Addendum: Comprehensive Bone Health FAQ
January 8, 2026
ADDENDUM: COMPREHENSIVE BONE HEALTH FAQ
(For Patients and Clinicians)
1. What is the difference between bone density and bone strength?
Bone density refers to the amount of mineral (primarily calcium) in bone and is what is measured by a DEXA scan. Bone strength, however, is a broader concept. It reflects not only mineral density but also bone microarchitecture, collagen matrix quality, cortical thickness, trabecular connectivity, muscle support, balance, and mechanical loading.
Fractures occur when bone strength fails — not simply when bone density is low. This explains why some individuals fracture with “normal” or mildly reduced DEXA scores, while others with lower bone density do not.
2. Why doesn’t increasing calcium intake reliably prevent fractures?
Calcium is a structural component of bone, but it is not a signaling molecule. Increasing calcium intake alone does not tell the body where or how to use that calcium.
Bone remodeling depends on:
- Magnesium for calcium utilization
- Vitamin D for absorption and regulation
- Vitamin K2 to direct calcium into bone
- Hormonal signaling to stimulate bone formation
- Mechanical loading to trigger osteogenesis
Without these, calcium may be poorly incorporated into bone and may instead contribute to soft tissue or vascular calcification. This is why high calcium intake has not consistently reduced fracture risk in adults.
3. Why do fractures occur in people with “osteopenia” or even normal DEXA scans?
DEXA scans do not measure:
- Bone collagen quality
- Microdamage accumulation
- Bone geometry
- Muscle mass or strength
- Balance or fall risk
Bone quality often deteriorates before measurable changes appear on DEXA, particularly during hormonal transitions such as menopause. Fracture risk is therefore influenced by factors that DEXA cannot capture.
4. Is osteoporosis always a calcium deficiency problem?
No. In most adults — especially those with secondary osteoporosis — bone loss reflects a combination of:
- Hormonal decline
- Sarcopenia (muscle loss)
- Chronic inflammation
- Medication effects (e.g., steroids, anticonvulsants)
- Nutrient imbalances
- Inadequate mechanical loading
Calcium deficiency is rarely the primary driver.
5. What role does magnesium play in bone health?
Magnesium is foundational for bone metabolism. It is required for:
- Activation of vitamin D
- Proper parathyroid hormone (PTH) signaling
- Calcium transport and incorporation into bone
- Formation of healthy bone crystals
Without adequate magnesium, calcium cannot be effectively utilized, regardless of intake.
A functional dosing framework commonly used in clinical practice is approximately 5 mg of magnesium per pound of body weight per day, individualized to tolerance and labs.
6. Why is vitamin D dosing individualized rather than fixed?
Vitamin D requirements vary widely based on:
- Body weight
- Sun exposure
- Absorption
- Medication use
- Inflammatory status
Vitamin D functions as a regulatory hormone, influencing calcium and magnesium metabolism, bone turnover, muscle strength, and fall risk. A weight-based framework of approximately 45–50 IU per pound of body weight per day is often used to achieve functional serum levels, with a common target range of 50–70 ng/mL for 25-OH vitamin D.
7. Why is vitamin K2 important for bone strength?
Vitamin K2 activates osteocalcin, a protein that allows calcium to be deposited into bone rather than remaining in circulation or depositing in soft tissues. Without adequate K2, calcium cannot be effectively directed to bone, even when vitamin D levels are adequate.
8. Does collagen really matter for bones?
Yes. Bone is approximately 30–40% collagen by volume. Collagen provides flexibility, tensile strength, and resistance to microfractures. Loss of collagen integrity makes bone brittle — a change not detected by DEXA scans.
Bone broth and whole-body collagen powders (typically 10–20 g/day) support collagen availability, particularly when paired with adequate vitamin C.
9. Why is muscle strength so important for preventing fractures?
Bones respond to mechanical strain, not nutrients alone. Resistance and impact loading stimulate osteoblast activity and improve bone geometry, particularly at the hip and femoral neck.
Additionally, muscle strength reduces fall risk — one of the strongest predictors of fracture. Sarcopenia significantly increases fracture risk independent of bone density.
