Dr Ritamarie
What if thinning bones, declining T scores, osteopenia, osteoporosis, or increased fracture risk are signs of a much bigger communication breakdown and not just a calcium problem after all?
What if it's a breakdown between the bones and the ovaries, the bones and the thyroid, the bones and the adrenals, the bones and the pancreas, the bones and the muscles, the bones and the immune system?
Most practitioners were taught to think about bone as structure with calcium, vitamin D, weight bearing exercise, maybe estrogen after menopause. Bone is not just a scaffold, it's a living endocrine tissue, and we forget that sometimes.
It's constantly breaking down, rebuilding, sensing, signaling, adapting, and communicating with the rest of the body. When we reduce bone health to take calcium and walk more, we miss the real story.
Today we're going to talk about bone as an endocrine and metabolic organ and why so many practitioners need to stop treating bone loss as if it only belongs in the orthopedic or gynecology box.
Bone loss is rarely just a bone problem. It's usually a hormone problem, a metabolic problem, a stress physiology problem, a thyroid problem, a muscle problem, a nutrient assimilation problem, an inflammation problem. All these things work together and very often it's a pattern recognition problem.
If you're a practitioner, this episode is especially for you. We're starting to take a deeper conversation about bone health, not from the usual calcium and DEXA scan perspective, but from the perspective of functional nutrition, endocrinology, metabolism, movement, and root cause pattern recognition.
If this topic is relevant for your clients, your patients, or even your own health, save this episode, because it's the first in a bone health series that's going to connect hormones and movement and nutrition and testing and clinical decision making.
In this series, we're going to look at bones from a root cause practitioner lens. We're going to talk about hormones, movement, nutrition, imaging, lab testing, and how to think through the client who's losing bone despite doing what looks like all the right things.
Today I want to start with the foundation. Bone isn't inert, it's endocrine, it's metabolic, and it's alive. The more we understand that, the more precise we can become in helping our clients to protect and rebuild bone health.
Let's start with the standard story. A woman goes through menopause, her estrogen drops, her bone density declines, and she's told to take calcium, vitamin D, and maybe even a medication, a bisphosphonate or others, and to do some weight-bearing exercise. Now, some of that's totally appropriate, Estrogen does matter, vitamin D does matter, and minerals matter, movement matters.
Medication may be necessary for some people, especially those with high fracture risk, but the problem is not that these pieces are wrong, but that they're incomplete.
Bone remodeling is regulated by a whole network of signals, hormones, nutrients, inflammation, mechanical load, muscle activity, circadian rhythm, thyroid function, insulin signaling, gut absorption, I'll keep going, stress physiology, all of this influences whether the bone is going to be built or broken down.
When a practitioner sees osteopenia or osteoporosis and thinks calcium deficiency, they miss the very pattern that's driving the bone loss. That's where functional health care and nutritional endocrinology becomes so powerful.
Bone is constantly remodeling, and it's not like building a frame that gets constructed once and simply stands there for the rest of your life. No, it's a dynamic conversation.
The osteoclasts break down the bone. Osteoblasts build it, and it's a constant ebb and flow. Osteocytes act as the embedded sensors inside the bone matrix that help detect mechanical strain and coordinate remodeling signals. The breakdown and rebuilding is normal, not bad. In fact, it's absolutely necessary. The problem happens when the rhythm becomes imbalanced. If we have too much breakdown and not enough rebuilding, if we have poor mineralization or poor matrix quality and high inflammation and low muscle signaling and pulling on that bone, or we have low hormone support, which does happen in menopause. We have poor protein status and poor absorption, which happens way more than we give it credit for. The bone density, bone strength, and bone resilience can all decline.
Here's the part that most practitioners were never taught deeply enough: bone is not just responding to hormones. Bone also participates in hormone signaling. Bone-derived molecules, including osteocalcin, have been studied for roles in glucose metabolism, insulin sensitivity, brain signaling, muscle function, and in men, testosterone production.
