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Type 2 diabetes is largely preventable with dietary and lifestyle changes. Current dietary recommendations for type 2 diabetes prevention focus mainly on total calories and macronutrients such as fat, carbohydrates and fiber. However, ample research suggests micronutrients, including magnesium, zinc and potassium, may be just as critical to offset risk. This article will highlight the importance of magnesium-rich foods, like bran, beans, seeds and nuts (which are also rich in fiber), as part of a healthful diet to fight off type 2 diabetes.
Magnesium and type 2 diabetes
Several meta-analyses (studies that aggregate data from previous studies on a similar topic and strive to draw a consensus) have concluded that dietary magnesium intake is significantly and inversely associated with risk of type 2 diabetes in a dose-response manner (Dong, Xun, He, & Qin, 2011; Schulze et al., 2007; Xu, Chen, Zhai, & Ke, 2015). Higher intake appears to improve insulin sensitivity and fasting glucose. In one meta-analysis involving over 500,000 people, those with the lowest magnesium intakes were 22% more likely to be diagnosed with type 2 diabetes than those people with the highest intakes. Furthermore, for every 100 mg of magnesium intake per day, there was a 14% reduction in relative risk of type 2 diabetes (Dong et al., 2011). Figure 1 shows the results of individual studies analyzed by one meta-analysis for magnesium’s effect on type 2 diabetes risk.
Fig 1. Results from individual studies in a meta-analysis by Xu et al. (2015). The relative risk of 1 is assigned to the reference group in each study (those with the highest magnesium intake). This group is then compared to other groups with the lowest magnesium intake. The relative increase or decrease in type 2 diabetes risk is shown in the graph.
Low magnesium intake combined with increased losses of magnesium in the urine underlies the majority of magnesium depletion in type 2 diabetes patients. Magnesium deficiency can worsen insulin resistance in those who are overweight/obese, creating a vicious cycle of more insulin resistance and more magnesium depletion for these people (Song, Manson, Buring, & Liu, 2004).
People with the lowest magnesium intake also have a 27% higher risk of metabolic syndrome compared to those with the highest intakes (Song et al., 2005). Metabolic syndrome is a collection of diseases within which insulin resistance is the common underlying mechanism. Those with metabolic syndrome have a five-fold greater chance of developing type 2 diabetes.
The pertinent question is: does supplementation with magnesium improve insulin resistance and fasting blood glucose levels? Experiments with otherwise healthy volunteers who had low blood magnesium levels showed that magnesium supplementation improved insulin sensitivity (Guerrero-Romero et al., 2004). Other studies in healthy volunteers that have risk factors for type 2 diabetes, such as being overweight/obese or suffering from insulin resistance, who took magnesium supplements showed improvements in insulin resistance and other metabolic parameters (Chacko et al., 2011; Mooren et al., 2011). A meta-analysis of clinical trials of type 2 diabetics given magnesium supplements showed some clinically-relevant reductions in blood sugar levels and improvements in HDL-cholesterol (“the good cholesterol”) levels (Song, He, Levitan, Manson, & Liu, 2006).
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Mechanisms for magnesium that affect glucose and insulin homeostasis
While the exact mechanisms involved in magnesium’s role in improving insulin resistance and glucose homeostasis remain to be elucidated, experimental evidence points to the roles of magnesium in both beta-cell dysfunction and insulin resistance in peripheral tissues.
One mechanism through which magnesium may be acting within peripheral tissue is via its effect on tyrosine kinase, a component of the insulin receptor for which magnesium is a co-factor. Activation of tyrosine kinase produces a signaling cascade that ultimately results in translocation of GLUT4 (the major insulin-regulated glucose transporter expressed in muscle and other insulin-responsive tissues) to the cells’ outer membrane, which allows the cell to take up glucose. If magnesium is deficient in these cells, insulin’s signal will be muted leading to a state of insulin resistance.
The carbohydrates that we eat are broken down into sugars that get further broken down by our cells to produce fuel (in the form of ATP or more precisely, MgATP). This fuel is used for a number of essential chemical reactions. The complex biological process used by our cells to convert sugar to ATP is called glycolysis (literally meaning the breakdown of sugar). The enzymes that carry out glycolysis require magnesium for proper function (Barbagallo & Dominguez, 2015). For this reason, magnesium deficiency could impair our ability to utilize sugar for energy.
Systemic, but especially regional, inflammation within our adipose tissues can promote insulin resistance through the production of several proinflammatory cytokines. Magnesium deficiency enhances this inflammatory response, which further contributes to insulin resistance (Malpuech-Brugere et al., 1998).
