Latest / Common Sense Health / Stop Fearing LDL: What They Don't Tell You

Transcript

Stop Fearing LDL: What They Don't Tell You · Common Sense Health

• Stephen Thomas BSc. Hons: Hello! Today I want to give you a slightly different way of thinking about cholesterol and lipoproteins, triglycerides, and the standard lipid panel, because this is probably one of the most discussed parts of a blood test, but also one of the most misunderstood. People often get handed their results, one or two numbers are highlighted, and suddenly the whole conversation becomes very dramatic. But biology is rarely that simple. The body is not a spreadsheet, it's not a plumbing system. And it's definitely not a cholesterol scoreboard where one number tells us everything we need to know. So let's slow it down and build this up properly. First, cholesterol itself is not a villain in the story. Cholesterol is an essential molecule. It is needed to build and maintain cell membranes. You need it to produce steroid hormones such as cortisol and Or estrogen, progesterone and testosterone. You need it to make vitamin D. You need it to make bile acids which help you digest and absorb fats. You need it for your brain and nerve function, and you need it to help maintain the structure and fluidity of your cells. So cholesterol is not some toxic waste product that your body accidentally forgot to remove. It is essential. The better question is not is cholesterol good or bad, the better question is How is cholesterol being transported? Why are certain transport particles higher or lower? And what is the broader metabolic context? And that word context is everything. Cholesterol and triglycerides are lipids. In simple terms, they are fat-based molecules. Blood is mostly water, and fat and water are not exactly best friends. If you have ever tried to mix olive oil into a glass of water, don't know why you do that, you would know roughly what I mean. You can shake it around and feel very scientific for a few seconds, but it gives you a moment and then it separates again. Just like two relatives at Christmas who should never have been seated together. So the body needs a clever transport system. It cannot just throw cholesterol and triglycerides into the bloodstream all loose and hope for the best. Instead it packages them into particles called lipoproteins. A lipoprotein is a transport particle. It is part lipid and part protein and its job is to move fat based substances safely through the watery bloodstream. I like to think of lipoproteins as biological courier parcels. The cargo might include cholesterol, triglycerides, phospholipids, fat soluble vitamins and other lipid based materials. The lipoprotein is the packaging and delivery system that allows that cargo to move around the body. So when we talk about LDL, HDL, V LDL, RDL, and LP LA, we are not actually talking about cholesterol itself, we are talking about transport particles. LDL stands for low density lipoprotein. HDL stands for high density lipoprotein. VLDL stands for very low density lipoprotein. IDL stands for intermediate density lipoprotein. An LP little A pronounced LP little A is a lipoprotein particle that looks a bit like LDL but has an extra protein attached. Now that distinction matters because if we get the language wrong, we often get the interpretation wrong. Now when you look at a standard lipid panel, you will usually see total cholesterol, triglycerides, HDL cholesterol and LDL cholesterol. Depending on the lab, you may also see non-LDL cholesterol, VLDL cholesterol, cholesterol to HDL ratio or other calculated values. Total cholesterol. is exactly what it sounds like. It is a broad total of cholesterol being carried in different lipoprotein particles. It includes cholesterol carried in LDL, HDL, VLDL, and other particles. The problem with total cholesterol is that it's very crude. It does not tell you where the cholesterol is being carried, why it is there, what triglycerides are doing, what glucose control looks like, whether someone's insulin management is poor, Whether they are inflamed, whether their blood pressure is high, or whether they are metabolically healthy. So total cholesterol can be interesting, but on its own it's not especially useful. Now, Several large observational studies have shown that the relationship between cholesterol and mortality is far more complex than the usual simplistic story. A large Korean prospective cohort study followed around 12.8 million adults and found a U-shaped relationship between total cholesterol and all-cause mortality. In other words, very low cholesterol was not necessarily associated with the best outcomes. The lowest mortality range was generally around two hundred ten to two hundred forty nine milligrams per deciliter, although this did vary by age and sex. A Norwegian population study also questioned the idea of using cholesterol as a simple mortality risk marker. The relationship between cholesterol and death was not straightforward, and in some groups lower cholesterol was associated with higher death rates. Then there was a twenty sixteen systematic review in BMJ, the British Medical Journal, looking at LDL cholesterol in people over sixty. It found either no association or an inverse association between LDL cholesterol and mortality in most of the included cohorts. Alright, what's that in plain English? In plain English, many older people with higher LDL appeared to live as long or longer than than those with lower LDL. Now