Diet - Inflammation - male pattern baldness- The Process...

[powersam]

well i can hem a floral flannel nightgown in under 15 minutes.. thats pretty super dont you think?

 

[docj077]

well i can hem a floral flannel nightgown in under 15 minutes.. thats pretty super dont you think?

With or without pockets?

 

[DammitLetMeIn]

You're still a noob at this whole debate thing..

Far from it.

I've never said that any doctor has been wrong...

Yes you have. On more than 4 occasions. I can retrieve the evidence from the other thread if you want me to.

I have no problem with you disagreeing with M.D.'s. My problem is that people reading you disagreeing with them believe you're a doctor from your screen name and thats very wrong.

In fact, I always point out that any given study that you post has the doctor agreeing with me no more than one to two paragraphs away from where you take your points out of context...

You've done that ONCE with a doctor's opinion and your point was invalid anyway.

I don't take my points out of context. On the contrary, it is you who takes them out of context and fails to recognise their significance.

In fact, many of the studies that you've posted clearly say that their is no correlation between two diseases or physiological abnormalities that you try so desperately to link. ...

There is no desperation. Baldness/male pattern baldness is quite clearly linked with heart disease, diabetes, prostate cancer and many other maladies.

If everyone is going to consider anything, have them consider a forumite without any formal scientific training trying to convince people that their diet is the source of all their problems. ...

Or perhaps consider this: what you eat has an impact upon your insulin levels and IGF-1 levels, your testosterone levels, your DHT levels, your SHBG levels which in turn have an impact upon what amount and quality of hair grows on your head.

You also have no formal scientific training. You are simply not qualified to claim otherwise.

Then, consider that this very same person posts studies that contradict the very points he attempts to make...

As I've said before - they don't. The information within them provides support to what I state.

Finally, consider his opinion, formulate your own opinion, and stop listening to the rantings of a person that really has no idea what he's talking about. ...

Or alternatively they could listen to you who, as a mere student feels he knows more than MD's with many years of experience who agree with the points I put forward.

Indeed, it IS THEIR points which I repeat on here.

For some reason you seem to think you have more knowledge than them. Perhaps you're scared of anything theysay which conflicts with your rather insecure view.

And yes, I can provide evidence. Want me to?

 

[Bertie]

I'm going to stick my nose in here to make one observation -- the Japan thing.

This whole "post war Japanese have male pattern baldness while pre war Japanese did not" seems to be the first line argument for any one arguing for a major connection between diet and male pattern baldness.

But not once have I seen any paper, any serious population study that makes this conclusion. Is the whole thing just anecdote? If if it be just anecdote, then the observation must be controlled by some highly relevant facts --

-- Japan has the world's highest life expectancy.
-- Japan has one of the world's lowest birth rates.

Put those two together -- and you get this -- Japan is an extremely old society. In fact, not only is modern Japan an extremely old society, it is quite possibly the oldest society there ever was. And old age means diabetes, heart disease -- and male pattern baldness. Pre-war Japanese simply who got sick simply didn't live into old age, while now they do.

Any one who is claiming that the Japanese are giving themselves diabetes, cancer, male pattern baldness and so forth by eating beef and white bread must account for all this. I doubt there is any serious study out there that does, or whether such a study would be even possible.

 

[docj077]

You're still a noob at this whole debate thing..

Far from it.

No, quite close to it.

I've never said that any doctor has been wrong...

Yes you have. On more than 4 occasions. I can retrieve the evidence from the other thread if you want me to.

I have no problem with you disagreeing with M.D.'s. My problem is that people reading you disagreeing with them believe you're a doctor from your screen name and thats very wrong.

Prove that I have said, "this doctor is wrong" on more than 4 occasions. Prove that I have used those exact words.

In fact, I always point out that any given study that you post has the doctor agreeing with me no more than one to two paragraphs away from where you take your points out of context...

You've done that ONCE with a doctor's opinion and your point was invalid anyway.

I don't take my points out of context. On the contrary, it is you who takes them out of context and fails to recognise their significance.

Nope, you keep taking them out of context. I've bolded the exact words of doctors and researchers for you on more than one occasion.

In fact, many of the studies that you've posted clearly say that their is no correlation between two diseases or physiological abnormalities that you try so desperately to link. ...

There is no desperation. Baldness/male pattern baldness is quite clearly linked with heart disease, diabetes, prostate cancer and many other maladies.

male pattern baldness is linked with those disorders, because it is the result of a hyperfunctional androgen receptor. That is proven. All downsteam effects associated with that hyperfunctional androgen receptor cause the physiological anomalies. IGF-1 is increased in the scalp in people with male pattern baldness, because that's the functional purpose of the androgen receptor. When androgens bind to the androgen receptor in men with male pattern baldness the result is going to be increased production of growth factors. However, they are also the possible substance that leads to the damage. Diet has no effect on this process.

