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Magnesium in Prevention and Therapy
3. Magnesium and Nutrition
Dietary surveys of people in Europe and in the United States still reveal that intakes of magnesium are lower than the recommended amounts . Epidemiological studies in Europe and North America have shown that people consuming Western-type diets are low in magnesium content, i.e. <30%–50% of the RDA for magnesium.
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²¤ÊƤαֳظ¦µæ¤Ë¤è¤ì¤Ð¡¢À¾Íη¿¿©»ö¤òÀݼ褹¤ë¿Í¡¹¤Ï¥Þ¥°¥Í¥·¥¦¥à´ÞÎ̤¬Ä㤯¡¢¤¹¤Ê¤ï¤Á¥Þ¥°¥Í¥·¥¦¥à¤Î1Æü¤¢¤¿¤ê¤Î¿ä¾©ÀݼèÎÌ¡ÊRDA¡Ë¤Î30〜50¡ó̤Ëþ¤Ç¤¢¤ë¤³¤È¤¬¼¨¤µ¤ì¤Æ¤¤¤Þ¤¹¡£ It is suggested that the dietary intakes of magnesium in the United States have been declining over the last 100 years from about 500 mg/day to 175–225 mg/day. This is likely a result of the increasing use of fertilizers and processed foods . In 1997, the Food and Nutrition Board (FNB) of the Institute of Medicine had increased the dietary references intakes (RDA) for magnesium, based on the results of controlled balance studies.
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Water accounts for ~10% of daily magnesium intake , chlorophyll (and thus green vegetables such as spinach) is the major source of magnesium. Nuts, seeds and unprocessed cereals are also rich in magnesium. Legumes, fruit, fish and meat have an intermediate magnesium concentration. Some types of food processing, such as refining grains in ways that remove the nutrient-rich germ and bran, lower magnesium content substantially. Low magnesium concentrations are found in dairy products, except milk .
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The United States NHANES 2005–2006 survey reported that nearly one half of all American adults have an inadequate intake from food and water of magnesium and do not consume the estimated average requirements (EAR) (set at 255–350 mg depending on gender and age group) . A chronic magnesium deficiency (serum magnesium <0.75 mmol/L) is associated with an increased risk of numerous preclinical and clinical outcomes, including atherosclerosis, hypertension, cardiac arrhythmias, stroke, alterations in lipid metabolism, insulin resistance, metabolic syndrome, type 2 diabetes mellitus, osteoporosis as well as depression and other neuropsychiatric disorders. Furthermore, magnesium deficiency may be at least one of the pathophysiological links that may help to explain the interactions between inflammation and oxidative stress with the aging process and many age-related diseases . ÊÆ¹ñ¤Î¹ṉ̃·ò¹¯±ÉÍÜÄ´ºº¡ÊNHANES¡Ë2005-2006¤ÎÄ´ºº¤Ë¤è¤ì¤Ð¡¢Á´ÊƤÎÀ®¿Í¤Î¤Û¤ÜȾ¿ô¤¬¿©Êª¤È¥Þ¥°¥Í¥·¥¦¥à¤ÎÀݼèÎ̤¬ÉÔ½½Ê¬¤Ç¡¢¿äÄêÊ¿¶Ñ½êÍ×ÎÌ¡ÊEAR¡Ë¤ò¾ÃÈñ¤·¤Æ¤¤¤Ê¤¤¤ÈÊó¹ð¤µ¤ì¤Æ¤¤¤Þ¤¹¡ÊÀÊ̤ª¤è¤ÓǯÎð¤Ë¤è¤Ã¤Æ255-350 mg¤ËÀßÄꤵ¤ì¤Æ¤¤¤ë ¥°¥ë¡¼¥×¡Ë¡£
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Magnesium homeostasis is maintained by the intestine, the bone and the kidneys. Magnesium is mainly absorbed in the small intestine, which was shown by 28Mg isotope measurements, although some is also taken up via the large intestine . Of the total dietary magnesium consumed, only about 24%–76% is absorbed in the gut the rest is eliminated in the faeces .
