Trying to be layperson freindly about science.

S Foote.

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Trying to be layperson friendly about science.

There are a lot of debates on hair loss forums, that involve what seems to be very complicated scientific issues and processes. Often people ask if these arguments can be described in a way lay people can better understand, and this is my attempt to explain my proposal in such terms.

On the surface science can seem very complicated. This is why the scientific method is taught as a way to work through the apparent complication. The scientific method is just basic common sense, and trying to keep things as simple as possible. Its really all about trying to find the simplest possible explanation. Any explanation that has to add unnecessary complication, is likely to be wrong according to the scientific method.

Keeping the descriptions here as simple as possible.

There is no disagreement on the central question about changes in hair growth. Every hair cycle a new follicle grows in the dermal tissue. The period of this growth phase and the size the follicle grows to, determines how much hair the follicle produces. A long growth phase means a larger follicle and more hair growth, a short growth phase means a smaller follicle and less hair growth. In most cases of hair loss the follicles become very small cycle by cycle.

So the basic question is what causes follicles to change their size in this way?

Most of the discussion about this, looks for changes at the molecular level that may explain the growth changes in follicles. From this point of view it seems very complicated, with lots of various interactions going on. But from another point of view, this process of change becomes very simple to understand.

You don't always need to know how something works at the molecular level, to know how it works at the functional level. I will make a simple analogy.

You don't need to know about the molecular basis of how your car works or all the interactions involved, to know that a certain control performs a certain function. Its what happens at the functional level that matters. It is the same in biology.

There is already a recognised tissue growth control in biology, that operates at the functional level.

This very simply explains the recognised growth changes in hair follicles. To understand how this is relevant here, you have to consider what we know about hair follicles in terms of evolution and their original purpose.

Hair or fur originally evolved as an insulator in mammals, and is an important part of the mammals temperature control system. To be effective hair has to be temperature responsive, increasing in cold conditions and reducing in warmer conditions. There has also got to be a way to shed hair when it matters, particularly around injuries. This is because hair close to injuries can hold dirt etc, and promote infection. Hair loss here allows the animal to clean the wound. So hair growth needs to be adjustable according to conditions.

How the hair cycle "builds" the follicle, and the finished structure is important here.

The first diagram here shows the changing size of follicles during the hair cycle. The second diagram shows the finished hair producing follicle, in the dermal system. The end product here is a pocket with the hair production area at its base, these are the significant features.


Dia 1
Hair_growth_stages_70132103.jpg



Dia2
fg201_1.jpg


The enlargement of the follicle within the dermal system, means the dermal tissue around it has to move out of the way. So the resistance, best thought of as "springiness" of the surrounding tissue is important. We know that tissue growth can be stopped by external pressure, and reducing that pressure allows tissue growth to continue.

http://www.pnas.org/content/111/15/5586.abstract

This normal external growth control, is all that is needed to explain the changes in hair follicle size. It is not necessary to know about all the molecular details involved!

The hair follicle wants to enlarge during the anagen period, what restricts this is the springiness of the tissue around it. The harder the spring, the earlier the switch off point is reached. This means a small follicle and reduced hair growth. The softer the spring, the more the follicle can enlarge before the switch off point is reached. You get a larger follicle and more hair growth. So it is the natural springiness of the dermal tissue around the follicle that determines follicle size and hair growth.

If all this is true, any changes in follicle size will be because of changes in the springiness of the surrounding tissue. We should also remember that even large follicles are small structures, so even small scale changes make a difference.

The primary response to cold in mammals, is to shift the dermal blood flow lower in the dermis to conserve heat. The reverse happens in a hot climate, and blood flow increases in the surface tissue to help get rid of body heat.

These changes in dermal blood supply change the tissue fluid pressures, and the springiness of the tissue around the follicles.

In hot conditions the increased fluid pressure around follicles, increases the springiness making it harder for follicles to enlarge and hair growth reduces. The reverse applies in cold conditions and the follicle can enlarge more. There is another effect based upon the pocket structure of follicles.

The hot response of increasing surface tissue fluid pressure, expands this tissue. This moves the surface of the skin and the attached pocket element of the follicle, away from the hair production area set in the lower tissue. You can see from diagram 2 that such movement would reduce the production area from the outside inwards. This reduces hair growth from follicles already in full anagen. In longer follicles this effect is magnified, and the production area reduces to zero. The hair detaches with the noted club hair shape, reflecting the reduced growth from the outside in to the centre.

