Latest / Common Sense Health / Don't Panic About Fasting Insulin: Here's What It Really Means
Transcript
- Stephen Thomas BSc. Hons: Hello and today's episode I'm calling the fasting insulin panic, how a low carb success story got mistaken for a problem. So let's go. There is a strange little panic during the rounds in the low carbon carnivore world. Someone gets their blood stun, their glucose is low or beautifully controlled, their inflammation markers are low, their triglycerides are low, their energy is good, and their waste is smaller or their appetite is stable. They are no longer riding the blood. Sugar roller coaster like a caffeinated squirrel on a trampoline. But then they see it. Fasted insulin, low. And cue that dramatic music. Suddenly, what could be a sign of metabolic improvement is being interpreted as a disaster. Your pancreas is shutting down. you have insulin suppression. You've lost your metabolic flexibility. You need to eat carbs to wake up your beta cells and get them back up to working. And just like that, a person who has improved their health starts worrying because their fasted insulin is doing exactly what fasted insulin is supposed to do. And it does it in a low glucose, low inflammatory, low carbohydrate environment. It's staying low. And the clue is in the word fasted. This is the part people keep skipping over. And fasting insulin test is not asking how much insulin can your pancreas produce. It is asking something much narrower. How much insulin is circulating while you are fasted? And that distinction matters enormously. If you have not eaten, if your blood glucose is stable, if your liver is not dumping huge amounts of glucose into circulation, if your body is not inflamed or stressed or sleep-deprived or insulin-resistant in inverted commas or drowning in processed carbohydrates, why would insulin need to be higher? Insulin is not meant to sit around waving at the camera just to make your lab report look reassuring. It has a job. If there is less glucose coming in, less need to store excess energy and less metabolic chaos to manage, then a lower fasting insulin can be entirely appropriate. The panic often comes from treating fasting insulin as though it is a beta cell capacity test, and it's not. It is a fasting snapshot. The insulin suppression story is ridiculous. I mean the theory goes something like this if you eat low carb or carnivore for long enough, your insulin gets suppressed. Your pancreas forgets how to produce it and you lose metabolic flexibility. And they can make it sound scientific enough to frighten people, but in many cases it is just a misunderstanding of context. A person eating very low carb will often have much lower glucose exposure, lower insulin demand, lower glycogen turnover, lower triglycerides, lower inflammatory burden, improved appetite control, reduced need for constant glucose disposal. So when that person takes a fasted insulin test, the result may be low. That does not automatically mean poor beta cell function. It may simply mean the pancreas is not being asked to produce much insulin at that moment. This is not witchcraft, this is basic physiology. Or to put it another way, if the fire is out, you do not criticize the fire brigade for not spraying water through the windows. I have a real world example here. Here is a perfect example. One person had genuinely fasted insulin a result of 1.6%. Micro international units per millilitre, where the reference range is 2.6 to 24.9. Well, that was flagged as low. The C peptide was also significantly below the lab's reference range. The C peptide, just for people who want to know, is 1.03 nanograms per milliliter, and the reference range is 1.1 to 4.4. Now, naturally, this could make someone worry if they were looking only at the red letter L beside the result. But then this same person did something rather clever. Before another insulin test, he ate. In his words, he had one pound of ribeye. Two hours later, his insulin was 10.9 international units per millilitre. Well, this was comfortably inside the lab's in control range of 2.6 to 24.9. now strictly speaking that second result was not a fasting insulin. It was an insulin response after food. But that is precisely the point. When actually fasted, insulin was low. When stimulated by food, insulin rose. That is not necessarily a broken pancreas. That looks far more like a system responding appropriately to context. Low insulin when fasted is not the same as no insulin response. And this is where many people get muddled. A low fasting insulin result does not prove that you cannot produce insulin. It only shows that at the fasting moment insulin output was low. If someone is worried about whether their pancreas can respond when challenged, then a fasting test is not the best tool for the question. A better question would be what happens to insulin and sea peptide after stimulation? And that can be assessed in several ways. Apart from what my my person did, you could do an official mixed meal tolerance test or an insulin and se peptide measured after food test, a glucose stimulated test, a glycogen stimulated C peptide test. More advanced research methods such as CLEMP studies are often used. But for practical purposes, the simplest informal version is exactly what This person did. Eat a meaningful meal, then measure the response. Now, a warning, obviously, if you eat before a test that is supposed to be fasted, you will invalidate all the other fasting markers. Glucose, triglycerides, insulin, C peptide, and other results may all be affected, which is the point when we're looking at insulin. So this should not be done casually as part of a full-fasted blood panel, unless the goal is specifically to observe an insulin response to food. In other words, Do not accidentally ruin a fasting panel. If you are testing stimulation, test stimulation deliberately. And the protein part of this matters too. Another missing piece in this debate is just protein. Many low carbon carnivore eaters are not just reducing carbohydrate, they are often eating decent amounts of protein. And protein can stimulate insulin. And that's normal. It is also not a problem by itself. Insulin is not merely a blood sugar hormone. It is involved in amino acid handling and protein metabolism and electrolyte balance and energy storage and tissue signaling. So the idea that a meat-based diet creates total insulin dormacy is it's just not very joined up thinking or anyway, it's not a way to look at physiology. A ribeye steak may not behave like a bowl of cereal, but it is it is food. It still produces digestive, hormonal, and metabolic responses. That is exactly what the 10.9 insulin result after that ribeye demonstrates. The reference range trap is another thing that we need to talk about because most people see a reference range and assume it means inside the range is healthy, outside the range is unhealthy. That is not always true. For many lab tests, the reference interval is built around a population. In simple terms, labs often use a central range that captures around 95% of the reference