Re: Conventional Hair Loss meets Alternative views: The role of inflammation in the gene expression and activation of sex hormone receptor sites

AS54 Fri Jun 01, 2012 10:33 am

Also, it could just be that DHT and other sex hormones are inflammatory incidentally, not because of some evolutionarily selected for effect. I mean, the body produces other inflammatory products. Peat has shown that serotonin, despite how critical for neurological and psychological function it is, is inflammatory. Perhaps certain sex hormones are likewise inflammatory secondarily to their beneficial effects in the body.

Now, someone will probably ask "Wouldn't evolution select against this in favor of hormones that don't exert inflammatory effects?"

Evolution by definition only selects for or against those genes or gene products that have some reproductive effect (whether pro- or against) that is exhibited prior to or during the reproductive phase of that organism. At the time of selection for mating, only those phenotypical qualities that effect one's "fitness" at that time are selected for or against. Something that might cause a late onset of unfit characteristics (disease) would be irrelevant, as that organism would have already served his evolutionary purpose and passed his/her genes along. Again, we have to remember that evolution and our genetics have little concern with how we fare after our respective reproductive phases (outside of a window for ensuring our offspring survive to self-sufficiency), assuming a male's reproductive maximum to be between puberty and somewhere in the 30s.

So consider the average 18 year old male. Despite the fact his DHT had spiked somewhere around 13 or 14, if DHT were primarily inflammatory, his own body's youthful vitality and protective systems would mitigate any real effects on his outward fitness. I mean how else can we explain that normal MPB takes so long to set in (in many cases) given the high levels of sex hormones during and after puberty?

I guess what I'm saying is if DHT were inflammatory by nature, this isn't something that evolution would necessarily weed out of the population because the cumulative effects of that inflammation typically show themselves physically much later than the age range of that person's reproductive continuum. Now, we know this isn't true as of late as younger and younger men are losing hair earlier, leading me to believe our normal background inflammation is being augmented by other environmental factors, and the cumulative effects of generations of epigenetic derangement being passed on to us.

a<r Fri Jun 01, 2012 10:45 am

Posting from my phone so bear with me, ill post more when I get to a computer.

Inflammation is so villified, even and possibly especially by natural health, but really once you look deeper into things, inflammation is a very important evolutionary trait, it is truly our immunity. Good posts Anthony, seriously, will also add more soonish.

AS54 Fri Jun 01, 2012 10:58 am

Thanks man. I love this topic. Lookin' forward to it.

LawOfThelema Fri Jun 01, 2012 11:30 am

Because remember getting us to that point of life, to the point of reproduction, is all our genes care about.

Your genes don't have a mind. As such they have no cares.

a<r Fri Jun 01, 2012 12:37 pm

LawOfThelema wrote:
Because remember getting us to that point of life, to the point of reproduction, is all our genes care about.

Your genes don't have a mind. As such they have no cares.

We're getting pretty deep there, but this is something talked about years ago by users like Prague and jdp.

Genes don't necessarily not have a mind, its easier to think of them and everything else in nature as shapes governed by and produced by tight mathematical law. One could get pretentious about it and see these shapes and algorithms in such seemingly different things as physics, music, geometry, visual presentation of organisms, molecular structures of the elements, and then take it a step further by seeing the same trends in how we perceive said things on a daily basis (ie dissonant notes in music, our distaste for objects and structures that aren't symmetrical). What the Takeaway is with all that, oncemore as devoid of pretension as possible, is perpetuation. Its a system that keeps moving and adapting. Our genes are probably pushed into a mode of self preservation like middle class citizens in a Japan subway car.

AS54 Fri Jun 01, 2012 4:09 pm

Lawofthelema,

I understand that. I didn't mean to say they literally had a mind. Its just difficult for people to talk about these things without suggesting some kind of goal oriented behavior and assigning concepts we understand to them. To put it in a way that might make more literal sense, the effects of genetic expression that occur after our respective reproductive phases have little effect on how those genes are perpetuated and carried into the future. The only thing with selective bearing on the capacity for these genes to be carried onward is how fit for reproduction the organism is made by those genes. So whatever positive or negative effects on longevity those genes may have after that organism can practically bear children are irrelevant. Hence, genetics doesn't "care" whether we live to be 100, only that our genetic material is transferred from one vehicle to a new one, and so on and so forth. In the context of what I was saying, this pertains to how certain things we know have a genetic component (like MPB) can be carried on in a population. The fact is that human beings at their reproductive phase often don't outwardly signal their predisposition to the condition and so the associated genes aren't selected for or against. Again though, many of us are observing people losing hair earlier and earlier.

