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Keloids - AA overload disease
Keloids - AA overload disease
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 ), compared with normal
individuals (n ). 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 ), compared with normal skin of keloid prone and non-
keloid prone patients (n 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
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 ), compared with normal
individuals (n ). 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 ), compared with normal skin of keloid prone and non-
keloid prone patients (n 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
Re: Keloids - AA overload disease
On May 8, 11:26 pm, Taka <taka0...@gmail . com > wrote: keloids <<
I think the latest is polycythemia and sun sensitivity issues ..
I just read it somewhere .. pretty new stuff ..
Who loves ya.
Tom
Jesus Was A Vegetarian!
* tinyurl . com /2r2nkh
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
> 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 ofkeloidpati=
ents.
>
> 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 ofkeloidpron=
e 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 ofkelo=
idformations 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-kelo=
idprone 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 ofkeloidfo=
rmations. 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/ derm=
al 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
On May 8, 11:26 pm, Taka <taka0...@gmail . com > wrote: keloids <<
I think the latest is polycythemia and sun sensitivity issues ..
I just read it somewhere .. pretty new stuff ..
Who loves ya.
Tom
Jesus Was A Vegetarian!
* tinyurl . com /2r2nkh
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
> 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 ofkeloidpati=
ents.
>
> 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 ofkeloidpron=
e 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 ofkelo=
idformations 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-kelo=
idprone 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 ofkeloidfo=
rmations. 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/ derm=
al 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
Re: Keloids - AA overload disease
Taka wrote:
> 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 ), compared with normal
> individuals (n ). 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 ), compared with normal skin of keloid prone and non-
> keloid prone patients (n 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
Incidentally, I saw a show on TV recently about Captain Cook's first
exploratory voyage (in 1768, searching for the hypothetical great
southern continent) in which it was stated that one of the signs of
scurvy is that "old wounds re-open." I can't help wondering whether
ascorbic acid might play an important role in the formation and
maintenance of scar tissue.
Assuming that the fatty acid connection (the "basic lipid model")
discussed in these articles is valid, I wonder whether ascorbyl
palmitate (which mixes with lipids) might help heal wounds with healthy
scars, and prevent keloid formation.
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.
It suggests that wound healing might be improved not only by fixing a
"raw" matrix of connective tissue in place, but also, perhaps, by
encouraging the formation of new connective tissue by nutritional
interventions.
--
Marshall Price of Miami
Known to Yahoo as d021317c
Taka wrote:
> 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 ), compared with normal
> individuals (n ). 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 ), compared with normal skin of keloid prone and non-
> keloid prone patients (n 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
Incidentally, I saw a show on TV recently about Captain Cook's first
exploratory voyage (in 1768, searching for the hypothetical great
southern continent) in which it was stated that one of the signs of
scurvy is that "old wounds re-open." I can't help wondering whether
ascorbic acid might play an important role in the formation and
maintenance of scar tissue.
Assuming that the fatty acid connection (the "basic lipid model")
discussed in these articles is valid, I wonder whether ascorbyl
palmitate (which mixes with lipids) might help heal wounds with healthy
scars, and prevent keloid formation.
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.
It suggests that wound healing might be improved not only by fixing a
"raw" matrix of connective tissue in place, but also, perhaps, by
encouraging the formation of new connective tissue by nutritional
interventions.
--
Marshall Price of Miami
Known to Yahoo as d021317c
Re: Keloids - AA overload disease
On May 18, 2:06 pm, Marshall Price <d0213...@yahoo . com > wrote:
> Taka wrote:
> > 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 ), compared with normal
> > individuals (n ). 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 ), compared with normal skin of keloid prone and non-
> > keloid prone patients (n 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
>
> Incidentally, I saw a show on TV recently about Captain Cook's first
> exploratory voyage (in 1768, searching for the hypothetical great
> southern continent) in which it was stated that one of the signs of
> scurvy is that "old wounds re-open." I can't help wondering whether
> ascorbic acid might play an important role in the formation and
> maintenance of scar tissue.
>
> Assuming that the fatty acid connection (the "basic lipid model")
> discussed in these articles is valid, I wonder whether ascorbyl
> palmitate (which mixes with lipids) might help heal wounds with healthy
> scars, and prevent keloid formation.
>
> 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.
>
> It suggests that wound healing might be improved not only by fixing a
> "raw" matrix of connective tissue in place, but also, perhaps, by
> encouraging the formation of new connective tissue by nutritional
> interventions.
