0
selected
-
1.
The Dietary Approach to the Treatment of the Rare Genetic Tubulopathies Gitelman's and Bartter's Syndromes.
Francini, F, Gobbi, L, Ravarotto, V, Toniazzo, S, Nalesso, F, Spinella, P, Calò, LA
Nutrients. 2021;(9)
Abstract
Gitelman's (GS) and Bartter's (BS) syndromes are rare, inherited autosomal recessive tubulopathies characterized by hypokalemia, metabolic alkalosis, renal sodium, chloride, and potassium and magnesium-wasting. While the treatment based on potassium, sodium, chloride, and magnesium supplementation in addition to other pharmacologic options are widely established, recommendations about the dietary approach to GS and BS still remain generic. In this review we focus on the dietary strategies to increase sodium, potassium, and magnesium intake in GS and BS patients. Potassium and magnesium-rich foods and supplements are considered together with those that may reduce through different mechanisms the potassium and magnesium plasma level. Magnesium supplementation is often poorly tolerated, causing abdominal pain and diarrhea in most patients. New formulations using liposome and, in particular, sucrosomial technology have been recently proposed for magnesium supplementation in order to increase magnesium supplement tolerability and intestinal absorption. The dietary approach to GS and BS may be very important in the therapeutic approach to these syndromes. Due to the relevance of the dietary approach to these syndromes, a nutritional counseling should always be recommended and the nutritionist should join nephrologists in the follow-up of GS and BS patient care.
-
2.
The Association between Excess Body Mass and Disturbances in Somatic Mineral Levels.
Banach, W, Nitschke, K, Krajewska, N, Mongiałło, W, Matuszak, O, Muszyński, J, Skrypnik, D
International journal of molecular sciences. 2020;(19)
Abstract
BACKGROUND Obesity and excess body weight are significant epidemiological issues, not only because they are costly to treat, but also because they are among the leading causes of death worldwide. In 2016, an estimated 40% of the global population was overweight, reflecting the importance of the issue. Obesity is linked to metabolism malfunction and concomitantly with altered mineral levels in the body. In this paper, we review alterations in somatic levels of iron, calcium, magnesium, copper, iodine, chromium, selenium, and zinc in relation to excess body mass. METHODOLOGY An electronic literature search was performed using PubMed. Our search covered original English research articles published over the past five years, culminating in 63 papers included for study. RESULTS The reviewed papers presented correlation between obesity and hypomagnesemia and hypozincemia. They also indicated that patients with excess body mass present increased body copper levels. Studies have similarly indicated that obesity appears to be associated with lower selenium levels in both blood and urine, which may be correlated with the decline and weakening of defenses against oxidative stress. It has been found that decreased level of chromium is connected with metabolic syndrome. Chromium supplementation influences body mass, but the effect of the supplementation depends on the chemical form of the chromium. It is hypothesized that obesity poses a risk of iodine deficiency and iodine absorption may be disrupted by increased fat intake in obese women. A range of studies have suggested that obesity is correlated with iron deficiency. On the other hand, some reports have indicated that excess body mass may coexist with iron excess. The relation between obesity and body iron level requires further investigation. Calcium signaling seems to be disturbed in obesity, due to the increased production of reactive oxygen species and low level of fast troponin isoform responsible for mediating calcium sensitivity of muscle relaxation. Correlation between excess body mass and calcium levels needs further research. CONCLUSIONS Excess body mass is associated with alterations in mineral levels in the body, in particular hypomagnesemia and decreased selenium (Se) and zinc (Zn) levels. Chromium (Cr) deficiency is associated with metabolic syndrome. Obese patients are at risk of iodine deficiency. Excess body mass is associated with elevated levels of copper (Cu). Data on the association between obesity and iron (Fe) levels are contradictory. Obesity coexists with disturbed calcium (Ca) signaling pathways. The association between obesity and body Ca levels has not been investigated in detail.
-
3.
Role of Magnesium in Vitamin D Activation and Function.
Uwitonze, AM, Razzaque, MS
The Journal of the American Osteopathic Association. 2018;(3):181-189
Abstract
Nutrients usually act in a coordinated manner in the body. Intestinal absorption and subsequent metabolism of a particular nutrient, to a certain extent, is dependent on the availability of other nutrients. Magnesium and vitamin D are 2 essential nutrients that are necessary for the physiologic functions of various organs. Magnesium assists in the activation of vitamin D, which helps regulate calcium and phosphate homeostasis to influence the growth and maintenance of bones. All of the enzymes that metabolize vitamin D seem to require magnesium, which acts as a cofactor in the enzymatic reactions in the liver and kidneys. Deficiency in either of these nutrients is reported to be associated with various disorders, such as skeletal deformities, cardiovascular diseases, and metabolic syndrome. It is therefore essential to ensure that the recommended amount of magnesium is consumed to obtain the optimal benefits of vitamin D.
