Help prevent osteoporosis by leading a bone-healthy lifestyle at all stages of life. Osteoporosis occurs when the ratio of bone synthesis to resorption is shifted towards resorption. In people with osteoporosis, the bones become porous and weaker, increasing the risk of fractures, especially in the hip, spinal vertebrae, and some peripheral joints, such as the wrists.
The hormones oestrogen and androgen protect bones from increased mineral loss. With menopause, however, women’s estrogen level decreases – making older women especially more prone to osteoporosis, contrary to men of the same age.
One of the risk factors for bone loss, and thus the development of osteoporosis, is an inadequate dietary intake of nutrients important to bones.
This review examines the impact of nutrition on bone health and compares the level of nutrient intake required as part of the dietary recommendations.
Over 99% of total body calcium is found in bones and teeth, where it functions as a key structural element. The remaining body calcium functions in metabolism, serving as a signal for vital physiological processes, including vascular contraction, blood clotting, muscle contraction and nerve transmission.
Inadequate intakes of calcium have been associated with increased risks of osteoporosis, nephrolithiasis (kidney stones), colorectal cancer, hypertension and stroke, coronary artery disease, insulin resistance and obesity. Most of these disorders have treatments but no cures. Owing to a lack of compelling evidence for the role of calcium as a single contributory element in relation to these diseases, estimates of calcium requirement have been made based on bone health outcomes, with the goal of optimising bone mineral density. Calcium is unique among nutrients, in that the body’s reserve is also functional: increasing bone mass is linearly related to the reduction in fracture risk.
To a great extent, individuals are protected from excess intakes of calcium by a tightly regulated intestinal absorption mechanism through the action of 1.25-dihydroxy vitamin D, the hormonally active form of vitamin D. When the amount of absorbed calcium is more than what the body needs, the excess is excreted by the kidney in most healthy people. If patients consume inadequate amounts of calcium, the body starts dissolving bones to release calcium and maintain adequate amounts in the blood. This leads to excess excretion in urine and crystallisation to form kidney stones.
Concern for excess calcium intake is directed primarily to those who are prone to milk-alkali syndrome (the simultaneous presence of hypercalcaemia, metabolic alkalosis and renal insufficiency).
Although calcium can interact with iron, zinc, magnesium and phosphorus within the intestine, thereby reducing the absorption of these minerals, available data do not suggest that these minerals are depleted when humans consume diets containing calcium above the recommended levels. For example, even though high intakes of calcium can exert acute effects on iron absorption, there is no evidence of reduced iron status or iron stores with long-term calcium supplementation.
Great heterogeneity exists in the formulation of dietary recommended intakes for calcium and magnesium, and future recommendations should ideally be based on established and common methodologies for respective age groups. Based on the survey data available, it is clear that very large numbers of people consume insufficient levels of these minerals that are to support the most conservative estimates of their physiological needs.
In fact, copper, magnesium, zinc and calcium status were measured in postmenopausal women with osteoporosis (n =23) and osteopenia (n = 28) as classified based on the T-score of the femur neck and dual-energy X-ray absorptiometry results. Anthropometric indices, dietary intake and serum copper, magnesium, zinc and calcium were assessed. The results of this study showed that the mean dietary intake of magnesium, zinc and calcium in postmenopausal women with low bone density was significantly lower than the recommended dietary allowance. The mean serum levels of zinc (P = 0.001) and copper (P = 0.000) were significantly lower than the normal range and 40% of these participants had serum magnesium levels lower than the normal range.
Due to the mineral deficiency in post-menopausal women with low bone density and the key role of minerals on bone health, supplementation with magnesium, calcium, zinc and perhaps copper are recommended.
Magnesium is the fourth most abundant mineral in the body overall and is essential for maintaining peak physical and mental functioning, yet dietary intake may be insufficient to meet the body’s demands. Magnesium deficiencies are relatively common and may lead to a range of symptoms including loss of energy, fatigue, muscle cramps, metabolic and mineral disturbances. Magnesium supplementation may be required to restore magnesium balance and consequently to improve overall health.
Magnesium is vital for the absorption and metabolism of calcium. In simple terms, magnesium converts vitamin D into its active form so that it can help calcium absorption. Magnesium deficiency impacts on the bone also indirectly by affecting the homeostasis of the two master regulator hormones of calcium homeostasis, ie, parathyroid hormone (PTH) concentrations and 1.25(OH)2-vitamin D3 thus leading to hypocalcaemia.
Magnesium also stimulates a particular hormone, calcitonin, which helps to preserve bone structure and draws calcium out of the blood and soft tissues back into the bones, preventing osteoporosis, some forms of arthritis and kidney stones.
