Did You Know Your Bones Affect Your Metabolism?
Join Dr. James Odell for Season 2 of the Science of Self-Healing Podcast! He's the medical and executive director for BRMI, as well as a practicing naturopathic doctor for over 35 years, and he's here to share with you his extensive knowledge of medicine from a different perspective.
You probably think of your bones as a frame that holds you up. But your skeleton is also sending hormones to your kidneys, pancreas, muscles, fat, and even your brain.
In this episode of The Science of Self-Healing, we look at bone as an active, hormone-producing organ. You’ll learn how a bone hormone called FGF23 helps control phosphate and vitamin D, why researchers think osteocalcin may affect blood sugar, and how bone might even play a role in appetite. We’ll also cover why people with diabetes can break bones even when their scans look normal, how undereating and rapid weight loss, including on GLP-1 medications, can quietly weaken the skeleton, and what progesterone, estrogen, and testosterone really do for bone. Along the way, we’ll take an honest look at the popular claim that progesterone cream can raise bone density by 15 percent.
You’ll walk away with a new way of seeing your skeleton, and the everyday habits that keep both your bones and your metabolism strong.
Transcript: Did You Know Your Bones Affect Your Metabolism?
Hello, everyone, and welcome to the Science of Self-Healing podcast. For health and wellness knowledge from a different perspective. Produced by the Bioregulatory Medicine Institute, also known as BRMI. We are your source for unparalleled information about how you can naturally support your body's ability to regulate, adapt, regenerate, and self-heal. I'm your host, Dr. James Odell, the medical and executive director for BRMI, as well as a practicing naturopathic doctor for over 35 years. And remember, this podcast is for informational purposes only and is not intended to be a substitute for the direct care of a qualified health professional who oversees and provides unique and individual care. The information here is to broaden our different perspectives and should not be construed as medical advice or treatment. Let's get started.
Most of us think about our bones the way we think about the frame of a house. They hold everything up, they store calcium, and as long as nothing breaks, we don’t give them much thought.
But your bones are doing far more than standing there. They’re alive, they rebuild themselves every day, and they send chemical messages to organs throughout your body. Some of those messages help control phosphate and vitamin D. Others may affect your blood sugar, your appetite, and how your muscles use fuel.
And the conversation between your bones and metabolism goes both ways. Diabetes, undereating, rapid weight loss, and shifting hormones can all change the health of your bones, sometimes without showing up on a scan.
Here’s what the science says, where it’s solid, where it’s still being worked out, and what you can do about it.
Your Bones Are Busier Than You Think
Bone is living tissue, and it’s constantly being taken apart and rebuilt. Three types of cells run the process. Osteoblasts lay down new bone. Osteoclasts remove older bone. And osteocytes, which are buried inside the bone itself, sense strain and help direct the work.
Most people reach their peak bone mass by around age 30. After that, the goal shifts from building bone to protecting what you have, which makes this constant remodeling even more important as we age.
While all of this rebuilding is happening, bone cells release chemical signals that reach the kidneys, pancreas, muscles, fat tissue, brain, and immune system. That’s why the skeleton belongs in conversations about metabolism, right alongside the liver, pancreas, gut, and fat tissue.
Some of these bone signals have well-established jobs in controlling phosphate and vitamin D. Others appear to affect insulin, appetite, muscle, inflammation, and energy use, although much of that research is still developing. Communication also runs in the other direction. Insulin, sex hormones, cortisol, nutrition, inflammation, and movement all shape the way bone is remodeled.
Seen this way, bone health and metabolic health aren’t separate problems. Diabetes can make bone more fragile even when a scan doesn’t show osteoporosis. Eating too little can slow bone formation. Kidney disease can disrupt hormones made by bone long before obvious skeletal symptoms appear. The skeleton isn’t the master controller of metabolism, but it is one important player in a much larger feedback system.
What We Know and What We’re Still Learning
Here’s a quick map before we get into the details.
One bone hormone, called FGF23, is accepted physiology with a clear clinical role. Another, osteocalcin, has strong animal evidence but a less certain role in people. And a handful of others, called lipocalin 2, sclerostin, RANKL, and osteoprotegerin, may widen the picture further, though researchers are still working out how much they matter outside bone.
This is an area where exciting early research sometimes gets presented as settled fact, so I’ll be clear about which is which as we go.
Osteocalcin: Can Your Bones Help Manage Blood Sugar?
Osteocalcin is the hormone that first made scientists wonder whether the skeleton might affect blood sugar.
