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synergy · 2
When muscles contract they pull on bone, and this loading is one of the main mechanical signals for rebuilding bone. With age, sarcopenia and osteoporosis often appear together (a combination called osteosarcopenia). Strength training loads muscle and bone at the same time, which makes it one way to look after both.
When older adults do strength training, contracting muscles pull on bone and give it a mechanical signal to remodel. Liu 2009 pooled 121 randomized trials: progressive strength training clearly improved strength and mobility in older adults, the very old and frail included; how much bone density rises is a question for trials that measure bone directly.
cofactor · 6
99% of your calcium is stored in bone as hydroxyapatite crystals grown along collagen fibers. When blood calcium dips, parathyroid hormone sends osteoclasts to draw calcium back out of bone into the blood. Bone is calcium's checking account, with money going in and out, not a vault that only takes deposits.
K2 adds carboxyl groups to the glutamate units of osteocalcin, and only then can osteocalcin grip calcium. Without this step, the osteocalcin that bone-building cells release is like a rope that cannot hold on to calcium.
The mineral in bone is hydroxyapatite itself, and phosphorus is the crystal's other half; about 85% of the body's phosphorus is stored in bone. Talking about calcium without phosphorus gives only half the recipe.
Prolyl hydroxylase needs vitamin C as its cofactor to twist the three strands of type I collagen into a stable triple helix. Collagen is roughly 30% of bone by weight and about 90% of its organic matrix. Mineral makes bone hard; collagen keeps it from being brittle.
Lysyl oxidase needs copper to build cross-links between neighboring collagen fibers; the firmer those links, the tougher the bone. When copper runs short, bone density can still look normal while the bone becomes brittle.
About 60% of the body's magnesium is stored in bone, some of it on the surface of the hydroxyapatite crystals, where it affects how large they grow. Magnesium is also a cofactor for the enzymes that activate vitamin D, so when magnesium is short, supplemented vitamin D may not be converted well.
regulates · 11
Perimenopause is the turning point for bone loss: as estrogen withdraws, the cells that remove bone outpace the cells that build it, and bone is lost fastest in the years around menopause. So attention to bone need not wait until 65.
The breakdown and building of bone is directed by several hormones: when blood calcium falls, parathyroid hormone draws calcium out of bone, and calcitonin works the other way; estrogen protects bone density; and cortisol that stays too high for a long time (including long-term glucocorticoid drugs) causes secondary osteoporosis.
In chronic kidney disease, phosphate cannot be cleared, vitamin D activation falters, parathyroid hormone rises in response, and bone suffers along with them. The whole set of changes is called chronic kidney disease–mineral and bone disorder, and its bone part is called renal osteodystrophy. Once kidney function declines, calcium and phosphate metabolism is a clinical problem that has to be managed.
Osteoporosis is an imbalance in bone rebuilding: bone is removed faster than it is laid down, bone mass falls, the bone's fine structure breaks down, and bone becomes fragile. The FRAX tool combines age, body mass index (BMI), a parent's hip fracture, smoking, drinking, glucocorticoid use and other factors with bone density to estimate the chance of fracture over the next 10 years (Kanis 2008), which doctors use to decide on treatment.
Estrogen holds back bone breakdown and keeps bone removal and bone building in balance; when estrogen falls in perimenopause, bone is lost fastest. Low testosterone in men likewise speeds up osteoporosis, though it is often overlooked.
Skin is where vitamin D starts: UVB in sunlight converts 7-dehydrocholesterol in the skin into a precursor of vitamin D, which the liver and kidney then process into the active form that helps the gut absorb calcium. Skin tone, sunscreen and latitude all affect bone at this first step in the skin.
The signaling pair RANKL and OPG regulates the osteoclasts that break down bone and is also used by the immune system: activated T cells release RANKL, which speeds up bone breakdown. The bone erosion next to joints in rheumatoid arthritis is tied to this mechanism.
In mice, undercarboxylated osteocalcin released by bone-building cells enters the blood and promotes insulin release and insulin sensitivity, which is why bone is regarded as an endocrine organ. How much this pathway matters in people is still unsettled.
The impact of each landing loads the bones, and bone remodels along those loads and grows stronger. But the impacts add up, and if they outpace the bone's repair, cumulative injuries such as stress fractures can follow. When van Gent 2007 pooled leg injuries in distance runners, the risk factors with the strongest evidence were a long weekly distance in men and a previous injury.
Bone is living tissue, and repeated but tolerable pressure along its long axis makes it stronger, so supervised, gradually progressed resistance training helps adolescents build bone density. Well-designed training has not been seen to affect growth in height or harm the growth plates; the injuries that get reported mostly happen in unsupervised settings with unsafe technique.
With long-term low energy availability, estrogen falls, so bone breakdown loses its brake while bone building runs short of energy, and bone density slides down round after round; when fine fatigue cracks in bone are not repaired in time, they join into a stress fracture. That is why missed periods and repeated stress fractures in training so often appear together: they are largely two results of the same energy gap.