Another molecule, lipocalin-2 or LCN2, has been studied as a possible bone-derived satiety signal. Now, this is where we need to be careful. Some of the research is exciting and still emerging. We don't want to say that osteocalcin fixes blood sugar or LCN2 is the missing appetite hormone. That'd be too simplistic. We can say that bone is not passive. It's part of the endocrine network, and it communicates with the pancreas, the brain, the muscles, the fat cells, the gonads, and the immune system.
What this means is that bone loss may be both a local skeletal issue and a systemic metabolic signal. That's a very different way of thinking.
Dr Ritamarie (06:34)
Let's talk a little bit about estrogen, because that's the hormone most closely associated with bone health. Estrogen helps restrain the osteoclast activity, so it helps bone breakdown from getting excessive. When estrogen declines during perimenopause and menopause, bone resorption can increase. That's one reason bone loss often accelerates in the years around menopause.
Here's where practitioners need nuance. It's not just estrogen good, estrogen bad. We need to think about estradiol levels. That's E2, estrogen receptor sensitivity, and that goes down as we age and as we are more metabolically sensitive and insulin resistant. That goes down as a result of inflammation and also cortisol and thyroid and progesterone and testosterone and insulin all have a role in this, as does nutrient status. It's not just about calcium, there's about 20 other nutrients that are important.
Gut health is super important. People with celiac disease have a higher risk of osteoporosis. Liver detoxification pathways and exposures need to be examined and the broader terrain that determines how the body uses and responds to hormones.
In some cases, we may want to look beyond local estrogen and consider estrone, estradiol, estriol, and estrogen metabolism patterns as is shown in a Dutch test or overnight twenty four hour test.
In functional practice, we look at estrogen metabolism as in 2-hydroxy, 4-hydroxy, and 16-hydroxyestrone. These are metabolites. These can be useful in understanding estrogen processing, methylation demand, oxidative stress, and possible risk factors.
Estrogen metabolites are not necessarily direct bone density predictors. The stronger bone story is still about estrogen signaling, especially estradiol and overall hormone terrain. That said, estrogen metabolism may give us clues about whether the body's clearing the estrogens well, whether methylation support is needed, whether oxidative stress is high, and whether a client has patterns that may influence hormone safety and hormone responsiveness.
In a practitioner framework, estrogen metabolites belong in the conversation, but they should not replace the basics. Menopause status, symptoms, estradiol, progesterone, testosterone, sex hormone binding globulin, thyroid, cortisol, insulin, inflammation, nutrient status, and clinical risk.
All of these are important. I like to say don't treat the hormone number. Interpret the hormone pattern. Definitely don't treat the bone number without asking why that bone number is changing.
Dr Ritamarie (09:20)
Estrogen often gets the spotlight, but it's not only sex hormone. It's not the only sex hormone that matters. Progesterone supports osteoblast activity, which means that they play a role in bone formation. The evidence isn't as definitive as it is for estrogen, but it's an important thing clinically nonetheless, and we need to not ignore it.
If estrogen prevents the breakdown and progesterone helps with the buildup, we really need to have them working in harmony. In perimenopause, progesterone actually declines earlier and more erratically than estrogen. A woman may still have good estrogen activity, but less progesterone, and that will cause more sleep disturbance, more anxiety, more cortisol activation, and more inflammatory signaling. All of that can influence bone remodeling in an indirect fashion.
Then there's testosterone. In men, testosterone matters for bone and muscle. We all know that intuitively, but it's also important to remember that estradiol matters in men, too, because some testosterone converts to estradiol depending on their aromatase activity. Estradiol plays an important role in male bone health. That's often overlooked.
In women, testosterone matters for muscle mass, obviously, strength, motivation, libido, connective tissue, and overall anabolic tone. Those things influence bone health. Low testosterone or low-free testosterone, so that would be excess sex hormone binding globulin. If the testosterone looks good, but the free testosterone is less because of the SHBG levels, then that can contribute to decreased muscle stimulus, which indirectly affects the bone.
