Study: Licorice, peppermint DECREASE sebum secretion
- Thread starter michael barry
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hair today gone tomorrow
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squeegee said:
ok then go take 2.5mg of dutasteride everyday
200mg of spironolactone everyday
and foam 2x a day.
ull have ur hair.
goata007 said:
I was unaware of the systemic absorption. Are you sure about that?
Even lavender is absorbed systemically. But how much is the question. So far we just have a few fat kids who got side effects. It is mostly fat people who get gyno from finasteride anyway. They have more estrogen to begin with.
collegechemistrystudent said:
I have no idea if it is absorbed systemically. I am planning on using this licorice stuff for body hair too, and since it is quite potent, thats why I asked if it absorbs systemically or not. Last thing I need is my manly hairy chest be replaced with a set of silky smooth boobs :nono:
hair today gone tomorrow
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for the guys who are looking for a licorice shampoo.
http://www.cvs.com/CVSApp/cvs/gateway/d ... iveCat=499^Query=licorice+shampoo^Click+to+go+to+search+results..x=0^Click+to+go+to+search+results..y=0^Click+to+go+to+search+results.=submit
it doesn't contain any peppermint oil...you could buy pure peppermint oil and pour a little bit in.
http://www.cvs.com/CVSApp/cvs/gateway/d ... iveCat=499^Query=licorice+shampoo^Click+to+go+to+search+results..x=0^Click+to+go+to+search+results..y=0^Click+to+go+to+search+results.=submit
it doesn't contain any peppermint oil...you could buy pure peppermint oil and pour a little bit in.
grove12345
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chore boy said:
i have that shampoo and i mix it with 50% water.
Saved my hair.
Not saying peppermint did it, just that my hair is SUPER sensitive so 99% of shampoos destroy my hair cause it to shed.
I shampoo 2-3xs a week with that stuff.
But now im trying peppermint oil on my hairline.
Ive been using Virile Mane which has peppermint and it helped me, not hurt my hair. So im pretty sure Peppermint doesnt hurt your hair.
patagonia
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michael barry said:
http://www.haircycle.com/catalog/Shampoo_dir.html
Looking at the ingredients on Dr. Coles "Haircycle" shampoo website it seems like Licorice and Peppermint are no longer listed in the ingredients list.
I wonder why this is?
I believe this two ingredients where part of the original shampoo formula.
I wonder if Dr. C decided against peppermint and licorice due to fears they might be harmful for hair?
squeegee
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Phytol directly activates peroxisome proliferator-activated receptor alpha (PPARalpha) and regulates gene expression involved in lipid metabolism in PPARalpha-expressing HepG2 hepatocytes.Goto T, Takahashi N, Kato S, Egawa K, Ebisu S, Moriyama T, Fushiki T, Kawada T.
Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Uji, Japan.
The peroxisome proliferator-activated receptor (PPAR) is one of the indispensable transcription factors for regulating lipid metabolism in various tissues. In our screening for natural compounds that activate PPAR using luciferase assays, a branched-carbon-chain alcohol (a component of chlorophylls), phytol, has been identified as a PPARalpha-specific activator. Phytol induced the increase in PPARalpha-dependent luciferase activity and the degree of in vitro binding of a coactivator, SRC-1, to GST-PPARalpha. Moreover, the addition of phytol upregulated the expression of PPARalpha-target genes at both mRNA and protein levels in PPARalpha-expressing HepG2 hepatocytes. These findings indicate that phytol is functional as a PPARalpha ligand and that it stimulates the expression of PPARalpha-target genes in intact cells. Because PPARalpha activation enhances circulating lipid clearance, phytol may be important in managing abnormalities in lipid metabolism.
Sebum production is key in the pathophysiology of acne, an extremely common condition, which when severe, may require treatment with isotretinoin, a known teratogen. Apart from isotretinoin and hormonal therapy, no agents are available to reduce sebum. Increasing our understanding of the regulation of sebum production is a milestone in identifying alternative therapeutic targets. Studies in sebocytes and human sebaceous glands indicate that agonists of peroxisome proliferator-activated receptors (PPARs) alter sebaceous lipid production. The goal of this study is to verify the expression and activity of PPARs in human skin and SEB-1 sebocytes and to assess the effects of PPAR ligands on sebum production in patients. To investigate the contribution of each receptor subtype to sebum production, lipogenesis assays were performed in SEB-1 sebocytes that were treated with PPAR ligands and isotretinoin. Isotretinoin significantly decreased lipogenesis, while the PPAR agonist-GW7647, PPAR agonist-GW0742, PPAR/ agonist-GW2433, PPAR agonist rosiglitazone, and the pan-agonist-GW4148, increased lipogenesis. Patients treated with thiazolidinediones or fibrates had significant increases in sebum production (37 and 77%, respectively) when compared to age-, disease-, and sex-matched controls. These data indicate that PPARs play a role in regulating sebum production and that selective modulation of their activity may represent a novel therapeutic strategy for the treatment of acne.
