Bone Health is NOT Just About Calcium!

For decades, most of us have been taught a very simple story about bone health. If bones weaken, it must mean we are not getting enough calcium. If a bone scan shows thinning, the solution is more calcium. If that is not enough, vitamin D is added. And if bone loss continues, medications are often prescribed to slow it down.

At first glance, this seems logical. Bones are made of minerals, so adding minerals should fix the problem. Right??? Well, here is where the story quietly falls apart…

If calcium were the main solution, osteoporosis would be rare. Calcium intake in modern societies is generally sufficient, and supplements are everywhere. Yet bone loss is common. Many people take calcium for years and still see declining bone density. Others develop calcium deposits in arteries, joints, or kidneys while their bones continue to weaken. The calcium is present. It is simply not going where it belongs.

That is because bone is not a rock. It is living tissue that constantly breaks down and rebuilds itself. Nearly a third of bone is made of collagen, a flexible protein framework that gives bones the ability to absorb force rather than shatter. Minerals harden this framework, but they are not the foundation. Without healthy collagen, adding more calcium can actually increase brittleness rather than strength.

Bone-building cells are also extremely energy-dependent. They rely on healthy mitochondria, the energy-producing structures inside cells, to do their work. When energy production is impaired by poor sleep, chronic stress, inflammation, or metabolic dysfunction, bone formation slows. Over time, the body shifts away from building strong bone and toward storing fat inside the bone marrow. This happens even when calcium intake appears adequate.

Vitamin D is often misunderstood in this process. It is usually treated as a simple vitamin deficiency, when it functions more like a hormone that reflects sunlight exposure and daily biological rhythm. Low vitamin D is often a signal that the body is not receiving enough natural light or that its internal timing system is disrupted. Taking vitamin D supplements can raise blood levels, but that does not always mean bone health improves, especially if sunlight exposure remains low.

This is where the parathyroid glands quietly enter the picture. The parathyroid glands are small, but they play a major role in bone health. Their job is to regulate calcium levels in the blood by deciding when calcium should be released from bone and when it should be stored. When parathyroid function is within normal limits, calcium is carefully balanced and bone is protected. When parathyroid signaling becomes chronically overstimulated, the body may pull calcium out of bone even when intake is adequate.

Parathyroid hormone is highly sensitive to vitamin D status, magnesium levels, and overall mineral balance. It is also influenced by circadian rhythm, meaning it responds to light and dark cycles. Sunlight helps regulate this system by supporting proper vitamin D signaling, while poor sleep, indoor living, and artificial light at night can disrupt it. Grounding, or regular contact with the earth, may also support electrical and hormonal balance in ways that are still being explored, particularly in tissues like bone that respond to electrical signals.

Vitamin A is another overlooked player. It helps regulate whether bone is built or broken down and assists in directing calcium into the right tissues. Traditionally, vitamin D from sunlight and vitamin A from animal foods were present together. When these signals are separated, calcium can lose its guidance system, and bone quality may suffer even if density numbers look acceptable.

This brings us to bone medications. These drugs are often presented as the primary solution, but full understanding matters. Many bone medications work by slowing the natural breakdown of bone. This can improve bone density measurements in the short term, but bone health depends on a balance between breakdown and rebuilding. When bone turnover is suppressed for too long, older bone remains in place longer than it should. Over time, this can increase the risk of unusual fractures, delayed healing, or jaw complications in some individuals.

Other bone medications stimulate bone formation, but once stopped, bone loss can accelerate rapidly if the underlying causes were never addressed. These medications may be appropriate in certain situations, but they do not restore normal bone signaling, parathyroid balance, mitochondrial health, or circadian rhythm. They manage risk, not root cause. BTW: read their package inserts. You might be surprised to find out that some increase the risk of femur fractures…OUCH!

It is also important to know that many commonly prescribed medications not intended for bone health can still make it harder to maintain strong bones. Long-term acid-suppressing drugs can interfere with mineral absorption. Steroids weaken collagen and accelerate bone loss. Some antidepressants affect balance and bone turnover. Thyroid medications, blood sugar drugs, and certain hormonal therapies can all influence bone metabolism depending on dose and duration. None of this means these medications should never be used, but it does mean their impact on bone should be considered over time.

