 5-year event risk and set targets accordingly. Higher risk leads to lower targets and more aggressive treatment.
Low cardiovascular risk (under 10% 5-yr)
Healthy adult with no risk factors or strong family history. Lifestyle focus, no medication. Recheck every 3-5 years.
Moderate risk (10-15% 5-yr)
Multiple risk factors but no event yet. Lifestyle change plus consider statin if LDL above target. Recheck every 12 months.
High risk (above 15% 5-yr or diabetes)
Diabetes, chronic kidney disease, established cardiovascular disease (CHD, stroke, PAD), or AusCVDRisk above 15%. Statin almost always indicated. Recheck 3-6 months after starting treatment.
Very high risk (recent event or FH)
Recent heart attack, stroke, or familial hypercholesterolaemia. High-intensity statin plus ezetimibe, with PCSK9 inhibitor if targets not met. Specialist or cardiac rehab guidance.
What Drives An Atherogenic Lipid Pattern
Cholesterol problems are mostly a mix of genetics, diet, body composition, and a few common medical and medication causes. Sorting out which factor is contributing matters for treatment choice.
Familial hypercholesterolaemia (FH)
Genetic LDL receptor defect affecting about 1 in 250 Australians. Most cases undiagnosed. Causes early heart attacks. Suspect when LDL is above 5.0, especially with family history of early CHD. Treat aggressively from young adulthood — often needs statin plus ezetimibe plus PCSK9 inhibitor.
High saturated and trans fat intake
Cream, butter, fatty red meat, processed and fried foods raise LDL by direct effect on liver lipid synthesis. The Mediterranean diet, with olive oil and fish replacing saturated fats, reliably lowers LDL by 10-20 percent.
Low fibre intake
Soluble fibre from oats, barley, legumes, apples and psyllium binds bile acids in the gut, forcing the liver to use cholesterol to make replacements. Each additional 10 g of fibre daily lowers LDL by roughly 5 percent.
Visceral obesity
Fat around the liver and intestines causes the classic metabolic syndrome lipid pattern: triglycerides up, HDL down, and small dense LDL up. Drops fast with even modest weight loss (5-7 percent).
Insulin resistance and type 2 diabetes
Insulin resistance produces excessive VLDL from the liver and impairs HDL maturation. LDL particle number (ApoB) is elevated even when LDL cholesterol looks normal. ApoB is the better risk marker in this group.
Hypothyroidism
Hypothyroidism slows LDL receptor expression in the liver and reduces clearance. Always check TSH in any new unexplained cholesterol elevation — treating thyroid often normalises lipids within 3 months.
Nephrotic syndrome
Kidney disease with heavy protein loss in urine causes the liver to overproduce LDL. Treat the kidney disease and the cholesterol usually follows. Persistent dyslipidaemia after remission needs statin therapy.
Alcohol effect on triglycerides
Even moderate daily alcohol raises triglycerides. Heavy alcohol can lift triglycerides above 5 mmol/L and risk pancreatitis. Cutting back is the fastest way to reduce a high triglyceride result.
Cholestasis (bile flow blockage)
Gallstones, primary biliary cholangitis, or biliary obstruction back up bile acids and lipoprotein-X into the blood, causing very high cholesterol. Liver function tests (raised ALP and bilirubin) point to this cause.
Medications
Oral corticosteroids, beta-blockers (some), thiazide diuretics in high doses, atypical antipsychotics, oestrogens, and certain HIV antiretrovirals can all raise lipids. Review your medication list with your GP if cholesterol rises on treatment.
Signs To Look For — Mostly Silent
High cholesterol is normally completely asymptomatic. By the time it produces a symptom, significant damage has often already occurred. That is why routine screening from age 35-45 (earlier with family history) is essential.
Asymptomatic in most people
High cholesterol itself causes no symptoms — that is precisely why it is so dangerous. Damage builds silently inside artery walls for decades before a heart attack or stroke makes itself known.
Xanthomas on tendons
Fatty deposits on the Achilles tendon, knuckles, or elbows. Highly suggestive of familial hypercholesterolaemia and warrant urgent specialist review. Often felt as firm yellowish lumps.
Xanthelasma around the eyes
Yellow plaques on the upper or lower eyelids near the inner corner. Not always associated with high cholesterol, but worth checking lipids if they appear.
Corneal arcus
A grey or white ring around the coloured part of the eye (cornea). In someone under 45-50, it can suggest familial hypercholesterolaemia. Common and benign in older adults.
