Few nutrients are as polarizing as fat. Sometimes it’s blamed for weight gain, sometimes it’s praised for protecting the heart and brain. Cholesterol, especially, tends to appear only in the same sentence as heart attack. No wonder many of us feel confused. If you’re interested in understanding fat metabolism, you’re not alone.
But fat is more than just energy. It also provides structure and enables communication. And it’s this variety that makes fat so fascinating and so vital.
This article takes a closer look:
What exactly are lipids? Why are omega-3 fatty acids so crucial for your brain? How does cholesterol transport work. And what’s really going on with ApoB, LDL, HDL, and Lp(a)?
You’ll get the background, the fun facts and the knowledge to help you make informed decisions. No panic, just lightbulb moments.
Fat Fun Facts
- Butter is less evil than palm oil. With ~55% saturated fats, it’s well below palm oil’s ~80%. And, it comes with fat-soluble vitamins.
- Olive oil? Still a star. Especially when it’s peppery, bitter, and a little scratchy: that’s the polyphenols at work. Oleocanthal irritates your throat like ibuprofen.
Oleuropein brings the bitterness. Hydroxytyrosol is a powerful antioxidant.
The more intense the flavor, the more protective compounds it contains. - Your body is picky. If it doesn’t get quality fats, it’ll make do with whatever’s around. But that’s like wrapping your cell membrane in plastic instead of silk.
- MCTs are fat in fast-forward.
Medium-chain fats (like in coconut oil) skip the lymphatic route and head straight to the liver via the portal vein. Instant fuel, like espresso, but fatty. - Plant oils don’t contain cholesterol. But that says nothing about their quality. Sunflower oil, for example, is rich in omega-6 and potentially pro-inflammatory.
- Triglycerides ride in style.
They don’t float freely but travel in lipoprotein particles like chylomicrons and VLDL complete with address tags (ApoB) and targeting systems. - Omega-3s are building blocks, not bonus features.
They’re woven into your cell membranes especially where flexibility matters: brain, retina, immune system. - DPA is the omega-3 ninja.
Hardly anyone knows about docosapentaenoic acid (DPA) but it moves flexibly between EPA and DHA, fighting inflammation and repairing vessels. - Your brain is fat.
No offense, it’s about 60% fat and highly sensitive to poor supply. - Fat isn’t just fuel.
It’s a communication hub that regulates inflammation, hormones, appetite, and sometimes even your inner peace. - Fat cells rarely disappear.
When you lose weight, they shrink. But the number stays the same. Even after 20 years. (Yes, really.) - Your body makes its own cholesterol: about 1–2 g per day.
Only ~20% comes from food. What you eat has less influence than you think. - HDL is the cleanup crew, LDL the delivery guy.
LDL brings cholesterol to your cells including inflamed vessel walls. HDL comes to pick it up again. A high HDL level used to be seen as protective but this matters more.
Lipid, Fat, Cholesterol?
When we talk about fat metabolism, what we actually mean is lipid metabolism. Specialists in this field are called lipidologists. A quick look at the basics is worth it to clear things up a bit. Because much of what we casually call “fat” is, chemically speaking, only one part of a larger family: the lipids.
Lipids are a class of molecules that all have one thing in common:
They are insoluble in water (hydrophobic) and dissolve well in fats and oils (lipophilic).
(A quick vocab detour: “hydro” = water, “lipo” = fat, “-phobic” = avoiding, “-philic” = loving.)1
In the human body, we mainly encounter three types of lipids in significant amounts. We’ll look at them one by one. First, the triglycerides, your classic storage fat. Then, the phospholipids, which make up our cell membranes. They are ultra-thin but highly versatile barriers, like clever soap bubbles: stable enough to hold a cell together, flexible enough to communicate with the outside world.
And finally, cholesterol, capable of far more than just triggering heart attack headlines. It’s an underrated all-rounder with a major PR problem.
All three play a central role in structure, function, and communication within your body.
But since they don’t behave well in water, they need clever transport systems to travel through the (very watery) bloodstream.
What that has to do with your blood test results: we’ll get to that in a bit.
Three-tailed energy storage
When we talk about “fat” in the context of diet we’re almost always referring to triglycerides. These molecules are the main form in which our body stores fat. Chemically, they consist of four parts: a glycerol backbone which is a three-carbon alcohol with three so-called hydroxyl groups; and three fatty acids that attach to it. The bond is formed through what’s called esterification: each OH group of the glycerol reacts with a fatty acid, releasing a molecule of water in the process.
Don’t worry too much about the chemistry here. I’m just giving you a feel for how organic molecules like to play. Because once you see the patterns, it all starts to make sense.
The result is a molecule with three fatty acid tails attached to a glycerol backbone ideal for compact energy storage.
There are smaller versions too: monoglycerides with just one fatty acid, or diglycerides with two which leaves one of glycerol’s OH groups free. These “unfinished” versions are less common as energy stores, but play more exciting roles elsewhere: as emulsifiers in the kitchen or signal molecules in the body.
