Any Alternative Treatments Worth It?
- Thread starter eshack
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Notcoolanymore
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Alternative treatments that help fight Androgenetic Alopecia are Dutasteride and Ketoconazole, which aren't FDA approved to treat androgenic alopecia though help to do so.
About natural treatments, sorry about that eshack, there are no known natural treatments that fight Androgenetic Alopecia.
Actually WE HAVE some.One is eclipta alba and castor oil.Both work to an extent to help not halt hair loss.I'd say you are better off using finasteride or minoxidil or both rahter then above.Those take a HUGE time and commitment with the results being not so satisfying in the end
MEVOYACURAR
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Any supportive information about eclipta alba or castor oil´ effectiveness?
HairShocka
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Not sure if this helps. I'm just pasting stuff from my evernote.
http://www.ncbi.nlm.nih.gov/pubmed/11263183
[h=4]RESULTS:[/h]The PGE2 levels in the portal vein increased, while the PGE2 levels in peripheral blood had no changes significantly, the PGE2 levels in the tissues of the intestinal mucosa, placenta, amnion and amniotic cells were increased significantly; Ricinoleic acid stimulated the synthesis of PGE2 in the above tissues in vitro, which had the positive correlations with the dose of ricinoleic acid and its lasting time. Indomethacin inhibited the synthesis of PGE2 in-vitro.
[h=4]CONCLUSION:[/h]The increased synthesis of PGE2 in the intrauterine tissues is a key of the initiation of labor induced by castor oil-diet, and ricinoleic acid in castor oil-diet might be the active component which induced the initiator of labor.
http://www.ncbi.nlm.nih.gov/pubmed/6141271
The effect of ricinoleic acid on prostaglandin E2 (PGE2)-evoked contractions was studied on guinea-pig isolated ileum. Addition of ricinoleic acid (10 micrograms ml-1) to the organ bath increased the amplitude of the PGE2-evoked responses. Ricinoleic acid (10 micrograms ml-1) also sensitized the guinea-pig isolated ileum to acetylcholine and histamine. The effect of the ricinoleic acid was greatly reduced by indomethacin either in-vivo (10 mg ml-1) or in-vitro (2 micrograms ml-1).
http://www.pnas.org/content/109/23/9179.full.pdf
These data suggest that ricinoleic acid can specifically activate a G protein-coupled receptor (GPCR). To identify a putative GPCR activated by ricinoleic acid, we screened a small interfering RNA (siRNA) library targeting all known and predicted nonolfactory human GPCRs for its ability to interfere with activation of MEG-01 cells by ricinoleic acid. Fig. 1C shows that siRNA pools directed against mRNAs encoding EP3 and EP4 (20–22) strongly reduced ricinoleic acid effects in MEG-01 cells. We verified that EP3 and EP4 receptors are expressed in MEG- 01 cells and that prostaglandin E2 (PGE2) has effects comparable to ricinoleic acid in these cells (Fig. S1). Consistent with a role of EP3 and EP4 receptors in mediating cellular effects of ricinoleic acid, the selective antagonists of EP3 and EP4 receptors, L-798,106 and L-161,982, respectively, at maximally active concentrations inhibited ricinoleic acid- and PGE2-induced calcium mobilization in MEG-01 cells (Fig. 1D). EP3/EP4-mediated effects of ricinoleic acid were not because of formation of PGE2 in response to ricinoleic acid (Fig. S2 A and B). Consistent with this finding, ricinoleic acid effects were not affected by inhibition of cyclooxygenase (COX)-1 and COX-2 (Fig. S2C).
To further characterize the effects of ricinoleic acid on prostanoid receptors, we heterologously expressed prostanoid receptors together with the promiscuous G protein α-subunit Gα15 isomer ricinelaidic acid was inactive (Fig. S3A). Whereas ricinoleic acid was about one order-of-magnitude less potent than PGE2, the efficacy of ricinoleic acid to activate EP3 and EP4 receptors was comparable with that of PGE2 (Fig. 1E). Ricinoleic acid also activated murine EP3 and EP4 receptors (Fig. S3B). None of the other prostanoid receptors, including IP, DP1, DP2, FP, and TP were activated by ricinoleic acid (Fig. 1F). In contrast to oleic acid, ricinoleic acid was able to displace 3 H-PGE2 from EP3 receptors expressed in CHO cells with an IC50 of 500 nM, but ricinelaidic acid hardly competed with PGE2 for binding (Fig. 1G). Taken together, these data show that ricinoleic acid is a selective agonist of EP3 and EP4 receptors.
