Higher Magnesium Intake Reduces Risk of Impaired Glucose and Insulin Metabolism and Progression From Prediabetes to Diabetes in Middle-Aged Americans
To assess 7-year associations between magnesium intake and incident prediabetes and/or insulin resistance (IR), and progression from these states to type 2 diabetes. In 2,582 community-dwelling participants 26-81 years old at baseline, magnesium intake and risk of incident "metabolic impairment...
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| Published in | Diabetes care Vol. 37; no. 2; pp. 419 - 427 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Alexandria, VA
American Diabetes Association
01.02.2014
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0149-5992 1935-5548 1935-5548 |
| DOI | 10.2337/dc13-1397 |
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| Abstract | To assess 7-year associations between magnesium intake and incident prediabetes and/or insulin resistance (IR), and progression from these states to type 2 diabetes.
In 2,582 community-dwelling participants 26-81 years old at baseline, magnesium intake and risk of incident "metabolic impairment," defined as impaired fasting glucose (FG) (≥5.6 to <7.0 mmol/L), impaired glucose tolerance (2-h postload glucose ≥7.8 to <11.1 mmol/L), IR, or hyperinsulinemia (≥90th percentile of homeostasis model assessment of IR or fasting insulin, respectively), was estimated among those with normal baseline status, and risk of incident diabetes was estimated among those with baseline metabolic impairment. In participants without incident diabetes, we examined magnesium intake in relation to 7-year changes in fasting and postload glucose and insulin, IR, and insulin sensitivity.
After adjusting for age, sex, and energy intake, compared with those with the lowest magnesium intake, those with the highest intake had 37% lower risk of incident metabolic impairment (P trend = 0.02), and in those with baseline metabolic impairment, higher intake was associated with 32% lower risk of incident diabetes (P trend = 0.05). In the combined population, the risk in those with the highest intake was 53% (P trend = 0.0004) of those with the lowest intake. Adjusting for risk factors and dietary fiber attenuated associations in the baseline normal population but did not substantially affect associations in the metabolically impaired. Higher magnesium intake tended to associate with lower follow-up FG and IR, but not fasting insulin, postload values, or insulin sensitivity.
Magnesium intake may be particularly beneficial in offsetting risk of developing diabetes among those at high risk. Magnesium's long-term associations with non-steady-state (dynamic) measures deserve further research. |
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| AbstractList | To assess 7-year associations between magnesium intake and incident prediabetes and/or insulin resistance (IR), and progression from these states to type 2 diabetes.OBJECTIVETo assess 7-year associations between magnesium intake and incident prediabetes and/or insulin resistance (IR), and progression from these states to type 2 diabetes.In 2,582 community-dwelling participants 26-81 years old at baseline, magnesium intake and risk of incident "metabolic impairment," defined as impaired fasting glucose (FG) (≥5.6 to <7.0 mmol/L), impaired glucose tolerance (2-h postload glucose ≥7.8 to <11.1 mmol/L), IR, or hyperinsulinemia (≥90th percentile of homeostasis model assessment of IR or fasting insulin, respectively), was estimated among those with normal baseline status, and risk of incident diabetes was estimated among those with baseline metabolic impairment. In participants without incident diabetes, we examined magnesium intake in relation to 7-year changes in fasting and postload glucose and insulin, IR, and insulin sensitivity.RESEARCH DESIGN AND METHODSIn 2,582 community-dwelling participants 26-81 years old at baseline, magnesium intake and risk of incident "metabolic impairment," defined as impaired fasting glucose (FG) (≥5.6 to <7.0 mmol/L), impaired glucose tolerance (2-h postload glucose ≥7.8 to <11.1 mmol/L), IR, or hyperinsulinemia (≥90th percentile of homeostasis model assessment of IR or fasting insulin, respectively), was estimated among those with normal baseline status, and risk of incident diabetes was estimated among those with baseline metabolic impairment. In participants without incident diabetes, we examined magnesium intake in relation to 7-year changes in fasting and postload glucose and insulin, IR, and insulin sensitivity.After adjusting for age, sex, and energy intake, compared with those with the lowest magnesium intake, those with the highest intake had 37% lower risk of incident metabolic impairment (P trend = 0.02), and in those with baseline metabolic impairment, higher intake was associated with 32% lower risk of incident diabetes (P trend = 0.05). In the combined population, the risk in those with the highest intake was 53% (P trend = 0.0004) of those with the lowest intake. Adjusting for risk factors and dietary fiber attenuated associations in the baseline normal population but did not substantially affect associations in the metabolically impaired. Higher magnesium intake tended to associate with lower follow-up FG and IR, but not fasting insulin, postload values, or insulin sensitivity.RESULTSAfter adjusting for age, sex, and energy intake, compared with those with the lowest magnesium intake, those