October is Cholesterol Awareness Month, and yet most of the conversations about cholesterol are still stuck in the past. You’ve heard it for decades: lower your cholesterol, save your heart. It’s a waxy molecule with a double life: vital for hormone production, brain health, and cell structure, but capable of harm when wrapped in the wrong particle or oxidised by the wrong conditions.
October is Cholesterol Awareness Month, and yet most of the conversations about cholesterol are still stuck in the past. You’ve heard it for decades: lower your cholesterol, save your heart. But the science isn’t that simple anymore. If you’ve ever had a “cholesterol chat” at your GP, you’ll know it’s usually a five-minute, ten if you're lucky, tick-box exercise: total cholesterol, LDL, HDL, triglycerides, here's statin with a vague warning to “eat less fat.” Yet cholesterol isn’t the villain it’s made out to be. It’s a waxy molecule with a double life: vital for hormone production, brain health, and cell structure, but capable of harm when wrapped in the wrong particle or oxidised by the wrong conditions. So, this week I’ve been diving deep into the cholesterol controversy - because understanding it could be the difference between a decade gained or a decade lost. Let’s dive in...
Where insight becomes impact
What I’ve been looking at this week…
Let’s start with a truth that often surprises people: Half of all heart attacks occur in people with normal cholesterol. Half That’s because total cholesterol and LDL are blunt tools. They measure quantity, not quality.
Which means the conventional tests are missing the mark - we're looking at the wrong thing.
What matters isn’t how much cholesterol you have, it’s how it travels.
Think of cholesterol as passengers on buses: 🚌 LDL buses deliver cholesterol from the liver to tissues, where it’s used for repair and hormone production. But when too many buses are on the road, or the arterial “roads” are inflamed with potholes, they start to crash into the lining of the arteries and deposit their cargo. 🚍 HDL buses make the return journey, collecting excess cholesterol (even from the artery walls) and bringing it back to the liver for recycling into hormones, vitamin D, and new cell membranes.
But not all buses are built the same. Some are big and buoyant, they cruise safely through the bloodstream. Others are small and dense, tthey weave through traffic, slip beneath the arterial lining, and crash into the vessel wall. The key marker here is ApoB - it counts how many “bad buses” are on the road. The more there are, the greater the chance of a pile-up inside your arteries, where those particles can trigger inflammation and plaque formation. Then there’s ApoA1, your clean-up crew; Lp(a), your genetically sticky wildcard; and homocysteine, the inflammatory spark that roughens artery walls. Add triglycerides, insulin and HOMA-IR, and you start to see how metabolism and inflammation shape your true cardiac risk, not just cholesterol.
That’s why I never stop at a basic lipid panel. The real insight comes when we go deeper.
And here's something else. You don’t just want to know whether a heart attack is imminent, you want to know whether it’s inevitable. And that’s the difference between looking at your risk of heart disease in the next 10 years and your risk across your whole lifetime. Most GP’s calculators predict the next decade. Your arteries, meanwhile, are keeping score for the next fifty years. A low 10-year risk can hide a high lifetime risk, especially if silent inflammation or insulin resistance is already at work.
A low-risk decade means little if plaque is quietly building for the next half-century.
What I've also seen is that most people don't start thinking about their heart health until their 40s or 50s. But if you're in your 20s or 30s, this is not the time to get complacent, it's the time to get curious. The first signs of arterial ageing start in your 20s, long before symptoms do, and early testing means early advantage.
Track it to hack it.
What I’ve been monitoring this week…
This week, I’ve been reviewing results from clients who completed my Comprehensive Cardiac Longevity Panel, the test I wish every adult would have annually. Because the truth is, 25% of you reading this will die from heart disease. It still remains our number one killer. Which means we've got to dig deeper, look harder together.
Here’s why each marker I test looks deeper:
ApoA1 & ApoB: The proteins that drive your cholesterol “buses.” ApoA1 shows the helpful drivers; ApoB counts the reckless ones. Too many ApoB particles = too much traffic in your arteries.
Lp(a): The genetic wildcard: glue on your LDL tyres that makes them more likely to stick to arterial walls. One in five people have high Lp(a) and never know it.
hs-CRP: The inflammation alarm bell. When this rises, your arterial lining is already under chemical stress.
Fasting insulin, triglycerides & HOMA-IR: Your metabolic dashboard. This picks up insulin resistance long before sugar levels change, one of the earliest signs of vascular ageing.
