July 2017 – Vol. 11, Issue 7

 In This Issue…

  • One third of Americans have at least one micronutrient deficiency
  • Can we modulate our gene expression with nutrients?
  • Research team suggests carnitine deficiency may be a root cause of autism
  • In healthy athletes, vitamin K supplementation may improve fitness
  • Vitamin B1 deficiency compromises health of egg cells

CLINICAL UPDATE – One third of Americans have at least one micronutrient deficiency
Using data from the National Health and Nutrition Examination Survey (NHANES), a group of researchers compiled data on seven vitamins from over 15,000 people in America. They determined that 31% of the United States population is at risk for at least one vitamin deficiency, 23% of Americans are at risk for deficiency in at least two vitamins and 6% are at risk for three or more vitamin deficiencies.
          The data came from several sources – dietary recall, supplement use, lab results – some less quantifiable than others.  They concluded that the most common vitamin deficiency in the United States is vitamin B6 although they concede that biomarkers of nutrient status are affected by inflammation, suggesting deficiency rates may be higher. In addition, the nutrient status did not correlate with dietary intake, according to their data.  A review of the extensive information supports the view that a one-size-fits-all approach to nutritional requirements is an outdated and inaccurate model. 
          Finally, this study states that “sub-clinical deficiency symptoms for many vitamins and minerals are non-specific, and may include fatigue, irritability, aches and pains, decreased immune function, and heart palpitations” further complicated the quantification of micronutrient deficiency.  Functional measurements of cellular nutritional status may gain attention as studies like this are published.
          (Nutrients, June 2017)
          LINK to ABSTRACT
Risk of Deficiency in Multiple Concurrent Micronutrients in Children and Adults in the United States.
          LINK to FREE FULL TEXT


CLINICAL UPDATE – Can we modulate our gene expression with nutrients?
Recent evidence suggests that the answer is yes.  Most people understand that we all have inherent genetic predispositions – some as benign as the shape of our nose and others more dangerous such as the tendency toward certain cancers.  However, as research on epigenetics grows, the ability to modulate the expression of certain genes is becoming clearer.  Epigenetics is the study of how our genetic expression is affected by factors other than changes in DNA sequence.  These factors include our environment, including what we eat, supplements we take, toxins, illnesses, even the amount of sunlight to which we are exposed. 
          In this study, variations (polymorphisms) in a specific gene that makes a protein called the zinc transporter 8 (ZNT8), which carries zinc into the hormone insulin, were studied. This protein ZNT8 is responsible for ensuring that pancreatic beta cells (the cells that make insulin which allows us to metabolize blood sugar) have adequate zinc available.  If cells in the pancreas do not have enough zinc, they will not function optimally which may ultimately result in higher risk of insulin resistance and the metabolic dysfunction that follows. 
          When participants with the (CC) genotype ingested more zinc and omega 3 fatty acids, they lowered their risk of metabolic syndrome consequences associated with their genotype. Stated differently, people with this specific genotype (CC) responded well (in terms of improved insulin sensitivity and metabolic health) to higher levels of zinc and omega 3 fatty acids, while other genotypes (CT or TT) did not show a meaningful improvement in metabolism.  Since over-supplementation has potentially negative consequences (too much zinc can cause copper deficiency, for example), knowing your genotype may lead to more informed supplementation decisions. 
          (Scientific Reports, May 2017)
LINK to ABSTRACT Some dietary factors can modulate the effect of the zinc transporters 8 polymorphism on the risk of metabolic syndrome. 
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CLINICAL UPDATE – Research team suggests carnitine deficiency may be a root cause of autism
Carnitine is a nutrient whose main function is to transport fatty acids into the cellular powerhouse – the mitochondria – so they can be used for energy.  Low carnitine, which is common in autism, can impair the ability to use fatty acids for learning and social development.  This paper hypothesizes that carnitine deficiency may cause symptoms of autism and goes on to suggest that up to 20% of autism may possibly be prevented by appropriate supplementation.  The author  points out that defects in carnitine biosynthesis is a risk factor for autism, and cites a gene (SLC6A14) that limits carnitine utilization in the brain which is only expressed in males, suggesting that this may be part of the reason autism is much more prevalent in boys than in girls. 
          (Bioessays, July 2017)
LINK to ABSTRACT Brain carnitine deficiency causes nonsyndromic autism with an extreme male bias: A hypothesis.



CLINICAL UPDATE – In healthy athletes, vitamin K supplementation may improve fitness
In this small study, 26 trained athletes (male and female) were given placebo or vitamin K2 supplements for eight weeks while they maintained their regular exercise routine. At the beginning of the study and after eight weeks, each person completed a fitness test on an exercise machine designed to quantify their physical work load, including oxygen consumption, respiratory rate, cardiac output and heart rate. 
          Vitamin K2 supplementation was associated with a 12% increase in cardiac output, which is the volume of blood the heart is capable of pumping each beat.  The authors suggest that vitamin K2, which has been shown previously to play a role in energy metabolism  especially in tissues with high energy requirements like skeletal muscle and the heart, might be considered in healthy athletes to improve performance.
          (Alternative Therapies in Health and Medicine, July 2017)
LINK to ABSTRACT Oral Consumption of Vitamin K2 for 8 Weeks Associated With Increased Maximal Cardiac Output During Exercise.




CLINICAL UPDATE – Vitamin B1 deficiency compromises health of egg cells
Mice were fed one of the following diets – (1) normal or (2) a diet lacking in vitamin B1. Not surprisingly, the vitamin B1 concentration in the ovaries from mice not given vitamin B1 was much lower than in mice fed vitamin B1.  Since the major source of cellular energy in oocytes (immature egge cells) comes from a compound (pyruvic acid) that is metabolized by a vitamin B1-dependent enzyme, the researchers wanted to investigate the effect of B1 deficiency on egg cell development.
          If the vitamin B1 deficiency was “mild” meaning that it was not severe enough to cause weight loss, the mice ovaries produced egg cells that were normal.  However, if the vitamin B1 deficiency reached severe levels, then the mice ovaries would produce abnormal egg cells more often – 44% of the eggs from the severely deficient animals were abnormal, compared to only 14% of the eggs from mice with adequate vitamin B1.  In addition, once the mice were put back on a vitamin B1 containing diet, the level of abnormal egg cells dropped from 44% to 23% suggesting that damage to the egg cell may occur as the cell matures but not in its immature stage. 
          (Nutrition and Metabolic Insights, March 2017)
LINK to ABSTRACT Effects of Mild and Severe Vitamin B1 Deficiencies on the Meiotic Maturation of Mice Oocytes.
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