I guess what I'm looking at is the duality of genetics and physiology. One one hand a hormone, like DHT, could have several positive aspects, contributing to genetic fitness to such a degree that it is perpetuated, if those effects contribute positively to reproductive value at the time of selection. It could also have negative effects such as inducing inflammation that would be neither selected for or against, because these effects do not show outwardly (typically) until after reproductive years, this process allowing for biological chemicals to exert both positive and negative effects simultaneously.

987 Sat Jun 02, 2012 1:09 am

How I see it, genetic susceptibility aside, we all were born growing hair and lived many many fully functional healthy years successfully growing hair, something along our path changed in our bodies, or the effects of long term low grade inflammation, built up toxicity, or deficiencies of any sort finally became detrimental enough to express itself through our hair. The only cure is to figure out what is affecting our own individual bodies the most, and I think we have to stop it before too many hair follicles are damaged for good because unfortunately I do believe once something fully dies it is dead, and a lot of bald guys on hair loss forums saying nothing is working for their hair loss is because they are acting way too late, rather than when they were still freshly nw1's and 2's. We just need to master upholding the environment inside of our bodies that achieve optimal health therefore not allowing poor hair genetics to express themselves...

AS54 Sat Jun 02, 2012 2:10 am

The way I see it, hair loss (if susceptibility is present) is a normal part of the aging process, the cumulative effects of inflammation over years of living. Like A < R has said, inflammation is vital to our health, a primal part of our physiology. It is how the body heals and restructures itself and also how it fights invaders. The duality of our genetics is that this inflammation can serve such a vital purpose while also eventually leading to the processes of our demise, because only the effects that are seen at the time of reproduction are selected for or against. So protection from infection and the healing aspects of inflammation (muscle building, MTOR), increase our "fitness" leading up to reproduction, our genes are passed on, we've done our evolutionary task, and the same inflammation shows the opposite side of the coin, and something so vital can actually do harm given enough time to proceed chronically. Yin and yang. That is why it is so essential that we try to manage these processes as we age and step in where our genetics are in essence, in "no selection" territory. Using the things CS and others have promoted here, we can mitigate the negative aspects of these processes and hopefully live healthier, fuller lives.

I think the onset of MPB too early is a signal of hyper aging. Something is augmenting that normal, low-level inflammation.

To me, hair loss is some function of total sex hormone concentration, those hormone's receptor status, and the state of the immune system all interacting with one another. The more sex hormone you produce (CS put up a good study yesterday on the effects of ARO and STAR in this process in the skin), the more sensitive and prevalent the receptors are, and how they are dispersed will determine your susceptibility. But I think the heart of this lies in the immune system status. We are really dealing with an inflammatory degradation of the hair bulb: DHT causes and is upregulated by inflammation. I think its really a case of compartmentalized hyperimmunity in the scalp. Perhaps its compartmentalized or systemic, but in systemic cases we see other skin issues ensue.

Consider what we know already to contribute to early hair loss: heavy metals, pathogens, lack of oxygen, poor blood flow. All of these eventually lead to hyper immunity in the scalp. Heavy metals are not only superoxidizers but provide the environment for infection, pathogens are the target of inflammation, lack of oxygen provides the envrionment for pathogens to survive and incite inflammation, vascular damage because of inflammation leads to lessened circulation, hence less oxygen delivery (exacerbated by thyroid problems). All cases lead to a state of hyper immunity with the not only sex hormones inciting inflammation, but pathogens as well who are able to evade the attacks.
So, the increase in poor diet and toxicity in the envrionment can increase that cumulative load of inflammatory stress and cause early hair loss, essentially the processes that leads to our normal aging pattern are occuring more heavily earlier.

We must also consider that a person could be in an "immune system hole" from birth. A lack of breastfeeding or improper foods too early will inoculate the infant at an improper stage of development, introducing a more adult immune system to the child too early. This could effect immunity for the rest of the child's life, in addition to gut function. The epigenetic choices of our parents and prior generations find their way to us, and immune development is a delicate thing.

