Stephen Foote and his Hydraulic Theory of Hair Loss

Earlier this month, an online hair loss legend (a word I generally dislike using) e-mailed me out of the blue. His name is Stephen Ian Foote. He is an independent researcher based in the UK. Even though he is now in his 60s, it seems like Stephen is still extremely interested in hair loss research. I do not know anyone more persistent than Stephen in our sector of the internet. Over three  decades of persistence and counting in his case.

Stephen Foote and the Hydraulic Theory of Hair Loss

Before I proceed to what Stephen sent me, below are some links of interest:

The below is written by Stephen for this blog’s readers:

My research into hair loss can be summed up very simply. Hair loss research is all about trying to find the cause of the restricted anagen growth of hair follicles within the dermal tissue, “within” the dermal tissue being the important point in my research.

In general tissue physiology, it is recognized that all normal tissue growth in vivo, is restricted by the growth control described here.

Hydraulic Theory of Hair LossThis in vivo growth restricting factor must apply to hair follicle enlargement in the dermis, but is very clearly not being taken account of in the historic or current research into hair loss. My research is about what happens when you apply this in vivo growth control, to the known data about hair loss. This clearly
explains why promising treatment indications in vitro and animal models, are just not working in the Human condition.

The Background

I am an English systems engineer, with over forty years’ experience of building and troubleshooting complex mechanical/hydraulic systems. On occasion I have acted as an expert witness in legal disputes in my field. I became involved with hair loss research entirely by chance, when I saw a TV science programme about this problem. Being affected by hair loss myself, I was keen to try to understand what was going on here.

From the information presented, what initially struck me about hair follicle enlargement from my systems engineering perspective, was the pocket based structure of the follicle, with the hair production area at its base. This means that any swelling or shrinkage of the surrounding tissue will distort the follicle in such a way as to change the size of the hair production area. This was in 1995, a time when I only had access to textbook physiology. My first article
about this was published in Medical Hypotheses, Hair Growth and the Fluid Factor, 1995 Jun; 44(6): 475-8.

Shortly after this, I developed a serious long term illness, and any further research into this had to be put on hold for a long time. In 2002 I got internet access, and getting hold of studies etc significantly improved, and I started to do more research into this issue.

I published another article in Medical Hypotheses, The hydraulic influence in androgen related hair growth, implications in autoimmune disease. doi:10.1016/S0306-9877(02)00259-1

I also joined the hair loss forums for links to further information, and to see if anyone could provide any scientific reason why I was on the wrong track here. There were a few posters who made such claims, but the so called science behind these claims was flawed in my opinion.

By this time I had contacted many expert scientists in the field about this issue in the current research, but just got a consistent no comment. It should be noted that this factor in follicle miniaturisation, predicted the failure of the established treatment research to produce results in the actual human condition.

Current Status

Seventeen years on, and so far this prediction has held true. As time passed, more and more information became available that further supported this dermal interaction, and in 2015 I published a more comprehensive review/discussion article on Researchgate.

Because of the continued refusal of the recognized experts to comment on this issue, I published my latest article that challenges scientists about this in Tissue Science and Engineering. This can also be read on Researchgate.

Ultimately there is a simple bottom line here. Any valid scientific theory is required to explain all the observations, without adding unnecessary complication (the rule of parsimony). In androgen related hair growth, any valid theory must therefore explain the following.

How DHT consistently increases hair growth in certain areas of the body, in something like a dose dependent manner. Also, why in just some individuals DHT has the opposite effect of reducing hair growth in certain scalp areas, in a none dose related way. Then you must explain all the related tissue changes.

These include significant changes in the sweating capacity of the affected tissues, reduced where hair growth is increased, and increased where hair growth is reduced. Also, the increased immune reactions, hypoxia, and fibrosis in the balding scalp. Then of course you must explain why certain hair transplantation procedures work, when others fail. The traditional claims about the role of DHT in changes in hair growth, cannot possibly conform to the established rules about valid scientific theories.

However, once you factor the currently overlooked spatial growth controls into the data about DHT related hair growth changes, it’s a very different story. Then you can explain all the factors described above, by just one initial action of DHT. You can do this using just accepted textbook physiology, and you don’t even need to know what is happening at the genetic/molecular level.

