Comparative transcriptome profiling provides new insights into mechanisms of AGA - BaldTruthTalk.com
+ Reply to Thread
Page 1 of 2 1 2 LastLast
Results 1 to 10 of 13
  1. #1
    Member
    Join Date
    Dec 2015
    Posts
    87

    Post Comparative transcriptome profiling provides new insights into mechanisms of AGA

    http://onlinelibrary.wiley.com/doi/1...bjd.14767/full

    Dear Editor, Androgenetic alopecia (AGA) is the most common progressive form of hair loss, occurring in more than half of men aged > 50 years.[1] AGA onset is dependent on genetic predisposition and presence of androgen.[2, 3] In patients with AGA, hair undergoes a shortened anagen phase, progressive miniaturization and subsequent vellus transformation of the terminal hair follicle.

    In this study, we present follicular bulb-centric transcriptome profiling of AGA and non-AGA control scalps. We sought to identify key transcriptomic differences among the hair bulbs of the occipital and vertex regions of 20 patients with AGA (Hamilton grade III–VI) and 10 controls aged 21–57 years (Table S1, Fig. S1; see Supporting Information). These were correlated with dermatoscopic scalp imaging and microscopic evaluation of follicular unit extractions (FUEs) from the leading edge of hair recession at the vertex and occipital regions. Patients had given informed consent and the study protocol was approved by the domain-specific review board of NHG Research.

    We found no significant difference in hair density among the vertex and occipital regions in patients (PV and PO, respectively) and controls (CV and CO, respectively) (Fig. 1a, c). The absence of reduction in hair density in patients with AGA is concordant with previous findings where hair thinning was observed.[4] Furthermore, the number of hairs per follicular unit (FU) was reduced in PV (Fig. 1h), which provides support to the hypothesis that a subset of hair follicles within an FU in AGA is more prone to undergoing a reduction in hair shaft size and miniaturization.[5]



    The hair shafts in PV (Fig. 1a, d), measured at the protrusion through the epidermis, were significantly thinner in all comparisons, while PO was thinner compared with CO samples. FUE samples from PV showed a well-correlated reduction in hair depth and hair bulb width compared with PO, which was comparable with CV and CO where no significant differences were found (Fig. 1e–g).

    We then interrogated the transcriptome profile of the hair bulb-containing lower portion (Fig. 1b) of one vertex and one occipital FUE from each subject by RNA sequencing. We found low numbers of differentially expressed transcripts between anatomical sites (PV vs. CV, PV vs. PO, PO vs. CO; Fig. 2b) due to transcriptome heterogeneity within samples of each anatomical site (Fig. 2a). Genes upregulated in the three comparison pairs were highly enriched in lipid synthesis and electron carrier activity/transport (Fig. 2c–e; Fig. S2 and Table S2; see Supporting Information). Interestingly, the transcriptome profiles of occipital and vertex FUEs of controls revealed a high degree of similarity (Fig. 2b), despite the difference in embryonic origins.[6] We validated five upregulated genes in PV compared with PO (CYB5R3, FADS2, PTGDS, INSR and SRD5A1) with reverse-transcriptase quantitative polymerase chain reaction, and found that the expression trend concurred with RNA-seq observations (Fig. 2h; Table S3).



    The transcriptomic heterogeneity observed within samples of each anatomical site (Fig. 2a) has shown that it is insufficient to classify and compare between them. Rather, identification of differentially expressed genes in clustered samples following unbiased transcriptome profile-based sample stratification was a more suitable approach. As such, we conducted principal-components analysis of all samples (all expressed transcripts; fragments per kilobase of transcript per million mapped reads > 0), and found that the majority of samples fell within three clusters (I, II, III; Fig. 2a). A mixture of samples from all anatomical sites was found in cluster I, suggesting that PV samples in cluster I are likely to be less advanced in AGA, as its transcriptome profile is more similar to non-AGA (CV and CO) samples. The distinct cluster II, consisting of five CV and six CO samples, was isolated from all patient samples and thus represented the healthiest hairs. Cluster III contained only morphologically miniaturized PV samples and thus represented hairs with advanced AGA profiles.

    We identified 1339 differential transcripts between samples from clusters III and II (Fig. 2b, g), and found upregulation of metabolism (electron carrier activity, respiratory chain and monosaccharide metabolic process), lipid biosynthesis, response to hormone stimulus and steroid hormone biosynthesis-related genes (Fig. 2f; Table S2; see Supporting Information). The upregulation of genes in the respiratory chain (CYB5R3, INSR) may impact on the redox state in AGA-affected hairs.[7, 8]

    Furthermore, the upregulation of antioxidation genes (GPX4 and PRDX3) suggests that PV scalps may be exposed to greater oxidative stress than control scalps, possibly resulting from increased respiratory chain activity.[9, 10] Increased levels of GPX4 would also protect the increased amount of lipid synthesized in the PV scalp from phospholipid hydroperoxide-mediated oxidation.[11] The occurrence of oxidative stress in dermal papilla cells may account for impaired hair growth in AGA, as elevated reactive oxidative species in balding dermal papilla cells are known to cause elevated secretion of the hair growth inhibitors, transforming growth factors β1 and β2, and cell senescence.[12, 13] Furthermore, it is proposed that low-level laser therapy alleviates AGA through increasing mitochondrial ATP production, providing support for the involvement of mitochondrial activity in AGA pathogenesis.[14]

    We found downregulation of genes related to keratin, epidermis development, cell cycle and hair follicle morphogenesis in cluster III compared with cluster II (Fig. 2b, f; Table S4; see Supporting Information), likely attributed to reduced proliferation and differentiation of matrix cells into keratin-rich hair inner root sheath cells in PV scalps. This is concordant with the significantly decreased hair depth (P = 0·012, Fig. 2i) and hair bulb width (P < 0·001, Fig. 2j) observed in cluster III compared with cluster II, suggesting that downregulation of these genes is a hallmark of advanced AGA.

    In conclusion, we present a potential link between altered redox state in the hair follicle and its potential contribution to AGA pathogenesis, which could be targeted in AGA treatments. Further studies to validate the spatial expression of candidate genes in hair follicle compartments is essential to address the contribution of different hair cell types to AGA pathogenesis. Our results emphasize that follicular-based transcriptomes should be compared and analysed with clinical and histological measurements. Evaluation by Hamilton score, while established as a robust clinical measurement of scalp hair pattern, is not designed to classify the state of individual hair follicles in the course of miniaturization and molecular changes in AGA progression. Our data illustrate the importance of evaluating each hair follicle individually, and suggest that future study designs should take these factors into consideration.




    CYB5R3 > High ROS in balding scalp
    FADS2 > Too much of Fatty acid production. Omega 3 and 6 r products of this gene
    PTGDS > Protaglandin d2 synthase. Thus, reafffirming other researcher's findings.
    INSR > Insulin receptor. Thus, too much of Insulin in balding scalp.
    SRD5A1 > 5-alpha redutase. Thus, DHT is indeed responsible.

  2. #2
    Junior Member
    Join Date
    Feb 2016
    Posts
    9

    Default

    Nice found and conclusion man.

    You had been missed.

  3. #3
    Member
    Join Date
    Dec 2015
    Posts
    87

    Default

    hey u still have the TM? dont sell it away! use it orally, dont apply it topically. pgd2 is really a causative factor, not a resultant 1. oh n i've 4gotten all my passwords

  4. #4
    Member
    Join Date
    Dec 2015
    Posts
    87

    Default

    atually i've even forgotten the URL as well. everything was in my cell phone(lost). n this site sucks.