It’s made mainly by osteoblasts, the bone-building cells, and most of it gets built into the bone itself. Vitamin K helps attach small chemical groups to osteocalcin, a process called carboxylation. That’s what lets it grip onto bone mineral.
When bone is broken down and remodeled, some osteocalcin is released into the blood. Some of it is fully carboxylated, and some has fewer of those chemical groups attached. That second form is called undercarboxylated osteocalcin, and animal research suggests it’s the form that acts as a metabolic signal.
What the Mouse Studies Found
In influential mouse studies, mice without osteocalcin made less insulin, responded to insulin less well, gained more fat, and handled glucose poorly. Giving osteocalcin, or boosting its activity, did the opposite. Researchers proposed that it acts on beta cells, the insulin-making cells of the pancreas, as well as on fat cells, muscle, and the liver.
One model suggests a loop. Insulin signals bone to break down a little, which creates an acidic environment that activates osteocalcin. Osteocalcin then travels back to the pancreas and helps it make more insulin.
Why People Aren’t Mice
In people, lower osteocalcin often shows up alongside higher fasting blood sugar, more insulin resistance, more belly fat, or type 2 diabetes. That’s an interesting pattern, but there are several possible explanations.
Osteocalcin is also a marker of how actively bone is being built, and its level changes with age, kidney function, vitamin K status, medications, and overall health. A low level might be a result of illness or slow bone turnover, rather than the reason blood sugar got worse.
Comparing studies is harder than it looks, too. Some researchers measure total osteocalcin, others measure only the undercarboxylated form, and those tests aren’t interchangeable. So far, no trial has shown that changing osteocalcin itself prevents or treats diabetes. So if you see claims that a supplement or a workout “activates osteocalcin,” know that they’re running ahead of the evidence.
More Bone Breakdown Isn’t a Good Thing
This research doesn’t mean that more bone turnover is always better. Releasing osteocalcin may be part of normal remodeling, but too much breakdown weakens the skeleton. Building and breaking down have to stay in balance.
Osteoporosis drugs that slow bone breakdown can lower osteocalcin levels, but there’s no good evidence that appropriate treatment causes diabetes by suppressing this protein.
The takeaway: osteocalcin is an important research bridge between bone and metabolism, not something to test and chase on its own. It helps explain how bone might report on the body’s nutritional and physical state to other organs. For now, blood sugar, A1c, cholesterol, blood pressure, body composition, kidney function, and overall risk are far more useful for making metabolic decisions than an osteocalcin test.
Muscle and Bone: A Two-Way Partnership
Muscle and bone are closely linked. When you load your skeleton through movement, osteocytes respond by encouraging new bone. At the same time, working muscles release their own signaling molecules, called myokines, that influence bone.
Experimental studies suggest osteocalcin may help muscles take up and use fuel during exercise and adapt to training. Exercise, in turn, increases the forces on bone and changes the signals bone sends out.
This two-way conversation is one reason strength training benefits both your skeleton and your metabolism, without needing a single-hormone explanation.
FGF23: Your Bones Talking to Your Kidneys
FGF23, short for fibroblast growth factor 23, is the clearest example of bone acting as a hormone-producing organ.
It’s made mainly by osteocytes and osteoblasts, then travels through the blood to the kidneys. To respond to it, the kidney needs a helper protein called alpha-Klotho. FGF23’s main job is simple: keep phosphate from building up. It tells the kidneys to release more phosphate into the urine, and it lowers the amount of active vitamin D the body makes.
FGF23 works in a feedback loop with parathyroid hormone, which comes from small glands in the neck, along with vitamin D, calcium, phosphate, and the kidneys. Active vitamin D can increase FGF23, and FGF23 then puts the brakes on active vitamin D. Parathyroid hormone also pushes phosphate out through the kidneys and interacts with FGF23.
Together, this system keeps calcium and phosphate in a narrow range, while still providing enough for building bone, cell signaling, energy production, and much more.
When the Signal Won’t Switch Off
In chronic kidney disease, the kidneys gradually lose the ability to clear phosphate. FGF23 often rises early to compensate, sometimes before blood phosphate even looks abnormal.
That helps for a while. But when FGF23 stays high for a long time, it goes along with low active vitamin D, overworked parathyroid glands (a condition called secondary hyperparathyroidism), abnormal bone remodeling, and higher heart disease risk. In this setting, high FGF23 is both a sign that mineral balance is off and possibly a contributor to the disease. That’s why it should always be read alongside kidney function, phosphate, calcium, vitamin D, and parathyroid hormone.