So, what does this mean in terms of treatments for hair loss? A primary role of spatial growth controls in hair follicle miniaturisation, explains why animal and in vitro studies have consistently failed to produce treatment results in Humans. The overruling nature of this in vivo growth control upon all “normal” tissue growth, predicts the same fate for all the current lines of treatment research.

Whilst the molecular details of this growth control are not fully understood, we do know that the Wnt’s pathway is involved here. This explains why manipulating Wnt’s does have an effect upon follicle size. But this is not a viable treatment strategy, because of the real danger of producing cancerous growth.

The in vivo spatial growth controls are also known to be relaxed somewhat during the healing process. This explains why scalp wounding can increase the local hair growth. But this is only a short term effect, and continuous wounding will increase the local fibrotic tissue, making the situation worse in the long term.

There is only ever going to be one way to significantly increase hair growth in these circumstances, and this is of course to significantly reduce the tissue pressure around the follicles. All the current treatments that have some effect upon increasing follicle size, all do this to some degree. Minoxidil, latanoprost, lasers, anti-inflammatories, massage, and reducing the androgen stimulus (Finasteride).

Knowing what the real target is, there are a few possible ways to reduce external tissue pressure a lot more effectively, with minimal side effects and probably quite cheaply. This would require however, that the people in the position to develop this kind of treatment, are prepared to pursue this.


I think people should be aware that in my papers the basic claim is not mine, it is the recognized science in general tissue growth physiology. According to this, the historic and current research into the restricted growth of hair follicles, is overlooking a basic in vivo growth control that must be involved. It is the current hair loss research that is at odds with the mainstream science here.

I do have a degree of hair loss myself, but now in my 60’s, it does not concern me as much. And I have regrown a fair amount from my personal experiments.

49 thoughts on “Stephen Foote and his Hydraulic Theory of Hair Loss”

  1. I’m not 100% sure what he means by external tissue pressure but I am intrigued. When I have more time I’ll check out those links. I’d like to know more about his personal experiments that lead to some regrowth for him.

  2. All good but what does he suggest we do after his 30 years of experience?

    Is it still the big 3 or did he encouter something new we could try?

  3. I applaud the effort, but he has more questions than answers.
    Some long serving members of this forum are probably more knowledgeable.

  4. Does he have his Foote in his mouth?

    I think innuendos and cryptic story is not credible. Give me cold hard facts with photos to back it up. How many hundreds of claims have been made regarding hairloss over the years turned out to be untrue.

    I saw the Real Photos from Aclaris for treatment of normal pattern hairloss using JAK. There is a strong possibility of a good treatment only time will tell by the end of 2020 after their next trial ends and with the photos of results. Either way, that is going to be the Cold Hard Truth.

    At this point I have given up on all other talk about being able to grow hair as I have been scammed enough. I am holding my hopes out for end summer of 2020. That hopefully will be it.

      1. They said JAK would Never work now they say at a higher dose it will Never work better. I say they are wrong – again.

        1. ok but still needs to go through stage II, stage III and approval.. how long you think it would take? ~4 years in my opinion.

    1. I want whatever works but tired of false promises. I can see results of JAK at low dose real photos the others are just words. Again anything that works I am first in line but just think the line is for JAK.

  5. I read some of his stuff and i’ts really interesting but on the other side a little crazy. Like I think somewhere on hairlosstalk forum he speculates that dht is good for hair and the future treatment could be to reduce dht in hairy places like beard and increase dht further in the scalp by using some dht cream :) so this is 180 degrees from the mainstream science :)

  6. “Knowing what the real target is, there are a few possible ways to reduce external tissue pressure a lot more effectively, with minimal side effects and probably quite cheaply. This would require however, that the people in the position to develop this kind of treatment, are prepared to pursue this.”

    Well then clearly explain these cheap, effective ways to reduce external tissue pressure. People will fall into position if you have anything of measurable value; a theory here, a speculation there, is of no help to those of us who just want to escape this labyrinth, not add more twists and turns.

  7. I think there’s definitely a place in medicine for the dedicated citizen-scientist. It’s not the credentials that matter.