If everyone is going to consider anything, have them consider a forumite without any formal scientific training trying to convince people that their diet is the source of all their problems. ...

Or perhaps consider this: what you eat has an impact upon your insulin levels and IGF-1 levels, your testosterone levels, your DHT levels, your SHBG levels which in turn have an impact upon what amount and quality of hair grows on your head.

You also have no formal scientific training. You are simply not qualified to claim otherwise.

Yes, I do have the training. I graduated Summa c*m Laude with a 3.9 GPA from SDSU. My major was Biology and my minors are chemistry and microbiology. Once I graduated, I spent one year in graduate school working towards my masters in biology. During that time I spent 8 hours per day in the lab as a laboratory technician working on toxin-antitoxin pairs in a post-segregational kill mechanism in enterococcus faecalis. I've had my work published in the papers of fellow laboratory personal and featured on the walls of my medical school. I am fluent in the processes and procedures involved with PCR, fusion PCR, northern blotting, southern blotting, DNA and RNA purification, and genetic cloning. I'm also a former anatomy teaching assistant and have been accepted as a member of the Golden Key International Honour Society. A society that only the elite in the nation and the world are welcomed into. I'm also a former licensed paramedic and just to throw it in there I'm also an A+ certified computer technician.


I forget. What are your qualifications again?

Then, consider that this very same person posts studies that contradict the very points he attempts to make...

As I've said before - they don't. The information within them provides support to what I state.

No, they really don't

Finally, consider his opinion, formulate your own opinion, and stop listening to the rantings of a person that really has no idea what he's talking about. ...

Or alternatively they could listen to you who, as a mere student feels he knows more than MD's with many years of experience who agree with the points I put forward.

Indeed, it IS THEIR points which I repeat on here.

For some reason you seem to think you have more knowledge than them. Perhaps you're scared of anything theysay which conflicts with your rather insecure view.

And yes, I can provide evidence. Want me to?

Do you want to know of three drugs that prove your point is ridiculous? Metformin, somatropin and mecasermin. Look them up and look at their effects on hair growth and loss, as well as, the side effects associated with their use.

 

[DammitLetMeIn]

No, quite close to it....

End your childishness

Prove that I have said, "this doctor is wrong" on more than 4 occasions. Prove that I have used those exact words....

I can show you many occasions when you totally disagreed with the MDs who have many years of experience.

Nope, you keep taking them out of context. I've bolded the exact words of doctors and researchers for you on more than one occasion. ...

You took out of them what you wanted to take out them.

male pattern baldness is linked with those disorders, because it is the result of a hyperfunctional androgen receptor. That is proven. All downsteam effects associated with that hyperfunctional androgen receptor cause the physiological anomalies. IGF-1 is increased in the scalp in people with male pattern baldness, because that's the functional purpose of the androgen receptor. When androgens bind to the androgen receptor in men with male pattern baldness the result is going to be increased production of growth factors. However, they are also the possible substance that leads to the damage. Diet has no effect on this process....

so diet has no effect on heart disease?

so diet has no effect on prostate cancer?

so diet has no effect upon diabetes?

you're dreaming.

Yes, I do have the training. I graduated Summa c*m Laude with a 3.9 GPA from SDSU. My major was Biology and my minors are chemistry and microbiology. Once I graduated, I spent one year in graduate school working towards my masters in biology. During that time I spent 8 hours per day in the lab as a laboratory technician working on toxin-antitoxin pairs in a post-segregational kill mechanism in enterococcus faecalis. I've had my work published in the papers of fellow laboratory personal and featured on the walls of my medical school. I am fluent in the processes and procedures involved with PCR, fusion PCR, northern blotting, southern blotting, DNA and RNA purification, and genetic cloning. I'm also a former anatomy teaching assistant and have been accepted as a member of the Golden Key International Honour Society. A society that only the elite in the nation and the world are welcomed into..

lol. Congratulations you have a biology degree. What college did you go to?

Its also worth remembering that if you do go through so much teaching and endless hours of indoctrination you're not going to be able to accept a conflicting view - even if forwarded by MD's. You become institutionalized. You want me to put up their views so you can disagree with them?

Frankly, I don't believe any of the other stuff. You've shown me enough to provide me with the belief that you'd twist the truth to try to prove a point. You're obviously very insecure about the whole issue.

Do you want to know of three drugs that prove your point is ridiculous? Metformin, somatropin and mecasermin. Look them up and look at their effects on hair growth and loss, as well as, the side effects associated with their use.

Every drug has a range of implications for a body. Relying on them for a specific action without taking into account what other effects they have on the body and actions which are not known is inadvisable and unnreliable.