group. That means about 2.5% may fall below and 2.5% may fall above. And this is the holy grail of health problem. Well, you know, basically imagine a bell curve. In the middle, you have the central 95%. That becomes the lab's reference interval. But the outer edges do not automatically mean disease. They mean the result is less common compared with the reference population. So if your fasting insulin is below the range, the first question should not be what disease do I have. It should be does this result make sense in my actual context? And that context includes what you ate in the days before, whether you were truly fasted, your glucose glucose, your HBA1C if you want that, but ideally fructose amine assays are better, your triglycerides, your waste circumference, your symptoms, your medication history, recent weight loss, inflammation, stress, sleep, yes. Your overall diet pattern, everything. And yeah, as I said, the HPA1C is not as good. Fructosamine assay deserves a mention because it reflects roughly the previous two to three weeks of glycemic exposure. I mean the HBA1C can be useful if you're a carb sort of driven person, but it's not perfect, especially when red blood cell lifespan or recent lifestyle change can affect that interpretation. You know, and reference ranges are not built around carnivore metabolism, are they? And that is the elephant in the laboratory. Most reference ranges are not built from a population of metabolically healthy, low-carb, ketogenic or carnivore eaters consuming adequate protein and living with low glucose variability. They are usually based on a broader population, often including people eating standard mixed diets. Depending on the test, the reference interval may come from assay manufacturers, published datasets, local lab verification, or other population-based methods. That does not make reference ranges useless, by the way, far from it, but it does mean they are not sacred tablets brought down from Mount Biochemistry. They are tools, useful tools, but tools that require interpretation. A low fasting insulin in a person eating a high carb diet with high glucose, weight loss and thirst and frequent urination and fatigue would raise a very different question from a low fasting insulin in a low carb diet. Person with low normal glucose, low triglyceride, stable energy, and improved metabolic markers. You get the same number, but you get completely different context. And that is a whole game. When low insulin might matter, just to be clear, this is not an argument for ignoring low insulin or low C peptide in every case. There are situations where low insulin and low C peptide may deserve a proper investigation, especially if it's accompanied by high fasted glucose. High post-mill glucose readings, unexplained weight loss, excessive thirst, frequent urination, fatigue, ketones in an inappropriate context, personal or family history or autoimmune disease, very low or declining C peptide over time, or suspicion of type 1 diabetes or LADA. In those cases, further testing may be sensible. That might include repeat glucose markers, C peptide, autoantibodies. stimulated testing and clinical review, but that is very different from scaring every low carb person because their fasted insulin is low. A low fasted insulin with excellent glucose control may be a sign of reduced demand for that insulin. A low fastet insulin with rising glucose and symptoms may be a sign of inadequate supply. So that context it separates the two. Metabolic flexibility is not proved by a fasted insulin result. One of the strangest claims is that low fast insulin proves you've lost metabolic flexibility, but metabolic flexibility means the ability to switch between fuels and respond appropriately to the changing conditions. Well a fast and insulin test does not measure that. If anything, someone who can run comfortably on fat derived energy, maintain that stable glucose, avoid sort of constant hunger, and then produce instant insulin appropriate. Appropriately, instantly, when food arrives, may actually be demonstrating rather good flexibility, which is what the case was there when I talked about the gentleman who did the test. So if you want to test a response, you need a response-based test. Using a fasting insulin result to prove less or loss of metabolic flexibility is like checking whether your oven works by looking at it while it's switched off. A more sensible interpretation. Let's have a look at that. Instead of saying your insulin is low, that's bad. A more intelligent interpretation would be your fasting insulin is low. What was your glucose? Were you genuinely fasted? What is your HBA1C? What is your fructose fructosamine assay? What are your triglycerides? What is your diet? Are you symptomatic? What happens after food? Does C peptide rise when you've stimulated it with food? And that's the joined up thinking. I'm always saying this the body is not a spreadsheet. It is a responsive system. Insulin should rise when needed and fall when not needed. A permanently high fasting insulin is often a sign the body is having to work hard just to keep glucose under control. A lower fastening insulin in the right context may reflect lower demand. So the simple takeaway is this. If your fasting insulin is low on a low carb, ketogenic, or carnivore diet, do not immediately assume disaster. Ask better questions. Firstly, was I truly fasted? If yes, Then low insulin may simply reflect low demand. It's not rocket science, is it? What was my glucose at the same time? Low insulin with controlled glucose is very different from low insulin with high glucose. What does my recent glycemic picture actually show? Like I say, HBA1C is useful, but fructosamine, as a test, can add a shorter term view of roughly two to three weeks, and that is better. Do you have any symptoms? Numbers, Without symptoms need careful interpretation. Symptoms plus abnormal numbers deserve more attention. And then get to am I asking the right question? If the concern is insulin response, consider a stimulated insulin and C peptide test rather than relying on a fasted value. Does the reference range fit my physiology? A standard range may not be built from people eating low carb keto or carnivore with adequate protein coming in. So, my final thoughts really are the insulin suppression panic is a is a perfect example of what happens when people worship the reference range but ignore the human being in front of them. A fasting insulin test is a fasting insulin test. It is not a crystal ball. A full beta cell function study or a certificate of metabolic flexibility, a fasting insulin test isn't that. Now, sometimes low insulin is not a problem. Sometimes that is the point. If your glucose is controlled, your inflammation is low, your energy is good, and your insulin rises when food arrives, the pancreas may not be asleep at the will. It may simply be doing something rare in modern life, responding appropriately. And if that confuses the lab range, perhaps the lab range needs a little context, or at least a decent stake and a sit-down. I'll be back.