science-jay
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I've been reading a lot of posts and articles on these forums for years and i'm beginning to believe it's all about fatty acids...
without these fatty acids Testosterone could be converted to DHT, it's a genetic thing if your body is able to convert the fatty acids in such a way DHT formation would be limited. Ofcourse DHT formation could be inhibited by a 5-alpha reductase inhibiter like finasteride, but i think the fatty acids play a more crucial underlying role.
Saw palmetto has only proven to be benefial to BPH (for the prostate), when it contains at least 80-95% fatty acids, probably if there could be benefits for hair it's also attributable to the fatty acids in Sawpalmetto...
Recent theories have been put to the light by Hogan on regrowth.com, who said he stopped his hairloss with borage- and fish oil.
Now Youghstah on hairlosshelp.com also has succes with a fatty acid based regimen.
critics would say these fatty acids will only play a role in the prostate or work when they are applied topically in a synthetic free structure (so not as triglyceride) but i highly doubt it!
have a look at these abstracts and you will see there is a connection...
Steroid 5alpha-reductase inhibitory activity and hair regrowth effects of an extract from Boehmeria nipononivea.
Shimizu K, Kondo R, Sakai K, Shoyama Y, Sato H, Ueno T.
Department of Forest Products, Faculty of Agriculture, Kyushu University, Fukuoka, Japan.
The acetone extract of Boehmeria nipononivea showed both potent 5alpha-reductase inhibitory activity and hair regrowth promotion effects on mice. 5alpha-Reductase inhibitory activity-guided fractionation led to six active fatty acids: alpha-linolenic, linoleic, palmitic, elaidic, oleic and stearic acids. The extract of B. nipononivea, and alphalinolenic, elaidic and stearic acids exhibited a hair regrowth effect.
Anti-androgenic and hair growth promoting activities of Lygodii spora (spore of Lygodium japonicum) I. Active constituents inhibiting testosterone 5alpha-reductase.
Matsuda H, Yamazaki M, Naruo S, Asanuma Y, Kubo M.
Faculty of Pharmaceutical Sciences, Kinki University, Higashiosaka, Osaka, Japan. matsuda@phar.kindai.ac.jp
The aqueous ethanol extract of Lygodii Spora (spore of Lygodium japonicum (Thunb.) Sw.) showed in vitro testosterone 5alpha-reductase inhibitory activity and in vivo anti-androgenic activity using growth of flank organ in castrated Syrian hamsters and hair regrowth after shaving in testosterone-treated C57Black/6CrSlc mice. From the lipophilic constituents of Lygodii Spora, oleic, linoleic and palmitic acids were identified as the main active principles inhibiting testosterone 5alpha-reductase.
Inhibition of type 1 and type 2 5alpha-reductase activity by free fatty acids, active ingredients of Permixon.
Raynaud JP, Cousse H, Martin PM.
D.R.I.T.T., Universite Pierre et Marie Curie, 4 Place Jussieu, Paris, France. jean-pierre.raynaud@admp6.jussieu.fr
In different cell systems, the lipido-sterolic extract of Serenoa repens (LSESr, Permixon inhibits both type 1 and type 2 5alpha-reductase activity (5alphaR1 and 5alphaR2). LSESr is mainly constituted of fatty acids (90+/-5%) essentially as free fatty acids (80%). Among these free fatty acids, the main components are oleic and lauric acids which represent 65% and linoleic and myristic acids 15%.To evaluate the inhibitory effect of the different components of LSESr on 5alphaR1 or 5alphaR2 activity, the corresponding type 1 and type 2 human genes have been cloned and expressed in the baculovirus-directed insect cell expression system Sf9. The cells were incubated at pH 5.5 (5alphaR2) and pH 7.4 (5alphaR1) with 1 or 3nM testosterone in presence or absence of various concentrations of LSESr or of its different components. Dihydrotestosterone formation was measured with an automatic system combining HPLC and an on-line radiodetector.The inhibition of 5alphaR1 and 5alphaR2 activity was only observed with free fatty acids: esterified fatty acids, alcohols as well as sterols assayed were inactive. A specificity of the fatty acids in 5alphaR1 or 5alphaR2 inhibition has been found. Long unsaturated chains (oleic and linolenic) were active (IC(50)=4+/-2 and 13+/-3 microg/ml, respectively) on 5alphaR1 but to a much lesser extent (IC(50)>100 and 35+/-21 microg/ml, respectively) on 5alphaR2. Palmitic and stearic acids were inactive on the two isoforms. Lauric acid was active on 5alphaR1 (IC(50)=17+/-3 microg/ml) and 5alphaR2 (IC(50)=19+/-9 microg/ml). The inhibitory activity of myristic acid was evaluated on 5alphaR2 only and found active on this isoform (IC(50)=4+/-2 microg/ml).The dual inhibitory activity of LSESr on 5alpha-reductase type 1 and type 2 can be attributed to its high content in free fatty acids.