An emulsifier is a molecule that gets along with everyone. It helps mix water- and fat-soluble substances. A real socialite, chemically speaking. One well-known example is lecithin, a phospholipid found in egg yolk. Without it, there’d be no mayonnaise.
You probably already know that fat provides more than twice as much energy per gram as carbohydrates or protein. That makes the compact, efficient, and calorie-rich triglycerides true energy experts. It’s actually quite practical to carry such a dense fuel source around at all times. Even if modern society has developed mixed feelings about that.
To illustrate: Butter and sugar have nearly the same density by volume. Here you see 250 grams of each. But while the sugar adds up to around 1,000 kilocalories, the butter easily hits over 1,800. As you can see: fat packs a punch.
Characterizing Fatty Acids – Variety with Impact
There’s a lot of talk about fatty acids and rightly so. Their exact structure determines how they behave in the body: Are they stable or flexible? Do they promote or reduce inflammation? And are they used more as building blocks, fuel, or signaling agents?
Things get even more interesting (and sometimes confusing) when you take a closer look at their names. Many fatty acids go by several labels: chemical names, abbreviations, and everyday terms. Here’s a quick guide so you know how to tell them apart when you next read a sensationalist headline.
Saturated and unsaturated?
A key distinction is saturation: Saturated fatty acids have no double bonds, are straight in structure, and can pack tightly together. That’s why they’re solid at room temperature. Kitchen fats with a lot of saturated fatty acids are for example butter or coconut oil. Monounsaturated fatty acids have one double bond that puts a kink in the chain, making them more fluid like in olive oil. Then there are the polyunsaturated fatty acids, with multiple double bonds that add flexibility and bendiness. Typical examples include the well-known omega-3 and omega-6 fatty acids.
Why is it called Omega-x?
The term “omega” refers to the position counting from the tail end of the carbon chain where the first double bond appears. For omega-3, it’s at the third carbon; for omega-6, at the sixth. Only unsaturated fatty acids get these names, since saturated ones have no double bonds worth mentioning.
And why does this matter? Because the human body can only insert double bonds at certain positions. At others, it can’t which is exactly what makes some fatty acids essential.
Essential means: You have to eat it. Period.
Essential means the body can’t produce it on its own. We have to get it through food. Two especially important examples are linoleic acid (LA), an omega-6 fatty acid found in sunflower and canola oil, and alpha-linolenic acid (ALA), a plant-based omega-3 fatty acid found in flaxseed, chia, and walnut oil.
But here comes the little plot twist: ALA isn’t the final form your body actually wants. For many vital processes, it needs eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). These two omega-3 fatty acids found mainly in oily sea fish like mackerel, herring, salmon, and sardines.
In theory, the body can convert ALA into EPA and DHA but in practice, it’s not very efficient. The conversion rate is often below 10%, sometimes even below 1%, and it drops further during times of stress, inflammation, pregnancy, or chronic illness. That’s why many professional health organizations now recommend getting EPA and DHA directly either by eating fish or using microalgae oil as a vegan alternative.
So you can see, it’s worth thinking beyond ALA and bringing in the final products directly.
Excursion: An Ode to Omega-3
Omega-3 fatty acids really deserve their glowing reputation. Their range of effects is truly impressive.
They influence blood clotting and vascular health. EPA inhibits platelet aggregation, meaning blood platelets are less likely to clump together. In other words, it makes the blood a little more fluid. At the same time, EPA soothes the cells lining your blood vessels (endothelial cells) and reduces oxidative stress. The result are fewer inflammatory processes and a lower risk of atherosclerosis.
Cell membranes incorporate DHA directly especially in the brain, the retina, and sperm cells. There, it increases membrane fluidity, which improves signal transmission and communication between cells. This is especially crucial in the nervous system.
EPA and DHA also serve as raw materials for a whole array of biologically active molecules. EPA, in particular, competes with arachidonic acid, a metabolite of the omega-6 fatty acid linoleic acid (LA) mentioned earlier, for the production of eicosanoids. When EPA wins this molecular race, the resulting signaling molecules are far less inflammatory.
Even more intriguing: EPA and DHA are also precursors to entirely unique mediators such as resolvins, protectins, and maresins. These not only help regulate inflammation but they actively support its resolution. That’s a crucial but often overlooked step in preventing chronic inflammatory conditions.
They even have an impact on gene activity2: omega-3s activate transcription factors called PPARs (Peroxisome Proliferator-Activated Receptors) that regulate genes involved in fat metabolism, glucose balance, and immune regulation. At the same time, they inhibit the NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) pathway which is a central switch in the inflammatory response. This results in fewer pro-inflammatory cytokines and less silent inflammation.
Info: How Do I Know If I’m Getting Enough Omega-3?
- Indirect signs: dry skin, trouble concentrating, low mood, increased tendency toward inflammation.