The overall effect in response to heat, is a moult and reduced hair growth. With the opposite effect in cold conditions of increased hair growth and volume, ie the winter coat. This is the most simple way possible to adjust hair growth in mammals, in hairs original function as an insulator.

Where you have a significant increase in tissue expansion such as swelling induced by an injury, all the local follicles will be distorted as described and the hair will be shed. Allowing cleaning and reduced risk of infection.

This simple interaction between the hair cycle, follicle structure, and pressure changes in the surrounding tissue, offers all that is required from mammalian hair growth in terms of evolution.

In modern humans, anything that changes these factors, will also change hair growth. The principles of this hair growth mechanism have wider implications than just hair growth. In my opinion this tells a story of human evolution, general physiology, and some gender related diseases. There is also testing that can be done here.

The principle is that hair growth is set by the springiness of the surrounding tissue, modified by changes in local tissue fluid pressure.

Most of the changes in human hair growth have a link with changes in tissue fluid pressure. Inflammatory processes increase tissue fluid pressures. Local edema or tissue swelling is a known effect of many hormone imbalances. In radiation sickness and chemotherapy, the cell damage causes rapid edema. Many treatments that improve hair growth are also known to reduce tissue fluid pressures.

We know that humans also lose hair around injuries, commonly called shock loss.

We can also get some insight here, on the changes necessary to produce modern human hair patterns. There is a clear example of this hair growth mechanism in humans, that anyone can check out for themselves.

Why is it that we get the isolated strips of increased hair growth, we call eyebrows?

If you raise your eyebrows and run your finger down from above them, you can feel the difference in the tissue they grow from. This tissue is softer than the surrounding tissue, you can feel the boundary. This allows increased follicle enlargement and the increased local hair growth.

In my opinion eyebrow growth perhaps reflects our original "fur", and understanding what makes the surrounding tissue different could be important in understanding human evolution.

I think this is as simple and as understandable, as i can make this proposal.
 

benjt

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Unbelievable. Just your bullshyt hypothesis on "fluid pressure" again. You are not trying to help laymen to understand science, you are just trying to sell your wacko ideas.

At least be honest about it when you try to sell your subjective, unconfirmed, and unsupported opinion, instead of pretending that this is the "scientific truth".
 

Armando Jose

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Human hair is more complex than it. the more intriguing issue is the asynchronic growth..., not only hot and cold ;)
 

Python

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Unbelievable. Just your bullshyt hypothesis on "fluid pressure" again. You are not trying to help laymen to understand science, you are just trying to sell your wacko ideas.

At least be honest about it when you try to sell your subjective, unconfirmed, and unsupported opinion, instead of pretending that this is the "scientific truth".

Haha, I like how boldly you put it.
 

Swoop

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Unbelievable. Just your bullshyt hypothesis on "fluid pressure" again. You are not trying to help laymen to understand science, you are just trying to sell your wacko ideas.

At least be honest about it when you try to sell your subjective, unconfirmed, and unsupported opinion, instead of pretending that this is the "scientific truth".

Well said.
 

manualswork

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S.foote , get on a open minded forum, this is dead.
You have an interesting theory and I'm sure people would like to hear more without your topics being trolled just because they don't share your view
 

manualswork

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What does it have to do with having an open mind? We should be able to discuss any theories, whether they have progressed on to treatment advice or not. This is a forum and free speech should be encouraged.
Also he has stuck to science by referencing a study.
Young balding guys can see the list of FDA approved treatments after a 3 second Google search, and it hasn't changed in longer than a lot of male pattern baldness sufferers lives.
This forum is full of old bitter men perched in their thrones, preaching of how finasteride is the only hope.
I remember the dermarolling days and how everyone was slated for believing in alternative treatments, then how admin shut down all the threads because of 2young2retire posting photos of some blood. The last time I saw a photo update from that guy he has fully restored his hair (NW4 to NW1).
I don't follow the same beliefs as S Foote, but that doesn't mean I can insult him. To be productive, I should counter his arguments like an adult.
Rant over
 

benjt

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Also he has stuck to science by referencing a study.
No he didn't, and that's the main point. Just by referencing one study his own ideas and interpretations, which are extremely far fetched and not even supported by the study, do not become true.

