Studies that help confirm my theory that balding = low oxygen + DHT

I have a good coating if body hair, but I also have super thick head hair.
Some random hairs here and there in my shoulders and back too.
My temples have receded to nw 1 or 2... After a serious bout of inflammation there
Where I had spots that wouldn't go. (Always wearing hats at the time even whilst
Exercising indoors)

My friend who is nearly full Norwood has pretty minimal body hair.
Yet he has bad stomach issues.

So like as said, it's multi factoral.

I was interested in a time when CS said body hair is negatively correlated with hair loss.
I still can't fathom that out.

Okay, this is going to be a long one. This is just an example of how multi-factorial this whole process is, and an example of how when you're bored your research can lead you down the rabbit hole. I will try to string these studies in some logical order so you can follow the arrows connecting the signaling molecules, or at least draw some connections and say, "Oh yeah, I see how that connects". Text in blue is taken from the linked page, black text is mine.

http://www.ncbi.nlm.nih.gov/pubmed/11595812

Androgens are the main regulator of normal human hair growth. After puberty, they promote transformation of vellus follicles, producing tiny, unpigmented hairs, to terminal ones, forming larger pigmented hairs, in many areas, e.g. the axilla. However, they have no apparent effect on the eyelashes, but can cause the opposite transformation on the scalp leading to the replacement of terminal hairs by vellus ones and the gradual onset of androgenetic alopecia. This paradox appears to be an unique hormonal effect. Hair follicles are mainly epithelial tissues, continuous with the epidermis, which project into the dermis. A mesenchyme-derived dermal papilla enclosed within the hair bulb at the base controls many aspects of follicle function. In the current hypothesis for androgen regulation, the dermal papilla is also considered the main site of androgen action with androgens from the blood binding to receptors in dermal papilla cells of androgen-sensitive follicles and causing an alteration of their production of paracrine factors for target cells e.g. keratinocytes. Studies of cultured dermal papilla cells from sites with different responses to androgens in vivo have confirmed the paradoxical responses. All dermal papilla cells from androgen-sensitive sites contain low capacity, high affinity androgen receptors. However, only some cells formed 5alpha-dihydrotestosterone, e.g. beard but not axillary cells, in line with hair growth in 5alpha-reductase deficiency. Incubation with androgens also stimulated the mitogenic capacity of beard cell media, but inhibited that produced by scalp cells. This suggests that the paradoxical differences are due to differential gene expression within hair follicles, presumably caused during embryogenesis.

Some material above relating to the androgen paradox. The only explanation is that the androgens, particularly DHT, are producing different genetic transcripts between the scalp and body.

http://www.ncbi.nlm.nih.gov/pubmed/23016593

Androgens stimulate beard growth but suppress hair growth in androgenetic alopecia (AGA). This condition is known as 'androgen paradox'. Human pilosebaceous units possess enough enzymes to form the active androgens testosterone and dihydrotestosterone. In hair follicles, 5α-reductase type 1 and 2, androgen receptors (AR) and AR coactivators can regulate androgen sensitivity of dermal papillae (DP). To regulate hair growth, androgens stimulate production of IGF-1 as positive mediators from beard DP cells and of TGF-β1, TGF-β2, dickkopf1 and IL-6 as negative mediators from balding DP cells. In addition, androgens enhance inducible nitric oxide synthase from occipital DP cells and stem cell factor for positive regulation of hair growth in beard and negative regulation of balding DP cells. Moreover, AGA involves crosstalk between androgen and Wnt/β-catenin signalling. Finally, recent data on susceptibility genes have provided us with the impetus to investigate the molecular pathogenesis of AGA.

Important to note: the different effectors produced by androgens in the different DP cells, i.e. more inflammatory signalling in the scalp from the same hormone! Particularly important, note that androgens promote more NO production in occipital scalp versus the balding scalp region. Remember this part.