    At the same time, non-professionals pushing psuedoscience-based agendas are responsible for a lot of misinformation and harm — think autism “cures,” fake cancer treatments, anti-vaccination movements, etc.

    Mr. Foote’s theory doesn’t seem to be misinformative. Signaling molecules are certainly the en vogue arena of research and experimentation for hair loss. DHT, prostaglandins, JAK/STAT, WNT… it’s all signaling. Foote is suggesting that medical interventions could target the structural changes caused by these signaling processes, rather than modifying the signals themselves, right?

  8. Firstly in response to the comments, I think most of these points are answered in my review/discussion paper linked above. This includes the study linked by Admin about the ligature of scalp arteries, and how this fits in. I suggest people read this paper, then I can answer specific points here. This paper covers the role of this dermal interaction in evolution, and also the pressure connection in other forms of rapid hair loss.

    I think it is important to make a couple of points about the historic and current research.

    It does not matter what anyone thinks about scientific issues, and this includes scientists themselves. There are strict scientific rules about valid research and valid peer review. In peer review one primary reason for the rejection of papers is described by Wiley publishers as quote, “Ignoring a process that is known to have a strong influence on the area under study”

    According to this rule, all the published papers about hair follicle miniaturisation that fail to consider spatial growth controls, should be retracted. As far as I can see, this means all of them. I have no issue with the technical correctness of what is in these published studies, it is what is missing from them that is important here, and this breaks a basic scientific rule.

    There is another scientific rule here. Any theory must be falsifiable, ie able to be proven wrong. The idea that the significant action of DHT is within the follicle itself, has been falsified many times over the last 50 years or so. How, because every single treatment proposal based upon this notion, has failed to produce the expected results in the Human condition. Everyone who uses the hair loss forums is well aware of this ongoing situation.

    Just to add something, it is perhaps easier for mechanical engineers to grasp the principle involved in this dermal interaction, because the enlarging pocket principle here is used by engineers to test the resistance or hardness of materials. A crude analogy may help people to better understand this. If you push your finger into an inflated party balloon with a fixed amount of force, the size of pocket formed is directly related to the pressure in the balloon. In engineering terms, enlarging anagen hair follicles are very sensitive pressure sensors.

    I will check here in a few days, to answer any specific questions about the points I raise in my papers.

    1. All the theory is great, but what are the **practical suggestions** I don’t get? Massage? Anything else? Anyone understood?

  9. Stephen Foote,

    I applaud your efforts. However, as someone going for their practitioner degree and as an indivual who has made two speeches at a university with academics on human physiology to a demographic that doesn’t fully understand human physiology in depth, more chemistry and physics…..I think you may need to break it down. When i spoke, it was off a research paper i which the university can use, I had to sign a waiver. Indeed a PH.D in a non related science used my work.

    However when I spoke, it was not off the research paper. It was a powerpoint, which failed to connect to the main big screen, so I had to make a speech with what was in my head, unscripted. The whole thing is I didn’t speak to the audience as if they knew what i was talking about. I broke it down.

    I think ppl on here are actually saying…break it down. For example, i specifically gave $ numbers for a health condition for the cost to treat in the top percentile and then compared that to the demographics median income for ppl to truly understand the significance of that particular disease. Then I went into more in-depth on the disease itself. So ppl who had no knowledge had an understanding of the financial aspects and disease itself. Kind of see what I am saying? A research paper and conveying information are two different birds, but in the same nest.

    So I think…and anyone correct me if i am wrong, but what are your suggested ways of approaching hairloss that one can do based on your theories and research…and why? Taking into account this doesn’t replace medical advice.

    Also I was not being insultive, just curious.

  10. Everyone has asked you what these personal regrowth experiments are. Your papers do not provide any details.

    We are here for a hairlossCURE (preferably in the next 18 months) …Do you have one? —That’s it.

  11. Admin must have hundreds of people on this forum. Stephen, if you could give us all one experiment each for your theory, maybe we’ll have the cure ! (-:

  12. Mr Foote, you point to anything that works in any way such as Minoxidil has an effect on hydraulics. Minoxidil is a vasodialator which by my understanding increases blood flow yet curbing blood flow by ligature was just pointed out. This all seems contradictory.
    Your point seem to be “too much pressure in the plumbing”, so is the goal to slow blood flow or increase blood flow with things such as vasodialation while also increasing lymphatic drainage?
    If you would be so kind as to simplify it for us, maybe someone might be able to pick up the ball and run it a bit further down the field so to speak.

