Top 10 Evidence-Based Recommendations

K2 activates osteocalcin via γ-carboxylation so it can bind hydroxyapatite—literally telling calcium to mineralize bone. MK-7 has a long half-life and superior bioavailability vs MK-4, making once-daily dosing effective. ^{[1] [2] [3]}

A 3-year RCT (n=244) showed MK-7 180 mcg/day slowed age-related loss at spine/femoral neck and improved bone strength indices vs placebo. A 2022 meta-analysis of 16 RCTs (6,425 women) found K2 improved lumbar spine BMD. ^{[4] [5]}

Polyphenols and potassium in prunes reduce osteoclast activity (resorption) and preserve trabecular structure. ^[7]

In a 12-month RCT (n=235), 50 g/day prunes preserved total hip BMD vs a −1.1% loss in controls; fracture risk (FRAX) worsened only in controls. Prior 6-month RCTs also prevented total-body BMD loss and lowered TRAP-5b. ^{[7] [8]}

Collagen forms ~90% of bone's organic matrix. Providing peptide fragments (rich in hydroxyproline) upregulates osteoblast activity and increases bone formation markers. ^[9]

12-month RCT (n=131) in post-menopausal women: 5 g/day SCP increased spine and femoral neck BMD vs placebo and improved P1NP/CTX profile. Calcium-collagen chelate trials also showed slower whole-body BMD loss vs calcium alone. ^{[9] [10]}

Supplies hydroxyapatite substrate; suppresses PTH and bone resorption when intake is sufficient. Citrate absorbs better than carbonate, especially with low stomach acid. ^{[12] [13] [14]}

Calcium alone or with D shows inconsistent fracture reduction in community-dwelling adults, but remains essential to avoid secondary hyperparathyroidism. Citrate is ~20–27% better absorbed than carbonate and works even with achlorhydria/PPIs. ^{[12] [13] [14] [15]}

Increases intestinal calcium absorption and supports mineralization; deficiency raises PTH and accelerates bone loss. ^[17]

In VITAL (25,871 adults), D3 2,000 IU/day did not reduce fractures in generally replete adults. Annual mega-doses (500,000 IU) increased falls and fractures—avoid boluses. Benefit likely when correcting deficiency or with institutionalized/low-intake groups. ^{[17] [18] [19]}

Required for 1-α-hydroxylase (activates vitamin D), PTH signaling, and bone matrix quality; many older adults are low. Citrate/glycinate absorb far better than oxide. ^{[20] [21]}

Human RCTs for BMD are limited, but pediatric/young adult trials and meta-analyses show better bioavailability with citrate vs oxide and improved hip BMC in supplementation trials; observational data link higher Mg intake to better BMD. ^{[20] [22]}

Orthosilicic acid stimulates type I collagen synthesis and early mineralization—improving the "rebar" collagen network so calcium can harden it. ^[11]

12-month RCT in osteopenic women: ch-OSA plus Ca/D improved bone formation marker PINP vs Ca/D alone and showed subgroup femoral neck BMD benefits; safe and well-tolerated. ^[11]

Modulates gut inflammation and calcium handling; reduces osteoclast activation via immune signaling. ^[23]

12-month RCT in women aged 75–80 with low BMD: L. reuteri 6475 reduced tibial vBMD loss vs placebo. A newer 2-year RCT in early post-menopause found no benefit overall—effects may depend on age/BMI. ^{[23] [24]}

Western diets create net acid; bone buffers it by dissolving mineral. Potassium alkali reduces urinary calcium loss and bone resorption. ^{[25] [26]}

NEJM balance studies and dose-finding RCTs show reduced urinary calcium and bone turnover. A 24-mo RCT in healthy elders saw lumbar BMD increases, but a large RCT in healthy post-menopausal women found no BMD benefit—results likely depend on dose and baseline acid load. ^{[25] [26] [27] [28]}

Protein raises IGF-1, supports collagen formation, and maintains muscle (fewer falls). Very low protein intake increases fracture risk. ^{[29] [30]}

NOF meta-analysis: higher protein intake is neutral-to-beneficial for BMD when calcium is adequate; cohort data show higher fracture risk with low protein. Protein supplements alone rarely raise BMD but help when baseline intake is low. ^{[29] [31]}