A little more elaboration on the androgen paradox:
http://www.endocrine-abstracts.org/ea/0007/ea0007s24.htm
A different perspective from D Roddy:
http://www.dannyroddy.com/main/2013/12/09/the-androgen-paradox-pregnancy-and-pattern-hair-loss



http://www.fasebj.org/content/16/14/1967.full.pdf
http://www.ncbi.nlm.nih.gov/pubmed/10744631

This study above shows TGF-B is upregulated by androgen in the scalp dermilla papilla cells. TGF-B is an apoptotic signal that inhibits keratin cell growth, aka it inhibits hair growth.
The second study shows a direct link that TGF-B is one of the primary signals for the hair follicle to enter catagen.

http://www.hairlosstalk.com/interact/showthread.php/33507-Dickkopf-vs-TGF-Beta

Forum post by Mumuka showing the 30 most upregulated gene transcripts by DHT. Some important ones:

• dickkopf homolog 1  :  inhibits crucial wnt protein signalling required for hair growth/cycling
  
• LPS-induced TGF-a  :  DHT appears to modulate the response to LPS by inducing TNF-a, an inflammatory peptide
  
• Cyclin-dependent kinase inhibitors :  important apoptotic factors leading to cell death
  
• HMOX1 :  gene encoding heme oxygenase type I, an important antioxidant response element protecting against oxidative damage from hypoxia!
  
• UGCG:  makes glucosylceramide, a membrane lipid upregulated during keratin differentiation
  
• TGF-B
  

http://www.nature.com/nutd/journal/v2/n3/full/nutd20121a.html

Indeed, elevated TGF-β has been previously reported in human adipose tissue during morbid obesity and diabetic neuropathy. In this review, we discuss the pleiotropic effects of TGF-β/Smad3 signaling on metabolism and energy homeostasis, all of which has an important part in the etiology and progression of obesity-linked diabetes; these include adipocyte differentiation, white to brown fat phenotypic transition, glucose and lipid metabolism, pancreatic function, insulin signaling, adipocytokine secretion, inflammation and reactive oxygen species production.


Evidence that androgen signalling, via TGF-B actually contributes to insulin resistance, and can promote endothelial dysfunction!


http://www.nature.com/jid/journal/v97/n4/full/5612328a.html


We conclude that low oxygen tension upregulates the synthesis of TGF-1 by human dermal fibroblasts, and leads to increased secretion of this peptide.


http://www.ncbi.nlm.nih.gov/pubmed/12223962



The mechanism by which the local dihydrotestosterone increase leads to hair follicle loss is not clearly demonstrated. Inhibition of cell proliferation in the dermal papilla and a vascular process based on the inhibition in local production of vascular endothelial growth factor (VEGF) have been proposed. The increase in 5 alpha reductase activity is genetic and depends on androgen receptor polymorphism, characterized by a decrease in the number of CAG sequences on the exon 1.



http://www.ncbi.nlm.nih.gov/pubmed/12855613


Dihydrotestosterone (DHT) activates HIF-1alpha nuclear protein expression in LNCaP cells but not in androgen receptor-negative PC-3 cells. Androgens activate HIF-1, driving VEGF expression in androgen-sensitive LNCaP cells.


http://www.ncbi.nlm.nih.gov/pubmed/23161568


Histamine also induced the expressions of HIF-1α and VEGF in BMMCs. H1 receptor antagonists significantly improved overall survival rates and substantially suppressed tumor growth as well as the infiltration of mast cells and levels of VEGF through the inhibition of HIF-1α expression in B16F10 melanoma-bearing mice.


The hypoxia inducible factor from mast cells also promotes VEGF. There seems to be a common element of hypoxia/oxidative stress damaging vessels. Combining it with the prior study, DHT in mast cells may be one of the important signals promoting the hypoxia inducible factor.


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2517379/



In rats exposed for 20 days, MMP-13 positive mast cells accumulated within the walls of conduit arteries and subpleurally. In recovered rats, MMP-13 positive mast cells gathered at the prealveolar arterial level as well as in the walls of small muscular arteries; these mast cells stayed also in the conduit part of the pulmonary vasculature. These data support the hypothesis that perivascular pulmonary mast cells contribute to the vascular remodelling in hypoxic pulmonary hypertension in rats by releasing interstitial collagenase.



Hypoxia attracts mast cells positive for MMP-13. The MMP's are proteins that break down collagen. Between the promotion of MMP-13 and VEGF, it would be reasonable to say that mast cells are being attracted to hypoxic regions to remodel damaged vessels there. The induction of DHT by hypoxia and DHT's role in inducing HIF implicate a relationship between the androgens and mast cells in ischemic arterial damage repair!

http://www.ncbi.nlm.nih.gov/pubmed/20808808

Our data suggests that mast cell survival, degranulation and cytokine release are sustained under hypoxia. This may be of importance for host defence where mast cells in a hypoxic tissue can react to intruders, but also in chronic inflammations where mast cell reactivity is not inhibited by the inflammatory associated hypoxia.


