Re: Essential Fatty Acid Metabolism

From: MikeV (mvidler_at_NOSPAMiname.com)
Date: 11/27/04 

Date: Sat, 27 Nov 2004 19:33:35 GMT

"montygram" <nazztrader@lycos.com> wrote in message
news:d60d7a6e.0411262235.6de59547@posting.google.com...

> who in the world decided that these extremely dangerous
> substances are "essential?" >

> "MikeV" <mvidler@NOSPAMiname.com> wrote in message
> news:<cAMpd.4716$Ua.3264@newsread3.news.atl.earthlink.net>...
>> Another in depth review for anyone interested. (44 pages; 300+
>> refs)
>>
>> http://www.ub.rug.nl/eldoc/dis/medicine/e.n.smit/c1.pdf
>>
>> MikeV
Look it up. There are plenty of references out there.
People like: AA Spector, and LS Harbige, I imagine:

      1: Lipids. 1999;34 Suppl:S1-3. Related Articles, Links

Essentiality of fatty acids.

Spector AA.

Department of Biochemistry, College of Medicine, University of Iowa,
Iowa City 52242, USA. arthur-spector@uiowa.edu

All fatty acids have important functions, but the term "essential"
is applied only to those polyunsaturated fatty acids (PUFA) that are
necessary for good health and cannot be completely synthesized in
the body. The need for arachidonic acid, which is utilized for
eicosanoid synthesis and is a constituent of membrane phospholipids
involved in signal transduction, is the main reason why the n-6
class of PUFA are essential. Physiological data indicate that n-3
PUFA also are essential. Although eicosapentaenoic acid also is a
substrate for eicosanoid synthesis, docosahexaenoic acid (DHA) is
more likely to be the essential n-3 constituent because it is
necessary for optimal visual acuity and neural development. DHA is
present in large amounts in the ethanolamine and serine
phospholipids, suggesting that its function involves membrane
structure. Because the metabolism of n-6 PUFA is geared primarily to
produce arachidonic acid, only small amounts of 22-carbon n-6 PUFA
are ordinarily formed. Thus, the essentiality of n-3 PUFA may be due
to their ability to supply enough 22-carbon PUFA for optimal
membrane function rather than to a unique biochemical property of
DHA.

Publication Types:
  a.. Review
  b.. Review, Tutorial

MeSH Terms:
  a.. Animals
  b.. Dietary Fats
  c.. Fatty Acids, Essential/pharmacology
  d.. Fatty Acids, Essential/physiology*
  e.. Fatty Acids, Unsaturated/pharmacology
  f.. Fatty Acids, Unsaturated/physiology*
  g.. Human
  h.. Signal Transduction
  i.. Support, U.S. Gov't, P.H.S.

Substances:
  a.. Dietary Fats
  b.. Fatty Acids, Essential
  c.. Fatty Acids, Unsaturated

Grant Support:
  a.. CA 66081/CA/NCI
  b.. HL 49264/HL/NHLBI

PMID: 10419080 [PubMed - indexed for MEDLINE]

      Lipids. 2003 Apr;38(4):323-41. Related Articles, Links

Fatty acids, the immune response, and autoimmunity: a question of
n-6 essentiality and the balance between n-6 and n-3.

Harbige LS.

School of Chemical and Life Sciences, University of Greenwich at
Medway, Chatham Maritime, Kent ME4 4TB, United Kingdom.
L.Harbige@gre.ac.uk

The essentiality of n-6 polyunsaturated fatty acids (PUFA) is
described in relation to a thymus/thymocyte accretion of arachidonic
acid (20:4n-6, AA) in early development, and the high requirement of
lymphoid and other cells of the immune system for AA and linoleic
acid (1 8:2n-6, LA) for membrane phospholipids. Low n-6 PUFA intakes
enhance whereas high intakes decrease certain immune functions.
Evidence from in vitro and in vivo studies for a role of AA
metabolites in immune cell development and functions shows that they
can limit or regulate cellular immune reactions and can induce
deviation toward a T helper (Th)2-like immune response. In contrast
to the effects of the oxidative metabolites of AA, the longer-chain
n-6 PUFA produced by gamma-linolenic acid (18:3n-6, GLA) feeding
decreases the Th2 cytokine and immunoglobulin (Ig)G1 antibody
response. The n-6 PUFA, GLA, dihomo-gamma-linolenic acid (20:3n-6,
DHLA) and AA, and certain oxidative metabolites of AA can also
induce T-regulatory cell activity, e.g., transforming growth factor
(TGF)-beta-producing T cells; GLA feeding studies also demonstrate
reduced proinflammatory interleukin (IL)-1 and tumor necrosis factor
(TNF)-alpha production. Low intakes of long-chain n-3 fatty acids
(fish oils) enhance certain immune functions, whereas high intakes
are inhibitory on a wide range of functions, e.g., antigen
presentation, adhesion molecule expression, Th1 and Th2 responses,
proinflammatory cytokine and eicosanoid production, and they induce
lymphocyte apoptosis. Vitamin E has a demonstrable critical role in
long-chain n-3 PUFA interactions with immune functions, often
reversing the effects of fish oil. The effect of dietary fatty acids
on animal autoimmune disease models depends on both the autoimmune
model and the amount and type of fatty acids fed. Diets low in fat,
essential fatty acid deficient (EFAD), or high in long-chain n-3
PUFA from fish oils increase survival and reduce disease severity in
spontaneous autoantibody-mediated disease, whereas high-fat LA-rich
diets increase disease severity. In experimentally induced T
cell-mediated autoimmune disease, EFAD diets or diets supplemented
with long-chain n-3 PUFA augment disease, whereas n-6 PUFA prevent
or reduce the severity. In contrast, in both T cell- and
antibody-mediated autoimmune disease, the desaturated/elongated
metabolites of LA are protective. PUFA of both the n-6 and n-3
families are clinically useful in human autoimmune-inflammatory
disorders, but the precise mechanisms by which these fatty acids
exert their clinical effects are not well understood. Finally, the
view that all n-6 PUFA are proinflammatory requires revision, in
part, and their essential regulatory and developmental role in the
immune system warrants appreciation.

  a..

PMID: 12848277 [PubMed - indexed for MEDLINE]

MikeV

Relevant Pages

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