Chest pain on exertion (angina)
Tightness, heaviness, or pressure across the chest with exertion that resolves with rest. Suggests significant coronary artery narrowing. Needs same-week GP review and cardiology assessment.
Calf pain on walking (intermittent claudication)
Cramping calf pain after walking a set distance that improves with rest. Marker of peripheral artery disease and high overall cardiovascular risk. Needs vascular assessment.
Acute severe abdominal pain
Pancreatitis from triglycerides above 11 mmol/L. Sudden, severe upper abdominal pain radiating to the back, nausea and vomiting. Emergency presentation. Cut alcohol and high-fat foods immediately.
Pancreatic warnings on bloods
A fasting triglyceride above 5.6 mmol/L raises pancreatitis risk; above 11 is high risk. Often picked up on routine bloods before symptoms. Lifestyle plus medication can rapidly reduce the risk.
Red Flags — When To See Your GP Promptly
These patterns are not routine. Each one carries enough cardiovascular risk to justify same-month review and likely treatment:
TC/HDL ratio above 6
Doubles cardiovascular event risk compared to below 4. Combined with smoking or diabetes, treats as a near-event level urgency. Statin almost always indicated.
LDL above 5 mmol/L
Likely familial hypercholesterolaemia. Genetic LDL receptor defect that causes early heart attacks if untreated. Needs lipid clinic referral and cascade screening of close relatives.
ApoB above 1.2 g/L
Very high atherogenic particle number regardless of other markers. Particularly important to flag in diabetes, insulin resistance, fatty liver, or when LDL looks falsely reassuring.
Triglycerides above 5.6 mmol/L
Acute pancreatitis risk. Above 11 mmol/L the risk is high enough for hospital admission. Fenofibrate plus dietary fat reduction and alcohol cessation are urgent.
Lipoprotein(a) above 100 nmol/L
Inherited cardiovascular risk factor. Largely genetic, not modifiable by diet. Aggressive control of every other modifiable risk factor (LDL, BP, smoking) becomes more important.
Family history of early CHD plus high LDL
Father, mother or sibling with heart attack or stroke before age 55 (men) or 60 (women), plus elevated lipids, raises FH suspicion. Lipid clinic referral and a CAC score help quantify risk.
What Your GP Will Do Next — The Workup
A modern Australian lipid workup goes beyond a single fasting panel. The full picture requires repeat testing, secondary cause screening, AusCVDRisk scoring, and sometimes CAC scoring in equivocal cases.
Confirm with a fasting lipid panel
A 12-hour fasting blood test gives the most accurate triglyceride and calculated LDL. If triglycerides are above 4.5 mmol/L, calculated LDL is unreliable and a directly measured LDL or ApoB is preferred. Repeat the panel after 4-6 weeks to confirm before any treatment decision.
Add ApoB and lipoprotein(a)
ApoB measures the number of atherogenic particles directly and is increasingly preferred over LDL. Lipoprotein(a) is a once-in-a-lifetime test — it is largely genetic and identifies people at high inherited cardiovascular risk regardless of LDL. Recommended at first cholesterol assessment in adults with family history of early CHD.
Calculate the four key ratios
Calculate TC/HDL, LDL/HDL, TG/HDL and non-HDL from the panel. SmarterBlood does this automatically from your uploaded results, with Australian targets visible alongside each. The pattern across the four ratios tells you more than any single number.
AusCVDRisk score
The AusCVDRisk calculator combines age, sex, blood pressure, total and HDL cholesterol, smoking, diabetes, and Indigenous status to give a 5-year cardiovascular event risk percentage. Above 10 percent usually triggers statin discussion; above 15 percent indicates high risk.
Check secondary causes
TSH (thyroid), HbA1c (diabetes), urine ACR (kidney), liver function tests (fatty liver), and full blood count are standard at first dyslipidaemia assessment. Many secondary causes are reversible, and treating them is often more effective than statin alone.
Family history and genetic screening
If LDL is above 5.0 or non-HDL above 5.5, suspect familial hypercholesterolaemia. The Dutch Lipid Clinic Score combines LDL level, family history, and physical signs (xanthomas, corneal arcus). Genetic testing is available through specialist lipid clinics. Cascade screening of relatives is highly effective.