with the highest intake had 37% lower risk of incident metabolic impairment (P trend = 0.02), and in those with baseline metabolic impairment, higher intake was associated with 32% lower risk of incident diabetes (P trend = 0.05). In the combined population, the risk in those with the highest intake was 53% (P trend = 0.0004) of those with the lowest intake. Adjusting for risk factors and dietary fiber attenuated associations in the baseline normal population but did not substantially affect associations in the metabolically impaired. Higher magnesium intake tended to associate with lower follow-up FG and IR, but not fasting insulin, postload values, or insulin sensitivity.Magnesium intake may be particularly beneficial in offsetting risk of developing diabetes among those at high risk. Magnesium's long-term associations with non-steady-state (dynamic) measures deserve further research.CONCLUSIONSMagnesium intake may be particularly beneficial in offsetting risk of developing diabetes among those at high risk. Magnesium's long-term associations with non-steady-state (dynamic) measures deserve further research. To assess 7-year associations between magnesium intake and incident prediabetes and/or insulin resistance (IR), and progression from these states to type 2 diabetes. In 2,582 community-dwelling participants 26-81 years old at baseline, magnesium intake and risk of incident "metabolic impairment," defined as impaired fasting glucose (FG) (≥5.6 to <7.0 mmol/L), impaired glucose tolerance (2-h postload glucose ≥7.8 to <11.1 mmol/L), IR, or hyperinsulinemia (≥90th percentile of homeostasis model assessment of IR or fasting insulin, respectively), was estimated among those with normal baseline status, and risk of incident diabetes was estimated among those with baseline metabolic impairment. In participants without incident diabetes, we examined magnesium intake in relation to 7-year changes in fasting and postload glucose and insulin, IR, and insulin sensitivity. After adjusting for age, sex, and energy intake, compared with those with the lowest magnesium intake, those with the highest intake had 37% lower risk of incident metabolic impairment (P trend = 0.02), and in those with baseline metabolic impairment, higher intake was associated with 32% lower risk of incident diabetes (P trend = 0.05). In the combined population, the risk in those with the highest intake was 53% (P trend = 0.0004) of those with the lowest intake. Adjusting for risk factors and dietary fiber attenuated associations in the baseline normal population but did not substantially affect associations in the metabolically impaired. Higher magnesium intake tended to associate with lower follow-up FG and IR, but not fasting insulin, postload values, or insulin sensitivity. Magnesium intake may be particularly beneficial in offsetting risk of developing diabetes among those at high risk. Magnesium's long-term associations with non-steady-state (dynamic) measures deserve further research. To assess 7-year associations between magnesium intake and incident prediabetes and/or insulin resistance (IR), and progression from these states to type 2 diabetes. In 2,582 community-dwelling participants 26-81 years old at baseline, magnesium intake and risk of incident "metabolic impairment," defined as impaired fasting glucose (FG) (≥5.6 to <7.0 mmol/L), impaired glucose tolerance (2-h postload glucose ≥7.8 to <11.1 mmol/L), IR, or hyperinsulinemia (≥90th percentile of homeostasis model assessment of IR or fasting insulin, respectively), was estimated among those with normal baseline status, and risk of incident diabetes was estimated among those with baseline metabolic impairment. In participants without incident diabetes, we examined magnesium intake in relation to 7-year changes in fasting and postload glucose and insulin, IR, and insulin sensitivity. After adjusting for age, sex, and energy intake, compared with those with the lowest magnesium intake, those with the highest intake had 37% lower risk of incident metabolic impairment (P trend = 0.02), and in those with baseline metabolic impairment, higher intake was associated with 32% lower risk of incident diabetes (P trend = 0.05). In the combined population, the risk in those with the highest intake was 53% (P trend = 0.0004) of those with the lowest intake. Adjusting for risk factors and dietary fiber attenuated associations in the baseline normal population but did not substantially affect associations in the metabolically impaired. Higher magnesium intake tended to associate with lower follow-up FG and IR, but not fasting insulin, postload values, or insulin sensitivity. Magnesium intake may be particularly beneficial in offsetting risk of developing diabetes among those at high risk. Magnesium's long-term associations with non-steady-state (dynamic) measures deserve further research. To assess 7-year associations between magnesium intake and incident prediabetes and/or insulin resistance (IR), and progression from these states to type 2 diabetes. In 2,582 community-dwelling participants 26-81 years old at baseline, magnesium intake and risk of incident "metabolic impairment," defined as impaired fasting glucose (FG) (=5.6 to <7.0 mmol/L), impaired glucose tolerance (2-h postload glucose =7.8 to <11.1 mmol/L), IR, or hyperinsulinemia (=90th percentile of homeostasis model assessment of IR or fasting insulin, respectively), was estimated among those with normal baseline