Also, what pisses me off: He pretends to be "layperson friendly about science", as states the title. He isn't. He is only explaining his ideas. Not translating "science" into "layperson friendly talk". He wasn't honest about his intentions one bit. And this isn't the first thread he made about his wacko theories. He just tried it with a "trojan horse" this time.

Talking about hypotheses? Yeah, sure, no problem. But selling them as scientific fact? Definitely not.
 

zdm632

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No point in insulting him.
I agree hair loss may not be that simple as he tries to pretend, but let's be honest : what he says makes perfect sense.
Everybody can notice that on top-in the male pattern baldness NW6 area, scalp is very tight, and on the sides and back it is more flexible.
What he says about the hair returning to anagen and having to enlarge, is also true. It's logical that, if the tissue is hard, the follicle can't enlarge.

- - - Updated - - -

No point in insulting him.
I agree hair loss may not be that simple as he tries to pretend, but let's be honest : what he says makes perfect sense.
Everybody can notice that on top-in the male pattern baldness NW6 area, scalp is very tight, and on the sides and back it is more flexible.
What he says about the hair returning to anagen and having to enlarge, is also true. It's logical that, if the tissue is hard, the follicle can't enlarge.
 

S Foote.

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No he didn't, and that's the main point. Just by referencing one study his own ideas and interpretations, which are extremely far fetched and not even supported by the study, do not become true.

Also, what pisses me off: He pretends to be "layperson friendly about science", as states the title. He isn't. He is only explaining his ideas. Not translating "science" into "layperson friendly talk". He wasn't honest about his intentions one bit. And this isn't the first thread he made about his wacko theories. He just tried it with a "trojan horse" this time.

Talking about hypotheses? Yeah, sure, no problem. But selling them as scientific fact? Definitely not.

Well i am not concerned about the ranting's of the forum poseurs who don't seem able to read properly apart from anything else. People should look at the drivel posted by Benjt above as an example of what seems to pass for scientific comments from these people.

So i am just pretending to be layperson friendly, but then only explaining my ideas? This is from the very first paragraph in my post.

" Often people ask if these arguments can be described in a way lay people can better understand, and this is my attempt to explain my proposal in such terms."

How can this possibly be interpreted by any sane person, as me not being honest about my intentions?

How can the basic physics that two things cannot occupy the same space at the same time be called a "wacky" theory?

That one study was the only one needed to give people an insight into the basic cell growth control involved. There are a lot more references in my other thread about this, and a discussion of possible treatments.

What is really pissing off the internet science poseurs, is that i dare to question their authority here. Instead of trying to answer valid questions about their own opinions, there are just these personal attacks. It doesn't bother me at all, and i suggest people do their own research on scientific principles so they are better placed to judge for themselves.

Below is my opinion on the sort of meaningless pseudo scientific crap, that has been posted on the forums for many years. These threads are not intended to address genuine scientific issues, just to make the author look good.

http://www.hairlosstalk.com/interact/showthread.php/89309-Understanding-Androgenetic-Alopecia

In this thread Swoop discovers a link with male pattern baldness and cell senescence. Well cell senescence in an "already" growth impaired tissue, who would have thought that! I am sure your Nobel prize is in the post Swoop.

When i pointed out that this is all after the fact in male pattern baldness, and there are major issues with this being caused by direct androgen action, there was a feet stamping session. Why because these people only want to post about other peoples work, not actually try to explain it themselves!

I expect a lot of the usual excuses to be made, but we have heard all this guesswork many times before.


Yes i have been involved in this for around 20 years on and off. The traditional notion (that doesn't even qualify as a theory) has been around for about 60 years, so how's it doing?

In this time the best scientists in the field have explored this direct action of DHT on male pattern baldness follicles idea, and performed many related studies. In the last 25 years or so, a lot of money has also been invested in cell therapy research based on this idea by various companies.

In all this time the traditional notion has produced nothing of any significance at all, and this situation continues. The honest scientists admit they are still no closer to a genuine understanding of the process of male pattern baldness.