 

[H/B]

agreed, none of those studdies PROVE Igf 1 is the cuase of vertex baldness. anyone can post a biasd hypothesis with WEAK supporting details, small sample size, ect. on pubmed to serve a personal agenda.

 

[docj077]

No, quite close to it....

End your childishness

No childishness has brought into these forums by me. Only the rantings of an inept forumite like yourself have plagued this place.

Prove that I have said, "this doctor is wrong" on more than 4 occasions. Prove that I have used those exact words....

I can show you many occasions when you totally disagreed with the MDs who have many years of experience.

Never disagree. I merely have pointed out the truth of what they are trying to say within their very research articles. Also, you haven't proven that I said those very words.

Nope, you keep taking them out of context. I've bolded the exact words of doctors and researchers for you on more than one occasion. ...

You took out of them what you wanted to take out them.

No, I took their very conclusions from either the abstract or the results of their very articles and posted them in bold for every person on these forums to see. That's the truth and everyone else sees that.

male pattern baldness is linked with those disorders, because it is the result of a hyperfunctional androgen receptor. That is proven. All downsteam effects associated with that hyperfunctional androgen receptor cause the physiological anomalies. IGF-1 is increased in the scalp in people with male pattern baldness, because that's the functional purpose of the androgen receptor. When androgens bind to the androgen receptor in men with male pattern baldness the result is going to be increased production of growth factors. However, they are also the possible substance that leads to the damage. Diet has no effect on this process....

so diet has no effect on heart disease?

so diet has no effect on prostate cancer?

so diet has no effect upon diabetes?

you're dreaming.

Diet impacts the regulation of defective genes that are already present. Heart disease, prostate cancer, and diabetes all have genetic abnormalities that correlated with their inheritance and severity. Different forms of heart disease are associated with HLA subtypes. So is diabetes. Prostate cancer is specifically associated with genetic alterations in the androgen receptor, estrogen receptor, or many other receptors including the IGF-1 receptor.

Diet merely influences that which is unstoppable to begin with. You can not change the concentrations of influencial hormones enough through diet to influence the receptor response if the receptor is already capable of above normal stimulation. The body will simply increase the number of receptors to compensate or increase the downstream response. That is the very essence of gene regulation.

Yes, I do have the training. I graduated Summa c*m Laude with a 3.9 GPA from SDSU. My major was Biology and my minors are chemistry and microbiology. Once I graduated, I spent one year in graduate school working towards my masters in biology. During that time I spent 8 hours per day in the lab as a laboratory technician working on toxin-antitoxin pairs in a post-segregational kill mechanism in enterococcus faecalis. I've had my work published in the papers of fellow laboratory personal and featured on the walls of my medical school. I am fluent in the processes and procedures involved with PCR, fusion PCR, northern blotting, southern blotting, DNA and RNA purification, and genetic cloning. I'm also a former anatomy teaching assistant and have been accepted as a member of the Golden Key International Honour Society. A society that only the elite in the nation and the world are welcomed into..

lol. Congratulations you have a biology degree. What college did you go to?

Its also worth remembering that if you do go through so much teaching and endless hours of indoctrination you're not going to be able to accept a conflicting view - even if forwarded by MD's. You become institutionalized. You want me to put up their views so you can disagree with them?

Frankly, I don't believe any of the other stuff. You've shown me enough to provide me with the belief that you'd twist the truth to try to prove a point. You're obviously very insecure about the whole issue.

So, now you mock the very institution that brings you the research that you cling so helplessly to for your less than satisfactory theories and rantings. Talk about biting the hand that feeds you on this one.

Since you do not accept the method that is used to bring you the research, then you are also incapable of understanding or using that research as a basis for your arguments. From now on, I'd appreciate it if you wouldn't belittle the scientific community with the very ignorance that prevents you from understanding the M.D.s and Ph.D. that you defend. It's an insult to them.

Do you want to know of three drugs that prove your point is ridiculous? Metformin, somatropin and mecasermin. Look them up and look at their effects on hair growth and loss, as well as, the side effects associated with their use.

Every drug has a range of implications for a body. Relying on them for a specific action without taking into account what other effects they have on the body and actions which are not known is inadvisable and unnreliable.

Actually, that's the complete opposite of what I'm saying. Look at what the mechanism of action is for those drugs and then look at your side effects. You'll see that the very use of those drugs and the outcome associated with their use goes against everything you continue to preach.

 

[docj077]

You still haven't posted your qualifications, Dammitletmein.

Surely, if anyone is to trust you, then you must have some sort of formal scientific training.

 

[DammitLetMeIn]

No childishness has brought into these forums by me. Only the rantings of an inept forumite like yourself have plagued this place.

Not only have you brought childishness, you have consistently brought insults, let other people think you're a doctor when you're not, and generally behaved totally inappropriately when you have posted.