I'm sorry for the long winded post (forgive me), but I feel hair loss is a natural process that can be kept at bay with proper lifestyle/diet/etc., but is really a combination of sex hormone induced inflammation and a hyper immune situation localized (hopefully) to the scalp. Trying to lower the inflammatory response by addressing those things that incite the immune response is the best we can do. The sex hormones determine your "clock" in a sense for developing hair loss in and of themselves, given a world free of the factors we've discussed. This clock can be sped up or slowed down, but trying to alter the clock by disturbing the hormones themselves in a bad idea in my opinion.

a<r Sat Jun 02, 2012 2:27 am

Quick one from my phone again. Anthony you'll like this, there was a drug a while back that basically shut down your immune system, lowering inflammation to nothing. What was an unsuspected side effect? It also grew back larger amounts of hair than anything else seen on the market up to that pointx including finasteride and minoxidil.,

AS54 Sat Jun 02, 2012 3:11 am

No shit? Veddy veddy interestinguh. But like you've discussed A < R, inflammation is a necessary process. Its the yin and yang of it all, something beneficial can also be harmful given enough time. I bet the negatives of that product outweighed the benefits. A process we so desperately need is also at the heart of why we're on this forum. I think the problem is more of a case of we're experiencing inflammation on warp drive so its a matter of trying to corral the immune system without compromising its function to the point of deficiency.

We'll never eliminate the inflammatory nature of sex hormones, it would take evolutionary processes thousands of years and evolution really isn't designed to select against something that has its effects later in life. And trying to eliminate the sex hormones altogether will have the same negative effects that trying to eliminate the immune reaction entirely does. We have to find a balance in the process that will preserve our hair and health for the maximum possible.

It's like a complex calculus problem trying to find the minimum of sex hormone and immune function possible for health and longevity while still having all of the benefits to our reproductive success and also minimizing the level of inflammation. I think what we're trying to do with our lifestyle and supplementation is to eliminate all of the exacerbating factors that make this inflammatory relationship worse.

By the way, thanks for this thread A < R, and your responses.

a<r Sat Jun 02, 2012 3:39 am

anthonyspencer54 wrote:No shit? Veddy veddy interestinguh. But like you've discussed A < R, inflammation is a necessary process. Its the yin and yang of it all, something beneficial can also be harmful given enough time. I bet the negatives of that product outweighed the benefits.

^ Oh Yeah, there's a reason why nobody talks about that product (I can't even remember what its called and google searches are bringing up scarce info on it), it's because of the oncological implications of having no immune system. Virus's and bacteria are major causes of mutations, cancer, etc.

A process we so desperately need is also at the heart of why we're on this forum. I think the problem is more of a case of we're experiencing inflammation on warp drive so its a matter of trying to corral the immune system without compromising its function to the point of deficiency.

We'll never eliminate the inflammatory nature of sex hormones, it would take evolutionary processes thousands of years and evolution really isn't designed to select against something that has its effects later in life. And trying to eliminate the sex hormones altogether will have the same negative effects that trying to eliminate the immune reaction entirely does. We have to find a balance in the process that will preserve our hair and health for the maximum possible.

It's like a complex calculus problem trying to find the minimum of sex hormone and immune function possible for health and longevity while still having all of the benefits to our reproductive success and also minimizing the level of inflammation. I think what we're trying to do with our lifestyle and supplementation is to eliminate all of the exacerbating factors that make this inflammatory relationship worse.

By the way, thanks for this thread A < R, and your responses.

No sweat, we're all in this thing together. And I agree with what you're saying, thanks for keeping this topic alive. Often, the bigger picture gets lost on a lot of users because of how many factors have to be balanced at once.

Mastery Sat Jun 02, 2012 3:38 pm

aNo sweat, its a good topic to really get everybody looking at this in a different perspective. Epigenetics really is fascinating either way.

Absolutely first rate.

Mastery Sat Jun 02, 2012 3:50 pm

a
LawOfThelema wrote:
Because remember getting us to that point of life, to the point of reproduction, is all our genes care about.

Your genes don't have a mind. As such they have no cares.

We're getting pretty deep there, but this is something talked about years ago by users like Prague and jdp.

Genes don't necessarily not have a mind, its easier to think of them and everything else in nature as shapes governed by and produced by tight mathematical law. One could get pretentious about it and see these shapes and algorithms in such seemingly different things as physics, music, geometry, visual presentation of organisms, molecular structures of the elements, and then take it a step further by seeing the same trends in how we perceive said things on a daily basis (ie dissonant notes in music, our distaste for objects and structures that aren't symmetrical). What the Takeaway is with all that, oncemore as devoid of pretension as possible, is perpetuation. Its a system that keeps moving and adapting. Our genes are probably pushed into a mode of self preservation like middle class citizens in a Japan subway car.

OK, lot's to say on this.

