Bone Fracture Healing

Question:  Can anyone advise me on how to help my brother who fractured his Tibia 17 weeks ago and had an IM rod inserted, but the bone is healing too slowly.   Is there anything he can do to speed the process up?  —AD

Three suggestions:   First, mineral therapy.  This should get many responses from the FACT group.  Featuring 1) vitamin D3 (>5K units) to facilitate calcium utilization (much better than calcium supplementation, 2) magnesium, 3) strontium (low dose), 4) manganese, 5) boron, 6) copper, 7) silicon (horsetail grass, or bamboo), and 8) other trace minerals (as identified as deficient by cellular mineral testing, not serum testing).  Also consider toxic minerals that might counteract any of these nutritional minerals (lead, for example, can sabotage calcium and deposit in bone).

Second, collagen therapy.  Bone healing is as much about protein as mineral.  Collagen protein requires lots of proline, lysine and glycine, which can be supplemented as free-form amino acids for vegetarians and vegans or as predigested (hydrolyzed) collagen protein for omnivores.  Collagen-protein maturation requires vitamin C and bioflavonoids.  For vitamin C, I’d suggest that you consider doses of 4 grams per day (1 gram with each meal, and one before bed), or more.  For bioflavonoids, low dose and broad spectrum is probably best.  I do not know of any formulations of this kind, but other FACT participants might have product recommendations.  When I broke my fibula, I used multiple high-dose bioflavonoid formulations on a daily-rotation basis (a different one each day of the week).  Collagen maturation also requires iron, copper and silicon.  Iron is rarely deficient, especially in men.  But type-II copper deficiencies (cytokine induced) are quite widespread.  Transdermal copper cream applied to the leg can mitigate type-II copper deficiencies.  Consider the back of the knee, the inside of the ankle and any unbroken skin immediately above the fracture for administration of copper cream.  Assessment of type-11 copper deficiency must involve cellular assessments via enzyme activities; ceruloplasmin is frequently inversely related to bioavailable copper.  Type-II iron deficiency (also cytokine mediated) can impair bone healing, particularly when serum iron storage (ferritin) hits saturation and “leaks” into plasma, thus sabotaging vitamin C’s effects on collagen maturation.  Subclinical hemochromatosis is routinely missed in the USA.

Third, reduce sources of inflammation.  Chronic inflammation activates WBC cytokine production which 1) turns on the liver sequestration mechanism for iron, copper and zinc, 2) turns on the aromatase enzyme, which converts bone-building progesterone and testosterone into protein-synthesis-suppressing estrone and estradiol, and 3) turns on IDO (indoleamine dioxygenase) which catabolizes serum tryptophan, decreases CNS serotonin, sabotages sleep architecture and sleep-induced melatonin release, and interferes with protein-mediated tissue healing during sleep.  Chronic exposure to molds, spores, dust mites (use HEPA air filter in the bedroom).  Food-based delayed hypersensitivities involving IgG, IgA and IgM antibodies (eliminate wheat, corn, milk, yeast, as most common “food allergies”).  Consider low-level chronic infection (bacterial, viral, fungal, etc.).  All of these may be aggravated by low basal metabolic rate and hypercoagulopathies, both of which result from increased estrogen influence.  I hope this helps.  —Steve

From the FACT site (

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