CAC score in equivocal cases
When risk is borderline or the patient and GP cannot agree on treatment, a coronary artery calcium (CAC) score offers a direct measure of subclinical atherosclerosis. A score of 0 in a 50-60 year old is strongly reassuring; above 100 is high risk and almost always justifies a statin.
Treatment — Lifestyle First, Then Medication
Mediterranean-style diet
Olive oil, oily fish twice weekly, nuts, legumes, plenty of vegetables and fruit, whole grains, less red meat and almost no ultra-processed food. The PREDIMED trial reduced cardiovascular events by 30 percent over 5 years. Lipid effect: LDL down 10-20 percent, triglycerides down 20-30 percent, HDL up slightly.
Aerobic plus resistance exercise
150 minutes per week of moderate aerobic exercise raises HDL by 5-10 percent and lowers triglycerides by 15-25 percent. Resistance training adds insulin sensitivity benefits and small additional HDL improvement.
Weight loss and smoking cessation
5-10 percent body weight loss in adults with central obesity lowers triglycerides, raises HDL, and reduces small dense LDL. Smoking cessation lifts HDL by 5-10 percent within 3 months and is the single largest reversible cardiovascular risk reduction.
Statin therapy
Indicated when AusCVDRisk is above 10 percent, LDL above 5 mmol/L (likely FH), established cardiovascular disease, diabetes with risk factors, or strong family history. Atorvastatin 20-80 mg or rosuvastatin 10-40 mg are the standard Australian choices. LDL drops 30-55 percent depending on dose and intensity. Annual liver and muscle monitoring is standard.
Ezetimibe and PCSK9 inhibitors
If statin alone does not reach target, ezetimibe 10 mg adds another 20 percent LDL reduction. PCSK9 inhibitors (evolocumab, alirocumab) add 50-60 percent further reduction and are PBS-funded in Australia for familial hypercholesterolaemia or established CHD when LDL stays above target despite optimal statin plus ezetimibe.
Foods That Improve Your Cholesterol Ratios
Olive oil (extra virgin)
Monounsaturated fat, polyphenolsCornerstone of the Mediterranean diet. Replacing butter and refined oils with extra virgin olive oil lowers LDL and inflammation. 30-60 mL daily as the main cooking and dressing fat.
Oily fish (salmon, mackerel, sardines)
Omega-3 fatty acidsTwo or three servings per week of oily fish lowers triglycerides by 20-30 percent, raises HDL slightly, and reduces inflammation. Australian Heart Foundation recommends this as a primary dietary intervention.
Oats and barley
Soluble fibre (beta-glucan)Beta-glucan binds bile acids in the gut. One serve of porridge or muesli daily lowers LDL by around 5-7 percent within 6 weeks. The cheapest cholesterol-lowering food available.
Legumes (lentils, chickpeas, beans)
Soluble fibre, plant proteinCup of lentils or chickpeas daily lowers LDL by 5-10 percent, and replacing some red meat with legumes adds another reduction. Cornerstone of the Portfolio diet.
Nuts (almonds, walnuts, pistachios)
Mono- and polyunsaturated fats, plant sterols30 g daily of mixed nuts lowers LDL by 5-7 percent. Walnuts are particularly good for omega-3 content. Almonds add plant sterols.
Plant sterol fortified spreads
Plant sterols (2 g/day)Margarines and yoghurts fortified with 2 g of plant sterols per day lower LDL by an additional 8-10 percent. Combined with low-saturated-fat diet, the effect adds to statin therapy.
Soy protein (tofu, tempeh, soy milk)
Plant protein, isoflavonesReplacing some animal protein with soy lowers LDL by 3-5 percent. 25 g of soy protein daily is the dose used in trials. Useful for vegetarians.
Dark berries and apples
Polyphenols, soluble fibreAnthocyanins and other flavonoids reduce LDL oxidation, a key step in plaque formation. Apple skin contains soluble fibre. Aim for two pieces of fruit per day.
Related Reading
See Your Four Cholesterol Ratios Automatically
SmarterBlood calculates TC/HDL, LDL/HDL, TG/HDL and Non-HDL automatically from your lipid panel, with Australian Heart Foundation targets shown alongside. Trends across multiple tests make subtle changes obvious.
This page provides general educational information about cholesterol ratios and cardiovascular risk. It is not a substitute for professional medical advice, diagnosis, or treatment. Always consult your GP about lipid results — they have access to your full medical history and can interpret your panel in context. SmarterBlood does not provide medical care.