    We then interrogated the transcriptome profile of the hair bulb-containing lower portion (Fig. 1b) of one vertex and one occipital FUE from each subject by RNA sequencing. We found low numbers of differentially expressed transcripts between anatomical sites (PV vs. CV, PV vs. PO, PO vs. CO; Fig. 2b) due to transcriptome heterogeneity within samples of each anatomical site (Fig. 2a). Genes upregulated in the three comparison pairs were highly enriched in lipid synthesis and electron carrier activity/transport (Fig. 2c–e; Fig. S2 and Table S2; see Supporting Information). Interestingly, the transcriptome profiles of occipital and vertex FUEs of controls revealed a high degree of similarity (Fig. 2b), despite the difference in embryonic origins.[6] We validated five upregulated genes in PV compared with PO (CYB5R3, FADS2, PTGDS, INSR and SRD5A1) with reverse-transcriptase quantitative polymerase chain reaction, and found that the expression trend concurred with RNA-seq observations (Fig. 2h; Table S3).


    https://www.ncbi.nlm.nih.gov/pubmed/12713571

    Identification of the delta-6 desaturase of human sebaceous glands: expression and enzyme activity.

    Abstract
    Delta-6 desaturase, also known as fatty acid desaturase-2 (FADS2), is a component of a lipid metabolic pathway that converts the essential fatty acids linoleate and alpha-linolenate into long-chain polyunsaturated fatty acids. Isolation of Delta-6 desaturase/FADS2 cDNA from human skin predicts an identical protein to that expressed in human brain and Southern analysis indicates a single locus, together suggestive of a single Delta-6 desaturase/FADS2 gene. Within human skin, Delta-6 desaturase/FADS2 mRNA and protein expression is restricted to differentiating sebocytes located in the suprabasal layers of the sebaceous gland. Enzymatic analysis using CHO cells overexpressing human Delta-6 desaturase/FADS2 indicates catalysis of a "polyunsaturated fatty acid type" reaction, but also an unexpected "sebaceous-type" reaction, that of converting palmitate into the mono-unsaturated fatty acid sapienate, a 16-carbon fatty acid with a single cis double bond at the sixth carbon from the carboxyl end. Sapienate is the most abundant fatty acid in human sebum, and among hair-bearing animals is restricted to humans. This work identifies Delta-6 desaturase/FADS2 as the major fatty acid desaturase in human sebaceous glands and suggests that the environment of the sebaceous gland permits catalysis of the sebaceous-type reaction and restricts catalysis of the polyunsaturated fatty acid type reaction.


    FADS2= reason for high sebum levels in balding scalp- at least in asian men(because this 2016 analysis study was done on Chinese men in Singapore)

  5. #5
    Member
    Join Date
    Dec 2015
    Posts
    87

    Default

    Quote Originally Posted by TheKingofFighters View Post
    atually i've even forgotten the URL as well. everything was in my cell phone(lost). n this site sucks.





    We then interrogated the transcriptome profile of the hair bulb-containing lower portion (Fig. 1b) of one vertex and one occipital FUE from each subject by RNA sequencing. We found low numbers of differentially expressed transcripts between anatomical sites (PV vs. CV, PV vs. PO, PO vs. CO; Fig. 2b) due to transcriptome heterogeneity within samples of each anatomical site (Fig. 2a). Genes upregulated in the three comparison pairs were highly enriched in lipid synthesis and electron carrier activity/transport (Fig. 2c–e; Fig. S2 and Table S2; see Supporting Information). Interestingly, the transcriptome profiles of occipital and vertex FUEs of controls revealed a high degree of similarity (Fig. 2b), despite the difference in embryonic origins.[6] We validated five upregulated genes in PV compared with PO (CYB5R3, FADS2, PTGDS, INSR and SRD5A1) with reverse-transcriptase quantitative polymerase chain reaction, and found that the expression trend concurred with RNA-seq observations (Fig. 2h; Table S3).


    https://www.ncbi.nlm.nih.gov/pubmed/12713571

    Identification of the delta-6 desaturase of human sebaceous glands: expression and enzyme activity.

    Abstract
    Delta-6 desaturase, also known as fatty acid desaturase-2 (FADS2), is a component of a lipid metabolic pathway that converts the essential fatty acids linoleate and alpha-linolenate into long-chain polyunsaturated fatty acids. Isolation of Delta-6 desaturase/FADS2 cDNA from human skin predicts an identical protein to that expressed in human brain and Southern analysis indicates a single locus, together suggestive of a single Delta-6 desaturase/FADS2 gene. Within human skin, Delta-6 desaturase/FADS2 mRNA and protein expression is restricted to differentiating sebocytes located in the suprabasal layers of the sebaceous gland. Enzymatic analysis using CHO cells overexpressing human Delta-6 desaturase/FADS2 indicates catalysis of a "polyunsaturated fatty acid type" reaction, but also an unexpected "sebaceous-type" reaction, that of converting palmitate into the mono-unsaturated fatty acid sapienate, a 16-carbon fatty acid with a single cis double bond at the sixth carbon from the carboxyl end. Sapienate is the most abundant fatty acid in human sebum, and among hair-bearing animals is restricted to humans. This work identifies Delta-6 desaturase/FADS2 as the major fatty acid desaturase in human sebaceous glands and suggests that the environment of the sebaceous gland permits catalysis of the sebaceous-type reaction and restricts catalysis of the polyunsaturated fatty acid type reaction.


    FADS2= reason for high sebum levels in balding scalp- at least in asian men(because this 2016 analysis study was done on Chinese men in Singapore)
    https://respiratory-research.biomedc...1465-9921-8-16

    It is intriguing to note that CRTH2 is not only activated by PGD2 and several of its metabolites the generation of which is dependent on the enzyme PGD synthase, but also by products of the arachidonic acid cascade that are generated independent of PGD2 production. Among the latter are the TXA2 metabolite 11-dehydro-TXB2, and PGF2α, that have recently been demonstrated to activate eosinophils and basophils [43, 55]. The possibility that CRTH2 can be activated in cellular contexts where PGD synthase is not present, i.e. in the absence of PGD2 production, further corroborates its importance as a regulator of allergic inflammation and underscores the potential usefulness of CRTH2 antagonists as anti-asthmatic agents.

    PGF2A(Bimatoprost analog) can also activate CRTh2

  6. #6
    Junior Member
    Join Date
    Jun 2016
    Posts
    4

    Default

    Great to see you back and posting again. I have a enormous post I can put up linking everything things together between AGA, insulin resistance/diabetes, and even the Parkinson's link where it all comes back to FOXA2 and how it links up in the gut. I suggest you check out these two studies one showing the link between the gut and Parkinson's along with this other study of FOXA2 levels being affected by probiotic administration.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4135721/

    "Principally, the administration of L. casei Zhang prevents the loss of pancreatic ClC-2 and FoxA2 expression in high-fat-sucrose fed rats. Low pancreatic FoxA2 expression level is proven to be positively correlated with insulin resistance and the risk of T2DM27. Interestingly, the liver of FoxA2-deficient mice had shown high bile acid accumulation28. In addition, it has been proposed that a high intracellular Cl– in the β-cell of pancreas is essential to electrical activity of β-cell membrane and insulin release29.Considering all these, we presumed that probiotic pretreatment protects the pancreas in high-fat-sucrose fed rats by enhancing pancreatic ClC-2 expression and eliminating bile acids in feces through a bile acid–chloride exchanging mechanism."