that does not prove cholesterol is protective in every situation and it does not mean cardiovascular risk in inverted commas should be ignored. But it does tell us that cholesterol markers need to be interpreted carefully, not emotionally. Now next on the lipid panel we have triglycerides. Triglycerides are a transport and storage form of fat. They are not automatically a problem. They are part of normal energy metabolism. But fasting triglycerides are extremely useful because they often tell us something about the metabolic state of the person. When triglycerides are persistently high, especially when this occurs alongside low HDL or raised glucose, raised fructisamine, fatty liver tendencies or central weight gain or high blood pressure, that is a very important pattern. It can suggest poor insulin management, poor carbohydrate tolerance, and Liver fat accumulation, increased VLDL production, alcohol effects, ultra processed food intake, or a body that is simply struggling to manage incoming energy. And this is where joined up thinking matters. When looking at blood results, and this is important, interpreting bloods in the context of a carnivore or ketogenic or low carb way of eating is crucial. A person eating a high carbohydrate, ultra processed diet and running mainly on glucose may show a very different lipid pattern pattern. From someone eating very low carbohydrate and running mainly on fat. The fuel system has changed, so the blood results may change too. This is why we cannot just take one number, rip it out of context, wave it around like a parking ticket, and declare the whole person is unhealthy. Now, HDL on the standard lipid panel is usually reported as HDLC, meaning the amount of cholesterol being carried within these HDL particles. Now, HDL particles are involved in reverse cholesterol transport, which means they help move cholesterol from tissues back towards the liver for recycling or excretion through bile. But HDL does more than that. It is involved in immune signalling, antioxidant activity, repair mechanisms, and lipid transport. So low HDL often appears as part of the same metabolic pattern as high triglycerides. That combination is commonly seen in Poor insulin management, type 2 diabetics with fatty liver and poor carbohydrate tolerance. So when we see high triglycerides and low HDL together, we should not view them as two random numbers that happen to be sitting near each other on a blood test. We should view them as a metabolic fingerprint. Next we have LDL cholesterol or LDLC. LDLC tells us much how much cholesterol is being carried inside LDL particles. It does not tell us how many LDL particles there are. It does not tell us whether these particles are large or small, or whether they're damaged or oxidized or glycated. It does not tell us the person has poor insulin management or high blood pressure or vascular injury or inflammation or poor glucose control or a clotting tendency. And this is one of the biggest problems with obsessing over LDLC alone. LDLC is one marker, it's not the whole story. Raised LDL in someone with high triglycerides, low HDL, poor glucose control, raised fructosamine, fatty liver markers, high blood pressure and inflammation may mean something very different from raised LDL in a lean, metabolically healthy person eating keto or carnivore with low triglycerides, strong HDL, excellent glucose markers, good blood pressure, and no signs of metabolic dysfunction. Same LDL number, very different person, very different interpretation. And this is why LDLC alone is a poor predictor. It's too blunt. It is a bit like judging the quality of a restaurant by counting how many plates are in the kitchen. It tells you something perhaps, but it does not tell you whether the food is any good, whether the chef knows what they're doing, whether the building's on fire, or whether the waiter has just dropped soup into someone's handbag. You need the wider picture. Now VLDO is also worth understanding. VLDO stands for very low density lipid protein. VLDL is produced by the liver and is mainly used to transport triglycerides from the liver out to the tissues. So if triglycerides are high, VLDL production is often part of that story. In simple terms, VLDL is one of the body's ways of moving triglyceride energy around. As VLDL particles travel through the bloodstream, they deliver triglycerides to tissues. As they lose triglyceride cargo, they become smaller and denser, and they become IDL. IDL is the intermediate density lipoprotein. It is a sort of transitional particle. It sits between VLDL and LDL in the lipoprotein life cycle. IDL can be taken back up by the liver or it could be remodeled further into LDL. So LDL does not just appear out of nowhere. It is part of a dynamic transport system. The liver sends out VLDL, it the VLDL delivers triglycerides. VLDL becomes IDL, IDL can become LDL. I mean that's the basic flow. And this is why triglycerides matter so much. If someone has poor insulin management or fatty liver, is producing or overproducing triglycerides or has poor carbohydrate tolerance, then the liver may be producing more triglyceride rich VLDL and that can then influence the entire lipoprotein transport system downstream. And this brings us to one of the most useful markers on the standard lipid panel, and that is the triglyceride to HDL ratio. The triglyceride to HDL ratio is very simple. You divide triglycerides by HDL. So in UK units, millivolts per litre, if triglycerides