Low serum magnesium levels and metabolic syndrome.
TL;DR: A cross-sectional population-based study reveals a strong relationship between decreased serum magnesium and MS and among the components of MS, dyslipidemia and HBP were strongly related to low serum magnesium levels.
Abstract: Low serum magnesium levels are related to diabetes mellitus (DM) and high blood pressure (HBP), but as far as we know, there are no previous reports that analyzed the serum magnesium concentration in individuals with metabolic syndrome (MS). We performed a cross-sectional population-based study to compare 192 individuals with MS and 384 disorder-free control subjects, matched by age and gender. Magnesium supplementation treatment and conditions likely to provoke hypomagnesemia, including previous diagnosis of diabetes mellitus (DM) and/or high blood pressure (HBP), were exclusion criteria. In this regard, only incident cases of DM and HBP were included. MS was defined by the presence at least of two of the following features: hyperglycemia (≥7.0 mmol/l); HBP (≥160/90 mmHg); dyslipidemia (fasting triglycerides ≥1.7 mmol/l and/or HDLcholesterol <1.0 mmol/l); and obesity (body mass index ≥30 kg/m2 and/or waist-to-hip ratio ≥0.85 in women or ≥0.9 in men). Low serum magnesium levels were identified in 126 (65.6%) and 19 (4.9%) individuals with and without MS, p<0.00001. The mean serum magnesium level among subjects with MS was 1.8±0.3 mg/dl, and among control subjects 2.2±0.2 mg/dl, p<0.00001. There was a strong independent relationship between low serum magnesium levels and MS (odds ratio (OR)=6.8, CI95% 4.2–10.9). Among the components of MS, dyslipidemia (OR 2.8, CI95% 1.3–2.9) and HBP (OR 1.9, CI95% 1.4–2.8) were strongly related to low serum magnesium levels. This study reveals a strong relationship between decreased serum magnesium and MS.
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TL;DR: The data support the argument that magnesium supplementation improves the metabolic status in hypomagnesemic CKD patients with pre-diabetes and obesity.
Abstract: Background/Aims: Magnesium is an essential mineral for many metabolic functions. There is very little information on the effect of magnesium supplementation on me
4,639 citations
TL;DR: Recommendation to increase whole-grain intake may reduce the risk of developing the metabolic syndrome and dietary glycemic index, largely attributed to the cereal fiber, is inversely associated with HOMA-IR and a lower prevalence of the metabolic Syndrome.
Abstract: OBJECTIVE —The aim of this study was to examine the relation between carbohydrate-related dietary factors, insulin resistance, and the prevalence of the metabolic syndrome in the Framingham Offspring Cohort. RESEARCH DESIGN AND METHODS —We examined cross-sectional associations between carbohydrate-related dietary factors, insulin resistance, and the prevalence of the metabolic syndrome in 2,834 subjects at the fifth examination (1991–1995) of the Framingham Offspring Study. Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated using the following formula (fasting plasma insulin × plasma glucose)/22.5. The metabolic syndrome was defined using the National Cholesterol Education Program criteria. RESULTS —After adjustment for potential confounding variables, intakes of total dietary fiber, cereal fiber, fruit fiber, and whole grains were inversely associated, whereas glycemic index and glycemic load were positively associated with HOMA-IR. The prevalence of the metabolic syndrome was significantly lower among those in the highest quintile of cereal fiber (odds ratio [OR] 0.62; 95% CI 0.45–0.86) and whole-grain (0.67; 0.48–0.91) intakes relative to those in the lowest quintile category after adjustment for confounding lifestyle and dietary factors. Conversely, the prevalence of the metabolic syndrome was significantly higher among individuals in the highest relative to the lowest quintile category of glycemic index (1.41; 1.04–1.91). Total carbohydrate, dietary fiber, fruit fiber, vegetable fiber, legume fiber, glycemic load, and refined grain intakes were not associated with prevalence of the metabolic syndrome. CONCLUSIONS —Whole-grain intake, largely attributed to the cereal fiber, is inversely associated with HOMA-IR and a lower prevalence of the metabolic syndrome. Dietary glycemic index is positively associated with HOMA-IR and prevalence of the metabolic syndrome. Given that both a high cereal fiber content and lower glycemic index are attributes of whole-grain foods, recommendation to increase whole-grain intake may reduce the risk of developing the metabolic syndrome.
790 citations
TL;DR: Analysis of the mitochondrial genome of the maternal lineage identified a homoplasmic mutation substituting cytidine for uridine immediately 5′ to the mitochondrial transfer RNAIle anticodon, which may have implications for the common clustering of these metabolic disorders.