- Diagnostically measurable: Omega-3 Index (blood test) → target range: 8–12%
- Prevention tip: 1–2 servings of fish per week or 250–500 mg EPA/DHA daily (e.g. via microalgae oil) 3
And what about Omega-6? Don’t worry: linoleic acid is more than abundant in the Western diet. Some would say too abundant. It occurs in many vegetable oils, processed foods, and snacks making a deficiency very unlikely. The real challenge lies in the ratio of omega-6 to omega-3 (see below) , because too much omega-6 without sufficient omega-3 to balance it can promote inflammation.
At this point, omega-6 has almost become the new dietary scapegoat. You know it from debates about so-called “seed oils.” But what’s really behind the controversy?
Excursion: Omega-6 and “Seed Oils”- justified criticism or just hysteria?
Omega-6 fatty acids are currently under heavy scrutiny especially in the form of so-called seed oils. Rapeseed (canola) oil, sunflower oil, and corn oil are frequently demonized across the board.
But as so often, the issue isn’t the substance itself but the quantity. These relatively cheap oils are widely used in industrial food processing, canteen cooking, and ready-made meals. Arachidonic acid in particular, a downstream product of linoleic acid, can promote inflammation when consumed in excess. It plays important roles in the body but we only need small amounts.
In Western diets, the ratio of omega-6 to omega-3 is often 20:1 or higher. Experts recommend a ratio closer to 4:1 or even lower. Too much omega-6 can disrupt the balance, especially if omega-3 intake is insufficient.
Another key point is that when we heat polyunsaturated fats repeatedly, such as during deep-frying, trans fats can form. And on those, the verdict is clear: they are harmful to your health.
By the way: the term “seed oils” originates in the U.S., a country known for its deep-fried foods, somewhat relaxed regulations, and (ahem) a strong taste for polarized black-and-white debates.
My takeaway is that in reasonable amounts, these oils aren’t inherently bad. What matters is the combination, the processing and the variety. For cooking and frying, olive oil is an excellent choice. And when it comes to salad dressings, variety pays off: walnut, hazelnut, or flaxseed oil don’t just add flavor, they bring valuable nutrients too.
Cis, trans – sounds chemical, and it is
Here’s another term that often sounds confusing but is worth understanding: the cis and trans forms of fatty acids. In the natural bendy cis form, the hydrogen atoms sit on the same side of the double bond. This creates a bend in the fatty acid chain, increasing its flexibility and making the fat more fluid. In the trans form, which is typically the result of industrial fat hardening, the hydrogens are on opposite sides. The molecule stays straight, making the fat more solid, but also more problematic for your health. These trans fats, sometimes nicknamed “Frankenfats”, raise LDL cholesterol, lower HDL, and promote inflammation.
Good to know: The classic method of fat hardening through partial hydrogenation, which is the main culprit behind industrial trans fats, is now rarely used in Europe. Modern margarine production usually relies on the targeted selection and combination of fatty acids, emulsifiers, and vegetable oils to achieve the desired consistency without trans fats. The historical image of margarine as a trans fat bomb persists, but it no longer applies to many of today’s products. Also, some trans fats do occur naturally.
Excursion: Why Not All Trans Fats Are the Same
Not all trans fats come from factories. Natural trans fats occur in dairy products like butter (3–6% of total fat), cheese (0.6–0.7g CLA per kg fat), and yogurt (5–9g CLA per kg fat), particularly conjugated linoleic acid (CLA). And here’s where it gets interesting: studies suggest that CLA may not only be harmless but potentially beneficial for health, helping to modulate inflammation, stabilize blood sugar, or even support muscle growth4. The research isn’t fully conclusive yet, but one thing is clear: we shouldn’t lump natural trans fats from animal sources together with industrially hardened fats.
In short: trans isn’t just trans. As so often, context matters and while milk fat isn’t a superfood, it’s also not a secret villain.
Chain Length – An Underrated Difference
Last but not least, the chain length of fatty acids plays a key role not just in their chemical behavior, but also in how the body uses them.
Short-chain fatty acids like butyric acid are mainly produced in the colon specifically when our gut bacteria ferment fiber. Curious what they do? You’ll find out in the sidebar Small But Mighty.
A bit longer but still speedy are the medium-chain fatty acids, also known as MCTs (medium chain triglycerides), especially caprylic acid (C8) and capric acid (C10). We absorb them particularly efficiently. More on that in the sidebar Energy Drink in Fat Form?
Often lumped in with them but a bit of an oddball is lauric acid (C12). Chemically, it’s still a medium-chain fatty acid, but in the body it behaves more like a long-chain one: it’s transported via the lymphatic system instead of heading straight to the liver. So, lauric acid is an MCT with an identity crisis. It makes up about half the fat content of coconut oil, but it’s not quite the “turbo fat” it’s often made out to be. Which means for you that if you want to try MCT oil then pure coconut oil is not a substitute even though technically it mostly contains fatty acids with medium chain length.
