Cholesterol: What Really Matters

Welcome back! In Part 1 of our lipid series, we established that LDL is not inherently evil. It acts as an essential escort vehicle carrying vital nutrients, fats, and cellular building blocks throughout your bloodstream.

When people get a standard blood test back with high total cholesterol or high LDL, the initial knee-jerk reaction is often to start cutting out dietary cholesterol and healthy fats. But to understand cardiovascular risk, we have to look upstream at where LDL comes from, how triglycerides fit into the picture, and why insulin sensitivity rules them all.

The Skinny for those who haven’t got time to read the whole thing right now

• LDL doesn’t simply come from the fat you eat. Your liver makes and packages fats into VLDL, which can eventually become LDL.
• Triglycerides matter. Excess energy, particularly from refined carbohydrates and sugars can increase triglyceride production in the liver.
• VLDL is part of the LDL story. As VLDL delivers its triglyceride cargo, it gets progressively smaller and can eventually become LDL.
• Insulin resistance changes the picture. It can drive increased VLDL production and is commonly associated with higher triglyceride levels and more small, dense LDL particles.
• LDL-C doesn’t tell you how many LDL particles you have. It tells you how much cholesterol they carry.
• ApoB helps us count the traffic. Each atherogenic particle carries one ApoB, so ApoB gives us a much better idea of how many potentially atherogenic particles are circulating.
• Triglycerides and HDL provide additional clues. The TG ratio can help us build a picture of insulin sensitivity and metabolicMetabolism is not a calorie-burning furnace that sits somewhere near your belly button, deciding whether you can fit into last year's jeans. Metabolism is the set of chemical processes taking place inside your body every second of every day, keeping you alive.Referenced in 35 articlesClick to read more → health.
• Lp(a) is different. It is largely genetically determined and is worth knowing rather than assuming your standard cholesterol panel tells you everything.
• Don’t treat one elevated LDL-C result as the whole story. Look at LDL-C alongside triglycerides, HDL, ApoB, Lp(a), glucose regulation and the wider metabolic picture.
• And importantly, look upstream. Food quality, refined carbohydrates, fibre, insulin sensitivity, muscle mass, movement and visceral fat can all influence the lipid picture.

Where does LDL come from? (It starts with sugar!)

It may seem counterintuitive to talk about sugar when discussing cholesterol, but the primary production line for problematic LDL begins with excess sugar, refined carbohydrates, and processed flours (and we are not even going down the folic acid topic). Here is how the process works in two simple steps:

• Step 1: Excess sugar turns into Triglycerides in the liver. When you eat refined carbohydrates or added sugars, your body rapidly breaks them down into glucose. When your liver takes in more glucose than it can store, it converts that excess sugar into fat, specifically, triglycerides. To ship these newly made fats into your bloodstream for energy, the liver packages them into large transport vehicles called VLDL (Very Low-Density Lipoproteins). Every VLDL vehicle carries an ApoB proteinProtein is one of the three main macronutrients, alongside fats and carbohydrates, yet for many years it was often the forgotten member of the trio. More recently, protein has become something of a celebrity in the nutrition world, appearing in everything from snack bars and cereals to coffee and desserts. Whilst the marketing can sometimes get a little carried away, the truth is that protein is essential for human health. Every cell in the body relies on it. Protein helps build and repair tissues, supports immune function, forms enzymes and hormones, transports nutrients, and helps maintain muscle mass, particularly as we age.Referenced in 35 articlesClick to read more → molecule, which acts as the structural frame for these delivery trucks (check part 1, if you missed it)

• Step 2: VLDL is converted to LDL. As VLDL trucks travel through your body dropping off triglycerides (fat cargo) to your cells, they shrink down and morph into LDL particles (biology is just mind-blowing!)

If you need a refresher on what LDL actually is, rather than the rather unhelpful label of “bad cholesterol” — we broke that down in Part 1.

When your body develops insulin resistance, meaning your cells stop responding efficiently to insulin due to consistently high sugar intake, the liver pumps out far too many VLDL vehicles. Worse yet, elevated insulin levels over time downregulate the liver’s ‘vacuum receptors’ (LDL receptors), making it harder for the liver to clear old LDL particles out of your bloodstream.

This leaves you with a higher traffic count of small, dense, long-lingering LDL particles that are far more likely to penetrate artery walls and cause plaque formation. This is not good.

Making sense of a blood test panel

Now that you know how sugar drives triglyceride and LDL creation, let’s decode a blood report using the sample panel below:

Triglycerides (0.90 mmol/L): Triglycerides measure the fat cargo circulating in your blood. High triglycerides directly reflect a diet high in refined carbs/sugar or underlying insulin resistance. Keeping this number low (like the optimal 0.90 mmol/L above) shows your liver is not over-producing fat packages from excess glucose.

Total Cholesterol (6.31 mmol/L) & LDL-C (3.88 mmol/L): Total cholesterol measures all the cholesterol in your blood, while LDL-C measures the weight/concentration of cholesterol inside your LDL taxis. Looking at these numbers in isolation doesn’t tell us how many physical particles (trucks) are on the road. You can have a high LDL-C count broken up into a few large, harmless particles, or a ‘normal’ LDL-C broken up into hundreds of small, dangerous ones.

We went into this distinction in much more detail in Part 1,  LDL is the escort; cholesterol is part of what it is carrying.

