If you’re a practitioner who sees people with normal glucose and A1c with elevated triglycerides, abdominal weight gain, fatty liver, blood pressure changes, or other metabolic clues, this episode will help you recognize when the numbers may warrant a closer look.
Dr Ritamarie
Have you ever looked at somebody’s lab results and thought something just isn’t adding up? Their fasting glucose looks relatively good, their A1C is within the normal range, but other things are out of balance. Their triglycerides may be elevated, or their waist circumference is increasing, and they’re trying everything and can’t lose weight. Maybe they’ve been dealing with fatty liver or high blood pressure or hormonal imbalances. Yet, because their blood sugar looks normal, they’ve been reassured that everything’s fine, and we stop looking at metabolic health.
Is it really? What if their pancreas is working overtime to keep those glucose numbers looking good? That often happens when the person’s healthcare team is waiting for the blood sugar to become abnormal and the metabolic dysfunction has already been developing for years, and it gets overlooked as an underlying cause.
In reality, we can recognize some of these patterns by looking at how insulin and glucose respond to the foods someone actually eats, rather than just looking at their fasting numbers, and that’s what we’re exploring today.
Which tests are the most useful? What are we missing when we only measure glucose? How can we put the pieces together to identify metabolic dysfunction much, much earlier? Because the goal isn’t to diagnose everyone with insulin resistance, although a good percentage of the population has it, and it’s not recognized. It’s really to recognize when the whole clinical picture is telling us something that the standard blood sugar tests are missing.
In a previous episode, we explored something I think every practitioner needs to understand. Two people can have exactly the same fasting glucose and A1C, but very, very different insulin regulation. One might be maintaining healthy glucose levels with relatively little insulin, and the other may require lots more insulin, because their tissues aren’t responding. They’re insulin resistant. Same glucose, different metabolic circumstances, and very different approaches.
That brings us to today’s question. How do we recognize that difference before we wait for somebody to be diagnosed with diabetes? How do we know when glucose is telling the whole story and when we need to investigate further? That’s where testing and clinical pattern recognition come together, and that’s why fasting glucose and A1C just aren’t enough. Both are valuable, but they have an important place, but neither directly measures the insulin sensitivity the person’s having.
Fasting glucose tells us the concentration of glucose at a particular point in time. It doesn’t tell us how much insulin the pancreas had to produce to maintain that, and it doesn’t tell us what happens when someone eats. The A1C gives us an estimate of the average glucose over two to four months. That’s useful too, but it doesn’t show the full pattern of glucose fluctuations.
Someone could have a high level of up and down and have the same level as somebody who maintains a relatively stable insulin. It also doesn’t tell us how much insulin we need to maintain that, and there are also circumstances where A1C can be less misleading, especially when somebody has a condition affecting red blood cells like anemia.
What we really need to do is look at what is going on in their metabolic health overall, not just looking at fasting glucose and A1C. Normal glucose regulation is totally important. We need that, but it doesn’t mean that they have normal insulin regulation, and that’s why fasting insulin deserves more attention.
When I’m evaluating metabolic health, fasting insulin is one of the measurements I like to have for most people, if not all, because I want to understand not just what the glucose is doing, but how much insulin is present while the body maintains that level.
The less insulin it takes to maintain ideal blood sugar, the better, because the downstream effects of too much insulin, including weight gain, blood pressure elevation, loss of magnesium, stiffening of blood vessel linings, and much more can be devastating.
If two people have fasting glucose of 88 and an A1C of 5.2, but one has a fasting insulin of three and the other has a fasting insulin of 19, these are very different metabolic situations. We owe it to people to be able to understand and help them with that. I want to understand why there’s so much more insulin needed in one person than the other. If the pancreas is compensating for reduced insulin sensitivity, that’s one situation. Or, if hepatic insulin clearance is slow and contributing, that’s different, too.
And also, what do the lipids look like, and what’s happening with liver function? What’s their body composition, their physical activity, their sleep, their hormonal history? All of these play in. I know that routine insulin testing isn’t part of conventional diabetes screening, but I think it should be.
Diagnosing diabetes and investigating early metabolic dysfunction aren’t necessarily the same clinical question. Diabetes diagnostic criteria are focused on establishing abnormalities and glucose regulation, but I’m interested in the physiologic changes that may occur before anyone reaches those thresholds, and they can be happening for a long time.
It doesn’t mean fasting insulin is a definitive diagnostic test, nothing is, or that measuring it is proven to improve outcomes in every population. What it means is that we can provide useful, additional context, when we interpret it correctly and when we advise people correctly based on that. I’d much rather consider that information alongside, well, of course, their history and other findings.