5 alpha-reductase-catalyzed conversion of testosterone to dihydrotestosterone is increased in prostatic adenocarcinoma cells: suppression by 15-lipoxygenase metabolites of gamma-linolenic and eicosapentaenoic acids.
Pham H, Ziboh VA.
Department of Dermatology, School of Medicine, University of California at Davis, TB-192, One Shields Avenue, 95616, USA.
Although the androgens, testosterone (T) and its highly active metabolite dihydrotestosterone (DHT) play a role in the development and progression of prostate cancer, the mechanism(s) are unclear. Furthermore, 5 alpha-reductase which catalyze the conversion of T to DHT, has been a target of manipulation in the treatment of prostatic cancer, hence synthetic 5 alpha-reductase activity inhibitors have shown therapeutic promise. To demonstrate that nutrients derived from dietary sources can exert similar therapeutic promise, this study was designed using benign hyperplastic cells (BHC) and malignant tumorigenic cells (MTC) derived from Lobund-Wistar (L-W) rat model of prostatic adenocarcinoma to test the effects of gamma-linolenic acid (GLA), eicosapentaenoic acid (EPA) and their 15-lipoxygenase metabolites on cellular 5 alpha-reductase activity. Our data revealed: (i) that incubation of MTC with [3H]-T resulted in marked conversion to [3H]-DHT when compared to similar incubation with BHC; (ii) that DHT-enhanced activity of 5 alpha-reductase was inhibited 80% by 15S-hydroxyeicosatrienoic acid, the 15-lipoxygenase metabolite of GLA, when compared to 55% by 15S-hydroxyeicosapentaenoic acid, the 15-lipoxygenase metabolite of EPA; and (iii) that their precursor fatty acids, respectively, exerted moderate inhibition. Taken together, the study underscores the biological importance of 15-lipoxygenase metabolites of polyunsaturated fatty acids (PUFAs) in androgen metabolism.
Growth suppression of hamster flank organs by topical application of gamma-linolenic and other fatty acid inhibitors of 5alpha-reductase.
Liang T, Liao S.
Ben May Institute for Cancer Research and the Department of Biochemistry and Molecular Biology, University of Chicago, Illinois 60637, U.S.A.
Certain unsaturated aliphatic fatty acids, such as gamma-linolenic acid, inhibit 5alpha-reductase activity in vitro and in vivo. Hamster flank organ growth, as measured by the increase in the area of pigmented macule, is dependent on androgen. When one of the paired flank organs of a castrated hamster was treated topically with testosterone, the treated organ, but not the contralateral flank organ, became larger and darker. Topical application of gamma-linolenic acid to the testosterone-treated flank organ suppressed this testosterone effect. Other fatty acids that were not inhibitors of 5alpha-reductases were not active. Topical treatment of hamster flank organs with 5alpha-dihydrotestosterone also stimulated the growth of the organ. This 5alpha-dihydrotestosterone-dependent activity, however, was not significantly affected by gamma-linolenic acid, suggesting that flank organ growth was dependent on 5alpha-dihydrotestosterone and that gamma-linolenic acid acted by inhibiting 5alpha-reductase. With intact male hamsters, the endogenous androgen-dependent growth of flank organs is also suppressed by topical treatment with gamma-linolenic acid. The effect of gamma-linolenic acid is localized at the site of its application; topical application of gamma-linolenic acid did not affect the androgen-dependent growth of other organs such as testis, epididymis, seminal vesicle, and prostate. gamma-Linolenic acid, with low toxicity and absence of systemic effect, therefore may be potentially useful for treatment of androgen-dependent skin disorders.
