Y not? U just need 1% of tea tree oil though. Too much burns your scalp.
100% pure tea tree oil is more for aromatherapy(the smell is heavenly)
Starting A New Regime As Of 1st July 2019
- Thread starter sktboiboi
- Start date
100% pure tea tree oil is more for aromatherapy(the smell is heavenly)
At 6 months, the group of the 5% minoxidil solution showed a mean improvement in anagen ratio of the trichogram of 11.68%, and the group of the 0.2% caffeine solution had an anagen improvement of 10.59%. The difference of mean values between both groups was 1.09%. The statistical analysis was performed and reported in accordance with the CONSORT Guidelines 2010 for reporting of noninferiority and equivalence randomized trials.
This in vitro study used scalp biopsy samples from male Androgenetic Alopecia patients which were cultivated using different concentrations of testosterone and/or caffeine for a period of 120-192 hours. Addition of caffeine in concentrations of 0.001% and 0.005% were found to counteract the suppressive effects of testosterone on hair growth, with a higher hair shaft elongation seen at 120 h after caffeine administration, compared to control group. This in vitrostudy thus clearly demonstrates that caffeine is a stimulator of human hair growth which may have importance in the treatment of Androgenetic Alopecia.[5]
This in vitro study used scalp biopsy samples from male Androgenetic Alopecia patients which were cultivated using different concentrations of testosterone and/or caffeine for a period of 120-192 hours. Addition of caffeine in concentrations of 0.001% and 0.005% were found to counteract the suppressive effects of testosterone on hair growth, with a higher hair shaft elongation seen at 120 h after caffeine administration, compared to control group. This in vitrostudy thus clearly demonstrates that caffeine is a stimulator of human hair growth which may have importance in the treatment of Androgenetic Alopecia.[5]
Among the most differentially expressed lncRNAs, some are closely related to
coding-genes, such as CTD-2636A23.2, which is associated with the coding gene HMGCS1.
This gene was shown to be associated with cellular responses to follicle-stimulating hormone
stimuli, cellular responses to cholesterol, cholesterol biosynthetic processes and male gonad
development, all of which are tightly associated with Androgenetic Alopecia mechanisms.
20-23 T
= lack of unmetabolised cholesterol(metabolised = downstream steroid hormones) in Androgenetic Alopecia scalp
Cellular cholesterol directly activates Smoothened in Hedgehog signaling
We demonstrate Hedgehog signaling requires sterol binding to Smoothened and define key residues for sterol recognition and activity. We also show that cholesterol itself binds and activates Smoothened. Furthermore, the effect of oxysterols is abolished in Smoothened mutants that retain activation by cholesterol and Hedgehog. We propose that the endogenous Smoothened activator is cholesterol, not oxysterols, and that vertebrate Hedgehog signaling controls Smoothened by regulating its access to cholesterol.
= cholesterol is the endogenous ligand for the start of hedgehog signalling
Abstract
The consumption of caffeinated beverages has been linked to elevated serum cholesterol and an increased risk of coronary disease, although the relationships are inconsistent across studies and remain controversial. The effect of caffeine on cholesterol and coronary disease risk may be modulated by other factors. Using cohort data from a subsample of the University of North Carolina Alumni Heart Study, we investigated whether the relationships between caffeinated beverage consumption and serum lipid and lipoprotein levels in middle-aged men and women were modulated by levels of trait hostility. After adjustment for other risk factors, higher caffeinated beverage intake was associated with higher low-density lipoprotein cholesterol levels and a higher ratio of total to high-density lipoprotein cholesterol, both indicative of greater coronary disease risk. The interactive effects of hostility and caffeine intake were ambiguous, although there were trends for caffeine intake to have stronger effects on low-density lipoprotein and on total cholesterol in people with less hostility. Additional studies of personality characteristics and other factors that can modulate the cholesterol-raising effects of coffee drinking may be warranted because they might clarify the health consequences associated with coffee drinking and lead to the identification of individuals who would benefit most from changes in their coffee drinking.
= caffeine increases cholesterol levels
Cholesterol activates hedgehog signalling
Affirmed by:
"Using real-time PCR, the results showed that caffeine induced robust overexpression of Shh(Sonic hedgehog) mRNA in both cell types without significantly modifying PKA RI alpha gene expression.
So caffeine grows hair by upregulating Sonic hedgehog, via increasing cholesterol levels, which is downregulated in Androgenetic Alopecia scalp.
ASHGV40021
887
69.75304
54 Up
NM_00128227
5 PRAC2 17
Hs.2365
57 Prostate cancer susceptibility candidate 2
= mrcna gene that causes prostate cancer is the most upregulated in Androgenetic Alopecia scalp.
Whatever it does, 1 of its effects would have to be causing the levels of DHT to increase, for high levels of DHT produced by the arenal glands/male gonads is the cause of prostate cancer/ BPH.
All steroid hormones, including DHT, ultimately comes from cholesterol via the
https://en.m.wikipedia.org/wiki/Steroidogenic_enzyme pathway.
Cholesterol is low in Androgenetic Alopecia scalps, yet DHT is high.
= cholesterol is constantly being metabolised to DHT in the balding scalp. Sex hormones are higher in Androgenetic Alopecia scalps.
Unchanged cholesterol are higher in hairy scalps.
= topical caffeine + 5 alpha redutase inhibitor
Dht increases sebocyte hyperprofileration via hyperinsulinemia(upregulation of insulin receptor)
Enlarged sebocytes = sebum hypersecretion
Sebum feeds Propionibacterium acnes and Malessazia furfur, goblosa and restricta.
Microbial overload = T cell receptor signalling hyperactivation
T cell receptor signalling upregulation = immune system upregulation = Inflammation
The T cell receptor signalling
pathway plays important roles in human immune functions.
19 It has been reported that this
pathway is associated with the generation of alopecia areata, which is an auto-immune
disease.19 However, a relationship between Androgenetic Alopecia and this pathway had not previously been
reported. Our results reveal that Androgenetic Alopecia might be significantly and importantly involved with
the immune system, but this requires further investigation.
= topical or oral anti-microbial
coding-genes, such as CTD-2636A23.2, which is associated with the coding gene HMGCS1.
This gene was shown to be associated with cellular responses to follicle-stimulating hormone
stimuli, cellular responses to cholesterol, cholesterol biosynthetic processes and male gonad
development, all of which are tightly associated with Androgenetic Alopecia mechanisms.
20-23 T
= lack of unmetabolised cholesterol(metabolised = downstream steroid hormones) in Androgenetic Alopecia scalp
Cellular cholesterol directly activates Smoothened in Hedgehog signaling
We demonstrate Hedgehog signaling requires sterol binding to Smoothened and define key residues for sterol recognition and activity. We also show that cholesterol itself binds and activates Smoothened. Furthermore, the effect of oxysterols is abolished in Smoothened mutants that retain activation by cholesterol and Hedgehog. We propose that the endogenous Smoothened activator is cholesterol, not oxysterols, and that vertebrate Hedgehog signaling controls Smoothened by regulating its access to cholesterol.
= cholesterol is the endogenous ligand for the start of hedgehog signalling
Abstract
The consumption of caffeinated beverages has been linked to elevated serum cholesterol and an increased risk of coronary disease, although the relationships are inconsistent across studies and remain controversial. The effect of caffeine on cholesterol and coronary disease risk may be modulated by other factors. Using cohort data from a subsample of the University of North Carolina Alumni Heart Study, we investigated whether the relationships between caffeinated beverage consumption and serum lipid and lipoprotein levels in middle-aged men and women were modulated by levels of trait hostility. After adjustment for other risk factors, higher caffeinated beverage intake was associated with higher low-density lipoprotein cholesterol levels and a higher ratio of total to high-density lipoprotein cholesterol, both indicative of greater coronary disease risk. The interactive effects of hostility and caffeine intake were ambiguous, although there were trends for caffeine intake to have stronger effects on low-density lipoprotein and on total cholesterol in people with less hostility. Additional studies of personality characteristics and other factors that can modulate the cholesterol-raising effects of coffee drinking may be warranted because they might clarify the health consequences associated with coffee drinking and lead to the identification of individuals who would benefit most from changes in their coffee drinking.
= caffeine increases cholesterol levels
Cholesterol activates hedgehog signalling
Affirmed by:
"Using real-time PCR, the results showed that caffeine induced robust overexpression of Shh(Sonic hedgehog) mRNA in both cell types without significantly modifying PKA RI alpha gene expression.
So caffeine grows hair by upregulating Sonic hedgehog, via increasing cholesterol levels, which is downregulated in Androgenetic Alopecia scalp.
ASHGV40021
887
69.75304
54 Up
NM_00128227
5 PRAC2 17
Hs.2365
57 Prostate cancer susceptibility candidate 2
= mrcna gene that causes prostate cancer is the most upregulated in Androgenetic Alopecia scalp.