  13. If we are only here for the cure then every other post on this site can be deleted because we don’t have one yet.

    Foote is simply stating that there is years of research, studies, trials etc that don’t account for a basic set of rules. A set of rules he believes may be holding back actually obtaining the cure.

    I want a cure as bad as anyone but coming down on someone that has their own theories, not ones they read online, is poor taste. Major corporations with billions of dollars haven’t cured us. Major universities and colleges with millions of dollars worth of grants haven’t cured us. 30 years of part time research and a theory as to why they haven’t obtained the cure yet? I’ll listen for sure.

    1. I believe most of us are very specifically only here for the cure and the most direct line of research and thought that leads to it. i.e.

      Foote: “And I have regrown a fair amount from my personal experiments.”

      – According to Foote, he has an effective experiment for regrowing hair. That he decided not to make that his primary point—on a blog that states, “latest news and developments in regards to a cure for hair loss”—but stay silent and instead redirect us to outside links to download his papers and biography is in poor taste.

      Foote: “all the published papers about hair follicle miniaturization that fail to consider spatial growth controls should be retracted. As far as I can see, this means all of them.”

      Is anyone here really interested in or capable of helping him overthrow the entire hair loss research establishment? Or are we more interested in putting to use this [experiment] to possibly grow our own hair?

  14. Loving the comments on here from some people. Happy to come on forums and complain about how little progress gets made and how it’s all a conspiracy. Then some guy comes along who has actually done hte research, come up with a theory and presented it, and suddenly everyone is furious that he dared to look in any ohter direction than what’s already commonly researched. Total lack of vision -well done!

    I need to read his papers in depth, but based on what I understand of them, I can actually see this being supported by a few studies showing novel treatments.

    Google HL and Botox, Galeatomy, Carboxytherapy, Ivory Dome Theory, high blood pressure, L-Arginin and Carnitin – all would support what he is saying, all have been shown to work against HL to an extent.

    Thanks Stephen for your input, look forward to understanding it more in depth and very keen to start more of a dialogue about it.

    1. gbh- I agree. HLC is an incredible resource of *vetted* information for the hair loss community. It doesn’t exist merely to serve as an echo chamber to re-affirm one’s personal pessimistic or optimistic attitudes towards current and potential future hair loss treatments. Bizarre to see some of these negative comments, but such is the nature of the internet…

      Admin – thank you for sharing Foote’s research. All vetted information & ideas are welcome and appreciated! :)

  15. “suddenly everyone is furious that he dared to look in any other direction than what’s already commonly researched.”

    I see no fury, no one here is actually challenging his theory, although I’m sure that’s what he wants. To quote his paper: “I would repeat my basic question to scientists. Is there any evidence that hair follicle enlargement is not significantly influenced by the normal pressure based spatial growth controls?” —Does anyone here have lab access and the tissue to explore this? Blog replies aren’t enough.

    I think everyone just wants to know what he did to regrow his hair. : )

  16. Off Topic.. I have a question. Can I apply minoxidil when topic is on the head. Today is my first day with topic and I have my full head of hair

    1. Thank you Mr Foote for your contribution to the research of androgenic alopecia that has plagued many across the globe and has certainly afflicted everyone visiting this blog.

      As a medical doctor I find his hypothesis to be interesting and a refreshing take to hair loss. I do believe microscopic evaluation of the hair follicles (histology) in normal patients vs patients afflicted with androgenic alopecia will lead to greater understanding and hopefully possible solutions with regard to androgenic alopecia.

      Briefly looking at histologic studies online (Google’s your best friend) in patients with normal hair vs patients with androgenic alopecia, these are the notable differences :
      1) Miniaturisation of the follicles.
      2) Prominence of the sebaceous glands
      3) Decrease in the anagen follicles and an increase in the telogen follicles.
      Among many others…

      Perhaps prominence of the sebaceous glands contributes to Foote’s hypothesis? Sebaceous gland hyperplasia/hyperfunctioning is something known to be caused by DHT (ask any pubertal teenager).