Long-chain fatty acids (C14–C24) make up the majority of the fats we eat. They’re crucial building blocks for cell membranes, nerve tissue, and energy storage. Saturated long-chain fats like palmitic acid are particularly well-suited for compact, long-term storage in adipose tissue. That’s likely one reason why animal fats tend to contain more saturated forms in their high-calorie tissues. And you have already met the omega-3 DHA earlier. Our bodies incorporate it into nerve cells and the retina, where it enhances membrane fluidity and signal transmission.
The longer the chain, the more sluggish the molecule but also the more stable in certain structures. In membranes, for example, long-chain fatty acids increase density and firmness. That’s great for stability but not so much for flexibility. Why this is a balancing act is something I’ll explain in the section on membrane structure (see here).
Welcome to the biochemistry ballet: everything dances on the fine line between too much and too little.
Excursion: Small but mighty – the power of short chains
One especially intriguing group are the short-chain fatty acids, or SCFAs. Unlike other fats, they don’t come directly from food. Instead, gut bacteria which ferment fiber that we can’t digest ourselves produce them for us.
Sounds like a side note? Far from it. SCFAs like butyrate, acetate, and propionate act locally in the gut: they fuel the intestinal lining, help regulate pH, tame inflammation, and even send satiety signals to the brain (via hormones like GLP-15 or PYY).
Butyrate is especially beloved. It’s often called the favorite fuel of gut cells and plays a central role in maintaining the intestinal barrier. In short: SCFAs are the unsung heroes of a healthy digestion.
Excursion: Energy Drink in Fat Form?
Medium-chain fatty acids, or MCTs, behave like a hybrid between fat and sugar combining the best of both worlds. As I mentioned above, caprylic acid (C8) and capric acid (C10)6 are found in coconut oil (making up 12-20% of the total fat) and specially processed MCT oil.
What makes them special: MCTs don’t follow the usual fat digestion route. They bypass the detour through the lymphatic system and chylomicrons, heading straight to the liver via the portal vein. There, they’re rapidly converted into energy or ketone bodies.
This makes them an ideal energy source for those with digestive issues, in epilepsy treatment, on a ketogenic diet or simply when the body needs a quick energy boost. Bonus: MCTs are less likely to be stored in fat tissue. In a way, they’re fat with a built-in turbo.
And now?
You saw already that fatty acids are more than just fuel. They’re building blocks, messengers, energy sources, and balancing agents. Their effects depend not only on how much you eat, but which ones, where they come from, and in what ratio. Some are flexible, some stable, some essential. And a few are surprisingly misunderstood.
I’ve explained all this because understanding gives you the freedom to choose well. And above all: to decide for yourself instead of getting swept up by the next low-fat hype. (A blog post for another time. Nutrition trends are just like fashion: the sugar ‘bell-bottom trousers’ or the keto ‘crop top’ always come back. It’s called a revolution for a reason – ha!)
What you can take away: Fat is not the enemy. It’s part of your body, your metabolism, your cell membranes and if you like, your breakfast too.
Speaking of cell membranes…
If fatty acids are the basic components, then phospholipids are their cleverly wired-up building blocks. Without them, there’d be no cell membranes, no communication, no inside or outside. It’s time to take a closer look at these multitaskers.
From Fat to Form: How Phospholipids Step Into the Spotlight
Fatty acids are versatile, but only when combined with a bit of chemistry magic do they become true architects of life. Welcome to the world of phospholipids – the molecules that not only fill our cells, but hold them together.
Structure: Two Tails and a Head
A typical phospholipid consists of one glycerol molecule, two fatty acids (usually one saturated and one unsaturated), and a phosphate group, which is in turn bound to another molecule like choline, serine, or inositol. This combo creates what’s known as an amphiphilic molecule: the head loves water (hydrophilic), the two tails avoid it (hydrophobic). And it’s exactly this behavior that makes phospholipids masters of self-organization.
When placed in water, their molecules spontaneously align into a double layer: the water-loving heads face outward toward both the inside of the cell and the external environment. The water-avoiding tails snuggle up together on the inside. This forms a flexible, semi-permeable barrier that protects, filters, and shapes all life: the cell membrane.
And what a membrane it is, not stiff like plastic, but supple like silk. Stable enough to preserve structure, yet flexible enough to transmit signals, allow substances in and out, and even rebuild itself when needed. The precise mix of saturated and unsaturated fatty acids determines its properties: more stability or more fluidity. And to give you a clearer picture: if a cell were the size of a watermelon, its membrane would be about as thin as a sheet of paper.
Excursion: Flexible Membranes Need Flexible Fats
Cell membranes should be supple, adaptable, and permeable not rigid like a board. And that depends heavily on the types of fatty acids embedded in them. Saturated fats are straight in structure and provide rigidity. Unsaturated fats, on the other hand, have kinks in their chains. That makes them more flexible and promotes membrane fluidity. Especially important here are omega-3 fatty acids like DHA. Our bodies preferentially incorporate them into nerve cells and the retina exactly where fast and precise communication is key.
A diet rich in high-quality unsaturated fats, like those from fish, nuts, or flaxseed oil, can therefore influence more than just your cholesterol levels. It directly helps shape the quality and function of your cell membranes.
