Starting A New Regime As Of 1st July 2019

sktboiboi

Banned
My Regimen
Reaction score
98
Androgenetic Alopecia =


1)upregulation of the T cell receptor signalling pathway(Th1 + Th2)
2)downregulation of the Hedgehog signalling pathway(Sonic hedgehog)

Upregulation of the T cell receptor signalling pathway = upregulation of the immune system against the hair follicles- or to be more specifically- against the pathogens feeding on the sebum enveloping the hair follicles. Activation of the immune system is a reactive step taken by the body to fend off the microbes.

Sebum is drastically increased by DHT


Androgenetic Alopecia =

Balding scalp area is genetically-patterned and predetermined to secrete large amounts of:

5 alpha redutase mainly type 1 and type 2 in some compartments of the hair follicle => DHT => androgen receptor => hyperinsulinemia => Adiponectin upregulation=> AMPK signalling upregulation => Sebocyte hyperprofileration => Malassezia(furfur, goblosa, restricta) + Propionibacterium acnes overgrowth => activation of both innate(Th1) and adaptive(Th2) immunity => chronic inflammation => Androgenetic Alopecia

SO:


*MODIFIED*

6 components:

Dermarolling just once as initial opener of new regime


5 Alpha redutase inhibitors for sebum:

Black tea sachets: 2/day, morning
Theaflavin 87.5mg: 1 capsule/day, night

Anti-Malessezia and anti-Propionibacterium acnes anti-microbials

Caffeine + Zinc PCA shampoo: 6days/week, 5mins leave on, morning

Ciclopirox olamine + Zinc prythione shampoo 6days/week, 5 mins leave on, night

Hedghog signalling upregulator:

Polygonum multiflorum Thunb extract serum: 6days/week, 2hrs leave on, morning

T cell receptor signalling downregulator:

Chondrotin sulfate 600mg: 2 capsules/day, day and night








WOniW7d
 
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sktboiboi

Banned
My Regimen
Reaction score
98
How i came up with this regime:

EGCG:

use sci-hub

https://www.ncbi.nlm.nih.gov/pubmed/27239811

We validated five up-regulated genes in PV compared to PO (CYB5R3, FADS2, PTGDS, SDHA and SRD5A1) with RT-qPCR, and found expression trend concurred with RNA-seq observations (Figure 2H).

= 5 Alpha redutase type 1 is elevated in balding scalp, which is affirmed by:

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2003001000024

The 5alpha-reductase type 1, but not type 2, gene is expressed in anagen hairs plucked from the vertex area (balding scalp) of the scalp of hirsute women and normal individuals







So:







https://www.ncbi.nlm.nih.gov/pubmed/11931850

Structure-activity relationships for inhibition of human 5alpha-reductases by polyphenols.
Hiipakka RA1, Zhang HZ, Dai W, Dai Q, Liao S.
Author information
Abstract

The enzyme steroid 5 alpha-reductase (EC 1.3.99.5) catalyzes the NADPH-dependent reduction of the double bond of a variety of 3-oxo-Delta(4) steroids including the conversion of testosterone to 5 alpha-dihydrotestosterone. In humans, 5 alpha-reductase activity is critical for certain aspects of male sexual differentiation, and may be involved in the development of benign prostatic hyperplasia, alopecia, hirsutism, and prostate cancer. Certain natural products contain components that are inhibitors of 5 alpha-reductase, such as the green tea catechin (-)-epigallocatechin gallate (EGCG). EGCG shows potent inhibition in cell-free but not in whole-cell assays of 5 alpha-reductase. Replacement of the gallate ester in EGCG with long-chain fatty acids produced potent 5 alpha-reductase inhibitors that were active in both cell-free and whole-cell assay systems. Other flavonoids that were potent inhibitors of the type 1 5alpha-reductase include myricetin, quercitin, baicalein, and fisetin. Biochanin A, daidzein, genistein, and kaempferol were much better inhibitors of the type 2 than the type 1 isozyme. Several other natural and synthetic polyphenolic compounds were more effective inhibitors of the type 1 than the type 2 isozyme, including alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates. The presence of a catechol group was characteristic of almost all inhibitors that showed selectivity for the type 1 isozyme of 5 alpha-reductase. Since some of these compounds are consumed as part of the normal diet or in supplements, they have the potential to inhibit 5 alpha-reductase activity, which may be useful for the prevention or treatment of androgen-dependent disorders. However, these compounds also may adversely affect male sexual differentiation.