I am not really concerned with trying to convince people on hair loss forums, people here can believe whatever they like. I made a prediction a long time ago on these forums, and so far this prediction has held. It is simply this.

There is a basic law of physics involved in hair follicle enlargement, and unless this is taken into account hair loss research will continue to go nowhere.
 

S Foote.

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Unbelievable. Just your bullshyt hypothesis on "fluid pressure" again. You are not trying to help laymen to understand science, you are just trying to sell your wacko ideas.

At least be honest about it when you try to sell your subjective, unconfirmed, and unsupported opinion, instead of pretending that this is the "scientific truth".


Your a complete fake, who thinks if you shout loud enough people are just going to take your word for anything. There's a clear example of just how good your scientific skills are in this very thread.

You claimed in a response to someone, that the only study i referenced in my first post did not support my theory anyway.

Even you should at least have realised, that my theory is all about external pressure controlling cell and tissue growth in hair follicles. The quoted study proves that external pressure controls cell and tissue growth.

So just how stupid are you? You have proved to everyone here, that you are either an idiot or a liar.

There are people on these forums, who are genuinely interested in hair loss research and raising related questions. But they never post in threads like this, because they know they will just get flamed by fools like you!


For those who are interested in genuine science, i would like to make an important point.

I have no issues with most of the studies relating to male pattern baldness. But most of these studies take things apart and look at the pieces. I am a systems engineer, and what i am doing here is putting the pieces together to build the finished system.

When you do that, the process of male pattern baldness becomes very simple and logical.

The "significant" effect of androgens in the male pattern baldness area, is to increase the local fluid pressure through lymphatic effects. This external pressure restricts hair follicle enlargement, by recognised tissue growth controls.

This same increased tissue fluid pressure, also explains all the other recognised changes in the male pattern baldness scalp. Increased immunology and fibrosis, tissue tightness, and increased sweating, are all recognised effects of increased tissue fluid pressure.

If this is true, there will be a common factor involved in any treatment that increases hair growth in male pattern baldness. These treatments will reduce tissue fluid pressure.

finasteride and dutasteride of course reduce the androgen action, whatever that may be.

Minoxidil has significant effects on the circulation dynamics, changing the fluid balance of tissues. What we see in the "system" is wrinkling of the surface tissue, and swelling or bloating of the deeper tissues. The fluid pressure is being reduced at the level of the hair follicles.

Latanoprost was actually developed to reduce tissue fluid pressure in the eyes.

Low level lasers have been shown to be effective in reducing tissue fluid pressure in lymphedema.

Anti-inflammatories reduce tissue fluid pressure.

Massage and anything else that increases the microcirculation, reduces tissue fluid pressure.

What we need to do to more effectively treat male pattern baldness, is to better target the reduction of the tissue fluid pressure.

- - - Updated - - -

I'm not even going to respond. But I want to say that I went briefly through your post history S. Foote and you are indeed a wacko, moreover I would call you a lunatic. Seriously had some good laughs, thanks for that.

Blah Blah Blah.

If you really want to impress people on hair loss forums (and i know you do), how about you try to do some actual science? Go on i dare you!

Study what we already know about the direct action of steroid hormones on target cells, then tell us all how this explains the "actual" male pattern baldness experience? The completely meaningless phrase of "it's genetic" is not allowed by the way.

- - - Updated - - -

Which scientists would those be?

Try reading the studies.
 

LayZ

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To add to bushbush's simple request...


Foote,

Do you have a genuine understanding of the process of male pattern baldness?
 

S Foote.

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Please define what constitutes an "honest" and a "dishonest" peer-reviewed scientist and how you objectively tell them apart.

The honest scientists are those professionals that are subject to peer review. In terms of male pattern baldness published papers, I have yet to see any scientist claim a definitive answer. To quote the Cotsarelis PGD2 study

"Testosterone is necessary for the development of male pattern baldness, known as androgenetic alopecia (Androgenetic Alopecia); yet the mechanisms for decreased hair growth in this disorder are unclear."

The scientists then go on to present evidence in support for whatever influence they claim. They do not ever claim that the study rules out other possible factors of greater significance.