Whatever it does, 1 of its effects would have to be causing the levels of DHT to increase, for high levels of DHT produced by the arenal glands/male gonads is the cause of prostate cancer/ BPH.
All steroid hormones, including DHT, ultimately comes from cholesterol via the
https://en.m.wikipedia.org/wiki/Steroidogenic_enzyme pathway.
Cholesterol is low in Androgenetic Alopecia scalps, yet DHT is high.
= cholesterol is constantly being metabolised to DHT in the balding scalp. Sex hormones are higher in Androgenetic Alopecia scalps.
Unchanged cholesterol are higher in hairy scalps.
= topical caffeine + 5 alpha redutase inhibitor
Dht increases sebocyte hyperprofileration via hyperinsulinemia(upregulation of insulin receptor)
Enlarged sebocytes = sebum hypersecretion
Sebum feeds Propionibacterium acnes and Malessazia furfur, goblosa and restricta.
Microbial overload = T cell receptor signalling hyperactivation
T cell receptor signalling upregulation = immune system upregulation = Inflammation
The T cell receptor signalling
pathway plays important roles in human immune functions.
19 It has been reported that this
pathway is associated with the generation of alopecia areata, which is an auto-immune
disease.19 However, a relationship between Androgenetic Alopecia and this pathway had not previously been
reported. Our results reveal that Androgenetic Alopecia might be significantly and importantly involved with
the immune system, but this requires further investigation.
= topical or oral anti-microbial
Last edited:
It has also been reported that one key role of PG, and more specifically CS, is to preserve hair follicle immune privilege during the anagen stage.24 PG would envelop the follicle and act as a protective screen to prevent natural cytotoxic cells from recognizing the lack of ‘self’ histocompatibility antigens on bulb cells in the anagen hair follicle.24 Interestingly, 4C3-CS and PG4-CS ⁄DS epitopes progressively disappeared during catagen, as previously observed for C6S and C4S.24 By contrast, this phenomenon did not occur for type D chondroitin and HS. During the catagen phase and concomitantly with decline of some CS expression, an increase in major histocompatibility complex class I expression was noted in the follicle epithelial column together with an increased numbers
of active macrophages around the dermal compartment.
In a similar way, in alopecia areata (a self-immune disease), the induction of these antigens seemed to be linked to the loss of CS57 parallel to a T-cell infiltration first restricted to the hair bulb including matrix cells58 and ultimately leading to hair loss. The lowermost part of the bulb thus appeared as a weakened area and the discontinuous distribution of GAGs, together with the disappearance of some of them in catagen,
might contribute to this overall degradation process.
It thus seems that GAG distribution around hair matrix results from contradictory needs. On the one hand, a weak expression of GAGs at the BM and in the CTS would support and favour a privileged nutrient diffusion, a decreased cell–BM adhesion and a high proliferation rate of matrix cells. On the other hand, the lack of some GAGs such as HS and CS would somehow weaken the hair follicle immune privilege. In conclusion, this complex and patterned PG and GAG distribution in the anagen hair is likely to reflect their strong involvement in hair biology. Differential expression suggests differential functionalities in nutrient diffusion, cell proliferation and differentiation, and hair growth maintenance.
= oral Chondroitin Sulfate(CS)
Reason:
To provide an immune privillege for the hair follicle to sustain anagen. Loss of Chondroitin sulfate protoglycans = T cells(T cell receptor signalling pathway aka immune cells) are free to attack the hair follicle along with the overloaded microbials living off the overabundant sebum enveloping the hair follicle
The outer root sheath is made up of Chondrotin sulfate-derived protoglycans. Androgenetic Alopecia-hairs have a lack of this structure.
The outer root sheath (ORS) is an extension of the epidermal basal layer which envelopes the entire hair follicle (HF). In addition, the ORS contains a number of functional compartments: the bulge, which serves as a reservoir for hair stem cells, and the sebaceous gland, responsible for hair lubrication(it is the primary area to be attacked by T cells)
Modulation of inflammation by chondroitin sulfate.
Review article
Vallières M, et al. Osteoarthritis Cartilage. 2010.
Show full citation
Abstract
OBJECTIVE AND METHODS: To evaluate the immune-modulator effect of chondroitin sulfate (CS) by means of the review of the literature.
RESULTS: Inflammatory reactions are primarily originated by infectious agents, immune reactions and by sterile tissue lesions that activate membrane receptors by means of pathogen-associated molecular patterns, tissue breakdown products and cytokines. The activation of membrane receptors triggers the phosphorylation of mitogen activated protein kinases and of the nuclear factor kappaB (NF-kappaB). The binding of NF-kappaB to the promoter of target genes enhances the expression of pro-inflammatory cytokines, inducible nitric oxide synthase, cyclooxygenase 2, phospholipase A2, and matrix metalloproteases, proteins that contribute to tissue damage and to the inflammatory reaction. The activation of NF-kappaB has a key role in the immune homeostasis and the inflammatory response and therefore, in the pathogenesis of numerous diseases. Chondroitin sulfate (CS) is able to diminish NF-kappaB activation and nuclear translocation in chondrocytes and synovial membrane, effects that may explain the benefits of CS in osteoarthritis. In addition, systemic CS reduces NF-kappaB nuclear translocation in macrophages and hepatocytes, raising the hypothesis that CS might be of benefit to treat other diseases with a strong inflammatory component. There is preliminary evidence in humans that CS improves moderate to severe psoriasis. Moreover, experimental and clinical data suggest that CS might be a useful therapeutic agent in diseases such as inflammatory bowel diseases, atherosclerosis, Parkinson's and Alzheimer's diseases, multiple sclerosis, amyotrophic lateral sclerosis(this is caused by the same mechanism of Androgenetic Alopecia), rheumatoid arthritis and systemic lupus erythematosus.
DISCUSSION: These results urge for double blinded placebo-controlled trials to confirm the utility of CS in diseases with immune and inflammatory components.
PS* the synovial fluid in our joints are also made of chondroin sulfate protoglycans. They serve the same purpose, and that is to stop T cells from attacking the joints
of active macrophages around the dermal compartment.
In a similar way, in alopecia areata (a self-immune disease), the induction of these antigens seemed to be linked to the loss of CS57 parallel to a T-cell infiltration first restricted to the hair bulb including matrix cells58 and ultimately leading to hair loss. The lowermost part of the bulb thus appeared as a weakened area and the discontinuous distribution of GAGs, together with the disappearance of some of them in catagen,
might contribute to this overall degradation process.
It thus seems that GAG distribution around hair matrix results from contradictory needs. On the one hand, a weak expression of GAGs at the BM and in the CTS would support and favour a privileged nutrient diffusion, a decreased cell–BM adhesion and a high proliferation rate of matrix cells. On the other hand, the lack of some GAGs such as HS and CS would somehow weaken the hair follicle immune privilege. In conclusion, this complex and patterned PG and GAG distribution in the anagen hair is likely to reflect their strong involvement in hair biology. Differential expression suggests differential functionalities in nutrient diffusion, cell proliferation and differentiation, and hair growth maintenance.
= oral Chondroitin Sulfate(CS)
Reason:
To provide an immune privillege for the hair follicle to sustain anagen. Loss of Chondroitin sulfate protoglycans = T cells(T cell receptor signalling pathway aka immune cells) are free to attack the hair follicle along with the overloaded microbials living off the overabundant sebum enveloping the hair follicle
The outer root sheath is made up of Chondrotin sulfate-derived protoglycans. Androgenetic Alopecia-hairs have a lack of this structure.
The outer root sheath (ORS) is an extension of the epidermal basal layer which envelopes the entire hair follicle (HF). In addition, the ORS contains a number of functional compartments: the bulge, which serves as a reservoir for hair stem cells, and the sebaceous gland, responsible for hair lubrication(it is the primary area to be attacked by T cells)
Modulation of inflammation by chondroitin sulfate.
Review article
Vallières M, et al. Osteoarthritis Cartilage. 2010.
Show full citation
Abstract
OBJECTIVE AND METHODS: To evaluate the immune-modulator effect of chondroitin sulfate (CS) by means of the review of the literature.
RESULTS: Inflammatory reactions are primarily originated by infectious agents, immune reactions and by sterile tissue lesions that activate membrane receptors by means of pathogen-associated molecular patterns, tissue breakdown products and cytokines. The activation of membrane receptors triggers the phosphorylation of mitogen activated protein kinases and of the nuclear factor kappaB (NF-kappaB). The binding of NF-kappaB to the promoter of target genes enhances the expression of pro-inflammatory cytokines, inducible nitric oxide synthase, cyclooxygenase 2, phospholipase A2, and matrix metalloproteases, proteins that contribute to tissue damage and to the inflammatory reaction. The activation of NF-kappaB has a key role in the immune homeostasis and the inflammatory response and therefore, in the pathogenesis of numerous diseases. Chondroitin sulfate (CS) is able to diminish NF-kappaB activation and nuclear translocation in chondrocytes and synovial membrane, effects that may explain the benefits of CS in osteoarthritis. In addition, systemic CS reduces NF-kappaB nuclear translocation in macrophages and hepatocytes, raising the hypothesis that CS might be of benefit to treat other diseases with a strong inflammatory component. There is preliminary evidence in humans that CS improves moderate to severe psoriasis. Moreover, experimental and clinical data suggest that CS might be a useful therapeutic agent in diseases such as inflammatory bowel diseases, atherosclerosis, Parkinson's and Alzheimer's diseases, multiple sclerosis, amyotrophic lateral sclerosis(this is caused by the same mechanism of Androgenetic Alopecia), rheumatoid arthritis and systemic lupus erythematosus.
