My dad rang me last year to tell me his GP had put him on a statin. He said it like he was confessing to something. Like he'd failed.

"I eat well. I exercise. I don't smoke. And now I'm on cholesterol medication."

He's sixty-three. Fit for his age. Eats better than most people half his age. But his LDL has sat stubbornly above 4 mmol/L for years. His father had a heart attack at sixty-one. So his GP finally said the numbers and the risk profile together warranted medication.

What struck me wasn't the clinical decision. It was how he felt about it. Like getting a prescription meant the lifestyle stuff didn't count. Like all those morning walks and the salmon dinners and the years of not smoking were somehow invalidated by a number on a blood test.

They weren't. But I understood the feeling. Cholesterol is weird like that. It's one of the few biomarkers where you can do everything "right" and still end up with results that need attention. Genetics load the gun in a way that lifestyle alone can't always override.

I wanted to write this article because I think the public conversation around cholesterol is simultaneously too simple and too confusing. Too simple in the sense that most people know "high cholesterol = bad." Too confusing in the sense that almost nobody can explain what the different markers mean, which ones matter most, or how their GP actually uses the numbers to make decisions.

This is my attempt to close that gap. Not as a clinician (I'm not one), but as someone who's watched his dad navigate this and who wants to understand the numbers well enough to have an informed conversation about his own.

A note before we get into it

What cholesterol actually is, and why your body needs it

Here's something that doesn't get said often enough: cholesterol isn't inherently bad. Your body makes it on purpose.

Cholesterol is a waxy, fat-like substance produced primarily by your liver. It's a structural component of every cell membrane in your body. It's needed for producing hormones like testosterone, oestrogen, and cortisol. It's required for making bile acids to digest fat. It's also a building block for vitamin D synthesis.

Your body produces most of the cholesterol it needs regardless of what you eat. Dietary cholesterol (from eggs, meat, shellfish) does contribute, but for most people the liver adjusts its own production to compensate. The relationship between dietary cholesterol and blood cholesterol is less direct than people assume. That's why the old "eggs are bad for you" message has been substantially revised.

The problem isn't that cholesterol exists. The problem is when certain types, especially LDL, accumulate in the bloodstream at levels that promote plaque formation in artery walls. That process, atherosclerosis, is what drives heart disease and stroke.

So the clinical question isn't "do you have cholesterol?" Everyone does. It's "is the balance of different cholesterol types contributing to cardiovascular risk?"

The lipid panel: what each marker tells you

When you get a cholesterol test (properly called a lipid panel or lipid studies), you'll typically receive four or five numbers. Here's what each one means and how clinicians use them together.

Why the "good" and "bad" labels are oversimplified

I should flag this because I find it genuinely interesting, and it changes how you think about the numbers.

Calling LDL "bad" and HDL "good" is a shorthand that's useful for public health messaging but misleading at the clinical level. LDL isn't inherently destructive. Your body uses it to deliver cholesterol to cells that need it. It becomes problematic when levels are elevated and particles accumulate in artery walls, triggering an inflammatory response that leads to plaque formation.

Even within LDL, there's variation. Smaller, denser LDL particles appear to be more atherogenic (more likely to penetrate artery walls) than larger, more buoyant ones. Standard lipid panels don't differentiate between these subtypes. They just give you a total LDL number. Advanced lipid testing exists but isn't part of routine clinical practice in Australia.

HDL, meanwhile, isn't straightforwardly protective. It performs a useful function (reverse cholesterol transport), but simply having more HDL doesn't guarantee that function is working optimally. That's why interventions that raise HDL numbers (like certain drugs) haven't translated into reduced cardiovascular events.

Think of your lipid panel as a pattern, not a collection of independent numbers. LDL matters most for risk reduction. But the full picture, including triglycerides, HDL, and your metabolic context, tells a richer story.

Who should be testing, and how often

Cholesterol is one of those markers where you can feel perfectly fine while your numbers are quietly drifting into high-risk territory. Unlike iron deficiency or thyroid dysfunction, high cholesterol doesn't typically produce symptoms until something goes wrong.

That's exactly why testing matters.