Never disagree. I merely have pointed out the truth of what they are trying to say within their very research articles.

Wrong, you have brought YOUR truth EVERY time. In some articles the facets of information which I have highlighted have sometimes been at odds with the final conclusions of the people who are doing the study. However, where I have felt that the facet of information is worth highlighting OF ITSELF you have went on to try to discredit it by pointing out the purpose of the study when it isn't related to the point I was trying to make.

When, however, I bring a study which is relevant for the PURPOSE of the study, you then go and pull a facet of information which serves your view and try to discredit the study with something totally irrelevant whether it be study size, country whatever.

Also, you haven't proven that I said those very words.

I never said you said those words. That is something you have made up and are now clinging on to, to cover up the fact that you have openly disagreed with M'D.s in favor of your own view (that of a student).

I shall be providing evidence in due course, so don't even try to deny it.

No, I took their very conclusions from either the abstract or the results of their very articles and posted them in bold....

I, on occasion, take things out of studies on occasion which are valuable info of themselves - you then point to the conclusion which is not relevant.

OR, I post a study and then you tell me the study is no good for some twitty pedantic reason.

for every person on these forums to see. That's the truth and everyone else sees that. ....

So now you speak for everyone on the forum as well?

Numerous people have disagreed with you if not directly (its hard to argue with someone who pretends to be a doctor as people wouldn't feel confident challenging the view of a purported medical profession, which of course- you are not) then at least withwhat you say. However, you are trying to create an atmosphere whereby people can't say what they really feel with regards to diet and hair loss. You make it unfair for other people who see and have experienced a link between the two. You create a condition whereby they will be derided for having the view they do.

The people who I see regularly agreeing with what you say are almost all on Finisteride (a pharamceutical drug) and many have shunned taking any responsibility for their diet. They have invested in a particular course of action so of course they'll set out to defend it. Having a 'doctor' on their saide (which of course you are not) makes them feel justified in doing so.

Diet merely influences that which is unstoppable to begin with.....

I have already shown you the latest research which is going on demonstrating that diet trumps genes and changes them.

You can not change the concentrations of influencial hormones enough through diet....

I disagree. Just look at the positive changes in women with symptoms of PCOS when they make changes in their diet.

So, now you mock the very institution that brings you the research that you cling so helplessly to for your less than satisfactory theories and rantings..

I didn't mock the institution. If you read properly I was saying that one can have so much concentrated education that it can blind one to the obvious just because one has been taught otherwise.

They're not theories, 'theories' would be t suggest it remains theoretical when I believe the link between diet, insulin, high testosterone and hairloss to be an actuality.

However, I am prepared to say its theoretical because it is not currently commonly accepted in all medical spheres.

Talk about biting the hand that feeds you on this one.

Your amateur dramatics are impressing no one.

Since you do not accept the method that is used to bring you the research, then you are also incapable of understanding or using that research as a basis for your arguments. .

What are you even talking about? ARe you really that much of a simpleton that you feel you can draw your own biased implications from anything I post?

From now on, I'd appreciate it if you wouldn't belittle the scientific community with the very ignorance that prevents you from understanding the M.D.s and Ph.D. that you defend. It's an insult to them.

And you say I rant? Listen, you're the one disagreeing with them. I shall provide evidence of that.

And I don't belittle the scientific community ever. I take issue with some of the medical community (i.e. YOU) who appear to feel they have a monopoloy over what is right and wrong.

There are many M.D.s whom I agree with and I intend to post what they have written so you can disagree with it again.

And, why do you always try to take childish courses of argument. You always try to stain a character rather than sticking to facts. Argue your point but don't try to bring scientific communities, 'every person on the forum', into a debate. Like I've said before - grow up.

Actually, that's the complete opposite of what I'm saying. Look at what the mechanism of action is for those drugs and then look at your side effects. You'll see that the very use of those drugs and the outcome associated with their use goes against everything you continue to preach.

Do you even know what you're trying to say?

 

[DammitLetMeIn]

You still haven't posted your qualifications, Dammitletmein. .

Worry about ACTUALLY becoming a doctor rather than worrying about my qualifications.

Surely, if anyone is to trust you, then you must have some sort of formal scientific training.

I merely provide information which medical professionals, scientific experts, dieticians, herbalists and naturopaths have already forwarded.

All I ask is people tell me what they think - not to agree.

You (unlike others) seem intent upon an agenda which you have to follow my posts and pick out irrelevant details in a desperate attempt to control the minds of others.

 

[DammitLetMeIn]

Posted by Wookster in the last thread:

Comparative Rates of Androgen Production and Metabolism in Caucasian and Chinese Subjects1

[...]


