N
Nick
Guest
That study Larry Hoover posted is actually quite interesting (go to
http://stroke.ahajournals.org/cgi/content/full/33/8/2086?ijkey=e89900b331f3a
e87567a16d6f2a7906f6f43eeda). When you think about it in the context of other studies, and of
course, in the context of the physiology of fatty acid metabolism, it makes sense. The people who
were more likely to have a stroke had lower serum levels of linoleic acid (omega 6 PUFA). The most
likely explanation is that they had a chronic, possibly systemic inflammatory condition. In fact, a
couple of days ago the local paper reported how "experts" now see lupus as a chronic inflammatory
disorder which shares this quality with heart disease, cancer, etc. (though it's well know to those
of us who have been reading studies). In that condition, linoleic gets metabolized to arachidonic
acid, which is the "fuel" for chronic inflammation. Here's a study that is consistent with this
situation, but there are plenty more. And the point I make in many of my posts is that if you eat
almost no omega 6 PUFAs, you rid your body of arachidonic acid, and hence, there will be very little
chance of developing a "chronic disease."
Prostaglandins Leukot Essent Fatty Acids. 2000 Nov;63(5):255-62. Keloids in rural black South
Africans. Part 3: a lipid model for the prevention and treatment of keloid formations.
Louw L.
Department of Anatomy and Cell Morphology, University of the Orange Free State, Bloemfontein,
South Africa.
In the third part of this study a basic lipid model (regarding phospholipids, triglycerides,
cholesterol esters and free fatty acids) for keloids (n=20), compared with normal skin of keloid
prone and non-keloid prone patients (n=20 of each), was constructed according to standard methods,
to serve as a sound foundation for essential fatty acid supplementation strategies in the prevention
and treatment of keloid formations. Essential fatty acid deficiency (EFAD) of the omega-6 series
(linoleic acid (LA), g-linolenic acid (GLA), and dihomo-g-linolenic acid (DGLA)) and the omega-3
series (a-linolenic acid (ALA) and eicosapentaenoic acid (EPA)), but enhanced arachidonic acid (AA)
levels, were prevalent in keloid formations. Enhanced AA, but a deficiency of AA precursors (LA, GLA
and DGLA) and inflammatory competitors (DGLA and EPA), are inevitably responsible for the
overproduction of pro-inflammatory metabolites (prostaglandin E(2)(PGE(2))) participating in the
pathogenesis of inflammation. Of particular interest was the extremely high free oleic acid (OA)
levels present, apart from the high free AA levels, in the keloid formations. OA stimulates PKC
activity which, in turn, activates PLA(2)activity for the release or further release of AA from
membrane pools. Interactions between EFAs, eicosanoids, cytokines, growth factors and free radicals
can modulate the immune response and the immune system in undoubtedly involved in keloid formation.
The histopathology of keloids can be adequately explained by: persistence of inflammatory- and cytokine-
mediated reactions in the keloid/dermal interface and peripheral areas, where fibroblast
proliferation and continuous depletion of membrane linoleic acid occur; microvascular regeneration
and circulation of sufficient EFAs in the interface and peripheral areas, where maintenance of
metabolic active fibroblasts for collagen production occur; microvessel occlusion and hypoxia in the
central areas, where deprivation of EFAs and oxygen with consequent fibroblast apoptosis occur,
while excessive collagen remain. All these factors contribute to different fibroblast populations
present in: the keloid / dermal interface and peripheral areas where increases in fibroblast
proliferation and endogenous TGF-b occur, and these metabolic active fibroblast populations are
responsible for enhanced collagen production: the central areas where fibroblast populations under
hypoxic conditions occur, and these fibroblasts are responsible for excessive collagen production.
It was concluded that: fibroblast membrane EFAD of AA precursors and inflammatory competitors, but
prevailing enhanced AA levels, can contribute to a chain of reactions eventually responsible for
keloid formations. Copyright 2000 Harcourt Publishers Ltd.