    Here is the other study

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4932209/

    "Recently, a study explored the relation of gut microbiota with clinical phenotype of PD and compared fecal microbiomes of patients with PD with control subjects and showed a reduction of Prevotellaceae in PD. Moreover, the relative abundance of Enterobacteriaceae was positively related with the severity of postural instability and gait difficulty[22]. These findings offer some insight into the possible effect of gut microbiota on PD."

    What this study is showing is how scoliosis seen in Parkinson's is originating from gut dysbiosis.

    Please check your PM's and let's connect there. I forgot my passwords along with the url too.

    Edit: Wow seems like I can't find the PMs on here.

  7. #7
    Member
    Join Date
    Dec 2015
    Posts
    87

    Default

    Quote Originally Posted by forgottenwarrior View Post
    Great to see you back and posting again. I have a enormous post I can put up linking everything things together between AGA, insulin resistance/diabetes, and even the Parkinson's link where it all comes back to FOXA2 and how it links up in the gut. I suggest you check out these two studies one showing the link between the gut and Parkinson's along with this other study of FOXA2 levels being affected by probiotic administration.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4135721/

    "Principally, the administration of L. casei Zhang prevents the loss of pancreatic ClC-2 and FoxA2 expression in high-fat-sucrose fed rats. Low pancreatic FoxA2 expression level is proven to be positively correlated with insulin resistance and the risk of T2DM27. Interestingly, the liver of FoxA2-deficient mice had shown high bile acid accumulation28. In addition, it has been proposed that a high intracellular Cl– in the β-cell of pancreas is essential to electrical activity of β-cell membrane and insulin release29.Considering all these, we presumed that probiotic pretreatment protects the pancreas in high-fat-sucrose fed rats by enhancing pancreatic ClC-2 expression and eliminating bile acids in feces through a bile acid–chloride exchanging mechanism."



    Here is the other study

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4932209/

    "Recently, a study explored the relation of gut microbiota with clinical phenotype of PD and compared fecal microbiomes of patients with PD with control subjects and showed a reduction of Prevotellaceae in PD. Moreover, the relative abundance of Enterobacteriaceae was positively related with the severity of postural instability and gait difficulty[22]. These findings offer some insight into the possible effect of gut microbiota on PD."

    What this study is showing is how scoliosis seen in Parkinson's is originating from gut dysbiosis.

    Please check your PM's and let's connect there. I forgot my passwords along with the url too.

    Edit: Wow seems like I can't find the PMs on here.
    remember i've been advocating, based on that fact that my paternal grandfather died due to complications from Parkinson's and he was of cos-bald

    that Parkinson's is linked with AGA since years back b4 this this study even came up?

    if u check out the excel document on the genes differently regulated between the vertex and occipital scalps of balding men study in the 1st post here:

    SP_PIR_KEYWORDS mitochondrion 5.686E-15
    GOTERM_CC_FAT GO:0005739~mitochondrion 1.092E-13
    GOTERM_CC_FAT GO:0044429~mitochondrial part 5.250E-11
    SP_PIR_KEYWORDS transit peptide 1.159E-10
    GOTERM_CC_FAT GO:0005740~mitochondrial envelope 4.293E-10
    GOTERM_CC_FAT GO:0031966~mitochondrial membrane 2.852E-08
    GOTERM_CC_FAT GO:0005743~mitochondrial inner membrane 7.211E-08
    GOTERM_CC_FAT GO:0031967~organelle envelope 1.095E-07
    GOTERM_CC_FAT GO:0031975~envelope 1.203E-07
    GOTERM_CC_FAT GO:0070469~respiratory chain 2.193E-07
    GOTERM_CC_FAT GO:0019866~organelle inner membrane 3.709E-07
    GOTERM_CC_FAT GO:0031090~organelle membrane 4.600E-06
    GOTERM_CC_FAT GO:0005759~mitochondrial matrix 1.146E-04
    GOTERM_CC_FAT GO:0031980~mitochondrial lumen 1.146E-04
    SP_PIR_KEYWORDS mitochondrion inner membrane 1.481E-04
    KEGG_PATHWAY hsa05012:Parkinson's disease 1.554E-03