>
> --
> Marshall Price of Miami
> Known to Yahoo as d021317c
What you need to regenerate tissue rather than scar it is
dedifferentiated fibroblasts with the local clues in which part of the
body they are. Scar formation is encouraged by oxygen and the
mediator here is likely AA. Also one organ which can completely
regenerate is the liver but when it is overloaded with AA it rather
forms scar tissue resulting in a disease. Immunity plays a major role
in regeneration versus scarring as demonstrated on the unusual
"autoimmune" MRL mouse strain ( * news.bbc.co.uk/2/hi/science/nature/4888080.stm
). I would love to see which lipids and eicosanoids this mouse versus
normal mouse use. I bet Mead acid is the major PUFA in the blastemas
such as in the growing deer antlers. Also look at what Monty has to
say about his wounds - perfect healing. Ray Peat also wrote an
interesting essay about regeneration:
* raypeat . com /articles/articles/adaptive-substance.shtml
Taka
On May 18, 2:06 pm, Marshall Price <d0213...@yahoo . com > wrote:
> Taka wrote:
> > 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 ), compared with normal
> > individuals (n ). 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 ), compared with normal skin of keloid prone and non-
> > keloid prone patients (n 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
>
> Incidentally, I saw a show on TV recently about Captain Cook's first
> exploratory voyage (in 1768, searching for the hypothetical great
> southern continent) in which it was stated that one of the signs of
> scurvy is that "old wounds re-open." I can't help wondering whether
> ascorbic acid might play an important role in the formation and
> maintenance of scar tissue.
>
> Assuming that the fatty acid connection (the "basic lipid model")
> discussed in these articles is valid, I wonder whether ascorbyl
> palmitate (which mixes with lipids) might help heal wounds with healthy
> scars, and prevent keloid formation.
>
> 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.
>
> It suggests that wound healing might be improved not only by fixing a
> "raw" matrix of connective tissue in place, but also, perhaps, by
> encouraging the formation of new connective tissue by nutritional
> interventions.
>
> --
> Marshall Price of Miami
> Known to Yahoo as d021317c
What you need to regenerate tissue rather than scar it is
dedifferentiated fibroblasts with the local clues in which part of the
body they are. Scar formation is encouraged by oxygen and the
mediator here is likely AA. Also one organ which can completely
regenerate is the liver but when it is overloaded with AA it rather
forms scar tissue resulting in a disease. Immunity plays a major role
in regeneration versus scarring as demonstrated on the unusual
"autoimmune" MRL mouse strain ( * news.bbc.co.uk/2/hi/science/nature/4888080.stm
). I would love to see which lipids and eicosanoids this mouse versus
normal mouse use. I bet Mead acid is the major PUFA in the blastemas
such as in the growing deer antlers. Also look at what Monty has to
say about his wounds - perfect healing. Ray Peat also wrote an
interesting essay about regeneration:
* raypeat . com /articles/articles/adaptive-substance.shtml
Taka
Re: Keloids - AA overload disease
Taka wrote:
> On May 18, 2:06 pm, Marshall Price <d0213...@yahoo . com > wrote:
>> Taka wrote:
>>> 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 ), compared with normal
>>> individuals (n ). 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 ), compared with normal skin of keloid prone and non-
>>> keloid prone patients (n 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
>> Incidentally, I saw a show on TV recently about Captain Cook's first
>> exploratory voyage (in 1768, searching for the hypothetical great
>> southern continent) in which it was stated that one of the signs of
>> scurvy is that "old wounds re-open." I can't help wondering whether
>> ascorbic acid might play an important role in the formation and
>> maintenance of scar tissue.
>>
>> Assuming that the fatty acid connection (the "basic lipid model")
>> discussed in these articles is valid, I wonder whether ascorbyl
>> palmitate (which mixes with lipids) might help heal wounds with healthy
>> scars, and prevent keloid formation.
>>
>> 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.
>>
>> It suggests that wound healing might be improved not only by fixing a
>> "raw" matrix of connective tissue in place, but also, perhaps, by
>> encouraging the formation of new connective tissue by nutritional
>> interventions.