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Doesn't minoxidil work via the EP(4) receptor?
http://www.ncbi.nlm.nih.gov/pubmed/11263183
[h=4]RESULTS:[/h]The PGE2 levels in the portal vein increased, while the PGE2 levels in peripheral blood had no changes significantly, the PGE2 levels in the tissues of the intestinal mucosa, placenta, amnion and amniotic cells were increased significantly; Ricinoleic acid stimulated the synthesis of PGE2 in the above tissues in vitro, which had the positive correlations with the dose of ricinoleic acid and its lasting time. Indomethacin inhibited the synthesis of PGE2 in-vitro.
[h=4]CONCLUSION:[/h]The increased synthesis of PGE2 in the intrauterine tissues is a key of the initiation of labor induced by castor oil-diet, and ricinoleic acid in castor oil-diet might be the active component which induced the initiator of labor.
http://www.ncbi.nlm.nih.gov/pubmed/6141271
The effect of ricinoleic acid on prostaglandin E2 (PGE2)-evoked contractions was studied on guinea-pig isolated ileum. Addition of ricinoleic acid (10 micrograms ml-1) to the organ bath increased the amplitude of the PGE2-evoked responses. Ricinoleic acid (10 micrograms ml-1) also sensitized the guinea-pig isolated ileum to acetylcholine and histamine. The effect of the ricinoleic acid was greatly reduced by indomethacin either in-vivo (10 mg ml-1) or in-vitro (2 micrograms ml-1).
http://www.pnas.org/content/109/23/9179.full.pdf
These data suggest that ricinoleic acid can specifically activate a G protein-coupled receptor (GPCR). To identify a putative GPCR activated by ricinoleic acid, we screened a small interfering RNA (siRNA) library targeting all known and predicted nonolfactory human GPCRs for its ability to interfere with activation of MEG-01 cells by ricinoleic acid. Fig. 1C shows that siRNA pools directed against mRNAs encoding EP3 and EP4 (20–22) strongly reduced ricinoleic acid effects in MEG-01 cells. We verified that EP3 and EP4 receptors are expressed in MEG- 01 cells and that prostaglandin E2 (PGE2) has effects comparable to ricinoleic acid in these cells (Fig. S1). Consistent with a role of EP3 and EP4 receptors in mediating cellular effects of ricinoleic acid, the selective antagonists of EP3 and EP4 receptors, L-798,106 and L-161,982, respectively, at maximally active concentrations inhibited ricinoleic acid- and PGE2-induced calcium mobilization in MEG-01 cells (Fig. 1D). EP3/EP4-mediated effects of ricinoleic acid were not because of formation of PGE2 in response to ricinoleic acid (Fig. S2 A and B). Consistent with this finding, ricinoleic acid effects were not affected by inhibition of cyclooxygenase (COX)-1 and COX-2 (Fig. S2C).
To further characterize the effects of ricinoleic acid on prostanoid receptors, we heterologously expressed prostanoid receptors together with the promiscuous G protein α-subunit Gα15 isomer ricinelaidic acid was inactive (Fig. S3A). Whereas ricinoleic acid was about one order-of-magnitude less potent than PGE2, the efficacy of ricinoleic acid to activate EP3 and EP4 receptors was comparable with that of PGE2 (Fig. 1E). Ricinoleic acid also activated murine EP3 and EP4 receptors (Fig. S3B). None of the other prostanoid receptors, including IP, DP1, DP2, FP, and TP were activated by ricinoleic acid (Fig. 1F). In contrast to oleic acid, ricinoleic acid was able to displace 3 H-PGE2 from EP3 receptors expressed in CHO cells with an IC50 of 500 nM, but ricinelaidic acid hardly competed with PGE2 for binding (Fig. 1G). Taken together, these data show that ricinoleic acid is a selective agonist of EP3 and EP4 receptors.
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Doesn't minoxidil work via the EP(4) receptor?
MEVOYACURAR
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Did you ever try Eclipta Alba or castor oil?
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Natural alternative treatments can certainly be effective though it is heavily based on anecdotal stories by people on the internet and maybe a study or two comparing them to say Minoxidil. Does not mean they are not effective, just means they have not been studied enough and the people saying 'X' worked for me tend to also be the wishy washy types.
I'm studying a natural medicine modality and have to say evidence is lacking in most areas due to lack of funding. Many small scale studies show promise for certain herbal medicines in various applications (not so much hair loss), but that's as far as they'll ever get. Who would invest money in such a study for something which cannot be patented or profited from?
The real discouraging fact is that there doesn't seem to be anecdotal evidence of anything natural delivering noticeable growth, aside from maybe Saw Palmetto which is just a poor man's Finasteride with the same side effects.
The real discouraging fact is that there doesn't seem to be anecdotal evidence of anything natural delivering noticeable growth, aside from maybe Saw Palmetto which is just a poor man's Finasteride with the same side effects.