= EGCG is a selective inhibitor of the Type1 isoenzyme of 5 alpha redutase(read the study to discover this)

For comparison,

Dutatasteride inhibits both Type 1 and Type 2 equally well
Finasteride inhibits Type 2 selectively
Isoflavones(biochanin a, genistein, daizein, equol) inhibits Type 2 selectively

Type 1 is mainly found in the skin, hair and liver
Type 2 is mainly found in the prostate, testicles and foreskin


EGCG's half life =

https://en.wikipedia.org/wiki/Epigallocatechin_gallate

0 to 8 hours
After consumption, EGCG blood levels peak within 1.7 hours. The absorbed plasma half-life is ~5 hours, but with majority of unchanged EGCG excreted into urine over 0 to 8 hours. Methylated metabolites appear to have longer half-lives and occur at 8-25 times the plasma levels of unmetabolized EGCG.

Bioavailability[edit]
When taken orally, EGCG has poor absorption even at daily intake equivalent to 8–16 cups of green tea, an amount causing adverse effects such as nausea or heartburn.[5] After consumption, EGCG blood levels peak within 1.7 hours.[6] The absorbed plasma half-life is ~5 hours,[6] but with majority of unchanged EGCG excreted into urine over 0 to 8 hours.[6] Methylated metabolites appear to have longer half-lives and occur at 8-25 times the plasma levels of unmetabolized EGCG.[7]


So twice/day is reasonable, ~2hrs before eating anything.




 
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sktboiboi

Banned
My Regimen
Reaction score
98
DHT increases sebum by enlarging sebocyte profileration. Bacteria and yeast uses sebum as nutrition.

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0216330

Microbiome in the hair follicle of androgenetic alopecia patients

Abstract
Androgenetic alopecia is the most common form of hair loss in males. It is a multifactorial condition involving genetic predisposition and hormonal changes. The role of microflora during hair loss remains to be understood. We therefore analyzed the microbiome of hair follicles from hair loss patients and the healthy. Hair follicles were extracted from occipital and vertex region of hair loss patients and healthy volunteers and further dissected into middle and lower compartments. The microbiome was then characterized by 16S rRNA sequencing. Distinct microbial population were found in the middle and lower compartment of hair follicles. Middle hair compartment was predominated by Burkholderia spp. and less diverse; while higher bacterial diversity was observed in the lower hair portion. Occipital and vertex hair follicles did not show significant differences. In hair loss patients, miniaturized vertex hair houses elevated Propionibacterium acnes in the middle and lower compartments while non-miniaturized hair of other regions were comparable to the healthy. Increased abundance of P. acnes in miniaturized hair follicles could be associated to elevated immune response gene expression in the hair follicle.

https://en.wikipedia.org/wiki/Cutibacterium_acnes

=the immune response in the balding scalp is a reaction to an increased quantity of pain-causing bacteria and itch-causing yeast, feeding off the increased sebum















https://link.springer.com/article/10.1007/s11046-019-00345-8

Investigation on Microecology of Hair Root Fungi in Androgenetic Alopecia Patients

Abstract
Background
This study focused on the differences in hairy root fungal microecology between androgenetic alopecia patients and healthy individuals.

Methods
Light microscopy was used to observe the morphology of hairy roots. Morphological observations were also performed in the positive specimens using scanning electron microscopy and transmission electron microscopy. The high-throughput sequencing method was used to detect the fungal microecology of hairy roots at different sites. Moreover, the comparison of fungal loads of Malassezia in different group and scalp area were tested by PCR.

Results
The fungi in the hair root observed by optical microscopy are mainly Malassezia yeast. The positive rate of Malassezia in the hair loss group (60%) was higher than that in the control group (40%). The detection efficiency of Malassezia examined by scanning electron microscopy was higher than that by light microscopy. Results acquired from high-throughput molecular sequencing of fungi suggested that Ascomycota was the dominant species, whereas in the occipital hair roots of the control group Basidiomycota was the dominant species in the hair loss group. Malassezia followed by Trichosporon were the most abundant fungal genera. The changes in abundance at the top and occipital region of the control group were more significant than those of the genus Fusarium, followed by Epicoccum and Malassezia. The load of Malassezia located on calvaria in the alopecia group was significantly higher than that in the control group. In the alopecia group, the load of Malassezia on the scalp was higher than that on the occipital region. The load of Malassezia globosa and Malassezia restricta in the hair loss group was higher on calvaria and occipital areas.

