加载中…
Place · Level 3 · Condition
DXA T + FRAX · 髋骨折 1 年死亡 20-30% · 钙+D+蛋白+力量 · 双膦/Denos/Romo · 围绝经窗口
synergy · 1
Older people should eat less protein is a mistaken cultural expectation, and it damages two things at once: bone matrix and muscle. Bone density and muscle mass decline together and jointly set fall risk, so they are managed together.
cofactor · 5
Calcium is the building material, but absorption has a ceiling: past roughly 500 mg in one dose the fraction absorbed falls, so take it with meals and split it. Food first, supplements for the gap — a large single dose mostly just passes through the kidney.
Vitamin D decides whether the calcium you eat is absorbed at all: the target is 25(OH)D held between 30 and 50 ng/mL, reached with food, sun and supplements where needed. Below that line, more calcium mostly does not stay.
Bone is not only mineral: its matrix is collagen, and collagen needs protein. In fracture recovery or chronic illness the target is 1.2-1.5 g/kg/day, delivered as 25-40 g per meal with at least 2.5 g of leucine to drive synthesis — the distribution is easier to overlook than the total.
K2 governs where calcium goes: osteocalcin and matrix Gla protein both need gamma-carboxylation to work — the first clamps calcium into bone, the second keeps it out of the arterial wall. The mechanism is clear; the fracture-endpoint trial evidence is still early.
Magnesium is a supporting role in bone health but not an optional one: 320-420 mg/day elemental, involved in hydroxyapatite crystal formation and a cofactor on the vitamin D activation pathway. Short of it, the calcium-and-D machinery runs at a discount.
depletes · 1
↮GERD
Long-term PPI (>1 yr) → reduced gastric acid → impaired Ca/Mg/B12 absorption → reduced BMD + fracture risk. FDA 2010 boxed warning. GERD step-up therapy should pair with bone health + Ca + D + deprescribing strategy.
regulates · 7
↔Bone
Osteoporosis = remodeling imbalance (resorption > formation) + mineralization ↓ + microarchitectural deterioration. FRAX (Kanis 2008) integrates age / BMI / parental hip fracture / smoking / alcohol / steroid + BMD into 10-yr fracture probability. NOF 2016: treatment thresholds + stepwise therapy.
Perimenopause + first 5 yr postmenopause is peak bone-loss window (~2-3%/yr, spine higher). MHT (especially transdermal E2) is the most effective bone-protective option (beats bisphosphonates) but has a timing window; missing it relegates MHT to second-line. Pre-50 evaluation matters.
Heavy RT reverses BMD loss in perimenopausal women: LIFTMOR RCT (Watson 2018, n=135, 8 mo) → lumbar BMD ↑2.9%. Intensity + compound lifts are critical — low-intensity protocols do not work.
After menopause estrogen withdraws and the RANKL/OPG balance tips toward resorption, so bone is removed faster than it is built. Menopause matters to bone not as 'getting older' but as a predictable — and treatable — window of accelerated loss.
Vertigo causes falls, especially in older people, and one fall can cost far more than the dizziness did. Repositioning manoeuvres are not just symptom relief — they remove the first link in the fall-to-fracture chain.
Male osteoporosis is systematically underdiagnosed: bisphosphonates plus calcium, vitamin D and strength training apply the same way, and where testosterone really is low it should be assessed as hypogonadism — not filed as a women's condition.
An abnormal blood calcium is not telling you about intake; it says the regulatory system itself is off — parathyroid, kidney, certain tumours — and that is a signal for a doctor. How calcium moves in and out of bone, and how to read bone density, is where skeletal status is actually judged.