new hair from sides put on top full of dht and grow for life how come ??????

side hairtop grow Sat Jul 07, 2012 9:52 am

hi was looking to no more about dht way does hair from sides grow for life when put on top rooney ?????

SlowMoe Sat Jul 07, 2012 10:44 am

shaes8 wrote:hi was looking to no more about dht way does hair from sides grow for life when put on top rooney ?????

Where is the proof that hairs last a lifetime up there?
From what I see they fail within 10-15 years or so..

LawOfThelema Sat Jul 07, 2012 11:57 am

what do you mean from what you see? do you have a dermatological practice where you review the progress of a HT after 15 yrs?

its pretty well established that donor dominance is real and that the transplanted hair is permanent. the non transplanted hair would continue to miniaturize, so unless you replace all the hair, yeah your overall quality will decline.

CausticSymmetry Sat Jul 07, 2012 12:07 pm

I know many who have had more than one transplant. They don't last and are subject to inflammation.

Answer to 1st question is: Hair sides grow throughout life because the vascular system is not subject to low oxygen.
DHT is upregulated to scalp area to boost vascularization, because there, oxygen deprivation is much more likely and consequently, the present infections that occur will calcify within the vascular system in that region.

Amaranthaceae Sat Jul 07, 2012 6:01 pm

Very interesting theory CausticSymmetry.

You are saying that DHT is upregulated in the balding areas, as a mean to increase
oxygen in that area, by the body itself?

CausticSymmetry Sat Jul 07, 2012 6:39 pm

cpio wrote:Very interesting theory CausticSymmetry.

You are saying that DHT is upregulated in the balding areas, as a mean to increase
oxygen in that area, by the body itself?

Yes, as crazy as it sounds, there is research that supports this. In an earlier thread, here's a quote (to save time)

Over the years a number of papers have documented that DHT lowers levels of endotoxins, cytokines, vascular inflammation from low oxygen conditions. In other words, DHT acts as an anti-inflammatory in a low oxygen environment in order to repair damage.

Amaranthaceae Sat Jul 07, 2012 6:46 pm

Wow - that is pretty f**** awesome !

It all comes together now, it seems.

CausticSymmetry wrote:
cpio wrote:Very interesting theory CausticSymmetry.

You are saying that DHT is upregulated in the balding areas, as a mean to increase
oxygen in that area, by the body itself?

Yes, as crazy as it sounds, there is research that supports this. In an earlier thread, here's a quote (to save time)

Over the years a number of papers have documented that DHT lowers levels of endotoxins, cytokines, vascular inflammation from low oxygen conditions. In other words, DHT acts as an anti-inflammatory in a low oxygen environment in order to repair damage.

SlowMoe Sun Jul 08, 2012 12:08 am

Well then why does lowering DHT cause hair to grow?

side hairtop grow Sun Jul 08, 2012 2:29 am

CausticSymmetry wrote:
cpio wrote:Very interesting theory CausticSymmetry.

You are saying that DHT is upregulated in the balding areas, as a mean to increase
oxygen in that area, by the body itself?

Yes, as crazy as it sounds, there is research that supports this. In an earlier thread, here's a quote (to save time)

Over the years a number of papers have documented that DHT lowers levels of endotoxins, cytokines, vascular inflammation from low oxygen conditions. In other words, DHT acts as an anti-inflammatory in a low oxygen environment in order to repair damage.

LawOfThelema Sun Jul 08, 2012 5:57 am

DHT certainly isnt repearing your hair.

dudebro Sun Jul 08, 2012 6:07 am

LOT, consider how dht is known to help grow hair on the legs and beard. as everyone above is speculating, there might be an extrinsic factor on the scalp, be oxygen or whatever.

CausticSymmetry Sun Jul 08, 2012 7:03 am

LawOfThelema wrote:DHT certainly isnt repearing your hair.

Correct, it's repairing the vascular system at the expense of our hair.

Paradox Sun Jul 08, 2012 7:17 am

CausticSymmetry wrote:
LawOfThelema wrote:DHT certainly isnt repearing your hair.

Correct, it's repairing the vascular system at the expense of our hair.

Is the inverse true then? Does 5AR inhibition save hair at the expense of the vascular system? If that is correct then how does the hair survive longer with less DHT, but a compromised vascular system?