Clinically apparent prostate cancer occurs more commonly among Caucasians living in Western countries than in Chinese in the Far East. Prior studies demonstrated diminished facial and body hair and lower levels of plasma 3-androstanediol glucuronide and androsterone glucuronide in Chinese than in Caucasian men. Based upon these findings, investigators postulated that Chinese men could have diminished 5-reductase activity with a resultant decrease in prostate tissue dihydrotestosterone levels and clinically apparent prostate cancer. An alternative hypothesis suggests that decreased 3-androstanediol glucuronide and androsterone glucuronide levels might reflect reduced production of androgenic ketosteroid precursors as a result of genetic or environmental factors. The present study examined 5-reductase activity, androgenic ketosteroid precursors, and the influence of genetic and environmental/dietary factors in groups of Chinese and Caucasian men. We found no significant differences in the ratios of 5ß-:5-reduced urinary steroids (a marker of 5-reductase activity) between Chinese subjects living in Beijing, China, and Caucasians living in Pennsylvania. To enhance the sensitivity of detection, we used an isotopic kinetic method to directly measure 5-reductase activity and found no difference in testosterone to dihydrotestosterone conversion ratios between groups. Then, addressing the alternative hypothesis, we found that the Caucasian subjects excreted significantly higher levels of individual and total androgenic ketosteroids than did their Chinese counterparts. To distinguish genetic from environmental/dietary factors as a cause of these differences, we compared Chinese men living in Pennsylvania and a similar group living in Beijing, China. We detected a reduction in testosterone production rates and total plasma testosterone and sex hormone-binding levels, but not in testosterone MCRs in Beijing Chinese as a opposed to those living in Pennsylvania. Comparing Pennsylvania Chinese with their Caucasian counterparts, we detected no significant differences in total testosterone, free and weakly bound testosterone, sex hormone-binding globulin levels, and testosterone production rates.

Taken together, these studies suggest that environmental/dietary, but not genetic, factors influence androgen production and explain the differences between Caucasian and Chinese men.

 

[DammitLetMeIn]

From Doctor Gabe Mirkin M.D.

HAIR LOSS AND INSULIN

Gabe Mirkin, M.D.

Exciting new research shows that high blood levels of insulin and its growth factors may cause male pattern baldness in which men and women lose hair from the top and front of their heads, while hair on the sides of their scalp continue to grow luxuriously. A study from Harvard School of Public Health shows that men who have the highest blood levels of insulin like growth factor-1 are the ones most likely to suffer male pattern baldness. Women who have high levels of insulin (polycystic ovary syndrome) are the ones most likely to lose hair from the tops of their heads. It still is early in the research, but evidence is accumulating that male-pattern baldness may be caused by high levels of insulin that are produced by eating huge amounts of sugary and floured foods such as bakery products and pastas. We need research to show if male pattern baldness can be prevented by avoiding flour and sugar, eating fruits only with meals and taking drugs such as Glucophage, Actos and Avandia that lower insulin levels.

Signorello LB et al. Hormones and hair patterning in men: A role for insulin-like growth factor-1. Journal of the American Academy of Dermatology February, 1999;40:200-203.

Checked 8/9/05

Agree with him Docj077?


This from Doctor Neil Barnard M.D.:

By the way, the enzyme (5-alphareductase) that turns testosterone into DHT is also found in the scalp,9 where it works mischief of a different sort. DHT plays a critical role in baldness. Without it, men will not lose their hair, no matter what their genetics may dictate. DHT activity in the scalp may be subject to dietary manipulation.


Doctor Mercola (fully trained as a MEdical Doctor as well as being an Alternative medical practitioner) often talks about the link between baldness and insulin. I'm sure Powersam could provide a link.

heres a quote from him:

Dr. Mercola's Comment:

If I had only known this earlier I would still have a full head of hair! Yes folks, up until five years ago I was a certified carb addict and had a terribly unbalanced excess of high grain foods. I really believe this is a landmark article that nails the association between eating sugar and breads and premature baldness.

So there you go guys. For those of you who still have a significant amount of hair left, CUT DOWN the grains if you want to keep your hair. It is far more effective than Rogaine and much less costly. However, you must be warned of the side effects of a low grain diet - you will achieve far higher levels of health, and decrease your risk of diabetes, heart attacks, and cancer. If, and only if, you are willing to accept such side effects in exchange for keeping your hair, I would suggest following the healthy eating plan.



From Doctor MacDougall:

3) Growth hormones adversely affect the sebaceous glands causing them to become easily plugged. Insulin-like growth hormone-1 (IGF-1) is known to be increased by dietary protein (meat, poultry, etc.), and especially by dairy products. Research shows elevated IGF-1 levels are associated with more acne.4

4) Cordain L. Acne vulgaris: a disease of Western civilization. Arch Dermatol. 2002 Dec;138(12):1584-90.