Over 60% of the body’s total magnesium supply is stored in our bones. Several studies have found a direct link between low magnesium levels and osteoporosis. However, low magnesium is not only about weakening bones or an issue for older women. Deficiency of this key mineral has also been linked to neuromuscular disorders, hypertension, cardiac arrhythmias, insulin resistance and eclampsia, mitral valve prolapse, atherogenesis and disordered bone metabolism.
One study of postmenopausal women with either osteoporosis or osteopaenia, which is when bones are weaker than normal prior to developing osteoporosis, found that over 40% of the study participants had low magnesium levels.
Why are so many of us lacking in magnesium? A Western diet rich in processed food and relatively poor in micronutrients seems to be one of the main reasons. By making better food choices, we can provide better nutrition for our bone health. Green vegetables are an excellent source of magnesium, as are nuts, seeds, unprocessed grains, and some legumes.
Supplementation can also play an important role in improving the health of our bones. A study of women with osteoporosis in Israel reported significantly increased bone mineral density amongst those women who took a supplement that contained magnesium.
Due to the apparent widespread deficiency of magnesium, and the ongoing recognition of the key role that certain minerals play with regards to bone health, supplementation with magnesium as well as calcium and even Vitamin D is often recommended. If the two biofactors vitamin D and magnesium, which are essential for bone synthesis, are not available, the course of osteoporosis can intensify. According to recent findings, magnesium is also credited with stabilising functions in bone building. If there is no stabilising magnesium during bone synthesis, this also decreases bone density.
However, healthy magnesium and calcium-rich diet and supplementation should not only start after menopause.
Studies have shown that sufficient magnesium intake in childhood positively relates to bone mass density as you grow older. The bottom line is that building healthy bones throughout your life is the best strategy to prevent osteoporosis later in life.
As with any vitamin and mineral, it is better to focus on a healthy, balanced diet to meet daily requirements of magnesium and to use supplements as a backup. But the reality is that not all of us will achieve the recommended daily intake of magnesium, let alone calcium.
Not only can a supplement containing these key minerals assist people who are predisposed to osteoporosis, but a supplement containing magnesium can also assist those who suffer from muscle cramps.
Another aspect to consider is the evidence that adults on a western diet develop a low-grade acidosis which is intensified by ageing. Recently, the acid load imposed by this diet has been suggested to play a role in the pathophysiology of osteoporosis. Indeed, metabolic acidosis has been shown to lead to calcium loss from bone, inhibit osteoblast function and stimulate osteoclast activity, and impaired bone mineralisation. Accordingly, a neutralising diet improves bone micro-architecture and bone mineral density. It is therefore feasible that part of the effects of magnesium on the skeleton is due to its capability to act as a buffer for the acid produced by the typical Western diet.
The calcium/magnesium bond
It is known that calcium can directly or indirectly compete with magnesium for (re)absorption in the intestine and kidney. Ionized magnesium (Mg2+) and calcium (Ca2+) also antagonise each other in many physiological activities. Studies have shown the importance of the balance between magnesium and calcium in relation to the physiological functions of these micronutrients. The same cell receptor that regulates calcium also senses magnesium. In the kidney, this calcium receptor can inhibit the re-absorption of magnesium such that excess magnesium can be passed into the urine. In the gut, calcium and magnesium may compete for intestinal absorption. If there is a small amount of calcium but an abundance of magnesium in the contents of the intestine, the magnesium gets more actively absorbed. However, a high intake of calcium can reduce the absorption of both calcium and magnesium. The amount of calcium or magnesium absorbed depends on the dietary ratio of calcium to magnesium.
Although clinical evidence is still fragmentary, the beneficial effects of the supplementation of these minerals in a manner that supports calcium and magnesium homeostasis is documented. In an article entitled, Decreased magnesium status may mediate the increased cardiovascular risk associated with calcium supplementation (DiNicolantonio, 2017), the following is noted:
In a series of magnesium balance studies conducted by Seelig about 50 years ago, she found that in men with recommended dietary allowance (RDA)-level magnesium intakes (6 mg/kg/day or above), increasing dietary calcium to high levels did not impair magnesium balance— consistent with more recent reports. However, in men with relatively low (magnesium) intakes, a high calcium intake did indeed decrease magnesium balance. Somewhat paradoxically, a low calcium intake also impaired magnesium availability in this group. If these observations are confirmed in women, they imply that a high supplemental intake of calcium might impair magnesium balance in the rather high proportion of the population who have relatively low magnesium intakes, reflecting high intakes of ‘empty calorie’ foods. However, an increased intake of calcium-rich natural foods would not necessarily have a negative impact on magnesium balance because these foods also would supply magnesium.