Conclusion
Malassezia had a positive correlation with the incidence of androgenic alopecia.

https://en.wikipedia.org/wiki/Malassezia

Role in human diseases[edit]
Identification of Malassezia on skin has been aided by the application of molecular or DNA-based techniques. These investigations show that the Malassezia species causing most skin disease in humans, including the most common cause of dandruff and seborrhoeic dermatitis, is M. globosa (though M. restricta is also involved).[8] The skin rash of tinea versicolor (pityriasis versicolor) is also due to infection by this fungus.

As the fungus requires fat to grow,[4] it is most common in areas with many sebaceous glands: on the scalp,[16] face, and upper part of the body. When the fungus grows too rapidly, the natural renewal of cells is disturbed, and dandruff appears with itching (a similar process may also occur with other fungi or bacteria).

A project in 2007 has sequenced the genome of dandruff-causing Malassezia globosa and found it to have 4,285 genes.[17] M. globosa uses eight different types of lipase, along with three phospholipases, to break down the oils on the scalp. Any of these 11 proteins would be a suitable target for dandruff medications.

M. globosa has been predicted to have the ability to reproduce sexually,[18] but this has not been observed.





















So:

Antimicrobial effects of tea-tree oil and its major components on Staphylococcus aureus, Staph. epidermidis and Propionibacterium acnes.
Raman A1, Weir U, Bloomfield SF.
Author information

Abstract
Major components of two tea-tree oil samples were identified using thin layer and gas-liquid chromatography (TLC and GLC). Using a TLC-bioautographic technique, the tea-tree oils, terpinen-4-ol, alpha-terpineol and alpha-pinene were found to be active against Staphylococcus aureus, Staph. epidermidis and Propionibacterium acnes whereas cineole was inactive against these organisms. The MIC values of the three active compounds increased in the order alpha-terpineol < terpinen-4-ol < alpha-pinene for all three micro-organisms. MIC values of the tea-tree oils and terpinen-4-ol were lower for P. acnes than for the two staphylococci. This study supports the use of tea-tree oil in the treatment of acne, and demonstrates that terpinen-4-ol is not the sole active constituent of the oil.


In Vitro Activities of Ketoconazole, Econazole, Miconazole, and Melaleuca alternifolia (Tea Tree) Oil against Malassezia Species

The MICs shown in Table 1 demonstrate that ketoconazole was the most active of the imidazoles, followed by miconazole and econazole, which were similar in activity. M. furfur was the species least susceptible to imidazoles: the remaining species were similar. Tea tree oil was active against allMalassezia species, for which the MICs were similar.


Tea tree oil and products containing the oil have been evaluated in vivo for the treatment of superficial fungal infections such as onychomycosis and oral candidiasis, with some favorable clinical outcomes (1, 9). Reports have been published previously describing the in vitro susceptibility of Malassezia species to tea tree oil (6, 17), and the present study confirms and extends these findings. However, there are no reports on the use of tea tree oil specifically for the treatment of Malassezia skin infections. Most tea tree oil products contain 5 to 10% tea tree oil, and this is likely to be adequate for clinical use. Different commercially available 100% tea tree oils vary little in their antimicrobial activity (2), however, the activity of tea tree oil can be antagonized by various excipients used in the formulation of products (7). In addition, as with many topical agents, there is a low risk of allergic reactions to 100% tea tree oil. We have recently shown the prevalence of such allergy to be approximately 5% (Greig et al., unpublished data).

In conclusion, this work has shown that individualMalassezia species vary in their susceptibility to several antifungal agents, with M. furfur being the least susceptible of the species tested. Tea tree oil may be a suitable alternative topical agent. In view of the apparent emergence ofMalassezia as opportunistic pathogens, these data may have clinical significance.