CausticSymmetry Sun Jul 08, 2012 7:23 am

If this seems absurd, then here is just one of many pieces of supporting evidence:

INFLAMMATION-INDUCED TLR4 EXPRESSION AND REACTIVE OXYGEN SPECIES ARE
ATTENUATED BY DIHYDROTESTOSTERONE IN HUMAN PRIMARY VASCULAR SMOOTH
MUSCLE CELLS

Basic Medical Sciences, University of Arizona COM Phoenix, Phoenix, AZ,
2 Biomedical Sciences, Colorado State University, Fort Collins, CO, USA
Experimental studies have demonstrated that androgens modulate vascular inflammation, a
critical regulator in the development and progression of cerebrovascular disease, particularly
stroke1. In rats, low doses of androgens have been shown to be protective during cerebral
ischemia 2 . Our most recent data has demonstrated that the potent endogenous androgen,
dihydrotestosterone (DHT), attenuated endotoxin-induced 3 and oxygen glucose deprivation
(OGD; in vitro model for ischemia)-induced cyclooxygenase-2 (COX-2) in human vascular
smooth muscle (VSM) cells. It has been implicated that COX-2 plays a role in vascular
inflammation and may serve as a source of reactive oxygen species (ROS) 4. Expression of
COX-2 as with many other proinflammatory mediators such as cytokines, chemokines and iNOS
can be regulated by the activation toll-like receptor 4 (TLR4) following exposure to endotoxin or
injury 5. TLR4 expression significantly increases after middle cerebral artery occlusion in rodents
and these increases in TLR4 correlate with increased damage 6,7.

I think it's important to understand that 95% of what is perceived about the human body is incorrect
with respect to how human healing in physiology works

I could spend hours explaining but there is no time. In short, the body does nothing for no good reason.
Everything it does is an attempt to heal. Inflammation is intended to be a corrective process. However,
when chronic it becomes a vicious cycle. The body considers less essential things like hair worthy of sacrifice
to spare its vascular system.

Other questions remain, such as does this protect against a travel of endotoxins to distal areas? Whatever the case
it seems that the vascular network within the cranial system relative to hair becomes calcified anyway. This probably occurs due to the calcium binding effect with pathogens.

LawOfThelema Sun Jul 08, 2012 8:49 am

So it's an adaptive control system of sorts. Under normal conditions it is proinflammatory, under hypoxia it swings the other way.

A couple of things.

Firstly, Seems fairly irrelevant for our purposes, really. Ok it's protecting my vascular system if there is hypoxia (and only if... under normal conditions it is not doing this), but it is still turning the key that turns on the biological program for my body to ravage my hair.

Secondly, is the top of the scalp at enough a state of oxygen deprivation for it to exert an antiinflammatory effect.

And finally the "at the expense of part" is unestablished. You make it sound as if it werent exerting the effect on your circulatory system then it wouldnt be negatively affecting your hair. No reason to believe this is the case.

JZ Sun Jul 08, 2012 9:03 am

Interesting. So, what about women? They don't upregulate DHT production to the top of their scalp when the vascular system is compromised (AFAIK). What happens to them? I guess the hair follicles on the top of their scalp would simply be deprived of oxygen/nutrients, and they would have diffuse hair loss (which might not even be noticeable, depending on the severity)? Whereas, with men, the DHT leads to more acute damage to the hair follicles, and also a compromised vascular system in the end? Is that the idea?

JZ Sun Jul 08, 2012 9:24 am

Firstly, Seems fairly irrelevant for our purposes, really. Ok it's protecting my vascular system if there is hypoxia (and only if... under normal conditions it is not doing this), but it is still turning the key that turns on the biological program for my body to ravage my hair.

Yeah. I think CS meant that it is protecting your vascular system (and also damaging your hair) if there is hypoxia. But under normal conditions, it is not upregulated and therefore does not cause significant inflammation. So I guess it's relevant for our purposes like this: if there is no hypoxia, then DHT is not an issue, and therefore addressing circulation problems prevents the potential problems that DHT causes.

But I'm still unclear what DHT actually does to hair follicles that causes damage. I've read that it isn't damaging to them at all (nor to the prostate) unless estrogen levels are high.

And what was it that causes the circulation problems in the first place? Adrenal problems? Thyroid problems? Excess estrogen (which I think can be caused by adrenal problems)?