International Journal of Dermatology
Volume 43 Page 701 - September 2004
doi:10.1111/j.1365-4632.2004.02200.x
Volume 43 Issue 9
Correspondence
Further insight into the pathomechanism of acne by considering the 5-α-reductase inhibitory effect of linoleic acid
M. R. Namazi, MD
Dear Sir,
Active sebaceous glands are prerequisite for the development of acne. Acne patients, male and female, excrete on average more sebum than normal subjects, and the level of secretion correlates reasonably well with the severity of the acne.1
Sebaceous activity is predominantly dependent on androgenic sex hormones of gonadal or adrenal origin. Sebaceous glands in acne-prone regions show abnormally high 5-α-reductase activity in vitro,1 suggesting the presence of an amplified target response mediated through 5-α-reduction of testosterone. Substances that inhibit the conversion of testosterone to dehydrotestosterone reduce sebum production, and of note is that isotretinoin reduces 5-α-reductase activity in skin.1
It is known that linoleic acid is significantly reduced in epidermal and comedonal lipids of acne patients1 and returns to normal with resolution of acne,1,2 and that acne-prone sebaceous glands contain less linoleic acid than normal.1 Linoleic acid is known to down-regulate neutrophil oxygen metabolism and phagocytosis, and therefore its low levels in acne-prone sebaceous glands and epidermal lipids of acne patients could contribute to the inflammation of acne.1,3 Low linoleic acid levels have also been related to ductal hypercornification.2
Another mechanism explaining the link between low sebum linoleic acid levels and severity of acne is that polyunstaturated fatty acids have been found to inhibit human and rat microsomal 5-α-reductase activity, with gamma-linoleic acid being the most potent compound tested.4
Therefore, given the potent 5-α-reductase inhibitory effect of linoleic acid, the low level of linoleic acid in acne-prone sebaceous glands could, at least partly, explain why these glands have abnormally high 5-α-reductase activity and therefore high sebum production.
without these fatty acids Testosterone could be converted to DHT, it's a genetic thing if your body is able to convert the fatty acids in such a way DHT formation would be limited. Ofcourse DHT formation could be inhibited by a 5-alpha reductase inhibiter like finasteride, but i think the fatty acids play a more crucial underlying role.
Saw palmetto has only proven to be benefial to BPH (for the prostate), when it contains at least 80-95% fatty acids, probably if there could be benefits for hair it's also attributable to the fatty acids in Sawpalmetto...
Recent theories have been put to the light by Hogan on regrowth.com, who said he stopped his hairloss with borage- and fish oil.
Now Youghstah on hairlosshelp.com also has succes with a fatty acid based regimen.
critics would say these fatty acids will only play a role in the prostate or work when they are applied topically in a synthetic free structure (so not as triglyceride) but i highly doubt it!
have a look at these abstracts and you will see there is a connection...
Steroid 5alpha-reductase inhibitory activity and hair regrowth effects of an extract from Boehmeria nipononivea.
Shimizu K, Kondo R, Sakai K, Shoyama Y, Sato H, Ueno T.
Department of Forest Products, Faculty of Agriculture, Kyushu University, Fukuoka, Japan.
The acetone extract of Boehmeria nipononivea showed both potent 5alpha-reductase inhibitory activity and hair regrowth promotion effects on mice. 5alpha-Reductase inhibitory activity-guided fractionation led to six active fatty acids: alpha-linolenic, linoleic, palmitic, elaidic, oleic and stearic acids. The extract of B. nipononivea, and alphalinolenic, elaidic and stearic acids exhibited a hair regrowth effect.
Anti-androgenic and hair growth promoting activities of Lygodii spora (spore of Lygodium japonicum) I. Active constituents inhibiting testosterone 5alpha-reductase.
Matsuda H, Yamazaki M, Naruo S, Asanuma Y, Kubo M.