DISCUSSION: These results urge for double blinded placebo-controlled trials to confirm the utility of CS in diseases with immune and inflammatory components.
PS* the synovial fluid in our joints are also made of chondroin sulfate protoglycans. They serve the same purpose, and that is to stop T cells from attacking the joints
Last edited:
So reversing hair loss in Androgenetic Alopecia =
1)Topical Caffeine(for Sonic hedgehog. oral increases systemic arterial cholesterol levels, so going crazy on coffee might help your hair, but it would also increases your chances of getting cardio issues)
2)Topical or oral 5AR inhibitor(for sebum)
3)Topical anti-microbials(for the trigger of inflammation)
4)Oral Chondrotin sulfate(for inflammation itself)
1)Topical Caffeine(for Sonic hedgehog. oral increases systemic arterial cholesterol levels, so going crazy on coffee might help your hair, but it would also increases your chances of getting cardio issues)
2)Topical or oral 5AR inhibitor(for sebum)
3)Topical anti-microbials(for the trigger of inflammation)
4)Oral Chondrotin sulfate(for inflammation itself)
Last edited:
ASHGV40051 13.55103 Up NM_018325 C9orf72 9 Hs.4936 Chromosome 9 open reading frame 72
=upregulated in Androgenetic Alopecia scalp.
The protein is found in many regions of the brain, in the cytoplasm of neurons as well as in presynaptic terminals. Disease-causing mutations in the gene were first discovered by two independent research teams, led by Rosa Rademakers of Mayo Clinic and Bryan Traynor of the National Institutes of Health, and were first reported in October 2011.[6][7] The mutations in C9orf72 are significant because it is the first pathogenic mechanism identified to be a genetic link between familial frontotemporal dementia(FTD) and of amyotrophic lateral sclerosis (ALS). It is the most common mutation identified that is associated with familial FTD and/or ALS.[8]
"Frontotemporal" dementia. Androgenetic Alopecia is highly- correlated with neurodegenerative diseases in old age.
Neurons die at the frontal lobe with loss of dopaminergic pathways(Parkinson's)
Our hair follicles also die at the front of our scalp.
Hints strongly at our skull shape n the way our brain develops
=upregulated in Androgenetic Alopecia scalp.
The protein is found in many regions of the brain, in the cytoplasm of neurons as well as in presynaptic terminals. Disease-causing mutations in the gene were first discovered by two independent research teams, led by Rosa Rademakers of Mayo Clinic and Bryan Traynor of the National Institutes of Health, and were first reported in October 2011.[6][7] The mutations in C9orf72 are significant because it is the first pathogenic mechanism identified to be a genetic link between familial frontotemporal dementia(FTD) and of amyotrophic lateral sclerosis (ALS). It is the most common mutation identified that is associated with familial FTD and/or ALS.[8]
"Frontotemporal" dementia. Androgenetic Alopecia is highly- correlated with neurodegenerative diseases in old age.
Neurons die at the frontal lobe with loss of dopaminergic pathways(Parkinson's)
Our hair follicles also die at the front of our scalp.
Hints strongly at our skull shape n the way our brain develops
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https://www.verywellhealth.com/side-effects-of-glucosamine-88199
Side Effects of Chondroitin Sulfate
Chondroitin sulfate is naturally present in the cartilage surrounding your joints. The chondroitin sulfate found in dietary supplements is usually produced from animal sources, such as cow cartilage.
Mild stomach pain and nausea are the two side effects most frequently caused by chondroitin sulfate.
Chondroitin sulfate may also trigger the following side effects:
- constipation
- diarrhea
- hair loss
- irregular heartbeat
- swelling of the eyelids or legs
i didnt find any hair loss on it. Furthermore, i realised it gave me a strange, but positive side effect: rock-hard morning woods- something that ceased happening a about 6-7years ago as i move into my 30s. I stopped taking it because it gave me hard stools, which i attributed to the my habit of not drinking enough fluids and that CS reduces lactobacilus numbers in the intestinal tract.https://www.verywellhealth.com/side-effects-of-glucosamine-88199
Side Effects of Chondroitin Sulfate
Chondroitin sulfate is naturally present in the cartilage surrounding your joints. The chondroitin sulfate found in dietary supplements is usually produced from animal sources, such as cow cartilage.
Mild stomach pain and nausea are the two side effects most frequently caused by chondroitin sulfate.
Chondroitin sulfate may also trigger the following side effects:
- constipation
- diarrhea
- hair loss
- irregular heartbeat
- swelling of the eyelids or legs
ALso, i remember reading some1 mentioning that he found he had increased hair growth while on it somewhere in this forum. The mechanism by how that could have happen could be due to this.
Also, people have reported regrowing their hair taking anti-arthritic drugs ( https://www.ncbi.nlm.nih.gov/pubmed/19171984 ) - this could be the same mechanism by how Chondrotin sulfate stopped inflammation in their joints, because it grants the them immune privillege protection from inflammation induced by T cells by growing a thick layer of synovial fluid
Found it. here u go:
https://www.hairlosstalk.com/intera...-sulfate-for-hair-growth.122152/#post-1792413
Last edited:
It has also been reported that one key role of PG, and more specifically CS(<== chondropitin sulfate), is to preserve hair follicle immune privilege during the anagen stage.24 PG would envelop the follicle and act as a protective screen to prevent natural cytotoxic cells from recognizing the lack of ‘self’ histocompatibility antigens on bulb cells in the anagen hair follicle.24 Interestingly, 4C3-CS and PG4-CS ⁄DS epitopes progressively disappeared during catagen, as previously observed for C6S and C4S.24 By contrast, this phenomenon did not occur for type D chondroitin and HS. During the catagen phase and concomitantly with decline of some CS expression, an increase in major histocompatibility complex class I expression was noted in the follicle epithelial column together with an increased number (a1) (b1) (c1) (d1) (e1) (f1) (a3) (b3) (c3) (d3) (e3) (f3) (a2) (b2) (c2) (d2) (e2) Fig 4. Distribution of hair bulb proteoglycans at the anagen to catagen transition. Immunofluorescent stainings were done for 10E4-heparan sulphate (HS) (a1–3), perlecan (b1–3), type D chondroitin (c1–3), 4C3- chondroitin sulphate (CS) (d1–3), PG4- CS ⁄dermatan sulphate (DS) (e1–3) and aggrecan (f1, 3) epitopes in anagen (a1–f1), early catagen (a2–e2) and late catagen (a3–f3) follicles. After anagen to catagen transition, 10E4-HS, perlecan and type D chondroitin continued to be expressed in basement membrane (BM) and dermal papilla (DP). HS-positive anagen cortex cells disappeared in catagen. Intense DP 4C3-CS staining in anagen DP disappeared totally in early and late catagen. PG4-CS ⁄DS was present in BM of anagen and early catagen. The staining decreased in late catagen. PG4-CS ⁄DS remained negative in DP. During regression, aggrecan staining remained intense around the club hair but totally disappeared around the epithelial column. The DP became aggrecan positive in late catagen. 2007 The Authors Journal Compilation 2007 British Association of Dermatologists • British Journal of Dermatology 2008 158, pp234–242 240 Proteoglycans in human hair follicle, S. Malgouries et al. of active macrophages around the dermal compartment.24 In a similar way, in alopecia areata (a self-immune disease), the induction of these antigens seemed to be linked to the loss of CS57 parallel to a T-cell infiltration first restricted to the hair bulb including matrix cells58 and ultimately leading to hair loss. The lowermost part of the bulb thus appeared as a weakened area and the discontinuous distribution of GAGs, together with the disappearance of some of them in catagen, might contribute to this overall degradation process
= chondrotin sulfate is rich and active in the anagen phase, but disappears in catagen
Last edited:
Highlights
1. Up-regulation of CHSY1 endowed HCC with poor prognosis and malignant cellular behaviors.
2. Silence of CHSY1 suppressed malignant cellular behaviors in HCC cells.
3. CHSY1 promoted hedgehog signaling in vitro and in vivo. (Chsy1= Enzyme for making chondrotin sulfate)
4. Inhibition of hedgehog signaling suppressed CHSY1-induced malignant phenotypes.
Our results indicated that CHSY1 enhanced SHH-induced Ptch1 and Gli-2 expression (all 3 arey downregulated in Androgenetic Alopecia scalp)(Figure
4A). In contrast, CHSY1 expression did not significantly alter TGF-β and HGF induced signaling
(Supplementary Figure 2). These results suggest that CHSY1 selectively enhances the SHH signaling
pathway.
