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What about osteoporosis?
Magnesium and osteoporosis

Osteoporosis is a serious progressive bone metabolism disease, a multifactorial disease, and a common disease of the elderly, especially postmenopausal women. It is known that calcium deficiency can lead to osteoporosis, but it should not be prevented. Few people know that it is as important as calcium in formation and prevention. Magnesium deficiency is also a risk factor for osteoporosis. Osteoporosis is not only calcium deficiency, but also osteomalacia in myopia. Osteoporosis is calcium deficiency and magnesium, boron, zinc, copper, silicon and other minerals and bone components, such as collagen. Here is just a brief introduction of magnesium and osteoporosis related issues.

Magnesium is the main component of bones. 60% of magnesium in human body exists in bones. When it is insufficient, it will be released from the bones and promote the formation of bones, teeth and cells. Magnesium is formed in the intercellular substance of normal bones. Magnesium plays a key role in regulating bone mineral metabolism and is also related to calmodulin. Magnesium deficiency can stimulate parathyroid hormone (PTH) secretion and promote bone absorption. The sensitivity of magnesium to PTH target tissue and the activation of vitamin D metabolism are the basis. Magnesium is an important element to help and promote calcium absorption. Magnesium deficiency can change calcium metabolism and calmodulin, and magnesium supplementation can improve bone mineral density.

1. magnesium is the key to promote calcium absorption.

1 and magnesium are necessary for the hydroxylation of vitamin d into bioactive 1, 25 (OH) 2D3. The key to calcium supplementation is absorption, which is affected by many factors. It is known that vitamin D can help the intestine absorb calcium. However, if magnesium is not enough, it will increase the demand for vitamin D and cause vitamin D incompatibility. It is known that vitamin D needs to be hydroxylated by 25- hydroxylase in liver and 1α- hydroxylase in kidney to form 1, 25 (OH) 2d3, and this hydroxylation process needs magnesium to promote. Magnesium deficiency can produce vitamin D resistance syndrome, and 1, 25 (OH) 2d3 and PTH can produce targets with vitamin D.

2. Magnesium can regulate the balance between parathyroid hormone and calcitonin: parathyroid hormone and calcitonin are known to regulate calcium levels in bones, soft tissues and blood. When tissues and blood are deficient in calcium, PTH is secreted, which releases calcium from bone and reduces bone calcium. The calcium released by bones is several hundred percent, which can make the blood calcium much higher than normal. High calcium enters the blood and deposits on various organs and tissues, thus forming related diseases, such as deposition on bones. If deposited around the joints, arthritis will form. If deposited on the blood vessel wall, it will form calcification of the blood vessel wall and promote arteriosclerosis. Magnesium can inhibit PTH, stimulate calcitonin to help calcium enter bones and prevent osteoporosis. When blood calcium is high, calcitonin can move blood calcium into bone and keep it. Adequate magnesium is an important mineral element to adjust this balance.

3. Lack of magnesium leads to calcium malabsorption: Without enough magnesium, calcium cannot be fully absorbed. According to the International Clinical Review, people who are given a low-magnesium diet and supplemented with calcium and vitamin D are all short of calcium except magnesium. When they take calcium intravenously, their blood calcium can increase, and when they stop taking calcium, their blood calcium drops rapidly. However, when they were given magnesium, they didn't get calcium supplement.

Hypocalcemia caused by magnesium deficiency is due to calcium malabsorption, and people with magnesium deficiency become refractory hypocalcemia, which may be due to the resistance of target organs (bones and kidneys) to PTH, and vitamin D cannot form active metabolism. Magnesium supplementation can restore the reactivity to vitamin D and PTH and correct hypocalcemia, so magnesium is considered as the key to calcium absorption.

Secondly, magnesium can prevent calcification of tissues and cells.

1, magnesium is a natural calcium antagonist: this is mainly because resistant calcium enters tissue cells, because there is a certain proportion of calcium inside and outside cells, and intracellular calcium is one tenth of that outside cells. If intracellular calcium increases and cells lose their vitality, cell function will be abnormal, which will lead to related diseases. Magnesium can regulate calcium levels inside and outside cells, and magnesium outside cells and cell membranes plays an important role in controlling calcium intake, content, combination and redistribution. When magnesium is low, it will enhance calcium inflow, while when magnesium is high, it will block calcium inflow. Experiments show that magnesium deficiency is accompanied by the increase of intracellular calcium, and calcium can not be squeezed out of cells through the activity of magnesium-dependent calcium -ATP magnesium, which leads to calcification of mitochondria and other tissues and cells. Therefore, magnesium and calcium must be balanced, and magnesium should be supplemented at the same time to prevent low magnesium and high calcium.

2. Harmfulness of high calcium-magnesium ratio: "The calcium-magnesium ratio in your cells is the biochemical age of people". If you pay attention to supplementing calcium instead of magnesium, cells will "commit suicide", and the formation of calcification depends on your biochemical state. In addition, a large amount of calcium supplementation may cause hypercalciuria, kidney calculi and imbalance of calcium-magnesium ratio, and magnesium supplementation can reduce this danger and improve mineralization.