Another thing to look at is HOMA IR. That’s a tool that a lot of people use, and it combines fasting insulin and fasting glucose into a calculated estimate of insulin resistance. It certainly can be helpful in research and selected clinical assessments, but it has limitations, too. It’s derived from the fasting measurements. And again, because most doctors aren’t doing fasting insulin, we can’t calculate it.
It doesn’t really tell us how the skeletal muscle responds after a meal. What’s the tissue-specific insulin sensitivity? How’s the hepatic sensitivity? And, it depends on the accuracy of the insulin assay. We don’t usually get that. It’s just information, and all the information we get puts together the clinical picture.
What happens when a person actually eats? That’s one of the things that isn’t typically measured. One of the traditional ways, and it’s usually done during pregnancy, is the glucose tolerance test, and I understand why the test exists. It’s standardized, and we’ve established diagnostic criteria for interpreting it. But, for the type of metabolic evaluation I’m doing in day to day life, it doesn’t answer the question I’m most interested in.
A standard glucose tolerance test gives somebody 75 grams of glucose in a drink. That’s a specific challenge, and it’s not a typical meal. It doesn’t replicate the complexity of a typical meal and of digestion, fiber, protein, fat, and the food structure overall, the micronutrients and the hormonal responses that occur when somebody eats a real food meal.
While the standardized test has an important role in diagnosing diabetes and prediabetes, especially gestational, I want different information. I want to know if somebody’s metabolism is responding appropriately to the foods they actually choose to eat, and ideally, I want to evaluate insulin and glucose together.
My preferred approach is a postprandial insulin glucose challenge. We begin with fasting measurement of both glucose and fasting insulin. Then a person eats a meal but not just any meal. I generally want it to be a high carbohydrate meal that consists of foods that they would normally eat as part of their dietary choices.
I’m not asking somebody who’s eliminated refined sugar to drink a sugary drink just to figure out how their body handles sugar. It’s not real, right?
I want to know if somebody, like say somebody eats a whole food plant-based diet, I might choose a meal that features lentils or other legumes and sweet potatoes, fruit like prunes. It might include several of those foods, depending on what they normally eat. The idea is to choose a higher carbohydrate meal with their usual healthy eating patterns. Why?
I want to know whether their insulin and glucose regulation is working effectively when they’re eating the kinds of foods we actually want them to continue to eat. If they drink sodas, and they eat sugar all the time, then we’re going to include those things to show them how their body responds. I’m interested in the insulin response and whether it appears appropriate to the level of carbohydrate and the glucose response.
Ideally, we get them to combine this with a CGM, so we’re watching the glucose throughout. Unfortunately, we don’t have CGMs for insulin.
I want to look at what’s happening after the meal. When the glucose peaks, how long does it take to come down? That’s what I look for on the CGM. For a similar thing when I’m doing a postprandial insulin test, I want to look to see what’s happening at about that hour, and then again at the two-hour mark after they eat.
Is the insulin going way too high, but coming right back down? Is it going up and staying high? Those are all really important things. I like to do the postprandial at an hour and then again, ideally at two hours.
It’s inconvenient, but it’s less convenient than staying in the hospital all day to do a glucose tolerance test. It’s important that they document the meal, portion sizes, and approximate carbohydrate count, because we want to see what’s happening when their body is challenged with carbohydrates.
The insulin can give us information about circulating insulin at fasting and then what happens when they eat. I’ve had people who have had really strange, in my opinion, responses, not strange, but it seemed strange at the time. They would have a fasting insulin of 2.2, which is excellent, but it also can indicate that they’re starting to have some lowered pancreatic function. So I don’t know, is it ideal, or is it a lowered pancreatic function? I want to do postprandial.
I had someone do that postprandial, and it went from 2.2 up to 62. That’s huge, and all she’d eaten was sweet potatoes, fruit, and she had some potato chips, but foods that were not overtly crazy. It was just foods that were high in carbohydrates.
She did that same test again but ate her normal meal, her normal glycemic control meal, and it only went up to five or six or seven, something in that range. We get to see what these foods are doing, and she got to see, “I guess I shouldn’t be doing this.” Because, one of her complaints was that she wasn’t losing weight.
Dr Ritamarie (12:00)
When we’re doing this testing, we want to answer questions like how much insulin is required to handle that? What does the glucose pattern suggest? Are they regulating it efficiently or not? Is the glucose going way too high? Is there a disproportionately high or prolonged insulin response that we need to look at further, especially given some of the symptoms that high insulin causes? How do these findings relate to other metabolic markers? That’s an important question to know.