Kuenzli S, Saurat JH.
Department of Dermatology, University HospitalUniversity Hospital, Geneva, Switzerland.
Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors that regulate the expression of target genes involved in many cellular functions including cell proliferation, differentiation and immune/inflammation response. The PPAR subfamily consists of three isotypes: PPAR alpha, PPAR beta/delta and PPAR gamma, which have all been identified in keratinocytes. PPAR beta/delta is the predominant subtype in human keratinocytes, whereas PPAR alpha and PPAR gamma are expressed at much lower levels and increase significantly upon keratinocyte differentiation. PPAR beta/delta is not linked to differentiation, but is significantly upregulated upon various conditions that result in keratinocyte proliferation, and during skin wound healing. In vitro and in vivo evidence suggests that PPARs appear to play an important role in skin barrier permeability, inhibiting epidermal cell growth, promoting epidermal terminal differentiation and regulating skin inflammatory response by diverse mechanisms. These proprieties are pointing in the direction of PPARs being key regulators of skin conditions characterized by hyperproliferation, inflammatory infiltrates and aberrant differentiation such as psoriasis, but may also have clinical implications in inflammatory skin disease (e.g. atopic dermatitis), proliferative skin disease, wound healing, acne and protease inhibitor associated lipodystrophia.
Tetradecylthioacetic acid prevents high fat diet induced adiposity and insulin resistance
Tetradecylthioacetic acid (TTA) is a non-ß-oxidizable fatty acid analog, which potently regulates lipid homeostasis. Here we evaluate the ability of TTA to prevent diet-induced and genetically determined adiposity and insulin resistance. In Wistar rats fed a high fat diet, TTA administration completely prevented diet-induced insulin resistance and adiposity. In genetically obese Zucker (fa/fa) rats TTA treatment reduced the epididymal adipose tissue mass and improved insulin sensitivity. All three rodent peroxisome proliferator-activated receptor (PPAR) subtypes were activated by TTA in the ranking order PPAR{alpha} > PPAR{delta} > PPAR{gamma}. Expression of PPAR{gamma} target genes in adipose tissue was unaffected by TTA treatment, whereas the hepatic expression of PPAR{alpha}-responsive genes encoding enzymes involved in fatty acid uptake, transport, and oxidation was induced. This was accompanied by increased hepatic mitochondrial ß-oxidation and a decreased fatty acid/ketone body ratio in plasma. These findings indicate that PPAR{alpha}-dependent mechanisms play a pivotal role, but additionally, the involvement of PPAR{alpha}-independent pathways is conceivable. Taken together, our results suggest that a TTA-induced increase in hepatic fatty acid oxidation and ketogenesis drains fatty acids from blood and extrahepatic tissues and that this contributes significantly to the beneficial effects of TTA on fat mass accumulation and peripheral insulin sensitivity
Good read : http://www.jlr.org/cgi/reprint/R700015-JLR200v1.pdf
http://www.klinikum-dessau.de/fileadmin ... ormres.pdf
Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Uji, Japan.
The peroxisome proliferator-activated receptor (PPAR) is one of the indispensable transcription factors for regulating lipid metabolism in various tissues. In our screening for natural compounds that activate PPAR using luciferase assays, a branched-carbon-chain alcohol (a component of chlorophylls), phytol, has been identified as a PPARalpha-specific activator. Phytol induced the increase in PPARalpha-dependent luciferase activity and the degree of in vitro binding of a coactivator, SRC-1, to GST-PPARalpha. Moreover, the addition of phytol upregulated the expression of PPARalpha-target genes at both mRNA and protein levels in PPARalpha-expressing HepG2 hepatocytes. These findings indicate that phytol is functional as a PPARalpha ligand and that it stimulates the expression of PPARalpha-target genes in intact cells. Because PPARalpha activation enhances circulating lipid clearance, phytol may be important in managing abnormalities in lipid metabolism.