If high calcium intakes in humans can indeed impair magnesium balance when magnesium intakes are low, the clear implication is that calcium, when supplemented, should be given in conjunction with a balanced dose of magnesium. Especially if existing calcium is high.
The conclusion includes that, “In the meantime, people (especially those consuming a relatively refined diet) who wish to supplement with calcium might be well advised to take a supplement that also includes highly bioavailable magnesium,” and “The concept of ‘balancing’ calcium and magnesium in supplements has, in fact, been the accepted wisdom in ‘health food’ circles for decades, owing to Seelig’s research and its promulgation by popular health food pundits”.
It should also be noted that the absorption and bioavailability of minerals can be affected by various factors such as age, sex, smoking status, alcohol use, physical activity, use of other vitamins and mineral supplements, etc and should be taken into consideration during patient assessment.
The role of vitamin D
For calcium to reach the bones in the first place, vitamin D is indispensable.
Both vitamin D and magnesium are responsible for calcium’s absorption and its incorporation into our bones. If they are not available, the locomotor system cannot function well. For optimal calcium supply as well as healthy bones and joints, calcium should always be purposefully taken, combined with magnesium and vitamin D.
One of the main tasks of vitamin D lies in regulating calcium in our body – cholecalciferol (vitamin D3). It controls the absorption and utilisation of calcium from the diet. If there is too little vitamin D available, not enough calcium reaches the blood through the intestinal walls and the calcium level decreases – regardless of the calcium quantity supplied with the food. Although calcium in high doses can also reach the blood passively (ie without the help of vitamin D), this occurs only to a negligible extent. With babies and toddlers, this can become critical because they must incorporate a lot of calcium into their growing bones. Therefore, vitamin D is often administered to them as a preventive measure against rickets. In this disease – also called ‘bone softening’ – bones need the essential calcium, as the consequence is their impaired mineralisation, which leads to shortened and crooked limbs. However, vitamin D deficiency can also intensify diseases of old age such as osteoporosis.
Vitamin D contributes to the principal factors that maintain calcium homeostasis. 1.25(OH)2-vitamin D, the hormonally active form of vitamin D, is the major controlling hormone of intestinal calcium absorption. Calcium homeostasis is also regulated by parathyroid hormone and ionized calcium.
Increasing evidence indicates that the reason for disturbed calcium balance with age is inadequate vitamin D levels in the elderly.
Thus, a diet that includes foods containing vitamin D and magnesium helps to counteract the deficiency of these important nutrients. Also beneficial is taking vitamin D-rich medications with the respective indication of preventing or alleviating osteoporosis.
Vitamin D is one of the few vitamins that humans can synthesize themselves. Vitamin D is activated through sunlight – to be more precise, UV-B radiation – on the skin. Vitamin D3 is synthesized from dehydrocholesterol. From the blood, it reaches the liver, where it is converted to its storage form.
A healthy Central European adult who walks daily for approximately 20-30 minutes in the sun can fully satisfy his vitamin D need. After about 30 minutes, approximately 250 micrograms of vitamin D have been synthesized on a summer’s day. The body then virtually stops the synthesis to rule out an overdose caused by excessive sunlight. Unneeded vitamin D can be stored in fatty tissue, to be retrieved and activated in the winter months when the sun cannot send us enough UV-B radiation to synthesize more.
What is vitamin K?
Most people have never heard of vitamin K2. This vitamin is rare in the Western diet and hasn’t received much mainstream attention. However, this powerful nutrient plays an essential role in many aspects of health. In fact, vitamin K2 may be the missing link between diet and several chronic diseases.
Vitamin K was discovered in 1929 as an essential nutrient for blood coagulation. The initial discovery was reported in a German scientific journal, where it was called ‘Koagulationsvitamin’ – which is where the ‘K’ comes from.
It was also discovered by the dentist Weston Price, who travelled the world in the early 20th century studying the relationship between diet and disease in different populations. He found that the non-industrial diets were high in some unidentified nutrient, which seemed to provide protection against tooth decay and chronic disease.
He referred to this mystery nutrient as ‘activator X’, which is now believed to have been vitamin K2.
Vitamin K is a cofactor of γ-carboxylase, an enzyme necessary for the γ-carboxylation of glutamic acid residues in proteins, including osteocalcin, the principal non-collagenous protein of bone. Vitamin K deficiency increases under-carboxylated osteocalcin, a less fully functional form, and detected in osteoporotic patients. Population studies have also shown an association between low vitamin K intake and lower BMD or higher fracture risk.
Conversely, vitamin K supplementation reduces under-carboxylated fractions of osteocalcin, urinary calcium excretion, and bone resorption and increases bone formation.