Shows that hypoxic conditions don't kill or hurt the function of mast cells (probably because of HIF-1). But this may be a particular reason why mast cells are homed in on hypoxic tissues. They are in effect, like the immune's systems special forces for hypoxic environments.


http://bloodjournal.hematologylibrary.org/content/86/7/2488.full.pdf


We have observed previously that transforming growth factor$ (TGF-P), a regulator of angiogenesis: also is a remarkably potent chemotactic factor for tissue mast cells.’ This prompted us to determine if other known angiogenic factors stimulate directed mast cell migration. In this study, we observed the ability of platelet-derived growth factor-AB (PDGF-AB), vascular endothelial cell 
growth factor (VEGF), basic fibroblast growth factor(bFGF), and platelet-derived endothelial cell growth factor (PD-ECGF) at picomolar (or less) concentrations to induce mast cell chemotaxis.

So after CS' post on mast cells the other day, we're left wondering what's attracting the mast cells to the scalp. We have a hint that hypoxia is the attractor, but this study shows the actual chemo-attractants, and wouldn't you know it: several of these are induced by DHT. All of these growth factors seem to be a hypoxia-related response, and mast cells (positive for MMP-13, histamine, PGD2) are being attracted to the region. DHT active in these mast cells is a player in the inflammatory/vessel-repairing response.


From the Wiki on NO:
Nitric Oxide (NO) reduction is considered the hallmark of endothelial dysfunction ^[8] A key and quantifiable feature of endothelial dysfunction is the inability of arteries and arterioles to dilate fully in response to an appropriate stimulus that stimulates release of vasodilators from the endothelium like NO. Endothelial dysfunction is commonly associated with decreased NO bioavailability, which is due to impaired NO production by the endothelium and/or increased inactivation of NO by reactive oxygen species. NO has the following physiological effects that contribute to the inhibition of atherosclerosis: 1) NO is released and produces vasodilation after shear stress in the vessel; the vasodilation NO mediated-response in turns decreases the shear stress. If the shear stress is chronically induced it leads to the upregulation of and release of inflammatory cytokines ^[10] 2) NO decreases LDL oxidation; 3) NO reduces platelet aggregation to the endothelium 4) NO Inhibits smooth muscle cell proliferation 5) NO prevents leukocyte adhesion and infiltration into the vessels.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1906415/

NO inhibits a number of mast cell-dependent inflammatory processes in vivo, including histamine mediated vasodilatation, vasopermeation and leucocyte-endothelial cell attachment. In human asthma and animal models of lung inflammation the role of NO is harder to define. However, although there are conflicting data, the balance of evidence favours a predominantly protective role for NO. Mimicking or targeting NO dependent pathways may prove to be a valuable therapeutic approach to mast cell mediated diseases.


NO appears to be an important signal/regulator of the mast cell mediated immune response. Of course, NO can be a problem by itself if there is too much produced by once, for example if a cell is exposed to LPS. But overall, it looks as though any oxidative stress to the vascular endothelium initiates an inflammatory response from mast cells and that NO works to dilate the vessel, which lowers stress on the endothelium.

http://www.ncbi.nlm.nih.gov/pubmed/1385162

These observations demonstrate that platelet-derived products such as TGF-beta and PDGFs inhibit the induction of nitric oxide synthase activity in vascular smooth muscle cells.

And now we have evidence that TGF-B, induced by DHT, inhibits NO.

http://www.pnas.org/content/100/21/12504.full

It is well documented that endothelial dysfunction is believed to play an important integral part in the clinical presentation of coronary artery disease (50). When the endothelium is damaged, the reduced NO and prostacyclin production at the site leads to platelet aggregation with the release of 5-HT and thromboxane A2, subsequently enhancing basal vascular tone and leading to a reduction of local blood flow and ischemia/hypoxia. Because NO production is increased by inducible NOS induction in neutrophils, macrophages, and cardiomyocytes in the inflammatory phase of myocardial ischemia and infarction (51–55), HbFe(II)NO is likely formed under these conditions. In fact, HbFe(II)NO has been detected during ischemia reperfusion (21, 24). NO consumption by RBCs bearing HbFe(II)NO is expected to increase, which would further potentiate vasoconstriction, as implicated in the present study. It has been suggested that endothelial vasodilator dysfunction plays a causative role for triggering myocardial ischemia in stable angina pectoris (56). Increased NO consumption by RBCs would aggravate the sequelae of acute ischemic syndrome and might be the primary underlying mechanism in some patients with syndrome X (56).

