NOVEMBER 2015 - Volume 2015, Issue 11                     

In This Issue….                     

  • Low levels of this mineral double the risk of hardened arteries
  • Inorganic form of selenium more beneficial than organic form when supplementing people with liver problems, says study
  • Vitamin D may increase the fat-burning hormone adiponectin
  • Biotin may help repair damage to pancreas
  • Zinc deficiency in mom may cause behavioral problems in offspring
  • Vitamin A – an underappreciated nutrient in the treatment of diabetes?

 

CLINICAL UPDATE – Low levels of this mineral double the risk of hardened arteries

Levels of magnesium were measured in 34,553 people who also underwent tomography – a procedure that measures calcification of the arteries. This study, which was performed on people who were considered to have low risk of cardiovascular disease, was part of a hospital health examination program. After adjusting for traditional heart disease risk factors such as age, body mass index, diabetes, hypertension on others, it was found that the people with the lowest levels of magnesium were over twice as likely to have coronary artery calcification, or hardening of the arteries as those with higher blood levels of magnesium. (Nutrition, Metabolism and Cardiovascular Disease, November 2015)


LINK to ABSTRACT 
Low serum magnesium is associated with coronary artery calcification in a Korean population at low risk for cardiovascular disease.

 

CLINICAL UPDATE – Inorganic form of selenium more beneficial than organic form when supplementing people with liver problems, says study

In this randomized controlled trial, patients with cirrhosis of the liver were divided into three groups: one group received placebo, one group received selenium in the inorganic form of selenate, and one group received selenium in the organic form of selenomethionine. After four weeks, researchers measured selenoproteins (typically made in the liver) and the powerful enzyme glutathione peroxidase (a selenium dependent enzyme) – both measures of functional selenium deficiency. They found that selenium repletion, as measured by glutathione peroxidase activity, was higher in the selenate-supplemented group, while those taking either placebo or selenomethionine demonstrated functional selenium deficiency. Researchers concluded that cirrhosis of the liver may cause “impaired metabolism of selenomethionine.” American Journal of Clinical Nutrition, November 2015)

LINK to ABSTRACT Selenium deficiency occurs in some patients with moderate-to-severe cirrhosis and can be corrected by administration of selenate but not selenomethionine: a randomized controlled trial.

 

 

 

CLINICAL UPDATE – Vitamin D may increase the fat-burning hormone adiponectin

Levels of three hormones produced by fat cells – adiponectin, leptin and resistin – were measured in fifty obese individuals along with their vitamin D levels. When vitamin D levels were high, the hormones leptin (and resistin (both of which are linked to obesity) were relatively lower – a good thing. Conversely, vitamin D increased the protective hormone adiponectin, which regulates energy and fat metabolism. In fact, an increase in vitamin D is accompanied by “an intensive increase in adiponectin concentrations,” according to the authors.  (Angiology, August 2015)

LINK to ABSTRACT Vitamin D and Dysfunctional Adipose Tissue in Obesity.

 

CLINICAL UPDATE – Biotin may help repair damage to pancreas

In this animal study, an acute deficiency of biotin – a B vitamin that regulates several metabolic processes – was induced by feeding rats raw egg whites for six weeks. It is well accepted that raw egg whites will cause avidin-induced biotin deficiency, as the protein avidin in egg whites bonds to biotin making it completely unavailable for use in the body. (Avidin is so named for its propensity to bind to biotin: avid + biotin = avidin)

After biotin deficiency was induced, animals were divided into two groups – one group that continued on the depletion diet and one group that received biotin supplements to correct biotin deficiency. After one week, the pancreases of the animals in each group were examined. Biotin depletion altered genes in a way that resulted in inflammation and decreased pancreatic function. Biotin repletion, on the other hand, turned on genes that repaired pancreatic cells, reduced inflammation and increased their functional capacity. The authors state “that biotin repletion, even after lengthy deficiency, results in the rapid induction of repair processes in the pancreas.” (Canadian Journal of Physiology and Pharmacology, December 2015)

LINK to ABSTRACT Microarray analysis of pancreatic gene expression during biotin repletion in biotin-deficient rats.

 

 

CLINICAL UPDATE – Zinc deficiency in mom may cause behavioral problems in offspring

In this animal study, pregnant rats were fed a normal or zinc-deficient diet during gestation. At the end of their pregnancy, researchers discovered that the fetuses born to zinc-deficient mothers had decreased cerebral brain growth. Specifically, they demonstrated a change in the activity of zinc-dependent proteins that are specific to brain cell development, leading the authors to conclude that “disruption of fetal neurogenesis could underlie irreversible neurobehavioral impairments observed after even marginal zinc nutrition during a critical period of early brain development.”  (Journal of Nutritional Biochemistry, November 2015)

LINK to ABSTRACT Gestational marginal zinc deficiency impaired fetal neural progenitor cell proliferation by disrupting the ERK1/2 signaling pathway.

 

 

CLINICAL UPDATE – Vitamin A: an underappreciated nutrient in the treatment of diabetes?

As type 2 diabetes rates continue to rise, focus on the body’s antioxidant defense systems and how they may be connected to diabetes is increasing, particularly since oxidative stress in various tissues causes many diabetic complications. In this review, the role of vitamin A as a potential therapy in type 2 diabetics is discussed. Since vitamin A has well-established roles in gene expression and antioxidant regulation, coupled with the fact that diabetes has been linked to vitamin A deficiency, the authors suggest that “vitamin A supplementation may have a role in type 2 diabetes mellitus biology.” (Nutrition, August 2015)

LINK to ABSTRACT Role of vitamin A in type 2 diabetes mellitus biology: effects of intervention therapy in a deficient state.