January 2017 – Vol. 11, Issue 1

In This Issue…

  • L-carnitine may help lower Lp(a) in people taking statins
  • Magnesium treatment may benefit glucose metabolism in diabetics
  • Supplemental calcium linked to dementia in certain women
  • Serum levels of folate may not tell the whole story
  • Folic acid link to neural tube defects gains attention

 

CLINICAL UPDATE – L-carnitine may help lower lipoprotein(a) in people taking statins
          Lipoprotein(a) is strongly linked to heart disease and blood clotting problems and consequently is one of the four specific lipid related risk factors cited by the National Institutes of Health National Cholesterol Education Program (NCEP) as worthy of monitoring.  Unfortunately, Lp(a) has been notoriously difficult to treat pharmacologically since statins have shown little efficacy in lowering Lp(a) levels.
          In this double-blind placebo controlled trial, patients with elevated cholesterol and elevated Lp(a) were divided into two groups, each with 29 people:  Group 1 received a statin only and Group 2 received the same statin plus 2 grams/day of L-carnitine.  After 12 weeks, the group receiving only a statin showed about a 7% reduction in Lp(a) but the group receiving both L-carnitine + the statin showed over 19% reduction in Lp(a) levels.  Authors suggest that co-administration of L-carnitine, whose main function is to assist with fatty acid metabolism, may enhance efforts to lower Lp(a) compared to using a statin alone.
          (Lipids, January 2017)
          
LINK to ABSTRACT L-Carnitine/Simvastatin Reduces Lipoprotein (a) Levels Compared with Simvastatin Monotherapy: A Randomized Double-Blind Placebo-Controlled Study.

 

CLINICAL UPDATE – Magnesium treatment may benefit glucose metabolism in diabetics
          In this meta-analysis, eighteen randomized controlled trials were reviewed that specifically looked at magnesium supplementation versus placebo in patients that either had diabetes or were at high risk of diabetes.  Compared to placebo, magnesium treatment reduced blood sugar levels in diabetics.  Similarly, in people that did not yet have diabetes but who were at higher risk of developing it, magnesium treatment lowered blood sugar after a glucose challenge and trended toward lower markers for insulin resistance, leading authors to conclude that “magnesium supplementation appears to have a beneficial role” in markers of glucose metabolism.
          (European Journal of Clinical Nutrition, December 2016)
         
LINK to ABSTRACT Effect of magnesium supplementation on glucose metabolism in people with or at risk of diabetes: a systematic review and meta-analysis of double-blind randomized controlled trials.

 

CLINICAL UPDATE – Supplemental calcium linked to dementia in certain women
          This study followed 700 Swedish women between the ages of 70-92 years old who were all initially free from dementia.  After five years, the researchers collected data on which women took calcium supplements (and dosage) as well as which women were clinically diagnosed with dementia.  The odds of women developing dementia who took supplemental calcium were twice that for women who did not take calcium.  Further, for the women who had a history of stroke, the odds of developing dementia for women who took calcium were six times the odds as women who did not take calcium.  Although limited in sample size, the study results suggest that in elderly women, calcium supplementation may potentially be harmful, especially if there is a history of stroke or vascular problems.
          (Neurology, October 2016)
           LINK to ABSTRACT
Calcium supplementation and risk of dementia in women with cerebrovascular disease.

 

CLINICAL UPDATE – Serum levels of folate may not tell the whole story
          Several metabolites were measured in plasma, urine and cerebral spinal fluid of 33 young adults with treatment-resistant depression and then compared to 16 healthy control subjects.  Folate deficiency in cerebral spinal fluid was the most common deficiency seen in the patients with pharmacological treatment resistant depression. Interesting, in these patients, serum levels of folate were normal.  Plus, all of the patients with cerebral folate deficiency showed improvement in depression symptoms when treated with folinic acid, suggesting serum measurement of folic acid may be misleading as it does not reflect a functional deficiency.  In fact, when folic acid deficiency was confirmed (in this case via cerebral spinal fluid), an unexpectedly large proportion of patients with potentially treatable depression were identified.
          (American Journal of Psychiatry, January 2017)
         
LINK to ABSTRACT Neurometabolic Disorders: Potentially Treatable Abnormalities in Patients With Treatment-Refractory Depression and Suicidal Behavior.

 

CLINICAL UPDATE – Folic acid link to neural tube defects gains attention
          Folic acid has long been credited for drastically reducing the risk of neural tube defects in babies, but new research sheds light on possible consequences of the “if some is good, more is better” approach to supplementation.  Scientists investigated the effects of moderate folic acid supplementation on reproductive outcomes in mice.
          Female mice were fed folic acid-supplemented diets or control diets prior to and during pregnancy. The researchers found that in female mice with a certain genetic deficiency involved in methylation (called MTHFD1 R653Q),  the incidence of embryonic defects and developmental delays actually increased when given supplemental folic acid, compared to those mice on a control diet.  The findings suggest gene-nutrient interactions (in this case, folic acid with MTHFD1 R653Q) may complicate recommendations for supplemental nutrients during pregnancy.
          (American Journal of Clinical Nutrition, November 2016)
          
LINK to ABSTRACT Moderate folic acid supplementation and MTHFD1-synthetase deficiency in mice, a model for the R653Q variant, result in embryonic defects and abnormal placental development.