First up, inflammation is just a word. By that I mean there will be subsets of inflammation, some good, some bad. For example your immune systems ability to respond to an invader is good, but obviously it is tiresome. Aubrey de Gray and barnacles et al. Jdp, Richard Wright etc.

Inflammation caused by working out with Cindy Crawford and then screwing her in the changing rooms. Your immune system's ability to raise its game for this is good, but not tiresome - it's joyful.

Point being yes inflammation comes first - I agree A>R - but I bet only certain types of inflammation (or acidity).

Second point: genes - yes, environment (epigenetics) is 80 - 90% of whether they get triggered or not. But what is environment? If you think of environment as total consciounsess surrounding the genes, you are close. Again back to joy, and exhaust fumes. Both are environment, at the spiralling missile (that is your DNA) level.

Put another way - food is critical, but so is what your heart says...

Third point: - but related to # 2, point your canoe down stream and the bible. Samson. Are you getting where I am heading with all of this.

Yup - the very best science does not exist indpenedent of great thought, and by that we must include the divine and the mundane.

So hence the paradox, inflammation is good and bad, but never both in the same instance. For it always come back to existentialism, i.e. why?

Master why do you speak in parables, so that those who do not understand may not understand.

Mastery Sat Jun 02, 2012 3:52 pm

A > R's signature says so much.

"When you have nothing left to burn ... you have to set yourself on fire"

TIBET. Terrible.

Thanks for another wonderful thread, A > R. Give me a call I am back in Canada - I'll skype you my new cell #.

Believe I have almost all the answers now. Many thanks to you, CS, jdp, OMG, WG and MC.

Conscisouness at, and within, and surrounding the heart of the true understanding of epignetics is # 1

DNA is but a mad spiral desperate for leadership.

But while I understand I do not yet embody. Yet the body creates itself from thoughts less than instantaneously so that gives relief. And space for commitment to work your magic, as I do with mine.

CS - Jung, freud et al., all play more of a role that we think. For as A>R hints at once that (negative subset of) inflammation has set in the joyless soul has to find it's way back home. Love, peace, enthusiasm, relentless overcoming of soul stirring challenges. Set your dreams on fire. Ahhh, epigenetics.

a<r Sat Jun 02, 2012 4:52 pm

Anthony, not much time to post right now (you too mastery, nice to hear from you!) but thought you'd like this.

The effects of inflammatory cytokines on steroidogenic acute regulatory protein expression in macrophages.
Ma Y, Ren S, Pandak WM, Li X, Ning Y, Lu C, Zhao F, Yin L.
Source

Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai, PR China.
Abstract
OBJECTIVE:

To investigate the expression of steroidogenic acute regulatory protein (StAR) in macrophages and the effects of inflammatory cytokines on StAR expression.
METHODS:

The macrophages isolated from ApoE knockout mice and C57BL/6J mice and RAW264.7 cells (a cell line from mouse macrophage. ATCC Number: TIB-71) were cultured in DMEM containing 10% fetal bovine serum. RAW264.7 cells were treated with different inflammatory cytokines (TNF-alpha, IFN-gamma and TGF-beta1) and 8-Br-cAMP, a cAMP analog. RT-PCR and Western blot analysis were applied to evaluate the effects of inflammatory cytokines on StAR expression.
RESULTS:

RT-PCR and Western blot analysis demonstrated the expression of StAR in the macrophages isolated from ApoE knockout mice, C57BL/6J mice and RAW264.7 cells. Proinflammatory cytokines TNF-alpha and IFN-gamma significantly decreased StAR mRNA and protein levels in RAW264.7 cells. The inhibition was dose- and time-dependent. In contrast, anti-inflammatory cytokine TGF-beta1 increased StAR mRNA and protein levels. At 1:15 molecular ratio, TGF-beta1 blocked the down-regulation of StAR expression mediated by TNF-alpha. cAMP also induced StAR expression in RAW264.7 cells. When the cells were co-treated with 8-Br-cAMP and TNF-alpha, 8-Br-cAMP failed to induce StAR expression.
CONCLUSION:

Our results provide interesting evidence that inflammatory cytokines regulate StAR expression in macrophages.

Mastery Sun Jun 03, 2012 4:16 pm

Heh A> R - you know me I don't do long scientific words, I do the great thoughts...!

What precisely did that study mean?