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The majority of magnesium is absorbed in the small intestine by a passive paracellular mechanism, which is driven by an electrochemical gradient and solvent drag (see Figure 1). Paracellular magnesium absorption is responsible for 80%–90% of intestinal magnesium uptake.
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It is worth noting that intestinal absorption is not directly proportional to magnesium intake but is dependent mainly on magnesium status. The lower the magnesium level, the more of the mineral is absorbed in the gut, thus relative magnesium absorption is high when intake is low and vice versa. The kidneys are crucial in magnesium homeostasis as serum magnesium concentration is primarily controlled by its excretion in urine. IJ¤ÎµÛ¼ý¤Ï¥Þ¥°¥Í¥·¥¦¥à¤ÎÀݼèÎ̤ËľÀÜÈæÎ㤹¤ë¤Î¤Ç¤Ï¤Ê¤¯¡¢¼ç¤Ë¥Þ¥°¥Í¥·¥¦¥à¤Î¾õÂ֤˰͸¤·¤Æ¤¤¤ë¤³¤È¤ÏÃíÌܤËÃͤ·¤Þ¤¹¡£
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Most of the filtered magnesium is reabsorbed in the loop of Henle, mostly in the thick ascending limb (up to 70% of total magnesium reabsorption). The reabsorption and excretion of magnesium is influenced by several not yet classified mechanisms.
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In this context, we could show that an overload of blood cells with magnesium in renal insufficiency can be avoided by a special cell membrane buffering system for magnesium. In severe forms of renal insufficiency, this buffering system for magnesium is destroyed and an overload with magnesium in human cells is observed . Furthermore, the exchange time for magnesium between intra- and extracellular pools is relatively long . Hypomagnesaemia is frequently linked with hypokalemia owing to disturbances in renal secretion of potassium in the connecting tubule and collecting duct . ¤³¤Î»ö¾ð¤Ç¡¢²æ¡¹¤Ï¡¢¥Þ¥°¥Í¥·¥¦¥à¤Î¤¿¤á¤ÎÆÃÊ̤ʺÙ˦Ëì´Ë¾×·Ï¤Ë¤è¤Ã¤Æ¿ÕÉÔÁ´¤Î¥Þ¥°¥Í¥·¥¦¥à¤òȼ¤¦·ì±ÕºÙ˦¤Î²áÉé²Ù¤¬²óÈò¤µ¤ìÆÀ¤ë¤³¤È¤ò¼¨¤¹¤³¤È¤¬¤Ç¤¤Þ¤·¤¿¡£
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¥Þ¥°¥Í¥·¥¦¥àÊäµë¤Ï¡¢¥Ó¥¿¥ß¥óD¼£ÎŤËÂФ¹¤ëÄñ¹³À¤ò¼Â¼ÁŪ¤ËµÕž¤µ¤»¤Þ¤·¤¿¡£ Next to 1,25(OH)2D, several other factors, such as oestrogen or parathyroid hormone (PTH), are involved in the magnesium excretion. Oestrogen is known to stimulate TRPM6 expression . Thus, oestrogen substitution therapy can normalize hypermagnesuria, which occurs frequently in postmenopausal women. Interestingly, TRPM6 expression appears to be regulated by serum magnesium levels and oestrogens, but not by 1,25(OH)2D or PTH action . 1,25¡ÊOH¡Ë2D¤Î¼¡¤Ë¡¢¥¨¥¹¥È¥í¥²¥ó¡ÊÃ𣳡ˤäÉû¹Ã¾õÁ£¥Û¥ë¥â¥ó¡ÊPTH¡Ë¤Ê¤É¤Î¤¤¤¯¤Ä¤«¤Î¾¤Î°ø»Ò¤¬¥Þ¥°¥Í¥·¥¦¥àÇÓÝõ¤Ë´ØÍ¿¤·¤Æ¤¤¤Þ¤¹¡£
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