 

[DammitLetMeIn]

If these Doctors (yes fully qualified and practising for many years unlike you who is a mere medical student) can accept the link between diet, insulin, DHT and hairloss.

WHY THE HECK CAN'T YOU?

AND WHAT MAKES YOU THINK THAT YOU CAN DISMISS THEIR VIEWS?


especially since you're a student

 

[DammitLetMeIn]

double post

 

[docj077]

From Doctor Gabe Mirkin M.D.

HAIR LOSS AND INSULIN

Gabe Mirkin, M.D.

Exciting new research shows that high blood levels of insulin and its growth factors may cause male pattern baldness in which men and women lose hair from the top and front of their heads, while hair on the sides of their scalp continue to grow luxuriously. A study from Harvard School of Public Health shows that men who have the highest blood levels of insulin like growth factor-1 are the ones most likely to suffer male pattern baldness. Women who have high levels of insulin (polycystic ovary syndrome) are the ones most likely to lose hair from the tops of their heads. It still is early in the research, but evidence is accumulating that male-pattern baldness may be caused by high levels of insulin that are produced by eating huge amounts of sugary and floured foods such as bakery products and pastas. We need research to show if male pattern baldness can be prevented by avoiding flour and sugar, eating fruits only with meals and taking drugs such as Glucophage, Actos and Avandia that lower insulin levels.

Signorello LB et al. Hormones and hair patterning in men: A role for insulin-like growth factor-1. Journal of the American Academy of Dermatology February, 1999;40:200-203.

Checked 8/9/05

Agree with him Docj077?


This from Doctor Neil Barnard M.D.:

This is from a cancer doctor Neil D. Barnard M.D.:

By the way, the enzyme (5-alphareductase) that turns testosterone into DHT is also found in the scalp,9 where it works mischief of a different sort. DHT plays a critical role in baldness. Without it, men will not lose their hair, no matter what their genetics may dictate. DHT activity in the scalp may be subject to dietary manipulation.

Do you even know the mechanism of IGF-1 production? I don't think that you do. Do you even know the effect of insulin in the body? Again, doubtful.

What those doctors are posting is interesting, but the cause of increased IGF-1 in the scalp is not diet.


What are your qualifications? I want to know how you can justify what you post.

 

[docj077]

If these Doctors (yes fully qualified and practising for many years unlike you who is a mere medical student) can accept the link between diet, insulin, DHT and hairloss.

WHY THE HECK CAN'T YOU?

AND WHAT MAKES YOU THINK THAT YOU CAN DISMISS THEIR VIEWS?


especially since you're a student

What are your qualifications? Your interpretations are merely the interpretations of an amateur.

 

[DammitLetMeIn]

What those doctors are posting is interesting.

Now we're getting somewhere. In what way is it interesting to you?

but the cause of increased IGF-1 in the scalp is not diet. .

They seem to be suggesting it is. Why would they be wrong. Surely their knowledge of medicine is good?

5 MD's!

What are your qualifications? I want to know how you can justify what you post.

I'm posting what the doctors (5 M'D's) are saying. Its written in plain enough English.

 

[docj077]

What those doctors are posting is interesting.

Now we're getting somewhere. In what way is it interesting to you?

but the cause of increased IGF-1 in the scalp is not diet. .

They seem to be suggesting it is. Why would they be wrong. Surely their knowledge of medicine is good?

5 MD's!

What are your qualifications? I want to know how you can justify what you post.

I'm posting what the doctors (5 M'D's) are saying. Its written in plain enough English.

Here is what I want you to understand(so you know where I'm coming from) and what I'm currently working on.

READ ALL OF THIS AND THINK ABOUT IT FOR A WHILE.

From what I can gather, there is indeed an increase in IGF-1 in the scalp of balding males. There is also an increase in TGF-beta. The cause of this increase is genetic and related to the sensitivity of the androgen receptor in balding males. If you do the research, you'll see that the receptor is more sensitive due to triplet repeat mutations in the gene encoding the androgen receptor on the x chromosome.

Normally, the response that the androgen receptor causes is one of IGF-1 production. IGF-1 is of course a pro-growth molecule (normally) in men with normally functioning androgen receptors. In men with hyperfunctinal receptors, the increased function of the receptor leads to increased IGF-1 production in the scalp. You have even posted the evidence for this phenomenon with the increase in IGF-1 found in men with vertex baldness. IGF-1 is normally a pro-proliferation and anti-apoptotic molecule. However, if you produce excess IGF-1 you will enduce a hyperproliferative state (remember your prostate studies) which will lead to either a cancerous outcome or complete cessation of cellular function as the cells approach their mitotic limits. The second choice is what is likely happening in men with male pattern baldness.