Another key point is that muscle and bone are a unit. You can't fully address bone health while ignoring muscle. Low muscle mass means less mechanical signal to the bone, and that means less bone remodeling and less signal of those osteocytes to actually build the bone and strengthen it.
Low protein intake means there's less substrate for the muscle and for those in the matrix. Low anabolic tone means poor rebuilding capacity. When I see bone loss, I'm also thinking about sarcopenia, protein intake, resistance training, insulin sensitivity, hormone patterns that influence muscle. Bone health is not just skeletal medicine, it's musculoskeletal endocrinology.
Let's move into cortisol, because this is a huge missing piece in many bone conversations. Chronic stress physiology can be catabolic. Let's get a catabolic breakdown. High cortisol over time can reduce the osteoblast activity, which increases bone resorption and interferes with collagen formation. It can worsen blood sugar and disrupt sleep, cause inflammation, and contribute to muscle loss.
Remember, bone needs muscle. Bone needs sleep. Bone needs time to repair itself. It needs stable blood sugar, and it needs enough nutrients in order to build, to have that bone-rebuild, break down, build, break down in a nice even flow. Bone needs the nervous system to feel safe enough to rebuild. We talk about that a lot. The nervous system needs to feel safe in order for appropriate physiologic function to be happening, for healing to happen.
With a client with osteoporosis who also has chronic stress and insomnia and are under-eating or over-exercising, has a trauma history or is a caregiver, has high inflammatory load or long-term steroid exposure, medications for inflammation breakdown bone, we need to think beyond just add more calcium.
How much calcium are you taking? Are you taking 1500 milligrams a day? That should be fine. No, it's not. Okay, we have to look at all of these factors. Steroid medications are one of the clearest examples of cortisol-like bone loss, but the broader stress physiology pattern matters, too.
Even if you're not taking a cortisone drug for inflammation, or for whatever, or for anabolic reasons, and we're stressed, so we're getting that same effect on the physiology.
It doesn't mean that every stressed person gets osteoporosis, but it means that cortisol and stress load can be part of the terrain that shifts the remodeling towards breakdown and away from rebuilding.
As a practitioner, you should be asking, “How is this person sleeping? Are they under-eating? Are they over fasting? Fasting is a popular thing these days. Are they losing weight too rapidly? Are they chronically inflamed? Are they over-training?”
A little bit is good, more is better, not necessarily. Are they recovering? Are they losing muscle? Are they living in sympathetic overdrive? I talk about sympathetic overdrive syndrome like SOS. We're all there, so many of us are there constantly. Because of the stress, the body is not prioritizing building strong bone when it receives danger signals. Stress is important.
The other thing that's super important is thyroid. Thyroid hormone is essential for metabolic health and normal bone remodeling, but too much thyroid can signal, accelerate the turnover. This can happen not just with hyperthyroidism, which isn't a common condition, but it can happen when someone is over-medicated with thyroid medication, because thyroid medication is just handed out like candy these days. Your TSH is high, here's your thyroid medication, without looking at the deeper factors there. That's especially important in postmenopausal women.
If the TSH becomes suppressed and the free T3 is high because of over medication, the symptoms might suggest excess thyroid stimulation, heart palpitations and sweating and heat and all that, or bone turnover markers are high. We need to really pay attention.
That's of course not saying that thyroid medication is bad, absolutely not, but it's not prescribed in the proper way. It needs to be dosed individually and monitored carefully. So many people are put on thyroid medication and not checked again for a year, and that's not a good thing.
The goal is not to push metabolism at the expense of bone, heart rhythm, sleep, and muscle integrity. It's dangerous to do that.
A practitioner that looks at bone health should not just stop at vitamin D. They should review other things like let's look at the TSH and the free T4 and the free T3. Those are super important factors. Maybe look at reverse T3. I don't look at that as much, but yes. Look at the thyroid function from the standpoint of antibodies, as well, and symptoms.