It is only the self elected "dishonest" scientists on internet forums that make these sort of claims.
 

bushbush

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The honest scientists are those professionals that are subject to peer review. In terms of male pattern baldness published papers, I have yet to see any scientist claim a definitive answer. To quote the Cotsarelis PGD2 study

"Testosterone is necessary for the development of male pattern baldness, known as androgenetic alopecia (Androgenetic Alopecia); yet the mechanisms for decreased hair growth in this disorder are unclear."

The honest scientists admit they are still no closer to a genuine understanding of the process of male pattern baldness.

It is false to suggest that scientists think we are no closer to understanding the process of male pattern baldness. I'm glad you chose the Garza et al., 2012 study as an example. You quote the first sentence from the abstract. If you read as far as the end of the abstract you will also find: "These results define PGD2 as an inhibitor of hair growth in Androgenetic Alopecia and suggest the PGD2-GPR44 pathway as a potential target for treatment."

If these are so-called "honest" scientists, how could you possibly interpret this as being "no closer to a genuine understanding"?

They do not ever claim that the study rules out other possible factors of greater significance.

It is only the self elected "dishonest" scientists on internet forums that make these sort of claims.

There is some irony to this statement.
 

Armando Jose

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The "significant" effect of androgens in the male pattern baldness area, is to increase the local fluid pressure through lymphatic effects. This external pressure restricts hair follicle enlargement, by recognised tissue growth controls.

This same increased tissue fluid pressure, also explains all the other recognised changes in the male pattern baldness scalp. Increased immunology and fibrosis, tissue tightness, and increased sweating, are all recognised effects of increased tissue fluid pressure.

If this is true, there will be a common factor involved in any treatment that increases hair growth in male pattern baldness. These treatments will reduce tissue fluid pressure.

is your theory only applied to scalp hair or all hairs over the skin,...., I am refering to body hair.
These hairs needs androgens to growth, cite in a lot of peer review studies. what do you think?
 

abovedagame

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lol I remember the days when s. Foote used to come onto the forums and start an argument with Bryan that would span pages and pages. Armando used to chime in on the threads too with his broken English and get totally ignored (just like this thread lol). Now that Bryan is gone he is trying to find someone else to argue with him.
 

IDW2BB

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Seems there is a way of determining lymph flow.

http://www.ncbi.nlm.nih.gov/pubmed/17853615


Lymphology. 2007 Jun;40(2):52-62.
Fluorescence microlymphography: diagnostic potential in lymphedema and basis for the measurement of lymphatic pressure and flow velocity.
Bollinger A1, Amann-Vesti BR.
Author information
Abstract
Fluorescence microlymphography (FML) is an almost atraumatic technique used to visualize the superficial skin network of initial lymphatics through the intact skin of man. Visualization was performed with an incident light fluorescence microscope following subepidermal injection of minute amounts of FITC-dextran 150,000 using microneedles. Emanating from the bright dye depot, the surrounding network of microvessels is filled, documentation performed by photography or video film. In congenital Milroy lymphedema, a lack of microlymphatics (aplasia) is typical while in other primary lymphedemas and in secondary lymphedema after mastectomy or irradiation of proximal lymph nodes, the network remains intact but the depicted area is enlarged. Lymphatic microangiopathy characterized by obliterations of capillary meshes or mesh segments develops in phleboedema with trophic skin changes, progressive systemic sclerosis and Fabry's disease. In lipedema, lymphatic microaneurysms are stained. Microlymphatic pressure may also be measured using FML. For this purpose, glass micropipettes are inserted into the capillaries by means of a micromanipulator and pressure is determined by the servo-nulling technique. Normal subjects produced significantly lower pressure (7.9 +/- 3.4 mmHg) compared to patients with primary lymphedema (15.0 +/- 5.1 mmHg, p<0.001). This characteristic lymphatic hypertension may be improved by complex physiotherapy or local application of prostaglandins. Additionally, a modification of the FML procedure can be used to measure lymphatic capillary flow velocity in controls and patients. FML is suited to confirm the clinical diagnosis of lymphedema, contributes to distinguish among various forms of edema, and is useful in clinical research. In addition, FML has also become a tool for experimental animal studies including the depiction of gastric microlymphatics, the measurement of flow velocity in the naked mouse tail, and in evaluation of lymphangiogenesis in a model of Milroy disease.
 
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