When all of these pieces are viewed together, bone loss looks far less like an unavoidable part of aging and far more like a systems issue. Bone health depends on energy production, protein structure, hormonal regulation, light exposure, electrical signaling, and mineral guidance working together. Calcium is part of the picture, but it was never meant to act alone.

Strong bones are built when the body’s signaling systems are supported, not just when supplements are added. This article doesn’t even cover the importance of sunshine, sleep, and exercise. Stay tuned for future articles.

Questions to Ask Your Doctor

If you are thinking about bone health or bone medications, these questions can help guide a more complete discussion:

·       Is my parathyroid hormone within normal limits, and how does it affect my bone health?

·       How does this medication influence bone quality over time, not just bone density measurements?

·       What are the long-term risks of staying on this medication, and how will we monitor them?

·       Are any medications I currently take making it harder to maintain healthy bones or mineral balance?

·       How do vitamin D, vitamin A, magnesium, protein intake, and sunlight exposure work together for my bone health?

·       How do sleep, daily light exposure, and movement factor into my bone health plan?

·       Is my bone loss being treated as a mineral issue, or are we addressing the underlying systems involved?

Bone health decisions are best made with full information. Understanding how bones actually work allows you to participate in those decisions with clarity rather than fear.

The real surprise for many people is not that calcium matters. It is that bone health was never meant to depend on calcium alone. So, what SHOULD one eat for bone health.  Well food high in the aforementioned nutrients amongst other and plenty of protein and real fat.  Yes, the updated and upside down pyramid isn’t as bad as most people seem to think. We sometimes have to unlearn and rethink a situation. Don’t be afraid to think outside of the popular lines. I’m here for you if you need help.

-Diane Kopelakis, MS, RD

(scroll further down for references)

IT’S YOUR BODY, YOUR INFORMED DECISION… You will never regret getting tested! Here are some labs to consider asking your trusted and informed practitioner…

Comprehensive Bone Health Blood Labs

Foundational / Commonly Covered

  1. 25-Hydroxyvitamin D [25(OH)D]
    Widely covered; commonly ordered

  2. Parathyroid Hormone (PTH, intact)
    Extremely important; usually covered but under-ordered

  3. Phosphorus (Phosphate)
    Inexpensive; often overlooked

  4. Alkaline Phosphatase (ALP)
    Standard metabolic panel test

  5. Magnesium (serum)
    Inexpensive, but limited sensitivity

  6. Albumin
    Helps interpret calcium and protein status

  7. Total Protein
    Reflects collagen building resources

  8. Thyroid-Stimulating Hormone (TSH)
    Widely covered; indirect bone impact

 

Moderate Cost / Sometimes Covered

  1. Free T4
    Needed if TSH is abnormal or bone loss is unexplained

  2. Free T3
    Less commonly ordered; useful in over-replacement scenarios

  3. Ionized Calcium
    More informative than total calcium; slightly higher cost

  4. High-Sensitivity C-Reactive Protein (hs-CRP)
    Covered but not always ordered for bone evaluation

  5. Fasting Insulin
    Coverage varies; often overlooked in bone discussions

  6. Sex Hormones (context-dependent)

    • Estradiol (women)

    • Total testosterone (men)
      May require age- or symptom-based justification

 

Specialized / Higher Cost

(often hardest to obtain but important if you feel that you’re at risk)

  1. RBC Magnesium
    Better reflection of magnesium status; frequently out-of-pocket

  2. Bone-Specific Alkaline Phosphatase (BSAP)
    More precise than ALP; limited availability

  3. C-Terminal Telopeptide (CTX)
    Bone breakdown marker; fasting morning draw required

  4. Procollagen Type 1 N-Terminal Propeptide (P1NP)
    Bone formation marker; often bundled with CTX

  5. Serum Retinol (Vitamin A)
    Usually only covered if deficiency or excess is suspected

 

Rarely Ordered / Very Context-Specific

  1. 1,25-Dihydroxyvitamin D
    Useful in select endocrine disorders; not routine

  2. Fibroblast Growth Factor-23 (FGF-23)
    Specialized phosphate regulation disorders

 

Which labs are most often denied or out-of-pocket

  • RBC Magnesium

  • CTX

  • P1NP

  • Bone-specific ALP

  • Vitamin A (retinol)

  • Fasting insulin (sometimes)

These are often considered “non-routine” unless osteoporosis, fracture risk, or medication monitoring is clearly documented.