    GOTERM_MF_FAT GO:0033293~monocarboxylic acid binding 9.121E-08
    GOTERM_MF_FAT GO:0031406~carboxylic acid binding 1.415E-07
    GOTERM_MF_FAT GO:0005504~fatty acid binding 1.658E-04
    SP_PIR_KEYWORDS lipid synthesis 3.883E-11
    GOTERM_BP_FAT GO:0006633~fatty acid biosynthetic process 2.231E-04
    SP_PIR_KEYWORDS Fatty acid biosynthesis 1.344E-03
    GOTERM_MF_FAT GO:0009055~electron carrier activity 3.516E-08
    SP_PIR_KEYWORDS FAD 9.296E-07
    SP_PIR_KEYWORDS Flavoprotein 2.290E-06
    GOTERM_MF_FAT GO:0050660~FAD binding 4.335E-04
    SP_PIR_KEYWORDS extracellular matrix 1.676E-09
    GOTERM_CC_FAT GO:0044421~extracellular region part 4.337E-07
    GOTERM_CC_FAT GO:0031012~extracellular matrix 1.021E-06
    GOTERM_CC_FAT GO:0005578~proteinaceous extracellular matrix 1.948E-06
    GOTERM_CC_FAT GO:0005604~basement membrane 2.291E-06
    GOTERM_CC_FAT GO:0044420~extracellular matrix part 2.446E-06
    SP_PIR_KEYWORDS basement membrane 1.227E-05
    PANTHER_PATHWAY P00034:Integrin signalling pathway 6.833E-02
    SP_PIR_KEYWORDS lipid synthesis 3.883E-11
    GOTERM_BP_FAT GO:0008610~lipid biosynthetic process 5.046E-09
    GOTERM_BP_FAT GO:0006694~steroid biosynthetic process 7.998E-08
    SP_PIR_KEYWORDS Steroid biosynthesis 1.364E-07
    GOTERM_BP_FAT GO:0008202~steroid metabolic process 6.505E-07
    GOTERM_BP_FAT GO:0016126~sterol biosynthetic process 1.202E-06
    SP_PIR_KEYWORDS sterol biosynthesis 4.731E-06
    GOTERM_BP_FAT GO:0016125~sterol metabolic process 1.002E-04
    GOTERM_BP_FAT GO:0006695~cholesterol biosynthetic process 1.477E-04
    SP_PIR_KEYWORDS Cholesterol biosynthesis 1.845E-03
    GOTERM_BP_FAT GO:0008203~cholesterol metabolic process 2.908E-03
    KEGG_PATHWAY hsa00900:Terpenoid backbone biosynthesis 2.683E-02
    PANTHER_PATHWAY P00014:Cholesterol biosynthesis 5.236E-02
    GOTERM_BP_FAT GO:0006091~generation of precursor metabolites and energy 1.835E-12
    GOTERM_CC_FAT GO:0005740~mitochondrial envelope 4.293E-10
    SP_PIR_KEYWORDS electron transport 3.487E-09
    GOTERM_BP_FAT GO:0015980~energy derivation by oxidation of organic compounds 7.309E-09
    GOTERM_BP_FAT GO:0045333~cellular respiration 1.210E-08
    SP_PIR_KEYWORDS leber hereditary optic neuropathy 1.450E-08
    GOTERM_CC_FAT GO:0031966~mitochondrial membrane 2.852E-08
    GOTERM_CC_FAT GO:0005743~mitochondrial inner membrane 7.211E-08
    GOTERM_BP_FAT GO:0022900~electron transport chain 1.435E-07
    SP_PIR_KEYWORDS membrane-associated complex 1.925E-07
    GOTERM_CC_FAT GO:0070469~respiratory chain 2.193E-07
    GOTERM_CC_FAT GO:0019866~organelle inner membrane 3.709E-07
    SP_PIR_KEYWORDS oxidative phosphorylation 4.487E-07
    GOTERM_CC_FAT GO:0005746~mitochondrial respiratory chain 1.541E-06
    SP_PIR_KEYWORDS respiratory chain 5.301E-06
    GOTERM_MF_FAT GO:0016651~oxidoreductase activity, acting on NADH or NADPH 1.121E-05
    GOTERM_BP_FAT GO:0022904~respiratory electron transport chain 3.614E-05
    GOTERM_BP_FAT GO:0042775~mitochondrial ATP synthesis coupled electron transport 7.061E-05
    GOTERM_BP_FAT GO:0042773~ATP synthesis coupled electron transport 7.061E-05
    SP_PIR_KEYWORDS mitochondrion inner membrane 1.481E-04
    SP_PIR_KEYWORDS melas syndrome 2.251E-04
    GOTERM_BP_FAT GO:0006119~oxidative phosphorylation 3.211E-04
    GOTERM_CC_FAT GO:0044455~mitochondrial membrane part 3.673E-04
    SP_PIR_KEYWORDS ubiquinone 1.503E-03
    KEGG_PATHWAY hsa05012:Parkinson's disease 1.554E-03
    KEGG_PATHWAY hsa00190:Oxidative phosphorylation 1.804E-03
    GOTERM_BP_FAT GO:0006120~mitochondrial electron transport, NADH to ubiquinone 1.104E-02
    GOTERM_MF_FAT GO:0003954~NADH dehydrogenase activity 1.122E-02
    GOTERM_MF_FAT GO:0008137~NADH dehydrogenase (ubiquinone) activity 1.122E-02
    GOTERM_MF_FAT GO:0050136~NADH dehydrogenase (quinone) activity 1.122E-02
    GOTERM_CC_FAT GO:0045271~respiratory chain complex I 1.409E-02
    GOTERM_CC_FAT GO:0005747~mitochondrial respiratory chain complex I 1.409E-02
    GOTERM_CC_FAT GO:0030964~NADH dehydrogenase complex 1.409E-02
    GOTERM_MF_FAT GO:0016655~oxidoreductase activity, acting on NADH or NADPH, quinone or similar compound as acceptor 1.906E-02
    8 4.797 SP_PIR_KEYWORDS Secreted 2.091E-07
    SP_PIR_KEYWORDS signal 3.554E-07
    GOTERM_CC_FAT GO:0005576~extracellular region 7.085E-06
    SP_PIR_KEYWORDS glycoprotein 1.400E-03
    SP_PIR_KEYWORDS disulfide bond 1.405E-03
    9 4.534 GOTERM_BP_FAT GO:0006631~fatty acid metabolic process 1.802E-06
    GOTERM_BP_FAT GO:0016053~organic acid biosynthetic process 4.263E-05
    GOTERM_BP_FAT GO:0046394~carboxylic acid biosynthetic process 4.263E-05
    GOTERM_BP_FAT GO:0006633~fatty acid biosynthetic process 2.231E-04
    10 3.325 GOTERM_CC_FAT GO:0042579~microbody 2.262E-06
    GOTERM_CC_FAT GO:0005777~peroxisome 2.262E-06
    SP_PIR_KEYWORDS peroxisome 9.893E-06
    GOTERM_CC_FAT GO:0044439~peroxisomal part 1.551E-02
    GOTERM_CC_FAT GO:0044438~microbody part 1.551E-02
    GOTERM_CC_FAT GO:0031903~microbody membrane 2.089E-02
    GOTERM_CC_FAT GO:0005778~peroxisomal membrane 2.089E-02
    11 3.324 GOTERM_BP_FAT GO:0009060~aerobic respiration 1.202E-06
    GOTERM_BP_FAT GO:0051186~cofactor metabolic process 1.898E-05
    SP_PIR_KEYWORDS tricarboxylic acid cycle 2.656E-04
    KEGG_PATHWAY hsa00020:Citrate cycle (TCA cycle) 3.379E-04
    GOTERM_BP_FAT GO:0051187~cofactor catabolic process 4.117E-04
    GOTERM_BP_FAT GO:0006732~coenzyme metabolic process 4.482E-04
    GOTERM_BP_FAT GO:0006099~tricarboxylic acid cycle 7.219E-04
    GOTERM_BP_FAT GO:0046356~acetyl-CoA catabolic process 7.219E-04
    GOTERM_BP_FAT GO:0009109~coenzyme catabolic process 1.303E-03
    GOTERM_BP_FAT GO:0006084~acetyl-CoA metabolic process 2.947E-03
    GOTERM_BP_FAT GO:0043603~cellular amide metabolic process 9.208E-03
    PANTHER_PATHWAY P00051:TCA cycle 1.876E-02
    12 2.884 SP_PIR_KEYWORDS sterol biosynthesis 4.731E-06
    GOTERM_MF_FAT GO:0004128~cytochrome-b5 reductase activity 1.898E-02
    GOTERM_MF_FAT GO:0016653~oxidoreductase activity, acting on NADH or NADPH, heme protein as acceptor 2.478E-02
    13 2.870 KEGG_PATHWAY hsa00280:Valine, leucine and isoleucine degradation 2.781E-07
    KEGG_PATHWAY hsa00650:Butanoate metabolism 6.165E-04
