Minoxidil and Insulin

[Bismarck]

There has been done an in-vitro study on follicles with Minoxidil. The authors say minoxidil inhibited hair growth in the absence of insulin.
Could that explain the reports of worsening of hairloss after minoxidil application ?
_________________________________

Limitations of human occipital scalp hair follicle organ culture for studying the effects of minoxidil as a hair growth enhancer.

Magerl M, Paus R, Farjo N, Muller-Rover S, Peters EM, Foitzik K, Tobin DJ.

Department of Biomedical Sciences, University of Bradford, Bradford, UK.

Minoxidil induces new hair growth in approximately one-third of patients with androgenetic alopecia after 1 year of treatment. With several conflicting reports in the literature based on small-scale studies, the current study aimed to clarify whether organ culture of human scalp anagen VI hair follicles is a suitable in vitro test system for reproducing, and experimentally dissecting, the recognized in vivo hair-growth-promoting capacity of minoxidil. Hair shaft elongation was studied in terminal anagen VI hair follicles microdissected from the occipital scalp of 36 healthy adults. A total of 2300 hair follicles, approximately 65 per individual, were tested using modifications of a basic organ culture protocol. It is shown here that minoxidil does not significantly increase hair shaft elongation or the duration of anagen VI in ex vivo culture despite several enhancements on the conventional methodology. This disparity to what is seen clinically in minoxidil responders may be explained by the following: (i) use of occipital (rather than frontotemporal or vertex) hair follicles; (ii) use of, already maximally growing, anagen VI hair follicles; (iii) a predominance of hair follicles from minoxidil unresponsive-donors; (iv) use of minoxidil rather than its sulfate metabolite; and/or (v) use of a suboptimal minoxidil dosage. This disparity questions the usefulness of standard human hair follicle organ culture in minoxidil research. Unexpectedly, minoxidil even inhibited hair shaft elongation in the absence of insulin, which may indicate that the actual hair-growth-modulatory effects of minoxidil depend on the concomitant local presence/absence of other growth modulators.

PMID: 15447724 [PubMed - in process]

 

[Armando Jose]

In my opinion, this is an unfortunate male pattern baldness study…., Why din't use frontotemporal hairs?, why only tested anagen VI hair follicles?. (Mr. Tobin is a good guy with no baldness)
By the way, it's interesting "that minoxidil does not significantly increase hair shaft elongation or the duration of anagen VI in ex vivo culture despite several enhancements on the conventional methodology". Could be the explanation of the observed in men using minoxidil reporting growth of vellus hair but not terminals?
Finally, the link between insulin and hair growth is stronger passing the days. I think there is another report regarding finasteride efficacy and insulin.

Armando

 

[Bismarck]

This is not insulin but IGF (insulin like grwoth factor) that seems to determine the efficiacy of Finasteride.

 

[Armando Jose]

Ah, yes, I remember.

Thank you

Armando

 

[Norwood2.5]

What is pretty strange is that it is reported high insulin levels are on the contrary linked with male pattern baldness, while here it is said that in order for minoxidil to be effective insulin presence is required.

 

[thin=depressed]

--------------------------------------------------------------------------------

M119 -- 6/5/99 updated 3/22/00

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

 

[thin=depressed]

Man! This is getting confusing! So let me get this streight. Gf1 is said to be responsable for pattern hair loss but Biz's posts say gf1 is needed for finasteride to work. WTF meanwhile we have guys who have posted that hgh use has grown back thier hair and its hgh that inspires gf1 production. sh*t I don't know what to think.

 

[thin=depressed]

Now this topic is getting interesting. Here's a portion of a hgh spray study...
------------------------------------------------------------------------------------
In a randomized, placebo controlled study, older adults between 45 and 86 were randomly assigned our HGH formula or a placebo. Subjects receiving the HGH treatment had a 10.8% decrease in body fat, 4% decrease in weight and 151.5% increase in IGF-1 levels. IGF-1, or insulin-like growth factor, is an indicator of growth hormone secretion. This means that our HGH formula actually stimulated the subjects' natural production of human growth hormone. Subjects receiving our HGH formula also had significant improvements in muscle tone, strength, hair growth, sex drive and performance, and energy levels
--------------------------------------------------------------------------------------
Note the 151% gf1 levels and its ig1 is what we don't want.Also note the improvement of hair by using hgh. Now go figure. :hairy: Also adenosine which is a ribose sugar (insulin) is toted as improving hair. :hairy: :hairy:

 

[thin=depressed]

Here's a thought. Does not diabetes constrict vesel blood flow and in which people with diabetes are at risk of limb amputations in severe cases. Is there a link between high levels of insulin and constriction of blood vessels in scalp and this would have an impact on hair count. I know a couple of guys with bad cases of diabetes that have hardly any hair at the age of 20!