 

High-yield, cost-aware “priority bundle”

If you can’t get everything from your doctor (or covered by insurance and you can’t pay for it yourself), the most informative combo is:

  • 25(OH)D

  • PTH

  • Phosphorus

  • Magnesium (serum or RBC)

  • ALP

  • hs-CRP

That cluster alone reveals mineral signaling, hormonal stress, inflammation, and remodeling direction.

 

References

Bonjour, J. P. (2011). Calcium and phosphate: A duet of ions playing for bone health. Journal of the American College of Nutrition, 30(5 Suppl 1), 438S–448S. https://doi.org/10.1080/07315724.2011.10719988

Burr, D. B. (2002). Targeted and nontargeted remodeling. Bone, 30(1), 2–4. https://doi.org/10.1016/S8756-3282(01)00619-6

Eastell, R., Rosen, C. J., Black, D. M., Cheung, A. M., Murad, M. H., & Shoback, D. (2019). Pharmacological management of osteoporosis in postmenopausal women: An Endocrine Society clinical practice guideline. The Journal of Clinical Endocrinology & Metabolism, 104(5), 1595–1622. https://doi.org/10.1210/jc.2019-00221

Heaney, R. P. (2000). Calcium, dairy products and osteoporosis. Journal of the American College of Nutrition, 19(2 Suppl), 83S–99S. https://doi.org/10.1080/07315724.2000.10718088

Holick, M. F. (2007). Vitamin D deficiency. The New England Journal of Medicine, 357(3), 266–281. https://doi.org/10.1056/NEJMra070553

Karsenty, G., & Olson, E. N. (2016). Bone and muscle endocrine functions: Unexpected paradigms of inter-organ communication. Cell, 164(6), 1248–1256. https://doi.org/10.1016/j.cell.2016.02.043

Manolagas, S. C. (2000). Birth and death of bone cells: Basic regulatory mechanisms and implications for the pathogenesis and treatment of osteoporosis. Endocrine Reviews, 21(2), 115–137. https://doi.org/10.1210/edrv.21.2.0395

Reid, I. R. (2015). Short-term and long-term effects of osteoporosis therapies. Nature Reviews Endocrinology, 11(7), 418–428. https://doi.org/10.1038/nrendo.2015.53

Rizzoli, R., Biver, E., & Bonjour, J. P. (2021). Protein intake and bone health. Calcified Tissue International, 109(2), 178–189. https://doi.org/10.1007/s00223-020-00732-4

Rosen, C. J. (2008). Bone remodeling, energy metabolism, and the molecular clock. Cell Metabolism, 7(1), 7–10. https://doi.org/10.1016/j.cmet.2007.12.002

Shapses, S. A., & Sukumar, D. (2012). Bone metabolism in obesity and weight loss. Annual Review of Nutrition, 32, 287–309. https://doi.org/10.1146/annurev-nutr-071811-150630

Souberbielle, J. C., Prié, D., Courbebaisse, M., Friedlander, G., & Souberbielle, J. C. (2010). Update on vitamin D and bone health. Joint Bone Spine, 77(2), 101–106. https://doi.org/10.1016/j.jbspin.2009.11.003

Weaver, C. M., Gordon, C. M., Janz, K. F., Kalkwarf, H. J., Lappe, J. M., Lewis, R., O’Karma, M., Wallace, T. C., & Zemel, B. S. (2016). The National Osteoporosis Foundation’s position statement on peak bone mass development and lifestyle factors. Osteoporosis International, 27(4), 1281–1386. https://doi.org/10.1007/s00198-015-3440-3

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