    KEGG_PATHWAY hsa00071:Fatty acid metabolism 7.950E-03
    KEGG_PATHWAY hsa00640:Propanoate metabolism 1.273E-02
    KEGG_PATHWAY hsa00410:beta-Alanine metabolism 2.574E-01
    14 2.833 GOTERM_CC_FAT GO:0070469~respiratory chain 2.193E-07
    SP_PIR_KEYWORDS respiratory chain 5.301E-06
    SP_PIR_KEYWORDS mitochondrion inner membrane 1.481E-04
    KEGG_PATHWAY hsa05012:Parkinson's disease 1.554E-03
    GOTERM_MF_FAT GO:0015077~monovalent inorganic cation transmembrane transporter activity 1.700E-03
    KEGG_PATHWAY hsa00190:Oxidative phosphorylation 1.804E-03
    GOTERM_MF_FAT GO:0015078~hydrogen ion transmembrane transporter activity 2.181E-03
    KEGG_PATHWAY hsa04260:Cardiac muscle contraction 2.213E-02
    GOTERM_MF_FAT GO:0022890~inorganic cation transmembrane transporter activity 2.215E-02
    KEGG_PATHWAY hsa05010:Alzheimer's disease 1.911E-01
    KEGG_PATHWAY hsa05016:Huntington's disease 4.124E-01
    15 2.587 GOTERM_BP_FAT GO:0022610~biological adhesion 1.269E-03
    GOTERM_BP_FAT GO:0007155~cell adhesion 1.273E-03
    SP_PIR_KEYWORDS cell adhesion 1.074E-02
    16 2.521 GOTERM_BP_FAT GO:0048545~response to steroid hormone stimulus 5.154E-04
    GOTERM_BP_FAT GO:0010033~response to organic substance 6.142E-04
    GOTERM_BP_FAT GO:0009719~response to endogenous stimulus 7.237E-04
    GOTERM_BP_FAT GO:0009725~response to hormone stimulus 1.977E-03
    GOTERM_BP_FAT GO:0043627~response to estrogen stimulus 6.973E-03
    GOTERM_BP_FAT GO:0042493~response to drug 2.374E-02
    GOTERM_BP_FAT GO:0032355~response to estradiol stimulus 3.000E-02
    17 2.493 GOTERM_BP_FAT GO:0033273~response to vitamin 2.593E-04
    GOTERM_BP_FAT GO:0009719~response to endogenous stimulus 7.237E-04
    GOTERM_BP_FAT GO:0009991~response to extracellular stimulus 8.221E-04
    GOTERM_BP_FAT GO:0007584~response to nutrient 1.975E-03
    GOTERM_BP_FAT GO:0009725~response to hormone stimulus 1.977E-03
    GOTERM_BP_FAT GO:0033189~response to vitamin A 2.173E-03
    GOTERM_BP_FAT GO:0031667~response to nutrient levels 4.921E-03
    GOTERM_BP_FAT GO:0043434~response to peptide hormone stimulus 6.289E-02
    GOTERM_BP_FAT GO:0032526~response to retinoic acid 9.003E-02
    18 2.393 GOTERM_BP_FAT GO:0046395~carboxylic acid catabolic process 6.032E-05
    GOTERM_BP_FAT GO:0016054~organic acid catabolic process 6.032E-05
    GOTERM_BP_FAT GO:0009062~fatty acid catabolic process 9.500E-04
    GOTERM_MF_FAT GO:0003995~acyl-CoA dehydrogenase activity 1.033E-03
    GOTERM_BP_FAT GO:0006635~fatty acid beta-oxidation 1.846E-03
    GOTERM_BP_FAT GO:0034440~lipid oxidation 8.084E-03
    GOTERM_BP_FAT GO:0019395~fatty acid oxidation 8.084E-03
    GOTERM_BP_FAT GO:0044242~cellular lipid catabolic process 1.139E-02
    SP_PIR_KEYWORDS lipid metabolism 3.033E-02
    SP_PIR_KEYWORDS fatty acid metabolism 3.242E-02
    GOTERM_BP_FAT GO:0016042~lipid catabolic process 5.494E-02
    GOTERM_BP_FAT GO:0030258~lipid modification 7.248E-02
    19 2.259 GOTERM_MF_FAT GO:0033764~steroid dehydrogenase activity, acting on the CH-OH group of donors, NAD or NADP as acceptor 1.654E-04
    GOTERM_MF_FAT GO:0016229~steroid dehydrogenase activity 3.695E-04
    KEGG_PATHWAY hsa00140:Steroid hormone biosynthesis 8.354E-04
    GOTERM_MF_FAT GO:0047115~trans-1,2-dihydrobenzene-1,2-diol dehydrogenase activity 5.777E-03
    GOTERM_MF_FAT GO:0050327~testosterone 17-beta-dehydrogenase activity 5.777E-03
    KEGG_PATHWAY hsa00150:Androgen and estrogen metabolism 2.303E-02
    GOTERM_MF_FAT GO:0004303~estradiol 17-beta-dehydrogenase activity 5.374E-02
    SP_PIR_KEYWORDS steroid metabolism 4.024E-01
    20 2.146 GOTERM_BP_FAT GO:0006006~glucose metabolic process 1.322E-04
    GOTERM_BP_FAT GO:0019318~hexose metabolic process 1.694E-04
    GOTERM_BP_FAT GO:0016052~carbohydrate catabolic process 8.005E-04
    GOTERM_BP_FAT GO:0005996~monosaccharide metabolic process 9.103E-04
    GOTERM_BP_FAT GO:0046164~alcohol catabolic process 4.619E-03
    GOTERM_BP_FAT GO:0044275~cellular carbohydrate catabolic process 6.181E-03
    GOTERM_BP_FAT GO:0006007~glucose catabolic process 3.920E-02
    GOTERM_BP_FAT GO:0006096~glycolysis 6.493E-02
    GOTERM_BP_FAT GO:0019320~hexose catabolic process 7.248E-02
    GOTERM_BP_FAT GO:0046365~monosaccharide catabolic process 7.980E-02
    SP_PIR_KEYWORDS glycolysis 3.614E-01
    21 2.143 GOTERM_BP_FAT GO:0006633~fatty acid biosynthetic process 2.231E-04
    GOTERM_BP_FAT GO:0006690~icosanoid metabolic process 3.883E-03
    GOTERM_BP_FAT GO:0033559~unsaturated fatty acid metabolic process 5.845E-03
    GOTERM_BP_FAT GO:0046456~icosanoid biosynthetic process 1.708E-02
    GOTERM_BP_FAT GO:0006692~prostanoid metabolic process 2.221E-02
    GOTERM_BP_FAT GO:0006693~prostaglandin metabolic process 2.221E-02
    GOTERM_BP_FAT GO:0006636~unsaturated fatty acid biosynthetic process 2.334E-02
    22 2.087 GOTERM_BP_FAT GO:0006732~coenzyme metabolic process 4.482E-04
    GOTERM_MF_FAT GO:0051287~NAD or NADH binding 6.465E-04
    GOTERM_BP_FAT GO:0019748~secondary metabolic process 9.957E-04
    GOTERM_BP_FAT GO:0046496~nicotinamide nucleotide metabolic process 8.999E-03
    GOTERM_BP_FAT GO:0006769~nicotinamide metabolic process 8.999E-03
    GOTERM_BP_FAT GO:0043603~cellular amide metabolic process 9.208E-03
    GOTERM_BP_FAT GO:0009820~alkaloid metabolic process 9.983E-03
    GOTERM_BP_FAT GO:0019362~pyridine nucleotide metabolic process 1.104E-02
    GOTERM_BP_FAT GO:0006733~oxidoreduction coenzyme metabolic process 2.597E-02
    GOTERM_BP_FAT GO:0006739~NADP metabolic process 9.311E-02
    GOTERM_BP_FAT GO:0019674~NAD metabolic process 1.933E-01
    23 2.050 KEGG_PATHWAY hsa00980:Metabolism of xenobiotics by cytochrome P450 2.719E-04
    GOTERM_MF_FAT GO:0016765~transferase activity, transferring alkyl or aryl (other than methyl) groups 1.906E-02
    KEGG_PATHWAY hsa00982rug metabolism 1.958E-02
    KEGG_PATHWAY hsa00480:Glutathione metabolism 2.276E-02
    GOTERM_MF_FAT GO:0004364~glutathione transferase activity 2.422E-02
    24 2.029 SP_PIR_KEYWORDS iron 6.127E-04
    GOTERM_MF_FAT GO:0005506~iron ion binding 8.403E-04
    SP_PIR_KEYWORDS metalloprotein 3.065E-03
    SP_PIR_KEYWORDS chromoprotein 3.242E-02
    GOTERM_MF_FAT GO:0020037~heme binding 3.876E-02
    GOTERM_MF_FAT GO:0046906~tetrapyrrole binding 5.302E-02