Function: Membranes, Signals, Transport
Phospholipids aren’t just structurally clever they also play active roles. They’re signal transmitters, packaging artists, and border crossers all at once. Some of their derivatives act as secondary messengers within the cell. Others help incorporate triglycerides and cholesterol into lipoproteins, so they can safely travel through the bloodstream.
Nutrition & Synthesis
Your body can synthesize phospholipids from basic building blocks like choline or ethanolamine. However, some components, especially omega-3 fatty acids must come from your diet so that your body can build them into your membranes. That means that there is a direct link between what we eat and the quality of our cell walls.
Choline and What (Else) We Need It For
Choline, a component of many phospholipids, is crucial for cell membranes. On top of that it’s also a precursor of the neurotransmitter acetylcholine, which plays a key role in focus, memory, and reaction speed. That makes choline more than a niche nutrient. Although it isn’t classed as a vitamin it is vitamin-like in importance and necessity.
One of the reasons for its non-vitamin status is that the body can and does produce some of the choline it needs. However, that’s not always sufficient (see excursion). This is why choline is conditionally essential. We need to get it through food, at least from time to time.
Excursion: Choline in Practice
How much choline we need depends on age, hormonal status, and life circumstances. The European Food Safety Authority (EFSA) recommends a daily intake of 400 milligrams for adults and adolescents aged 15 and older. For children, the requirement ranges from 140 to 340 milligrams depending on age. Pregnant women should aim for about 480 milligrams, and breastfeeding women around 520 milligrams.7
For people with a mixed diet, this is usually not an issue. Just one egg can cover a third to half of the daily requirement. It’s more challenging for those following a strictly plant-based diet. While some plant foods do provide notable amounts such as soybeans (100–115 mg per 100 g), wheat germ (120 mg), shiitake mushrooms (50 mg), or quinoa (40 mg), the total often falls short of meeting daily needs.
Soy or sunflower lecithin found in processed foods also contains choline, but the amount is rarely specified and generally too low to rely on.
Tip: If you’re vegan or in a phase of increased need, you might consider targeted supplementation such as Alpha-GPC or Citicoline.
If we’re already talking about building blocks for cell membranes, signaling, and transport then we can’t skip a molecule that spent decades with a bad reputation and is only slowly making a comeback as the biological all-rounder it is: cholesterol.
It’s not a fat in the classic sense, but a so-called sterol; chemically related, but structurally and functionally distinct. And although it’s often cast as a scapegoat, cholesterol plays so many essential roles in the body that you have to wonder how it ended up with such a bad image in the first place. Time to take a closer look.
Cholesterol – From Villain to Multitalent
Few substances have a worse reputation – and few are so misunderstood. Cholesterol is not a neurotoxin. It’s a vital building block, signaling molecule, and protective factor. We can’t live without it – and the body knows it: it produces cholesterol on its own, every single day, and in surprisingly large amounts.
What Is Cholesterol, Really?
Contrary to common belief, cholesterol does not store energy. It’s not made of fatty acids either, but belongs to the group of sterols, a class of substances closely related to steroid hormones. If you’re thinking of estrogen, testosterone, or cortisol, you’re spot on: these hormones strucrurally derive from cholesterol.
Why Does the Body Need Cholesterol?
Cholesterol plays multiple key roles in the body. It stabilizes cell membranes and influences how flexible and fluid they are which is an important factor for cell function and communication. Moreover, it is the precursor to bile acids, which are essential for digesting fats. Hence the name, derived from the Greek word chole for bile.
It also serves as the raw material for a range of vital hormones, including cortisol, estrogen, testosterone, and aldosterone. Even vitamin D is synthesized from cholesterol in the skin, with the help of UVB light.
And here’s a particularly fascinating fact: the brain is highly dependent on cholesterol. The protective sheath around nerve cells ,the so-called myelin sheath, is largely made of cholesterol. When this sheath breaks down, as in multiple sclerosis, serious neurological symptoms can result.
Cholesterol Production: Homemade!
The good news: we don’t have to eat cholesterol to have enough of it. The body produces about one to two grams daily on its own primarily in the liver, but also in other tissues. Only about 20 percent comes from food. And the body actively regulates this: when we consume less cholesterol, it ramps up its own production. When we eat more, it can slow things down.
Can is the key word here because it doesn’t always work that way. At some point, internal regulatory mechanisms can become exhausted or overwhelmed, for example in cases of genetic disorders or persistently unhealthy lifestyles. That’s one reason cholesterol levels vary so much from person to person, depending on diet and habits.
Transport in the Blood: Lipoproteins
Cholesterol is a lipid and like most fats, it’s hydrophobic. In other words, it can’t just float freely through the bloodstream like a tiny fat dolphin. It needs a ride and that’s where lipoproteins come in.
Lipoproteins are transport particles that consist of proteins (apoproteins) and phospholipids forming the outer shell, with a mix of triglycerides and cholesterol inside. Depending on their composition and density, they serve different roles in lipid metabolism.