There are two main forms of vitamin K:
- Vitamin K1 (phylloquinone): Found in plant foods like leafy greens
- Vitamin K2 (menaquinone): Found in animal foods and fermented foods.
Some scientists have suggested that the roles of vitamins K1 and K2 are quite different, and many feel that they should be classified as separate nutrients altogether. Controlled studies observe that vitamin K2 supplements generally improve bone and heart health and plays a central role in the metabolism of calcium.
Vitamin K2 can be further divided into several different subtypes, the most important ones being MK-4 and MK-7. Vitamin K2 occurs in nature in several forms. Each form is designated by the length of the side chain (the number of isoprenoid units) of this fat-soluble molecule. MK-4, a relatively short-chain menaquinone, is found in foods of animal origin, such as butter and egg yolks. Longer-chain menaquinones such as MK-7 is found in fermented foods, such as cheese, yoghurt, in the Japanese fermented soy food natto. MK-7 is superior to MK-4 in terms of biological activity and half-life. It remains biologically active in the body for longer and allows for better distribution and activation of extra-hepatic K2-dependent proteins such as osteocalcin and matrix gla-protein. MK-7 reaches bones and vessel walls easier than MK-4.
Osteoblasts and osteoclasts are the two types of bone cells that break down and build up bone in the bone remodelling process. Osteoclasts are the bonedisassembly cells, osteoblasts are the bone-building cells. Osteoblasts secrete a protein called osteocalcin into the blood. Vitamin K2 activates the calcium-binding actions of two proteins – matrix GLA protein and osteocalcin. When osteocalcin is in an activated state (activated by vitamin K2 MK-7), osteocalcin binds to calcium and transports it from the blood and into the bone. Osteoblasts then integrate this calcium into the bone matrix, thereby increasing the bone‘s mineral density and strength. As part of the remodelling cycle, osteoclasts remove old or damaged bone, so that it can be replaced with new bone.
Vitamin K also activates proteins that play a role in blood clotting, calcium metabolism and heart health. One of its most important functions is to regulate calcium deposition, promoting the calcification of bones and preventing the calcification of blood vessels and kidneys.
In support of the above, there is also substantial evidence from controlled studies that K2 may provide major benefits for bone health. A three-year study in 244 postmenopausal women found that those taking vitamin K2 supplements had much slower decreases in age-related bone mineral density.
Long-term studies in Japanese women have observed similar benefits. Seven of these trials, which took fractures into consideration, found that vitamin K2 reduced spinal fractures by 60%, hip fractures by 77% and all non-spinal fractures by 81%.
In line with these findings, vitamin K supplements are officially recommended for preventing and treating osteoporosis in Japan.
In summary, Vitamin D3 aids the absorption of calcium from the intestine and into the bloodstream. Vitamin K2 MK7 activates osteocalcin proteins which binds to the calcium and transports it from the blood and into the bone where it incorporates calcium into the bone matrix instead of being deposited in the arteries in the form of plaque (a risk for heart disease). This vitamin plays a vital role in bone health by regulating the transport and distribution of calcium in the body.
The missing ingredient has long been vitamin K2 MK7.
Vitamin C is a cofactor in the hydroxylation of lysine and proline (these are amino acids, building blocks of protein). They are essentially required for collagen synthesis: prolyl hydroxylase (to stabilise the collagen molecule) and lysyl hydroxylase (to give structural strength cross-linking) and is required in the cross-linking of collagen fibrils in bone. Collagen is a hard, insoluble, and fibrous protein that makes up one-third of the protein in the human body, responsible for maintaining the structural integrity of bones.
Vitamin C also stimulates alkaline phosphatase activity, a marker for osteoblast formation.
Several studies have reported a beneficial effect of vitamin C intake on BMD in children, early postmenopausal women consuming at least 500mg of calcium, and post-menopausal women. The RDA for vitamin C was recently increased to 75mg/d in women and 90mg/d in men. It is still based primarily on the prevention of deficiency, rather than the prevention of chronic disease and the promotion of optimum health. However, intakes higher than the RDAs have been related to better bone health. In postmenopausal women, greater BMD was reported as vitamin C intake from supplements increased to 1000mg/d.
Vitamin C is also an important antioxidant and cofactor which is involved in the regulation of development, function, and maintenance of several cell types in the body. Deficiencies in vitamin C can lead to conditions such as scurvy, which, among other ailments, causes gingivia, bone pain and impaired wound healing.
Our bones support us and allow us to move. They protect our brain, heart, and other organs from injury. The health of bones is increasingly important as we age. Older adults often have bone loss, which leads to an increased risk of fractures and debilitating effects on quality of life. It’s never too early to start thinking about bone health, as maximising bone health during younger years helps to lower fracture risk later in life.
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