    SP_PIR_KEYWORDS heme 5.981E-02
    25 1.832 GOTERM_BP_FAT GO:0048545~response to steroid hormone stimulus 5.154E-04
    GOTERM_BP_FAT GO:0014823~response to activity 5.963E-03
    GOTERM_BP_FAT GO:0051384~response to glucocorticoid stimulus 1.083E-01
    GOTERM_BP_FAT GO:0031960~response to corticosteroid stimulus 1.412E-01
    26 1.827 GOTERM_CC_FAT GO:0000267~cell fraction 3.560E-03
    SP_PIR_KEYWORDS microsome 1.132E-02
    GOTERM_CC_FAT GO:0005792~microsome 1.734E-02
    GOTERM_CC_FAT GO:0042598~vesicular fraction 2.180E-02
    GOTERM_CC_FAT GO:0005626~insoluble fraction 2.275E-02
    GOTERM_CC_FAT GO:0005624~membrane fraction 3.140E-02
    27 1.752 GOTERM_BP_FAT GO:0034637~cellular carbohydrate biosynthetic process 1.680E-03
    GOTERM_BP_FAT GO:0006090~pyruvate metabolic process 1.104E-02
    GOTERM_BP_FAT GO:0019319~hexose biosynthetic process 1.708E-02
    GOTERM_BP_FAT GO:0016051~carbohydrate biosynthetic process 2.277E-02
    GOTERM_BP_FAT GO:0046364~monosaccharide biosynthetic process 3.083E-02
    GOTERM_BP_FAT GO:0006094~gluconeogenesis 4.575E-02
    GOTERM_BP_FAT GO:0046165~alcohol biosynthetic process 5.323E-02
    28 1.739 GOTERM_CC_FAT GO:0016323~basolateral plasma membrane 2.341E-05
    GOTERM_CC_FAT GO:0030055~cell-substrate junction 1.636E-03
    GOTERM_CC_FAT GO:0005925~focal adhesion 8.490E-03
    GOTERM_CC_FAT GO:0005924~cell-substrate adherens junction 1.080E-02
    GOTERM_CC_FAT GO:0070161~anchoring junction 1.587E-02
    GOTERM_CC_FAT GO:0005912~adherens junction 4.173E-02
    GOTERM_CC_FAT GO:0030054~cell junction 4.203E-01
    SP_PIR_KEYWORDS cell junction 4.782E-01
    GOTERM_CC_FAT GO:0005911~cell-cell junction 4.819E-01
    29 1.723 GOTERM_BP_FAT GO:0009081~branched chain family amino acid metabolic process 1.447E-03
    GOTERM_BP_FAT GO:0009083~branched chain family amino acid catabolic process 4.581E-03
    GOTERM_BP_FAT GO:0009310~amine catabolic process 1.083E-01
    GOTERM_BP_FAT GO:0009063~cellular amino acid catabolic process 1.779E-01
    30 1.659 GOTERM_CC_FAT GO:0005750~mitochondrial respiratory chain complex III 1.618E-02
    GOTERM_CC_FAT GO:0045275~respiratory chain complex III 1.618E-02
    KEGG_PATHWAY hsa04260:Cardiac muscle contraction 2.213E-02
    GOTERM_MF_FAT GO:0008121~ubiquinol-cytochrome-c reductase activity 2.478E-02
    GOTERM_MF_FAT GO:0016681~oxidoreductase activity, acting on diphenols and related substances as donors, cytochrome as acceptor 2.478E-02
    GOTERM_MF_FAT GO:0016679~oxidoreductase activity, acting on diphenols and related substances as donors 3.120E-02
    31 1.654 GOTERM_MF_FAT GO:0015077~monovalent inorganic cation transmembrane transporter activity 1.700E-03
    GOTERM_MF_FAT GO:0015078~hydrogen ion transmembrane transporter activity 2.181E-03
    SP_PIR_KEYWORDS electron transfer 1.400E-02
    KEGG_PATHWAY hsa04260:Cardiac muscle contraction 2.213E-02
    GOTERM_MF_FAT GO:0022890~inorganic cation transmembrane transporter activity 2.215E-02
    GOTERM_MF_FAT GO:0015002~heme-copper terminal oxidase activity 5.785E-02
    GOTERM_MF_FAT GO:0004129~cytochrome-c oxidase activity 5.785E-02
    GOTERM_MF_FAT GO:0016676~oxidoreductase activity, acting on heme group of donors, oxygen as acceptor 5.785E-02
    GOTERM_MF_FAT GO:0016675~oxidoreductase activity, acting on heme group of donors 5.785E-02
    SP_PIR_KEYWORDS mitochondrial inner membrane 1.020E-01
    32 1.629 SP_PIR_KEYWORDS transmembrane 5.339E-04
    SP_PIR_KEYWORDS membrane 1.339E-03
    GOTERM_CC_FAT GO:0016021~integral to membrane 6.092E-01
    GOTERM_CC_FAT GO:0031224~intrinsic to membrane 6.981E-01
    33 1.556 SP_PIR_KEYWORDS pyroglutamic acid 3.127E-04
    GOTERM_MF_FAT GO:0048407~platelet-derived growth factor binding 4.329E-03
    SP_PIR_KEYWORDS collagen 5.984E-03
    SP_PIR_KEYWORDS hydroxylation 1.614E-02
    GOTERM_CC_FAT GO:0005581~collagen 3.124E-02
    SP_PIR_KEYWORDS trimer 1.706E-01
    SP_PIR_KEYWORDS triple helix 2.231E-01
    SP_PIR_KEYWORDS hydroxylysine 2.231E-01
    SP_PIR_KEYWORDS hydroxyproline 2.873E-01
    34 1.524 SP_PIR_KEYWORDS annexin 6.756E-03
    SP_PIR_KEYWORDS calcium/phospholipid-binding 8.267E-03
    SP_PIR_KEYWORDS calcium binding 2.884E-02
    SP_PIR_KEYWORDS endonexin fold 3.809E-02
    GOTERM_MF_FAT GO:0005544~calcium-dependent phospholipid binding 4.807E-02
    GOTERM_MF_FAT GO:0005543~phospholipid binding 5.577E-02
    SP_PIR_KEYWORDS phospholipid binding 1.304E-01
    35 1.503 GOTERM_MF_FAT GO:0008092~cytoskeletal protein binding 1.831E-02
    GOTERM_MF_FAT GO:0003779~actin binding 3.158E-02
    SP_PIR_KEYWORDS actin-binding 5.358E-02
    36 1.450 GOTERM_MF_FAT GO:0009374~biotin binding 9.427E-03
    SP_PIR_KEYWORDS biotin 1.142E-02
    GOTERM_MF_FAT GO:0016885~ligase activity, forming carbon-carbon bonds 1.898E-02
    SP_PIR_KEYWORDS ligase 7.759E-01
    37 1.427 GOTERM_MF_FAT GO:0016667~oxidoreductase activity, acting on sulfur group of donors 1.322E-03
    SP_PIR_KEYWORDS Redox-active center 1.189E-01
    GOTERM_BP_FAT GO:0045454~cell redox homeostasis 3.342E-01
    38 1.394 GOTERM_MF_FAT GO:0042803~protein homodimerization activity 2.009E-02
    GOTERM_MF_FAT GO:0042802~identical protein binding 5.310E-02
    GOTERM_MF_FAT GO:0046983~protein dimerization activity 6.160E-02
    39 1.372 GOTERM_MF_FAT GO:0030247~polysaccharide binding 2.499E-02
    GOTERM_MF_FAT GO:0001871~pattern binding 2.499E-02
    GOTERM_MF_FAT GO:0005539~glycosaminoglycan binding 3.433E-02
    GOTERM_MF_FAT GO:0030246~carbohydrate binding 5.924E-02
    GOTERM_MF_FAT GO:0008201~heparin binding 1.092E-01
    40 1.321 KEGG_PATHWAY hsa04512:ECM-receptor interaction 3.900E-03
    PANTHER_PATHWAY P00034:Integrin signalling pathway 6.833E-02
    KEGG_PATHWAY hsa04510:Focal adhesion 4.085E-01
    41 1.311 GOTERM_BP_FAT GO:0048585~negative regulation of response to stimulus 1.577E-02
    GOTERM_BP_FAT GO:0002673~regulation of acute inflammatory response 2.907E-02
    GOTERM_BP_FAT GO:0032101~regulation of response to external stimulus 3.408E-02
    GOTERM_BP_FAT GO:0050727~regulation of inflammatory response 3.634E-02
    GOTERM_BP_FAT GO:0031348~negative regulation of defense response 1.099E-01
    GOTERM_BP_FAT GO:0032102~negative regulation of response to external stimulus 2.197E-01