Chylomicrons form in the intestine right after a high-fat meal and transport freshly absorbed dietary fats to muscles and fat tissue. The liver produces VLDL (very low-density lipoprotein) which delivers triglycerides to the body. When VLDL drops off most of these fats, a smaller, denser particle remains: LDL (low-density lipoprotein). This delivers cholesterol directly to body cells which is a useful job in principle, but its tendency to accumulate in blood vessel walls has given it a bad reputation.
In contrast, HDL (high-density lipoprotein) acts like a cleanup crew: it collects excess cholesterol from the tissues and returns it to the liver, which either reuses or excretes it.
In short: LDL is the delivery van, HDL is the taxi after the party.
LDL – The Bad Reputation
LDL = bad? Not quite. Without LDL, cholesterol wouldn’t reach the places it’s needed like cells, hormone factories, and nerve tissue. It plays a vital role in transport throughout the body. But, as so often, too much of a good thing can become a problem.
When doctors measure “LDL cholesterol,” they’re not actually counting the number of LDL particles. They’re only measuring how much cholesterol those particles carry on average. That may sound like a technicality, but it’s important. Because it’s not just the amount that matters, but also the form and behavior of these particles.
It becomes problematic when LDL particles oxidize meaning free radicals or chronic inflammation chemically alters them. Glycation also plays a role: when blood sugar levels are consistently high, sugar molecules attach to proteins in the LDL shell, a process that makes the particles more prone to oxidation. Oxidized LDL is seen by the immune system as “foreign” and is taken up by scavenger cells. These cells then form what’s known as foam cells, which can embed in the vessel walls.
Over time, this leads to plaque buildup – the start of atherosclerosis, a narrowing of the arteries that increases the risk of heart attack and stroke.
When cholesterol tries to help – but inflammation fuels the fire
So cholesterol itself isn’t the villain. It actually helps repair damaged blood vessels. But if this repair job becomes constant due to ongoing micro-injuries, inflammation, or oxidative stress then the whole system becomes unbalanced.
Chronic low-grade inflammation acts like an accelerant: it raises the demand for cholesterol, weakens vessel walls, and boosts LDL oxidation. The real danger arises when several risk factors overlap: high blood sugar, stress, smoking, sedentary lifestyle, poor fat intake, or a lack of protective antioxidants. That’s when this once-helpful building block can become a key player in the formation of arterial plaques.
Excursion: High Blood Pressure and Atherosclerosis – Who Came First?
High blood pressure can damage the delicate inner lining of blood vessels mechanically, through the constant force of elevated pressure. These tiny injuries trigger repair mechanisms that bring LDL cholesterol into play. If that LDL becomes oxidized, it attracts immune cells, which settle into the vessel wall. This can lead to atherosclerosis: the buildup of fats, immune cells, and connective tissue in the arterial wall.
But the reverse is also true: when blood vessels become narrowed and stiff due to atherosclerotic plaques, the heart has to pump harder to maintain proper blood flow. The pressure rises and high blood pressure develops.
In short: high blood pressure and atherosclerosis can reinforce each other. Which one comes first often depends on an individual’s risk profile but in the end, they’re rowing the same boat. That’s why prevention strategies are most effective when they target both together: protecting blood vessels and regulating blood pressure go hand in hand.
Aside from how much cholesterol is circulating: fewer taxis, lower risk regardless of their cargo. Because in the end, it’s not just how much cholesterol is floating around in your blood that matters, but how many particles are carrying it. This is exactly where more modern risk markers come in. They reveal more than the traditional cholesterol number.
ApoB & Lp(a) – the better markers?
If you really want to know what’s going on, forget total cholesterol and look at these two:
- ApoB (Apolipoprotein B-100): Each atherogenic lipoprotein particle (VLDL, LDL, IDL, Lp(a)) contains exactly one ApoB. So the ApoB level tells you how many potentially risky particles are circulating – regardless of how much cholesterol each one carries. If you paid attention you know that Chylomicrons also carry apoB albeit a shorter version. However, they are only in your blood if you have eaten recently and blood tests are carried out fasted (no food for 8-10 hours).
- Lp(a) (Lipoprotein little a): Structurally similar to LDL, but with a dangerous addition – Apolipoprotein(a). This variant is genetically determined, barely influenced by lifestyle, and particularly atherogenic. And the kicker (for better or worse): Lp(a) isn’t even measured in standard cholesterol tests. So, you could have “perfect” LDL levels – and still carry a hidden risk.
This variant is carried by 20–30% of the population, so it’s not exactly a niche issue. And that raises an intriguing question: why would the body even do that? Why produce a lipoprotein so strongly linked to cardiovascular disease?
Maybe because it used to be useful.
Lp(a) resembles a rescue helicopter equipped with special gear and a throw line: it can quickly fly to where a blood vessel has been damaged and help with the repair. Apo(a) resembles the enzyme plasminogen, which normally helps dissolve blood clots. Researchers therefore suspect that Lp(a) played an evolutionary role in wound healing and clotting, especially in times when injuries were common and survival depended on how quickly bleeding could be stopped.