- Bran
- Pumpkin seeds
- Hemp and chia seeds
- Cashews and almonds
- Soy and black beans
- Chocolate
- Salmon and mackerel
Concluding thoughts
Studies in model systems and human volunteers show that magnesium deficiency is linked to insulin resistance and other risk factors for type 2 diabetes. Magnesium supplementation improves these parameters. Interestingly, foods that are good sources of magnesium, like beans, seeds and bran, are also good sources of fiber and have a low glycemic index. Therefore, eating these foods may provide a double or triple advantage in helping ward off type 2 diabetes.
An outstanding question that has yet to be answered is whether magnesium deficiency is a cause or a consequence of type 2 diabetes. Reduced magnesium levels may be due to increased urinary excretion due to osmotic diuresis and this problem can be exacerbated by taking diuretics (medications frequently prescribed to people with hypertension).
Whether a cause or a consequence, it is prudent to make sure you get adequate magnesium from your diet. This is particularly important if you are overweight/obese, have polycystic ovary syndrome (PCOS) (link: https://www.gbhealthwatch.com/science-portal-PCOS-science.php) or other risk factors that increase your risk of type 2 diabetes. The HealthWatch 360 tool allows you to track how much magnesium you are getting from your diet and gives you tips to help you improve your overall diet.
We invite you to share your thoughts in the comments section below.
References
Barbagallo M., & Dominguez, L. J. (2015). Magnesium and type 2 diabetes. World J Diabetes, 6(10), 1152-1157. doi: 10.4239/wjd.v6.i10.1152
Chacko S. A., Sul, J., Song, Y., Li, X., LeBlanc, J., You, Y., . . . Liu, S. (2011). Magnesium supplementation, metabolic and inflammatory markers, and global genomic and proteomic profiling: a randomized, double-blind, controlled, crossover trial in overweight individuals. Am J Clin Nutr, 93(2), 463-473. doi: 10.3945/ajcn.110.002949
Dong J. Y., Xun, P., He, K., & Qin, L. Q. (2011). Magnesium intake and risk of type 2 diabetes: meta-analysis of prospective cohort studies. Diabetes Care, 34(9), 2116-2122. doi: 10.2337/dc11-0518
Guerrero-Romero F., Tamez-Perez, H. E., Gonzalez-Gonzalez, G., Salinas-Martinez, A. M., Montes-Villarreal, J., Trevino-Ortiz, J. H., & Rodriguez-Moran, M. (2004). Oral magnesium supplementation improves insulin sensitivity in non-diabetic subjects with insulin resistance. A double-blind placebo-controlled randomized trial. Diabetes Metab, 30(3), 253-258.
Malpuech-Brugere C., Rock, E., Astier, C., Nowacki, W., Mazur, A., & Rayssiguier, Y. (1998). Exacerbated immune stress response during experimental magnesium deficiency results from abnormal cell calcium homeostasis. Life Sci, 63(20), 1815-1822.
Mooren F. C., Kruger, K., Volker, K., Golf, S. W., Wadepuhl, M., & Kraus, A. (2011). Oral magnesium supplementation reduces insulin resistance in non-diabetic subjects - a double-blind, placebo-controlled, randomized trial. Diabetes Obes Metab, 13(3), 281-284. doi: 10.1111/j.1463-1326.2010.01332.x
Schulze M. B., Schulz, M., Heidemann, C., Schienkiewitz, A., Hoffmann, K., & Boeing, H. (2007). Fiber and magnesium intake and incidence of type 2 diabetes: a prospective study and meta-analysis. Arch Intern Med, 167(9), 956-965. doi: 10.1001/archinte.167.9.956
Song Y., He, K., Levitan, E. B., Manson, J. E., & Liu, S. (2006). Effects of oral magnesium supplementation on glycaemic control in Type 2 diabetes: a meta-analysis of randomized double-blind controlled trials. Diabet Med, 23(10), 1050-1056. doi: 10.1111/j.1464-5491.2006.01852.x
Song Y., Manson, J. E., Buring, J. E., & Liu, S. (2004). Dietary magnesium intake in relation to plasma insulin levels and risk of type 2 diabetes in women. Diabetes Care, 27(1), 59-65.
Song Y., Ridker, P. M., Manson, J. E., Cook, N. R., Buring, J. E., & Liu, S. (2005). Magnesium intake, C-reactive protein, and the prevalence of metabolic syndrome in middle-aged and older U.S. women. Diabetes Care, 28(6), 1438-1444.
Xu T., Chen, G. C., Zhai, L., & Ke, K. F. (2015). Nonlinear Reduction in Risk for Type 2 Diabetes by Magnesium Intake: An Updated Meta-Analysis of Prospective Cohort Studies. Biomed Environ Sci, 28(7), 527-534. doi: 10.3967/bes2015.075