PMID: 11090251 [PubMed - indexed for MEDLINE]
http://stroke.ahajournals.org/cgi/content/full/33/8/2086?ijkey=e89900b331f3a
e87567a16d6f2a7906f6f43eeda). When you think about it in the context of other studies, and of
course, in the context of the physiology of fatty acid metabolism, it makes sense. The people who
were more likely to have a stroke had lower serum levels of linoleic acid (omega 6 PUFA). The most
likely explanation is that they had a chronic, possibly systemic inflammatory condition. In fact, a
couple of days ago the local paper reported how "experts" now see lupus as a chronic inflammatory
disorder which shares this quality with heart disease, cancer, etc. (though it's well know to those
of us who have been reading studies). In that condition, linoleic gets metabolized to arachidonic
acid, which is the "fuel" for chronic inflammation. Here's a study that is consistent with this
situation, but there are plenty more. And the point I make in many of my posts is that if you eat
almost no omega 6 PUFAs, you rid your body of arachidonic acid, and hence, there will be very little
chance of developing a "chronic disease."
Prostaglandins Leukot Essent Fatty Acids. 2000 Nov;63(5):255-62. Keloids in rural black South
Africans. Part 3: a lipid model for the prevention and treatment of keloid formations.
Louw L.
Department of Anatomy and Cell Morphology, University of the Orange Free State, Bloemfontein,
South Africa.
In the third part of this study a basic lipid model (regarding phospholipids, triglycerides,
cholesterol esters and free fatty acids) for keloids (n=20), compared with normal skin of keloid
prone and non-keloid prone patients (n=20 of each), was constructed according to standard methods,
to serve as a sound foundation for essential fatty acid supplementation strategies in the prevention
and treatment of keloid formations. Essential fatty acid deficiency (EFAD) of the omega-6 series
(linoleic acid (LA), g-linolenic acid (GLA), and dihomo-g-linolenic acid (DGLA)) and the omega-3
series (a-linolenic acid (ALA) and eicosapentaenoic acid (EPA)), but enhanced arachidonic acid (AA)
levels, were prevalent in keloid formations. Enhanced AA, but a deficiency of AA precursors (LA, GLA
and DGLA) and inflammatory competitors (DGLA and EPA), are inevitably responsible for the
overproduction of pro-inflammatory metabolites (prostaglandin E(2)(PGE(2))) participating in the
pathogenesis of inflammation. Of particular interest was the extremely high free oleic acid (OA)
levels present, apart from the high free AA levels, in the keloid formations. OA stimulates PKC
activity which, in turn, activates PLA(2)activity for the release or further release of AA from
membrane pools. Interactions between EFAs, eicosanoids, cytokines, growth factors and free radicals
can modulate the immune response and the immune system in undoubtedly involved in keloid formation.
The histopathology of keloids can be adequately explained by: persistence of inflammatory- and cytokine-
mediated reactions in the keloid/dermal interface and peripheral areas, where fibroblast
proliferation and continuous depletion of membrane linoleic acid occur; microvascular regeneration
and circulation of sufficient EFAs in the interface and peripheral areas, where maintenance of
metabolic active fibroblasts for collagen production occur; microvessel occlusion and hypoxia in the
central areas, where deprivation of EFAs and oxygen with consequent fibroblast apoptosis occur,
while excessive collagen remain. All these factors contribute to different fibroblast populations
present in: the keloid / dermal interface and peripheral areas where increases in fibroblast
proliferation and endogenous TGF-b occur, and these metabolic active fibroblast populations are
responsible for enhanced collagen production: the central areas where fibroblast populations under
hypoxic conditions occur, and these fibroblasts are responsible for excessive collagen production.
It was concluded that: fibroblast membrane EFAD of AA precursors and inflammatory competitors, but
prevailing enhanced AA levels, can contribute to a chain of reactions eventually responsible for
keloid formations. Copyright 2000 Harcourt Publishers Ltd.
PMID: 11090251 [PubMed - indexed for MEDLINE]