= Chondrotin sulfate upregulates Sonic hedgehog
1. Up-regulation of CHSY1 endowed HCC with poor prognosis and malignant cellular behaviors.
2. Silence of CHSY1 suppressed malignant cellular behaviors in HCC cells.
3. CHSY1 promoted hedgehog signaling in vitro and in vivo. (Chsy1= Enzyme for making chondrotin sulfate)
4. Inhibition of hedgehog signaling suppressed CHSY1-induced malignant phenotypes.
Our results indicated that CHSY1 enhanced SHH-induced Ptch1 and Gli-2 expression (all 3 arey downregulated in Androgenetic Alopecia scalp)(Figure
4A). In contrast, CHSY1 expression did not significantly alter TGF-β and HGF induced signaling
(Supplementary Figure 2). These results suggest that CHSY1 selectively enhances the SHH signaling
pathway.
= Chondrotin sulfate upregulates Sonic hedgehog
Last edited:
Upon further researching, several compounds addresses multiple causes of Androgenetic Alopecia. The goal here is to use as little compounds as possible.
1)Topical Caffeine shampoo
2)Oral Theaflavins and black tea
3)Topic cholesterol conditioner OR 'He shou wu' extract serum
4)Oral Chondrotin sulfate(=< 400mg/day)
Based what i can feel in myself now, i can vonfirm oral theaflavins n black tea + chondroitin sulfate is working excellently. No pain, no itch., Skin feels great. My mood is excellent. The black tea polyphenols r doing incredibly alot- its giving me positive neurogenic effects.
Black tea sachets x 3 in the morning(1 sachet = 3 cups of tea. about 10 cups equivalent)
Theaflavin capsule x 1 at night.
1)Topical Caffeine shampoo
2)Oral Theaflavins and black tea
3)Topic cholesterol conditioner OR 'He shou wu' extract serum
4)Oral Chondrotin sulfate(=< 400mg/day)
Based what i can feel in myself now, i can vonfirm oral theaflavins n black tea + chondroitin sulfate is working excellently. No pain, no itch., Skin feels great. My mood is excellent. The black tea polyphenols r doing incredibly alot- its giving me positive neurogenic effects.
Black tea sachets x 3 in the morning(1 sachet = 3 cups of tea. about 10 cups equivalent)
Theaflavin capsule x 1 at night.
Last edited:
- Reaction score
- 239
I dunno man, if any of these had any potency, they would have shown some results already. Black tea and coffee have been around forever.
Regime update:
After close to 3 weeks of experimenting, I have narrowed down and simplified to:
1)Alpecin Sports shampoo(Caffeine and Taurine)
The cDNA microarray analysis provided information about the gene transcripts of the components of signaling pathways involved in cell proliferation that were regulated in the taurine-containing cultures. The transcripts involved in the Wnt and Sonic hedgehog (Shh) pathways exhibited an increase between 1.5 and 4-fold in the taurine-containing cultures. The Wnt signaling pathway is a highly conserved pathway that plays an important role in brain development (Faigle and Song, 2013, Wei et al., 2012). The functional role of this pathway in NPCs derived from the hippocampus and SVZ has been demonstrated, in which Wnt promotes cell proliferation (Lie et al., 2005, Yu et al., 2006). The involvement of Shh in adult NPC proliferation is also well documented. Recent studies have shown that Shh overexpression in the adult hippocampus increases progenitor cell proliferation, whereas inhibition or conditional knock-out of elements of the Shh signaling pathway reduces this process (Lai et al., 2003, Machold et al., 2003). The activity of these two pathways might be regulated by taurine, as suggested by the DNA microarray analysis and corroborated by RT-PCR results, thus enhancing the proliferation of NPCs. However, taurine did not affect cell proliferation if present in cultures for only 1.5 h, a time that is likely sufficient to activate directly these proliferation pathways. A direct effect on nuclear transcription was also excluded because taurine was confined to the cytosol.
Caffeine ups SHH
Taurine ups SHH
2)Loreal serioxyl black and full (mixed with Astragaloside IV 98% raw powder) once daily, morning.
He Shou Wu extract ups SHH. The activate molecule in it that does this is THSG, a compound related to resveratrol.
3)Lipton Black tea sachets x 3 daily, throughout the day.
Total = 3 components- a beverage, a shampoo and a topical serum.
As stated, my ultimate goal is to simply my regime into a managable one for maintaiNing a high degree of self-compliance. Too cumbersome, and I will sometimes get lazy.
1)The black tea part is easy to maintain- I just drink and reuse the sachets (about 7-8 cups in total of tea) as my daily water intake.
2)Upon reaching home, I will shower and leave on the shampoo for 3 mins, before washing off and wait for another 10mins for it to exert its effects- and then:
3)apply the serum and leave it on for at least 45mins and go about using my com.
4)I bought my pure Astragaloside IV powder from a lab(not Astragaloside membranaceus extract- I got the active constituent that's in it)
https://en.m.wikipedia.org/wiki/Astragaloside
Astragaloside IV promotes the proliferation and migration of osteoblast-like cells through the hedgehog signaling pathway.
Guo LH, et al. Int J Mol Med. 2019.
Show full citation
Abstract
The present study aimed to investigate the effects of astragaloside IV on osteoblast‑like cell proliferation and migration, in addition to the underlying signaling pathway. In order to observe the effect on proliferation, a Cell Counting Kit‑8 assay and flow cytometry were used. To detect cell migration ability, cell scratch and Transwell cell migration assays were performed. The RNA and protein expression levels of hedgehog signaling molecules, including Sonic hedgehog (SHH) and GLI family zinc finger 1 (GLI1), were examined by reverse transcription‑quantitative polymerase chain reaction and western blot analyses. To inhibit the hedgehog signaling pathway, cyclopamine was used. Astragaloside IV, at a dosage of 1x10‑2 µg/ml in MG‑63 cells and 1x10‑3 µg/ml in U‑2OS cells, resulted in the enhanced proliferation and migration of cells, and the gene expression levels of the SHH and GLI1 were significantly increased. The combination of astragaloside IV and cyclopamine reduced MG‑63 and U‑2OS cell proliferation and migration, and inhibited the gene expression of SHH and GLI1. Astragaloside IV enhanced the proliferation and migration of human osteoblast‑like cells through activating the hedgehog signaling pathway. The results of the present study provide a rational for the mechanistic link in astragaloside IV promoting the proliferation and migration of osteoblasts via the hedgehog signaling pathway.
PMID
30535481 [Indexed for MEDLINE]
PMCID
PMC6317662
Beneficial effects of Astragaloside IV for hair loss via inhibition of Fas/Fas L-mediated apoptotic signaling.
Kim MH, et al. PLoS One. 2014.
Show full citation
Abstract
Apoptosis with premature termination of hair follicle growth induces several types of hair loss and is one of the crucial factors of hair loss. Astragaloside IV, which is a major component of Astragalus membranaceus, is a cycloartane triterpene saponin. Although an anti-apoptotic effect of Astragaloside IV has been reported, its effects against hair loss have not been investigated. To explore the underlying mechanisms of Astragaloside IV on apoptotic signaling in hair follicle, the dorsal skin of depilated C57BL/6 mice was topically treated with 1 and 100 μM Astragaloside IV for 14 days. In Astragaloside IV-treated group, TUNEL-positive cells were reduced. We found that Astragaloside IV blocked the procaspase-8, resulting in the inhibition of caspase-3 and procaspase-9 activities. The changes were accompanied with down-regulation of Bax and p53, and up-regulation of Bcl-2 and Bcl-xL by Astragaloside IV treatment. In addition, activation of NF-κB and phosphorylation of IκB-α were inhibited, along with decreases in three MAPKs: ERK, SAPK/JNK and p38 by Astragaloside IV. The expressions of KGF, p21, TNF-α and IL-1β, which are keratinocyte terminal differentiation markers associated with catagen, were modulated by treatment with Astragaloside IV. These results demonstrated that Astragaloside IV is concerned with blocking the Fas/Fas L-mediated apoptotic pathway, which would be an alternative therapy for hair loss.
PMID
24676213 [Indexed for MEDLINE]
PMCID
PMC3968031
Full text
= Astragaloside iv reduces cell death(by increasing SHH).
Astragaloside IV and cycloastragenol stimulate the phosphorylation of extracellular signal-regulated protein kinase in multiple cell types.
Yung LY, et al. Planta Med. 2012.
