Latest / Common Sense Health / Don't Believe the Hype: The Truth About LDL Cholesterol and Heart Health
Transcript
- Stephen Thomas BSc. Hons: Hello. This article comes from a recent podcast interview with Dr. Anthony Jay. And if you've ever been told your LDL is too high, then handed a statin leaflet and given that solemn GP face usually reserved for lottery winners who forgot to buy a ticket, this one is for you. We got into cholesterol, LDL, statins, heart disease, insulin resistance, which I prefer to call carbohydrate toxicity. CSE scores, pharma influence and the curious modern habit of turning apparently healthy people into patients by changing the numbers on a spreadsheet. And I do mean just simply changing the numbers because one of the key points Dr. Anthony J. made early in the interview was this. The definition of high cholesterol has not remained fixed. It has been repeatedly lowered over time. According to Anthony, before statins entered the picture, Total cholesterol above 300 milligrams per deciliter was considered high. Then that threshold was lowered to 240 and then 200. Then when total cholesterol had already been pushed low enough, the focus shifted more aggressively towards LDL. Convenient really, isn't it? Almost as if the goalposts were not so much moved as packed into a van, driven three counters away and reinstalled outside a statin factory. Now, of course, the official story is that this was all done to save lives. That's the line. Lower cholesterol, lower LDL, reduce risk, job done. But this is where the conversation became much more interesting because LDL is not cholesterol. LDL is a lipoprotein particle. It transports lipids, cholesterol, fat soluble nutrients and other substances around the body. Cholesterol itself is a molecule. It is present in different lipoproteins, including LDL, HDL, IDL and VLDL. When people say LDL cholesterol, we already have slightly muddled that phrase. It is not quite as simple as saying LDL is some kind of free floating villain roaming the bloodstream with a tiny black cape and a bag marked artery damaged. Your body makes LDL. You need it. You cannot live without it. So the question should not be how low can we force LDL? The better question is What is actually damaging the arteries in the first place? I mean, that is the nub of it. And in the interview, Anthony made the point that the artery matters. If LDL were inherently destructive, why would we not see the same problems everywhere? Why not in the veins? Why is it the arterial environment that's so important? And that takes us away from the cartoon version of cardiovascular disease and towards a more useful conversation. Arterial damage, blood pressure, insulin resistance, like I say, carbohydrate toxicity, inflammation, metabolic dysfunction, clotting, plaque formation and repair mechanisms. In other words, the whole context. The context is the thing that tends to get thrown out of the window when medicine becomes a numbers game. A person walks in feeling well, eating well, improving their weight, reversing markers of metabolic disease, normalizing blood glucose, dropping triglycerides, improving their energy. And then one tiny number on the lipid panel flashes up in red and suddenly everyone panics. It's a lab report whack-a-mole. But if we're going to talk about cardiovascular risk, surely we should be asking which markers are actually associated most strongly with events such as heart attacks and deaths from coronary artery disease. Anthony referred to a study involving around 28,000 people and we looked at actual heart disease outcomes. His point was that insulin resistance came out as the major risk factor with a hazard ratio around 6.4, hypertension came next at around 2.3, triglycerides are also high on the list and As he said, triglycerides tend to track strongly with insulin resistance, which I call carbohydrate toxicity. Now, LDL by comparison was described as being much lower down the risk list with a hazard ratio around 1.38. Now, people can make 1.38 sound frightening if they want to. A 38 % increase, they might cry while clutching their pulls and reaching for their prescription pad. But when insulin resistance is sitting there at 6%, point for ignoring it while obsessing over LDL is like worrying about a squeaky garden gate while the house is on fire. And that was one of the strongest educational points from the interview. If someone has high triglycerides, high fasting insulin, raised blood glucose, abdominal fat, fatty liver, hypertension, low metabolic flexibility and a diet built around refined carbs. seed oils and ultra processed foods, then there is a very real cardiovascular conversation to be had. But if someone is eating low carb ketogenic or carnival has low triglycerides, good glycemic control, stable energy, reduced inflammation, improved waste circumference and a slightly seen this LDL rise in the context of that adaptation. You know, that is a different