-
4.
Essential Nutrient Interactions: Does Low or Suboptimal Magnesium Status Interact with Vitamin D and/or Calcium Status?
Rosanoff, A, Dai, Q, Shapses, SA
Advances in nutrition (Bethesda, Md.). 2016;(1):25-43
-
-
Free full text
-
Abstract
Although much is known about magnesium, its interactions with calcium and vitamin D are less well studied. Magnesium intake is low in populations who consume modern processed-food diets. Low magnesium intake is associated with chronic diseases of global concern [e.g., cardiovascular disease (CVD), type 2 diabetes, metabolic syndrome, and skeletal disorders], as is low vitamin D status. No simple, reliable biomarker for whole-body magnesium status is currently available, which makes clinical assessment and interpretation of human magnesium research difficult. Between 1977 and 2012, US calcium intakes increased at a rate 2-2.5 times that of magnesium intakes, resulting in a dietary calcium to magnesium intake ratio of >3.0. Calcium to magnesium ratios <1.7 and >2.8 can be detrimental, and optimal ratios may be ∼2.0. Background calcium to magnesium ratios can affect studies of either mineral alone. For example, US studies (background Ca:Mg >3.0) showed benefits of high dietary or supplemental magnesium for CVD, whereas similar Chinese studies (background Ca:Mg <1.7) showed increased risks of CVD. Oral vitamin D is widely recommended in US age-sex groups with low dietary magnesium. Magnesium is a cofactor for vitamin D biosynthesis, transport, and activation; and vitamin D and magnesium studies both showed associations with several of the same chronic diseases. Research on possible magnesium and vitamin D interactions in these human diseases is currently rare. Increasing calcium to magnesium intake ratios, coupled with calcium and vitamin D supplementation coincident with suboptimal magnesium intakes, may have unknown health implications. Interactions of low magnesium status with calcium and vitamin D, especially during supplementation, require further study.
-
5.
Hypomagnesemia: an evidence-based approach to clinical cases.
Assadi, F
Iranian journal of kidney diseases. 2010;(1):13-9
Abstract
Hypomagnesemia is defined as a serum magnesium level less than 1.8 mg/dL (< 0.74 mmol/L). Hypomagnesemia may result from inadequate magnesium intake, increased gastrointestinal or renal losses, or redistribution from extracellular to intracellular space. Increased renal magnesium loss can result from genetic or acquired renal disorders. Most patients with hypomagnesemia are asymptomatic and symptoms usually do not arise until the serum magnesium concentration falls below 1.2 mg/dL. One of the most life-threatening effects of hypomagnesemia is ventricular arrhythmia. The first step to determine the likely cause of the hypomagnesemia is to measure fractional excretion of magnesium and urinary calcium-creatinine ratio. The renal response to magnesium deficiency due to increased gastrointestinal loss is to lower fractional excretion of magnesium to less than 2%. A fractional excretion above 2% in a subject with normal kidney function indicates renal magnesium wasting. Barter syndrome and loop diuretics which inhibit sodium chloride transport in the ascending loop of Henle are associated with hypokalemia, metabolic alkalosis, renal magnesium wasting, hypomagnesemia, and hypercalciuria. Gitelman syndrome and thiazide diuretics which inhibit sodium chloride cotransporter in the distal convoluted tubule are associated with hypokalemia, metabolic alkalosis, renal magnesium wasting, hypomagnesemia, and hypocalciuria. Familial renal magnesium wasting is associated with hypercalciuria, nephrocalcinosis, and nephrolithiasis. Asymptomatic patients should be treated with oral magnesium supplements. Parenteral magnesium should be reserved for symptomatic patients with severe magnesium deficiency (< 1.2 mg/dL). Establishment of adequate renal function is required before administering any magnesium supplementation.
-
6.
Magnesium and aging.
Barbagallo, M, Dominguez, LJ
Current pharmaceutical design. 2010;(7):832-9
Abstract
Over the past decades, the clinical relevance and biological significance of magnesium (Mg) have been documented. Deficiency in Mg, aside from having a negative impact on the energy production pathway required by mitochondria to generate ATP, also reduces the threshold antioxidant capacity of the aging organism and its resistance to free-radical damage. Mg also acts as an antioxidant against free radical damage of the mitochondria. Chronic inflammation and oxidative stress have both been identified as pathogenic factors in aging and in several age-related diseases. Chronic Mg deficiency results in excessive production of oxygen-derived free radicals and low grade inflammation. Aging is very often associated with Mg inadequacy and with increased incidence of many chronic diseases, with muscle loss and sarcopenia, altered immune responses, and vascular and metabolic conditions, such as atherosclerosis, diabetes and the cardiometabolic syndrome. The most common cause of Mg deficit in the elderly population is dietary Mg deficiency, although secondary Mg deficit in aging may also results from many different mechanisms. The aim of the present manuscript is to discuss the mechanisms and consequences of the modifications of Mg metabolism with age, the difficulties in the measurement of Mg status, and to review the current evidences suggesting that age-related chronic Mg deficits may be proposed as one of the physiopathological links that may help to explain the interactions between inflammation, oxidative stress with the aging process and many age-related diseases.