The essential ratios and advanced markers

To get the true story of your metabolic health, we look at key ratios:

• Triglycerides / HDL Ratio (0.42): This is one of the single best indirect markers for insulin sensitivity. A low ratio (well under the <0.92 threshold) indicates that you do not have a high concentration of small, dense, dangerous LDL particles.
• ApoB (1.13 g/L) and ApoB / ApoA-1 Ratio (0.58): As we learned in Part 1, ApoB counts the actual number of atherogenic (potentially dangerous) particles floating in your blood. ApoA-1 counts your protective HDL escorts. An ApoB / ApoA-1 ratio of 0.58 (well under <0.96) shows an excellent balance between cholesterol delivery and cellular cleanup
• Lp(a) (0.29 µmol/L): Lp(a) is a specific type of LDL particle with a sticky protein attached. Because it is largely genetic rather than dietary, a low result confirms no inherited specific risk factor.

While a standard doctor looking solely at LDL-C (3.88 mmol/L) might flag it in red, the advanced markers (ApoB, ApoA-1, Triglycerides, and all the ratios) confirm that her metabolic health is excellent, her particle count is safe, and her cardiovascular risk profile is very favorable.

How to support your metabolism and lipid health naturally

Addressing lipid health isn’t about fearing natural dietary fats or restricting whole foods. It’s about creating an environment where your body remains insulin sensitive.

1. Reduce refined sugars and processed grains: Cutting back on added sugars, sodas, and refined flours directly slows down the liver’s production of VLDL and ApoB particles.
2. Embrace dietary fibre: Fibre acts like a natural sponge in the digestive tract. It binds to cholesterol-rich bile salts, prompting your liver to pull ApoB particles from circulation to make new bile, while also slowing sugar absorption to prevent insulin spikes.
3. Choose quality fats wisely: Focus on whole-food fats like olive oil, avocados, and nuts. Avoid ultra-processed fast foods that combine high levels of saturated fats with refined carbs, which spike insulin and slow LDL clearance simultaneously.
4. Build muscle mass (resistance training): Skeletal muscle is your body’s largest ‘glucose sink’. Muscles burn through excess glucose without relying heavily on insulin. The more muscle mass you maintain, the larger your glucose sink, keeping your body insulin-sensitive 24/7, even while resting!
5. Target visceral fat: Losing even 8–12% of total body weight, specifically reducing central or abdominal fat, significantly calms down systemic inflammation and lowers circulating ApoB particles.

When you look at a blood panel, don’t let a single elevated ‘LDL-C’ number cause unnecessary alarm. As we saw in Part 1, LDL-C is only one piece of the story. Here in Part 2, we can start looking upstream at what may be driving that picture in the first place.

By reducing refined sugars, increasing dietary fibre, building lean muscle mass, and evaluating key markers like Triglycerides, ApoB, and the TG/HDL ratio, you take true ownership of your metabolic and cardiovascular health!

The New School of Nutritional Medicine

At the New School, we teach our students to look beyond the standard cholesterol panel. We look at ApoB, Lp(a), triglycerides, insulin resistance and glucose regulation. But we also consider homocysteine, inflammation, omega-3 and omega-6 fatty acids, fatty acid balance, and the microbiomeWhen you hear the word microbiome, you probably think of the gut. Fair enough, it gets most of the attention. But what if we told you that microbes are not just hanging out 'down under'? They are everywhere. There is the oral microbiome living in your mouth, the skin microbiome covering every inch of your body, the urogenital microbiome, the lung microbiome, and, of course, the celebrity of the microbial world, the gut microbiome. These tiny organisms are not unwanted guests infact, truth be known, we are their guests. They are part of you, which helps keep you alive.Referenced in 31 articlesClick to read more →, including the oral microbiome.

And we don’t stop there. We look at stress and psychological health, the HPA axisThe HPA Axis stands for the Hypothalamic-Pituitary-Adrenal Axis. Sounds complicated, but it is essentially one of the body's main communication systems for responding to stress. It is like your body’s internal stress-response network, linking the brain and adrenal glands in a constant conversation about what is happening in your environment. Whether you are running late for work, worrying about finances, doom-scrolling at midnight, or genuinely facing danger, the HPA Axis helps coordinate the release of stress hormones such as cortisol and adrenaline to help you adapt and survive.Referenced in 9 articlesClick to read more →, cortisol, sleep, movement and muscle mass because all of these can influence metabolic and cardiovascular health.

Simply telling someone that their cholesterol is “high” doesn’t tell us enough. We need more to their story.

• What is happening with their blood sugar?
• Are they insulin resistant?
• Are they sleeping?
• Are they chronically stressed?
• What is happening with inflammation?
• Their fatty acids?
• Their gut and oral microbiome?
• Their homocysteine?
• And what is happening in their life?

It is never about ONE marker. If this is how you want to learn by questioning, exploring and joining the dots rather than looking at one marker in isolation come and study with us at the New School of Nutritional Medicine. Our next cohort starts 19th September, 2026. One intake for the integrated diploma per year. 

Come and dive deeper with us. APPLY NOW.

To WHOLE-ness!

From the team at The New School Of Nutritional Medicine

Learn about the Founder & Principal of the New School of Nutritional Medicine, Dr Khush Mark PhD HERE.