A food-based meal challenge isn’t a validated replacement. It’s not condoned by insurance companies, but it is an important diagnostic criteria for me when I’m trying to understand a person’s metabolic status.
The amount of carb, fat, protein, fiber in a meal all affect the glucose response, but the meal timing, the sleep, the activity, their medications, and so many other factors go into that. Even when the glucose curve looks similar, the underlying insulin dynamics may differ dramatically, and we can tell the glucose curve from the CGM. We’re trying to gather information so that we can help a person edit their lifestyle and edit their food choices. It’s a great assessment for that. Not everybody needs it, but I’m using it more and more.
For someone taking insulin or medications that can cause hypoglycemia, we need to have somebody that’s supervising it, because we don’t want them to go into a low that’s dangerous.
Doing a test like this really fits the way I think about personalized nutrition. I don’t want to know whether somebody can tolerate a laboratory glucose challenge with 75 grams of glucose sugar. I want to understand how their lifestyle is affecting them, because that’s what I’m helping them to shift around to optimize.
Dr Ritamarie (13:46)
Another test that can be helpful in this evaluation is C peptide. To understand why this may be useful, let’s go over and review a little bit about how insulin is made.
The pancreatic beta cells initially produce a precursor called proinsulin. Proinsulin is then split into insulin and C peptide. When the beta cells secrete mature insulin, C peptide is released along with it, so it’s usually in equal pmol amounts, but something interesting happens next. A lot of the insulin is extracted by the liver, before it even reaches the general circulation. C peptide, on the other hand, undergoes very little extraction.
When we look at C peptide, it gives us a better understanding of the beta cell capacity. It’s cleared mainly by the kidney, so C peptide can give us another perspective on how much insulin the pancreas is actually producing, especially if the numbers just seem off.
Why might we want to look at it? Well, it can be helpful when we need to evaluate the pancreas’ ability if we’re questioning whether the pancreatic function is declining. In somebody with diabetes whose insulin production might be declining, we will see the C peptide declining as well, but it can also be useful in evaluating certain types of hypoglycemia.
Unlike an insulin measurement, C peptide isn’t directly increased by injecting insulin. If somebody’s on insulin, the insulin measures the endogenous plus what’s taken, so these are things that we can look at. I think of C peptide as a more selective test rather than something everybody needs alongside the fasting insulin, but I do it quite a number of times in people with the right history. There’s things that affect it like everything else, kidney function affects the C peptide clearance, because they have different half-life clearance pathways. You can’t just compare the amounts of each, but it gives us a little bit more information, yet another clue.
What about pro insulin? Hardly anybody ever measures pro insulin. I’ve hardly ever measured it, but it’s the precursor, and we can measure it. Normally it’s processed, before it’s secreted, but when beta cell function becomes disrupted or when insulin production and processing are under greater demand, a larger proportion of incompletely processed pro insulin may enter the circulation.
If we’re looking at numbers and not really making sense of it, we can look to see if there’s elevated pro insulin or the ratio of pro insulin to insulin or C peptide. Those are just another way to look if the numbers start to kind of be baffling you.
Pro insulin isn’t usually measured, but it can be helpful if we’re looking for insulin-producing tumors and certain disorders of pro-insulin processing. It’s just something to keep in mind. I wouldn’t put it into everybody’s routine metabolic panel, although it isn’t super expensive.
In summary, glucose tells us about the outcome, insulin gives us information about the circulating signal, and C peptide helps us evaluate the endogenous insulin secretion. Pro insulin can provide clues about beta cell processing. They’re all related, but they’re not all interchangeable, and when we have the full picture, obviously we have more data to go on.
Dr Ritamarie (17:03)
Let’s pull this all together into a clinical framework. Imagine somebody who’s fasting glucose and A1C look great, but their triglycerides are elevated and their HDL is low. They’ve been developing more abdominal fat. They claim that they can’t lose weight no matter how much they starve themselves, and maybe liver imaging or testing shows that the liver needs some attention.
It’s important that we look at the numbers, yes, and we look at their history. We look at other metabolic markers, we look at medications, we look at possible other factors affecting insulin clearance, before we jump to they’re making too much, and they have insulin resistance.
It’s really important, I think, to look at the whole pattern rather than just treating fasting numbers as the final answer, and that’s why I think that there’s so much error in, or misdiagnosis, or late diagnosis, when we just look at fasting glucose like the conventional medical approach.
While insulin resistance isn’t the explanation for everything going wrong in the body, I find that it’s one of those core upstream drivers that we really need to look at, and I think it’s just overlooked so many times as we focus on the downstream effects like hormonal imbalances or thyroid or other things, as opposed to making sure that this is working.
