March 2016 – Vol. 10, Issue 3


In This Issue…

  • Mechanism behind vitamin E’s protection against breast cancer is elucidated
  • Zinc mitigates alcohol-induced liver damage
  • Vitamin D levels correlate with adiponectin, the fat-burning hormone
  • Magnesium reduces risk of metabolic syndrome
  • CoQ10 may protect liver function in pre-term babies


CLINICAL UPDATE – Mechanism behind vitamin E’s protection against breast cancer is elucidated
When treated with γ-tocotrienol (one of the eight forms of vitamin E), breast cancer cell activation was inhibited, according to recent in vitro studies.  According to this study, there is a specific section in the cell membrane of breast cancer cells that turns on a cancer-promoting gene called HER2 (human epidermal growth factor).  When vitamin E was added to these cells, activation of this section of the cell membrane was inhibited, rendering the cancer-causing protein inactive.  (Journal of Nutritional Biochemistry, January 2016)
 Antiproliferative effects of γ-tocotrienol are associated with lipid raft disruption in HER2-positive human breast cancer cells.

 CLINICAL UPDATE – Zinc mitigates alcohol-induced liver damage
Three groups of rats were measured for liver inflammation and gut permeability:  (1) a control group, (2) an alcohol fed group and (3) alcohol plus zinc group.  The group given alcohol only had much higher levels of inflammation (cytokine production and macrophage activation).  In addition, the permeability of their gastrointestinal lining was compromised.  However, administration of zinc mitigated the damage to their gut and consequently reduced liver inflammation.  The authors stated that “preserving the intestinal barrier contributes to the protective effect of zinc on alcohol-induced steatohepatitis.”(Journal of Nutrition, December 2015)
LINK to ABSTRACT Preventing Gut Leakiness and Endotoxemia Contributes to the Protective Effect of Zinc on Alcohol-Induced Steatohepatitis in Rats.



 CLINICAL UPDATE – Vitamin D levels correlate with adiponectin, the fat-burning hormone
In this animal study, researchers demonstrated that feeding dietary resistant starch to rats resulted in an increase in blood levels of the fat-burning hormone, adiponectin, which were highly correlated to blood levels of vitamin D.  Furthermore, the researchers showed that this relationship – between adiponectin and vitamin D – was mediated by hormones specifically involved in blood pressure and kidney function (angiotensin and nephrin). (Nutrition Research, April 2016)
 Circulating adiponectin concentrations are increased by dietary resistant starch and correlate with serum 25-hydroxycholecalciferol concentrations and kidney function in Zucker diabetic fatty rats.


 CLINICAL UPDATE – Magnesium reduces risk of metabolic syndrome
In this systematic review of almost 32,000 people, higher magnesium intake was linked to lower incidence of metabolic syndrome, which will not surprise many since magnesium is a cofactor to over 100 enzymatic biological reactions in the human body, many of which directly impact metabolic health.  Similarly, when researchers looked at actual serum levels of magnesium (versus intake) in over 3400 people and its correlation to metabolic syndrome, the link still existed, but was less consistent.   This may suggest that serum levels may not adequately reflect magnesium intake, and by extension, serum levels may not reflect functional status of magnesium in cells, thus accounting for the heterogeneous results in this meta-analysis. (Nutrition, April 2016)
LINK to ABSTRACT Magnesium status and the metabolic syndrome: A systematic review and meta-analysis.




CLINICAL UPDATE – CoQ10 may protect liver function in pre-term babies
Previous studies have shown that low birth weight may increase the risk of liver dysfunction later in life.  In this controlled animal study, coenzyme Q10 was administered to pre-term offspring and liver function via several biomarkers was measured.  The administration of coenzymeQ10 had dramatic and beneficial effects on liver function in the offspring.  Specifically, coQ10 reduced inflammation (lower interleukin-6, tumor necrosis factor alpha and lipid peroxidation), reduced fibrosis (an indicator of damaged hepatic tissue) and reduced oxidative stress in the liver when compared with a control group. (American Journal of Clinical Nutrition, February 2016)
LINK to ABSTRACT Coenzyme Q10 prevents hepatic fibrosis, inflammation, and oxidative stress in a male rat model of poor maternal nutrition and accelerated postnatal growth. FREE FULL TEXT