The Australian guideline (AusCVDRisk) recommends cardiovascular risk assessment, including lipid testing, for:

All adults from age 45 (or 35 for Aboriginal and Torres Strait Islander peoples).

Younger adults with specific risk factors: family history of premature cardiovascular disease, familial hypercholesterolaemia, diabetes, chronic kidney disease, smoking, or established cardiovascular disease.

Here's where it stands in Australia:

An estimated 6.5 million Australian adults have high cholesterol, according to ABS data. Nearly half of Australians under 45 already have at least one lipid risk factor. Three in four Australians aged 45 and over are either taking cholesterol medication or have abnormal lipid results. High cholesterol is responsible for more than one-third of all years of healthy life lost to heart disease in Australia.

Despite this, almost half of Australians presenting to general practice with cardiovascular disease aren't achieving recommended cholesterol targets, even when prescribed lipid-lowering medication.

If you haven't had your cholesterol checked and you're over 35, this is probably overdue.

How to prepare for a cholesterol test

Understanding your results

Here's a general framework for interpreting your lipid panel. These are based on Heart Foundation and AusCVDRisk guidelines.

Marker	Desirable	Borderline	High Risk
Total Cholesterol	Below 5.5 mmol/L	5.5-6.5 mmol/L	Above 6.5 mmol/L
LDL Cholesterol	Below 2.0 mmol/L (high risk) / Below 3.5 mmol/L (low risk)	3.5-4.5 mmol/L	Above 4.5 mmol/L
HDL Cholesterol	Above 1.0 mmol/L (men) / Above 1.3 mmol/L (women)	—	Below these thresholds
Triglycerides	Below 1.7 mmol/L	1.7-2.0 mmol/L	Above 2.0 mmol/L
TC/HDL Ratio	Below 4.5	4.5-6.0	Above 6.0

These numbers are guidelines, not verdicts. Your clinician will interpret them alongside your full cardiovascular risk profile.

The absolute risk conversation your GP is having

This is the bit most people miss, and it's arguably the most important section in this article.

Your GP does not look at your cholesterol numbers in isolation. They calculate your absolute cardiovascular risk: the probability that you'll have a heart attack or stroke in the next five years. That calculation factors in age, sex, blood pressure, cholesterol levels, smoking status, diabetes, and sometimes additional markers.

Two people with identical LDL levels can get completely different clinical advice. A 35-year-old nonsmoker with an LDL of 3.8 and no other risk factors might be told to focus on diet and exercise. A 55-year-old with the same LDL plus diabetes, hypertension, and a family history might be started on medication immediately. Same number. Completely different risk profile.

The Australian absolute risk calculator (AusCVDRisk) is the tool GPs use to make these assessments. It replaced the older Framingham-based model and better reflects the Australian population.

The threshold for "high risk" is generally a 10% or greater five-year risk of a cardiovascular event. "Moderate risk" is 5-10%. Below 5% is considered low risk.

Why does this matter for you? A "high" cholesterol number on a lab report doesn't automatically mean you need medication. A "normal" number doesn't automatically mean you're safe. Context is everything — and that context is what your GP is trained to assess.

What actually moves the numbers

If your lipid results warrant attention, lifestyle interventions are the first-line approach. Here's what the evidence supports.

Diet, but not the way you think. The biggest dietary driver of LDL isn't dietary cholesterol (from eggs, prawns, etc.). It's saturated fat. Reducing saturated fat (fatty meats, full-fat dairy, processed foods, baked goods) and replacing it with unsaturated fats (olive oil, avocado, nuts, oily fish) has a meaningful effect on LDL. The Mediterranean dietary pattern has the strongest evidence base for cardiovascular risk reduction overall.

Physical activity. Regular exercise, both aerobic and resistance, improves HDL, lowers triglycerides, and contributes to better metabolic health. The effect on LDL is more modest but still clinically relevant. The Heart Foundation recommends at least 150 minutes of moderate-intensity activity per week.

Weight management. Excess weight, especially around the abdomen, is strongly associated with higher triglycerides, lower HDL, and insulin resistance. Even modest weight loss (5-10% of body weight) can produce meaningful improvements in the lipid profile.

Alcohol. Alcohol raises triglycerides. If your triglycerides are elevated, reducing or eliminating alcohol is one of the fastest ways to bring them down.