physiological picture, isn't it? So. When we're interpreting blood in the context of carnivore or ketogenic way of eating, this context is crucial. This does not mean ignore everything. It means stop pretending that one marker viewed in isolation tells the whole story. One of the biggest problems in modern medicine is that reference ranges often become more of a moral judgment. You are even normal or abnormal, but reference ranges are not commandments from Mount Sinai. They are statistical tools and they can be changed. Anthony made the point that this happened not only with cholesterol, but also with familiar hypocalesterolemia. The definition is there. He mentioned Brown and Goldstein's work where familiar hypocalesterolemia was historically described as extremely high levels around 740 milligrams per deciliter or approximately 19 millimoles per liter. and contrasted that with how modern definitions have broadened over time, especially with genetic variants and LDL focused thresholds. And that broadening matters because if you keep lowering the threshold for a disease, you create more patients. And when the standard response to that new label is a lifelong medication, we are allowed, in fact, we're morally obliged to, ask who benefits? And Anthony was very direct about the role of the American Heart Association. He claimed the AHA was involved in lowering cholesterol thresholds and noted that it received very large sums from pharmaceutical and medical device companies. In the transcript to the video, you can see that he stated figures of around seven, sorry, $70 million per year. And he also referred to a 12 year study suggesting an average of something like 61 US dollars from biotech and pharma companies. Now, regardless of where someone sits on the cholesterol debate, it should matter to everyone because financial influence does not automatically prove that a recommendation is wrong. But it absolutely means we should be alert to any bias. If a biscuit company founded a national guideline on breakfast, we would all be suspicious when the conclusion was eat more biscuits. Yet when pharmaceutical money sits behind organizations influencing the drug-centered guidelines, we are told to be mature, stop asking awkward questions and take the medicine. No thank you. Awkward questions are often the healthiest ones. Then we moved on to statins. Now, Anthony did not exactly sit on the fence here either. In fact, I'm not sure he was in exactly the same county as the fence. His view was that statins are vastly over promoted, that the benefits are often exaggerated. and that the downsides are frequently under discussed. One of the key issues was raised. That was the increase in diabetes risk. That point matters enormously because if insulin resistance is one of the biggest drivers of cardiovascular disease and if a medication increases the risk of diabetes in some people, then we cannot simply wave away that as an inconvenient footnote. Diabetes is not a minor administrative inconvenience. It is the body saying A of paperwork sort out, nothing to see here. No, diabetes, properly understood, is chronically elevated blood glucose or carbohydrate intolerance. It is a serious metabolic state with wide ranging implications for blood vessels and nerves and your kidneys and your eyes and energy production and cardiovascular risk overall. So if the cholesterol conversation pushes people towards a drug while ignoring insulin resistance, we have a problem, a very big problem. this is where we have to return to joined up thinking. If someone is metabolically unwell, the priority should be restoring metabolic health. That means looking at blood glucose, fasted insulin where available, HbA1c, triglycerides, waist circumference, blood pressure, inflammatory markers, liver enzymes, kidney markers, lifestyle, sleep, stress, alcohol intake and diet quality. By the way, when discussing HbA1c, I also think it's worth remembering the fructosamine assay because It reflects roughly the previous three weeks of someone's lifestyle rather than the longer period captured by HbA1c. That can be particularly useful when someone has recently changed their diet or is actively improving their metabolic health. This is the kind of detail that gets missed when health care becomes LDO high prescribed statin. Next patient, please. Ding. So, Antony also discussed the CAC scores, coronary artery calcium scores. And this was another important part of the conversation. The CAC scan looks at calcified plaque and he referenced the dose response relationship between higher CAC scores and higher rates of major coronary events. In simple terms, a CAC score of zero is generally associated with very low risk over the following years, while higher numbers, especially above a hundred and three hundred, show progressively greater risk in inverted commas. But he also made a very important practical point. Very low CAC scores, such as 5 or 7, 10 or 20, can