are 0.8 and HDL is 1.6, the ratio is 0.5. That is generally a strong-looking pattern. Now if triglycerides are 2.4, And the HDL is one, the ratio is 2.4, and that is a very different picture. Now in the US, the measurements are milligrams per deciliter. Now the calculation is still triglycerides divided by HDL, but the numbers look different because the units are different. As a rough guide, in millimoles per litre, I generally like to see the triglyceride to HDL ratio below one. Between one and two, I would want to look carefully at the whole picture. Above two, I would be asking more serious questions about insulin management, carbohydrate tolerance, fatty liver, alcohol intake, ultra processed food intake, sleep, stress, thyroid function, medication use and overall metabolic health. Now, in milligrams per deciliter, under about two tends to look strong, and between two and four is worth investigating, and above four often suggests a more concerning metabolic pattern that we just spoke about. Now these are not diagnostic cutoffs, they are practical. Pattern recognition tools. And that is what blood testing should be pattern recognition, not number worship. The triglyceride to HDL ratio is useful because it gives us a window into the metabolic health. When triglycerides are low and HDL is higher, that often suggests better insulin management, better fat metabolism, better glucose handling, and better metabolic flexibility. But when triglycerides are high and LDL is low. The oppos the opposite is often true. It suggests the body may be struggling with energy processing. It suggests carbohydrate intolerance, increased triglyceride rich VLDL production, fatty liver tendency and metabolic dysfunction. And that is exactly the metabolic environment where cardiovascular risk tends to rise. This is why I often find the triglyceride to HDL ratio more useful than LDL cholesterol on its own. In fact, in many cases I think it can be more useful as a starting point than even advanced particle testing or LDL fraction testing. Not because particle testing is useless, can be useful, but because the triglyceride to HDL ratio tells us something about the terrain. Imagine a river system. LDL C tells you how much cargo is floating in one type of boat. Apo B or LDL particle numbers just tells you how many boats there are. Subfractions tell you whether those boats are large barges or small speed boats, but triglyceride and HDL together give us a clue about the condition of the river itself. Is the river flowing smoothly or is it full of debris, of flooding or sewage, and someone trying to paddle upstream in a shopping trolley? The underlying environment matters because damaged environments create damaged outcomes. Several studies support the importance of this pattern. In men with conventional risk factors for ischemic heart disease, those with low triglycerides combined with higher HDL appear to have much lower risk in inverted commas. Another study found that ischemic ECG changes were more predictive for phatoeschemic heart disease when they occurred alongside high triglycerides and low HDL. And in elderly women, triglycerides and HDL were independent predictors of coronary heart disease. Mortality with the combination of high triglycerides and low HDL being associated with a much higher risk in inverted commas pattern. So again, it is the pattern that matters, not one isolated number. Now let's talk about particle counts because once we've moved beyond the standard lipid panel, we get into more advanced testing. LDLC tells us the amount of cholesterol inside LDL particles, but LDL particle number, often called LDLP, tells us how many LDL particles are present. These are not the same thing. You could have fewer particles carrying more cholesterol each, or you could have more particles carrying less cholesterol each. That is why LDL-C and LDL particle numbers can sometimes disagree. Apo B is another useful marker here. Apo B or Apolipoprotein B is a structural protein found on VLDL, IDL, LDL and LP Litlay particles. Each of these particles generally carries one Apo B marker, which can give us an estimate of the amount of ApoB containing particles that are in circulation. If LDLC is like measuring how much luggage is being transported, Apo B is more like counting the number of taxis carrying luggage through towns. So that can be useful because from a conventional cardiovascular risk perspective, more Apo B containing particles may mean more particles interacting with the artery wall. But again, context matters. Apo B tells us particle number, but it does not does not tell us why particle number is high. It does not tell us whether the person has poor insulin management, whether triglycerides are high, whether glucose is damaging proteins through glycation, whether blood pressure is damaging the vascular wall, or whether inflammation or clotting activity or endothelial injury are part of the picture. So APAB is useful, but it is still not the whole story. Then we have LDL subfractions. You may hear about large buoyant LDL and small dense LDL. Small dense LDL is often considered more concerning because it is commonly associated with poor insulin management, high triglycerides, low HDL, and metabolic dysfunction. Is there a theme coming here? Can you see? But this is important because small dense LDL is often not the original problem. It may be a downstream sign of the metabolic environment. When triglycerides are high, VLDL production is