Show full citation
Abstract
Two Chinese herb-derived small molecule telomerase activators, astragaloside IV (AG-IV) and cycloastragenol (CAG), have recently been shown to improve the proliferative response of CD8+ T lymphocytes from HIV-infected patients by upregulating telomerase activity. Here, we examined the signaling mechanism of AG-IV and CAG. Telomerase activity in human embryonic kidney HEK293 fibroblasts was increased upon treatment with increasing concentrations of AG-IV or CAG. Both compounds induced the phosphorylation of extracellular signal-regulated protein kinase (ERK) in a time- and dose-dependent manner in HEK293 cells and HEK-neo keratinocytes. AG-IV and CAG also stimulated ERK phosphorylation in other cell lines of lung, brain, mammary, endothelial, and hematopoietic origins. Use of selective inhibitors and dominant negative mutants revealed the involvement of c-Src, MEK (ERK kinase), and epidermal growth factor receptor in CAG-induced ERK phosphorylation. Our data indicate that AG-IV and CAG may exert their cellular effects through the activation of the Src/MEK/ERK pathway.
© Georg Thieme Verlag KG Stuttgart · New York.
= Astragaloside extends telomeres
https://en.m.wikipedia.org/wiki/Telomerase
Astragaloside IV is a bioactive saponin first isolated from the dried plant roots of the genus Astragalus, which is used in traditional Chinese medicine.1 It dose-dependently inhibits human adenovirus type 3 (HAdV-3) in A549 cells (IC50 = 23 µM; LC50 = 865 µM).2 It inhibits replication of HAdV-3 and decreases HAdV-3-induced apoptosis. It has diverse protective effects for the cardiovascular, immune, digestive, and nervous systems.1,3 In particular, it reduces myocardial infarct size in dogs when administered prior to coronary ligation and reduces reperfusion arrhythmias in isolated rat hearts.4
Astragaloside iv is a kind of saponin and sanponins are a type of plant cholesterol.
As we know cholesterol is the ligand for hedgehog signalling.
Dumped 90mg of it into the serum(90ml) to make a 0.1% formulation.
After close to 3 weeks of experimenting, I have narrowed down and simplified to:
1)Alpecin Sports shampoo(Caffeine and Taurine)
The cDNA microarray analysis provided information about the gene transcripts of the components of signaling pathways involved in cell proliferation that were regulated in the taurine-containing cultures. The transcripts involved in the Wnt and Sonic hedgehog (Shh) pathways exhibited an increase between 1.5 and 4-fold in the taurine-containing cultures. The Wnt signaling pathway is a highly conserved pathway that plays an important role in brain development (Faigle and Song, 2013, Wei et al., 2012). The functional role of this pathway in NPCs derived from the hippocampus and SVZ has been demonstrated, in which Wnt promotes cell proliferation (Lie et al., 2005, Yu et al., 2006). The involvement of Shh in adult NPC proliferation is also well documented. Recent studies have shown that Shh overexpression in the adult hippocampus increases progenitor cell proliferation, whereas inhibition or conditional knock-out of elements of the Shh signaling pathway reduces this process (Lai et al., 2003, Machold et al., 2003). The activity of these two pathways might be regulated by taurine, as suggested by the DNA microarray analysis and corroborated by RT-PCR results, thus enhancing the proliferation of NPCs. However, taurine did not affect cell proliferation if present in cultures for only 1.5 h, a time that is likely sufficient to activate directly these proliferation pathways. A direct effect on nuclear transcription was also excluded because taurine was confined to the cytosol.
Caffeine ups SHH
Taurine ups SHH
2)Loreal serioxyl black and full (mixed with Astragaloside IV 98% raw powder) once daily, morning.
He Shou Wu extract ups SHH. The activate molecule in it that does this is THSG, a compound related to resveratrol.
3)Lipton Black tea sachets x 3 daily, throughout the day.
Total = 3 components- a beverage, a shampoo and a topical serum.
As stated, my ultimate goal is to simply my regime into a managable one for maintaiNing a high degree of self-compliance. Too cumbersome, and I will sometimes get lazy.
1)The black tea part is easy to maintain- I just drink and reuse the sachets (about 7-8 cups in total of tea) as my daily water intake.
2)Upon reaching home, I will shower and leave on the shampoo for 3 mins, before washing off and wait for another 10mins for it to exert its effects- and then:
3)apply the serum and leave it on for at least 45mins and go about using my com.
4)I bought my pure Astragaloside IV powder from a lab(not Astragaloside membranaceus extract- I got the active constituent that's in it)
https://en.m.wikipedia.org/wiki/Astragaloside
Astragaloside IV promotes the proliferation and migration of osteoblast-like cells through the hedgehog signaling pathway.
Guo LH, et al. Int J Mol Med. 2019.
Show full citation
Abstract
The present study aimed to investigate the effects of astragaloside IV on osteoblast‑like cell proliferation and migration, in addition to the underlying signaling pathway. In order to observe the effect on proliferation, a Cell Counting Kit‑8 assay and flow cytometry were used. To detect cell migration ability, cell scratch and Transwell cell migration assays were performed. The RNA and protein expression levels of hedgehog signaling molecules, including Sonic hedgehog (SHH) and GLI family zinc finger 1 (GLI1), were examined by reverse transcription‑quantitative polymerase chain reaction and western blot analyses. To inhibit the hedgehog signaling pathway, cyclopamine was used. Astragaloside IV, at a dosage of 1x10‑2 µg/ml in MG‑63 cells and 1x10‑3 µg/ml in U‑2OS cells, resulted in the enhanced proliferation and migration of cells, and the gene expression levels of the SHH and GLI1 were significantly increased. The combination of astragaloside IV and cyclopamine reduced MG‑63 and U‑2OS cell proliferation and migration, and inhibited the gene expression of SHH and GLI1. Astragaloside IV enhanced the proliferation and migration of human osteoblast‑like cells through activating the hedgehog signaling pathway. The results of the present study provide a rational for the mechanistic link in astragaloside IV promoting the proliferation and migration of osteoblasts via the hedgehog signaling pathway.
PMID
30535481 [Indexed for MEDLINE]
PMCID
PMC6317662
Beneficial effects of Astragaloside IV for hair loss via inhibition of Fas/Fas L-mediated apoptotic signaling.
Kim MH, et al. PLoS One. 2014.
Show full citation
Abstract
Apoptosis with premature termination of hair follicle growth induces several types of hair loss and is one of the crucial factors of hair loss. Astragaloside IV, which is a major component of Astragalus membranaceus, is a cycloartane triterpene saponin. Although an anti-apoptotic effect of Astragaloside IV has been reported, its effects against hair loss have not been investigated. To explore the underlying mechanisms of Astragaloside IV on apoptotic signaling in hair follicle, the dorsal skin of depilated C57BL/6 mice was topically treated with 1 and 100 μM Astragaloside IV for 14 days. In Astragaloside IV-treated group, TUNEL-positive cells were reduced. We found that Astragaloside IV blocked the procaspase-8, resulting in the inhibition of caspase-3 and procaspase-9 activities. The changes were accompanied with down-regulation of Bax and p53, and up-regulation of Bcl-2 and Bcl-xL by Astragaloside IV treatment. In addition, activation of NF-κB and phosphorylation of IκB-α were inhibited, along with decreases in three MAPKs: ERK, SAPK/JNK and p38 by Astragaloside IV. The expressions of KGF, p21, TNF-α and IL-1β, which are keratinocyte terminal differentiation markers associated with catagen, were modulated by treatment with Astragaloside IV. These results demonstrated that Astragaloside IV is concerned with blocking the Fas/Fas L-mediated apoptotic pathway, which would be an alternative therapy for hair loss.
PMID
24676213 [Indexed for MEDLINE]
PMCID
PMC3968031
Full text
= Astragaloside iv reduces cell death(by increasing SHH).
Astragaloside IV and cycloastragenol stimulate the phosphorylation of extracellular signal-regulated protein kinase in multiple cell types.
Yung LY, et al. Planta Med. 2012.
Show full citation
Abstract
Two Chinese herb-derived small molecule telomerase activators, astragaloside IV (AG-IV) and cycloastragenol (CAG), have recently been shown to improve the proliferative response of CD8+ T lymphocytes from HIV-infected patients by upregulating telomerase activity. Here, we examined the signaling mechanism of AG-IV and CAG. Telomerase activity in human embryonic kidney HEK293 fibroblasts was increased upon treatment with increasing concentrations of AG-IV or CAG. Both compounds induced the phosphorylation of extracellular signal-regulated protein kinase (ERK) in a time- and dose-dependent manner in HEK293 cells and HEK-neo keratinocytes. AG-IV and CAG also stimulated ERK phosphorylation in other cell lines of lung, brain, mammary, endothelial, and hematopoietic origins. Use of selective inhibitors and dominant negative mutants revealed the involvement of c-Src, MEK (ERK kinase), and epidermal growth factor receptor in CAG-induced ERK phosphorylation. Our data indicate that AG-IV and CAG may exert their cellular effects through the activation of the Src/MEK/ERK pathway.
