Joints & Bones
Bones do a lot more than just provide some shape to our bodies; they also produce blood cells, store and release minerals, and help regulate blood acid-base balance. Joints are the places where bones meet. Diet, vitamins, minerals, and other supplements all can play a role in bone and joint health.
Bones not only provide shape to our bodies and protection for our organs but also produce red and white blood cells, act as a store for minerals like calcium and phosphorus, and help regulate blood acidity. Joints are simply the spaces where bones meet. Some joints allow for a movement, such as knee joints, whereas others don’t, such as the joints between skull bones. The most common type of joint in the body — and the one that probably most easily comes to mind — are synovial joints, which are surrounded by a fluid-filled cavity and also contain cartilage to help with smooth movement.
A healthy diet high in fruits, vegetables, whole grains, fish and poultry, nuts, legumes, and low-fat dairy is associated with better bone health. Getting enough vitamin D, vitamin A, and calcium is particularly important for bone health. A healthy diet — along with weight loss in people with obesity — is also important for joint health.  On the other end of the spectrum, being underweight decreases bone density while raising the risk of osteoporosis. Increasing oily fish intake and good sources of vitamin K like leafy greens, Brussels sprouts, and broccoli may also be helpful in slowing osteoarthritis, which is the most prevalent form of arthritis.
For bone health, vitamin d and calcium together have evidence supporting their use, although vitamin D on its own may not do much in this regard. vitamin k supplements may also help prevent fractures to a small extent. Supplements for joint health include glucosamine, chondroitin, boswellia, turmeric, type ii collagen, fish oil, and more.
Supplement GuideClick here to read the Joint Health Supplement Guide
Bone is much more dynamic than it may appear, constantly undergoing a remodeling process of resorption and new bone formation. Whether or not bone mass is lost through resorption or gained is determined by the balance between osteoclast cells, which carry out bone resorption, and osteoblast cells, which form new bone tissue. The ability of bone to undergo dynamic remodeling is important for regulating calcium and phosphate levels in the body, as well as healing bone fractures and adapting to different mechanical stimuli.
osteoporosis, which literally means “porous bone”, is caused by an imbalance between osteoblasts and osteoclasts, favoring the bone- resorbing activity of the latter. The risk of such an imbalance greatly increases after about age 50, particularly so in women at the time of menopause. Osteoporosis is a common cause of bone fractures in older adults.
Since weight-bearing exercise increases mechanical loading on bones, such exercises act as a positive stimulus for increased bone mass. It would follow that obesity might have a similar effect, promoting increased bone mass in response to the higher forces on the skeleton imposed by moving around at a higher body weight. Although some human studies have indicated that bone mass does increase with obesity, results have been mixed, with other studies finding the opposite effect: a paradoxical decrease in bone mineral density (BMD) and an increase in fracture risk.
The reason for variation in associations between obesity and BMD across different studies and populations is an ongoing area of research. Animal studies have shed further light on the complex effects of obesity on bones, with one mouse study revealing an increase in bone mass during the early stages of obesity, but impaired bone formation with chronic obesity. In populations where it occurs, obesity-associated loss of BMD may be partially explained by the effects of obesity on mesenchymal stem cells (MSCs), a stem cell population in bone marrow capable of differentiating into a number of different tissues including muscle, bone (osteoblasts), fat (adipocytes), and cartilage. Since adipocytes and bone-building osteoblast cells arise from the same MSC progenitor cells, a shift in the differentiation of MSCs to adipocytes causes a reciprocal decrease in the number of osteoblasts. A change in the balance of osteoblasts to osteoclasts would reduce bone mineral density over time and increase risk of osteoporosis.
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