Women tend to have slightly higher Lp(a) levels on average than men. That, too, could be biologically meaningful: the greatest risk of bleeding in a woman’s life was (and still is) childbirth. A fast clotting response could mean the difference between life and death. What we now see as a risk factor may once have been a survival advantage.
In a world full of low-grade inflammation, chronic stress, and constant metabolic stimuli, this rescue helicopter gets called out far too often – even when there’s no real emergency. And that’s when a once protective function becomes a burden on the arteries.
What does that mean for you?
If Lp(a) was originally a useful repair helper, then maybe the key isn’t so much to lower its level. Either way it’s considered relatively stable and not influenced much by lifestyle. Instead, the goal should be to prevent the body from needing to send it out so often in the first place.
And that brings us to one of the most important influencing factors of all: inflammation.
Because particles like LDL, Lp(a) only become a problem in an inflammatory environment. That’s when they attach to vessel walls, oxidize, get “eaten” by immune cells, and end up embedded in the arteries.
That’s why it’s so important to pay attention to the quality of your diet, to move your body, to get good sleep, and to manage stress. It’s trendy wellness advice but you’re actively shaping the environment in which your blood vessels either age or manage to stay young.
So let’s take a closer look: what exactly is inflammation? And how can you tell if it’s quietly smoldering inside you?
Excursion: Inflammation and Fat Metabolism – Friend or Foe?
The word inflammation brings to mind swollen red patches, throbbing pain, and feverish drama. And yes, that’s exactly what classic acute inflammation looks like. Think cuts, infections, or sprained ankles. The immune system jumps into action like a well-trained emergency crew: it sends out messengers, opens blood vessels, allows immune cells to flood in, and clears out the mess. Once the job’s done, the team retreats, the body heals, and everything calms down again.
But what happens when that retreat never comes?
That’s when we enter the territory of chronic, low-grade inflammation. No drama. No obvious pain or hot, swollen area. Just a body stuck in constant alert mode. These processes can smolder beneath the surface for years. And that’s what makes them so sneaky. They drive oxidative stress, mess with repair processes, and increase the chances that otherwise harmless substances like cholesterol start showing up in the wrong places.
This type of inflammation is often fueled by a mix of modern-life stressors that overwhelm the system over time: chronically elevated blood sugar, a diet full of ultra-processed foods, too little movement, poor sleep, or ongoing emotional strain. Environmental toxins, lingering infections, or an overloaded gut can add to the fire.
The good news is there’s a lot that helps to calm things down. Regular movement. A colorful, plant-rich diet. Enough Omega-3s. Sleep. Sunlight. Slow breaths. True breaks. And the occasional honest conversation. (Let’s be real: a well-placed “no” often helps more than the seventh to-do list.)
Inflammation, then, isn’t the enemy. It’s a signal. A biological SOS that says: Something needs care. And when we learn to listen, something deeply healing can begin.
Side note: Funny, isn’t it? We often rush to suppress acute inflammation- ice swollen ankles, lower fevers – even though that’s our immune system doing exactly what it’s supposed to do (I am not denying that acute inflammation can escalate, too). But meanwhile, the slow-motion car crash of chronic inflammation quietly builds in the background… and we barely notice we’re fueling it.
Excursion: How do I know if I have low-grade inflammation?
The tricky thing about chronic, low-grade inflammation is: you don’t feel it. No fever, no redness, no classic pain. And yet, the body can remain on high alert for years. So how do you know if something’s quietly smoldering in the background?
There are a few clues if you know where to look. Certain inflammatory markers can be measured in the blood, most notably CRP, or more precisely: hsCRP, the high-sensitivity C-reactive protein. It spikes during acute inflammation, but in this more sensitive version, it can also detect low-grade, chronic processes. Values below 1 are considered low risk, above 3 are elevated though always to be interpreted in context.
Other lab values can also hint at inflammation, such as the neutrophil-to-lymphocyte ratio or elevated triglycerides paired with low HDL. But no single value can definitively prove or rule out chronic inflammation.
Sometimes, inflammation makes itself known indirectly through fatigue, diffuse pain, poor recovery after exertion, low mood, or unexplained weight gain. None of these are dramatic on their own but taken together, they can be a signpost.
So if you feel like your body is somehow out of balance, it might be worth checking in on those inflammatory markers. Not out of panic but out of curiosity and care. Because the earlier you notice something stirring inside, the easier it is to course-correct.
I wanted to show you what an amazing system your body is. We often look outward in search of fascinating things to discover but there’s this spectacular organism you’re wired into, always with you, quietly doing its job. It deserves admiration, care, and deep respect. And no matter what’s going on, your body is always trying to do right by you.
I hope I’ve convinced you how unfair it is to pin all the blame on cholesterol.