= Tea tree oil kills both acne-causing bacteria and dandruff-causing yeast


 
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sktboiboi

Banned
My Regimen
Reaction score
98
I have covered the rationale for using the 2 natural solutions, egcg, which is found in the leaves of the https://en.wikipedia.org/wiki/Camellia_sinensis aka green tea and tee tree oil, which is extracted from the leaves of the https://en.wikipedia.org/wiki/Melaleuca_alternifolia (the tree secretes the substances found in its leaves to ward off fungus growing on it)


while their roles are addressing the trigger of Androgenetic Alopecia, they are not the atual solution though. Clobetasol propionate and pimecrolimus are the 1s that will be regrowing hair(hopefully)




to be continued on the remaining 2 when i have the time.
 
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sktboiboi

Banned
My Regimen
Reaction score
98
*MODIFIED*

5 components:

Dermarolling just once as initial opener of new regime


Lipton Black tea(unsweetened and unflavored): 2 sachets/day
Tea Tree oil shampoo: once/day, 6days/week, 15 mins leave on
Clobetasol propionate shampoo(Clobex): once/day, 3 days/week, 15 mins(max) leave on
Caffeine + EGCG serum: 6days/week, 2 hrs leave on
Polygonum multiflorum Thunb extract serum: 6days/week, 2hrs leave on




WOniW7d
Why black tea:

this is atually more for my body than hair.

Abstract
Although high doses of single bioactive agents may have potent anticancer effects, the chemopreventive properties of the Asian diet may result from interactions among several components that potentiate the activities of any single constituent. In Asia, where intake of soy products and tea consumption are very high, aggressive prostate cancer is significantly less prevalent in Asian men. The objective of the present study was to identify possible synergistic effects between soy and tea components on prostate tumor progression in a mouse model of orthotopic androgen-sensitive human prostate cancer. Soy phytochemical concentrate (SPC), black tea and green tea were compared with respect to tumorigenicity rate, primary tumor growth, tumor proliferation index and microvessel density, serum androgen level and metastases to lymph nodes. SPC, black tea and green tea significantly reduced tumorigenicity. SPC and black tea also significantly reduced final tumor weights. Green tea did not reduce final tumor weight, although it tended to elevate (P = 0.14) the serum dihydrotestosterone (DHT) concentration. The combination of SPC and black tea synergistically inhibited prostate tumorigenicity, final tumor weight and metastases to lymph nodes in vivo. The combination of SPC and green tea synergistically inhibited final tumor weight and metastasis and significantly reduced serum concentrations of both testosterone and DHT in vivo. Inhibition of tumor progression was associated with reduced tumor cell proliferation and tumor angiogenesis. This study suggests that further research is warranted to study the role of soy and tea combination as effective nutritional regimens in prostate cancer prevention.


=

Green tea increases testeterone and DHT
Black tea also increases testerone, but decreases DHT

Mice treated with black tea tended to have a greater serum testosterone concentration (34.4%, P = 0.50) and had a 72% lower DHT concentration than controls (P < 0.05), suggesting that black tea may contain components that inhibit the activity of 5α-reductase, an enzyme that converts testosterone to the more bioactive DHT. Green tea tended to increase serum testosterone and DHT levels by 73.8% (P = 0.14) and 194% (P = 0.076), respectively. The combination of SPC and green tea reduced serum levels of DHT (P < 0.05).




Type1 5AR is mainly expressed in the scalp and liver. it is still found in the genitalia and other parts of the body.

Type 2 5AR is mainly expressed in the genitalia. It is still found in the scalp and other parts of the body.


Green tea increases DHT probably because there's some other constituents in it that does so, not EGCG, as can be seen in:

"On the other hand, green tea did not reduce the serum level of DHT, but instead tended to increase it (P = 0.076) (Fig. 2D), and we found that green tea treatment did not inhibit tumor growth (Fig. 1A). Green tea contained more EGCG than black tea (Table 1), and studies have shown that EGCG inhibits the activity of 5α-reductase (38). These results derived from our animal model suggest that, although EGCG may be a potent antitumor agent in green tea and inhibit 5α-reducatase activity, green tea contains other constituents that may counteract EGCG's antitumor activity, in part by counteracting its modulation of 5α-reducatase activity."


=

it's been established that EGCG inhibits 5AR type 1 selectively- and type 1 is only weakly expressed in the genitalia. Hence, this is why it does not significantly reduced prostate tumors. Black tea does significantly reduce prostate tumors- . a likelihood is it inhibits the Type 2 isoenzyme way more than whatever is in Green tea


So Black tea gives a 35% increase in testoerone levels, while reducing DHT levels by 72%

EGCG itself gives a reduction in DHT levels(via selective inhibition of Type1 5AR), but its unknown co-constituents in Green tea increases it. So it's ok to take just EGCG, but not Green Tea extract as a whole.