What else does that mean for us? Increased sensitivity of the androgen receptor also leads to increased production of TGF-beta from dermal fibroblasts. They have androgen receptors, as well. TGF-beta is a pro-apoptotic molecule that causes fibroblasts to increase their production of collagen. IGF-1 and TGF-beta also work synergistically together to increase the production and deposition of type I collagen.

What the studies that you keep posting are actually showing us is that it's not only diet that increases serum IGF-1 in balding men. Take a balding man with a diet that will increase IGF-1 and then take a non-balding man with the same diet and the non-balding man's IGF-1 levels will be lower. This is due to the increased production of IGF-1 secondary to androgen receptor hypersensitivity. The diet can increase IGF-1 levels, but not in the manner we see in balding men without a genetic abnormality to produce those effects. Remember, the body normally has a negative feedback mechanism that allows IGF-1 to decrease the production of growth hormone, and thus, decrease the release of IGF-1, as well. So, the increase in IGF-1 must be tissue specific, so as to not cause a decrease in IGF-1 production systemically.

So, the end result is increased IGF-1 production in scalp tissue secondary to androgen/hypersensitive androgen receptor binding with the eventual increase in TGF-beta, as well. This process causes the death of keratinocytes and the deposition of collagen (perifollicular fibrosis) to take their place.

I have the studies to demonstrate the androgen receptor hypersensitivity, the increase in IGF-1 in the scalp, the increase in TGF-beta in the scalp, the presence of androgen receptors in the dermal papillae and on dermal fibroblasts, and the synergistic effect of IGF-1 and TGF-beta on fibrosis.


That's what I believe and I'm sticking to it.



Again, lowering IGF-1 levels in the serum through diet will not stop a hyperfunctioning androgen receptor from causing the production of increased IGF-1 at the tissue level. You can decrease the amount of 5 alpha reductase, but the receptors are in place, both testosterone and dihydrotestosterone can bind, and the required inhibition of potent androgen creation and binding is far too high to overcome through mere diet. Herbal or targeted drug therapy must be used as decreasing the production of potent androgens through diet will simply increase androgen receptor production and the binding of less potent androgens to maintain the cellular response.

 

[docj077]

If you want a few of the studies I'm basing my work on, here's some to read over. Forgive the abundance of extra material. I've tried to bold a few important points. Also, forgive my poor reply time. I have a final tomorrow.

These studies will show you that androgen binding causes TGF-beta. I can't find my study that demonstrates that androgen binding causes IGF-1 production, so you'll have to either find that yourself or take my word for it. They will also show you that IGF-1 increases proliferation and decreases differentiation (a process needed for hair growth). Lastly they will show you that these molecules and work alone or together to increase follicular fibrosis.

Study#1: Basically demonstrates that IGF-1 and TGF-beta work both together and alone to cause fibrosis through the processes that inhibit extracellular matrix degradation by inhibiting collagenase. Androgens increase both IGF-1 and TGF-beta, so any increased sensitivity in the androgen receptor will increase the amount of these two molecules.

Study#2: Testosterone increases the production of TGF-beta and the expression of type 1 collagen mRNA. So, adding to the pro-fibrotic response of androgens.

Study#3: This whole study can be summed up by the last line. Increased IGF-1 receptor signaling leads to increased proliferation and decreased differentiation of keratinocytes. A process that will be increased with androgen receptor hypersensitivity.

Wound Repair Regen. 2007 Mar-Apr;15(2):236-44.
Keratinocyte conditioned medium abrogates the modulatory effects of IGF-1 and TGF-beta1 on collagenase expression in dermal fibroblasts.
• Kilani RT,
• Guilbert L,
• Lin X,
• Ghahary A.
BC Professional Fire Fighters' Burn & Wound Healing Laboratory, Edmonton, Alberta, Canada.
Overexpression of wound healing-promoting factors such as transforming growth factor-1 (TGF-beta1) and insulin-like growth factor-1 (IGF-1) during the healing process has been implicated in the development of dermal fibrosis in patients following thermal injury, surgical incision, and deep trauma. However, the mechanism through which the expression of these two fibrogenic factors is slowed down and/or abrogated in the late stages of the healing process is not known. Here, we hypothesize that keratinocyte-releasable factors counteract the fibrogenic role of both IGF-1 and TGF-beta1 in fibroblasts. To test this hypothesis, the levels of collagenase (MMP-1), as an index for extracellular matrix degradation, in dermal fibroblasts in response to either keratinocyte-conditioned medium (KCM) or our recently identified keratinocyte-releasable stratifin in the presence and absence of either IGF-1, TGF-beta1, or both were evaluated. The results of Northern analysis showed a significant increase in collagenase mRNA expression in cells treated with KCM in the presence of both IGF-1 and TGF-beta1. The effect was, at least in part, due to keratinocyte-derived stratifin that was present in KCM. This was ascertained as the levels of MMP-1 mRNA were markedly reduced when cells were treated with stratifin-immuno-depleted KCM. The results of Western blot analysis showed an increase in the level of MMP-1 protein in stratifin-treated fibroblasts and this was consistent with the level of MMP-1 mRNA expression detected by Northern analysis. However, in contrast to KCM, whose efficacy on MMP-1 expression was modestly reduced by either IGF-1 and TGF-beta1, or a combination of both, these factors abrogated the MMP-1 stimulatory effect of stratifin in fibroblasts. In summary, the results of this study revealed that both stratifin and KCM stimulate the expression of MMP-1-in fibroblasts and this effect can be abrogated by either IGF-1, TGF-beta1, or a combination of both.
PMID: 17352756 [PubMed - in process]