It’s neither the villain nor the hero of the story but rather a multifunctional building block of life that only becomes a problem in the wrong context. The molecule itself isn’t the risk. It’s how many of them are circulating, how they’re packaged, whether they oxidize, and whether your internal environment promotes inflammation. If you’re only looking at total cholesterol, you’re only seeing half the picture and missing the chance to take smarter, more personalized steps for prevention. Cholesterol isn’t the end. It’s the beginning of a much more fascinating journey through metabolism, immunity, and modern risk diagnostics.
Practical Tips for Supporting Your Fat Metabolism
The good news? You have more influence over your lipid metabolism than you might think without needing statins. (That said, don’t stop any medications on your own! But ideally, find a doctor who’s at least heard of ApoB.)
A lot starts with what you do every day. Movement, for instance, works like an internal cleanup crew and reduces silent inflammation. A diet rich in colorful vegetables, healthy fats, and low in sugar also supports a calmer, more resilient system. Fiber plays multiple roles: it feeds your gut microbiome, helps regulate blood sugar, and binds bile acids in the gut which can help lower cholesterol levels.
Try to avoid trans fats, which are found in industrially hardened oils and disrupt fat metabolism on many levels. And if you’ve never had your cholesterol checked, remember: the classic total cholesterol number doesn’t tell you much. More informative markers include ApoB, LDL-P, and Lp(a), which give you a clearer picture of how many atherogenic particles are actually circulating.
Some people also use plant sterols or niacin. These can be helpful, but not for everyone, and never without guidance. As so often, the smartest hacks are the least spectacular. But they work, if you stick with them.
My Personal Case Study
I’ve tried a lot of things including keto. Afterwards, I had my labs done: my LDL has always been on the higher end of the normal range, but my ApoB is completely unremarkable, and my triglycerides are in a good place. What is genetically elevated for me, though, is Lp(a). That’s why I no longer just look at numbers in isolation but at the bigger picture of my metabolism. Because my transport taxis are a bit stickier than average they could get stuck in the vessel walls. That part I can’t change.
My focus now is on keeping inflammation low and staying metabolically flexible. I practice “intermittent intermittent fasting”. I generally like to eat a lower-carb diet, because it keeps my hunger signals calm and helps me stay steady throughout the day. But not during the luteal phase of my cycle. And especially not in the final week.
I eat fats, but intentionally. I go for high-quality plant-based fats like nuts, olive oil, avocados, and seeds but I avoid large amounts of sunflower oil and the like. Animal products are part of my diet too. I do not exclude anything in fact. Not even cake as you know from my front page. I do prefer fermented dairy and occasionally organ meats, for their nutrient density.
What I consciously include on a regular basis: fatty sea fish twice a week for Omega-3s (EPA and DHA). Plenty of vegetables, some fruit. And a few times a week, chia or flaxseed pudding for fiber, plant-based Omega-3 (ALA), and satiety.
I don’t believe in the perfect diet and I certainly don’t have one. But I do believe in self-observation, good data. And in the idea that our metabolism thrives on variety grounded in rhythm.
- If you’re a chemist, please forgive me for not diving into polarity, partial charges, and dipole moments right now. We’re not in an organic chemistry seminar, after all. We’re here to get a clearer picture of what fat actually does in the body. ↩︎
- It’s now well established that it’s not the genome alone that sets the tone, but rather its patterns of activation known as gene expression. Our genetic material isn’t a rigid blueprint but a dynamic system that responds to environment, nutrition, stress, and many other factors. Unlike bacteria, whose evolution depends on rapid generational turnover, long-lived organisms like us rely more heavily on flexible regulation. Our epigenetics isn’t a switch. It’s a dance. ↩︎
- EFSA Panel on Dietetc Products, Nutrition and Allergies (2012): Scientific Opinion on the Tolerable Upper Intake Level of EPA, DHA and DPA. ↩︎
- Marianne Raff, Tine Tholstrup, Samar Basu, Pernille Nonboe, Martin Tang Sørensen, Ellen Marie Straarup (2008).
A diet rich in conjugated linoleic acid and butter increases lipid peroxidation but does not affect atherosclerotic, inflammatory, or diabetic risk markers in healthy young men.
The Journal of Nutrition, Volume 138, Issue 3, March 2008, Pages 509-514. ↩︎ - Wenn dir GLP-1 bekannt vorkommt, ganz genau: Das Prinzip hinter den derzeit so populären Diätspritzen. Ozempic, Wegovy und Mounjaro sind sogenannte GLP-1-Agonisten – sie verstärken also genau dieses Signal. ↩︎
- Die Namen Capronsäure (C6), Caprylsäure (C8) und Caprinsäure (C10) leiten sich alle vom lateinischen capra (= Ziege) ab – weil sie erstmals aus Ziegenfett isoliert wurden. Und ja: Capronsäure riecht tatsächlich ein bisschen nach Stall. Wer sie mal pur gerochen hat, vergisst das nicht mehr, deshalb ist sie auch nicht Bestandteil von MCT-Ölen im Handel. ↩︎
- EFSA Panel on Dietetic Products, Nutrition and Allergies (2016): Scientific Opinion on the dietary reference values for choline. ↩︎