May 2017 – Vol. 11, Issue 5

Micronutrient of the Month:  VITAMIN A

In This Issue…
                                                                           

  • Vitamin A deficiency in utero may increase risk of Alzheimer’s later in life
  • Lack of vitamin A may play a major role in developing diabetes
  • Conventional methods for assessing vitamin A status may be misleading
  • For eye problems, vitamin A solves more than just night blindness
  • Deficiency in vitamin A increases risk of tuberculosis 10-fold when exposed
  • New research demonstrates the role of vitamin A in gut flora

 

CLINICAL UPDATE – Vitamin A deficiency in utero may increase risk of Alzheimer’s later in life
          In this interesting animal study, female rats with marginal vitamin A deficiency – defined as less severe than clinical deficiency – gave birth to babies who were then subjected to a controlled diet that was marginally deficient in vitamin A. After weaning, a type of protein known to cause Alzheimer’s (called amyloid β) was injected into the rats’ brains.  The animals with vitamin A deficiency had more learning and memory problems than those who were not deficient.  Further, the authors found that vitamin A deficiency caused a change in the expression of certain genes linked to the vitamin A receptor.
          This suggests that vitamin A deficiency during embryonic development has major long-term implications.  Deficiency of this important vitamin can alter genetic expression and, according to the authors, enhance the risk of developing Alzheimer’s disease later in life.  This research supports the practice of correcting vitamin deficiencies before pregnancy, as the result can affect both mother and baby.   
          (Current Alzheimer’s Report, April 2017)
          LINK to ABSTRACT
Marginal Vitamin A Deficiency Exacerbates Memory Deficits Following Aβ1-42 Injection in Rats.  LINK to FREE FULL TEXT

 

CLINICAL UPDATE – Lack of vitamin A may play a major role in developing diabetes
          Diabetes – both type 1 and 2 – is characterized by an inability to appropriately respond to glucose in the bloodstream, notably from an impaired insulin response.  One factor that causes dysfunctional insulin response is defective pancreatic beta cells, also termed loss of beta cell function.  In this research, when vitamin A receptors were inactivated, the pancreatic beta cells ceased working properly.
          The authors explain the mechanism behind this clinical effect: pancreatic cells have high levels of a special protein called G-protein coupled receptor C5C, or GPRC5C, which happens to bind with vitamin A, which makes it appropriately called a vitamin A receptor protein.  Vitamin A allows GPRC5C to be expressed, and although its exact function is not totally understood, its high levels in pancreatic tissue suggest a link to insulin response. In fact, blocking this protein, which might occur due to vitamin A deficiency, reduces the amount of insulin secreted. 
          The paper states that vitamin A improves pancreatic β-cell function and may even prevent the progression of pre-diabetes to full-blown type 2 diabetes.   
          (Endocrinology Journal, March 2017)
          LINK to ABSTRACT
Anti-diabetic action of all-trans retinoic acid and the orphan G protein coupled receptor GPRC5C in pancreatic β-cells. LINK to FREE FULL TEXT

 

 

CLINICAL UPDATE – Conventional methods for assessing vitamin A status may be misleading
          The conventional way to measure vitamin A deficiency is often by assessing retinol-binding protein levels in the blood of a person.  However, some scientists consider this an indirect measure of vitamin A since retinol-binding protein is really a carrier protein – in other words, it binds to vitamin A in order to transport it to various tissues.  Complications in determining vitamin A status arise because during an acute-phase inflammatory response, retinol-binding protein will decrease in the blood.  A study on 8803 children confirmed this conclusion – when inflammation is present, concentrations of RBP do not necessarily reflect vitamin A status.
          (American Journal of Clinical Nutrition, June 2017)
          LINK to ABSTRACT
Adjusting retinol-binding protein concentrations for inflammation: Biomarkers Reflecting Inflammation and Nutritional Determinants of Anemia (BRINDA) project.

 

 

CLINICAL UPDATE – For eye problems, vitamin A solves more than just night blindness
          Lack of vitamin A is a well-documented cause of night blindness.  This is because vitamin A combines with a protein (rhodopsin) to create the light absorbing cells in the eye.  However, a recently published case report on a 47 year old woman with a progressive loss of vision demonstrates that vitamin A deficiency may directly cause other eye problems.  The patient suffered from extreme dry eye, the inability to produce tears, and “spots” on the cornea caused by keratin deposits, likely due to vitamin A’s role in regulating growth of epithelial tissue.  The authors attributed the vision problems to vitamin A deficiency.
          In a different case report, a 69 year old woman presented with dry eye and vision loss.  As she had a bowel resection surgery that likely impaired her ability to absorb nutrients, it was concluded that her vision problems were likely due to vitamin A deficiency.  She was given sublingual vitamin A (sublingual because intestinal malabsorption was an issue) and after 5 months, her peripheral vision and ability to see in low light not only improved, but actually normalized.  These cases highlight the impact a systemic vitamin A deficiency has on a variety of vision problems.
          (British Medical Journal Case Reports, May 2017)
          LINK to ABSTRACT
Vitamin A deficiency due to chronic malabsorption: an ophthalmic manifestation of a systemic condition. 
          (Advances in Ophthamology,  April 2016)
          LINK to ABSTRACT
Treatment of vitamin A deficiency retinopathy with sublingual vitamin A palmitate.

 

 

CLINICAL UPDATE – Deficiency in vitamin A increases risk of tuberculosis 10-fold when exposed
          A case-control study was conducted in Lima, Peru where tuberculosis rates are relatively high, in which 6751 people who lived in a household of someone who had contracted tuberculosis were monitored for rates of infection.  180 cases of tuberculosis occurred and it was found that vitamin A deficiency was associated with a 10-fold increase in risk of contracting tuberculosis when living with a relative who already had it.   In addition, the risk was dose-dependent meaning that the more severe the deficiency, the more severe the risk of getting tuberculosis.
          (Clinical Infectious Diseases, May 2017)
          LINK to ABSTRACT
Impact of Vitamin A and Carotenoids on the Risk of Tuberculosis Progression.

 

 

CLINICAL UPDATE – New research demonstrates the role of vitamin A in gut flora
         
Several bacteria known to exist in the human gastrointestinal tract were cultured and then introduced into gnotobiotic mice, which are mice where only certain strains of bacteria are present – essentially a sterile biologic canvas for the purpose of measuring which bacteria flourish.  After specific bacteria were introduced in the animals’ gut, they were fed a very controlled diet that was deficient in key nutrients: vitamin A, folate, iron and zinc.  Acute vitamin A deficiency had the largest effect on the bacteria community with certain species flourishing wildly in the absence of vitamin A.  Further experiments demonstrated that this effect was likely mediated by altered gene expression in the deficient animals, suggesting vitamin A deficiency plays a larger role in the human microbiome than previously thought.
          (Science Translational Medicine, May 2017)
          LINK to ABSTRACT
The effects of micronutrient deficiencies on bacterial species from the human gut microbiota.