S Foote. said:
Ok i am not an unreasonable person, if you want to continue to call yourself "Doctor" for sentimental reasons, go ahead.
But put a disclaimer in your posts like many other people do, so that vunerable newbies are not given the wrong idea you seem to want them to have :roll:
I personaly think you are a dangerous misleading individual on these forums. You read your medical textbooks, then shout about them like you are preaching from a pulpit!
You read all this information, but you haven't got a clue on how to put together a scientific argument from it!
I appreciate your willingness to allow me to keep my name. As I said, I may not be a "Doctor", but Doctor is still my nickname and it really was given to me by my grandfather before he passed away due to complications from glioblastoma multiforme.
I typically strive to only post relevant articles and interpretations. I find that I have a little more insight into the world of research than most people as I've worked in a lab and done the experiments that everyone seems to argue about. It's rather frustrating to see someone like you post that androgen receptors were added during cellular culturing when my biochemistry and research training tells me that it's simply an impossibility. That's why I was very grateful that michael barry posted the article that demonstrated how they used a vector with the androgen receptor gene. They not only used it, but they upregulated it. So, any andrognen response in that study was quite likely equal to the response in balding scalp.
So, when you post your interpretations and I come along and tear you down, I'm not doing it, because those are my interpretations. I'm doing it, because I know what needs to be done for it to be done right. I worked with vectors, vector cloning, and PCR for a long time. I hope that you can understand that.
S Foote. said:
Even Bryan has pointed out to you my argument on pre-didposition about three times, but still you just don't understand it!
When i first told you in this thread about the problems with the in-vitro tests and androgen seeding, you said yourself that such testing would be completely misleading. But now you try to use these "SAME" in-vitro tests as proof of your androgen inducable TGF beta-1 "cause" of male pattern baldness! :roll:
You're right, Mr. Foote, I did say that. That's why I came up with a logical explanation of why exogenous androgen receptor can not be added to cellular culture. Michael simply proved my point when he posted the study, I read the methods section, and it clearly pointed out that they used a vector system. That's how I would have done it, but I either misinterpreted what you said or you simply didn't explain it correctly.
S Foote. said:
You clearly claim in this thread that androgens are creating male pattern baldness by increasing TGF beta-1 from DP cells in a dose dependent manner.
Your whole argument about androgen inducable TGF beta-1 from DP cells "causing" male pattern baldness, is completely refuted by The immuno deficient mice study.
http://www.hairlosshelp.com/forums/mess ... &forumid=1
In this study, there was no maintained effect of androgen inducable TGF beta-1 in a dose dependant, or any other manner! The results were the same in both male and female mice.
Your whole argument falls down with that one study :wink:
Of course you wiil come up with your usual tirade of disjointed medical textbook phrases, but the reality is right there for all to see.
Now, seeing you post what you just posted above really hurts my eyes. I know that you're better than this and I know that you understand how to read studies. Nowhere in that study do they mention TGF-beta, so one can not assume anything regarding that molecule as they did not measure it. There are rules that need to followed here, Mr. Foote. You're breaking them with your interpretations.
The way I understand this article is probably quite different from you. They are taking balding and non-balding hair follicles and putting them into immunodeficient mice. In both cases, the hair follicles demonstrate very similar growth characteristics at 22 weeks. Now, by taking balding follicles out of their balding environment and putting them into a immunodeficient and "normal" environment, you do two things. You remove one of the very characteristics of molecules like Il-1, TNF-alpha, and TGF-beta in that you remove their pro-inflammatory and chemotactic capabilities, because the mice are immune deficient. Not only is this true, but you remove the balding follicles from their normal inhibitory environment. Remember, the action of TGF-beta is inhibitory and it also causes increased collagen deposition to the point of growth and contact inhibition. This inhibition is no longer surrounding the follicle, so obviously, it is going to resume normal growth characteristics. You know and I know that no study demonstrates follicular inhibition at 22 weeks. Do this same study for a year and then you can come and talk to me about interpretations. male pattern baldness is a prolonged, aggressive, and gradually worsening disease. As far as I'm concerned, this study is inappropriate. Not because of their interpretations, but because there is no possible way that such a study would demonstrate anything other than growth. It should demonstrate such findings, because that is exactly what it is set up to do. The mechanism takes time to set up. I know, Bryan knows, and you should know it, as well.