Dr Ritamarie (15:58)
We always need to do a good medication history summary and look at their heart rate and their sleep and bone turnover markers. A lot of doctors are just doing DEXAs, and they're not looking at bone turnover markers, which we'll be talking about in another episode in this series. We're not looking at CTX, NTX, P1NP and a bunch of others. There's a lot of things you can look at to see what's happening with the bone, because you have to wait a year, or at least six months, before you see major changes on a DEXA.
We need to get the full clinical picture when we're talking about bone health, and it has to do with all the other endocrine systems. Sometimes their bone protocol is less about adding another mineral and more about correcting an excess catabolic signal.
Let's talk about insulin and blood sugar and how they affect bone. This is a place where bone intersects beautifully with metabolic health. When we look at the stats, 93% of the population is metabolically out of balance.
Insulin is anabolic, yes. We need adequate anabolic signaling for tissue maintenance and repair, yes, but insulin resistance and chronic inflammation, hyperglycemia, high blood sugar, and glycation, the sugar coating of our body parts, impairs bone quality. It's super important, because fracture risk is not just about bone density, which many of the docs will have you believe when they do a DEXA and say, it's bad. It's also about the quality of that bone.
We can have thickened bone, and a lot of times when people are on medication that prevents the breakdown of the bone, the bone gets thicker, but the quality isn't improving. It's old, worn-out bone that just keeps getting thicker. In diabetes and insulin resistance, bone density may not always look as low as expected, but fracture risk can be elevated, because of the collagen quality, the microarchitecture, the inflammation, the oxidative stress, and the fall risk.
When practitioners look only at a T-score, they may miss the metabolic pattern. We will have a segment on imaging. Bone is mineral, but bone is also a collagen matrix. If blood sugar is high and collagen is being glycated, sugar-coated, that matters a lot. If insulin resistance is there and inflammatory signaling is high, that matters. If muscle mass is low and glucose disposal is poor, that matters. Again, this is why bone health belongs in the metabolic conversation.
Fat tissue we know is also endocrine. The adipocytes, the fat cells, release leptin, and adiponectin, and inflammatory cytokines, and other signaling molecules that are important. Fat is an endocrine tissue, bone is an endocrine system. This is why nutritional endocrinology deals with the body, the whole body, and the endocrine system is the master controller, because it's part of each and every tissue and system in the body.
It's not as simple as more body weight protects bones. Higher body weight may increase mechanical loading, but visceral adiposity, inflammation, insulin resistance, and poor muscle quality increase risk. If the additional body weight helps, because it's muscle weight versus someone who's very, very lean and doesn't have the muscle pull, that's an issue,
And leptin, we talk a lot about leptin with the satiation and appetite, but it has a complex central and peripheral effect on bone. Adiponectin and inflammatory cytokines and metabolic health, they all matter.
When we evaluate bone, we need to look at all of these factors. We need to look to see if the client is inflamed, do they have visceral fat? Do they have low muscle with high fat mass? Do they have insulin resistance or chronic immune activation? All these things matter, as does autoimmune disease and gut derived inflammation.
Many people are running around with gut dysbiosis and microbiome imbalances. What about inflammatory dietary patterns? The standard American diet, the ultra-processed diet, is highly inflammatory. These inflammatory cytokines increase osteoclasts activity and shift the body towards bone breakdown.
Let's just pause and make an important distinction. Some of what we're talking about is clinically established. Estrogen loss increases bone resorption. We know that. Thyroid signals can accelerate bone turnover. We know that. Glucocorticoids can cause bone loss. We know that. Metabolic loading influences bone remodeling. We know this. We know vitamin D and K2 and calcium, magnesium, protein, and other nutrients matter.
Dr Ritamarie (20:38)
We know that inflammation affects bone turnover, and there's patterns we can assess and patterns we can address. Some other parts of the bone story and the signaling are emerging and fascinating, and they help us to understand why bone is more than structure.
One of them is osteocalcin, a protein made primarily by osteoblasts, the cells that build bone, and traditionally we thought of osteocalcin mostly as a bone formation marker that tells us osteoblasts are active and bone is being built.
