Prostaglandins Leukot Essent Fatty Acids. 2000 Nov;63(5):237-45.

Keloids in rural black South Africans. Part 1: general overview and
essential fatty acid hypotheses forkeloidformation and prevention.

Louw L.
Department of Anatomy and Cell Morphology, University of the Orange
Free State, Bloemfontein, South Africa.

In the first part of this study a general overview on the hypertrophic
scar andkeloidphenomena regarding history, epidemiology,
histopathology and aetiology, in general, together with an essential
fatty acid approach as basis for hypotheses ofkeloidformation and
prevention are given. Upon reviewing the literature in planning a
strategy for prevention and treatment of keloids, one encounters an
overwhelming amount of hypotheses on this topic. Based on a
preliminary study on total fatty acid compositions in keloids,
compared with normal skin ofkeloidprone and non-keloidprone
patients, there can be argued as follows: an essential fatty acid
deficiency of precursors and inflammatory competitors for arachidonic
acid may be a factor in the multifactorial aetiology ofkeloid
formations, and apart from a local essential fatty acid deficiency in
the wound area, nutrition may also be a contributing factor in rural
black South Africans. To confirm or refute the stated hypotheses of
the role of essential fatty acids inkeloidformation and prevention
(outlined in this part of the study), dietary questionnaires and blood
(plasma and red blood cell) phospholipid analyses for general
information and true fatty acid intake and metabolism, respectively,
in the diets of these patients (outlined in part II of this study), as
well as a lipid model forkeloidformations regarding phospholipids,
triglycerides, cholesterol esters and free fatty acids (outlined in
part III of this study), are given. The purpose of this comprehensive
fatty acid study was an attempt to assess the enigma surrounding
keloids and to end the nightmare of the plastic and reconstructive
surgeon, since these dermal tumours are notoriously recurrent.
PMID: 11090249

Prostaglandins Leukot Essent Fatty Acids. 2000 Nov;63(5):247-53.

Keloids in rural black South Africans. Part 2: dietary fatty acid
intake and total phospholipid fatty acid profile in the blood ofkeloidpatients.

Louw L, Dannhauser A.
Department of Anatomy and Cell Morphology, University of the Orange
Free State, Bloemfontein, South Africa.

In the second part of this study, emphasis is placed on nutritional
intakes (fatty acids and micronutrients) and fatty acid intake and
metabolism in the blood, respectively, according to a combined 24 h
recall and standardized food frequency questionnaire analyses ofkeloidprone patients (n=10), compared with normal black South
Africans (n=80), and total phospholipid blood (plasma and red blood
cell ) analyses ofkeloidpatients (n=20), compared with normal
individuals (n=20). Lipid extraction and fractionation by standard
procedures, total phospholipid (TPL) separation with thin layer
chromatography, and fatty acid methyl ester analyses with gas liquid
chromatography techniques were used. Since nutrition may play a role
in several disease disorders, the purpose of this study was to confirm
or refute a role for essential fatty acids (EFAs) in the hypothesis ofkeloidformations stated in part 1 of this study. (1)According to the
Canadian recommendation (1991), we observed that inkeloidpatients
linoleic acid (LA) and arachidonic acid (AA) dietary intakes, as EFAs
of the omega-6-series, are higher than the recommended 7-11 g/d.
However, the a-linolenic acid (ALA), eicosapentaenoic acid (EPA) and
docosahexaenoic acid (DHA) dietary intakes, as EFAs of the omega-3
series, are lower than the recommendation of 1.1-1.5 g/d. This was
also the case in the control group, where a higher dietary intake of
the omega-6 fatty acids and a slightly lower dietary intake of the
omega-3 fatty acids occurred. Thus, we confirm a high dietary intake
of LA (as a product of organ meats, diary products and many vegetable
oils) and AA (as a product of meats and egg yolks), as well as lower
dietary intakes of ALA (as a product of grains, green leafy
vegetables, soy oil, rapeseed oil and linseed), and EPA and DHA (as
products of marine oils). Lower micronutrient intakes than the
recommended dietary allowances were observed in thekeloidgroup that
may influence EFA metabolism and/or collagen synthesis. Of cardinal
importance may be the lower intake of calcium in thekeloidpatients
that may contribute to abnormal cell signal transduction in
fibroblasts and consequent collagen overproduction, and the lower
copper intake that may influence the immune system, or perhaps even
the high magnesium intake that stimulates metabolic activity.
Micronutrient deficiencies also occurred in the diets of the normal
black South Africans that served as a control group. In the case of
plasma TPLs, deficiency of the omega-3 EFA series (ALA, EPA and DHA)
occurred, and this is in accordance with the apparent lower omega-3
EFA intake in the diets of these patients. In the case of the red
blood cell TPLs, as a true and reliable source of dietary fatty acid
intake and metabolism, sufficient EFAs of the omega-6 series (LA and
AA) and the omega-3 series (ALA, EPA and DHA) occurred. For this study
group a relative deficiency of nutritional omega-3 EFA intake
apparently did occur, but was probably compensated for by blood fatty
acid metabolism.
PMID: 11090250

