March 2017 – Vol. 11, Issue 3

In This Issue…

  • More evidence confirms that omega 3 fatty acids protect telomeres
  • Can weight loss improve vitamin D status?
  • High BMI increases risk for vitamin B1 deficiency
  • Functional indicator of vitamin B2 is more telling than blood levels
  • Supplemental selenium affects immune response to flu vaccine


CLINICAL UPDATE – More evidence confirms that omega 3 fatty acids protect telomeres
          In a double-blind, placebo-controlled trial, 85 patients with chronic kidney disease were given omega 3 fatty acids, the antioxidant coenzyme Q10, a combination of these or neither of these.  The patients’ telomeres were measured at baseline and then again after eight weeks of supplementation.  At first glance, no difference in telomere length was seen between patients who had or had not taken omega 3 fatty acids.  However, when correcting for cell counts, omega 3 fatty acids did, in fact, protect telomeres.  Specifically, the number of white blood cells (neutrophils) with shorter telomeres decreased.  
          Neutrophils are the most abundant type of white blood cell in the body and are important in fighting off infections. They typically travel to an infection site in the body, fight pathogens, then die – thus, neutrophils are short-lived. In this study, when the authors corrected for the number of neutrophil cells, supplementation with omega 3 fatty acids did increase average telomere length.  They postulated that the mechanism of this beneficial effect on telomere length via omega 3 fatty acid supplementation was due to the omega 3 fatty acids’ role in reducing oxidative stress, and in doing so, helped clear neutrophils with shorter telomeres from the blood.
          (Nutrients, March 2016)
LINK to ABSTRACT n-3 Fatty Acid Supplementation and Leukocyte Telomere Length in Patients with Chronic Kidney Disease.  LINK to FREE FULL TEXT



CLINICAL UPDATE – Can weight loss improve vitamin D status?
          According to a review of trials on the effects of weight loss on vitamin D, the answer may be yes, but only marginally so.  Former research has linked obesity to vitamin D deficiency, but the causal link has remained elusive.  Does vitamin D deficiency contribute to obesity or does obesity cause vitamin D deficiency?  This review suggests the latter conclusion is more likely – that increasing adiposity leads to suboptimal levels of circulating vitamin D.
          When comparing people from several studies who actually lost weight to people who simply maintained their weight (over 3400 people total), there was a slight improvement in vitamin D status in those that lost weight, leading the authors to conclude that lower vitamin D “may be due to reversed causation.”  Simply put, obesity may contribute to vitamin D deficiency, not the other way around.
          (American Journal of Clinical Nutrition, October 2016)
LINK to ABSTRACT Vitamin D status and weight loss: a systematic review and meta-analysis of randomized and nonrandomized controlled weight-loss trials.



CLINICAL UPDATE – High BMI increases risk for vitamin B1 deficiency
          In this observational study, 400 patients with a BMI (body mass index) of at least 35 were evaluated for vitamin B1 status before undergoing bariatric surgery.  Vitamin B1 (also known as thiamine) was measured in blood, and clinical symptoms associated with B1 deficiency – neuropathy, cardiac abnormalities (congestive heart failure) and psychiatric symptoms – were recorded.  Any patients that had already had bariatric surgery or had a history of heavy alcohol use (something that can deplete vitamin B1 levels) were excluded from this study.
          Of the 400 obese patients, 17% were confirmed to be deficient in vitamin B1.  More than half of the patients that were deficient in vitamin B1 manifested clinically with cardiac or neurologic complications.  The authors concluded that a higher body mass index is a risk factor for clinical thiamine (vitamin B1) deficiency.
          (Nutrition Research, January 2017)
          LINK to ABSTRACT
Prevalence of clinical thiamine deficiency in individuals with medically complicated obesity.




CLINICAL UPDATE – Functional indicator of vitamin B2 is more telling than blood levels
          When researchers fed rats a riboflavin-deficient or riboflavin-replete diet for 13 days and then measured the amount of a key metabolite called formate that was synthesized, they found that blood levels and functional status did not correlate.  Formate is a metabolite produced by mitochondria that is needed for methylation reactions in the body, since it contributes methyl groups to the folate cycle – that is, formate assists cellular metabolism by enhancing the efficient recycling of micronutrients.
          In this study, researchers showed that vitamin B2 deficiency significantly decreased the rate of formate production in liver cells.  Specifically, B2 deficiency lowered the activity of the enzyme MTHFR (methylenetetrahydrofolate reductase) which is key to cellular detoxification.  However, what they found interesting is that although enzymatic function was clearly decreased, blood levels of formate did not change, suggesting that plasma levels are not indicative of functional status when it comes to micronutrients or metabolites.
          (Journal of Nutrition, March 2017)
          LINK to ABSTRACT
Riboflavin Deficiency in Rats Decreases de novo Formate Production but Does Not Affect Plasma Formate Concentration.




CLINICAL UPDATE – Supplemental selenium affects immune response to flu vaccine
          A group of 117 healthy adults were given supplemental selenium from two different sources – either from selenium-enriched yeast or selenium-containing onions – and their cellular immune response was measured before and after they were administered the flu vaccine.  In addition, the amount of selenium was given at different doses from both the yeast and onion sources.  Two weeks after the flu vaccine was given, all groups taking selenium showed enhanced T cell proliferation, indicating an increased immune response.  In other words, T cell proliferation is an indication that the lymphocytes (a type of white blood cells responsible for immunity) are responding robustly to a threat, such that immune function is working well.  In fact, the T cell proliferation responded dose-dependently to supplemental selenium.
          However, in the same people, some aspects of cellular immunity seemed to be down-regulated after supplemental selenium. For example, the production of proteins (TNF-α) involved in acute phase reactions were decreased after vaccination.  Ultimately, this led the researchers to conclude that supplemental selenium had both “beneficial and detrimental effects on cellular immunity to flu.” 
          This research highlights three key points when it comes to micronutrients’ effects on immunity: (1) the complexity of the immune response should not be underestimated and (2) a comprehensive evaluation of nutritional status on immunity may be more useful than measuring a single nutrient and (3) blind supplementation (versus targeting specific micronutrient deficiencies) may not be the best course of action.  
          (Clinical Nutrition, April 2017)
LINK to ABSTRACT Selenium supplementation has beneficial and detrimental effects on immunity to influenza vaccine in older adults.  LINK to FREE FULL TEXT