September 2017 – Vol. 11, Issue 9

 In This Issue…

  • Vitamin B3 may help prevent birth defects
  • Vitamin E supplementation may help some women who struggle with infertility
  • Biotin may help optimize carbohydrate metabolism 3
  • Increasing vitamin B5 intake may lower chronic inflammation
  • Beriberi outbreak occurs in South America

CLINICAL UPDATE – Vitamin B3 may help prevent birth defects   
A group of scientists recently found several genes that may contribute to birth defects that result in heart, bone and kidney abnormalities.  In addition, they helped confirm that correcting a nutritional deficiency could be the key to correcting these genetic defects.   How they accomplished this was quite interesting.
          Seeking to determine the specific genes responsible for several congenital defects, they first identified several potentially harmful gene variants in human patients that shared the birth defects but were not related.  Then the scientists tested enzyme activity associated with each of these genes and once they found enzymes that were functioning sub-optimally due to the gene variants, they created a mouse model with the potentially harmful genes.  Using a new technology for precisely cutting genes (called CRISPR), they “engineered” these mice and were subsequently able to accurately determine the metabolic pathways that were connected to birth defects.
          The birth defects stem from disruption of metabolic pathways caused by a deficiency in the coenzyme NAD (nicotinamide adenine dinucleotide), which is an enzyme found in all living cells that is critical in DNA repair.  A precursor to this enzyme is vitamin B3 (also called niacin).  After the genes that affect NAD enzyme activity were identified and then inserted into mice, the mice offspring were born with congenital defects.  However, when the scientists gave the mice vitamin B3 supplementation during gestation, it prevented the malformations in the mice.  This study lends credence to the practice of micronutrient repletion for pregnant women in order to correct for genetically-induced nutritional deficiencies.  The implications are that targeted nutritional repletion in pregnancy may ultimately decrease birth defects.
          (New England Journal of Medicine, August 2017)
          LINK to ABSTRACT 
NAD Deficiency, Congenital Malformations, and Niacin Supplementation.


CLINICAL UPDATE – Vitamin E supplementation may help some women who struggle with infertility
In this study, 40 women, ages 18-37, who had experienced implantation failure (where a fertilized egg does not successfully implant into the uterine wall thus ending a pregnancy) were randomly divided into two groups.   The first group (20 women) took 400 IU of vitamin E daily and the second group (also 20 women) took  a placebo pill.  Before and after the trial, several measures of oxidative stress that potentially affect implantation rates were recorded.  After twelve weeks, women who took vitamin E had increased endometrial thickness, which is generally beneficial and increases the probability of a successful embryo implantation. In addition, oxidative stress that is linked to lower uterine receptivity was decreased.  Specifically, interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-α) were decreased in the women taking vitamin E, suggesting that the supplement may quell some of the inflammation that affects implantation rates in women.
          (Journal of Maternal and Fetal Neonatal Medicine, September 2017)
LINK to ABSTRACT The effects of vitamin E supplementation on endometrial thickness, and gene expression of vascular endothelial growth factor and inflammatory cytokines among women with implantation failure.



CLINICAL UPDATE – Biotin may help optimize carbohydrate metabolism
Biotin (also known as vitamin B7) serves as a key cofactor in many metabolic pathways, particularly in energy metabolism and glycemic control.  Past research indicates that high doses of biotin may benefit glucose metabolism but it is unknown how biotin affects the hormone glucagon, which is produced in the pancreas.  Glucagon has the opposite action of insulin – it is secreted by the pancreas when blood glucose levels dip too low in order to raise glucose levels in the bloodstream.  It does this by telling the liver to covert the stored form of glucose (known as glycogen) into glucose in the bloodstream for use throughout the body.
           In this animal study, male mice were fed one of two diets – a control diet or a biotin-supplemented diet.  Three facets of glucagon function were evaluated: (1) expression of genes that up-regulate glucagon synthesis, (2) glucagon secretion by the pancreas into the bloodstream and (3) glucagon action.  After eight weeks, the mice that were fed supplemental biotin increased glucagon production and secretion compared to the control group.  However, the action of glucagon did not increase – only the amount produced and secreted.  In other words, fasting blood sugar and levels of an enzyme that prevents dramatic blood sugar dips (called PcK1 for phosphoenolpyruvate carboxykinase) did not change, even though the hormone (glucagon) that regulates them did change.  This research suggests that biotin may help optimize glycemic control, albeit via indirect mechanisms.
          (Nutrition, November 2017)
          LINK to ABSTRACT
Effects of dietary biotin supplementation on glucagon production, secretion, and action.



CLINICAL UPDATE – Increasing vitamin B5 intake may lower chronic inflammation
908 healthy men and women living in rural South Korea that were over 40 years old were assessed for vitamin B5 intake (also called pantothenic acid) and  CRP (c-reactive protein) which is a well established biomarker for chronic inflammation.  Vitamin B5 plays a key role in energy metabolism, buffers the negative effects of stress on cellular health, and is needed for the manufacture of many important cellular enzymes which led this team to investigate its correlation to inflammation.  They measured CRP three times – at baseline then after two additional visits to the community.  At the same time, they assessed dietary intake of vitamin B5 and found that over the long-term, higher intake of vitamin B5 was linked to a lower CRP value, suggesting B5 may help lower chronic inflammation over time.
          (Nutrition, Metabolism and Cardiovascular Disease, September 2017)
LINK to ABSTRACT The long-term relationship between dietary pantothenic acid (vitamin B5) intake and C-reactive protein concentration in adults aged 40 years and older.




CLINICAL UPDATE – Berberi outbreak occurs in South America
An outbreak of beriberi, which is a disease caused by severe vitamin B1 deficiency, occurred in 2014 in the small South American country of French Guiana that borders Brazil and the Atlantic Ocean.  A group of gold miners working in the tropical forest went to a local health center for severe swelling and signs of heart failure.  42 cases of beriberi were diagnosed in the workers, of which one was fatal. 
          Lab results showed that most of the men were severely deficient in vitamin B1 to the point that heart failure had begun to set in.  Seventy percent of the men (30) responded favorably when given vitamin B1 (thiamin) either intravenously or intramuscularly at a single high dose (500 mg).  According to the authors, the cause of the vitamin B1 deficiency was due to several confounding factors  including insufficient intake and possibly malaria. In 2016, beriberi cases were still being reported in the region.  Since the treatment of vitamin B1 was both effective and relatively inexpensive, they suggested more screening for B1 deficiency related symptoms in these workers.
          (The American Journal of Tropical Medicine and Hygiene,  Ma, 2017)
LINK to ABSTRACT A Large Outbreak of Thiamine Deficiency Among Illegal Gold Miners in French Guiana.