If you work with people experiencing osteopenia, osteoporosis, fractures, menopause-related bone loss, or unexplained bone decline, this episode will help you move beyond the diagnosis and investigate the patterns driving the problem.
Dr Ritamarie
When someone gets a DEXA scan and they’re told you have osteopenia, or you have osteoporosis, almost immediately the conversation becomes do you need more calcium? What about vitamin D? Should you exercise more? Do you need medication? And of course, these are important questions, but there’s a question I think needs to be coming out much earlier. Why is this person losing bone in the first place? The why, the big why.
Osteoporosis isn’t a calcium deficiency diagnosis. It’s the end result of something that’s been happening in the body sometimes for many years. Maybe bone is being broken down too quickly, or new bone isn’t being built efficiently, or maybe both are happening at the same time.
There can be hormonal, digestive, inflammatory, metabolic, nutritional, renal, immune, medication related, or other factors that are driving that imbalance that’s leading to bone loss.
Throughout this bone health series, I’ve been wanting to change the way we look at bone, the way we think about bone, because it isn’t an inert structure that just slowly gets thinner as we age. It’s a living metabolically active tissue that’s constantly responding to hormones, to nutrients, to inflammation, to mechanical load and metabolic signaling, to the gut and the kidneys and the rest of the body’s internal environment. That’s exactly why a bone density number can never tell us the whole story.
The DEXA scan is super useful. It helps us to assess bone mineral density and fracture risk, but think about what it’s actually giving us. It’s essentially a snapshot of the accumulated results of what has happened to the bone over time. It doesn’t really tell us what’s happening now.
Is bone breakdown accelerated or is bone formation inadequate? What about nutrients like calcium? Is it being absorbed? Is it being lost? Is parathyroid hormone causing the body to go towards resorption?
Is thyroid signaling involved? Is there poor protein or mineral status related to malabsorption? Is there inflammation that’s interfering with bone remodeling? Maybe it’s insulin resistance that’s changing the quality of bone, even if the density doesn’t look terrible. Lab testing can be helpful here.
Today, I want to organize these tests into a framework, not simply giving you a big long list of labs. I want to help you understand when to use which tests and why.
One of the biggest missing pieces in conventional bone evaluation is that we often measure how much bone is there, but not how actively it’s being remodeled. It’s constantly undergoing a cycle.
Osteoclasts break down the older bone, osteoblasts build new bone. Ideally these processes happen, and they stay in equilibrium, but osteoporosis can develop when the balance shifts.
One of the questions I want practitioners to be asking is, “Is this predominantly an excessive resorption problem, an inadequate formation problem, or both?” That’s where bone turnover markers become really interesting and really important.
One of my favorite markers to look at is the serum CTX or C terminal telopeptide. It’s released when type I collagen in bone is broken down. Think about CTX as a window into what’s happening with bone resorption.
When CTX is high, it can suggest that bone breakdown is happening at an accelerated rate, and that changes the questions I like to ask. Why are those osteoclasts breaking down the bone so actively? It could be menopause-related estrogen loss, it could be hyperparathyroidism, or hyperthyroidism, or inflammation. It can also be excessive stress and glucocorticoid exposure that can play a role, as can immobilization or medication.
Labs need to be looked at in a relationship. High CTX does not equal osteoporosis. CTX has significant circadian and food-related variations, so we have to be testing it over time, not just once. If you’re testing it over time, we want to be consistent about when we do it, if we’re comparing it in the morning, or we’re comparing it in the afternoon. They need to be collected under similar situations, or we don’t really get apples to apples comparisons.
If we’re not consistent, we can create changes in the CTX value that aren’t related to their metabolism or their bone.
For the other side of the equation, I like to look at P1NP, procollagen type 1 N-terminal pro peptide, P1NP for short. It reflects type 1 collagen formation and gives us information about the bone building side of the equation.
We have two pieces of information. CTX tells us how much bone appears to be getting broken down, and P1NP is looking at what’s happening with bone formation. When we look at these two together, that gives us a good idea of the balance between things. It’s not just static. This is where the bone is now.
You can imagine that if there’s two people with the exact same T-score, and one has a very elevated resorption and another has a low bone formation. They aren’t necessarily the same metabolic situation. Even though the DEXA score is similar, we’re going to want to use different approaches to what we do with them.