A cheap and simple method to know whether black tea increases testosterone for you.


1)buy a small box of unsweetened and unflavored black tea sachets( i use Lipton). u can get them from the supermarket and they are cheap.
2)drink 4-5 cups by simply reusing 1-2 sachets. do it at least 2hrs before u eat anything.(if u drink green/black tea with a meal, u are going to get a noticeable stomach bloatedness. this is likely the compoennts in teas inhibit some cytochrome enzymes in the liver and results in inproper digestion)
3) after 1-2 hrs of ingesting, listen for any changes in your own voice. If there's a noticeable added deep bass to it other than how it normally sounds- that's a sign that your body's testerone has increased.

"High testosterone levels predict low voice pitchamong men
Author links open overlay panelJames MDabbsJr.1AlisonMallinger1
https://doi.org/10.1016/S0191-8869(98)00272-4Get rights and content
Abstract
We measured salivary testosterone levels and voice pitch, or fundamental frequency,among 61 male and 88 female college students. Higher levels of testosterone were significantlyassociated with lower pitched voices among males but not among females. The magnitude of theeffect was approximately the same as the magnitude of other relationships that have beenreported between testosterone and behavior. There are two plausible explanations of a linkbetween testosterone and pitch. One explanation is physiological, in which testosterone changesthe bulk, length, or tension of the vocal folds. The other is psychological, in which testosteroneaffects the vocal style that an individual uses as part of a social interaction strategy."
 
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sktboiboi

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Why caffeine:

Caffeine induces sonic hedgehog gene expression in cultured astrocytes and neurons.
Sahir N1, Evrard P, Gressens P.
Author information
Abstract
Caffeine affects early in vivo murine brain development by accelerating the evagination of the primitive neuroepithelium into telencephalic vesicles. In this model, caffeine induces the expression of the regulatory subunit alpha of protein kinase A (PKA RI alpha) and of Sonic hedgehog (Shh). The understanding of the molecular mechanisms linking caffeine and neural gene expression would benefit from a reproducible in vitro model. Accordingly, the present study aimed to determine whether caffeine modulated the expression of these genes in primary neuronal and astroglial cultures derived from developing murine neocortex. Using real-time PCR, the results showed that caffeine induced robust overexpression of Shh mRNA in both cell types without significantly modifying PKA RI alpha gene expression.




Also, there are tons of hair growth products out in the market already including caffeine as a component, likely via other mechanisms that's conducive to hair growth in Androgenetic Alopecia, which is caused by 2 factors:

Downregulation of the Hedgehog signalling pathway(Sonic hedgehog)
Upregulation of the T cell receptor signalling pathway(Th1 and Th2, but not Th17)
 
Last edited:

sktboiboi

Banned
My Regimen
Reaction score
98
Why caffeine:

Caffeine induces sonic hedgehog gene expression in cultured astrocytes and neurons.
Sahir N1, Evrard P, Gressens P.
Author information
Abstract
Caffeine affects early in vivo murine brain development by accelerating the evagination of the primitive neuroepithelium into telencephalic vesicles. In this model, caffeine induces the expression of the regulatory subunit alpha of protein kinase A (PKA RI alpha) and of Sonic hedgehog (Shh). The understanding of the molecular mechanisms linking caffeine and neural gene expression would benefit from a reproducible in vitro model. Accordingly, the present study aimed to determine whether caffeine modulated the expression of these genes in primary neuronal and astroglial cultures derived from developing murine neocortex. Using real-time PCR, the results showed that caffeine induced robust overexpression of Shh mRNA in both cell types without significantly modifying PKA RI alpha gene expression.




Also, there are tons of hair growth products out in the market already including caffeine as a component, likely via other mechanisms that's conducive to hair growth in Androgenetic Alopecia, which is caused by 2 factors:

Downregulation of the Hedgehog signalling pathway(Sonic hedgehog)
Upregulation of the T cell receptor signalling pathway(Th1 and Th2, but not Th17)
So the study stated thESE:

The present results are in agreement with our previous work (Sahir et al., 2001), showing that caffeine increases Shh gene expression. In contrast, caffeine did not induce significant PKA RI α gene overexpression in primary cortical cultures, whereas in an
earlier study caffeine increased PKARIαgene expression in early postimplantatory neural tubes

The mechanisms by which caffeine induces Shh
gene expression remain unknown. Caffeine has been shown to block adenosine receptors. Adenosine receptors are G protein-coupled receptors that caninhibit or enhance neuronal communication, interact with other types of receptors, and are involved
in a large variety of normal and pathological functions of neural cells (Ribeiro et al., 2002). One hypothesis, which could be tested in the present model, is that caffeine indirectly induces Shh gene expression by interfering with adenosine receptors.