© Georg Thieme Verlag KG Stuttgart · New York.
= Astragaloside extends telomeres
https://en.m.wikipedia.org/wiki/Telomerase
Astragaloside IV is a bioactive saponin first isolated from the dried plant roots of the genus Astragalus, which is used in traditional Chinese medicine.1 It dose-dependently inhibits human adenovirus type 3 (HAdV-3) in A549 cells (IC50 = 23 µM; LC50 = 865 µM).2 It inhibits replication of HAdV-3 and decreases HAdV-3-induced apoptosis. It has diverse protective effects for the cardiovascular, immune, digestive, and nervous systems.1,3 In particular, it reduces myocardial infarct size in dogs when administered prior to coronary ligation and reduces reperfusion arrhythmias in isolated rat hearts.4
Astragaloside iv is a kind of saponin and sanponins are a type of plant cholesterol.
As we know cholesterol is the ligand for hedgehog signalling.
Dumped 90mg of it into the serum(90ml) to make a 0.1% formulation.
Last edited:
Root cause of Androgenetic Alopecia
= increased Insulin sensitivity in the sebocytes of the balding scalp
Onset of puberty > suppressed FOXA2 in the balding scalp and pancreas> Insulin hyper secretion from b cells in the pancreas > enhanced Insulin/IGF-1 signalling > PGD2 upregulation + SOX9 downregulation in prostate > alox15 > 15 PGJ2 > PGC1A + PPAR gamma + Androgen receptor > chrebp Alpha > enhanced glucose uptake via GLU4 > etopic + enhanced lipogenesis aka lipid accumulation in sebocytes and at where the arrector pili muscle is > sebocyte hyperprofileration resulting in morphologically large, lipid-filled droplets accumulated in sebocytes > Malassezia fungi + Propiones acnes colony hyperexpansion at the lower half of the hair follicle in both the inner and outer root sheath, due to the increased sebum available as food source> lipase-generated oxidated free fatty acid > Crth2 from PGD2 >epidermal kerotinocyte hyperprofileration > dandruff + Androgenetic Alopecia + shiny scalp
An 'Antigen' = the presence of a foreign substance that provokes a immunity reponse from the body. So the microinflammation in the hair follicles is due to the immune system attacking that 'antigen'.
Here, the antigen is either the Malassezia/Propiones acnes themselves, or the oxidated free fatty acid byproduct generated by the lipase they produce.
The body is able to harmoniously tolerate the presence of these microbes living on our scalp in small amounts https://en.m.wikipedia.org/wiki/Microbiota , but when they grow out of proportion, the body switches to an eradication mode and starts attacking them.
= increased Insulin sensitivity in the sebocytes of the balding scalp
Onset of puberty > suppressed FOXA2 in the balding scalp and pancreas> Insulin hyper secretion from b cells in the pancreas > enhanced Insulin/IGF-1 signalling > PGD2 upregulation + SOX9 downregulation in prostate > alox15 > 15 PGJ2 > PGC1A + PPAR gamma + Androgen receptor > chrebp Alpha > enhanced glucose uptake via GLU4 > etopic + enhanced lipogenesis aka lipid accumulation in sebocytes and at where the arrector pili muscle is > sebocyte hyperprofileration resulting in morphologically large, lipid-filled droplets accumulated in sebocytes > Malassezia fungi + Propiones acnes colony hyperexpansion at the lower half of the hair follicle in both the inner and outer root sheath, due to the increased sebum available as food source> lipase-generated oxidated free fatty acid > Crth2 from PGD2 >epidermal kerotinocyte hyperprofileration > dandruff + Androgenetic Alopecia + shiny scalp
An 'Antigen' = the presence of a foreign substance that provokes a immunity reponse from the body. So the microinflammation in the hair follicles is due to the immune system attacking that 'antigen'.
Here, the antigen is either the Malassezia/Propiones acnes themselves, or the oxidated free fatty acid byproduct generated by the lipase they produce.
The body is able to harmoniously tolerate the presence of these microbes living on our scalp in small amounts https://en.m.wikipedia.org/wiki/Microbiota , but when they grow out of proportion, the body switches to an eradication mode and starts attacking them.
Last edited:
Malassezia and Propiones acnes are microbes that are lipid-dependent organisms. They can't make their own lipids, so they have to rely on parasiting n subsisting on host lipid sources to grow l. Everyone has them
In Androgenetic Alopecia scalps, they are overabundant due to the increased lipid food source(sebum)
They reside on the lower half of our hair follicle and in Androgenetic Alopecia, the t cells attack them and the hair follicle gets caught in the crossfire.
So the real question is:
Why does the balding scalp's sebobytes(but not those of the non-balding scalp of the same person) have an increased reponse to insulin, resulting in enhanced lipid accumulation?
In Androgenetic Alopecia scalps, they are overabundant due to the increased lipid food source(sebum)
They reside on the lower half of our hair follicle and in Androgenetic Alopecia, the t cells attack them and the hair follicle gets caught in the crossfire.
So the real question is:
Why does the balding scalp's sebobytes(but not those of the non-balding scalp of the same person) have an increased reponse to insulin, resulting in enhanced lipid accumulation?
Last edited:
- Reaction score
- 65
Adenosine increase hair growth, 0.75% adenosine solution is equal to 5% minoxidil https://www.ncbi.nlm.nih.gov/pubmed/24183218 plus some minoxidil effects are mediated through Adenosine 2b receptor https://www.ncbi.nlm.nih.gov/pubmed/11886528. Adenosine in scalp increases cAMP, caffeine blocks adenosine receptor but also it is PDE inhibotor which increases cAMP. PDE inhibitors which dont block adenosine receptor ( like sildenafil) also work for hair loss.
whatintheworld
Senior Member
- Reaction score
- 1,214
Notice any progress with this regimen?
Update:
after more research:
Hedgehog signalling => Wnt signalling => hair growth
so Wnt signalling is downstream of Gli2, a component of hedgehog signalling
so hedgehog signalling activates hair growth via wnt signalling
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5716664/
my newest regime:
Resveratrol
EGCG 0.05%
Baicalin 0.05%
Asthaxanthin 12mg x 2/day
after more research:
Hedgehog signalling => Wnt signalling => hair growth
so Wnt signalling is downstream of Gli2, a component of hedgehog signalling
so hedgehog signalling activates hair growth via wnt signalling
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5716664/
my newest regime:
Resveratrol
EGCG 0.05%
Baicalin 0.05%
Asthaxanthin 12mg x 2/day
Last edited:
Asthaxanthin is a must for any regime. it's a potent natural antioxidant that is heavily present in the Japanese diet which is seafood-based.
Pros:
1)Long half life-
72 hours (not half life, but remaining trace residues in the body)
"In the case of Astaxanthin, one dose has been shown to be detectable in serum for up to 72 hours and the known elimination half-life (T 1/2) - which is the time it takes for a substance to lose half of its original dose - is 16 hours.Mar 7, 2012"
Smoking significantly reduces the half life of asthaxanthin. So 1 can expect the mean half life to be between 10-16 hrs. That means 2 capsules/day, spaced 12hrs apart is good enough.
Now WHY is asthaxanthin important?
2 studies:
1) Abstract
Inhibition of 5alpha-reductase has been reported to decrease the symptoms of benign prostate hyperplasia (BPH) and possibly inhibit or help treat prostate cancer. Saw Palmetto berry lipid extract (SPLE) is reported to inhibit 5alpha-reductase and decrease the clinical symptoms of BPH. Epidemiologic studies report that carotenoids such as lycopene may inhibit prostate cancer. In this investigation the effect of the carotenoid astaxanthin, and SPLE were examined for their effect on 5alpha-reductase inhibition as well as the growth of prostatic carcinoma cells in vitro. These studies support patent #6,277,417 B1. The results show astaxanthin demonstrated 98% inhibition of 5alpha-reductase at 300 microg/mL in vitro. Alphastat, the combination of astaxanthin and SPLE, showed a 20% greater inhibition of 5alpha-reductase than SPLE alone n vitro. A nine day treatment of prostatic carcinoma cells with astaxanthin in vitro produced a 24% decrease in growth at 0.1 mcg/mL and a 38% decrease at 0.01 mcg/mL. SPLE showed a 34% decrease at 0.1 mcg/mL.
CONCLUSIONS:
Low levels of carotenoid astaxanthin inhibit 5alpha-reductase and decrease the growth of human prostatic cancer cells in vitro. Astaxanthin added to SPLE shows greater inhibition of 5alpha-reductase than SPLE alone in vitro.