1: Biol Pharm Bull. 2006 Jun;29(6):1246-50
Perifollicular fibrosis: pathogenetic role in androgenetic alopecia.
• Yoo HG,
• Kim JS,
• Lee SR,
• Pyo HK,
• Moon HI,
• Lee JH,
• Kwon OS,
• Chung JH,
• Kim KH,
• Eun HC,
• Cho KH.
Department of Dermatology, Seoul National University College of Medicine, Laboratory of Cutaneous Aging and Hair Research, Clinical Research Institute, Seoul National University Hospital, and Institute of Dermatological Science, Seoul National University.
Androgenetic alopecia (Androgenetic Alopecia) is a dihydrotestosterone (DHT)-mediated process, characterized by continuous miniaturization of androgen reactive hair follicles and accompanied by perifollicular fibrosis of follicular units in histological examination. Testosterone (T: 10(-9)-10(-7) M) treatment increased the expression of type I procollagen at mRNA and protein level. Pretreatment of finasteride (10(-8) M) inhibited the T-induced type I procollagen expression at mRNA (40.2%) and protein levels (24.9%). T treatment increased the expression of transforming growth factor-beta 1 (TGF-beta1) at protein levels by 81.9% in the human scalp dermal fibroblasts (DFs). Pretreatment of finasteride decreased the expression of TGF-beta1 protein induced by an average of T (30.4%). The type I procollagen expression after pretreatment of neutralizing TGF-beta1 antibody (10 mug/ml) was inhibited by an average of 54.3%. Our findings suggest that T-induced TGF-beta1 and type I procollagen expression may contribute to the development of perifollicular fibrosis in the Androgenetic Alopecia, and the inhibitory effects on T-induced procollagen and TGF-beta1 expression may explain another possible mechanism how finasteride works in Androgenetic Alopecia.
PMID: 16755026 [PubMed - in process]


Molecular and Cellular Biology, April 2006, p. 2675-2687, Vol. 26, No. 7
0270-7306/06/$08.00+0 doi:10.1128/MCB.26.7.2675-2687.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Insulin-Like Growth Factor 1 Receptor Signaling Regulates Skin Development and Inhibits Skin Keratinocyte Differentiation

Marianna Sadagurski,1 Shoshana Yakar,2 Galina Weingarten,1 Martin Holzenberger,3 Christopher J. Rhodes,4 Dirk Breitkreutz,5 Derek LeRoith,2 and Efrat Wertheimer1*
Department of Pathology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel,1 Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland,2 INSERM U515, Saint-Antoine Hospital, Paris, France,3 Pacific Northwest Research Institute, Seattle, Washington,4 German Cancer Research Center, Division A080, Heidelberg, Germany5
Received 15 September 2005/ Returned for modification 21 October 2005/ Accepted 22 December 2005

The insulin-like growth factor 1 receptor (IGF-1R) is a multifunctional receptor that mediates signals for cell proliferation, differentiation, and survival. Genetic experiments showed that IGF-1R inactivation in skin results in a disrupted epidermis. However, because IGF-1R-null mice die at birth, it is difficult to study the effects of IGF-1R on skin. By using a combined approach of conditional gene ablation and a three-dimensional organotypic model, we demonstrate that IGF-1R-deficient skin cocultures show abnormal maturation and differentiation patterns. Furthermore, IGF-1R-null keratinocytes exhibit accelerated differentiation and decreased proliferation. Investigating the signaling pathway downstream of IGF-1R reveals that insulin receptor substrate 2 (IRS-2) overexpression compensates for the lack of IGF-1R, whereas IRS-1 overexpression does not. We also demonstrate that phosphatidylinositol 3-kinase and extracellular signal-regulated kinase 1 and 2 are involved in the regulation of skin keratinocyte differentiation and take some part in mediating the inhibitory signal of IGF-1R on differentiation. In addition, we show that mammalian target of rapamycin plays a specific role in mediating IGF-1R impedance of action on keratinocyte differentiation. In conclusion, these results reveal that IGF-1R plays an inhibitory role in the regulation of skin development and differentiation.