Faculty of Pharmaceutical Sciences, Kinki University, Higashiosaka, Osaka, Japan. matsuda@phar.kindai.ac.jp
The aqueous ethanol extract of Lygodii Spora (spore of Lygodium japonicum (Thunb.) Sw.) showed in vitro testosterone 5alpha-reductase inhibitory activity and in vivo anti-androgenic activity using growth of flank organ in castrated Syrian hamsters and hair regrowth after shaving in testosterone-treated C57Black/6CrSlc mice. From the lipophilic constituents of Lygodii Spora, oleic, linoleic and palmitic acids were identified as the main active principles inhibiting testosterone 5alpha-reductase.
Inhibition of type 1 and type 2 5alpha-reductase activity by free fatty acids, active ingredients of Permixon.
Raynaud JP, Cousse H, Martin PM.
D.R.I.T.T., Universite Pierre et Marie Curie, 4 Place Jussieu, Paris, France. jean-pierre.raynaud@admp6.jussieu.fr
In different cell systems, the lipido-sterolic extract of Serenoa repens (LSESr, Permixon inhibits both type 1 and type 2 5alpha-reductase activity (5alphaR1 and 5alphaR2). LSESr is mainly constituted of fatty acids (90+/-5%) essentially as free fatty acids (80%). Among these free fatty acids, the main components are oleic and lauric acids which represent 65% and linoleic and myristic acids 15%.To evaluate the inhibitory effect of the different components of LSESr on 5alphaR1 or 5alphaR2 activity, the corresponding type 1 and type 2 human genes have been cloned and expressed in the baculovirus-directed insect cell expression system Sf9. The cells were incubated at pH 5.5 (5alphaR2) and pH 7.4 (5alphaR1) with 1 or 3nM testosterone in presence or absence of various concentrations of LSESr or of its different components. Dihydrotestosterone formation was measured with an automatic system combining HPLC and an on-line radiodetector.The inhibition of 5alphaR1 and 5alphaR2 activity was only observed with free fatty acids: esterified fatty acids, alcohols as well as sterols assayed were inactive. A specificity of the fatty acids in 5alphaR1 or 5alphaR2 inhibition has been found. Long unsaturated chains (oleic and linolenic) were active (IC(50)=4+/-2 and 13+/-3 microg/ml, respectively) on 5alphaR1 but to a much lesser extent (IC(50)>100 and 35+/-21 microg/ml, respectively) on 5alphaR2. Palmitic and stearic acids were inactive on the two isoforms. Lauric acid was active on 5alphaR1 (IC(50)=17+/-3 microg/ml) and 5alphaR2 (IC(50)=19+/-9 microg/ml). The inhibitory activity of myristic acid was evaluated on 5alphaR2 only and found active on this isoform (IC(50)=4+/-2 microg/ml).The dual inhibitory activity of LSESr on 5alpha-reductase type 1 and type 2 can be attributed to its high content in free fatty acids.
5 alpha-reductase-catalyzed conversion of testosterone to dihydrotestosterone is increased in prostatic adenocarcinoma cells: suppression by 15-lipoxygenase metabolites of gamma-linolenic and eicosapentaenoic acids.
Pham H, Ziboh VA.
Department of Dermatology, School of Medicine, University of California at Davis, TB-192, One Shields Avenue, 95616, USA.
Although the androgens, testosterone (T) and its highly active metabolite dihydrotestosterone (DHT) play a role in the development and progression of prostate cancer, the mechanism(s) are unclear. Furthermore, 5 alpha-reductase which catalyze the conversion of T to DHT, has been a target of manipulation in the treatment of prostatic cancer, hence synthetic 5 alpha-reductase activity inhibitors have shown therapeutic promise. To demonstrate that nutrients derived from dietary sources can exert similar therapeutic promise, this study was designed using benign hyperplastic cells (BHC) and malignant tumorigenic cells (MTC) derived from Lobund-Wistar (L-W) rat model of prostatic adenocarcinoma to test the effects of gamma-linolenic acid (GLA), eicosapentaenoic acid (EPA) and their 15-lipoxygenase metabolites on cellular 5 alpha-reductase activity. Our data revealed: (i) that incubation of MTC with [3H]-T resulted in marked conversion to [3H]-DHT when compared to similar incubation with BHC; (ii) that DHT-enhanced activity of 5 alpha-reductase was inhibited 80% by 15S-hydroxyeicosatrienoic acid, the 15-lipoxygenase metabolite of GLA, when compared to 55% by 15S-hydroxyeicosapentaenoic acid, the 15-lipoxygenase metabolite of EPA; and (iii) that their precursor fatty acids, respectively, exerted moderate inhibition. Taken together, the study underscores the biological importance of 15-lipoxygenase metabolites of polyunsaturated fatty acids (PUFAs) in androgen metabolism.