It may not be the underlying cause in somebody, but you have to rule it out. It’s a very big contributing factor, and our job is really to investigate, not to just assume what’s going on. This is the difference between pattern recognition and jumping to conclusions.
That’s why I created my Free Beyond Protocols Guide, A Practitioner’s Guide to Root Cause Pattern Recognition. Collecting the data doesn’t actually give us answers necessarily. We need to be able to put the frameworks together and look at it as a clue. I recommend that you go to the show notes and download that as a free guide. We need to know what questions to ask, what patterns to look for, and what is really going on in this person that we’re trying to help.
Let me leave you with five questions I think that we all as practitioners need to be asking.
First, what are the glucose markers actually telling us? Are fasting glucose and A1C reassuring? Do they match the person’s history and other findings? Is there anything that could make those results less reliable?
Secondly, what’s happening with insulin? Could there be compensatory insulin secretion? I see it a lot. Are there reasons to suspect altered insulin clearance, like some diagnosed or suspected liver dysfunction? Would fasting insulin or another selected measurement help clarify it?
The third is how is this person responding to their actual food choices? Do we know what’s happening with their glucose? Have we gotten them to use a CGM or postprandial testing? Would a carefully planned food-based assessment with glucose and insulin measurements add information to this case? Would it change the kind of things that we’re going to be recommending?
Fourth, what are the other metabolic clues? What’s happening with triglycerides and HDL? Triglyceride-HDL ratio is really recognized as a good marker. What’s happening with their liver, their blood pressure, their body composition, and other things? Are there several findings pointing towards a common physiologic problem?
Fifth, what can we address now? How can we improve dietary quality? How can we improve healthy muscle mass so that it’s uptaking the glucose better? How do we address sleep and circadian disruption and evaluate medication effects, identify other medical or hormonal contributors ,because we don’t have to wait until somebody develops diabetes to address their metabolic risk factors?
That’s all what we do in our Metabolic Mastery program. There’s details about that in the show notes. There’s not the same protocol for everybody. We need to understand the person.
Here’s what I want you to remember from today’s episode. Normal blood sugar doesn’t automatically mean optimal metabolic regulation. I think you get that. Fasting glucose and A1C are very useful, but they don’t tell us everything about what’s going on, particularly about the insulin physiology. Fasting insulin can add more information, especially when we interpret it in context, and a CGM helps us understand glucose patterns, but it doesn’t measure insulin.
When appropriate, I believe in doing postprandial insulin and glucose testing in response to carbohydrate-rich foods that are actually what the person will eat, not just a fabricated jelly beans and ice cream diet.
C peptide and pro insulin can add information about pancreatic insulin secretion and processing in certain circumstances. Choose them wisely. None of these tests should be interpreted in isolation. The goal is to recognize patterns and understand the mechanisms underneath them.
Here’s a question I want you to keep asking. What information do I need to understand what’s really happening? Will that affect what I do and what I recommend that this client do? That’s how we move beyond simply collecting lab results, and that’s how we begin to practice truly personalized root cause health care.
In some upcoming episodes, I’m going to be looking more deeply at the effects of insulin and the surprising ways that it shows up throughout the body. We’re going to look at all the underlying connections that affect metabolic health and how we as practitioners can become better clinical detectives. I hope you join me for these episodes.
This is what reinventing healthcare is all about, looking beyond isolated symptoms and lab numbers, connecting the dots and understanding the underlying physiology, so we can create more personalized root cause approaches to care.
I believe the future of healthcare depends on practitioners who ask better questions, recognize meaningful patterns, and understand the whole person rather than simply following protocols.
If you’re a practitioner who wants to strengthen those skills, download my Free Beyond Protocols Guide. The link is in the show notes.
If today’s episode gave you a newer perspective on metabolic testing, please follow reInvent healthcare and share it with another practitioner who you think will benefit. Thank you for joining me on my quest to reinvent healthcare, and until next time, shine on.
What’s Inside This Episode? Why normal glucose doesn’t always mean normal metabolism What insulin can…
What’s Inside This Episode? Why a diagnosis of osteoporosis doesn’t explain why bone is being…
What’s Inside This Episode? Why having more tools does not always lead to better outcomes…
What’s Inside This Episode? Why the T-score is important but never the complete bone health…
What’s Inside This Episode? Why your client’s sleep problem may not actually be a sleep…
What’s Inside This Episode? Why bone is a living collagen matrix, not simply a place…
This website uses cookies.