Together, these markers reveal mechanical, chemical, and metabolic stress, the three silent forces that age your arteries.
Then comes the imaging. 🩶 The Coronary Artery Calcium (CAC) Scan If blood tests tell you what’s happening in your bloodstream, the CAC tells you what’s been etched into your artery walls. It’s a five-minute, low-radiation CT scan that measures microscopic calcium deposits - the scars left by inflammation. The result is your CAC score:
0: No calcified plaque: pristine arteries, low risk.
1–99: Mild plaque: early warning lights; time to act.
100–399: Moderate plaque: active reversal needed.
400+: Significant plaque: advanced arterial ageing, high event risk.
A CAC of 0 means youthful arteries and an exceptionally low short-term risk. Anything above zero provides a crucial baseline, the chance to stabilise and reverse the process.
For soft plaque (younger, unstable, more rupture-prone), in select patients, particularly those with multiple risk factors and co-morbidities, and those with strong family histories, I also use CT angiography, a dynamic map of arterial integrity.
🏠 Home Devices Matter Too The best heart health tracking happens daily:
Blood-pressure monitor: I use continuous wrist monitoring to show vascular load trends.
HRV tracker (Oura, Whoop): Reveals your stress-recovery rhythm to give you a window into your arterial tone.
Sleep tracker: Your arteries rejuvenate overnight; deep sleep literally keeps them flexible.
When you combine biomarkers, imaging, and home metrics, you move from I think I’m fine to I know I’m protected.
BOOK YOUR COMPREHENSIVE CARDIAC TEST AND CONSULTATION
From knowing to doing.
What this means for YOU…
Don’t panic - profile. Precision beats panic every time.
Here’s a simple framework to guide your daily heart decisions:
❤️ C.A.R.D.I.A.C: Seven Daily Decisions for a Younger Heart C: Cholesterol Context Don’t chase low numbers, chase clarity. Your ApoB/ApoA1 and triglyceride/HDL ratios tell the real story of lipid quality and balance. A: Anti-Inflammatory Food Eat to heal, not to harm. Omega-3s, olive oil, avocados, walnuts, and dark chocolate feed your arteries instead of clogging them. R: Resilient Rhythm Cortisol spikes harden arteries faster than cholesterol. Check your cortisol levels, and smooth your stress curve with the 6-60 Breathflow and consistent sleep. D: Daily Fibre & Fasting Aim for 30 g of soluble fibre and a 12-hour overnight fast. Together, they lower LDL and triglycerides naturally. and keep your microbiome on your side. I: Insulin Insight Carbs need a chaperone. Eat protein and fat first to flatten glucose peaks and reduce endothelial stress. A: ActivateVO₂ Your VO₂max, oxygen efficiency, predicts heart longevity better than cholesterol ever will. Move daily, combine with short bursts of intensity. C: CoQ10 Care Optimise your CoQ10 levels through food (beef, salmon, spinach) or supplements, especially if you’re on statins - they deplete this vital mitochondrial molecule.
💼 Case in point: A 46-year-old CEO came to me panicked by a total cholesterol of 7.4 mmol/L and an instant statin prescription. We ran the full panel: ApoB normal, Lp(a) low, CAC = 0. His problem wasn’t cholesterol. it was cortisol. Once we re-trained his sleep, stress rhythm, and VO₂max, his lipid ratios normalised within twelve weeks. No medication. No side effects. That’s the power of precision: from presumption to precision, from guessing to knowing.
🎯 If you'd like to protect your heart, make decisions with precision based on your personal data and use devices that are specific for you, then book a private consultation and let's start to decode your health.
Where you’ll find me…
Last week: Had some of the most exciting collaborative conversations I've had all year... watch this space!!
This week: Delivering a talk to Whistle on the Power of The Pause, then jet-setting to Lisbon for another keynote - very exciting!
Next week: Off to Bahrain for the week!
A thought to pause on…
"We spend decades measuring wealth in pounds and profit. But the true currency of a rich life is health...and the heartbeat that sustains it. Your heart remembers every beat, every breath, every choice. Know your numbers, and you’ll know your future." Wishing you a wonderful week ahead! (that's 168 hours of your million hour life!) 😊 Dr Alka
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Take the free LQThis article is general education, not medical advice, and reading it does not create a doctor-patient relationship. If something has been going on for a while, please get it properly looked at by your own doctor.