This one is important. It is showing that NO is reduced at sites of vascular damage and hypoxia, and that other inflammatory mediators are produced. During the inflammatory phase of the damage, NO produced by immune cells increases formation of HbFe(II)NO, reducing NO overall. This leads to vasoconstriction which can create hypoxic conditions in the local tissue.

This is direct evidence that endothelial dysnfunction (oxidative stress) in arteries/veins leads directly to a hypoxic state, which lowers NO availability. This translates into a heightend immune response and based on all the former studies, a greater migration of mast cells to the area. DHT induced HIF promotes release of several growth factors that attract even more mast cells. DHT induced TGF-B inhibits hair growth and promotes catagen. TGF-B also lowers NO even further. This promotes mast cell degranulation in a viscious circle of inflammation, releasing products like the MMP (breaking down collagen) and PGD2 (hair's enemy). This mechanism for vascular repair should be being off-set by NO, but the damage to the endothelium is taking this check-and-balance system out the window. So there is just a runaway inflammation going on. This last study is even suggesting that the reduced NO might be one of the causes of syndrome X (high blood sugar, insulin resistance). Another paradox, however, is a protective role of DHT suggested by Slowmoe in some earlier posts. There is evidence that DHT PROMOTES NO in the dermal papilla. Could it be DHT is upregulated in response to hypoxia and that its many roles in the body are just getting "mushed" up here? Estradiol, also shown to increase NO in the endothelium, this might be the primary reason it is protective of hair.

The combination of inflammatory factors like TGF-B, TNF-a, and lowered NO is going to inhibit other growth factors important to hair, namely IGF-1.


And the beauty: this doesn't even begin to scratch the surface of how stupid and convoluted this all is.   But to me there is at least a clear hint that MPB is either (A) a genetically pre-programmed event  (B) the effect of oxidative damage to blood vessels (which can be tied to mitochondrial dysfunction) leading to hypoxia

But that still leaves out why the vessels in the scalp are particularly vulnerable: again either its genetically pre-programmed (X-chromosome shows a lowered number of CAG repeats which sensitizes androgen receptors in the scalp) or there is something particular to the scalp environment that's responsible.

this is not based on facts other than observation, but i suspect it is likely when hair grows in one spot of the body another spot has to suffer for it.
i'm regrowing hair on top, so a little has to go from the sides..

also i wonder if thick hair grows slower than thin hair, would be logical. could be even thick BECAUSE it's growing slower.

Thanks loads AS.

The genetic part of this, i would love to know the reason.
As in, i would accept this as evolution if it wasnt specifically in the area its in.

Live Forever,

Yes, it is frustrating. The pattern of loss suggests something particular to the environment there.

So its either something about the landscape or we're dealing with something with an evolutionary purpose.

Most people don't want to hear that theory. That there might be a social effect of hair loss, something evolutionarily perpetuating it is a thought
most people wouldn't want to accept.

It could also be a mutation in a couple of genes, pure randomness, that just hasn't had enough evolutionary pressure against it to wipe it out.

I have found some interesting studies on smoking and its effects.
http://peatarian.com/24183/tobacco-is-an-aromatase-inhibitor
http://www.elitefitness.com/bodybuilding/anabolic-steroids/01-2001/042790.html

*Smoking is known for its aromatase inhibiting effects. (Yes, zinc can reduce aromatase as well, but smoking is IMHO easier way to get it).
*In one study nicotine was able to reduce the side effects of the prostaglandin PGF2a (one of CSs goals + you do not need an extra omega 3 for it)
*Nicotin decreases levels of vit. C + E. (I think that the key is smoking tabacco because of smoking increases the levels of several antioxidants).
Note that many of the oldest people smokes as well.