Overall, is there anything much more to it in totality in your view than this - TOXICITY = PATHOGENS = INFLAMMATION = BALDING

AS54 Mon Jun 04, 2012 3:39 am

Awesome find A < R,

So it looks like inflammation could play a big role in how estrogen and testosterone are expressed, could have interesting implications for how the sex hormones are expressed in the dermis too. But doesn't STAR typically upregulate sex hormones? So what this study is pointing at is that the anti-inflammatory cytokines might be what maintain proper levels? Does this also mean that their inflammatory counterparts are creating sex hormone imbalances?

a<r Mon Jun 04, 2012 5:51 am

anthonyspencer54 wrote:Awesome find A < R,

So it looks like inflammation could play a big role in how estrogen and testosterone are expressed, could have interesting implications for how the sex hormones are expressed in the dermis too. But doesn't STAR typically upregulate sex hormones? So what this study is pointing at is that the anti-inflammatory cytokines might be what maintain proper levels? Does this also mean that their inflammatory counterparts are creating sex hormone imbalances?

That is the trend with all the studies I have read Anthony, your interpretation is right on the money.

Mastery Mon Jun 04, 2012 3:36 pm

And isn't it the case that pathogens and toxicity are the two huge drivers of inflammation (the other being "bad" food, but as JDP has proved if you lower the pathogenic load the food intolerance reduces, possibly to very low)...

M

a<r Mon Jun 04, 2012 6:13 pm

Mastery wrote:And isn't it the case that pathogens and toxicity are the two huge drivers of inflammation (the other being "bad" food, but as JDP has proved if you lower the pathogenic load the food intolerance reduces, possibly to very low)...

M

Very good post. Pathogens, toxicity, bad diet all are major drivers of inflammation, and eachother. It all starts with one, but you need to deal with all three to get a complete hold on things.

a<r Mon Jun 04, 2012 6:22 pm

I've been entertaining the thought that mpb could have a viral component ...

This stidy has been proposed before, but it doesn't delve into the particulars, the how, why and what, of what we already know to be associated with androgenic alopecia, such as androgens, increased risk of certain cancers, heart disease, etc.

The role of inflammation and immunity in the pathogenesis of
androgenetic alopecia.
Magro CM, Rossi A, Poe J, Manhas-Bhutani S, Sadick N.
Department of Pathology and Laboratory Medicine, Weill Medical College
of Cornell University, New York, NY, USA.

BACKGROUND: Female pattern hair loss affects many women; its
pathogenetic basis has been held to be similar to men with common
baldness. OBJECTIVE: The objective of this study was to determine the
role of immunity and inflammation in androgenetic alopecia in women and
modulate therapy according to inflammatory and immunoreactant profiles.
MATERIALS AND METHODS: 52 women with androgenetic alopecia (AA)
underwent scalp biopsies for routine light microscopic assessment and
direct immunofluroescent studies. In 18 patients, serologic assessment
for antibodies to androgen receptor, estrogen receptor and cytokeratin
15 was conducted. RESULTS: A lymphocytic folliculitis targeting the
bulge epithelium was observed in many cases. Thirty-three of 52 female
patients had significant deposits of IgM within the epidermal basement
membrane zone typically accompanied by components of complement
activation. The severity of changes light microscopically were more
apparent in the positive immunoreactant group. Biopsies from men with
androgenetic alopecia showed a similar pattern of inflammation and
immunoreactant deposition. Serologic assessment for antibodies to
androgen receptor, estrogen receptor or cytokeratin 15 were negative.
Combined modality therapy with minocycline and topical steroids along
with red light produced consistent good results in the positive
immunoreactant group compared to the negative immunoreactant group.
CONCLUSION: A lymphocytic microfolliculitis targeting the bulge
epithelium along with deposits of epithelial basement membrane zone
immunoreactants are frequent findings in androgenetic alopecia and could
point toward an immunologically driven trigger. Cases showing a positive
immunoreactant profile respond well to combined modality therapy
compared to those with a negative result.
PMID: 22134564

This is the most straightforward study of many like it showing viral activation of androgen receptor transcription, or upregulation. What is present in balding areas? more prominent androgen receptor activity and immune activity. What is present with viral infection? more prominent androgen receptor activity and immune activity.