 

[S Foote.]

This is yet another study to support the idea that male pattern baldness is not initiated, or affected `directly' within follicle cells.

One thing we know for sure about Minoxidil is that it creates significant Hydro-dynamic changes in fluid balance in-vivo. Minoxidil `shifts' fluid towards the central blood volume, that is away from the the body surface and hair follicles.

http://www.hairsite4.com/dc/dcboard.php ... 051&page=2

This shift in fluid levels away from the follicles, is why Minoxidil grows hair in-vivo, according to the Hydraulic theory.

S Foote.

 

[thin=depressed]

This is yet another study to support the idea that male pattern baldness is not initiated, or affected `directly' within follicle cells.

One thing we know for sure about Minoxidil is that it creates significant Hydro-dynamic changes in fluid balance in-vivo. Minoxidil `shifts' fluid towards the central blood volume, that is away from the the body surface and hair follicles.

http://www.hairsite4.com/dc/dcboard.php ... 051&page=2

This shift in fluid levels away from the follicles, is why Minoxidil grows hair in-vivo, according to the Hydraulic theory.

S Foote.

very interesting, so minoxidil's abilities are indirect by removing excess fluid and perhaps the gf1 and dht in the process.

 

[S Foote.]

http://www.hairsite4.com/dc/dcboard.php ... 051&page=2[/url]

This shift in fluid levels away from the follicles, is why Minoxidil grows hair in-vivo, according to the Hydraulic theory.

S Foote.

very interesting, so minoxidil's abilities are indirect by removing excess fluid and perhaps the gf1 and dht in the process.[/quote:23638]

I personally think that DHT or any other substance for that matter, has no significant `direct' effect on hair follicle growth `in-vivo'. I think that the vast majority of evidence including this study, supports some kind of `in-direct' action of DHT in the miniaturization of hair follicles. I suggest that this in-direct effect is related to `early' normal contact inhibition of follicle growth, because of DHT induced changes in the `pressure' conditions around the follicles. http://www.hairsite2.com/library/abst-167.htm

I think the big problem with current hair loss research, is that the results of the various studies are still trying to be reconciled with a 60 year old `assumption'!! This assumption is that DHT `MUST' act directly on follicles because of the transplantation results.

In my opinion, this assumption failed to take account of other induced changes in transplantation, and therefore other possible explainations for follicle survival. Now this `direct theory' continues to struggle to try to explain experiments like this that just don't support it!

This is the danger of jumping to conclusions in the absense of a `proper' scientific theory, which the direct theory never was!

You only have to consider one thing here. This is that the recognised effect of Minoxidil in increasing hair growth in male pattern baldness, just `CANNOT' be reconciled with any `direct' effect of DHT on hair follicles. In fact, in the `real world', Minoxidil dis-proves the current theory!

The current theory is saying that DHT acts `directly' on follicle cells to restrict their growth at the very center of growth control within the cells genetic structure. This means quite simply that it dosen't matter what growth factors are `thrown' at the follicle, it makes no difference because the genetic `response' to these growth stimulants is `turned off' by DHT.

So the only factors that could possibly change the situation (according to the current theory), are factors that influence this DHT `strangle hold' on the follicles.

Minoxidil has `NO' effect on the DHT pathway, so how can it possibly increase hair growth if the current theory is right?

The simple answer is Minoxidil cannot increase hair growth in male pattern baldness if the current theory is right. We know that Minoxidil does increase hair growth in male pattern baldness, so the current theory is therefore wrong in any proper scientific interpretation!!

This is just one more study, that should indicate to people how increasingly questionable the current theory is!

S Foote.

 

[Bryan]

One thing we know for sure about Minoxidil is that it creates significant Hydro-dynamic changes in fluid balance in-vivo. Minoxidil `shifts' fluid towards the central blood volume, that is away from the the body surface and hair follicles.

This shift in fluid levels away from the follicles, is why Minoxidil grows hair in-vivo, according to the Hydraulic theory.

Oh come on, Stephen... It can cause general fluid retention (your favorite topic), that's why it's also generally used with diuretics, as that study mentioned. You can sometimes see posts on the hairloss sites from guys complaining about "puffiness" in the face after using minoxidil. Sometimes it's bad enough that they have to quit using it! That doesn't jive very well with your theory, does it? :wink:

Bryan

 

[Bryan]

You only have to consider one thing here. This is that the recognised effect of Minoxidil in increasing hair growth in male pattern baldness, just `CANNOT' be reconciled with any `direct' effect of DHT on hair follicles. In fact, in the `real world', Minoxidil dis-proves the current theory!