What Rare Disorders Reveal
Rare genetic disorders, and certain rare tumors, show just how powerful this hormone is. Too much FGF23 can cause the kidneys to waste phosphate, along with low active vitamin D, muscle weakness, and bone pain. It can also cause softened bones, called rickets in children and osteomalacia in adults. Too little FGF23 activity can do the opposite, leading to phosphate buildup and calcium deposits in places they don’t belong.
These conditions prove that the bone-kidney connection isn’t just a theory. A hormone made in bone can shift mineral balance throughout the whole body.
Phosphate: Essential, but Not Without Limits
Phosphate itself is essential. It’s part of ATP, the molecule your cells use for energy. It’s in your cell membranes and your DNA. And it’s part of hydroxyapatite, the mineral crystal that makes bone hard.
The goal isn’t to push phosphate as low as possible. Healthy kidneys usually handle normal ups and downs in the diet very well. Problems show up when kidney function is impaired, hormone control is disrupted, or the amount of phosphate coming in is more than the system can handle.
Phosphate additives in processed foods are absorbed very easily, and they can add a large phosphate load, especially for people with kidney disease. Even then, any dietary restriction should be tailored to the person, because cutting back too hard can lower protein quality and overall nutrition. FGF23 testing is useful for specific disorders, but it isn’t a general wellness test.
Do Your Bones Help Decide When You’re Full?
This is one of the more surprising areas of research.
Lipocalin 2 is a protein made in several tissues, and its levels rise during inflammation. In mouse studies, osteoblasts turned out to be an important source. Bone-made lipocalin 2 was able to cross into the brain and reach the hypothalamus, the area that manages hunger. There, it acted on receptors called melanocortin 4 receptors, which help switch hunger off, and the mice ate less. The same experiments linked bone-made lipocalin 2 with better insulin release and glucose handling.
That raises an intriguing possibility: bone may help tell the brain whether the body has enough energy coming in.
But lipocalin 2 is nowhere near ready to be used as an appetite treatment or a simple metabolic marker. Its blood level is affected by inflammation, obesity, infection, kidney function, and tissue injury, so you can’t assume what’s in the blood came from bone.
Sclerostin: Why Your Bones Need You to Move
Sclerostin is released mainly by osteocytes, and it acts as a brake on bone building. It works by blocking a signaling pathway called Wnt, which normally tells bone cells to build.
When you put load on your bones, sclerostin tends to drop, which lets bone building pick up. When bones aren’t loaded, like during bed rest, sclerostin tends to rise. So sclerostin is part of how bone adapts to what you ask of it, and one more reason movement matters so much.
Studies have also found links between sclerostin levels and body fat, insulin resistance, heart disease, and diabetes, but the direction and meaning vary from one population to the next. Higher sclerostin can reflect age, sex, kidney function, how much bone is producing, or how slowly it’s being cleared.
There’s now an osteoporosis drug that blocks sclerostin, and it works well for bone. But that confirms sclerostin’s role in bone, not that blocking it treats metabolic disease. Heart safety concerns with this drug class are another reason to avoid simple conclusions.
Where Bone Meets the Immune System
RANKL, which stands for receptor activator of nuclear factor kappa-B ligand, helps form osteoclasts, the cells that break bone down. Osteoprotegerin acts as a decoy that soaks up RANKL and limits its effect.
This system controls bone breakdown, but it also overlaps with the immune system, because many immune cells use related signals. Chronic inflammation can ramp up osteoclast activity and cause bone loss. In obesity and type 2 diabetes, inflammatory signals, oxidative stress, changes in the hormones made by fat tissue (called adipokines), and shifts in sex hormones may disturb both metabolism and bone remodeling.
Bone marrow adds another layer. It holds hematopoietic stem cells, the stem cells that make all of your blood cells, along with immune cells, blood vessels, nerves, and marrow fat. Osteoblasts and other support cells help maintain the spaces where blood and immune cells develop.
And marrow fat isn’t just filler. It changes with age, starvation, diabetes, medications, and bone disease. Its exact role as a hormone source is still being worked out.
Good Signal or Bad Signal? It Depends
These pathways rarely sort neatly into good and bad.
FGF23 is necessary, but chronically high levels can become part of a disease process. Lipocalin 2 helps fight infection and drives inflammation, as well as showing up in appetite research. Sclerostin keeps bone building from running out of control, even though too much of it can hold bone building back.