be affected by noise in the machine. In his view, tiny scores like that are often functionally close to zero. That does not mean people should ignore the results. It means people should not be terrified by tiny numbers without understanding the scale, the context and the measurement variability. Because a CAC score is not a percentage blockage. A score of 20 does not mean 20 % of your data is a block. Yet plenty of people hear a number like that and immediately imagine their arteries are like old plumbing in a student house. The panic begins, the statin discussion starts and once again fear becomes the sales assistant. This is not how health care should work. mean, people need education. They don't need this intimidation. We also touched on the strange modern attempt to reframe hard plaques as somehow protective. Anthony challenged that idea strongly, pointing to evidence that Higher coronary artery calcification is associated with higher risk of major coronary event. Now, there is a nuance here. Plaque biology is complex. Soft plaque, calcified plaque, plaque stability, endothelial health, clotting, inflammation, blood pressure and metabolic health all matter. But the broader point remains, pretending calcification is automatically good is far too simplistic. And that brings us back to the central message of the whole interview. LDL is not the whole story. It was never the whole story. The mainstream model often presents this cardiovascular disease as if it is largely a story of LDL particles crashing into arteries and causing chaos. But that model leaves too many questions unanswered. Why arteries more than veins? Why the strong relationship with insulin resistance? Why the role of hypertension? Why triglycerides? Why smoking, stress, sleep, alcohol, clotting, inflammation and metabolic dysfunction? Why do they play a role? And why, after decades of cholesterol lowering obsession, are we still surrounded by metabolic disease? Perhaps because we have been staring at the wrong part of the map. It is not that LDL is irrelevant in every context. That would be too simplistic as well. But making LDL the supreme villain has allowed far too many people to ignore the bigger terrain. Insulin resistance, or as I say, carbohydrates, toxicity is significant. Blood pressure is important. Triglycerides are relevant. Glycemic control is crucial. Inflammation plays a role. Smoking obviously is detrimental. Sleep is vital. Stress is impactful and body composition is essential. Food quality. I mean, that's critical. And yes, this context matters, especially in people eating low carb, ketogenic or carnivore diets. Someone thriving on a ketogenic or carnival way of eating may present with a lipid pattern that looks different from someone eating a standard high carbohydrate ultra-processed diet. That does not mean we ignore the numbers. It means we interpret them intelligently. A high LDL in the context of high triglycerides, high HbA1c, high fasting insulin, hypertension and central obesity is not the same conversation as high LDL with low triglycerides and excellent glucose control. low inflammation and robust metabolic health. The problem is that many conventional systems do not make that distinction. So they see LDL. That's what they see. They see red. They reach for the script and the patient is often left frightened, confused and feeling as though all their health improvements have somehow been invalidated by this one marker. And that's not medicine. That is spreadsheet theatre. The hard-hitting point from this interview is this. People deserve better than fear-based cholesterol reduction. Patients deserve a proper conversation about cardiovascular risk. They need to understand that LDL is a transport particle, not simply a death sentence. Just as they must grasp the realities of carbohydrate toxicity, it is vital for them to know that triglycerides offer powerful health clues. and that blood pressure is never just a trivial detail. Furthermore, individuals have a right to understand what a CAC score can and cannot tell them, alongside the potential downsides of statins, including the risks of diabetes. Now, finally, public health messages must be delivered with total transparency regarding the organisational financial conflicts of interest. And they deserve transparency about financial conflicts of interest. in the organisations that shape public health messages. This does not mean rejecting all medicine, does not mean ignoring risk, and it does not mean telling everyone to do the same thing. It just means returning to common sense. If the house is smoking, find the fire. Don't spend all day polishing the smoke alarm. For many people, the fire is insulin resistance, like I said, carbohydrate intolerance. And this is where low carb, ketogenic and carnivore approaches can be so powerful. They directly address the thing mainstream conversations. often dance around carbohydrate intolerance, chronically elevated