By no stretch of the imagination does it "disprove" the current theory. That's one of the oddest of all your claims.

The current theory is saying that DHT acts `directly' on follicle cells to restrict their growth at the very center of growth control within the cells genetic structure. This means quite simply that it dosen't matter what growth factors are `thrown' at the follicle, it makes no difference because the genetic `response' to these growth stimulants is `turned off' by DHT.

No, it DOESN'T mean that. If you can supply the necessary growth factors EXTERNALLY that are switched-off internally by androgens, then in principle, that could be sufficient for the normal growth of the follicle.

So the only factors that could possibly change the situation (according to the current theory), are factors that influence this DHT `strangle hold' on the follicles.

No. You can either influence the DHT strangle-hold, or you can supply the missing factors directly. Or both.

Minoxidil has `NO' effect on the DHT pathway, so how can it possibly increase hair growth if the current theory is right?

By directly stimulating its growth via unknown growth factors (possibly VEGF, which is known to be upregulated by minoxidil).

The simple answer is Minoxidil cannot increase hair growth in male pattern baldness if the current theory is right. We know that Minoxidil does increase hair growth in male pattern baldness, so the current theory is therefore wrong in any proper scientific interpretation!!

Wrong, wrong, wrong. Stephen, you're stuck in a rut...

Bryan

 

[thin=depressed]

Can I have a go at this? I have a basic idea compared to yours. What part of our bodies sees the least amount of blood flow? I would think our heads would, so with that in mind poor circulation allows for stagnation and thus allows dht to accumulate in levels high enough to effect hair cells that are already programmed to be sensitive to ANY negative influence. Perhaps the hairs on top are geneticly more sensitive. Insulin and gf1 have been linked to pattern baldness. Could it be that gf1 encouraged dht production. And insulin restricts blood flow all be it miniscule but enough to trigger higher dht stagnation in the scalp where blood vessels are geneticly at a minimum to begin with.
So let me recap. At birth we are exposed to male pattern baldness when genetics gives us a poor amount of circulation in scalp area but this isn't damning. Then our diet giving us large insulin surges that only encourage accumulation of the dht (high levels of gf1 may have produced)stagnation in scalp and everything is in place for male pattern baldness.
Note:Its a known fact that muscles need dht to grow, well surprise surprise men have more muscle due to the fact we are very good dht producing machines. Gf1 is in fact linked to male pattern baldness and interesting enough intake of HGH increases gf1 greatly BUT its not the gf1 that directly inhibits hair growth its the DHT that the gf1 helps produce.
Or perhaps gf1 and insulin TOGETHER produce dht

 

[S Foote.]

Snip all the hocus pocus!


S Foote. wrote:
The current theory is saying that DHT acts `directly' on follicle cells to restrict their growth at the very center of growth control within the cells genetic structure. This means quite simply that it dosen't matter what growth factors are `thrown' at the follicle, it makes no difference because the genetic `response' to these growth stimulants is `turned off' by DHT.

Bryan wrote:
No, it DOESN'T mean that. If you can supply the necessary growth factors EXTERNALLY that are switched-off internally by androgens, then in principle, that could be sufficient for the normal growth of the follicle.<<


No Bryan that just isn't the direct theory you support is it!

In male pattern baldness there is no change in the available growth factors necessary for normal hair growth. The change is in the ability of follicle cells to use these growth factors to grow a large follicle!

The current theory says that this is because of an internal action of DHT with the genetics of `pre-disposed' follicle cells, that alters the growth control program of the cell.

So it is just not possible for anything that does not effect this DHT/cell interaction to change things, according to the direct theory, Simple!

If you want to argue the point Bryan, you will have to be specific about the mechanism you propose?

And please Bryan no more fantasy mechanisms that have no recognised precidents in physiology!

S Foote.

 

[S Foote.]

One thing we know for sure about Minoxidil is that it creates significant Hydro-dynamic changes in fluid balance in-vivo. Minoxidil `shifts' fluid towards the central blood volume, that is away from the the body surface and hair follicles.

This shift in fluid levels away from the follicles, is why Minoxidil grows hair in-vivo, according to the Hydraulic theory.

Oh come on, Stephen... It can cause general fluid retention (your favorite topic), that's why it's also generally used with diuretics, as that study mentioned. You can sometimes see posts on the hairloss sites from guys complaining about "puffiness" in the face after using minoxidil. Sometimes it's bad enough that they have to quit using it! That doesn't jive very well with your theory, does it? :wink:

Minoxidil alters the reletive fluid levels in the various tissues. So if it's moving fluid out of the surface tissue, there is going to be an increase in fluid retension in the deeper tissues. You can have a bloated face because of increased fluid in the deeper dermis, whilst the fluid levels around the hair follicle are reduced.