Abstract: Hypertension and dyslipidemia are risk factors for atherosclerosis and occur together more often than expected by chance. Although this clustering suggests shared causation, unifying factors remain unknown. We describe a large kindred with a syndrome including hypertension, hypercholesterolemia, and hypomagnesemia. Each phenotype is transmitted on the maternal lineage with a pattern indicating mitochondrial inheritance. Analysis of the mitochondrial genome of the maternal lineage identified a homoplasmic mutation substituting cytidine for uridine immediately 5′ to the mitochondrial transfer RNAIle anticodon. Uridine at this position is nearly invariate among transfer RNAs because of its role in stabilizing the anticodon loop. Given the known loss of mitochondrial function with aging, these findings may have implications for the common clustering of these metabolic disorders.
345 citations
TL;DR: Benefits of Mg supplementation on metabolic profile in diabetic subjects have been found in most, but not all clinical studies, and larger prospective studies are needed to support the potential role of dietary Mg supplements as a possible public health strategy in diabetes risk.
339 citations
TL;DR: Magnesium intake was inversely associated with incidence of metabolic syndrome after adjustment for major lifestyle and dietary variables and baseline status of each component of the metabolic syndrome.
Abstract: Background— Studies suggest that magnesium intake may be inversely related to risk of hypertension and type 2 diabetes mellitus and that higher intake of magnesium may decrease blood triglycerides and increase high-density lipoprotein (HDL) cholesterol levels. However, the longitudinal association of magnesium intake and incidence of metabolic syndrome has not been investigated. Methods and Results— We prospectively examined the relations between magnesium intake and incident metabolic syndrome and its components among 4637 Americans, aged 18 to 30 years, who were free from metabolic syndrome and diabetes at baseline. Metabolic syndrome was diagnosed according to the National Cholesterol Education Program/Adult Treatment Panel III definition. Diet was assessed by an interviewer-administered quantitative food frequency questionnaire, and magnesium intake was derived from the nutrient database developed by the Minnesota Nutrition Coordinating Center. During the 15 years of follow-up, 608 incident cases of t...
334 citations
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TL;DR: The correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.
Abstract: The steady-state basal plasma glucose and insulin concentrations are determined by their interaction in a feedback loop. A computer-solved model has been used to predict the homeostatic concentrations which arise from varying degrees beta-cell deficiency and insulin resistance. Comparison of a patient's fasting values with the model's predictions allows a quantitative assessment of the contributions of insulin resistance and deficient beta-cell function to the fasting hyperglycaemia (homeostasis model assessment, HOMA). The accuracy and precision of the estimate have been determined by comparison with independent measures of insulin resistance and beta-cell function using hyperglycaemic and euglycaemic clamps and an intravenous glucose tolerance test. The estimate of insulin resistance obtained by homeostasis model assessment correlated with estimates obtained by use of the euglycaemic clamp (Rs = 0.88, p less than 0.0001), the fasting insulin concentration (Rs = 0.81, p less than 0.0001), and the hyperglycaemic clamp, (Rs = 0.69, p less than 0.01). There was no correlation with any aspect of insulin-receptor binding. The estimate of deficient beta-cell function obtained by homeostasis model assessment correlated with that derived using the hyperglycaemic clamp (Rs = 0.61, p less than 0.01) and with the estimate from the intravenous glucose tolerance test (Rs = 0.64, p less than 0.05). The low precision of the estimates from the model (coefficients of variation: 31% for insulin resistance and 32% for beta-cell deficit) limits its use, but the correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.
29,217 citations
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...was used to determine insulin action [15]....
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TL;DR: A WHO Consultation has taken place in parallel with a report by an American Diabetes Association Expert Committee to re‐examine diagnostic criteria and classification of diabetes mellitus and is hoped that the new classification will allow better classification of individuals and lead to fewer therapeutic misjudgements.