2) Abstract
Background
Maintaining endogenous testosterone (T) levels as men age may slow the symptoms of sarcopenia, andropause and decline in physical performance. Drugs inhibiting the enzyme 5α-reductase (5AR) produce increased blood levels of T and decreased levels of dihydrotestosterone (DHT). However, symptoms of gynecomastia have been reported due to the aromatase (AER) enzyme converting excess T to estradiol (ES)(such as dutasteride and finasteride) The carotenoid astaxanthin (AX) from Haematococcus pluvialis, Saw Palmetto berry lipid extract (SPLE) from Serenoa repens and the precise combination of these dietary supplements, Alphastat® (Mytosterone(™)), have been reported to have inhibitory effects on both 5AR and AER in-vitro. Concomitant regulation of both enzymes in-vivo would cause DHT and ES blood levels to decrease and T levels to increase. The purpose of this clinical study was to determine if patented Alphastat® (Mytosterone(™)) could produce these effects in a dose dependent manner.
Results
ANOVA-RM showed significant within group increases in serum total T and significant decreases in serum DHT from baseline in both dose groups at a significance level of alpha = 0.05. Significant decreases in serum ES are reported for the 2000 mg/day dose group and not the 800 mg/day dose group. Significant within group effects were confirmed using ANOVA-2 analyses after baseline subtraction. ANOVA-2 analyses also showed no significant difference between dose groups with regard to the increase of T or the decrease of DHT. It did show a significant dose dependant decrease in serum ES levels.
Conclusion
Both dose groups showed significant (p = 0.05) increases in T and decreases in DHT within three days of treatment with Alphastat® (Mytosterone(™)). Between group statistical analysis showed no significant (p = 0.05) difference, indicating the effect was not dose dependent and that 800 mg/per day is equally effective as 2000 mg/day for increasing T and lowering DHT. Blood levels of ES however, decreased significantly (p = 0.05) in the 2000 mg/day dose group but not in the 800 mg/day dose group indicating a dose dependant decrease in E levels.
and there is a patent for using Asthaxanthin as a 5 alpha inhibitor:
https://patents.google.com/patent/US6277417B1/en
Method of inhibiting 5α-reductase with astaxanthin
Abstract
A method for inhibiting the activity of the enzyme 5α-reductase in a human subject is provided which comprises administering to the subject a composition comprising the carotenoid astaxanthin. Administration of the composition to inhibit the enzyme is useful to prevent and treat benign prostate hyperplasia (BPH) and prostate cancer in human males.
I'm using this:
So there u go, a natural proven DHT blocker without the deleterious side effect of finasteride and dutasteride(though i can feel their similarities and difference myself)
PPAR gamma causes Androgenetic Alopecia:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6584672/
Abstract
Current opinion views androgens as the pathogenic driver in the miniaturization of hair follicles of androgenetic alopecia by interfering with the dermal papilla. This cannot be the sole cause and therefore it is important for therapeutic and diagnostic purposes to identify additional pathways. Comparative full transcriptome profile analysis of the hair bulb region of normal and miniaturized hair follicles from vertex and occipital region in males with and without androgenetic alopecia revealed that next to the androgen receptor as well the retinoid receptor and particularly the PPAR pathway is involved in progressive hair miniaturization. We demonstrate the concurrent up-regulation of PPARGC1a in the epithelial compartment and androgen receptor in the dermal papilla of miniaturized hair. Dynamic Ppargc1a expression in the mouse hair cycle suggests a possible role in regulating hair growth and differentiation. This is supported by reduced proliferation of human dermal papilla and predominantly epithelial keratinocytes after incubation with AICAR, the agonist for AMPK signaling which activates PPARGC1a and serves as co-activator of PPARγ. In addition, miRNA profiling shows enrichment of miRNA-targeted genes in retinoid receptors and PPARGC1α/PPARγ signaling, and antigen presentation pathways.
hsa-miR-98-5p 0.00000126 −2.271 PPARGC1B 2.893 LPS/IL-1 Mediated Inhibition of RXR Function
hsa-miR-301b-3p 0.0000118 −6.39 PPARG 6.658 Adipogenesis pathway, ERK/MAPK Signaling, FXR/RXR Activation,
hsa-miR-138-5p 0.00781 −5.901 PPARGC1A 8.296 AMPK Signaling, Estrogen Receptor Signaling, FXR/RXR Activation
hsa-miR-27b-3p 6.84E-07 −2.189 PPARG 6.658 Adipogenesis pathway, ERK/MAPK Signaling, FXR/RXR Activation,
hsa-miR-92a-1-5p 0.00329 −5.08 PPARGC1A 8.296 AMPK Signaling, Estrogen Receptor Signaling, FXR/RXR Activation
hsa-miR-92a-1-5p 0.00329 −5.08 PPARGC1B 2.893 LPS/IL-1 Mediated Inhibition of RXR
Asthaxanthin does this:
The natural carotenoid astaxanthin, a PPAR-α agonist and PPAR-γ antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes.
Abstract
SCOPE:
A natural carotenoid abundant in seafood, astaxanthin (AX), has hypolipidemic activity, but its underlying mechanisms of action and protein targets are unknown. We investigated the molecular mechanism of action of AX in hepatic hyperlipidemia by measuring peroxisome proliferator-activated receptors (PPAR) activity.
METHODS AND RESULTS:
We examined the binding of AX to PPAR subtypes and its effects on hepatic lipid metabolism. AX binding activated PPAR-α, but inhibited PPAR-γ transactivation activity in reporter gene assay and time-resolved fluorescence energy transfer analyses. AX had no effect on PPARδ/β transactivation. AX bound directly to PPAR-α and PPAR-γ with moderate affinity, as assessed by surface plasmon resonance experiments. The differential effects of AX on PPARs were confirmed by measuring the expression of unique responsive genes for each PPAR subtype. AX significantly reduced cellular lipid accumulation in lipid-loaded hepatocytes. Transcriptome analysis revealed that the net effects of stimulation with AX (100 μM) on lipid metabolic pathways were similar to those elicited by fenofibrate and lovastatin (10 μM each), with AX rewiring the expression of genes involved in lipid metabolic pathways.
CONCLUSION:
AX is a PPAR-α agonist and PPAR-γ antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes.
https://benthamopen.com/FULLTEXT/TOMCJ-13-7
2.5. Astaxanthin
Astaxanthin is a natural carotenoid, found in a great variety of red-colored aquatic organisms, as salmon, crustaceans and microalgae (Fig. 4) [42]. It is structurally similar to beta-carotene, but it does not work as a precursor of vitamin A in the human organism. Thanks to its antioxidant activity, it is mainly used as a dietary supplement for human consumption, but also as a food colorant. Astaxanthin protects against lipid peroxidation and contrasts the oxidative damage of cells and tissues; its antiatherogenic effects were studied in animal models of cardiovascular diseases [43]. Additional beneficial activity of astaxanthin has been described in different studies, where it demonstrated hypolipidemic and antiatherogenic effects [44, 45]. In high cholesterol diet fed rats, astaxanthin induced a marked decrease of total cholesterol, Low-density Lipoprotein Cholesterol (LDL-C), Very Low-density Lipoprotein Cholesterol (VLDL-C) and triglycerides, and increased High-density Lipoprotein Cholesterol (HDL-C). A significant reduction in atherosclerotic lesions was observed on aorta of high cholesterol-fed rats, after treatment with astaxanthin [45]. The effects of astaxanthin on serum lipids prompted researchers to investigate about a possible mechanism of action involving PPAR receptors; the study by Jia and coworkers showed that astaxanthin works as moderate PPARα agonist (EC50 3.9 µM) and PPARγ antagonist (IC50 607.8 µM), whereas it is inactive versus PPARδ [46]. These findings were confirmed analyzing the expression profile of specific target genes for PPARα and PPARγ. In lipid-loaded hepatocytes, the treatment with astaxanthin produced a strong reduction of cellular lipid accumulation: these data support the potential of astaxanthin as nutritional prevention of obesity and metabolic disorders.
Pros:
1)Long half life-
72 hours (not half life, but remaining trace residues in the body)
"In the case of Astaxanthin, one dose has been shown to be detectable in serum for up to 72 hours and the known elimination half-life (T 1/2) - which is the time it takes for a substance to lose half of its original dose - is 16 hours.Mar 7, 2012"
Smoking significantly reduces the half life of asthaxanthin. So 1 can expect the mean half life to be between 10-16 hrs. That means 2 capsules/day, spaced 12hrs apart is good enough.
Now WHY is asthaxanthin important?
2 studies:
1) Abstract
Inhibition of 5alpha-reductase has been reported to decrease the symptoms of benign prostate hyperplasia (BPH) and possibly inhibit or help treat prostate cancer. Saw Palmetto berry lipid extract (SPLE) is reported to inhibit 5alpha-reductase and decrease the clinical symptoms of BPH. Epidemiologic studies report that carotenoids such as lycopene may inhibit prostate cancer. In this investigation the effect of the carotenoid astaxanthin, and SPLE were examined for their effect on 5alpha-reductase inhibition as well as the growth of prostatic carcinoma cells in vitro. These studies support patent #6,277,417 B1. The results show astaxanthin demonstrated 98% inhibition of 5alpha-reductase at 300 microg/mL in vitro. Alphastat, the combination of astaxanthin and SPLE, showed a 20% greater inhibition of 5alpha-reductase than SPLE alone n vitro. A nine day treatment of prostatic carcinoma cells with astaxanthin in vitro produced a 24% decrease in growth at 0.1 mcg/mL and a 38% decrease at 0.01 mcg/mL. SPLE showed a 34% decrease at 0.1 mcg/mL.
