follicept - what's this?
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No ,guys Dr. Okajima is legit. The guy has a scholarship of a god (magna cum laude) compared to someone like Cotsarelis. Follicept seems damn legit to if I look at the credentials of the poeple involved. I was too short sighted.
I'm definately going to buy the products, I can't wait for follicept to come in with possibly better working IGF-1 products. Btw Theradome lately is getting some damn good results. Now using blue light instead of red actually stimulates IGF-1! Maybe we should concentrate on that too, to maximize our IGF-1 levels. Really looking awesome this.Comment
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Nope, seems legit:
Quote Originally Posted by Swooping View Post
No ,guys Dr. Okajima is legit. The guy has a scholarship of a god (magna cum laude) compared to someone like Cotsarelis. Follicept seems damn legit to if I look at the credentials of the poeple involved. I was too short sighted.
I'm definately going to buy the products, I can't wait for follicept to come in with possibly better working IGF-1 products. Btw Theradome lately is getting some damn good results. Now using blue light instead of red actually stimulates IGF-1! Maybe we should concentrate on that too, to maximize our IGF-1 levels. Really looking awesome this.Comment
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Nope, seems legit:
Quote Originally Posted by Swooping View Post
No ,guys Dr. Okajima is legit. The guy has a scholarship of a god (magna cum laude) compared to someone like Cotsarelis. Follicept seems damn legit to if I look at the credentials of the poeple involved. I was too short sighted.
I'm definately going to buy the products, I can't wait for follicept to come in with possibly better working IGF-1 products. Btw Theradome lately is getting some damn good results. Now using blue light instead of red actually stimulates IGF-1! Maybe we should concentrate on that too, to maximize our IGF-1 levels. Really looking awesome this.Comment
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Wait...creatine? Really? First I've ever heard of that. Would you mind elaborating a bit?Comment
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Objective: This study investigated resting concentrations of selected androgens after 3 weeks of creatine supplementation in male rugby players. It was hypothesized that the ratio of dihydrotestosterone (DHT, a biologically more active androgen) to testosterone (T) would change with creatine supplementation.
Design: Double-blind placebo-controlled crossover study with a 6-week washout period.
Setting: Rugby Institute in South Africa.
Participants: College-aged rugby players (n = 20) volunteered for the study, which took place during the competitive season.
Interventions: Subjects loaded with creatine (25 g/day creatine with 25 g/day glucose) or placebo (50 g/day glucose) for 7 days followed by 14 days of maintenance (5 g/day creatine with 25 g/day glucose or 30 g/day glucose placebo).
Main Outcome Measures: Serum T and DHT were measured and ratio calculated at baseline and after 7 days and 21 days of creatine supplementation (or placebo). Body composition measurements were taken at each time point.
Results: After 7 days of creatine loading, or a further 14 days of creatine maintenance dose, serum T levels did not change. However, levels of DHT increased by 56% after 7 days of creatine loading and remained 40% above baseline after 14 days maintenance (P < 0.001). The ratio of DHT:T also increased by 36% after 7 days creatine supplementation and remained elevated by 22% after the maintenance dose (P < 0.01).
Conclusions: Creatine supplementation may, in part, act through an increased rate of conversion of T to DHT. Further investigation is warranted as a result of the high frequency of individuals using creatine supplementation and the long-term safety of alterations in circulating androgen composition.
Statement of Clinical Relevance: Although creatine is a widely used ergogenic aid, the mechanisms of action are incompletely understood, particularly in relation to dihydrotestosterone, and therefore the long-term clinical safety cannot be guaranteed.Comment
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No ,guys Dr. Okajima is legit. The guy has a scholarship of a god (magna cum laude) compared to someone like Cotsarelis. Follicept seems damn legit to if I look at the credentials of the poeple involved. I was too short sighted.
I'm definately going to buy the products, I can't wait for follicept to come in with possibly better working IGF-1 products. Btw Theradome lately is getting some damn good results. Now using blue light instead of red actually stimulates IGF-1! Maybe we should concentrate on that too, to maximize our IGF-1 levels. Really looking awesome this.Comment
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I think he actually is being sarcastic. the guy has gone from being a doubty thomas to a straight up troll. He's spewing sarcasm on another topic too. It's great to have valid criticism and skepticism based on hard facts or even opinions(even I'm not sold on this approach yet), but man, first he hates on this idea based on a misunderstanding of causation and on anecdotal evidence, insults the very kind and helpful representative of follicept as if he were a dime a dozen shill, and then switches up to obnoxious sarcasm on every comment. I really have no care to get into personal shit here, but he is particularly unpalatable. Moderator should nix that guy, it's horrid people like that who scare serious scientists away from here.
Sorry for going offtopic follicept. Btw what is also good from IGF-1 is that it is a potent activator of the AKT pathway. That is basically a stimulator of cell growth and cell proliferation. This can only have impact on signalling pathways which attribute positively on hair growth. IGF-1 has broader actions, also on downstream signalling. I jumped to fast to a conclusion, without reviewing the broad action of IGF-1. Sorry for that.Comment
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I also reviewed the hypothesis of follicept and it is seems legit.
