May 2018 – Vol. 12, Issue 5

 In This Issue…                                                                            

  • Study sheds light on the link between biotin deficiency and inflammation
  • Fish oil, chocolate and green tea may help patients reduce their statin dose
  • Vitamin A alleviates ethanol-induced cellular stress
  • Magnesium may beneift blood vessel health by facilitating an artery’s ability to dilate
  • Trans fats may be associated with shortened telomeres


CLINICAL UPDATE – Study sheds light on the link between biotin deficiency and inflammation
            Previous research has shown that biotin deficiency increases inflammation but since there are so many causes of inflammation – physiologically speaking – the actual metabolic pathways between biotin deficiency and inflammation are unclear.  In this study, researchers subjected human immune cells to biotin deficiency and compared the result to human immune cells living in a biotin-rich environment.  Biotin, also known as vitamin B7, is a key vitamin necessary for proper cellular metabolism. It is a cofactor to cellular energy production and therefore important to cellular health at a fundamental level. 
            When the human immune cells were biotin deficient, expression of inflammatory proteins increased.  Specifically, CD4+T cells were used, which are also known as T-helper cells because they are a type of white blood cell that directs the function of other immune cells.  In other words, T-helper cells supervise immune cells, sending signals to attack viruses and bacteria, for example. In biotin deficiency, the number of these regulatory immune cells (CD4+T) decreased.  At the same time, biotin deficiency caused an increase in the metabolic pathway (called mTOR) that regulates cell growth.  mTOR (mammalian target of rapamycin) is a protein that senses the nutrient and energy status of cells and regulates their metabolism accordingly.  A decrease in mTOR is generally good and can lead to a longer lifespan.  An increase in mTOR is generally bad and can lead to tumors or cancerous growths. 
            The results of this study – both in vivo and in vitro – showed that biotin deficiency increased the mTOR pathway, which then resulted in an increase in several inflammatory compounds.  This, combined with the fact that biotin deficiency decreased the number of T-helper cells, meaning fewer immune cells were around to regulate everything, ultimately induced the increase in inflammation seen in biotin deficiency.
          (Journal of Immunology, April 2018)
LINK to ABSTRACT Biotin Deficiency Induces Th1- and Th17-Mediated Proinflammatory Responses in Human CD4+ T Lymphocytes via Activation of the mTOR Signaling Pathway.
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CLINICAL UPDATE – Fish oil, chocolate and green tea may help patients reduce their statin dose
            This pilot study sought to find out whether patients who were taking high-dose statins could reduce their dosage when supplemented with a combination of fish oil, chocolate and green tea.  The study was broken up into two phases:  Phase 1 included 53 type 2 diabetics who were taking a statin.  They remained on their statin therapy at their prescribed dosage but were also given the following every day for 6 weeks:  fish oil (1.7 grams EPA + DHA daily) + special chocolate containing plant sterols + green tea.  In Phase 2, ten patients (out of the original 53) were selected because they were “good responders” to the fish oil/ chocolate/ green tea regimen.   These ten patients continued the fish oil/ chocolate/ green tea therapy for another 6 weeks (for a total of 12 weeks), but they reduced their statin dosage by 50%.
            After 12 weeks, the ten patients who completed Phase 2 showed no difference in the level of blood lipids from before their statin was reduced.  In other words, cutting the statin dose in half had no adverse effect on blood lipids.  Nor did the dose reduction alter inflammation levels, their ability to metabolize cholesterol or change high-density lipoprotein (HDL) levels.  This study underscores the growing interest ina “personalized medicine” approach, especially for patients who cannot tolerate high dose statin therapy and are looking for alternatives in treatment.  Further studies may elucidate the profile parameters of the “good responders” as candidates for this personalized approach.
          (Molecular Metabolism, May 2018)
LINK to ABSTRACT Statin dose reduction with complementary diet therapy: A pilot study of personalized medicine.
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CLINICAL UPDATE – Vitamin A alleviates ethanol-induced cellular stress
            This animal study sought to determine the effect vitamin A supplementation might have on liver cells that were stressed by exposure to ethanol.   Vitamin A helps the immune system function properly, plays a role in the maintenance of epithelial barriers throughout the body, regulates gene expression and facilitates hormone production.   Ethanol is a known competitive inhibitor of vitamin A metabolism, meaning that ethanol will block vitamin A receptors in the liver rending the vitamin incapable of normal function.
            In this study, four groups of mice were studied: (1) a control group, (2) a group given ethanol, (3) a group given vitamin A and (4) a group given ethanol and vitamin A.   After 90 days, the livers of all animals were evaluated.  Not surprisingly, the mice fed ethanol showed signs of liver damage, including fatty liver, damage to liver cell membranes and an increased activity of an enzyme that signals cellular stress.  Ethanol in the mice also inactivated the vitamin A receptors in their livers.  However, when the mice were given the active metabolite of vitamin A via supplementation along with the ethanol, the ethanol-induced cellular stress was reversed.  In other words, supplementation with vitamin A blunted the negative effects ethanol had on liver cells in these mice.
          (Archives of Physiology and Biochemistry, May 2018)
LINK to ABSTRACT Supplementation of all trans retinoic acid ameliorates ethanol-induced endoplasmic reticulum stress.