CONCLUSIONS:
Low levels of carotenoid astaxanthin inhibit 5alpha-reductase and decrease the growth of human prostatic cancer cells in vitro. Astaxanthin added to SPLE shows greater inhibition of 5alpha-reductase than SPLE alone in vitro.
2) Abstract
Background
Maintaining endogenous testosterone (T) levels as men age may slow the symptoms of sarcopenia, andropause and decline in physical performance. Drugs inhibiting the enzyme 5α-reductase (5AR) produce increased blood levels of T and decreased levels of dihydrotestosterone (DHT). However, symptoms of gynecomastia have been reported due to the aromatase (AER) enzyme converting excess T to estradiol (ES)(such as dutasteride and finasteride) The carotenoid astaxanthin (AX) from Haematococcus pluvialis, Saw Palmetto berry lipid extract (SPLE) from Serenoa repens and the precise combination of these dietary supplements, Alphastat® (Mytosterone(™)), have been reported to have inhibitory effects on both 5AR and AER in-vitro. Concomitant regulation of both enzymes in-vivo would cause DHT and ES blood levels to decrease and T levels to increase. The purpose of this clinical study was to determine if patented Alphastat® (Mytosterone(™)) could produce these effects in a dose dependent manner.
Results
ANOVA-RM showed significant within group increases in serum total T and significant decreases in serum DHT from baseline in both dose groups at a significance level of alpha = 0.05. Significant decreases in serum ES are reported for the 2000 mg/day dose group and not the 800 mg/day dose group. Significant within group effects were confirmed using ANOVA-2 analyses after baseline subtraction. ANOVA-2 analyses also showed no significant difference between dose groups with regard to the increase of T or the decrease of DHT. It did show a significant dose dependant decrease in serum ES levels.
Conclusion
Both dose groups showed significant (p = 0.05) increases in T and decreases in DHT within three days of treatment with Alphastat® (Mytosterone(™)). Between group statistical analysis showed no significant (p = 0.05) difference, indicating the effect was not dose dependent and that 800 mg/per day is equally effective as 2000 mg/day for increasing T and lowering DHT. Blood levels of ES however, decreased significantly (p = 0.05) in the 2000 mg/day dose group but not in the 800 mg/day dose group indicating a dose dependant decrease in E levels.
and there is a patent for using Asthaxanthin as a 5 alpha inhibitor:
https://patents.google.com/patent/US6277417B1/en
Method of inhibiting 5α-reductase with astaxanthin
Abstract
A method for inhibiting the activity of the enzyme 5α-reductase in a human subject is provided which comprises administering to the subject a composition comprising the carotenoid astaxanthin. Administration of the composition to inhibit the enzyme is useful to prevent and treat benign prostate hyperplasia (BPH) and prostate cancer in human males.
I'm using this:
So there u go, a natural proven DHT blocker without the deleterious side effect of finasteride and dutasteride(though i can feel their similarities and difference myself)
PPAR gamma causes Androgenetic Alopecia:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6584672/
Abstract
Current opinion views androgens as the pathogenic driver in the miniaturization of hair follicles of androgenetic alopecia by interfering with the dermal papilla. This cannot be the sole cause and therefore it is important for therapeutic and diagnostic purposes to identify additional pathways. Comparative full transcriptome profile analysis of the hair bulb region of normal and miniaturized hair follicles from vertex and occipital region in males with and without androgenetic alopecia revealed that next to the androgen receptor as well the retinoid receptor and particularly the PPAR pathway is involved in progressive hair miniaturization. We demonstrate the concurrent up-regulation of PPARGC1a in the epithelial compartment and androgen receptor in the dermal papilla of miniaturized hair. Dynamic Ppargc1a expression in the mouse hair cycle suggests a possible role in regulating hair growth and differentiation. This is supported by reduced proliferation of human dermal papilla and predominantly epithelial keratinocytes after incubation with AICAR, the agonist for AMPK signaling which activates PPARGC1a and serves as co-activator of PPARγ. In addition, miRNA profiling shows enrichment of miRNA-targeted genes in retinoid receptors and PPARGC1α/PPARγ signaling, and antigen presentation pathways.
hsa-miR-98-5p 0.00000126 −2.271 PPARGC1B 2.893 LPS/IL-1 Mediated Inhibition of RXR Function
hsa-miR-301b-3p 0.0000118 −6.39 PPARG 6.658 Adipogenesis pathway, ERK/MAPK Signaling, FXR/RXR Activation,
hsa-miR-138-5p 0.00781 −5.901 PPARGC1A 8.296 AMPK Signaling, Estrogen Receptor Signaling, FXR/RXR Activation
hsa-miR-27b-3p 6.84E-07 −2.189 PPARG 6.658 Adipogenesis pathway, ERK/MAPK Signaling, FXR/RXR Activation,
hsa-miR-92a-1-5p 0.00329 −5.08 PPARGC1A 8.296 AMPK Signaling, Estrogen Receptor Signaling, FXR/RXR Activation
hsa-miR-92a-1-5p 0.00329 −5.08 PPARGC1B 2.893 LPS/IL-1 Mediated Inhibition of RXR
Asthaxanthin does this:
The natural carotenoid astaxanthin, a PPAR-α agonist and PPAR-γ antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes.
Abstract
SCOPE:
A natural carotenoid abundant in seafood, astaxanthin (AX), has hypolipidemic activity, but its underlying mechanisms of action and protein targets are unknown. We investigated the molecular mechanism of action of AX in hepatic hyperlipidemia by measuring peroxisome proliferator-activated receptors (PPAR) activity.
METHODS AND RESULTS:
We examined the binding of AX to PPAR subtypes and its effects on hepatic lipid metabolism. AX binding activated PPAR-α, but inhibited PPAR-γ transactivation activity in reporter gene assay and time-resolved fluorescence energy transfer analyses. AX had no effect on PPARδ/β transactivation. AX bound directly to PPAR-α and PPAR-γ with moderate affinity, as assessed by surface plasmon resonance experiments. The differential effects of AX on PPARs were confirmed by measuring the expression of unique responsive genes for each PPAR subtype. AX significantly reduced cellular lipid accumulation in lipid-loaded hepatocytes. Transcriptome analysis revealed that the net effects of stimulation with AX (100 μM) on lipid metabolic pathways were similar to those elicited by fenofibrate and lovastatin (10 μM each), with AX rewiring the expression of genes involved in lipid metabolic pathways.
CONCLUSION:
AX is a PPAR-α agonist and PPAR-γ antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes.
https://benthamopen.com/FULLTEXT/TOMCJ-13-7
2.5. Astaxanthin
Astaxanthin is a natural carotenoid, found in a great variety of red-colored aquatic organisms, as salmon, crustaceans and microalgae (Fig. 4) [42]. It is structurally similar to beta-carotene, but it does not work as a precursor of vitamin A in the human organism. Thanks to its antioxidant activity, it is mainly used as a dietary supplement for human consumption, but also as a food colorant. Astaxanthin protects against lipid peroxidation and contrasts the oxidative damage of cells and tissues; its antiatherogenic effects were studied in animal models of cardiovascular diseases [43]. Additional beneficial activity of astaxanthin has been described in different studies, where it demonstrated hypolipidemic and antiatherogenic effects [44, 45]. In high cholesterol diet fed rats, astaxanthin induced a marked decrease of total cholesterol, Low-density Lipoprotein Cholesterol (LDL-C), Very Low-density Lipoprotein Cholesterol (VLDL-C) and triglycerides, and increased High-density Lipoprotein Cholesterol (HDL-C). A significant reduction in atherosclerotic lesions was observed on aorta of high cholesterol-fed rats, after treatment with astaxanthin [45]. The effects of astaxanthin on serum lipids prompted researchers to investigate about a possible mechanism of action involving PPAR receptors; the study by Jia and coworkers showed that astaxanthin works as moderate PPARα agonist (EC50 3.9 µM) and PPARγ antagonist (IC50 607.8 µM), whereas it is inactive versus PPARδ [46]. These findings were confirmed analyzing the expression profile of specific target genes for PPARα and PPARγ. In lipid-loaded hepatocytes, the treatment with astaxanthin produced a strong reduction of cellular lipid accumulation: these data support the potential of astaxanthin as nutritional prevention of obesity and metabolic disorders.
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action is better than inaction, even if the former is futile.