Research over the last few years, and a few decades actually, has suggested that osteocalcin can also act like a hormone. In other words, it may not stay in the bone. Some forms of osteocalcin can circulate through the bloodstream and communicate with other tissues.
Here's where animal research may give us some clues. Osteocalcin has been linked with glucose metabolism, insulin production, insulin sensitivity, exercise capacity, brain development, cognition, and male fertility in animal studies.
Human research is a little bit more mixed and nuanced and still evolving. I won't say we can use osteocalcin to treat blood sugar, cognition, and testosterone, but it gives us a powerful clue and a powerful message, and I think should be tested in anyone in the age where bone and osteoporosis tends to be a risk factor.
The bone building cell is not just building bone, it may be sending metabolic signals. This is important. That means that the osteoblasts may matter for more than just bone density. It may be part of the bigger whole body communication network.
The other signal is LCN2, which is short for lipocalin 2. LCN2 is also called NGAL in other areas of medicine, especially kidney and inflammation research. It's not produced only by bone, immune cells, fat tissue, kidney tissue, and other cells, but it's especially produced under inflammatory conditions.
In the bone endocrine research world, LCN2 became fascinating, because osteoblasts produce it. Some research suggests that osteoblast derived LCN2 may communicate with the brain through appetite and satiety channels. Aha, including the melanocortin 4 receptor, which is often abbreviated MC4R.
This means that the body's production of bone may be part of the energy balance conversation. The same cells involved in building bone may also help signal the brain about appetite, and fuel status, and metabolism. This is where I want you to hear the nuance. I'm not saying we should run out and start testing LCN on every client with osteopenia.
I'm not saying that LCN is the missing appetite hormone, although maybe we'll find some more about it in the future. I'm not even saying that osteocalcin is the answer to insulin resistance, low testosterone, or brain aging. What I'm saying is that these discoveries help us see bone differently. Bone's not just receiving instructions from the rest of the body. Bone may also be giving instructions. That brings us to a deeper bone, brain, gut, muscle, fat communication. All of these are connected,
The thigh bones are connected to the brain. All of these things are connected, and the more research we do, the more we find out about it. Bone talks to muscle, muscle releases myokines. They're signaling molecules produced during contraction of the muscle. The myokines can influence inflammation and insulin sensitivity and therefore metabolism and bone remodeling. Muscle talks back to bones through mechanical force.
Every single squat and carry and jump and resistance exercise sends a signal through the muscle into the bone. Bone talks to the brain through emerging signals like osteocalcin and LCN2. The brain talks back to the bone through the nervous system, the stress pathways, the thyroid regulation, appetite regulation, and hormone rhythms. It's a lot more complex than we're led to believe. Fat tissue talks to bone through leptin, adiponectin, and inflammatory cytokines, and insulin resistance-related signals, and bone and fat interact inside the marrow, where bone marrow fat can reflect changes in the bone-building environment.
Dr Ritamarie (25:02)
Now the gut talks to the bone through nutrient absorption. We need nutrient absorption to get all those good nutrients to build this stuff. The microbiome, the immune signaling, inflammation, minerals, protein, digestion, vitamin K, and gut-derived hormones.
If someone is not absorbing minerals, and they're not absorbing amino acids or fat-soluble vitamins or phytonutrients, the skeleton will feel that. Not immediately, but over time we're going to see changes there. When I say bone is part of the bone, brain, gut, muscle, fat communication network, I mean bone health reflects the messages coming from the whole body.
The muscles tell the bone whether it's being used. The gut determines whether bone has the raw material it needs. The brain and the nervous system influence stress chemistry, appetite, sleep, and repair. Fat tissue influences inflammation, leptin, insulin signaling. All of this stuff matters, and the bone sends signals back into that network.
This research is really exciting, because it helps us see bone as a whole body organ.
As practitioners, we need to be clear about what's ready for direct clinical decision making and what's still part of the growing model. Estrogen loss, excess thyroid, glucocorticoid exposure, low protein intake, low vitamin D, low magnesium, inflammation, insulin resistance, low muscle mass, poor balance, and lack of progressive loading are clinically actionable right now.
