November 2016 – Vol. 10, Issue 11

In This Issue…

  • High dose vitamin E reduced kidney inflammation in diabetics
  • Folic acid deficiency exacerbates damage from stroke
  • Low selenium before a heart bypass may increase risk of complications
  • Researchers suggest a disease-specific reference range for vitamin B1 in heart failure patients
  • Low vitamin D linked to erectile dysfunction
  • Study sheds light on zinc’s role in protecting the liver

CLINICAL UPDATE – High dose vitamin E reduced kidney inflammation in diabetics
          In this randomized double-blind placebo-controlled trial, sixty diabetics with confirmed kidney disease were divided into two groups:  one group (n=30) took 1200 IU/d of vitamin E while the other group (n=30) took placebo.  After 12 weeks, the group taking vitamin E showed a significant reduction in several biomarkers of renal inflammation and although glucose levels and insulin resistance showed no improvement, there was a significant decrease in insulin concentration. 
          (Journal of Clinical Lipidology, August 2016)
          LINK to ABSTRACT
The effects of high-dose vitamin E supplementation on biomarkers of kidney injury, inflammation, and oxidative stress in patients with diabetic nephropathy: A randomized, double-blind, placebo-controlled trial.

 

CLINICAL UPDATE – Folic acid deficiency exacerbates damage from stroke
          Previous studies have linked low folic acid with an increased risk of ischemic stroke (stroke caused by oxygen deprivation) but new research sheds light on how damage occurs.  In this animal study, scientists demonstrated that after a stroke, brain tissue is damaged not only from lack of oxygen, but also through the prolonged activation of a process called autophagy, whose function is to degrade dysfunctional parts of a cell. When folic acid is deficient, this entire process (autophagy) is accelerated to the point where nerve cells die, thus exacerbating damage to the brain after an initial stroke.
          (Journal of Nutritional Biochemistry, December 2016)
          LINK to ABSTRACT
Folic acid deficiency increases brain cell injury via autophagy enhancement after focal cerebral ischemia.

 

CLINICAL UPDATE – Low selenium before a heart bypass may increase risk of complications
         Fifty patients who underwent a heart bypass operation (coronary artery bypass graft surgery) were evaluated for post-operative atrial fibrillation, a common complication of cardiac surgery. Since selenium is a key micronutrient for very powerful antioxidant enzymes and oxidative stress plays a major role in atrial fibrillation, researchers decided to measure selenium levels on these fifty patients at five different points in their treatment: (1) right before the operation, (2) at the end of the operation, (3) three hours after the operation, (4) one day after the operation and (5) five days after the operation.
          Seventeen patients developed atrial fibrillation complications following surgery. Preoperative selenium levels were lower in these patients leading the authors to conclude that “low preoperative selenium levels may be at a greater risk of developing post-operative atrial fibrillation.”
          (European Journal of Clinical Nutrition, October 2016)
          LINK to ABSTRACT
Low preoperative selenium is associated with post-operative atrial fibrillation in patients having intermediate-risk coronary artery surgery.

 

CLINICAL UPDATE – Researchers suggest a disease-specific reference range for vitamin B1 in heart failure patients
          Vitamin B1 (thiamine), which is a cofactor to at least 24 known enzymes many of which are involved in cellular energy metabolism, was measured in 30 heart failure patients at the Mayo Heart Failure Clinic. Although vitamin B1 deficiency has been strongly linked to heart failure in previous studies – some reports suggest that as many as 96% of heart failure patients are thiamine deficient – in this group less than 12% were thiamine deficient according to standard reference values.
          The authors note that high dose thiamine supplementation has improved cardiac function in heart failure patients in previous studies, regardless of thiamine blood levels, suggesting two things:  (1) that thiamine may become conditionally essential with heart failure and (2) a disease-specific reference range for thiamine should exist because the “normal” reference range does not identify heart failure patients that would benefit from supplementation.
          (Clinical Nutrition, February 2016)
          LINK to ABSTRACT
Prevalence of thiamine deficiency in a stable heart failure outpatient cohort on standard loop diuretic therapy.

 

CLINICAL UPDATE – Low vitamin D linked to erectile dysfunction
          Blood levels of vitamin D were measured in 3390 men who were free of atherosclerotic heart disease, which has been linked to erectile dysfunction in previous studies.  Men with erectile dysfunction had approximately 6% lower levels of vitamin D than men who did not.  Also, after adjusting for several variables such as medication and other health problems, the men who had vitamin D deficiency were one-third more likely to have problems with erectile dysfunction than those with adequate vitamin D (defined as levels above 30 ng/mL), regardless of whether or not they also suffered from heart disease.
          (Atherosclerosis, September 2016)
          LINK to ABSTRACT
Vitamin D deficiency is independently associated with greater prevalence of erectile dysfunction: The National Health and Nutrition Examination Survey (NHANES) 2001-2004.

 

CLINICAL UPDATE – Study sheds light on zinc’s role in protecting the liver
          In this study, mice were fed either a zinc-deficient or zinc-adequate diet and subsequently evaluated for stress-induced biomarkers related to protein synthesis in the liver. The mice that were fed a zinc deficient diet did not exhibit any additional cellular stress in the liver or pancreas than those given adequate zinc. 
          However, a second part of the study compared zinc-deficient, zinc-adequate, or zinc-supplemented mice exposed to a chemical that induces a cellular stress response by thwarting the correct manufacture of proteins.  When exposed to this exogenous chemical stressor, zinc deficiency – even though it did not directly initiate stress to liver cells – did impair the cells’ ability to stop the destructive stress response once it had started suggesting that adequate dietary zinc intake is required to suppress this process in mice.
          (Journal of Nutrition, November 2016)
          LINK to ABSTRACT
Dietary Zinc Regulates Apoptosis through the Phosphorylated Eukaryotic Initiation Factor 2α/Activating Transcription Factor-4/C/EBP-Homologous Protein Pathway during Pharmacologically Induced Endoplasmic Reticulum Stress in Livers of Mice.