|If Mg is the solution, then in form of high Mg foods, not supplements.|
In his review, Mooren doesn't make the same mistake, instead he provides a brief, but in-depth overview of the regulation of intra- and extracellular Mg and the regulatory role of Mg in important metabolic pathways involved in energy metabolism and glycaemic control.
An overview Mooren concludes by stating that a "critical consideration of the pros and cons of a Mg replacement therapy" that accounts for various "parameters such as Mg status, stage of disease and glycaemic control" is still lacking.
The fact that we do not yet understand all the confounding factors, though, does not mean that we are still completely in the dark. Rather than that we do know that,,,
- ...diabetes predisposes to magnesium deficiency - It may seem to be a chicken or egg question, but an impartial review of the evidence suggests that diabetes or rather pre-diabetes comes first and hypomagnesaemia = low magnesium levels are a consequence of the development of diabetes.
Next to the low magnesium content of the pro-diabetic junkfood Western diet (Pham. 2014), recent data indicate that hyperglycaemia and resulting osmotic diuresis overwhelm the kidneys’ reabsorption capacity for Mg leading to hypermagnesuria. In conjuction with various disturbances of metabolic and electrolyte variables, such as hypokalaemia and metabolic acidosis, which are common among diabetics, the elevated glucose levels trigger a redistribution of Mg within its compartments that will eventually lead to the depletion of intracellular Mg and an enhanced urinary Mg excretion (Pham. 2014).
- ...hypomagnesaemia accelerates the transition from pre- to full-blown diabetes - The hyperglycemia-induced depletion of magnesium levels triggers a viscous cycle, because a balanced Mg status seems to be an important prerequisite for an adequate carbohydrate metabolism.
Are we talking serum of intracellular Mg levels? Both serum and intracellular Mg levels were reduced in patients with metabolic syndrome and were inversely correlated with BMI. Hypomagnesaemia (=low serum levels) as well as intracellular Mg depletion have been shown to be more prevalent (23.2 % and 36.1 %, respectively) in T2DM patients than in control group (3.3 % and 9.8 %, respectively | de Lourdes Lima. 2009). The reason that intra-cellular levels may still be a better predictors of future disturbances in glucose metabolism is the time-course of magnesium depletion which will begin in the cells and surface in form of low serum magnesium levels only when the intracellular stores are already critically low.Six cross sectional studies have also reported associations between magnesium intake and risk of metabolic syndrome were reviewed in a recent meta-analysis by Diaba et al. (2014). More than 24,000 individuals of both sexes have been included.
|Figure 1: Multivariable adjusted odds ratios (95% CI) of having prevalent metabolic syndrome in participants with the highest level of dietary magnesium intake compared with those with the lowest (Diba. 2014).|
In a similar vein, most of the studies did not observe significant improvements in glucose control and the long-term glucose measure HbA1c in response to magnesium supplementation (only 23% and 18%, respectivels). The closely related triglyceride levels were not affected in any of the studies.
Fourteen randomized controlled studies have been identified which investigated the effect of Mg supplementation on type 2 diabetes (Table 3). In total, 825 people with diabetes were enrolled, who had suffered from the disease for a mean duration of about 10.8+4.1 years. 10 studies reported values for glycosylated haemoglobin (HbA1c) at study onset. Their long term glucose control failed the recommended values for diabetic patients (target range HbA1c from 6.5-7.5 %) as indicated by a mean HbA1c of 9.3+2.1 %. 3 studies included patients with initial HbA1c levels lower than 7.5 %. Serum Mg concentrations at study onset have been reported in 12 studies. 5 out of 12 studies included diabetic people with hypomagnesaemia (Mg < 0.74mmol/l), while patients of another 5 studies showed serum Mg levels in the lower segment of the normal range (between 0.74 and 0.85 mmol/l).
Table 1: Absolute changes in fasting plasma glucose after Mg supplementation in people with impaired glucose regulation | FPG – Fasting plasma glucose; * indicates the inclusion of hypomagnesaemic subjects only (Mooren. 2015).
Different Mg salts (Mg-pidolate; Mg-lactate-citrate; Mg-oxide; Mg-chloride; Mg-aspartate; Mg sulfate) were applied during a wide range of treatment periods which lasted from 4-16 weeks (mean treatment duration 9.6 weeks). After Mg supplementation, only 50 % of the studies reported significant improvements in serum Mg (7 out of 14 studies). Such a limited supplementation efficacy might partially result from different bioavailabilities of the various Mg salts (organic vs. inorganic) applied" (Mooren. 2015).
- de Lourdes Lima, Maria, et al. "Serum and intracellular magnesium deficiency in patients with metabolic syndrome—evidences for its relation to insulin resistance." Diabetes research and clinical practice 83.2 (2009): 257-262.
- Dibaba, D. T., et al. "Dietary magnesium intake and risk of metabolic syndrome: a meta‐analysis." Diabetic Medicine 31.11 (2014): 1301-1309.
- Mooren, Frank C. "Magnesium and disturbances in carbohydrate metabolism." Diabetes, Obesity and Metabolism (2015): Accepted Article.
- Pham, Phuong-Chi T., et al. "Hypomagnesemia: a clinical perspective." International journal of nephrology and renovascular disease 7 (2014): 219.