CLINICAL UPDATE – Magnesium may benefit blood vessel health by facilitating an artery’s ability to dilate
            In this meta-analysis, seven randomized controlled trials that measured the effect of magnesium supplementation on blood vessel health were evaluated. Since previous studies on the effect of magnesium on endothelial function were inconsistent, this review sought to distinguish between two different markers of endothelial function – flow mediated dilation (FMD) and carotid intima media thickness (CIMT).  Endothelial function refers to the ability of the arteries to respond to chemical or physical cues to contract or dilate, depending on the circumstances.  The more responsive the artery, the healthier the blood vessel.  But the response of the artery depends on more than one specific factor – for example, FMD refers to the ability of the artery to appropriately respond to chemical cues in the blood due to release of nitric oxide (NO).  CIMT, however, measures the thickness of the carotid artery and the presence of atherosclerosis (arterial plaque) which would negatively affect endothelial function albeit by a different mechanism, more physical than chemical. 
            In the trials studied, magnesium supplementation significantly increased FMD, thus benefiting blood vessel health by improving endothelial function.  However, in the same studies, magnesium supplementation did not affect CIMT suggesting that the improvement in blood vessel health resulting in magnesium supplementation studies came from improvements in the blood vessels’ ability to respond to chemical cues for dilation versus an improvement from clearing the arteries of plaque.
          (Atherosclerosis, June 2018)
LINK to ABSTRACT Effect of magnesium supplementation on endothelial function: A systematic review and meta-analysis of randomized controlled trials.



CLINICAL UPDATE – Trans fats may be associated with shortened telomeres
            In a database of over 5400 people, the levels of trans fatty acids were measured and compared to the telomere length in a typical sample population of Americans.  Telomeres are sections of DNA found in all cells at the tips of our chromosomes that serve to protect our chromosomes from “unraveling”.  As we age, our cells’ telomeres get shorter to the point that eventually a cell dies because the telomeres protecting it is too short to do its job.  Several things affect telomere attrition rate – both positive (good nutrient status, healthy blood sugar and lipid metabolism, normal weight, exercise, etc.) and negative (micronutrient deficiencies, inflammation, cellular stress, etc.).
            This study revealed that the level of trans fatty acids in a person’s blood – in both men and women – was negatively correlated to telomere length.  In other words, the higher the trans fatty acid levels in a person’s blood, the shorter their telomeres.  Since shortened telomeres are associated with aging and chronic disease, these results suggest that reducing trans fatty acid consumption may be something to consider when looking to achieve optimal health.
          (European Journal of Clinical Nutrition, April 2018)
LINK to ABSTRACT Association between plasma trans fatty acids concentrations and leucocyte telomere length in US adults.