S Foote. said:
Bryan also tried a quick U turn regarding this study when he realised it supported my arguments! But if people take the time to read his original posts in that link, yet again they will see how the rules of evidence get "changed" when it doesn't suit! Just like the donor dominance argument! :roll: :roll:
I got involved in this thread because people were having a go at Armando. I also do not agree with Armando for reasons i have explained before.
But there has been a lot of "pot calling kettle black" here. If you are going to demand other people conform to the rules of scientific evidence, you have to stick to these yourself!
Both you and Bryan regularly show everyone that you both don't mind breaking these rules when it suits your personal arguments. So there is really no point going on with yet another boring repetitive thread, where people just ignore true science :roll:
S Foote.
I'm glad and you and I agree when it comes to Armando. You have to agree that science and evidence are funny things on these forums. For the most part, they seem to be up to personal interpretation when I don't even know if any of us are truly qualified. I've worked in a lab and I'm two years away from my M.D. I have no idea what sort of training that you, Bryan, Michael, or Armando have, so I rarely play the education card. I simply post what I think is right, because that is my interpretation based upon a two years studying medical biochemistry, medical physiology, and medical pathology. I have a 3.6 GPA in medical school, so obviously I've learned something along the way and I frequently score in the top 85% of medical students in this country on board examinations. So, when you think that my opinion is worthless, don't be surprised when I think you're wrong. I've earned my opinion and my current top 15 ranking in my medical school class.
There are no rules to conform to here, but when somebody posts a study that refutes your argument, you should be just as willing to go out and find the right scientific evidence to back your claims. You do that, but I think that sometimes you use your own interpretation of the study instead of the actual authors to come to a conclusion that backs your opinion.
You claim contact inhibition is the cause. I claim androgen induced production of TGF-beta is the cause. I have studies that clearly show that TGF-beta is upregulated as a result of androgen action. I also have studies that show that TGF-beta is associated with increased collagen deposition as a result of increased procollagen expression and decreased collagenase production. Plus, I have studies that demonstrate that TGF-beta upregulates the necessary inhibitor molecules to cause the arrest of proper follicular cycling. Lastly, I have studies that demonstate that collagen is a molecule that promotes contact inhibition.
As far as hair cycling and differences in follicular capabilities go, I have proof of that, as well. The study that I posted early for Armando demonstrates that different hair from different areas of the body including the scalp and the beard require differing concentrations of androgens to achieve the type of hair growth that is readily observed. The only answer for that is an initial different in the intrinsic growth response.
Not only that, but in the total absence of androgen action (like in AIS), scalp hair grows at a different rate from all other hair of the human body including axillary and pubic hair which will still grow in the absence of androgens, but WILL ONLY GROW once puberty begins.
Mr. Foote, you bring a lot of good thoughts to this forum and I appreciate your willingness to step out and say that there is vascular insufficiency and contact inhibition. Unfortunately, the action of TGF-beta and subsequent increase in collagen deposition around the follicle and in vessels resulting in contact inhibition and a lack of vessel flexibility combined with increased vessel obliteration more than makes up for what you currently believe in.
So, believe what you want, but I can explain the whole process from the time the androgen binds to the mutated receptor all the way up to the formation of a vellus hair follicle with an increased sebaceous unit/follicle ratio with ease using what I know about biochemistry and the studies that I've read.
Believe what you want, but that doesn't mean that I'm going to believe it along with you. Sorry, but the journey and the interpretations that I believe in are very different from yours.
Also, I apologize that I responded to you in such a way with multiple responses like this. I get annoyed when people do it to me, but I really have no choice as I had a lot to say. Only reply to what you want to reply to.