SlowMoe Sun Jul 08, 2012 10:31 am

So are you saying that under hypoxia, the cell walls "open" and let DHT in? And when tree is hypoxia, then the "holes" are closed?

Also, what is the cause of the inflammation? Too much DHT in the cell?

JZ Sun Jul 08, 2012 12:17 pm

Well, at this point I get confused.

CausticSymmetry wrote:
cpio wrote:Very interesting theory CausticSymmetry.

You are saying that DHT is upregulated in the balding areas, as a mean to increase
oxygen in that area, by the body itself?

Yes, as crazy as it sounds, there is research that supports this. In an earlier thread, here's a quote (to save time)

Over the years a number of papers have documented that DHT lowers levels of endotoxins, cytokines, vascular inflammation from low oxygen conditions. In other words, DHT acts as an anti-inflammatory in a low oxygen environment in order to repair damage.

So, CS is saying that DHT is upregulated as a means to increase oxygen into an oxygen-deprived area. Then he also says that DHT helps reduce inflammation.

Aren't these two distinct functions? CS, can you clarify how DHT helps repair the vascular system? Is it simply by reducing inflammation, or does it have a further role in, for example, promoting the flow of NO or enhancing angiogenesis?

CausticSymmetry wrote:
INFLAMMATION-INDUCED TLR4 EXPRESSION AND REACTIVE OXYGEN SPECIES ARE
ATTENUATED BY DIHYDROTESTOSTERONE IN HUMAN PRIMARY VASCULAR SMOOTH
MUSCLE CELLS

Alright, so this paper is more evidence that DHT can reduce inflammation in vascular tissue.

CausticSymmetry wrote:
LawOfThelema wrote:DHT certainly isnt repearing your hair.

Correct, it's repairing the vascular system at the expense of our hair.

OK, well how is it hurting our hair?? DHT reduces inflammation. So what is the process by which DHT hurts our hair?

SlowMoe wrote:So are you saying that under hypoxia, the cell walls "open" and let DHT in? And when tree is hypoxia, then the "holes" are closed?

The information CS posted just said that DHT reduces the effects of COX-2, a vascular inflammatory agent. It didn't say how. I don't know if it's that more DHT is allowed to enter the cells (the "holes" open) or if more testosterone is converted to DHT in the inflamed tissue, but I guess either way, yeah, under hypoxia it happens more. According to this theory as I am trying to understand it.

SlowMoe wrote:Also, what is the cause of the inflammation? Too much DHT in the cell?

That's a great question. CS?

Xenon Sun Jul 08, 2012 2:28 pm

"DHT is upregulated to scalp area to boost vascularization"

I know it's true that DHT triggers the release of nitric oxide so the penis has more oxygen to help it stay erect. I'm not disputing your theory here, as this is interesting to ponder over; but if DHT did increase oxygen and lower inflammation to the scalp, then why is it that this area is most susceptible to inflammation and thinning hair? Yet when DHT levels have been reduced through finasteride, then hair has been known to grow back.

I did also consider (prior to the clogging theory) that too much nitric oxide could cause cellular ATP to go into 'overdrive', cause the cell to then generate far too much metabolic heat and provoke an inflammatory response. However, I feel that a build up of DHT within the cytoplasm could gradually cause hypoxia, and thus cause cell asphyxiation. To me, this seems to be the most likely issues caused by an overload of DHT.

LawOfThelema Sun Jul 08, 2012 3:01 pm

OK, well how is it hurting our hair?? DHT reduces inflammation. So what is the process by which DHT hurts our hair?

Please, just read a recent scientific review of androgenetic alopecia. In those with androgenetic alopecia, the DHT/androgen receptor complex changes the gene expression of androgen sensitive genes which gives rise to biological factors that cause the body to attack the hair. The entire process of this attack isn't fully understood. DHT turns on the process by which your own body attacks its hair follicle. It is only anti-inflammatory under conditions of oxygen deprivation. Because it is ant-iinflammatory under some condition doesn't mean that it is capable of stopping the own triggered attack on the hair follicle that it itself has brought about.

This is why I disagree with the Caustic theory that DHT isn't as important as everyone says it is in hair maintance. While we may have some inkling about the 1000s of factors involved in the bodies attack on the hair after that process has been turned on by the DHT/AR complex, we know that blocking DHT from binding the receptor prevents or drastically slows this process, by effectively addressing the primum movens or initial cause.

a<r Sun Jul 08, 2012 3:38 pm

LawOfThelema wrote:
OK, well how is it hurting our hair?? DHT reduces inflammation. So what is the process by which DHT hurts our hair?