      With regards to oedema of the scalp, perhaps I misunderstood the article, but I believe this may not be a mechanism as patients with androgenic alopecia demonstrate a typical “tightness of the scalp” rather than pitting edema (pictures on Google will be more than explanatory to those unfamiliar). However that being said the lymphatic drainage patterns addressed in Mr Foote’s articles are something to consider for scientists. Again histology and further evaluation may help answer these questions.

      I do look forward to further research into this hypothesis and yes hopefully a timeous solution for us all!

  17. Hi Stephen,

    Can you elaborate on how your theory explains (if at all): (1) body hair to head hair transplants working; and (2) regular hair transplants working. Thanks.

  18. “I would repeat my basic question to scientists. Is there any evidence that hair follicle enlargement is not significantly influenced by the normal pressure based spatial growth controls?

    This is inverted. You should begin with a null hypothesis, that is no significant influence. Then you would seek to find sufficient evidence (statistically significant) to reject the null hypothesis.

    You have to find the evidence in the affirmative not the opposite. All swans are white until you find a black one.

  19. Wow! Bad Aclaris News for Areata

    Aclaris Shares dropped minus 50 percent to yesterday and and are now at 2,25 USD coming from 33 USD Two years ago!

    On the other Hand does this mean good News for Androgenetic Alopecia? …

    “We look forward to advancing our other development programs.”

    1. I got that email…glad they are honest about the failures. Don’t remember any other hair related company saying they got bad results in Phase 2 so openly! All we can do is wait for the 12 month AGA results and hope for the best.

      1. This doesnt make sense. I thought JAK were anti-inflammatory and therefore more likely to work for AA than AGA? But it doesnt seem so. Can anyone explain this?

        1. The biology is too complex to know for sure.

          Do note that for AA, they probably need a miracle result on people who are mostly all Norwood 7 bald. For AGA, even maintenance + 10 percent new hair growth can lead to a bestselling product.

    2. “ATI-502 did not achieve statistical superiority at the primary or secondary endpoints due to high rates of disease resolution in vehicle-treated patients”

      Seems the vehicle had good results by itself.. anyone knows what was the vehicle used?

  20. The leading international companies in the development of baldness treatment /
    Dr. Alexey Terskikh had this to say of the presentation made today.
    “Our new protocol described today overcomes key technological challenges that kept our discovery from real-world use,”
    “Now we have a robust, highly controlled method for generating natural-looking hair that grows through the skin using an unlimited source of human iPSC-derived dermal papilla cells. This is a critical breakthrough in the development of cell-based hair-loss therapies and the regenerative medicine field.”

    1. Yes replied to that before too to someone else…it is based on a study from 2018, but clearly important.

    2. Yes replied to that before to someone else I think…it is based on a study from 2018, but clearly important. Have not looked into Christiano’s company recently, but will check soon. Not too keen to cover her or Cotsarelis lately, but maybe I should !?

  21. Thanks for your comments, to address your points.

    Firstly about the science here. People have mentioned methodologies, and the interpretation of particular studies. This is all very well, but what really matters is what happens when you apply these interpretations to treatments. Everyone who follows the research knows that so far these treatment predictions just don’t work out in the real world.

    A note about Minoxidil. This changes the dermal fluid dynamics, reducing the surface tissue fluid pressures. This is demonstrated by the noted bad skin and wrinkling. The crazing effect upon scalp skin, is a sign that a treatment is reducing tissue fluid pressure.

    According to the recognised science about tissue growth in vivo (remember this is not just my opinion), this ongoing failure to produce results in Humans, is because there is a major scientific flaw in the current research. The issue here in the published studies, is going to be investigated by the scientific powers that be, and I will pass on any further information I get about this.

    On the issue of transplantation.

    In my opinion, there are variables here that have not been taken into account. Importantly how much of the original tissue around the follicles is also transplanted? The Holy grail of hair loss treatment, is to get your miniaturised follicles to significantly re-enlarge. This is what makes this mouse study most are aware of very important.

    I contacted one of the authors about this, and he said that all the original tissue was stripped from around all the Human follicles. I think this was important in getting these results. I will come back to this study shortly.