>>
>> --
>> Marshall Price of Miami
>> Known to Yahoo as d021317c
>
> What you need to regenerate tissue rather than scar it is
> dedifferentiated fibroblasts with the local clues in which part of the
> body they are. Scar formation is encouraged by oxygen and the
> mediator here is likely AA. Also one organ which can completely
> regenerate is the liver but when it is overloaded with AA it rather
> forms scar tissue resulting in a disease. Immunity plays a major role
> in regeneration versus scarring as demonstrated on the unusual
> "autoimmune" MRL mouse strain ( * news.bbc.co.uk/2/hi/science/nature/4888080.stm
> ). I would love to see which lipids and eicosanoids this mouse versus
> normal mouse use. I bet Mead acid is the major PUFA in the blastemas
> such as in the growing deer antlers. Also look at what Monty has to
> say about his wounds - perfect healing. Ray Peat also wrote an
> interesting essay about regeneration:
> * raypeat . com /articles/articles/adaptive-substance.shtml
That's "an interesting essay about regeneration"? Whatever it is,
it's too long and kooky for me. I read about a quarter of it before I
realized I had no idea what he was going on about.
I liked the mouse article, though.
About livers, it isn't true that they can completely regenerate
themselves. Once a lobe is gone, the other two can grow bigger, but
that lobe will never grow back, and if all three are sick enough, the
whole organ is lost.
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.
--
Marshall Price of Miami
Known to Yahoo as d021317c
Taka wrote:
> On May 18, 2:06 pm, Marshall Price <d0213...@yahoo . com > wrote:
>> Taka wrote:
>>> 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 ), compared with normal
>>> individuals (n ). 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 ), compared with normal skin of keloid prone and non-
>>> keloid prone patients (n 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
>> Incidentally, I saw a show on TV recently about Captain Cook's first
>> exploratory voyage (in 1768, searching for the hypothetical great
>> southern continent) in which it was stated that one of the signs of
>> scurvy is that "old wounds re-open." I can't help wondering whether
>> ascorbic acid might play an important role in the formation and
>> maintenance of scar tissue.
>>
>> Assuming that the fatty acid connection (the "basic lipid model")
>> discussed in these articles is valid, I wonder whether ascorbyl
>> palmitate (which mixes with lipids) might help heal wounds with healthy
>> scars, and prevent keloid formation.
>>
>> 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.
>>
>> It suggests that wound healing might be improved not only by fixing a
>> "raw" matrix of connective tissue in place, but also, perhaps, by
>> encouraging the formation of new connective tissue by nutritional
>> interventions.
>>
>> --
>> Marshall Price of Miami
>> Known to Yahoo as d021317c
>
> What you need to regenerate tissue rather than scar it is
> dedifferentiated fibroblasts with the local clues in which part of the
> body they are. Scar formation is encouraged by oxygen and the
> mediator here is likely AA. Also one organ which can completely
> regenerate is the liver but when it is overloaded with AA it rather
> forms scar tissue resulting in a disease. Immunity plays a major role
> in regeneration versus scarring as demonstrated on the unusual
> "autoimmune" MRL mouse strain ( * news.bbc.co.uk/2/hi/science/nature/4888080.stm
> ). I would love to see which lipids and eicosanoids this mouse versus
> normal mouse use. I bet Mead acid is the major PUFA in the blastemas
> such as in the growing deer antlers. Also look at what Monty has to
> say about his wounds - perfect healing. Ray Peat also wrote an
> interesting essay about regeneration:
> * raypeat . com /articles/articles/adaptive-substance.shtml
That's "an interesting essay about regeneration"? Whatever it is,
it's too long and kooky for me. I read about a quarter of it before I
realized I had no idea what he was going on about.
I liked the mouse article, though.
About livers, it isn't true that they can completely regenerate
themselves. Once a lobe is gone, the other two can grow bigger, but
that lobe will never grow back, and if all three are sick enough, the
whole organ is lost.
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.
--
Marshall Price of Miami
Known to Yahoo as d021317c
Re: Keloids - AA overload disease
On May 20, 9:28 pm, Marshall Price <d0213...@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
On May 20, 9:28 pm, Marshall Price <d0213...@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
Re: Keloids - AA overload disease
Taka wrote:
> On May 20, 9:28 pm, Marshall Price <d0213...@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
Not to mention the finger extensionists. I wonder if they've tried
zinc fingers, or are they stuck in a homeobox?
(Personally, I have no intention of progressing beyond the pupal
stage. It's just asking for trouble.)
--
Marshall Price of Miami
Known to Yahoo as d021317c
Taka wrote:
> On May 20, 9:28 pm, Marshall Price <d0213...@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
Not to mention the finger extensionists. I wonder if they've tried
zinc fingers, or are they stuck in a homeobox?
(Personally, I have no intention of progressing beyond the pupal
stage. It's just asking for trouble.)