This is one of the essential themes I want us to do as we go beyond bone health. The diagnosis may be the same, osteoporosis, osteopenia, while the underlying physiology is different,
Dr Ritamarie (06:33)
Other bone health bone tests in the blood are NTX or N-terminal telopeptide, bone-specific alkaline phosphatase, and osteocalcin. Each of these gives us additional information about remodeling. I don’t think practitioners need to order every available bone marker. Start with the CTX and the P1NP, because that gives us an excellent look at bone breakdown versus bone building.
CTX and P1NP give us an excellent starting point, and if we need more, we can always order more to try to get a little bit more precise.
We want to know why we may have accelerated loss or decreased bone building. Why does the pattern exist? Calcium’s important, but it’s tightly regulated, because it’s so important in cardiovascular health. When we look at the blood calcium, the serum calcium, it’s not really reflective of the level in the skeletal system, because most people are going to have relatively normal calcium results, but they may not have normal calcium in the bones.
When the body maintains serum calcium, it’s by pulling calcium out of the bone. If somebody’s on a calcium restrictive diet, but they have normal calcium, it may be that they’re releasing it from the bone. We have to pay attention to albumin, because a lot of the calcium in the blood is protein bound. In certain situations, ionized calcium can give us an additional bit of information.
We also need to look at parathyroid hormone. When calcium availability drops, parathyroid rises in an effort to restore serum calcium. Parathyroid can increase calcium mobilization from the skeleton and increase renal calcium conservation.
If parathyroid is elevated, we need to look at vitamin D level and the things that impact calcium, including their intake, the absorption, the kidney dysfunction, and whether it’s holding on to it, and, magnesium, which is super important.
We want to know if we are dealing with primary hyperparathyroidism. If vitamin D is low, we need to ask about intakes, sun exposure, and increased demands based on genetic SNPs. We also need to look at vitamin D metabolism and what balances that.
Phosphorus is another important one. Calcium and phosphorus combined to form hydroxyapatite, which gives bone much of its mineral strength. Abnormal phosphorus can point towards vitamin D issues, parathyroid dysfunction, renal losses or retention, malnutrition, and other metabolic issues.
Magnesium participates in bone mineral structure, vitamin D metabolism, parathyroid physiology, and hundreds of enzymatic activities that are important.
Calcium loss needs to be considered. That’s where a twenty-four hour urine calcium may be done, We’re not doing all of these tests. We start with the two, we look at the DEXA, and then we decide whether we need to go further.
If we do a 24-hour urine calcium, we want to look at what does it really mean? If it’s high, it indicates loss. If it’s low, it can answer questions about inadequate intake or poor absorption. Those are things related to minerals.
Dr Ritamarie (09:56)
Let’s look at thyroid. Most people, most of us, what we see is mostly hypothyroid, but in the case of bone, we want to be looking for excess thyroid signaling, hyperthyroidism, because it accelerates bone turnover and that can lead to bone loss over time.
It’s not just about hyperthyroidism, but people that are treated with hypothyroid hormone, and that’s a really common thing we have to look at.
If someone is overtreated with thyroid hormone, they will look like hyperthyroid, and it may not be that they show obvious signs like the racing heart and sweaty and losing weight, but it might be subtle enough that it is eating away at their bones. We really do need to look at that. We want to keep the TSH in a place where it’s normal, not chronically suppressed.
Sex hormones are important as well, not just estrogen. We talk about estrogen as women going through perimenopause and menopause, but it’s not just estradiol, it’s estradiol, progesterone, testosterone, DHEA, sex hormone binding globulin. In men, it’s the total and free testosterone and estradiol and sex hormone binding globulin.
Chronic stress leading to chronic glucocorticoid excess is another major contributor to osteoporosis. We know this very clearly from people taking steroid medications, but endogenous cortisol excess matters, too. People are stressed out all the time.
Dr Ritamarie (11:29)
These systems we’ve been talking about don’t operate independently, and that brings us to one of my favorite topics which is metabolic health. We have to be careful here, because bone density can actually be misleading in metabolic dysfunction.
If somebody has type 2 diabetes, they may have normal or even higher bone mineral density and still have increased fracture risk. The density isn’t the same thing as quality.
Chronic hyperglycemia, elevated blood sugar, advanced glycation end products, oxidative stress, inflammation, and altered insulin signaling can all affect the collagen and bone quality.
A full metabolic panel is critical, including glucose, A1C, insulin, and postprandial, not just fasting glucose. All of these interactions are a perfect example of what I mean when I talk about going beyond protocols.
