Guerrero-Romero, F. and M. Rodriguez-Moran (2000). “Hypomagnesemia is linked to low serum HDL-cholesterol irrespective of serum glucose values.” J Diabetes Complications 14(5): 272-6.
Hypomagnesemia is common in diabetic subjects, and is especially common in poorly controlled diabetes, suggesting that diabetes low serum magnesium status is osmotic diuresis-dependent. To assess the relationship between serum magnesium and HDL-cholesterol concentration adjusted by serum glucose values. We assessed the serum magnesium levels of 50 controlled (HbA(1c)7.5% and FPG>/=126 mg/dl) type II diabetic patients, 40 subjects with impaired fasting glucose (IFG) (FPG>/=110 mg/dl and <126 mg/dl) and 190 healthy volunteers (FPG<110 mg/dl). Healthy volunteers were required to have normal blood pressure and normal laboratory tests. Subjects in the groups included were matched by age and body mass index (BMI). The average of diabetes duration was of 11.4+/-6.6, and 10.9+/-6.2 years, P=NS, for the controlled and non-controlled diabetic patients, respectively. Thirty (60.0%) controlled diabetic subjects, 58 (52. 7%) non-controlled diabetic patients, 21 (52.5%) subjects with IFG, and 39 (20.5%) healthy volunteers had serum magnesium levels Serum HDL-cholesterol value showed significant graded increase with serum magnesium levels irrespective of glucose values. Results of this study suggest that hypomagnesemia by an etiopathogenic pathway glycemia independent seems to be involved to decrease HDL-cholesterol.
He, K., K. Liu, et al. (2006). “Magnesium intake and incidence of metabolic syndrome among young adults.” Circulation 113(13): 1675-82.
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 the metabolic syndrome were identified. 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. Compared with those in the lowest quartile of magnesium intake, multivariable-adjusted hazard ratio of metabolic syndrome for participants in the highest quartile was 0.69 (95% confidence interval [CI], 0.52 to 0.91; P for trend <0.01). The inverse associations were not materially modified by gender and race. Magnesium intake was also inversely related to individual component of the metabolic syndrome and fasting insulin levels. CONCLUSIONS: Our findings suggest that young adults with higher magnesium intake have lower risk of development of metabolic syndrome. https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16567569
Rasmussen, H. S., P. Aurup, et al. (1989). “Influence of magnesium substitution therapy on blood lipid composition in patients with ischemic heart disease. A double-blind, placebo controlled study.” Arch Intern Med 149(5): 1050-3.
In a double-blind, placebo-controlled study, 47 patients with ischemic heart disease and acute myocardial infarction were allocated to 3 months’ treatment with peroral magnesium (15 mmol/d) or placebo. Before, during, and after treatment, blood samples were taken to determine serum concentrations of cholesterol; triglyceride; high-density, low-density, and very-low-density lipoprotein; apolipoprotein A1 and B; and magnesium. We found a 13% increase in molar ratio of apolipoprotein A1:apolipoprotein B after magnesium treatment, as compared with a 2% increase in the placebo group (for mean differences between changes of the magnesium and the placebo groups). This increase was caused by a decrease in apolipoprotein B concentrations, which were reduced by 15% from 1.44 to 1.23 mmol/L in the magnesium group as compared with a slight increase in the placebo group. Triglyceride, and thereby very-low-density lipoprotein concentrations decreased by 27% after magnesium treatment (from 2.41 to 1.76 mmol/L, and from 1.1 to 0.79 mmol/L, respectively) as compared with much smaller decrements in the placebo group. Likewise, we found tendencies toward an increase in high-density lipoprotein cholesterol and in high-density lipoprotein cholesterol ratio/(low-density lipoprotein cholesterol:very-low-density lipoprotein cholesterol) after magnesium treatment. The observed findings support the hypothesis that magnesium deficiency might be involved in the pathogenesis of ischemic heart disease by altering the blood lipid composition in a way that disposes to atherosclerosis.
Singh, R. B., S. S. Rastogi, et al. (1990). “Can dietary magnesium modulate lipoprotein metabolism?” Magnes Trace Elem 9(5): 255-64. In a randomized, single-blinded, controlled study (430 patients aged 25-63 years, 394 males), 214 subjects were administered a magnesium-rich diet and 216 subjects were administered a usual diet for 12 weeks. Age, sex, body weight, hypertension, diabetes, hyperlipidemia, smoking, obesity, diuretic therapy and hypomagnesemia were comparable between the two groups as were laboratory data at entry to the study. The intervention group A received a significantly higher amount of dietary magnesium (1,142.0 +/- 225 mg/day) compared to group B which received the usual diet (438 +/- 118 mg/day). After 12 weeks, there was a significant decrease in total serum cholesterol (10.7%), low-density-lipoprotein (LDL) cholesterol (10.5%) and triglyceride (10.1%) in group A compared to the values at entry to the study; no such changes were evident in group B subjects. HDL-cholesterol showed a marginal mean decrease of 0.8 mg/dl in group B and 2.0 mg/dl increase in group A. However, in hypomagnesemic patients (26 cases) of the intervention group, there was a 10.9% increase in high-density-lipoprotein (HDL) cholesterol in association with a decrease in other lipids. Although a general blood-lipid-reducing effect of a high-fiber, low-cholesterol diet cannot be excluded, dietary magnesium may have contributed to the reduction of total serum cholesterol, LDL-cholesterol, and triglyceride as well as to the marginal rise in HDL-cholesterol. More studies with a longer follow-up are needed in order to confirm the role of magnesium in preventing a decrease in HDL-cholesterol in association with reduction in other lipoproteins. https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2130823
Sprecher, D. L. (2000). “Raising high-density lipoprotein cholesterol with niacin and fibrates: a comparative review.” Am J Cardiol 86(12A): 46L-50L. A growing number of trials that used fibrates and niacin alone or in combination with other lipid-altering agents have shown that both these drugs are effective for reducing total cholesterol, low-density lipoprotein cholesterol (LDL-C) and triglycerides, and for increasing high-density lipoprotein cholesterol (HDL-C) levels. These lipid changes are associated with a reduction in events such as fatal and nonfatal myocardial infarction, stroke, and transient ischemic attack. In angiographic trials, they are associated with disease regression, increased minimal luminal diameter, and protection from risk of new lesions. In a head-to-head comparison study, niacin 2,000 mg/day increased HDL-C more than gemfibrozil 1,200 mg/day, and decreased the total cholesterol-to-HDL-C ratio, lipoprotein (a) (Lp[a]), and fibrinogen levels significantly more. Combination therapies of niacin plus a resin or statin are effective, well tolerated, and safe.