10. How do hormones influence bone health in both women and men?
Bone remodeling is hormonally regulated in both sexes. Key hormones include:
- Testosterone
- DHEA
- Estrogen
- Progesterone
- Cortisol
The biology is the same; what differs is which hormones decline first and most significantly.
In men, testosterone decline is often dominant.
In women, loss of progesterone, estrogen, and androgens contributes to bone fragility.
Supplementation strategies remain the same; hormone evaluation does not.
11. Why do women need testosterone and DHEA for bone health?
Testosterone and DHEA are not male-only hormones.
In women, they:
- Support osteoblast activity
- Preserve cortical bone thickness
- Maintain muscle mass and balance
- Reduce fall and fracture risk
Relative androgen deficiency after menopause contributes to sarcopenia and bone fragility, even when estrogen is addressed.
12. What role does cannabidiol (CBD) play in bone health?
Bone tissue expresses CB1 and CB2 receptors, part of the endocannabinoid system. These receptors influence osteoblast (bone-building) and osteoclast (bone-resorbing) activity.
Preclinical research demonstrates that cannabidiol (CBD):
- Supports bone formation
- Enhances fracture healing
- Helps normalize bone turnover by reducing excessive resorption while supporting bone-building pathways
CBD is considered adjunctive and is not a replacement for foundational bone-strength strategies.
13. Does CBD work differently than pain relief alone?
Yes. While CBD is often associated with pain and inflammation modulation, its effects on bone appear to involve direct signaling pathways within bone tissue, independent of analgesia.
When used clinically, bioavailable formulations, such as nano-emulsified capsules or liquids, are often preferred to support consistent absorption.
14. Is this bone-strength approach appropriate for both women and men?
Yes. The supplementation framework and nutritional principles are identical for both sexes. The difference lies in which hormones require evaluation and optimization.
Bone biology does not change by sex — hormone patterns do.
15. How does testing fit into a bone-strength strategy?
Because bone loss is often hormonally driven, testing is essential. Symptoms and age alone are unreliable.
At-home testing options available through VitalHealthPharmacist.com may include:
- Testosterone
- DHEA-S
- Estradiol
- Progesterone
- Cortisol
- Vitamin D (25-OH)
Testing allows targeted intervention rather than guesswork.
16. What is the most important takeaway about bone health?
Bone strength is built through:
- Hormonal balance
- Magnesium, vitamin D, vitamin K2, and collagen
- Adequate protein and micronutrients
- Mechanical loading and muscle strength
- Inflammation control
Calcium plays a supporting role — it is not the driver
17. Why are bisphosphonate drugs not emphasized in a functional health model of bone care?
*Bisphosphonates work by suppressing bone resorption, not by restoring bone quality or strength. While they may increase bone mineral density on a DEXA scan, they do so by inhibiting normal bone remodeling, a process that is essential for repairing microdamage and maintaining healthy bone architecture.
From a functional health perspective, several concerns are considered:
- Bone is a living, adaptive tissue that requires ongoing turnover to remain resilient
- Long-term suppression of remodeling may allow microcracks to accumulate, potentially increasing fracture risk over time
- Bisphosphonates do not address underlying contributors to bone fragility such as hormonal deficiency, sarcopenia, nutrient imbalance, inflammation, or impaired collagen quality
- Rare but serious adverse effects — including atypical femoral fractures and osteonecrosis of the jaw — highlight the consequences of excessive turnover suppression
In functional care, the goal is bone strength, resilience, and repair, not simply higher bone density scores. This approach prioritizes restoring the biological signals that drive healthy bone remodeling — including hormonal balance, mechanical loading, collagen matrix support, and nutrient regulation — before or alongside consideration of anti-resorptive medications.
Bisphosphonates may be appropriate in select high-risk situations, but they are not considered first-line tools when the objective is long-term bone strength rather than short-term density changes.
Footnote
Bisphosphonates primarily reduce fracture risk through suppression of osteoclast-mediated resorption. In patients with very high fracture risk or recent fragility fractures, anti-resorptive therapy may be appropriate as part of a broader, time-limited strategy.
This content is intended for educational and informational purposes only and should not be construed as medical advice. The information presented reflects current evidence and clinical perspectives but does not substitute for individualized medical care. Readers should consult their physician or qualified healthcare provider before making changes to medications, supplements, exercise programs, or treatment plans.