high, HDL is low and glucose control is poor. The lipoprotein system can become remodeled in a way that leads to smaller, denser LDL particles. So if someone has a high triglyceride to HDL ratio, you can often predict that their particle pattern may not be ideal. That is one of the reasons the triglyceride to HDL ratio is so useful. Gives you a simple marker that often predicts and reflects what the advanced tests will later confirm. But again it's not perfect, but it is practical. Then we have oxidized LDL and glycated LDL. These are damaged forms of LDL. Oxidization refers to damage from oxidative stress and glycation refers to sugar related damage, where glucose binds to proteins and lipoproteins in a way that can impair normal function. This is one of the reasons glucose control matters so much. If someone has raised glucose or raised fluctosamine or blood sugar spikes, poor insulin management and inflammation, then Lipoproteins are travelling through a much more hostile metabolic environment. They are more likely to become damaged and damaged particles may behave very differently from healthy transport particles. This is why I always want to see glucose markers alongside lipids. Now some people use HBA1C here, but I find that reading a little unreliable and prefer a fructosamine assay because fructosamine reflects roughly the previous three weeks of someone's lifestyle. That can be extremely useful when someone has recently changed their diet, move towards keto or carnivore, reduced carbohydrates, lost weight, or improve their metabolic health. HBA1C may give us one window, but fructosamine often gives us a much more useful short term picture. Together with fasting glucose and the wider clinical context, it can help us understand what is happening now rather than relying too heavily on a single long term marker. Now, we also need to discuss LP little A. LP little A is an LDL-like particle with an additional protein attached called apolipropriatein A. LP litl A is strongly genetically influenced and it is often discussed in relation to cardiovascular risk, but it is not just another cardiovascular risk cholesterol marker. LPA may be linked to clotting biology, vascular repair, and wound healing processes. The extra apolipoprotein A component has structural similarities to plasminogen, which is involved in clot breakdown. That is one reason LP little A is often discussed in relation to clotting and repair. So LP little A may be particularly relevant when we think about cardiovascular disease, not just as a cholesterol problem, but as a vascular injury clotting and repair problem. Which brings us neatly to plaque formation because one of the biggest misunderstandings in cardiovascular disease is the idea that plaque is just cholesterol clogging an artery like lard blocking a drain. That is far too simplistic. Arteries are not pipes, they are living responsive tissue. They contain endothelial cells, smooth muscle cells, immune cells, collagen, extracellular matrix, clotting activity, repair mechanisms, and their own tiny blood supply. Aphrosclerotic disease. Plaque is much better understood as part of a complex process involving vascular injury, disturbed blood flow, high pressure, inflammation, clotting, immune cell activity, tissue repair, calcification, and scar formation. From a thrombotic perspective, plaque development is heavily linked to clotting and repair processes inside the artery wall. And this is where the vasovesaurum become very interesting. The Vasovisorum are the tiny blood vessels that supply the walls of larger arteries. If these tiny vessels become damaged or dysfunctional, they may contribute to bleeding, to tissue injury, to inflammation and repair activity within the artery wall itself. This gives us a very different way of thinking about plaque. Instead of imagining cholesterol drifting around and sticking to the inside of an artery like candle wax, we can think of plaque more like a messy repair site inside. a living tissue. It involves clotting, immune cells, inflammation, smooth muscle cells, collagen, calcium and lipoproteins. Lipoproteins may not simply be causing the problem, they may also be arriving as part of the repair process, bringing cholesterol and lipid soluble materials needed for cell membranes, healing and reconstruction. So a plaque is not just a blob of cholesterol, it is more like a scarred, calcified, clot related repair patch inside the artery wall. And if we want to understand why that repair patch formed, we need to ask better questions. We need to ask whether high blood pressure has been damaging the vessel wall, whether poor glucose control has been causing glycation, whether insulin management is part of the picture, whether oxidative stress and chronic inflammation are present, whether there is a clotting tendency, whether the vasovosaurum are involved, and whether Disturbed blood flow or smoking or poor sleep or stress or infection or autoimmune activity or nutrient deficiencies may be contributing to this vascular injury. And those questions matter far more than simply shouting at LDL like it has been caught stealing biscuits. So let's bring this back to practical interpretation. When I look at a lipid panel, I do not want to see one isolated number. I want to see the pattern. I want to know whether triglycerides are high or low, what HDL is doing. what the triglyceride to HDL ratio looks like and whether LDLC fits with the rest of the metabolic picture. If FOB has been