Smoking cessation. Smoking lowers HDL and damages blood vessel walls, accelerating atherosclerosis. Quitting improves HDL and reduces overall cardiovascular risk substantially.

Fibre. Soluble fibre (oats, legumes, psyllium, barley) has a modest but consistent LDL-lowering effect. It's not dramatic, but it's additive and works alongside other dietary changes.

One thing I've noticed (anecdotal, not clinical) is that people often focus on adding "cholesterol-lowering foods" while continuing to eat a diet high in saturated fat. The addition doesn't offset the foundation. The foundation is the intervention.

When medication enters the conversation

Statins are the first-line pharmacological treatment for elevated LDL, and they're among the most well-studied medications in existence. They work by reducing the liver's production of cholesterol, which in turn upregulates LDL receptors and pulls more LDL out of the blood.

In Australia, more than a quarter of adults over 50 are prescribed lipid-lowering medication. That's a lot of people.

Whether medication is right for you depends on your absolute cardiovascular risk, not your cholesterol number alone. General thresholds for considering medication include:

High absolute risk (10% or greater five-year risk): medication typically recommended alongside lifestyle changes.

Moderate risk (5-10%): may be recommended depending on specific factors, patient preference, and clinical judgement.

Low risk (below 5%): lifestyle modification is generally the primary approach, unless there's a specific indication like familial hypercholesterolaemia.

If your GP recommends a statin, it's worth understanding why. Ask what your calculated absolute risk is, what target LDL they're aiming for, and what the expected benefit is in your case. That's not questioning their judgement. It's being an informed participant in the decision.

My dad, for what it's worth, is three months into his statin now. His LDL has dropped from 4.2 to 2.1 mmol/L. He still eats salmon. He still walks every morning. The medication didn't replace the lifestyle. It filled the gap the lifestyle couldn't close.

Tests to consider through Bloody Good

The standard cholesterol test:

Cholesterol (Lipid Studies inc. HDL) Blood Test covers total cholesterol, LDL, HDL, triglycerides, and TC/HDL ratio. This is the full standard lipid panel.

Related tests for a more complete cardiovascular and metabolic picture:

HbA1c measures blood sugar control. Metabolic health and cardiovascular risk are deeply connected. Insulin resistance drives the triglyceride-high / HDL-low pattern.

High-Sensitivity CRP adds an inflammatory dimension to cardiovascular risk assessment. Some clinicians use it alongside lipid results.

Lipoprotein(a) is a genetically determined cardiovascular risk marker that's independent of LDL. You can't change it with lifestyle, but knowing about it can change how aggressively your risk is managed.

Fasting Glucose provides metabolic context alongside your lipid results.

Liver Function Test (LFT) is relevant if starting or monitoring statin therapy, and for assessing fatty liver which often coexists with dyslipidaemia.

If you want the full picture:

The Bloody Good Test covers 100 biomarkers including the full lipid panel alongside liver, kidney, thyroid, iron, vitamin D, blood sugar, and inflammation markers. If you're doing a cardiovascular baseline, doing it all at once makes sense.

Biomarker info: Total Cholesterol · LDL Cholesterol · HDL Cholesterol · Triglycerides

When to retest

If your results are normal and you're low risk: Retest every 2-5 years, or sooner if risk factors change (weight gain, new diagnosis, family history events).

If results are borderline and you're making lifestyle changes: Retest in 8-12 weeks. Lipids are one of the faster-responding markers. You can see meaningful shifts in LDL and triglycerides within 2-3 months of sustained dietary and exercise changes.

If you've started medication: Your GP will typically retest at 6-8 weeks to assess response and determine whether the dose needs adjusting. Then periodically thereafter.

If you have familial hypercholesterolaemia or known cardiovascular disease: Regular monitoring as directed by your specialist, typically every 6-12 months or more frequently if treatment is being adjusted.

After significant life changes: Major weight fluctuation, new medication, change in diet, new diagnosis (diabetes, thyroid issues). All warrant retesting.

Explore more biomarkers

If you want to go deeper into any of the markers covered here, the Bloody Good biomarker directory has detailed pages on what each test measures and how to think about results.

Browse the Bloody Good Biomarker Directory