3. As early as 1940, studies have shown that magnesium has anticoagulant effect, and calcium is known to play a certain role in the process of blood coagulation. If the ratio of calcium to magnesium increases, the risk of blood coagulation and thrombosis will increase. When estrogen and calcium are used to treat osteoporosis, the demand for magnesium will increase, because estrogen increases intravascular coagulation, promotes thrombosis, and magnesium antagonizes calcium and enhances fibrinolysis. Platelet aggregation needs calcium and magnesium, but it is dependent on calcium. Magnesium is needed for platelet depolymerization and morphology maintenance. Aggregating platelets releases serotonin, which leads to vasoconstriction. Calcium enhances the release of serotonin from platelets, magnesium inhibits the release of serotonin, and magnesium also inhibits the vasoconstriction caused by serotonin. Experiments have proved that magnesium can resist the thrombosis of atherosclerotic plaque and the microthrombosis related to arterial spasm.

Third, magnesium deficiency can lead to osteoporosis.

1. Bone magnesium and blood magnesium in patients with osteoporosis are decreased. There is evidence that postmenopausal women are accompanied by low magnesium, and magnesium retention is obvious during magnesium load test. Female advanced osteoporosis is a "skeletal manifestation of chronic magnesium deficiency". Among 20 cases of advanced osteoporosis, 12 cases showed decreased trabecular magnesium and abnormal bone crystallization, and (secondary) O in postmenopausal osteoporosis, senile osteoporosis, alcoholic osteoporosis and diabetes mellitus was also related to magnesium deficiency. As we all know, the intake and absorption rate of magnesium in the elderly are low. Diabetic patients have polyuria and increased magnesium excretion, which leads to magnesium deficiency. Insulin is beneficial to the uptake of magnesium by cells. Chronic insulin deficiency can reduce tissue magnesium, including bone magnesium. The decrease of bone magnesium and cellular magnesium has been detected in diabetic patients, so osteoporosis is a common complication of insulin-dependent diabetes. Cohen et al. detected the bone magnesium of human bone and upper femur, and observed that the bone magnesium of patients with osteoporosis and diabetes decreased significantly by 65,438+00%, while that of alcoholics decreased by 65,438+08%. The magnesium residue in patients with osteoporosis was more.

2. Experimental magnesium deficiency leads to bone loss: American expert Seelig described the early scholars' research on the relationship between magnesium and bone. Experimental magnesium deficiency can reduce bone, narrow bone and thin tibia, and magnesium deficiency can reduce bone collagen and bone alkaline phosphatase. Magnesium deficiency can cause hyperosteogeny, periosteoma and osteolysis, and disappear after magnesium supplementation.

In recent years, Rude pointed out that magnesium deficiency is usually related to osteoporosis. Magnesium deficiency leads to hypocalcemia, impaired PTH secretion and resistance of end organs to PTH, and the level of serum 1, 25 (OH) 2D3 decreases. The deficiency of these two hormones will affect bone formation; In addition, magnesium deficiency can also lead to the decrease of immunoglobulin. In acute magnesium deficiency rats, substance P increased rapidly with the increase of inflammatory cytokines, which contributed to the increase of bone resorption of osteoclasts and explained the decoupling of bone formation and bone resorption.

Fourthly, the effect of magnesium supplementation on osteoporosis.

1, magnesium in the treatment of osteoporosis: magnesium plays an important role in many physiological processes, which fails to activate osteoblasts, increase bone mineralization and enhance the sensitivity of target tissues to PTH and 1, 25 (OH) 2D3.

2. Magnesium supplementation can inhibit bone turnover. The author gave 12 young people Mg 15mmol/d, and checked it two hours after intake. Results: The biochemical indexes of bone formation, namely osteocalcin, decreased by 65438 05%, PICP by 20% and ICTP by 30%. Serum PICP and osteocalcin are obviously related to serum levels, that is, magnesium supplementation can inhibit bone turnover, while reducing bone loss can increase bone peak, which is beneficial to prevent osteoporosis.

3. Effect of magnesium supplementation: Stanley et al. gave magnesium supplementation to chickens, which activated the activity of bone pyrophosphatase. The reaction of rabbits is similar to that of chickens. Magnesium supplementation reduces bone calcification and maturation. After magnesium supplementation, the weight of ashes is obviously reduced. The effect of magnesium supplementation on bones varies from race to race. Under the agreed model, mice with vitamin D deficiency and magnesium deficiency in bones are more beneficial, which may be due to the increase of PTH response or the direct effect of magnesium on skeletal system.

To sum up, magnesium deficiency and calcium deficiency are the same factors leading to osteoporosis. Magnesium is the key to help calcium absorption. Magnesium is necessary for hydroxylation of vitamin D into bioactive 1, 25 (OH) 2D3. Magnesium deficiency can produce vitamin D low resistance syndrome. Magnesium supplementation can prevent bone loss, increase bone density and inhibit bone turnover. To treat osteoporosis, we should not only supplement calcium, but also supplement magnesium.