You know I don’t like protocols. I talk about that all the time. Protocols imply that we’re treating a condition as opposed to a person, a person with a condition or a set of conditions that’s unique.
We need to put together beyond protocols, a customized plan.
Somebody can have accelerated resorption related to hormonal changes. Another might have malabsorption and nutrient deficiencies. Another might have hyperparathyroidism or medication-induced hyperthyroidism. Inflammatory conditions play a part as well. Another may have more poor metabolic health.
All these different things are patterns that can exist together, and our jobs as functional practitioners is to really look at what’s going on with people and figure out what the imbalances are and what the imbalances accumulate to present as in terms of their metabolic bone health. Bone is a metabolic tissue.
I created a guide called Beyond Protocols, and I’ll put the link in the show notes if you want to download that, because it’s really an important aspect of what we do as functional practitioners. What all practitioners should be doing is looking at the body and the function and how those things get out of balance.
A diagnosis of osteoporosis doesn’t really tell us much. It doesn’t tell us about the underlying absorption problem, the malabsorption. It doesn’t tell us about the underlying metabolic imbalances and nutrient imbalances and celiac disease, even.
Celiac is big. You can prescribe a perfect bone supportive diet and recommend all the supplements, protein, and all the things, but it doesn’t help if that person can’t digest and absorb adequately. A lot of people I see have celiac disease that went undiagnosed for a long time, and now they have very bad osteoporosis and started getting it very young. We cannot overlook celiac disease.
Celiac disease is one thing, but there’s also non-celiac gluten intolerance. Really look at the gluten intake of people, because that might be contributing to their bone loss..
In an unexplained case, celiac screening is important, and a lot of times when we look at this, we look for transglutaminase enzymes, but that’s not necessarily going to be elevated. We really have to look at the big picture and things that affect the gut, If somebody has chronic diarrhea or pancreatic insufficiency or malabsorption or bariatric surgery, gastric surgery, long-term restrictive diets with low protein intake and poor appetite, these are going to have chronic, digestive dysfunction, and that’s going to affect the quality of the bone.
It’s more than just what supplements they are taking, it’s what they are absorbing and how much they are absorbing.
Tests that I think everybody should run on somebody when they get a low DEXA or just in general to screen include a CBC and CMP, including total protein, albumin, liver enzymes, renal function. And, we need to look at their clinical diet history, body composition, muscle mass, and weight changes over time.
Are they chronically under-eating? A lot of people these days are, especially if they’re on GLP medications. They suppress the appetite. If they’re losing muscle and strength, then removing mechanical load from the skeleton, it can lead to unexplained bone loss in inflammatory conditions.
Depending on the case, I also recommend inflammatory markers like hs-CRP and erythrocyte sedimentation rate, ESR and CBC, and all the kidney and the and the liver enzymes, because we want to see the big picture. The kidneys are important in vitamin D activation and regulation of phosphate. Those are important for bones.
Chronic kidney disease can dramatically alter parathyroid hormone, calcium, phosphorus, and bone metabolism, so creatinine and eGFR aren’t just boring components of a panel, those are critical to be looking at. I think they’re so inexpensive that we should be running them consistently to compare.
The liver function, as well, because the liver participates in vitamin D metabolism as well and produces many of the proteins that we need for strong bones,
The other thing is a CBC can give us clear ideas if there is anemia, is there hematological disorders and other systemic problems? Are there problems with the immune system and inflammatory conditions?
We have to look at these when we’re looking at fracture risk. Some of the things that are additional, people can do serum protein electrophoresis with extra testing, because occasionally it’s not just osteoporosis. There’s a lot of other metabolic conditions underlying it that lead to osteoporosis.
The responsibility that comes with root cause thinking is that we look at everything. We don’t just have our tests that we run for this condition or tests that we run for this other condition.
Before you order an exotic laboratory panel, make sure you look at the basics, and also look at their medications, because a lot of medications interfere with bone health.
Look at their celiac situation and their gut situation. There’s a bunch of different meds that can affect the bones, things that affect sex hormones and thyroid and gastric acid and seizure control, all these meds can have an effect on bone health. We do need to do a thorough history and really look at what people are taking. We want to look at what they were taking when the bone loss accelerated, if it did? And, don’t forget to ask about previous osteoporosis medications, because they can change the bone term over markers and give us a rebound bone loss.