-
7.
[Magnesium homeostasis. Etiopathogeny, clinical diagnosis and treatment of hypomagnesaemia. A case study].
González, EP, Santos, F, Coto, E
Nefrologia : publicacion oficial de la Sociedad Espanola Nefrologia. 2009;(6):518-24
Abstract
Magnesium is the fourth-most abundant cation in the human body and the second-most abundant intracellular cation after potassium. Magnesium is pivotal in the transfer, storage, and utilization of energy as it regulates and catalyzes more than 300 enzyme systems. Hypomagnesemia may thus result in a variety of metabolic abnormalities and clinical consequences. It results from an imbalance between gastrointestinal absorption and renal excretion of magnesium. The main consequence related directly to hypomagnesemia is cardiovascular arrhythmias secondary to hipokaliemia and if this is not recognized and treated it may be fatal. In this article we review the hypomagnesemic disorders in children with emphasis on the molecular mechanisms responsible for abnormalities in magnesium homeostasis, differential diagnosis and appropriate therapy, and we describe the clinical and biochemical manifestations as well as the genetic defect in a family with Gitelman syndrome.
-
8.
[Magnesium and hypertension].
Rosanoff, A
Clinical calcium. 2005;(2):255-60
Abstract
Magnesium status has a direct effect upon the relaxation capability of vascular smooth muscle cells and the regulation of the cellular placement of other cations important to blood pressure - cellular sodium:potassium (Na:K) ratio and intracellular calcium (iCa(2+)). As a result, nutritional magnesium has both direct and indirect impacts on the regulation of blood pressure and therefore on the occurrence of hypertension. Hypertension occurs when cellular Na:K ratios become too high, a consequence of a high sodium, low potassium diet or, indirectly, through a magnesium deficient state which causes a pseudo potassium deficit. Like wise, magnesium deficiency alters calcium metabolism, creating high iCa(2+), low serum calcium and low urinary calcium states even when calcium intake is adequate. High iCa(2 + ) and high cellular Na:K ratio both occur when cellular magnesium becomes too low and the Mg-ATP driven sodium-potassium pump and calcium pump become functionally impaired. High iCa(2+) has several vasoconstrictive effects which lead to hypertension, an indirect result of low magnesium status. Dietary calcium is directly proportional to dietary magnesium. Serum magnesium does not reflect true magnesium status as do intracellular magnesium measurements. Several studies on the effect of calcium on blood pressure need these added considerations of magnesium status to fully understand the impact of the Mg:Ca ratio as the primary cause of hypertension and other aspects of Syndrome X. Magnesium supplementation above 15 mmol per day are required to normalize high blood pressure in unmedicated hypertensive patients while 15 mmol per day will lower high blood pressure in patients treated with anti-hypertensive medications. In most humans, healthy blood pressure depends upon a balance of both Na:K and Mg:Ca ratios at both cellular and whole body levels which, in turn, require adequate, long-term intakes of nutritional magnesium. The knowledge that low magnesium causes imbalance in both cellular and physiological calcium widens our view of the studies showing hypertensives have abnormal calcium metabolism.
-
9.
[Magnesium and insulin resistance].
Higashiura, K, Shimamoto, K
Clinical calcium. 2005;(2):251-4
Abstract
Recently, there are some reports about correlations between insulin resistance and deficiency of magnesium. It is considered that the some of mechanisms of those correlations are magnesium deficiency fail to activate tyrosine kinase of insulin receptor and hyperinsulinemia stimulates magnesium excretion. It is expected that the exact mechanisms between insulin resistance, metabolic syndrome and magnesium metabolism.
-
10.
[Fetus and magnesium].
Takaya, J, Kaneko, K
Clinical calcium. 2005;(11):105-10
Abstract
Chronic magnesium deficiency in pregnant women is frequently seen because of inadequate or low intake of magnesium. Magnesium deficiency during pregnancy can induce not only maternal and fetal nutritional problem, but also pediatric consequences that might last throughout life. Many epidemiological studies have disclosed that restricted fetal growth, i.e., intrauterine growth retardation (IUGR) is associated with an increased risk of insulin resistance in adult life. We previously postulated that intracellular magnesium of cord blood platelets is lower in the small for gestational age than in the appropriate for gestational age group, suggesting chronic intrauterine magnesium deficiency may result in IUGR. Taken together, chronic intrauterine magnesium deficiency in the fetus may lead to or program the insulin resistance after birth. Prospective study whether the children born with magnesium induced IUGR are at high-risk for metabolic syndrome in childhood or adulthood is currently undertaken.