--
Marshall Price of Miami
Known to Yahoo as d021317c
Re: Keloids - AA overload disease
On May 18, 6:06 am, Marshall Price <d0213...@yahoo . com > wrote:
> 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 think you need to read this: * w w w .badscience . net /?p=664
MattLB
On May 18, 6:06 am, Marshall Price <d0213...@yahoo . com > wrote:
> 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 think you need to read this: * w w w .badscience . net /?p=664
MattLB
Re: Keloids - AA overload disease
MattLB wrote:
> On May 18, 6:06 am, Marshall Price <d0213...@yahoo . com > wrote:
>> 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 think you need to read this: * w w w .badscience . net /?p=664
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.
Incidentally, I'll betray a secret my father told me a long time ago.
He was in the habit of giving advice to aspiring young entertainers,
and had all his teeth removed when he was about 20, which would have
been in 1919. He advised FDR and Eleanor to go to his surgeon, Maxwell
Maltz, for plastic surgery, and they did. Later, I found out that they
retired to Hyde Park for a whole month, avoiding the press. That must
have been the month after the surgery. I haven't found any evidence
that the secret has gotten out, but I'm sure Dad was telling the truth.
--
Marshall Price of Miami
Known to Yahoo as d021317c
MattLB wrote:
> On May 18, 6:06 am, Marshall Price <d0213...@yahoo . com > wrote:
>> 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 think you need to read this: * w w w .badscience . net /?p=664
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.
Incidentally, I'll betray a secret my father told me a long time ago.
He was in the habit of giving advice to aspiring young entertainers,
and had all his teeth removed when he was about 20, which would have
been in 1919. He advised FDR and Eleanor to go to his surgeon, Maxwell
Maltz, for plastic surgery, and they did. Later, I found out that they
retired to Hyde Park for a whole month, avoiding the press. That must
have been the month after the surgery. I haven't found any evidence
that the secret has gotten out, but I'm sure Dad was telling the truth.
--
Marshall Price of Miami
Known to Yahoo as d021317c
Re: Keloids - AA overload disease
On May 20, 9:42 pm, Marshall Price <d0213...@yahoo . com > wrote:
> 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.
As for the extracellular matrix (ECM) growth factors supporting proper
regeneration I suggest the cat ECM membranes would be even better than
any pig bladder, cats are incredible healers. Also the latest hit is
using own platelet rich plasma (PRP) which promotes proper
regeneration/healing of e.g. connective tissues:
* drreeves . com /Blood%20and%20PRP.html
Again I guess the AA metabolites termed leukotrienes act destructively
while certain prostaglandins may support proper regeneration. But
"antioxidants" such as resveratrol or Aloe vera gel are known to
prevent scar formation and promote proper healing and they do so by
being AA metabolization inhibitors (resveratrol is a potent COX
inhibitor) so AA is no go here at least at an early stage when
proliferation and proper positioning of stem cells is needed.
Allantoin (present e.g in comfrey) is far better stem cell attractant
than any AA-derived eicosanoid (coincidentally higher primates cannot
manufacture allantoin from uric acid). The regenerating animals
having adult blastemas may be equipped with mechanisms postponing the
production of AA metabolites till the new organ scaffold has been put
in place.
Taka
(BTW the company manufacturing the pig bladder powder is * w w w .acell . com /
)
On May 20, 9:42 pm, Marshall Price <d0213...@yahoo . com > wrote:
> 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.
As for the extracellular matrix (ECM) growth factors supporting proper
regeneration I suggest the cat ECM membranes would be even better than
any pig bladder, cats are incredible healers. Also the latest hit is
using own platelet rich plasma (PRP) which promotes proper
regeneration/healing of e.g. connective tissues:
* drreeves . com /Blood%20and%20PRP.html
Again I guess the AA metabolites termed leukotrienes act destructively
while certain prostaglandins may support proper regeneration. But
"antioxidants" such as resveratrol or Aloe vera gel are known to
prevent scar formation and promote proper healing and they do so by
being AA metabolization inhibitors (resveratrol is a potent COX
inhibitor) so AA is no go here at least at an early stage when
proliferation and proper positioning of stem cells is needed.
Allantoin (present e.g in comfrey) is far better stem cell attractant
than any AA-derived eicosanoid (coincidentally higher primates cannot
manufacture allantoin from uric acid). The regenerating animals
having adult blastemas may be equipped with mechanisms postponing the
production of AA metabolites till the new organ scaffold has been put
in place.
Taka
(BTW the company manufacturing the pig bladder powder is * w w w .acell . com /
)
