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Zinc Deficiency & Essential Fatty Acids

Friday, August 04, 2017


Zinc deficiency was first described in humans in the early 1960s in people consuming plant-based diets. Since then, tremendous advances have been made both in our basic and clinical understand of zinc metabolism, and we now understand that zinc is used in ​more than 300 enzymatic reactions and multiple biochemical structural processes in the body.


White spots under nails like  you see above can be a symptom of zinc deficiency.

  

The World Health Organization now suggests that more sensitive and specific biological markers of zinc status are needed. A review just published in the peer-reviewed journal Nutrients titled "The linoleic acid: dihomo-y-linolenic acid ratio (LA:DGLA)—an emerging biomarker of zinc status" provides evidence to demonstrate that the LA:DGLA ratio may be a useful additional indicator for assessing zinc status more precisely.


Science now proves that dietary deficiency of zinc in humans is a widespread phenomenon suggested to affect 17 percent of the world’s population.


Delta 6 Desaturase: structure, regulation, and function


Delta 6 desaturase is a membrane-bound desaturase enzyme required for the synthesis of polyunsaturated fatty acids (PUFA). The enzyme is molecularly identical across all living organisms. It’s widely expressed in human tissues in the liver, the membrane of red blood cells, lungs, and heart, with the highest levels being present in the brain.


Linoleic acid (LA) is an essential omega 6 fatty acid that cannot be synthetized in the human body and must be obtained from the diet to ensure the appropriate development of various cells throughout the body. 


​LA is the most abundant PUFA in human tissues. It’s a metabolic precursor of dihomo-y-linolenic acid (DGLA), which converts to the anti-inflammatory, gamma-linolenic acid (GLA).

  

Over the years, it has been noted that zinc is an important co-factor for the metabolism of fatty acids, particularly in the conversion of LA to DGLA to GLA to arachidonic acid (AA), which should be abundant in the brain, muscles, and liver. 


AA is also required for cellular signaling, particularly signaling enzymes involved in life-saving inflammatory responses, including vasodialation and brain function.


Zinc deficiency and the metabolism of linoleic acid via desaturase enzymes partial summary:


  • Zinc deficiency decreases the mobilization of DGLA from tissue stores.
  • Zinc is needed in the formation of GLA.
  • EFA supplementation worsens the effect of zinc deficiency.
  • Zinc deficiency decreases the esterification of essential fatty acids into phospholipids.
  • During zinc deficiency, linoleic acid accumulates in tissues when EFA supplements are administered.
  • Zinc-deficient subjects have an increased beta-oxidation of linoleic acid, resulting in decreased amounts of linoleic acid available to be metabolized into arachidonic acid.
  • The most important EFA functions are carried out by molecules downstream of GLA.
  • The inhibition of the desaturases by zinc deficiency is so strong that it causes a more rapid decline in tissue arachidonic acid and docosahexaenoic acid than does the direct dietary deficiency of all the omega 6 or omega 3 polyunsaturated fatty acids.


Ellen Troyer with Spencer Thornton, MD, David Amess and the Biosyntrx staff



PEARL

Zinc has a direct role in the modulation of desaturase activities involved in fatty acid metabolism and absorption and oxidation, which suggests the ratio of LA:DGLA could be an important biomarker of zinc status in humans. Foods high in zinc include oysters, beef, lamb, wheat germ, spinach, pumpkin seeds, nuts, dark chocolate, pork, chicken, beans, and mushrooms. Again, we recommend consumption of a junk-food free, well-balanced diet to avoid the need for excessive fish oil supplementation to balance fatty acid intake, and to save our seas. 






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