    seems like i was right after all. early-onset AGA is a prognosis to later-onset Parkinson's

  8. #8
    Member
    Join Date
    Dec 2015
    Posts
    87

    Default

    Not only that, AGA is actually a prognosis to many health disorders in later life.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5344973/

    Meta-analysis identifies novel risk loci and yields systematic insights into the biology of male-pattern baldness <== done by the same authors who have conducted the most comprehensive gene comparisons of AGA to date, including the 1st 1 of thread. This study is done on men of European-descent in London.


    Overlap with other human traits

    On an epidemiological level, early-onset MPB has been associated with several severe late-onset somatic disorders, such as cardiovascular disease (CVD)48; prostate hyperplasia and cancer49,50,51; Parkinson's disease10; and amyotrophic lateral sclerosis52. We therefore investigated a possible genetic overlap between MPB and other phenotypes, and compared our data to reported GWAS signals from the NHGRI GWAS catalogue. The results are summarized in Supplementary Data 3. A total of 124 GWAS catalogue entries mapped to MPB-risk loci (r2≥0.3 and/or D′>0.8). These included the above mentioned associations with hormone-dependent traits and a reduced pigmentation of facial skin, scalp hair and eyes. As regards to the well-established associations between MPB and CVD and prostate cancer, a total of seven overlapping associations were identified. These were found between MPB and: (i) blood pressure (N=3); (ii) QT-interval length (N=1); (iii) atrial fibrillation (N=1); (iv) sudden cardiac arrest (N=1); (v) and prostate cancer (N=1). Here, our analysis confirmed the positive epidemiological association between prostate cancer and MPB at Xq12 (AR/EDA2R-locus), pointing towards a shared pathophysiological mechanism that may involve EDA2R-signalling and AR-transactivation53. Surprisingly, for the majority of CVD GWAS SNPs, the direction of effect for MPB and CVD differed, thus opposing the reported positive association between MPB and CVD at an epidemiological level. This was not the case for the positive associations between MPB and diastolic blood pressure at 4q21.21, and sudden cardiac arrest at 12q13.12. Here, further analyses are warranted to elucidate the exact underlying genes and biological pathways, and how they relate to the epidemiological findings. Notably, while the 4q21.21 locus pointed towards a positive association between MPB and diastolic blood pressure levels, opposite effect direction were observed for a second overlapping association between these traits on 5q33.3. This indicates that the effect direction of the genetic correlation between two complex traits may differ between individual loci or pathways. This finding highlights the need for systematic studies to assess not only the quantitative genetic overlap but also individual overlapping genetic factors and the underlying genes and pathways. In addition, associations with four loci were found for MPB and lower body height, which may be driven by an accelerated progression of puberty and premature induction of epiphyseal closure54. MPB-risk alleles at 17q21.31 and 6q22.32 were associated with increased bone mineral density, which may be a consequence of optimized UVR-induced vitamin D synthesis in subjects with MPB. This is consistent with the observation that MPB-associated alleles confer a reduced risk for immune related phenotypes, such as type 1 diabetes; multiple sclerosis (MS); and rheumatoid arthritis (Supplementary Data 3). An increased incidence of these diseases has been reported in subjects with poor vitamin D intake and low serum vitamin D levels55. Furthermore, a recent Mendelian-randomization study by Mokry et al.56, found an association between genetically lowered 25-hydroxyvitamin D levels and increased susceptibility to MS. Moreover, our data indicate shared genetic determinants for MPB and a reduced risk for ovarian cancer, colorectal cancer, and chronic lymphatic leukaemia, as well as overlapping associations with progressive supranuclear palsy and decreased intracranial volume. The indispensability of sex hormones for the MPB phenotype is supported by the identification of overlapping genetic association between MPB and other hormone-dependent traits, such as an earlier age-at-onset of menarche in females and earlier sexual maturation and higher serum androgen levels in males (6q22.32, 16p13.12, Xp22.31)12,57,58,59,60.


    Acute lymphoblastic leukemia (childhood)
    Adolescent idiopathic scoliosis
    Androgen levels
    Atrial fibrillation
    Black vs. blond hair color
    Black vs. red hair color
    Blood pressure measurement (high sodium intervention)
    Blood pressure measurement (high sodium intervention)
    Bone mineral density
    Bone mineral density (hip)
    Bone mineral density (paediatric, skull)
    Bone mineral density (paediatric, skull)
    Bone mineral density (paediatric, skull)
    Bone mineral density (paediatric, upper limb)
    Bone mineral density (paediatric, upper limb)
    Bone mineral density (spine)
    Celiac disease
    Chronic lymphocytic leukemia
    Chronic lymphocytic leukemia
    Chronic lymphocytic leukemia
    Chronic lymphocytic leukemia
    Cocaine dependence
    Colorectal cancer
    Hair curl
    Diastolic blood pressure
    Diastolic blood pressure
    Dupuytren's disease
    Epithelial ovarian cancer
    Erectile dysfunction after prostate cancer treatment
    Ewing sarcoma
    Eye color
    Facial pigmentation
    Fibrinogen
    Freckling
    Hair color
    Hair color
    Hair color
    Hair curl
    Hair morphology
    Head circumference (infant)
    Height
    Height
    Height
    Height
    Height
    Height
    Height
    Height
    Height
    Height
    Height
    Height
    Height
    Height
    Height
    Height
    Hypertension
    Idiopathic pulmonary fibrosis
    Infant length
    Infant length
    Inflammatory biomarkers
    Interstitial lung disease
    Intracranial volume
    Intracranial volume
    Intracranial volume
    Intracranial volume
    Intracranial volume
    LDL cholesterol
    Male-pattern baldness
    Male-pattern baldness
    Male-pattern baldness
    Male-pattern baldness
    Male-pattern baldness
    Male-pattern baldness
    Male-pattern baldness
    Male-pattern baldness
    Male-pattern baldness
    Male-pattern baldness
    Male-pattern baldness
    Mammographic density (non-dense area)
    Menarche (age at onset)
    Menarche (age at onset)
    Menarche (age at onset)
    Menarche (age at onset)
    Morbidity-free survival at age 65years
    Multiple sclerosis
    Non-melanoma skin cancer
    Obesity-related traits (Sitting height)
    Ossification of the posterior longitudinal ligament of the spine
    Osteosarcoma
    Ovarian cancer in BRCA1 mutation carriers
    Ovarian cancer in BRCA1 mutation carriers
    Ovarian cancer in BRCA1 mutation carriers
    Ovarian cancer in BRCA1 mutation carriers
    Parkinson's disease
    Parkinson's disease
    Parkinson's disease
    Parkinson's disease
    Parkinson's disease
    Parkinson's disease
    Parkinson's disease
    Parkinson's disease
    Parkinson's disease
    Parkinson's disease
    Parkinson's disease
    Parkinson's disease
    Parkinson's disease
    Parkinson's disease
    Periodontitis (Mean PAL)
    Progressive supranuclear palsy
    Progressive supranuclear palsy
    Progressive supranuclear palsy
    Prostate cancer
    Puberty onset (genital enlargement)
    Pulmonary function
    QT interval
    Rheumatoid arthritis
    Sudden cardiac arrest
    Sunburns
    Systolic blood pressure
    Tanning
    Type 1 diabetes
    Type 2 diabetes
    White matter hyperintensity