Pathway diagram. IGF-1 or insulin binding to IGF1R (IGF-1 Receptor) results in activation of signaling pathways which in turn causes Akt or another PIP3-dependent kinase to translocate to the nucleus and phosphorylate Foxo1 at three sites Ser-253, Ser-316, Thr-24). The phosphorylation prevents Foxo1 from binding to its substrates normally, attenuating its usual deactivation of the AR (androgen receptor). Ligands binding to AR stimulates expression of IGF1R, creating a positive feedback loop.15The androgen-androgen receptor (AR) system plays vital roles in a wide array of biological processes, including prostate cancer development and progression. Several growth factors, such as insulin-like growth factor 1 (IGF1), can induce AR activation, whereas insulin resistance and hyperinsulinemia …
Basically this means that it can antagonize the androgen receptor. FOXO1 is a downstream pathway that is way more interesting actually. IGF-1 has an impact on this one as you can read.
The most important factor in AGA is the genetic link. Unfortunately, we cannot change our genetics.
It seems that the second most important factor in AGA is the forkhead box (foxo) family. It regulates pretty much everything in AGA.
1) How androgens interact
2) Interacts will various factos p16,p27,p53,akt, mapk, ampk, and much more
3) Regulates cell cycle, quiescence, senescence, etc
4) Involved with estrogen receptor
5) Involved with SIRT1, autophagy, mitochondria, antioxidant formation, apoptosis, stat3, almost everything if not everything involved with AGA
Examples of forkhead box family FOXA2. FOXA2, for example, causes androgen sensitivity in which even free testosterone can bind to the androgen receptor and cause hair loss. There are others as well, I posted about some of them already here and in the androgenetic alopecia update thread.
I recommend anyone serious about AGA to read and do some searches about Forkhead box (foxo, fox, etc)
Minoxidil for instance has impact on these factors too;
We demonstrated here that minoxidil plus ATRA additively increased the phosphorylation of Erk in both dermal papilla cells and NHK, compared with minoxidil alone. The role of the Erk signaling pathway in cell growth has been well established (20). The diverse involvement of retinoic acid has been demonstrated in the regulation of developmental processes and the modulation of differentiation in various cellular models by the MAPK pathways (21, 22). The MAPK pathway is also involved in maintaining cell survival by modulating apoptotic molecules including Bcl-2 family (23). The PI3 kinase/ Akt cascade plays a crucial role in cell survival and the prevention of apoptosis (24, 25). The crosstalk between Erk and PI3K/Akt pathway has been demonstrated to prolong cell survival (26). Our results thus suggest that the activation of Akt, an anti-apoptotic molecule, by minoxidil plus ATRA may prolong survival of DPCs and epithelial counterpart.In summary, our data suggest that the enhanced hair growth by minoxidil plus ATRA in our short-term organ culture may be explained through prolonged survival of epithelial cells and dermal papilla cells, which mediate signals for follicular epithelium. Minoxidil plus ATRA more increased the phosphorylation of Erk and Akt early 1 hr after the treatment than minoxidil alone. The change of Bcl-2/Bax ratio, P53 and P21 were also detected later 24 hr after the treatments. Minoxidil plus ATRA could work together to prolong the survival of cultured dermal papilla cells and epithelial cells and to protect them from apoptosis by dual mechanisms with different kinetics: 1) the activation of Erk- and Akt-dependent pathways and 2) the increase of the ratio of Bcl-2/Bax and the suppression of the expression of P53 and its downstream target P21.Comment
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Is this swooping guy for real? I don't think anyone on here has a problem with me but you dude. First you call me a baboon for calling you out on generalized and misinformed criticism, then you get all sarcastic, and now you seem to have completely turned around and actually support folicept's line of thinking, all the while claiming that I have a low IQ. No one can follow you anymore. Maybe you're just a crazy person? Either way, can you please stop with the broscience overload on the forum? I have my ideas too, but I'm not polluting the thread with them. let the professionals do their work.Comment
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Is this swooping guy for real? I don't think anyone on here has a problem with me but you dude. First you call me a baboon for calling you out on generalized and misinformed criticism, then you get all sarcastic, and now you seem to have completely turned around and actually support folicept's line of thinking, all the while claiming that I have a low IQ. No one can follow you anymore. Maybe you're just a crazy person? Either way, can you please stop with the broscience overload on the forum? I have my ideas too, but I'm not polluting the thread with them. let the professionals do their work.Comment
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Swooping, you call him a baboon because he was open to the possibility of follicepts potential,
then you realize there may very well be potential in their product,
yet you still maintain that he's a baboon?
....and then you report him for harassment?...and proceed to call him a monkey, again.
it is quite apparent that your raw IQ may be quite high, but dude you are emotionally immature.
Man up and apologise.Comment
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Swooping, you call him a baboon because he was open to the possibility of follicepts potential,
then you realize there may very well be potential in their product,
yet you still maintain that he's a baboon?
....and then you report him for harassment?...and proceed to call him a monkey, again.
it is quite apparent that your raw IQ may be quite high, but dude you are emotionally immature.
Man up and apologise.Comment
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