blood glucose, high levels of insulin, fat storage, high triglycerides, fatty liver and metabolic dysfunction. When those markers improve, the person has not become less healthy because LDL has moved up. They may well have become more metabolic, metabolic resilient. Again, the key is context. A blood test is not a personality test, it is not a moral verdict, it is a set of clues, but the clues need interpretation. This is why I keep saying that blood results should be assessed as a pattern, not as an isolated number. LDL, HDL, triglycerides, HbA1c, fructosamine, say probably better, fasted insulin, liver markers, kidney markers, inflammatory markers, thyroid markers, iron status, they all sit within a broader physiological story. For instance, when looking at kidney function, EGFR can be useful, but a cyst statin C tends to give a more accurate assessment, particularly when muscle mass or dietary context may influence the level of creatinine, which has a knock on effect. When looking at the thyroid markers, especially T3, we also have to remember dietary context. On a low carb diet, there may be a lower requirement for T3 because there is less reliance on glycolysis. T3 has a relationship with pyruvate metabolism, so reduced carbohydrate flux can change the picture, although a T3 is not automatically a thyroid disaster in someone who is otherwise thriving, or warm, or energetic and metabolically stable. This is the same principle again and again. I'm always talking about context, context, context. If you eat steak and eggs, lose weight, reverse type 2 diabetes, reduce hunger, improve energy, lower your triglycerides, improve your blood pressure, reduce inflammation and then get told off because you're LDL rose, you are allowed to ask whether the model being used to judge you is fit for purpose. And if the answer is, well, the guideline just says so, then perhaps the guideline deserves a harder stare, maybe even two hard stares and a raised eyebrow. Because as Anthony made clear in the interview, There has been a long history of shifting definitions, powerful institutions, drug centred thinking and selective focus. And that should not make us cynical about everything, but it should make us a little bit more careful. Health is not achieved by chasing one number ever lower. Health is achieved by understanding the body as a system. The artery is not a passive pipe. Plaque is not a random cholesterol spillage. LDL is not a cartoon villain. Statins are not a free lunch. Guidelines are not sacred texts and metabolic disease cannot be solved by ignoring metabolism. And that for me was the strength of the conversation with Dr. Anthony Jay. It was not just another cholesterol chat. It was a challenge to think more deeply, to ask more questions and to stop outsourcing common sense to a committee and to remember that the body usually gives us patterns, not isolated headlines. So If your LDL has been waved in your face like a parking fine, take a breath. Look at the bigger picture. What are your triglycerides doing? What is your blood glucose doing? What does your HbA1c show us? What was your blood pressure when you had your blood taken? What is your CAC score, if appropriate? What is your inflammatory picture? What is your blood glucose control? How is your waist circumference? How do you feel? I mean, that's a Great question. How are you sleeping? That's another one. Are you metabolically healthier than you were six months ago? Because those questions matter. They may matter far more than whether your LDL has offended a reference range that keeps getting revised downwards like a supermarket special offer in reverse. The cholesterol conversation is not going away, nor should it, but it desperately needs more honesty, more nuance and more physiology and perhaps a little less panic. After all, if fear were medicine, we would be the healthiest society in human history. Clearly we're not. Anyway, I'll be back. by the way, if you like more common sense support around carnivore, keto fasting, blood tests, weight loss, metabolic health and all that, these little things do actually matter. You can join my common sense carnivore community online. There's a link in the description. And if you'd like more personal help, you can also book a one to one consultation with me. And again, there's links in the description. And if you're ready, to use fasting properly without making it weird or miserable or turning into a competitive starvation event. You can join my fasting challenge. I run one every single month, the first Monday of every month. Link in the description. And if you want a structured program to help you reset your appetite, improve your metabolic health, simplify your food and get you back in control, you could join my metabolic reset program. Again, there's a link in the description to help you find out all about that. Thanks for watching. Do consider liking, sharing and subscribing. See you on the next one.