Abstract: The classification of diabetes mellitus and the tests used for its diagnosis were brought into order by the National Diabetes Data Group of the USA and the second World Health Organization Expert Committee on Diabetes Mellitus in 1979 and 1980. Apart from minor modifications by WHO in 1985, little has been changed since that time. There is however considerable new knowledge regarding the aetiology of different forms of diabetes as well as more information on the predictive value of different blood glucose values for the complications of diabetes. A WHO Consultation has therefore taken place in parallel with a report by an American Diabetes Association Expert Committee to re-examine diagnostic criteria and classification. The present document includes the conclusions of the former and is intended for wide distribution and discussion before final proposals are submitted to WHO for approval. The main changes proposed are as follows. The diagnostic fasting plasma (blood) glucose value has been lowered to > or =7.0 mmol l(-1) (6.1 mmol l(-1)). Impaired Glucose Tolerance (IGT) is changed to allow for the new fasting level. A new category of Impaired Fasting Glycaemia (IFG) is proposed to encompass values which are above normal but below the diagnostic cut-off for diabetes (plasma > or =6.1 to or =5.6 to <6.1 mmol l(-1)). Gestational Diabetes Mellitus (GDM) now includes gestational impaired glucose tolerance as well as the previous GDM. The classification defines both process and stage of the disease. The processes include Type 1, autoimmune and non-autoimmune, with beta-cell destruction; Type 2 with varying degrees of insulin resistance and insulin hyposecretion; Gestational Diabetes Mellitus; and Other Types where the cause is known (e.g. MODY, endocrinopathies). It is anticipated that this group will expand as causes of Type 2 become known. Stages range from normoglycaemia to insulin required for survival. It is hoped that the new classification will allow better classification of individuals and lead to fewer therapeutic misjudgements.
15,167 citations
TL;DR: No associations were observed between intakes of energy, protein, sucrose, carbohydrate, or fiber and risk of diabetes among women with BMIs less than 29 kg/m2 and inverse associations were attenuated among obese women (BMIs greater than or equal to 29).
442 citations
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...This relationship is supported by epidemiological studies in which deficient magnesium intake was an independent risk factor for the development of type 2 DM [7, 20, 21]....
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TL;DR: That low dietary magnesium intake does not confer risk for type 2 diabetes implies that compartmentalization and renal handling of magnesium may be important in the relationship between low serum magnesium levels and the risk forType 2 diabetes.
Abstract: Background Experimental studies in animals and cross-sectional studies in humans have suggested that low serum magnesium levels might lead to type 2 diabetes; however, this association has not been examined prospectively. Methods We assessed the risk for type 2 diabetes associated with low serum magnesium level and low dietary magnesium intake in a cohort of nondiabetic middle-aged adults (N=12,128) from the Atherosclerosis Risk in Communities Study during 6 years of follow-up. Fasting serum magnesium level, categorized into 6 levels, and dietary magnesium intake, categorized into quartiles, were measured at the baseline examination. Incident type 2 diabetes was defined by self-report of physician diagnosis, use of diabetic medication, fasting glucose level of at least 7.0 mmol/L (126 mg/dL), or nonfasting glucose level of at least 11.1 mmol/L (200 mg/dL). Results Among white participants, a graded inverse relationship between serum magnesium levels and incident type 2 diabetes was observed. From the highest to the lowest serum magnesium levels, there was an approximate 2-fold increase in incidence rate (11.1, 12.2, 13.6, 12.8, 15.8, and 22.8 per 1000 person-years; P =.001). This graded association remained significant after simultaneous adjustment for potential confounders, including diuretic use. Compared with individuals with serum magnesium levels of 0.95 mmol/L (1.90 mEq/L) or greater, the adjusted relative odds of incident type 2 diabetes rose progressively across the following lower magnesium categories: 1.13 (95% CI, 0.79-1.61), 1.20 (95% CI, 0.86-1.68), 1.11 (95% CI, 0.80-1.56), 1.24 (95% CI, 0.86-1.78), and 1.76 (95% CI, 1.18-2.61) (for trend, P =.01) In contrast, little or no association was observed in black participants. No association was detected between dietary magnesium intake and the risk for incident type 2 diabetes in black or white participants. Conclusions Among white participants, low serum magnesium level is a strong, independent predictor of incident type 2 diabetes. That low dietary magnesium intake does not confer risk for type 2 diabetes implies that compartmentalization and renal handling of magnesium may be important in the relationship between low serum magnesium levels and the risk for type 2 diabetes.
431 citations
"Low serum magnesium levels and meta..." refers background or methods in this paper
...On the other hand, magnesium seems to play an important role in glucose metabolism [7]....
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...This relationship is supported by epidemiological studies in which deficient magnesium intake was an independent risk factor for the development of type 2 DM [7, 20, 21]....
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...In addition, recent data show a graded and inverse independent relationship between serum magnesium levels and the development of type 2 DM [7]....
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TL;DR: There is no readily available test to determine intracellular/total body magnesium status and the clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium.
Abstract: Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
333 citations
"Low serum magnesium levels and meta..." refers background in this paper
...Magnesium is the second most abundant intracellular cation [1], its serum concentration is remarkably constant in healthy subjects [2], it activates more than 300 enzymes, and it is a critical cofactor in many enzymatic reactions of the carbohydrate metabolism [3, 4]....
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