Dr Ritamarie (18:15)
My opinion is never interpret a bone turnover marker without knowing what treatment the person is receiving. Okay, so let me pull it together into a framework you can actually use.
When I see osteopenia, osteoporosis, unexpected bone loss, or fragility fracture, fracture because the bone is fragile, I’m thinking in layers.
Layer one, what’s the structural status? That would be the DEXA, that would be fracture history, that would be assessment of the vertebrae, and when it’s appropriate, an additional assessment of the bone structure quality when it’s clinically useful. What has happened?
Layer two, what is the bone doing now? That’s where we look at CTX and P1NP and the ratios between them. The CTX should be no more than 10 times the P1NP. These are really important things that we look at. And, we want the P1NP to be no less than thirty five.
The other labs that we can do, if those don’t give us a clear picture, osteocalcin, bone-specific alkaline phosphatase, but we want to know, is the abnormal remodeling happening now? Or is it in the past?
Layer three is what’s getting in the way. We investigate the major regulatory systems like mineral and regulatory physiology, like calcium and albumin, its carrier, phosphorus and magnesium, and 25-OH vitamin D. The 125 is for a different story.
Look at the parathyroid, the alkaline phosphatase, renal function, 24-hour urine calcium when it’s indicated, and then we have to look at the endocrine system.
So many people have thyroid imbalance, and that suppressing TSH can lead to bone loss. Sex hormones need to be looked at, and of course cortisol, because stress, everybody’s under stress. These are important.
We need to look at the metabolic markers like glucose and insulin and A1C. So many doctors are not doing insulin. We’re not looking to see what’s happening here. The metabolic health markers are super important and digestion markers, like testing for celiac, but also testing for malabsorption and leaky gut and things like that.
Then look at the inflammatory markers. The CBC is the basics, but inflammatory markers like C-reactive protein, hs-CRP. We can look at ESR, we can look at GGT. There’s a lot of inflammatory markers.
Then, we have to look at their history. How’s their diet? How’s their exercise? What’s going on with them? Are they losing weight, gaining weight? Do they have a digestive history?
Testing isn’t just useful in figuring out what went wrong. It helps us determine whether what we’re doing is actually changing physiology. The DEXA changes slowly. We’re not going to see changes in that for a good six months, but the P1NP and the CTX can change very rapidly. We can do those once a month and see, are we moving in the right direction?
Establish a baseline, intervene appropriately, then repeat the marker under compatible testing conditions and ask, did the resorption change? Did bone formation improve? Is this intervention moving the needle in the direction that we expected and desire? This is more useful than saying, take this supplement and come back for another DEXA in two years or even a year or six months.
One question that keeps coming up from me is why are they losing bones? Why? A DEXA scan tells us the bone densities decline, but it can’t by itself tell us why. Ask if the bone breakdown is accelerated? Is bone formation inadequate? And what’s happening with calcium regulation and all the nutrients we discussed so far?
All the systems are important. What about parathyroid? And, what about magnesium? And, what about thyroid and sex hormones? All these things are important. Metabolic function is super important. Inflammation, digestion, absorption, kidney function, all this stuff’s important. We have to ask good questions to get good answers to lead us to understanding what’s going awry in this person’s body, what medications might be interfering.
Ultimately, osteoporosis isn’t a cause, it’s the manifestation. You broke your leg, because you have osteoporosis. That doesn’t say much. You broke the leg, because you had bone loss, and that was diagnosed as osteoporosis. But why? Why? We always have to ask why and go deeper and deeper.
That’s what this bone health series has been all about. We’re not chasing a T-score, although that’s used and revered in medicine. We’re not trying to reduce bone health to just calcium, and we’re not waiting until somebody has a fracture, because before we start asking better questions, we need to understand that bone is a living tissue. It’s responsive, metabolically active tissue. We have to look at the whole person that owns the skeleton and what are they doing that’s causing their skeleton not to be worthwhile. This is where healthcare needs to go.
The future of healthcare isn’t just identifying disease, making a diagnosis, and giving somebody something. No, it’s understanding all the connections between all the systems and asking why long before the dysfunction progresses to become a diagnosis. That’s the essence of what I teach, which is nutritional endocrinology. It’s the way we’re training practitioners to think differently, to connect the dots, and help reinvent healthcare one patient at a time.
If you would like help developing that thinking, download our Beyond Protocols Guide to Root Cause Pattern Recognition. I’ll put the link in the show notes. And until next time, shine on.
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