Effects of Coffee Consumption, Smoking, and Hormones on Risk for Primary Sclerosing Cholangitis

Andersen, I. M., Tengesdal, G., Lie, B. A., Boberg, K. M., Karlsen, T. H., & Hov, J. R. (2013). Effects of Coffee Consumption, Smoking, and Hormones on Risk for Primary Sclerosing Cholangitis. Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association. doi:10.1016/j.cgh.2013.09.024

BACKGROUND & AIMS: Little is known about nongenetic risk factors for primary sclerosing cholangitis (PSC), except a possible protective effect of smoking. We investigated the relationship between environmental risk factors and susceptibility to PSC. METHODS: A questionnaire was distributed to patients with PSC, recruited from Oslo University Hospital Rikshospitalet in Norway through 2011, and randomly chosen individuals from the Norwegian Bone Marrow Donor Registry (control subjects). Data were analyzed from 240 patients with PSC and 245 control subjects, matched for gender and age. RESULTS: A lower proportion of patients with PSC were daily coffee drinkers than control subjects, both currently (76% vs 86%; odds ratio [OR], 0.52; 95% confidence interval [CI], 0.32-0.82; P = .006) and at the age of 18 years (35% vs 49%; OR, 0.58; 95% CI, 0.40-0.83; P = .003). The associations were mainly attributed to differences observed in men. Twenty percent of the patients were ever (current or former) daily smokers compared with 43% of control subjects (OR, 0.33; 95% CI, 0.22-0.50; P < .001). Ever daily smoking before PSC diagnosis was associated with older age at diagnosis (42 years vs 32 years; P < .001). Ever daily smoking (P < .001) and being a coffee drinker at the age of 18 years (P = .048) were independently and negatively associated with PSC. Fewer female patients with PSC than control subjects reported ever use of hormonal contraception (51% vs 85%; P < .001). Among female patients, there was a strong correlation between increasing number of children before the diagnosis of PSC and increasing age at diagnosis (r = 0.63; P < .001). CONCLUSIONS: Coffee consumption and smoking might protect against development of PSC. In women, the disease might be influenced by hormonal factors.

Thyroid cancer was negatively associated with tobacco smoking and alcohol drinking
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2220030/

Nicotine primarily suppresses lung Th2 but not goblet cell and muscle cell responses to allergens

Mishra, N. C., Rir-Sima-Ah, J., Langley, R. J., Singh, S. P., Peña-Philippides, J. C., Koga, T., … Sopori, M. L. (2008). Nicotine primarily suppresses lung Th2 but not goblet cell and muscle cell responses to allergens. Journal of immunology (Baltimore, Md. : 1950), 180(11), 7655–63. Retrieved from http://www.jimmunol.org/content/180/11/7655.full

Allergic asthma, an inflammatory disease characterized by the infiltration and activation of various leukocytes, the production of Th2 cytokines and leukotrienes, and atopy, also affects the function of other cell types, causing goblet cell hyperplasia/hypertrophy, increased mucus production/secretion, and airway hyperreactivity. Eosinophilic inflammation is a characteristic feature of human asthma, and recent evidence suggests that eosinophils also play a critical role in T cell trafficking in animal models of asthma. Nicotine is an anti-inflammatory, but the association between smoking and asthma is highly contentious and some report that smoking cessation increases the risk of asthma in ex-smokers. To ascertain the effects of nicotine on allergy/asthma, Brown Norway rats were treated with nicotine and sensitized and challenged with allergens. The results unequivocally show that, even after multiple allergen sensitizations, nicotine dramatically suppresses inflammatory/allergic parameters in the lung including the following: eosinophilic/lymphocytic emigration; mRNA and/or protein expression of the Th2 cytokines/chemokines IL-4, IL-5, IL-13, IL-25, and eotaxin; leukotriene C(4); and total as well as allergen-specific IgE. Although nicotine did not significantly affect hexosaminidase release, IgG, or methacholine-induced airway resistance, it significantly decreased mucus content in bronchoalveolar lavage; interestingly, however, despite the strong suppression of IL-4/IL-13, nicotine significantly increased the intraepithelial-stored mucosubstances and Muc5ac mRNA expression. These results suggest that nicotine modulates allergy/asthma primarily by suppressing eosinophil trafficking and suppressing Th2 cytokine/chemokine responses without reducing goblet cell metaplasia or mucous production and may explain the lower risk of allergic diseases in smokers. To our knowledge this is the first direct evidence that nicotine modulates allergic responses.