Please, just read a recent scientific review of androgenetic alopecia. In those with androgenetic alopecia, the DHT/androgen receptor complex changes the gene expression of androgen sensitive genes which gives rise to biological factors that cause the body to attack the hair. The entire process of this attack isn't fully understood. DHT turns on the process by which your own body attacks its hair follicle. It is only anti-inflammatory under conditions of oxygen deprivation. Because it is ant-iinflammatory under some condition doesn't mean that it is capable of stopping the own triggered attack on the hair follicle that it itself has brought about.

This is why I disagree with the Caustic theory that DHT isn't as important as everyone says it is in hair maintance. While we may have some inkling about the 1000s of factors involved in the bodies attack on the hair after that process has been turned on by the DHT/AR complex, we know that blocking DHT from binding the receptor prevents or drastically slows this process, by effectively addressing the primum movens or initial cause.

I agree with Law here in some ways, and disagree with him in others, and its a perspective thing that has a lot to do with time and experience.

Law is right when he says that its the receptors that seem to be upregulated, there is a rise in DHT via the aromatization that happens during inflammation / insulin resistance / SHBG lowering, but whether its a factor that is upstream or downstream isn't that important when other factors are addressed, especially when you see how limited the lowering of DHT becomes as a treatment for hairloss and BHP as one ages, it just loses effectiveness.

Somebody asked why this isn't a problem in women, and the answer is simple, I've posted a large amount of information confirming estrogens (the less potent ones that aren't problematic, as we see as women become menopausal) protective role on the microvascular system, and its effects on hair via WNT signalling, I believe it also downregulates DKK-1.

The last point I want to make is that of perspective, there is a lot of talk on this site now from new users about microvascular circulation, wounding, etc, but I hear nothing about some major topics that were all the rage this time last year, such as how DKK-1 is upregulated in MPB areas. Leaving out these factors from posts yonder makes it hard to see the "bigger picture". DKK-1 is also upregulated in the tissues of other inflammitory conditions, such as in heart valves that are diseased, what upregulates them? the combo of oxidation (a good and bad thing) from certain pathogens and sexual steroid hormones which just perfectly happen to get a boost during inflammation. Once you get all the available details, it's readily apparent that this is a very streamlined system, nothing is without duality.

LawOfThelema Sun Jul 08, 2012 3:45 pm

Well, wounding does bring into play WNT signalling. I guess that was Cotsarelis big insight, and it looks like it figured a lot into his latest patent. Using a peturbation or distruption on the skin to control the growth of the hair, either stopping it or starting. Wounding can reactivate the prior "dead" hair follicles.

^ This reminds me of something a professor I had said

one starts on simplicity, then gradually adds complexity and things look very untractable then you add some organizing principles and reach a higher level of simplicity that accounts for the complexity with the organizing principles. the discussion context was semiconductor devices an area where duality principles interstingly pop up a lot and help to organize all the information.

CausticSymmetry Sun Jul 08, 2012 7:34 pm

Well, this has turned into an interesting thread.

Yes, as A > R has pointed out quite well, a lot of background information is needed to fully understand this twist of a concept.

Women and men do not have identical estrogen receptor activity.

Moreover, there is the effect on DHT via the ERbeta agonist, 5α- androstane 3β, 17β Diol (3β-Diol). This converts DHT and can convert it into an anti-inflammatory.

With that said, have a look at this:

Steroids. 2012 Jul;77(8-9):835-44. Epub 2012 Apr 20.
Estrogen receptor beta dependent attenuation of cytokine-induced cyclooxygenase-2 by androgens in human brain vascular smooth muscle cells and rat mesenteric arteries.
Zuloaga KL, O'Connor DT, Handa RJ, Gonzales RJ.

Department of Basic Medical Sciences, University of Arizona College of Medicine, Phoenix, AZ 85004-2157, United States.