What a signal does depends on how much there is, when it’s released, where it comes from, and the condition of the tissue receiving it. Keep that in mind whenever you see one lab value presented as the answer to everything.
When Metabolism Fights Back
So far, we’ve looked at how bone talks to the rest of the body. Now let’s look at what happens when metabolic disease talks back.
Why People With Diabetes Break Bones With “Normal” Scans
Both major forms of diabetes raise fracture risk, though not in quite the same way.
In type 1 diabetes, lack of insulin, autoimmune activity, lower body weight, and reduced bone building can all interfere with making and keeping bone.
Type 2 diabetes is more of a puzzle. Bone density may look normal or even high, yet fractures still happen more often. That’s because a bone density scan measures how much mineral is there. It doesn’t measure collagen quality, tiny cracks, bone structure, or how likely you are to fall.
When blood sugar stays high, sugar molecules stick to the collagen in bone, forming compounds called advanced glycation end products, or AGEs. These make bone more brittle. Diabetes can also impair bone-building cells, change osteocyte signaling, damage small blood vessels, and slow healing after an injury. On top of that, nerve damage, vision problems, muscle weakness, and certain medications all raise the risk of falling.
This is a clear example of why metabolic health and bone health can’t be looked at separately. If you have diabetes and a “normal” bone scan, it’s still worth talking with your practitioner about fracture and fall risk.
The Hidden Cost of Not Eating Enough
Not eating enough can lower reproductive hormones, reduce thyroid signaling, raise stress hormones, and slow bone building. We see this in the female athlete triad, and in the broader condition called relative energy deficiency in sport.
A person can exercise regularly and look fit while still losing bone if they’re not eating enough to cover their needs. Missed periods are an important warning sign, but bone effects can start even before periods stop.
Weight, Weight Loss, and GLP-1 Medications
Obesity doesn’t automatically protect bone. Extra body weight does put more load on the skeleton, but belly fat, inflammation, insulin resistance, fat buildup inside muscle, and a higher risk of falls can cancel out that advantage.
Rapid weight loss can also reduce bone, especially when protein, calcium, vitamin D, and strength training are lacking. If weight loss is needed for metabolic health, it has to be balanced with protecting muscle and bone.
This matters more than ever now that so many people are losing weight quickly on GLP-1 medications. Fast weight loss, from any cause, can take muscle and bone along with fat. That makes protein and strength training even more important.
Simple Habits That Protect Bones and Metabolism
The good news is that the steps that help are familiar, because they work on several systems at once.
Load your bones. Progressive strength training and weight-bearing activity load the skeleton, preserve muscle, improve insulin sensitivity, and lower fall risk. Think squats, lunges, step-ups, carrying heavy groceries, climbing stairs, and brisk walking.
“Progressive” is the key word: gradually asking your body for a little more over time. If you’re new to strength training or have osteoporosis, a physical therapist or qualified trainer can help you start safely.
Eat enough, including protein. Protein provides the raw material for both muscle and bone. And eating enough overall matters, since undereating slows bone building.
Get your calcium and vitamin D. Calcium is needed to mineralize bone, and vitamin D3 helps the body absorb it. But more isn’t always better. Unnecessary high-dose supplements can create their own problems.
Don’t forget vitamin K. Vitamin K, especially K2, is what allows osteocalcin to lock calcium into bone. One caution: if you take a blood thinner like warfarin, talk to your doctor before adding vitamin K.
Protect your sleep and manage stress. Ongoing sleep loss and stress can impair blood sugar control and change appetite, cortisol, and your ability to train.
Skip the smoking and heavy drinking. Both damage bone and raise many other health risks.
Look for underlying causes. Thyroid disease, celiac disease, kidney disease, low sex hormones, and eating disorders should be identified and treated, not covered up with supplements.
Know your medications. Long-term steroid use is the best-known example of a medication that harms bone. Others include pioglitazone, a diabetes drug linked to more fractures in women; high doses of thyroid medication; long-term acid blockers called proton pump inhibitors; and aromatase inhibitors used after breast cancer. If you take any of these, don’t stop them on your own. Just ask your doctor whether your bones should be checked.
There’s no supplement proven to “balance bone hormones” as a group. A more sensible plan starts by finding which part of the system is actually off. That might mean treating diabetes or kidney disease, correcting a real nutritional deficiency, eating enough to meet your needs, or choosing exercise that safely loads your skeleton.