In the end, I think that good coffee (lots of magnesium) and chocolate (lots of copper + antistress) could have a positive effects as well.

AS, the head cooling theory has merit, but then why is it dominant in males, why dont more women suffer aside from usually after menopause.

And again, the pattern... Grrr frustrating and interesting in equal measure.

Interesting what you mentioned about nutrients and keratin xenon, although ive not looked into it.
Im sure i once read that reducing facial hair with anti androgens would plausibly be an effective treatment for male hair loss.

AS54 wrote:http://www.ncbi.nlm.nih.gov/pubmed/10025745

Men with higher levels of testosterone were more likely to have vertex baldness (odds ratio [OR] = 2.5, 95% confidence interval [CI: 0.9 to 7.8] per 194 ng/dL increment of testosterone). In addition, for each 59 ng/mL increase in IGF-1, the odds of having vertex baldness doubled (95% CI [1.0 to 4.6]). Those who were found to have higher circulating levels of SHBG were less likely to have dense hair on their chest (OR = 0.4, 95% CI [0.1 to 0.9] per 24 nmol/L increment in SHBG]).

Admittedly though, this was with older subjects so the situation with senescene could be much different than for a guy losing at 25.

http://www.ncbi.nlm.nih.gov/pubmed/10827403

Of the 431 men, 128 had vertex balding at age 45. Compared with men who were not balding, for a 1 standard deviation increase in plasma IGF-1 level (72.4 ng/mL), the OR for vertex balding was 1. 31 (95% CI, 0.95-1.81). For a 1 standard deviation increase in plasma IGFBP-3 (957 ng/mL), the OR for vertex balding was 0.62 (95% CI, 0.44-0.88).

Older men with vertex balding have lower circulating levels of IGFBP-3 and higher levels of IGF-1 when controlling for IGFBP-3 level.

Again, we're talking older men here, so it may be that I am extrapolating a bit by assuming the situation with MPB is the same between age groups.

http://www.ncbi.nlm.nih.gov/pubmed/12894070

IGF-1 was up-regulated by finasteride treatment in 4 of 9 patients. Among the patients with increased IGF-1 expression, 3 of them showed moderate clinical improvement after 12 months of treatment and another patient remained unchanged. In contrast, 3 patients with decreased IGF-1 expression in the balding scalp showed clinical worsening after 12 months. The other 2 patients without noticeable change in IGF-1 expression showed either slight improvement or no change in their hair condition.

In a small uncontrolled study of 9 patients with AGA, an increased expression of IGF-1 messenger RNA levels in the DP was associated with patient response to finasteride.

Now here's some evidence the other way. I realize the problem is I worded that in a stupid way in my former post. IGF-1 is growth promoting...the reason it isn't in the scalp is that DHT inhibits it. However, we do have evidence to show irrespective of DHT, IGF-1 is associated with vertex balding in older subjects. There is obviously something more complicated happening up there. Because despite this, we still have androgen promoting hair growth on the face body, but what would seem to be programmed androgen inhibition of hair on the scalp. What is the mediator that is causing DHT to either promote/inhibit growth factor in the scalp versus the face.

There are some dense journal articles out there about the IGF family and hair cycling. If I get a bit of time later on tonight I can post them, but they are a relatively easy find on Google. They'll for the most part confirm what you are saying. In any other context outside of the vertex of the scalp, IGF-1 is promoting growth. It just seems its signal isn't being heard in the scalp because of DHT.

If you look at the results of the study CS posted yesterday:
https://immortalhair.forumotion.com/t9882-a-prostaglandin-d-synthase-positive-mast-cell-gradient-characterizes-scalp-patterning#101418

These data indicate that scalp is spatially programmed via mast cell prostaglandin d-synthase distribution in a manner reminiscent of the pattern seen in androgenetic alopecia.

This suggests that the immune system is programming MPB. That might be stated a little exceptionally, but mast cells have to migrate from the lymph tissue. Why are mast cells targeting the MPB area directly? Is it a chemotaxic attraction? If so, to what? Either way, this study shows there is programmed process happening on the scalp, at least from the perspective of the immune system. Again, we're back at the problem of wondering what the antigen is though, or what the physical damage is that's attracting the mast cells, or whether it could just be a genetic thing (no outright damage).

