Starting A New Regime As Of 1st July 2019

[Otis Mack]

Those upregulated gene studies are garbage because the hair follicle needs to be analyzed in a scaffold type environment. Failure to do this and putting cells in a flat petri dish gives erroneous results.

I'm out of time but IIRC something like 200 gene expressions are changed by not following an "in-vivo"like culturing approach. All genes are effected by the tiniest of things too even if say homocysteine was too high in male pattern baldness this would not be reflected in this gene culture.




Dr. Christiano's research:

Tissue engineering of human hair follicles using a biomimetic developmental approach

 

[sktboiboi]

Those upregulated gene studies are garbage because the hair follicle needs to be analyzed in a scaffold type environment. Failure to do this and putting cells in a flat petri dish gives erroneous results.

I'm out of time but IIRC something like 200 gene expressions are changed by not following an "in-vivo"like culturing approach. All genes are effected by the tiniest of things too even if say homocysteine was too high in male pattern baldness this would not be reflected in this gene culture.




Dr. Christiano's research:

Tissue engineering of human hair follicles using a biomimetic developmental approach

that article u've quoted isnt even talking about Androgenetic Alopecia genetic etiological causes- it's only discussing on how to grow hair in the lab using lef-1(which is a downstream target gene of Beta catenin of the wnt signalling pathway)

hence, we are on a different page

 

[Otis Mack]

I was in a hurry when I posted that.

What I said is true what Dr. Christiano's said but will get back on finding the correct article.

Anyways....for an accurate gene expression you would have to have the medium EXACTLY like serum from male pattern balding patients combined with a 3-d growth process like what occurs naturally in our bodies.

Lion Corportation I think already pursued these "bad" genes and found not much of importance.

 

[Timii]

Dude, no offence but no one is going to read all these studies. You see , this forum has an extensive history of suggestions that sounded good on paper but turned out to be useless in practice, so if you really wanna know if your approach works try it, then come back here after 6 months and report your results.

 

[sktboiboi]

My barber said the 'hole' at my top has become smaller(i cut my hair every fortnight, so he knows best). The circled part use to be empty. I have a chronic OCD using my fingers to touch that part all the time(cos like i said, it was bald). Now it feels hairy to the touch.


I must be doing something right.

 

[sktboiboi]

Dude, no offence but no one is going to read all these studies. You see , this forum has an extensive history of suggestions that sounded good on paper but turned out to be useless in practice, so if you really wanna know if your approach works try it, then come back here after 6 months and report your results.

No offence too , but i wasnt expecting any1 to read them. I merely treat this forum as a sort of diary, writing my experience with my hairloss.

This form is full of lazy shitters who just want somebody or something to give them the 'cure' on a sliver platter anyway.

 

[inmyhead]

Dude, no offence but no one is going to read all these studies. You see , this forum has an extensive history of suggestions that sounded good on paper but turned out to be useless in practice, so if you really wanna know if your approach works try it, then come back here after 6 months and report your results.

There are people reading the studies. I'm one of them.

 

[sktboiboi]

latest update:

EGCG 20mg powder twice/day, morning and night
+
Ketoconazole 2% shampoo twice/day, 5 mins leave on, day and night




EGCG upregulates Sonic hedgehog

Green tea epigallocatechin-3-gallate (EGCG) promotes neural progenitor cell proliferation and sonic hedgehog pathway activation during adult hippocampal neurogenesis.
Wang Y1, Li M, Xu X, Song M, Tao H, Bai Y.
Author information
1
Department of Medical Genetics, Third Military Medical University, Chongqing, P. R. China.
Abstract
SCOPE:
Adult hippocampal neurogenesis is a lifelong feature of brain plasticity that appears to be critically involved in adult brain function and neurological disease. Recent studies suggest that (-)-epigallocatechin-3-gallate (EGCG), which is the main polyphenolic constituent of green tea, may be used for the prevention and treatment of various neurodegenerative diseases. We hypothesized that EGCG promotes adult neurogenesis, which may be beneficial to hippocampus-dependent learning and memory.

METHODS AND RESULTS:
We show that EGCG treatment significantly increased the number of 5-bromo-2'-deoxyuridine (BrdU)-labeled cells in adult hippocampal neural progenitor cell (NPC) cultures and in the dentate gyrus of adult mice. Meanwhile, EGCG markedly improved spatial cognition in mice. These events are associated with the sonic hedgehog (Shh) signaling pathway. We observed that EGCG triggered a robust upregulation of Shh receptor (Patched) mRNA and protein expression in cultured NPCs as well as an upregulation of the downstream Shh transcriptional target Gli1. These changes were further confirmed in the hippocampus of mice administered EGCG. The blockage of the Shh signal with the pharmacological inhibitor cyclopamine attenuated EGCG-induced hippocampal neurogenesis.

CONCLUSION:
Our results provide strong evidence that EGCG enhances adult hippocampal neurogenesis.

Ketoconazole Blocks AR and kills Malassezia/Propiones acnes

Abstract
The common skin disease acne vulgaris is caused by Propionibacterium acnes. A lipase secreted by this microorganism metabolizes sebum and the resulting metabolites evoke inflammation in human skin. The antifungal drug ketoconazole inhibits P. acnes lipase activity. We previously showed that the drug also inhibits the growth of P. acnes. Thus, ketoconazole may serve as an alternative treatment for acne vulgaris, which is important because the number of antibiotic-resistant P. acnes strains has been increasing.

© 2017 The Societies and John Wiley & Sons Australia, Ltd.