    From this, we see why Caucasian men(might apply to Asian men as well) have a much higher and severe magnifestation of AGA:


    1)Height. Caucasian bald men are phenotypically almost always tall.
    2)Caucasian mphenotypically have bigger bones and BMI.
    3)Very likely to suffer from Parkinson's in senility.
    4)will come to suffer from various heart conditions metabolic- sepcially insulin ensitivities.
    5)Skin pigmentation. ligther skin colour = higher chances for balding

  9. #9
    Member
    Join Date
    Dec 2015
    Posts
    87

    Default

    Quote Originally Posted by forgottenwarrior View Post
    Great to see you back and posting again. I have a enormous post I can put up linking everything things together between AGA, insulin resistance/diabetes, and even the Parkinson's link where it all comes back to FOXA2 and how it links up in the gut. I suggest you check out these two studies one showing the link between the gut and Parkinson's along with this other study of FOXA2 levels being affected by probiotic administration.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4135721/

    "Principally, the administration of L. casei Zhang prevents the loss of pancreatic ClC-2 and FoxA2 expression in high-fat-sucrose fed rats. Low pancreatic FoxA2 expression level is proven to be positively correlated with insulin resistance and the risk of T2DM27. Interestingly, the liver of FoxA2-deficient mice had shown high bile acid accumulation28. In addition, it has been proposed that a high intracellular Cl– in the β-cell of pancreas is essential to electrical activity of β-cell membrane and insulin release29.Considering all these, we presumed that probiotic pretreatment protects the pancreas in high-fat-sucrose fed rats by enhancing pancreatic ClC-2 expression and eliminating bile acids in feces through a bile acid–chloride exchanging mechanism."



    Here is the other study

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4932209/

    "Recently, a study explored the relation of gut microbiota with clinical phenotype of PD and compared fecal microbiomes of patients with PD with control subjects and showed a reduction of Prevotellaceae in PD. Moreover, the relative abundance of Enterobacteriaceae was positively related with the severity of postural instability and gait difficulty[22]. These findings offer some insight into the possible effect of gut microbiota on PD."

    What this study is showing is how scoliosis seen in Parkinson's is originating from gut dysbiosis.

    Please check your PM's and let's connect there. I forgot my passwords along with the url too.

    Edit: Wow seems like I can't find the PMs on here.
    Mechanism of AGA = Fatty acid dysregulation + Hormones

    good news is i've figured out a simple solution to tackle: CYB5R3, FADS2, PTGDS, INSR.

    5AR type 1 is the 1 responsible for Asian men, as can be seen in:

    We then interrogated the transcriptome profile of the hair bulb-containing lower portion (Fig. 1b) of one vertex and one occipital FUE from each subject by RNA sequencing. We found low numbers of differentially expressed transcripts between anatomical sites (PV vs. CV, PV vs. PO, PO vs. CO; Fig. 2b) due to transcriptome heterogeneity within samples of each anatomical site (Fig. 2a). Genes upregulated in the three comparison pairs were highly enriched in lipid synthesis and electron carrier activity/transport (Fig. 2c–e; Fig. S2 and Table S2; see Supporting Information). Interestingly, the transcriptome profiles of occipital and vertex FUEs of controls revealed a high degree of similarity (Fig. 2b), despite the difference in embryonic origins.[6] We validated five upregulated genes in PV compared with PO (CYB5R3, FADS2, PTGDS, INSR and SRD5A1) with reverse-transcriptase quantitative polymerase chain reaction, and found that the expression trend concurred with RNA-seq observations (Fig. 2h; Table S3).

    E.G.Y.C. and B.S.Y.H. contributed equally to this work.
    Funding sources: Agency for Science, Technology and Research (A*STAR). <== Public science institute funded by the Government of Singapore
    Conflicts of interest: none declared.


    5AR type 2 is the 1 responsible for Caucasian men, as can be seen in :

    Here, we report the results of the largest genome-wide association studies (GWAS) meta-analysis of MPB to date, that comprised a total of 22,518 individuals from eight independent GWAS samples of European descent. The analysis identifies 63 genome-wide significant loci that explain ∼39% of the phenotypic variance in MPB. More than one-third of these loci (N=23) have not been reported previously. Our data highlight highly plausible candidate genes and pathways that are likely to contribute to key-pathophysiological characteristics of MPB such as the deregulation of anagen-to-catagen transition (FGF5, EBF1, DKK2, adipogenesis); increased androgen sensitivity (SRD5A2, melatonin signalling); and the transformation of pigmented terminal hair into unpigmented vellus hair (IRF4). Some of these genes and pathways may represent promising targets for the development of novel therapeutic options. In addition, our data provide molecular evidence that MPB shares a substantial biological basis with numerous other human phenotypes, which may have major implications in terms of the evaluation of MPB as an early prognostic marker for different phenotypes such as prostate cancer, sudden cardiac arrest or neurodegenerative disorders.


    There's another private forum that we used to post in- cant rem the name. any idea what is it? lets talk there.

  10. #10
    Member
    Join Date
    Dec 2015
    Posts
    87

    Default

    Taking 5AR inhibitors = boosting Testosterone + Estradiol levels.
    Estradiol is a direct regulator of PGE2/PGE1.

    Thus, u r already boosting pge2/pge1 by taking 5ar inhibitors.

    when using DUtasteride on a chronic basis, Gynaecomastia, with varying severity- happens sooner or later because the amount of Estradiol being boosted is more than the amount of Testosterone being boosted with the ratio getting worse as 1 ages with indigenous testosterone production levels dipping:

    https://www.researchgate.net/publica...ic_hyperplasia

    My guess why Glaxosmith didnt report their 2.5mg Dut for AGA results is because of this- that Gynaecomastia will happen sooner or later(as seen in myself)


    Finasteride will suffice for Asian men, because only type 1 is the culprit.
    Caucasian men need Dutasteride. Finasteride will not help, becos the latter inhibits only type 1 and type 2 is the culprit.

Similar Threads

  1. Can we get some 7.5 month post-op insights here?
    By ZooMass in forum Men's Hair Loss: Start Your Own Topic
    Replies: 1
    Last Post: 06-28-2017, 07:51 AM
  2. Electric stimuli induces mechanisms activation of Wnt/β-catenin and MAPK pathway
    By noisette in forum Cutting Edge / Future Treatments
    Replies: 2
    Last Post: 10-20-2015, 06:51 PM

Posting Permissions

  • You may not post new threads
  • You may not post replies
  • You may not post attachments
  • You may not edit your posts

» IAHRS

hair transplant surgeons

» The Bald Truth

» Recent Threads

Which is the best Salesforce institutes in Hyderabad?
03-17-2024 09:59 AM
Last Post By palashmim2022
03-17-2024 09:59 AM
The Resveratrol microneedling process study - enroll now
04-11-2022 02:38 AM
Last Post By Briam1930
03-16-2024 05:43 AM
What wedding packages are offered in Tbilisi?
01-27-2024 04:13 AM
by Jiromen
Last Post By Henryclark
03-16-2024 03:12 AM
Tour Operator's Treasures in Bangladesh
09-28-2023 06:48 AM
by davidm
Last Post By Briam1930
03-16-2024 12:49 AM