Osteocalcin and LCN2 are fascinating, but they're not, yet, routine clinical targets in the same way. You can still test osteocalcin. It's not an expensive test. It gives you a clue, but we don't want to just jump ahead until we have some more evidence.
The established science is so powerful, even without the LCN and the osteocalcin. We already know that bone responds to hormones, nutrients, inflammation, to muscle, to movement, to stress, to thyroid signaling, to insulin signaling, and gut function.
It responds to everything that we talk to people about in terms of diet and lifestyle. It's not just isolated to bone. When we're looking at somebody who comes in because they have osteoporosis or osteopenia, we don't just look for bone therapies. We don't just look for the latest herb or supplement. We've got to look at the whole picture. That's how we should be practicing. This is part of the nutritional endocrinology method.
Dr Ritamarie (27:36)
That's what we look at for everyone, in spite of what actually is being out of balance. I keep coming back to the importance of moving beyond protocols. A generic protocol with all the nutrients, the calcium and D and magnesium and K2, and weight bearing exercise. They're all useful. I’m not saying not to do it, but what if the client's primary driver is thyroid overreplacement? We don't want to overlook that.
What if it's high cortisol and poor sleep? No, don't overlook that. What if it's low protein and sarcopenia? What if it's gut inflammation and malabsorption? We need to look at all of these factors in order to help people to improve their bones. If it's postmenopausal estrogen loss combined with low testosterone and low muscle and no impact loading, there's things that we can do.
The client doesn't need a generic handout with a list of all these things and is sent off to do this. They can go on the internet and find that. They need pattern recognition. They need a capable practitioner who can look beyond protocols and help them to put together a personalized plan, to look at the patterns underneath. Don't throw the same supplement list at everyone and just really start asking better questions.
Let's just bring this all together. If you are practitioners, the key takeaway from today's episode, or takeaways actually, bone is not inert. It's a living endocrine and metabolic tissue.
Second, bone loss is not always a calcium problem. It may reflect changes in estrogen, progesterone, testosterone, cortisol, thyroid, insulin, inflammation, muscle, gut health, nutrient status, or mechanical loading. Hormones are important.
Third, estrogen matters deeply, but the hormone bone story is much bigger than estrogen alone.
Fourth, bone-derived hormones like osteocalcin and LCN2 are exciting, but we need to distinguish emerging research from direct clinical application.
Fifth, fracture risk is not just about bone density. It has to do with bone quality, muscle, balance, fall risk, inflammation, glycation, and medications. We have to do a thorough history. We have to find all the underlying causes.
When you see bone loss, ask what the body is trying to tell you, not just what supplement I should give.
Today, we opened the door to a bigger way of thinking about bone health. Bone's not just structure, it's an endocrine organ, it's a metabolic organ, it's a mineral reservoir loaded with minerals if everything's going right. It's a blood cell-producing tissue, it's a mechanosensitive tissue, sensitive to the pulls of the muscles.
It's part of a hormone network, the muscle network, the immune network, and the metabolic network. If we want to help clients build resilient bones, we need to understand the signals that tell the bone to break down and the signals that tell the bone to rebuild.
In the next episode, we're going to look at one of the most powerful signals of all movement. We'll talk about jumping and resistance, training and impact and weighted vests and yoga balance and contraindications for all and why walking alone is often not enough.
If this episode helped you see bone health differently, this is exactly the kind of root cause thinking we explore in Beyond Protocols because practitioners don't need another generic protocol. So go ahead to the show notes, click on the link, and download the Beyond Protocols booklet that I put together. It's a great way to help you to learn to recognize patterns.
Keep listening to this bone series and watch for the practitioner training that will go deeper into labs and imagery and bone turnover markers and hormone patterns, etc.
Thank you for joining me on this mission to reinvent healthcare. Let's keep reinventing the way we think about bone health, hormones, and real root cause patient care. And until next time, shine on.
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