KEYWORDS:
Propionibacterium acnes; ketoconazole; lipase



So EGCG for the stimulating factor/inhibitory(by virtue that it downs PPAR gamma)

Epigallocatechin-3-gallate inhibits adipogenesis through down-regulation of PPARγ and FAS expression mediated by PI3K-AKT signaling in 3T3-L1 cells.
Wu M1, Liu D1, Zeng R1, Xian T1, Lu Y1, Zeng G1, Sun Z2, Huang B2, Huang Q3.
Author information
1
Key Provincial Laboratory of Basic Pharmacology, Nanchang University, Nanchang 330006, Jiangxi Province, P.R. China; Department of Pharmacology, School of Pharmaceutical Science, Nanchang University, Nanchang 330006, Jiangxi Province, P.R. China.
2
Jiangxi Medical School, Nanchang University, Nanchang 330006, Jiangxi Province, P.R. China.
3
Key Provincial Laboratory of Basic Pharmacology, Nanchang University, Nanchang 330006, Jiangxi Province, P.R. China; Department of Pharmacology, School of Pharmaceutical Science, Nanchang University, Nanchang 330006, Jiangxi Province, P.R. China. Electronic address: qrhuang@ncu.edu.cn.
Abstract
Epigallocatechin-3-gallate (EGCG), a major component in green tea, functions as extensive bioactivities including anti-inflammation, anti-oxidation, and anti-cancer. However, little is known about its anti-adipogenesis and underlying mechanisms. The purport of this study sought to investigate effects of EGCG on 3T3-L1 preadipocyte differentiation and to explore its possible mechanisms. The 3T3-L1 cells were induced to differentiate under the condition of pro-adipogenic cocktail with or without indicated EGCG concentrations (10, 50, 100, 200µM) for 2, 4, 6 and 8 days, respectively. Also, another batch of 3T3-L1 cells was induced under the optimal EGCG concentration (100µM) with or without SC3036 (PI3K activator, 10µM) or SC79 (AKT activator, 0.5µM) for 8 days. Subsequently, the cell viability was examined by MTT assay and the cell morphology was visualized by Oil red O staining. Finally, the mRNA levels including peroxisome proliferator activated receptor γ (PPARγ) and fatty acid synthase (FAS) were detected by quantitative real time PCR, while the protein levels of PPARγ, FAS, phosphatidylinositol 3 kinase (PI3K), insulin receptor substrate1(IRS1), AKT, and p-AKT were measured by immunoblotting analysis. Our results showed that EGCG inhibited adipogenesis of 3T3-L1 preadipocyte in a concentration-dependent manner. Moreover, the inhibitory effects were reversed by SC3036 or SC79, suggesting that the inhibitory effects of EGCG are mediated by PI3K-AKT signaling to down-regulate PPARγ and FAS expression levels. The findings shed light on EGCG anti-adipogenic effects and its underlying mechanism and provide a novel preventive-therapeutic potential for obesity subjects as a compound from Chinese green tea.


= EGCG inhibits adipogenesis



of hair growth and ketoconzole for the inhibitory factor of hair growth. Simple.

 

[-G-]

Really have to say, I admire your enthusiasm. Now that I have some free time, I too am going to try and look at some studies and try to understand why we lose hair loss and perhaps natural methods.

I am curious if you have other additional pictures as there isn't a cosmetic difference there that is not worthy...

 

[Xander94]

Really have to say, I admire your enthusiasm. Now that I have some free time, I too am going to try and look at some studies and try to understand why we lose hair loss and perhaps natural methods.

I am curious if you have other additional pictures as there isn't a cosmetic difference there that is not worthy...

Waste of time imo. Just do massage min dermaroll maybe corticosteroid and finasteride if u can handle and pray for future

 

[Xander94]

tbh I also research alot and take supplements but dont forget about proven treatments !

 

[Jakejr]

Wow, quite extensive reasoning. Bottom line does this regimen grow hair.
Can’t tell because you have so much.

 

[EndlessPossibilities]

@sktboiboi dude you are a genius. You should check out my thread over here. You and I are on similar wave lengths. Literally discovered so much of the same things you discovered.


there was one thing that always confused me with your findings however. From all the studies it’s clear that steroidgensis was very high in androgenic scalp by default in men this will be androgens. Why would u say we needed to increase hmgcoa when that directly would lead to more cholesterol which would lead to more steroidgensis? Unless the cholesterol can go somewhere else?

pm me. You and I should chat this out

https://raypeatforum.com/community/threads/some-solid-bro-science-on-balding.32518/

 

[killDHT]

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.

sildenafil increases cAMP.If it will make face aging likes min

 

[MikeJay]

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:

View attachment 129116

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.

How's.the astaxanthin working for u

 

[jamesbooker1975]

Ok, If I inhibit DHT with Finasteride or Dutasteride is bad, but if I inhibiting ( also by blocking 5-alpha reductase ) with potatoes are good. Lol. Can somebody explain me this logic ? If like , If Somebody die cause a bullet, is no natural , so is bad. But is somebody hang out, the rope is natural, is good .
Really, some people pretend to be stupid or are really that stupid ?!

 

[jamesbooker1975]

No offence too , but i wasnt expecting any1 to read them. I merely treat this forum as a sort of diary, writing my experience with my hairloss.

This form is full of lazy shitters who just want somebody or something to give them the 'cure' on a sliver platter anyway.

Are all useless in VITRO studies, anyway.

 

[Aethas]

Why you being rude ? He share freely usefull information to the community..