Enhancement of gene transactivation activity of androgen receptor by
hepatitis B virus X protein
Yanyan Zheng a, Wen-ling Chen a, W.-L. Maverick Ma b,
Chawnshang Chang b, J.-H. James Ou a,⁎
a Department of Molecular Microbiology and Immunology, University of Southern California, Keck School of Medicine, 2011 Zonal Avenue,
HMR-401, Los Angeles, CA 90033, USA
b George Whipple Lab for Cancer Research, Department of Pathology, Urology, Radiation Oncology and the Cancer Center,
University of Rochester Medical Center, Rochester, NY, USA
Received 8 January 2007; returned to author for revision 22 January 2007; accepted 30 January 2007
Available online 28 February 2007
Abstract
Hepatitis B virus (HBV) X protein (HBx) is a regulatory protein that is required for efficient replication of HBV in its natural host. In this
report, we demonstrate by co-immunoprecipitation experiments that HBx can physically bind to the androgen receptor (AR), which is a nuclear
hormone receptor that is expressed in many different tissues including the liver. This observation is further supported by confocal microscopy,
which reveals that HBx can alter the subcellular localization of the AR both in the presence and in the absence of dihydrotestosterone (DHT).
Further studies indicate that HBx can enhance the gene transactivation activity of AR by enhancing its DNA binding activity in a DHT-dependent
manner. However, HBx does not remain associated with AR on the DNA. As AR can regulate the expression of a number of cellular genes, our
results raise the possibility that HBV pathogenesis may be mediated in part via the interaction between HBx and AR.
© 2007 Elsevier Inc. All rights reserved.

Mastery Mon Jun 04, 2012 6:42 pm

Yes and that is the secret...

And on viruses - agree too.

Basically any negative load on the body, once it overwhelms the immune system's ability to **EASILY** handle it, you have to shut down energy or leach stuff from elsewhere and whose body really needs hair more than e.g. a good key organ - liver; so we dump it as we age.

Regrowing hair is a core marker of succesful anti aging. It is a brilliant one.

Aubrey de Gray eat your heart out, here we come. It's simpler than he makes it and yet more profound.

Land, sea and sky. Easy right?

Not if stupido humans keep polluting the crap out of it as you are made up of what you eat, literally - even that sack of skin you are wearnig, its not protecting you from your environment, its made up from it....!

EPI GENETICS is perhaps a misnomer then, there is only the environment. Your DNA will spiral away anyway, whatever way you and your environment shape it.

AS54 Tue Jun 05, 2012 1:49 am

Mastery,

I wouldn't mock Aubrey. His beard will find you.

A > R,

You've been on one for this thread. Another good set of studies. I remembered the first one from a while back, but I think its important enough to be reminded of again.

The virus theory is extremely interesting. But the rabbit hole goes even deeper. Many types of viruses secrete their own type of interleukins that alter the host's T-cell response to them. Because they are intracellular parasites, eliminating them requires a primarily T1 response. The interleukins they secrete trick the immune system into believing they are extracellular invaders and incite a T2 response, inflaming the region but not effectively eliminating the virus. Its an amazing evolutionary adaptation, and for me, puts us in our place because many of these microorganisms (yup, I bunched viruses in here) are beginning to adapt faster than we can keep up.

Anyhow, in trying to connect the INFLAMMATION/SEX HORMONE/IMMUNITY/HAIR LOSS thing, this could be a player. The T2 dominance would upregulate antibody production, probably in a mistaken fashion to the degree of autoimmunity because the proper antigens are not being targeted. This could implicate structural parts of the hair bulb in the attack, because the body is basically firing buck shot. The viruses can literally modulate the body's local inflammatory condition.

In the context of what we've been talking about, it could truly be: viral infection > improper antigen recognition > inflammatory augmentation > imbalance of sex hormone synthesis and receptor sensitivity > further inflammation/immune reaction> thinning hair

SlowMoe Thu Jun 07, 2012 5:12 am

Let me add something from my point of view..

What I'm reading here sounds very believable, and I think you guys are on point. But there is one thing that hasn't been brought up..Why are the inflammatory responses/ sex hormone receptors not pronounced on any other part of the body..? Why are they only pronounced on the top of the head?

To me it makes sense that the reason ONLY the hairs on top of the head fall prey to the devastating effects of sex hormones and inflammation is the fact that blood flow in balding scalps is 60% less than in non-balding scalps.

To me, that is the missing piece of the puzzle. The lack of bulk blood flow to the order of 60% and the excess toxin accumulation to nearly that extent could be the trigger for sex hormone sensitivity/ inflammation.

Does it make sense that an environment devoid of oxygen and abundant in toxic waste would be a perfect breeding ground for pathogens or other undesirable conditions?

AS54 Thu Jun 07, 2012 5:43 am

Hey Floppy,

I think there are more appropriate forums for you to be on. I believe there is hope for you to solve
your problem, and if not, there are plenty of people out there who are completely fine with a small penis.