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 ofkeloidformations.

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 ofkeloidprone and non-keloidprone 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 ofkeloidformations. 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 inkeloidformations. 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 thekeloidformations.
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 inkeloidformation. The histopathology of
keloids can be adequately explained by: persistence of inflammatory-
and cytokine-mediated reactions in thekeloid/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: thekeloid/ 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 forkeloidformations.
PMID: 11090251

Prostaglandins Leukot Essent Fatty Acids. 2000 Nov;63(5):237-45.

Keloids in rural black South Africans. Part 1: general overview and
essential fatty acid hypotheses for keloid formation and prevention.

Louw L.
Department of Anatomy and Cell Morphology, University of the Orange
Free State, Bloemfontein, South Africa.

In the first part of this study a general overview on the hypertrophic
scar and keloid phenomena regarding history, epidemiology,
histopathology and aetiology, in general, together with an essential
fatty acid approach as basis for hypotheses of keloid formation and
prevention are given. Upon reviewing the literature in planning a
strategy for prevention and treatment of keloids, one encounters an
overwhelming amount of hypotheses on this topic. Based on a
preliminary study on total fatty acid compositions in keloids,
compared with normal skin of keloid prone and non-keloid prone
patients, there can be argued as follows: an essential fatty acid
deficiency of precursors and inflammatory competitors for arachidonic
acid may be a factor in the multifactorial aetiology of keloid
formations, and apart from a local essential fatty acid deficiency in
the wound area, nutrition may also be a contributing factor in rural
black South Africans. To confirm or refute the stated hypotheses of
the role of essential fatty acids in keloid formation and prevention
(outlined in this part of the study), dietary questionnaires and blood
(plasma and red blood cell) phospholipid analyses for general
information and true fatty acid intake and metabolism, respectively,
in the diets of these patients (outlined in part II of this study), as
well as a lipid model for keloid formations regarding phospholipids,
triglycerides, cholesterol esters and free fatty acids (outlined in
part III of this study), are given. The purpose of this comprehensive
fatty acid study was an attempt to assess the enigma surrounding
keloids and to end the nightmare of the plastic and reconstructive
surgeon, since these dermal tumours are notoriously recurrent.
PMID: 11090249


Prostaglandins Leukot Essent Fatty Acids. 2000 Nov;63(5):247-53.

Keloids in rural black South Africans. Part 2: dietary fatty acid
intake and total phospholipid fatty acid profile in the blood of
keloid patients.

Louw L, Dannhauser A.
Department of Anatomy and Cell Morphology, University of the Orange
Free State, Bloemfontein, South Africa.