status, and risk of incident diabetes was estimated among those with baseline metabolic impairment. In participants without incident diabetes, we examined magnesium intake in relation to 7-year changes in fasting and postload glucose and insulin, IR, and insulin sensitivity. After adjusting for age, sex, and energy intake, compared with those with the lowest magnesium intake, those with the highest intake had 37% lower risk of incident metabolic impairment (P trend = 0.02), and in those with baseline metabolic impairment, higher intake was associated with 32% lower risk of incident diabetes (P trend = 0.05). In the combined population, the risk in those with the highest intake was 53% (P trend = 0.0004) of those with the lowest intake. Adjusting for risk factors and dietary fiber attenuated associations in the baseline normal population but did not substantially affect associations in the metabolically impaired. Higher magnesium intake tended to associate with lower follow-up FG and IR, but not fasting insulin, postload values, or insulin sensitivity. Magnesium intake may be particularly beneficial in offsetting risk of developing diabetes among those at high risk. Magnesium's long-term associations with non-steady-state (dynamic) measures deserve further research. |
| Audience | Professional |
| Author | Meigs, James B. McKeown, Nicola M. O’Donnell, Christopher J. Jacques, Paul F. Hruby, Adela |
| Author_xml | – sequence: 1 givenname: Adela surname: Hruby fullname: Hruby, Adela organization: Nutritional Epidemiology Program, Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA – sequence: 2 givenname: James B. surname: Meigs fullname: Meigs, James B. organization: General Medicine Division, Department of Medicine, Massachusetts General Hospital (MGH) and Harvard Medical School, Boston, MA – sequence: 3 givenname: Christopher J. surname: O’Donnell fullname: O’Donnell, Christopher J. organization: National Heart, Lung, and Blood Institute (NHLBI) Division of Intramural Research and NHLBI’s Framingham Heart Study, Framingham, MA, Cardiovascular Division, Department of Medicine, MGH and Harvard Medical School, Boston, MA – sequence: 4 givenname: Paul F. surname: Jacques fullname: Jacques, Paul F. organization: Nutritional Epidemiology Program, Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA – sequence: 5 givenname: Nicola M. surname: McKeown fullname: McKeown, Nicola M. organization: Nutritional Epidemiology Program, Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA |
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| References | American Diabetes Association (2022031219301677200_B2) 2013; 36 Dong (2022031219301677200_B5) 2011; 34 Guerrero-Romero (2022031219301677200_B10) 2011; 41 Schulze (2022031219301677200_B6) 2007; 167 Nadler (2022031219301677200_B14) 1993; 21 Ye (2022031219301677200_B30) 2012; 142 Kannel (2022031219301677200_B27) 1979; 139 Humphries (2022031219301677200_B37) 1999; 12 Burnett-Hartman (2022031219301677200_B31) 2009; 109 Song (2022031219301677200_B33) 2004; 27 Rumawas (2022031219301677200_B35) 2006; 25 Rimm (2022031219301677200_B20) 1992; 135 Lopez-Ridaura (2022031219301677200_B32) 2004; 27 Hadjistavri (2022031219301677200_B11) 2010; 16 Ma (2022031219301677200_B18) 2006; 164 Willett (2022031219301677200_B22) 1985; 122 Matthews (2022031219301677200_B25) 1985; 28 Song (2022031219301677200_B12) 2006; 23 Pratley (2022031219301677200_B15) 2001; 44 American Diabetes Association (2022031219301677200_B24) 2010; 33 van Dam (2022031219301677200_B29) 2006; 29 Yokota (2022031219301677200_B34) 2004; 23 Rutter (2022031219301677200_B16) 2005; 54 American Diabetes Association (2022031219301677200_B3) 2010; 33 Willett (2022031219301677200_B23) 1998 Salvini (2022031219301677200_B21) 1989; 18 Suárez (2022031219301677200_B38) 1995; 38 Feinleib (2022031219301677200_B19) 1975; 4 Gutt (2022031219301677200_B26) 2000; 47 Bhupathiraju (2022031219301677200_B28) 2013; 97 Mooren (2022031219301677200_B13) 2011; 13 Guerrero-Romero (2022031219301677200_B9) 2004; 30 Fung (2022031219301677200_B36) 2003; 22 Günther (2022031219301677200_B40) 2010; 23 Meigs (2022031219301677200_B17) 2002; 25 Kim (2022031219301677200_B4) 2010; 33 2022031219301677200_B1 Barbagallo (2022031219301677200_B39) 2007; 458 Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, Institute of Medicine (2022031219301677200_B8) 1997 2022031219301677200_B7 |
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| SubjectTerms | Adult Aged Aged, 80 and over Biological and medical sciences Development and progression Dextrose Diabetes Diabetes Mellitus, Type 2 - epidemiology Diabetes Mellitus, Type 2 - prevention & control Diabetes. Impaired glucose tolerance Disease Progression Endocrine pancreas. Apud cells (diseases) Endocrinopathies Epidemiology/Health Services Research Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Glucose Glucose Intolerance - prevention & control Glucose metabolism Homeostasis Humans Incidence Insulin Insulin - metabolism Insulin resistance Magnesium Magnesium - administration & dosage Male Medical sciences Metabolic diseases Metabolism Middle Aged Physiological aspects Prediabetic state Prediabetic State - epidemiology Prediabetic State - prevention & control Type 2 diabetes United States |
| Title | Higher Magnesium Intake Reduces Risk of Impaired Glucose and Insulin Metabolism and Progression From Prediabetes to Diabetes in Middle-Aged Americans |
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