The quoted study clearly refers to this shift of fluid away from the surface tissue Bryan!

Again Bryan, i am arguing using precidents for differences in fluid levels in the tissue layers. There are also case histories of lymphatic drainage weakness creating hair loss, which is the basis of my Hydraulic theory in male pattern baldness.

http://www.amjdermatopathology.com/pt/r ... 31!9001!-1

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

http://www.lymphedemapeople.com/thesite ... hedema.htm

http://www.pdg.cnb.uam.es/UniPub/iHOP/pm/9659245.html

S Foote

 

[Bryan]

In male pattern baldness there is no change in the available growth factors necessary for normal hair growth. The change is in the ability of follicle cells to use these growth factors to grow a large follicle!

The current theory says that this is because of an internal action of DHT with the genetics of `pre-disposed' follicle cells, that alters the growth control program of the cell.

So it is just not possible for anything that does not effect this DHT/cell interaction to change things, according to the direct theory, Simple!

Oh, is THAT all you're going to do, Stephen? Just keep repeatig the same thing over and over, even after I've told you how VEGF is altered by androgens and antiandrogens? That's a pretty boring response on your part...

And please Bryan no more fantasy mechanisms that have no recognised precidents in physiology!

We BOTH have mechanisms that we can't explain in detail, and have no "recognized precedent". One of yours is that you are unable to explain how and why contact inhibition in hair follicles would alter their response to androgens in vitro.

Bryan

 

[S Foote.]

In male pattern baldness there is no change in the available growth factors necessary for normal hair growth. The change is in the ability of follicle cells to use these growth factors to grow a large follicle!

The current theory says that this is because of an internal action of DHT with the genetics of `pre-disposed' follicle cells, that alters the growth control program of the cell.

So it is just not possible for anything that does not effect this DHT/cell interaction to change things, according to the direct theory, Simple!

Oh, is THAT all you're going to do, Stephen? Just keep repeatig the same thing over and over, even after I've told you how VEGF is altered by androgens and antiandrogens? That's a pretty boring response on your part...

[quote="S Foote.":d035a]And please Bryan no more fantasy mechanisms that have no recognised precidents in physiology!

We BOTH have mechanisms that we can't explain in detail, and have no "recognized precedent". One of yours is that you are unable to explain how and why contact inhibition in hair follicles would alter their response to androgens in vitro.

Bryan[/quote:d035a]

The effect of Minoxidil on VEGF (vascular endothelial growth factor), is far more likely to support my theory rather than yours Bryan. This effects the vasculature and therefore the local fluid dynamics!

Again i will ask you how an influence of Minoxidil on VEGF, or any other growth factor can increase hair production, when your theory says DHT is shutting down the cells growth response internally?

Apart from anything else Bryan, the original Minoxidil study in this thread shows that minoxidil is `not' increasing hair growth directly!!

I have as you well know Bryan, explained my opinion of how contact inhibition `could' be altering the in-vitro response to androgens. I argued this point in our last debate here, using recognised precedents in support of the principle. You may not agree with me Bryan, but please don't try to suggest that i am `unable' to respond to the points.

On the other hand, despite me asking on many occasions, you are unable to offer any precedent or any other support for your `genetic clock' speculation!

S Foote.

 

[Bryan]

Again i will ask you how an influence of Minoxidil on VEGF, or any other growth factor can increase hair production, when your theory says DHT is shutting down the cells growth response internally?

I've already explained to you numerous times: if androgens are downregulating the internal production of certain critical growth factors, then you can presumably circumvent that by supplying those same growth factors EXTERNALLY. I'll keep repeating that for you until you understand it.

I have as you well know Bryan, explained my opinion of how contact inhibition `could' be altering the in-vitro response to androgens. I argued this point in our last debate here, using recognised precedents in support of the principle. You may not agree with me Bryan, but please don't try to suggest that i am `unable' to respond to the points.

Oh, you're responding all right, but you're unable to respond WELL to those points! :wink:

Your claim above that you've cited "precedents" is a complete sham, Stephen. I don't care what you think COULD be happening from contact inhibition, all I care about is what is obviously so embarrassing to you; namely, that there is not a shred of evidence that contact inhibition can alter the way that hair follicle cells (ANY kind of cell, for that matter) respond to androgens. That is pure and utter speculation on your part. It's not based on ANY kind of biological "precedent".

On the other hand, despite me asking on many occasions, you are unable to offer any precedent or any other support for your `genetic clock' speculation!

Yep, you're right: we BOTH have things we can't explain in detail! :wink:

Bryan