In the second part of this study, emphasis is placed on nutritional
intakes (fatty acids and micronutrients) and fatty acid intake and
metabolism in the blood, respectively, according to a combined 24 h
recall and standardized food frequency questionnaire analyses of
keloid prone patients (n=10), compared with normal black South
Africans (n=80), and total phospholipid blood (plasma and red blood
cell ) analyses of keloid patients (n=20), compared with normal
individuals (n=20). Lipid extraction and fractionation by standard
procedures, total phospholipid (TPL) separation with thin layer
chromatography, and fatty acid methyl ester analyses with gas liquid
chromatography techniques were used. Since nutrition may play a role
in several disease disorders, the purpose of this study was to confirm
or refute a role for essential fatty acids (EFAs) in the hypothesis of
keloid formations stated in part 1 of this study. (1)According to the
Canadian recommendation (1991), we observed that in keloid patients
linoleic acid (LA) and arachidonic acid (AA) dietary intakes, as EFAs
of the omega-6-series, are higher than the recommended 7-11 g/d.
However, the a-linolenic acid (ALA), eicosapentaenoic acid (EPA) and
docosahexaenoic acid (DHA) dietary intakes, as EFAs of the omega-3
series, are lower than the recommendation of 1.1-1.5 g/d. This was
also the case in the control group, where a higher dietary intake of
the omega-6 fatty acids and a slightly lower dietary intake of the
omega-3 fatty acids occurred. Thus, we confirm a high dietary intake
of LA (as a product of organ meats, diary products and many vegetable
oils) and AA (as a product of meats and egg yolks), as well as lower
dietary intakes of ALA (as a product of grains, green leafy
vegetables, soy oil, rapeseed oil and linseed), and EPA and DHA (as
products of marine oils). Lower micronutrient intakes than the
recommended dietary allowances were observed in the keloid group that
may influence EFA metabolism and/or collagen synthesis. Of cardinal
importance may be the lower intake of calcium in the keloid patients
that may contribute to abnormal cell signal transduction in
fibroblasts and consequent collagen overproduction, and the lower
copper intake that may influence the immune system, or perhaps even
the high magnesium intake that stimulates metabolic activity.
Micronutrient deficiencies also occurred in the diets of the normal
black South Africans that served as a control group. In the case of
plasma TPLs, deficiency of the omega-3 EFA series (ALA, EPA and DHA)
occurred, and this is in accordance with the apparent lower omega-3
EFA intake in the diets of these patients. In the case of the red
blood cell TPLs, as a true and reliable source of dietary fatty acid
intake and metabolism, sufficient EFAs of the omega-6 series (LA and
AA) and the omega-3 series (ALA, EPA and DHA) occurred. For this study
group a relative deficiency of nutritional omega-3 EFA intake
apparently did occur, but was probably compensated for by blood fatty
acid metabolism.
PMID: 11090250


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.
PMID: 11090251

Another thought. There was a report on TV recently about a man who'd
lost a significant amount of the distal portion of one of his fingers in
an accident. By grafting on some sort of artificially-formed connective
tissue, his medical team encouraged the finger to regrow perfectly.
Considering the complexity of fingertips, I found this very impressive.

I happen to have cut off a much smaller portion of my right index
finger. (A young doctor at the emergency room cut off even more of it.)

But even though I was a fast healer, it never grew back perfectly.
That's why I was impressed by the pixie dust story, and I still am. I
have a lot of respect for cosmetic surgery. It's come a long, long way.

On May 20, 9:28 pm, Marshall Price <d0213... at (no spam) yahoo.com> wrote:
I remember reading a disappointing passage in my pathology textbook,
where I discovered that contrary to my intuition, there is no "ideal
pattern" that an organism constantly strives to complete. Instead,
healing consists of many mechanisms for dealing with specific problems
which have evolved over time to promote survival. If a broken bone is
improperly aligned, the organism will adapt in multifarious ways to cope
with the new shape, but the fracture itself won't gradually straighten
out. The forces on it will always be different from those on a newly
developing bone.

That's why it is better doing it the Salamander way - cut the whole
injured part off and regrow it from beginning according to the
embryonic developmental plan The lifeextensionists are working
hard on this ... Also the reconstructive surgeries would be more
successful if the scar tissue formation can be somehow inhibited.

Taka