tested, I want to know what if what it suggests about particle number. If LPA l or sorry, LP little A has been tested, I want to know whether there may be an inherited clottingovascular repair component to consider. But I also want to see the non lipid markers, because They are just as important. I want to know what fasting glucose looks like, fasting insulin, what fructosamine is showing, what blood pressure is doing, whether liver markers suggest fatty liver or metabolic stress, whether thyroid function is relevant, whether inflammatory markers are raised, and whether the person's body composition, diet and clinical history fit the pattern we are seeing. In other words, I want to interpret the blood results in the context of the actual person. Are they eating a high carbohydrate, ultra-processed diet and showing signs of metabolic dysfunction? Or are they eating low carb keto or carnivore, using fat as a primary fuel source, improving glucose control, reducing their waste circumference, improving blood pressure and reversing signs of carbohydrate intolerance? And that difference is enormous. Let's use two examples. Person one has LDLC of 180 milligrams per deciliter. Triglycerides of 70 mg per deciliter and HDL of 70 mg per deciliter. Normal blood pressure, normal fasting glucose, good fructosamine, normal liver markers, low waist circumference, and no signs of fatty liver. And person 2 has LDLC of 110 mg per deciliter, triglycerides of 220 mg per deciliter, HDL of 35 mg per deciliter. raised blood pressure, raised fasting glucose, raised fructosamine, fatty liver markers, and central obesity. If we only look at LDLC, we might panic about person one and relax about person two. But metabolically that would be the wrong way round. P person two has the classic pattern associated with poor insulin management and higher cardiovascular risk. Person one has a much stronger metabolic picture despite higher LDLC. And this is why LDL cholesterol alone can be so misleading and it is why the triglyceride to HDL ratio is a lot more valuable. It helps us see the metabolic context. It helps us understand whether we are looking at a fuel handling problem. It gives us clues about insulin management and carbohydrate tolerance and fatty liver tendency and metabolic flexibility. It also often helps us make sense of why more advanced markers such as Apo B, LDL particle numbers, and LDL subfractions may look the way they do. So if you're looking at a lipid panel, do not start to panic. Start with physiology. Cholesterol is essential. Lipoproteins are transport particles. Triglycerides are transportable fat fuel. VLDL carries triglycerides away from the liver. IDL is a transitional particle. LDL carries cholesterol and other lipid soluble materials to tissues. HDL is involved in transport, recycling, immune function, and repair. Apo B gives an estimate of the number of Apo B containing particles. LP little A may relate to inherited cardiovascular risk patterns and maybe clotting and vascular repair and plaque is not simply cholesterol blocking a pipe. It is part of a complex process involving vascular injury, clotting, inflammation and repair. The triglyceride to HDL ratio is one of the simplest and most useful markers for understanding the metabolic terrain. And that is the key phrase, metabolic terrain. Disease does not happen in a vacuum. Lifer proteins travel through an environment. If that environment is low glucose, well managed from an insulin perspective, low inflammatory, with good blood pressure, good nutrient status, and good metabolic health, that is one situation. If that environment is high glucose, poorly managed from an insulin perspective, inflamed Hypertensive, oxidative, fatty liver prone, and metabolically chaotic, that is another situation entirely. Same lipoprotein name, different biological setting, different interpretation. So the next time someone points a LDL cholesterol on a blood test and acts as though the entire mystery of cardiovascular disease has been solved. Remember this. The lipid panel is not a verdict, it is a conversation. It is asking us to think about transport, fuel metabolism, glucose control. Vascular health, clotting, repair, and the wider clinical picture. The best interpretation comes from patterns, not panic. If we are serious about understanding lipids, we have to move beyond single number thinking. We need to stop treating cholesterol like a cartoon villain in a cape and start understanding lipoproteins as part of a dynamic transport and repair system. That means looking at triglycerides and HDL as metabodic clues. It means using Apo B, LP little A, particle count and subfractions. When they genuinely add some value. And most importantly, it means interpreting blood results in the context of the person sitting in front of us. Not just cholesterol number, but their diet, glucose control, insulin management, blood pressure, liver health, thyroid function, body composition, symptoms, history, lifestyle, and actual biology. Because the body is not trying to confuse us, it's giving us signals. We just have to learn how to read them properly. And once you start seeing the lipid panel this way, it becomes much less frightening and much more useful. It becomes less about panic and more about pattern recognition, less about cholesterol theatre and more about physiology. And on that note, thank you for listening. I hope if you did like it, please consider liking, sharing, and subscribing. I'll be back.