Androgens may provide protective effects in the vasculature under pathophysiological conditions. Our past studies have shown that dihydrotestosterone (DHT) decreases expression of cyclooxygenase-2 (COX-2) during cytokine, endotoxin, or hypoxic stimulation in human vascular smooth muscle cells, in an androgen receptor (AR)-independent fashion. Classically DHT is regarded as a pure AR agonist; however, it can be endogenously metabolized to 5α-androstane-3β, 17β-diol (3β-diol), which has recently been shown to be a selective estrogen receptor (ERβ) agonist. Therefore, we hypothesized that DHT's anti-inflammatory properties following cytokine stimulation are mediated through ERβ. Using primary human brain vascular smooth muscle cells (HBVSMC), we tested whether DHT's effect on IL-1β induced COX-2 expression was mediated via AR or ERβ. The metabolism of DHT to 3β-diol is a viable pathway in HBVSMC since mRNA for enzymes necessary for the synthesis and metabolism of 3β-diol [3alpha-hydroxysteroid dehydrogenase (HSD), 3β-HSD, 17β-HSD, CYP7B1] was detected. In addition, the expression of AR, ERα, and ERβ mRNA was detected. When applied to HBVSMC, DHT (10nM; 18h) attenuated IL-1β-induced increases in COX-2 protein expression. The AR antagonist bicalutamide did not block DHT's ability to reduce COX-2. Both the non-selective estrogen receptor antagonist ICI 182,780 (1μM) and the selective ERβ antagonist PHTPP (1μM) inhibited the effect of DHT, suggesting that DHT actions are ERβ-mediated. In HBVSMC and in rat mesenteric arteries, 3β-diol, similar to DHT, reduced cytokine-induced COX-2 levels. In conclusion, DHT appears to be protective against the progression of vascular inflammation through metabolism to 3β-diol and activation of ERβ.
Published by Elsevier Inc.

CausticSymmetry Sun Jul 08, 2012 7:37 pm

Now, here is where this gets interesting: Note, this also requires back ground information (think of the effects of stress, cortisol, etc.)

Front Endocrinol (Lausanne). 2011;2:65. Epub 2011 Nov 10.
A role for the androgen metabolite, 5alpha androstane 3beta, 17beta diol (3β-diol) in the regulation of the hypothalamo-pituitary-adrenal axis.
Handa RJ, Sharma D, Uht R.

Department of Basic Medical Sciences, University of Arizona College of Medicine - Phoenix Phoenix, AZ, USA.

Activation of the hypothalamo-pituitary-adrenal (HPA) axis is a basic reaction of animals to environmental perturbations that threaten homeostasis. These responses are ultimately regulated by neurons residing within the paraventricular nucleus (PVN) of the hypothalamus. Within the PVN, corticotrophin-releasing hormone (CRH), vasopressin (AVP), and oxytocin (OT) expressing neurons are critical as they can regulate both neuroendocrine and autonomic responses. Estradiol (E2) and testosterone (T) are well known reproductive hormones; however, they have also been shown to modulate stress reactivity. In rodent models, evidence shows that under some conditions E2 enhances stress activated adrenocorticotropic hormone (ACTH) and corticosterone secretion. In contrast, T decreases the gain of the HPA axis. The modulatory role of testosterone was originally thought to be via 5 alpha reduction to the potent androgen dihydrotestosterone (DHT) and its subsequent binding to the androgen receptor, whereas E2 effects were thought to be mediated by estrogen receptors alpha (ERalpha) and beta (ERbeta). However, DHT has been shown to be metabolized to the ERbeta agonist, 5α- androstane 3β, 17β Diol (3β-Diol). The actions of 3β-Diol on the HPA axis are mediated by ERbeta which inhibits the PVN response to stressors. In gonadectomized rats, ERbeta agonists reduce CORT and ACTH responses to restraint stress, an effect that is also present in wild-type but not ERbeta-knockout mice. The neurobiological mechanisms underlying the ability of ERbeta to alter HPA reactivity are not currently known. CRH, AVP, and OT have all been shown to be regulated by estradiol and recent studies indicate an important role of ERbeta in these regulatory processes. Moreover, activation of the CRH and AVP promoters has been shown to occur by 3β-Diol binding to ERbeta and this is thought to occur through alternate pathways of gene regulation. Based on available data, a novel and important role of 3β-Diol in the regulation of the HPA axis is suggested.

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new hair from sides put on top full of dht and grow for life how come ??????

new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

ha was lookin to no were is the research to support this ?

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????

Re: new hair from sides put on top full of dht and grow for life how come ??????