    In the traditional donor dominance claim, the transplanted follicles retain their original growth characteristics. What we now know about the requirements of tissue engineering in vivo, far better explains this than any genetic differences in the follicles themselves. If you want to grow tissues in vivo, you have to use some kind of supporting scaffold. This protects multiplying cells from the early onset of spatial growth controls, and provides guidance for this new tissue growth.

    According to this principle, when hair follicles are transplanted, the healing process creates a fibrotic shell around the follicles. This acts as a natural scaffold, and dictates the maximum size that future anagen follicles can grow. This creates the donor dominance effect noted. There was a significant notable difference in that mouse study.

    The immune status of the mice used here, means that no fibrotic tissue was formed around the transplanted follicles. As all the original tissue had been removed from the follicles, this allowed all the follicles to be size controlled by the pressure conditions in the mouse tissue. This is the only credible explanation for the results here. The MPB follicles enlarged, and the so called androgen resistant follicles shrank, resulting in the one maximum size of follicle allowed by the spatial controls.

    There are two important things here that are clear beyond any reasonable doubt. Firstly, the Human MPB follicles are not being held in the miniaturised state by any direct action of androgens. Secondly the so called donor suitable androgen resistant follicles, are just as reactive to spatial growth controls as the MPB follicles.

    There has been some recent publicity about yet another stem cell breakthrough to generate new hair follicles. This claims to use biodegradable scaffolds to guide this new growth. This could work initially, but there is a problem. When the scaffold goes, come the next hair cycle so will the new hair growth. That will be the big issue with the cell based treatments. It may be possible to get reasonable initial results, but you could pay a lot of money for an invasive treatment that only lasts for one hair cycle.

    According to this dermal interaction, DHT is the most powerful hair growth stimulator there is, and given the right conditions it will regrow miniaturised scalp follicles. In MPB the problem is too much DHT being produced in the wrong place. I am not going to go into the long and complex fluid dynamics at work here, just what could be done about it.

    The indication is you need to change the balance of levels of DHT in the vascular system of the head. Reducing production in the hairy areas of the scalp and beard, and increasing DHT levels in the balding areas. I think nature is already trying to reduce edema in the bald scalp by producing the noted higher levels of DHT in bald tissue. The problem is the drains are blocked lower down the system, by the action of DHT there. Topicals to achieve this correct balance of DHT levels could be developed, avoiding any adverse systematic effects.

    This mechanism of MPB also explains why topical Finasteride does not work as well as systematic Finasteride. The topical is being used in the wrong place. Such topical 5ARi’s should be used on the hairy scalp and beard area. I think it is also fair to say that Nazarol shampoo’s effect on hair loss, exceeds expectations, because its a quite weak 5ARi. According to this mechanism the enhanced effect of Nazarol, is because it is being used in the right place, that is the hairy areas of the scalp.

    There is something I have found to make a difference in maintaining what you have, and in my case at least, getting some regrowth. This costs nothing only a few minutes a day. The issue here is scalp edema ,and there are physical ways to reduce edema that are used by medical practitioners. This is my personal adaptation.

    The goal is to increase the circulation “through” the scalp. This helps to drain the tissue fluid. Lie on your back with your legs up a wall for 2 or three minutes no longer, this increases the blood levels in the scalp. The treatment effect happens when you stand up, the increased blood drainage from the scalp takes more tissue fluid with it. You just stand up and gently massage the scalp for a couple of minutes to boost the effect, do this twice a day.

    I found that just a couple more minutes after this using a laser comb/brush, can increase the effect. Low level lasers are licensed for edema treatment, as they have been found to stimulate the lymphatic vessels, which is what is needed.

    If I have any further news about this matter, I will post here again. I sincerely wish everyone the best in your quest to grow more hair.

    1. Hi Stephen,

      I like the fact you responded. However, why would increasing DHT in the balding areas be a good thing in your theory? Body builders, as an example, there would be little doubt their hairloss would be a result of increase DHT levels.

      Just getting your thoughts.

    2. Hi Stephen,

      The above example seems to simple to be true. Surely by the same mechanism, alternating hot and cold water would have the same effect?

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