This is affirmed by other studies:

Imiquimod directly inhibits Hedgehog signalling by stimulating adenosine receptor/protein kinase A-mediated GLI phosphorylation

Abstract
Imiquimod (IMQ), a nucleoside analogue of the imidazoquinoline family, is used in the topical treatment of basal cell carcinoma (BCC) (this pathway is downregulated in Androgenetic Alopecia tissues, because the causative pathway that causes BCC- the Hedgehog signalling pathway, is downregulated)and other skin diseases. It is reported to be a TLR7 and TLR8 agonist and, as such, initiates a Th1 immune response by activating sentinel cells in the vicinity of the tumour. BCC is a hedgehog (HH)-driven malignancy with oncogenic glioma-associated oncogene (GLI) signalling activated in a ligand-independent manner. Here we show that IMQ can also directly repress HH signalling by negatively modulating GLI activity in BCC and medulloblastoma cells. Further, we provide evidence that the repressive effect of IMQ on HH signalling is not dependent on TLR/MYD88 signalling. Our results suggest a mechanism for IMQ engaging adenosine receptors (ADORAs) to control GLI signalling. Pharmacological activation of ADORA with either an ADORA agonist or IMQ resulted in a protein kinase A (PKA)-mediated GLI phosphorylation and reduction in GLI activator levels. The activation of PKA and HH pathway target gene downregulation in response to IMQ were abrogated by ADORA inhibition. Furthermore, activated Smoothened signalling, which positively signals to GLI transcription factors, could be effectively counteracted by IMQ. These results reveal a previously unknown mode of action of IMQ in the treatment of BCC and also suggest a role for ADORAs in the regulation of oncogenic HH signalling.













Caffeine and adenosine.
Review article
Ribeiro JA, et al. J Alzheimers Dis. 2010.
Show full citation
Abstract
Caffeine causes most of its biological effects via antagonizing all types of adenosine receptors (ARs): A1, A2A, A3, and A2B and, as does adenosine, exerts effects on neurons and glial cells of all brain areas. In consequence, caffeine, when acting as an AR antagonist, is doing the opposite of activation of adenosine receptors due to removal of endogenous adenosinergic tonus. Besides AR antagonism, xanthines, including caffeine, have other biological actions: they inhibit phosphodiesterases (PDEs) (e.g., PDE1, PDE4, PDE5), promote calcium release from intracellular stores, and interfere with GABA-A receptors. Caffeine, through antagonism of ARs, affects brain functions such as sleep, cognition, learning, and memory, and modifies brain dysfunctions and diseases: Alzheimer's disease, Parkinson's disease, Huntington's disease(all three neurodegenerative diseases are associated with Androgenetic Alopecia), Epilepsy, Pain/Migraine, Depression, Schizophrenia. In conclusion, targeting approaches that involve ARs will enhance the possibilities to correct brain dysfunctions, via the universally consumed substance that is caffeine.



= adenosine downregulates sonic hedgehog.
Caffeine blocks the adenosine receptors.

Hence, caffeine upregulatEs sonic hedgehog
 
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yayapapaya

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Thank you for compiling this. I appreciate it.

Do you think tea tree oil can replace polysorbate 80 in ethanol-pg vehicle or added to liquid minoxidil?
 

Jakejr

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It seems I change or modify my protocol every week.
Good luck..
 

sktboiboi

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Omg 34$ for its too expensive, I'm not from US
U dont have to buy that brand, there are so many caffeine shampoos out in the market n most of thwm r fairly cheap. I only linked that brand becos its widely available in my country
 

yayapapaya

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Why would u do that? There tons of caffeine shampoos out there. Just Google 'caffeine shampoo'
I'd rather use 1 master topical then several shampoos. So far, I have seti+minoxidil topical. Looking to add tea tree oil+ caffeine.
 
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