Growth suppression of hamster flank organs by topical application of gamma-linolenic and other fatty acid inhibitors of 5alpha-reductase.
Liang T, Liao S.
Ben May Institute for Cancer Research and the Department of Biochemistry and Molecular Biology, University of Chicago, Illinois 60637, U.S.A.
Certain unsaturated aliphatic fatty acids, such as gamma-linolenic acid, inhibit 5alpha-reductase activity in vitro and in vivo. Hamster flank organ growth, as measured by the increase in the area of pigmented macule, is dependent on androgen. When one of the paired flank organs of a castrated hamster was treated topically with testosterone, the treated organ, but not the contralateral flank organ, became larger and darker. Topical application of gamma-linolenic acid to the testosterone-treated flank organ suppressed this testosterone effect. Other fatty acids that were not inhibitors of 5alpha-reductases were not active. Topical treatment of hamster flank organs with 5alpha-dihydrotestosterone also stimulated the growth of the organ. This 5alpha-dihydrotestosterone-dependent activity, however, was not significantly affected by gamma-linolenic acid, suggesting that flank organ growth was dependent on 5alpha-dihydrotestosterone and that gamma-linolenic acid acted by inhibiting 5alpha-reductase. With intact male hamsters, the endogenous androgen-dependent growth of flank organs is also suppressed by topical treatment with gamma-linolenic acid. The effect of gamma-linolenic acid is localized at the site of its application; topical application of gamma-linolenic acid did not affect the androgen-dependent growth of other organs such as testis, epididymis, seminal vesicle, and prostate. gamma-Linolenic acid, with low toxicity and absence of systemic effect, therefore may be potentially useful for treatment of androgen-dependent skin disorders.
International Journal of Dermatology
Volume 43 Page 701 - September 2004
doi:10.1111/j.1365-4632.2004.02200.x
Volume 43 Issue 9
Correspondence
Further insight into the pathomechanism of acne by considering the 5-α-reductase inhibitory effect of linoleic acid
M. R. Namazi, MD
Dear Sir,
Active sebaceous glands are prerequisite for the development of acne. Acne patients, male and female, excrete on average more sebum than normal subjects, and the level of secretion correlates reasonably well with the severity of the acne.1
Sebaceous activity is predominantly dependent on androgenic sex hormones of gonadal or adrenal origin. Sebaceous glands in acne-prone regions show abnormally high 5-α-reductase activity in vitro,1 suggesting the presence of an amplified target response mediated through 5-α-reduction of testosterone. Substances that inhibit the conversion of testosterone to dehydrotestosterone reduce sebum production, and of note is that isotretinoin reduces 5-α-reductase activity in skin.1
It is known that linoleic acid is significantly reduced in epidermal and comedonal lipids of acne patients1 and returns to normal with resolution of acne,1,2 and that acne-prone sebaceous glands contain less linoleic acid than normal.1 Linoleic acid is known to down-regulate neutrophil oxygen metabolism and phagocytosis, and therefore its low levels in acne-prone sebaceous glands and epidermal lipids of acne patients could contribute to the inflammation of acne.1,3 Low linoleic acid levels have also been related to ductal hypercornification.2
Another mechanism explaining the link between low sebum linoleic acid levels and severity of acne is that polyunstaturated fatty acids have been found to inhibit human and rat microsomal 5-α-reductase activity, with gamma-linoleic acid being the most potent compound tested.4
Therefore, given the potent 5-α-reductase inhibitory effect of linoleic acid, the low level of linoleic acid in acne-prone sebaceous glands could, at least partly, explain why these glands have abnormally high 5-α-reductase activity and therefore high sebum production.
