Psoriasis: Zinc Deficiency May Be an Omega 6 Deficiency
A deficiency of any essential nutrient may be the cause of every disease possible including psoriasis.
The problem is that people get often so hooked up with some idea that they stop thinking about the deficiencies logically.
A lot of “health gurus” are OK with fooling you and selling you the supplements over and over even though you did not improve even after months on them.
But the similar scenario as I describe in this article is very possible in case of any nutrient including magnesium, calcium, iodine, B-vitamins and so on.
So even though I am striving on importance of B-vitamins for reversal of psoriasis keep in mind that low bile flow impairs the fat digestion dramatically so you may be very well deficient not just in omega 3 but even in omega 6 fatty acids.
I would say mostly omega 6 fatty acids since many psoriatics avoid them intentionally in order to decrease the production of inflammatory molecules which may not be the best idea. Not all omega 6 fatty acids are alike.
Zinc deficiency vs. Omega 6 deficiency
The Zinc deficiency and Fatty Acids deficiency both share these symptoms:
- dry skin, scaling, bumps
- weak nails
- visual symptoms (blurring, daylight/bright light sensitivity)
- excessive hunger
- weight loss
- impaired immune system (immunodeficiency, allergies) – inflammation
- mental disorders
The first study – “Most biological effects of zinc deficiency corrected by γ-linolenic acid (18: 3ω6) but not by linoleic acid (18: 2ω6)” – I am going to refer to in this article was published in 1982, but many of you probably never though or heard about something like this up to this day.
Just read the next abstract of the study “Most biological effects of zinc deficiency corrected by γ-linolenic acid (18: 3ω6) but not by linoleic acid (18: 2ω6)”.
Zinc deficiency mimics many of the clinical features of essential fatty acid (EFA) deficiency in rats. Since zinc appears to be needed for the Δ-6-desaturase step in EFA metabolism, experiments were conducted to determine whether bypassing this step with γ-linolenic acid (18 : 3ω6) would alleviate the biological effects induced by a zinc-deficient diet. In pair-fed rats over a period of 5 weeks the deficient diet impaired growth and changed the relative weights of internal organs. It also induced hypolipidemia but had little effect on the fatty acid composition of tissue lipids.
Daily subcutaneous injection of primrose oil containing 10% 18: 3ω6 reversed most of the effects of zinc deficiency on tissue weights, growth and plasma lipids. In contrast, injection of safflower oil, which has a similar content of linoleic acid (18 : 2ω6) but is devoid of 18 : 3ω6, had only a partial effect on some tissue weight changes. Neither oil affected the plasma fatty acid pattern, but both of them increased liver triglyceride concentrations. They also elevated the proportion of 18 : 2ω6 in liver, skin and epididymal fat. The latter effects were not observed in the absence of zinc deficiency.