When to Ask About a Bone Density Scan
Bone density scans and lab tests are useful when your age, history, medications, or symptoms call for them, not as broad wellness screening. In the U.S., current guidelines recommend a bone density scan for women 65 and older, and for younger women after menopause who have extra risk factors. A fracture from a minor fall, long-term steroid use, or a family history of hip fracture are all good reasons to ask about one sooner.
Hormones That Shape Your Bones
Now let’s talk about the hormones that have some of the biggest effects on bone.
Estrogen Protects, Progesterone Builds
Estrogen slows down osteoclasts, the cells that break bone down. When estrogen falls at menopause, bone loss speeds up. That drop is the main driver of bone loss in women after menopause.
Progesterone plays a different role. Osteoblasts, the bone-building cells, have receptors for progesterone. Lab studies suggest it helps them mature and lay down new bone. So, estrogen mainly protects the bone you have, while progesterone may help build new bone.
Your Cycle Is a Bone Health Signal
In younger women, progesterone depends on ovulation. If a cycle doesn’t ovulate, or the second half of the cycle is too short, progesterone stays low. Studies have linked these cycles to a slow loss of bone at the spine, roughly one percent a year. That’s one more reason a regular cycle is a sign of overall health, not just fertility.
During perimenopause, progesterone usually drops and swings before estrogen does. Some practitioners use progesterone on its own during this stage.
Should You Consider Progesterone?
Bioidentical progesterone has the same structure as the hormone your body makes. It comes as oral micronized capsules or as a cream. It behaves differently from synthetic progestins, which tend to carry more side effects. Oral progesterone often causes drowsiness, so it’s usually taken at bedtime, and some women find it helps them sleep.
What About the 15 Percent Claim?
You may have heard that progesterone cream can raise bone density by about 15 percent. That number comes from Dr. John Lee’s work in the late 1980s and early 1990s.
It was an important early observation, but it wasn’t a controlled study. The women were also changing their diet, exercise, and supplements, and some were taking estrogen. When researchers later compared a progesterone cream to a placebo cream for a full year, bone density didn’t differ between the groups.
So, progesterone may support bone, but the strongest evidence for protecting bone after menopause is still for estrogen, often combined with progesterone.
Safety and Testing Matter
A woman who still has her uterus and takes estrogen also needs enough progesterone to protect the uterine lining, and creams may not reliably provide that.
Testing matters as well. Blood levels can look low with a cream even when the hormone is reaching your tissues, so the type of test should match the type of progesterone you use. These decisions belong with a practitioner who can monitor you.
Men Lose Bone Too
In men, testosterone, along with the estrogen the body makes from it, protects bone. Low testosterone is a common and often overlooked cause of bone loss in men.
The Bottom Line on Bones and Metabolism
Bone gives the body structure, but it also sends signals. Its cells sense force, mineral levels, nutrition, and messages from other organs, and they answer by adjusting remodeling and releasing hormones of their own. Your skeleton isn’t just waiting for instructions from somewhere else.
The evidence isn’t equally strong for every claim. The FGF23-kidney connection, which controls phosphate and active vitamin D, is established physiology. Osteocalcin has opened a credible link between bone remodeling and blood sugar, but how much it matters in people is still unsettled. Lipocalin 2 offers early evidence that bone may influence appetite. And sclerostin and the RANKL system connect bone remodeling with movement, the immune system, and possibly metabolism.
That connection has real consequences. A plan for diabetes or weight loss shouldn’t ignore bone, and osteoporosis care shouldn’t ignore metabolism. Diabetes can lower bone quality. Undereating can slow bone building. Kidney disease can disrupt mineral hormones. And inactivity affects muscle, fat, and bone all at once. Following one lab value without looking at the rest of the system can easily miss what’s really driving the problem.
Supporting this network doesn’t require exotic testing. Enough food, progressive strength and weight-bearing exercise, good sleep, and proper treatment of real hormonal, kidney, inflammatory, or metabolic disease remain the foundation. They may sound simple, but they create the conditions your bones need to stay strong and keep doing their regulatory work.
Coming up: In a future episode of The Science of Self-Healing, I’ll cover the foods and supplements that support your skeletal system.
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This article is for informational purposes only and is not intended to be a substitute for the direct care of a qualified health practitioner who oversees and provides unique and individualized care. The information provided here is to broaden our different perspectives and should not be construed as medical advice, diagnosis, or treatment.