Sebum production is key in the pathophysiology of acne, an extremely common condition, which when severe, may require treatment with isotretinoin, a known teratogen. Apart from isotretinoin and hormonal therapy, no agents are available to reduce sebum. Increasing our understanding of the regulation of sebum production is a milestone in identifying alternative therapeutic targets. Studies in sebocytes and human sebaceous glands indicate that agonists of peroxisome proliferator-activated receptors (PPARs) alter sebaceous lipid production. The goal of this study is to verify the expression and activity of PPARs in human skin and SEB-1 sebocytes and to assess the effects of PPAR ligands on sebum production in patients. To investigate the contribution of each receptor subtype to sebum production, lipogenesis assays were performed in SEB-1 sebocytes that were treated with PPAR ligands and isotretinoin. Isotretinoin significantly decreased lipogenesis, while the PPAR agonist-GW7647, PPAR agonist-GW0742, PPAR/ agonist-GW2433, PPAR agonist rosiglitazone, and the pan-agonist-GW4148, increased lipogenesis. Patients treated with thiazolidinediones or fibrates had significant increases in sebum production (37 and 77%, respectively) when compared to age-, disease-, and sex-matched controls. These data indicate that PPARs play a role in regulating sebum production and that selective modulation of their activity may represent a novel therapeutic strategy for the treatment of acne.
Kuenzli S, Saurat JH.
Department of Dermatology, University HospitalUniversity Hospital, Geneva, Switzerland.
Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors that regulate the expression of target genes involved in many cellular functions including cell proliferation, differentiation and immune/inflammation response. The PPAR subfamily consists of three isotypes: PPAR alpha, PPAR beta/delta and PPAR gamma, which have all been identified in keratinocytes. PPAR beta/delta is the predominant subtype in human keratinocytes, whereas PPAR alpha and PPAR gamma are expressed at much lower levels and increase significantly upon keratinocyte differentiation. PPAR beta/delta is not linked to differentiation, but is significantly upregulated upon various conditions that result in keratinocyte proliferation, and during skin wound healing. In vitro and in vivo evidence suggests that PPARs appear to play an important role in skin barrier permeability, inhibiting epidermal cell growth, promoting epidermal terminal differentiation and regulating skin inflammatory response by diverse mechanisms. These proprieties are pointing in the direction of PPARs being key regulators of skin conditions characterized by hyperproliferation, inflammatory infiltrates and aberrant differentiation such as psoriasis, but may also have clinical implications in inflammatory skin disease (e.g. atopic dermatitis), proliferative skin disease, wound healing, acne and protease inhibitor associated lipodystrophia.
Tetradecylthioacetic acid prevents high fat diet induced adiposity and insulin resistance
Tetradecylthioacetic acid (TTA) is a non-ß-oxidizable fatty acid analog, which potently regulates lipid homeostasis. Here we evaluate the ability of TTA to prevent diet-induced and genetically determined adiposity and insulin resistance. In Wistar rats fed a high fat diet, TTA administration completely prevented diet-induced insulin resistance and adiposity. In genetically obese Zucker (fa/fa) rats TTA treatment reduced the epididymal adipose tissue mass and improved insulin sensitivity. All three rodent peroxisome proliferator-activated receptor (PPAR) subtypes were activated by TTA in the ranking order PPAR{alpha} > PPAR{delta} > PPAR{gamma}. Expression of PPAR{gamma} target genes in adipose tissue was unaffected by TTA treatment, whereas the hepatic expression of PPAR{alpha}-responsive genes encoding enzymes involved in fatty acid uptake, transport, and oxidation was induced. This was accompanied by increased hepatic mitochondrial ß-oxidation and a decreased fatty acid/ketone body ratio in plasma. These findings indicate that PPAR{alpha}-dependent mechanisms play a pivotal role, but additionally, the involvement of PPAR{alpha}-independent pathways is conceivable. Taken together, our results suggest that a TTA-induced increase in hepatic fatty acid oxidation and ketogenesis drains fatty acids from blood and extrahepatic tissues and that this contributes significantly to the beneficial effects of TTA on fat mass accumulation and peripheral insulin sensitivity
Good read : http://www.jlr.org/cgi/reprint/R700015-JLR200v1.pdf
http://www.klinikum-dessau.de/fileadmin ... ormres.pdf