Very good finding AS54 !

I think control igf1 blood level doesnt make sense since indeed its implied in any hair growth cycle: make it in anagen. Since it will also control body hair its hard to conclude anything.

DHT promotes ROS expression, DKk1 etc, this is why I also believe in the CS theory wich is to increase GSH and SOD in the scalp naturally. GHK does it in a very few % topically. Problem is to increase GSH and SOD in the body with supplement, you often increase by the same your androgen level like its the case with ashwagwandha..

Isn't the pattern that men lose hair in later in life... the same pattern that hair grows in for newborn babies? Just in reverse? Could be some significance there.

I thought the exact same thing. my nephew is 2 and has receding hairline that is growing in

FWIW - it may be in your interest to sleep with the lights out as much as possible. Artificial light has been shown to suppress melatonin levels. Melatonin not only has very powerful antioxidant / anti-inflammatory properties, but greatly increases human growth hormone by up to 157 percent. HGH stimulates the production of IGF-1 also.

*note: I remember reading a story about some guy who slept with the light on every night for years and it caused him to age rapidly. Perhaps lack of melatonin = increased ROS.

"On a daily basis, millions of people choose to keep the lights on prior to bedtime and during the usual hours of sleep," said Joshua Gooley, PhD, of Brigham and Women's Hospital and Harvard Medical School in Boston, Mass. and lead author of the study. "Our study shows that this exposure to indoor light has a strong suppressive effect on the hormone melatonin. This could, in turn, have effects on sleep quality and the body's ability to regulate body temperature, blood pressure and glucose levels."

In this study, researchers evaluated 116 healthy volunteers aged 18-30 years who were exposed to room light or dim light in the eight hours preceding bedtime for five consecutive days. An intravenous catheter was inserted into the forearms of study participants for continuous collection of blood plasma every 30-60 minutes for melatonin measurements. Results showed exposure to room light before bedtime shortened melatonin duration by about 90 minutes when compared to dim light exposure. Furthermore, exposure to room light during the usual hours of sleep suppressed melatonin by greater than 50 percent."

http://www.sciencedaily.com/releases/2011/01/110113082716.htm

Live Forever,

I don't think we can argue this is not an androgen dependent issue. This is the reason we still see the pattern occurring in men much more than we do in women, although hormonal alterations in women that favor androgens do lead to hair loss in the same type of pattern, although it tends to be more of a diffuse loss.

The fact that women usually display increased hair growth and density during pregnancy is indicative of the protective role of estrogens here, although the situation is more complicated than just saying estrogen is "all good".

Some of the information I posted earlier shows that DHT may play a critical role in the response to hypoxia. It would appear transcripts that are increased by DHT are protective in some cases, while in others they are damaging. For example the increase in TGF-B appears to be detrimental to hair, and DHT increases it. The damage of TGF-B appears to contribute to the endothelial dysfunction that may be partially responsible for the hypoxic conditions that attract mast cells to the region. When LPS is present, DHT is an initiator of an inflammatory response. But in other ways, DHT can independently decrease COX-2 levels. So we're seeing a double-edged sword situation. DHT increases dickkopf proteins, which directly lower wnt signalling. So irregardless of whether we are taking all of the anti-inflammatories in the world, androgen activity is still always going to be promoting negative growth factors. That's just the plain reality of it.

But at any rate, I still don't think we've got a viable hair loss solution if it doesn't address the androgen issue, unless we discover that there is some penultimate molecule in the chain that if blocked stops the process. If/when we do that, then the androgens become irrelevant. The talk is that this signal is PGD2, so if we have a means of blockading the paracrine action if PGD2 at the DP, perhaps that's the key.

To me, the merit of all of these other upstream approaches is that I have no doubt other systems have an impact on the process. LPS has a huge impact on hair loss. So the environment of the gut is a major factor. Leaky gut in particular. The gut bacteria are probably having impacts we can't even begin to predict and I won't try. The liver's role in detoxing excess hormone. Thyroid and its impact on oxygen utilization. It all interacts somewhere if you connect the dots, so its obvious if there is something we can do to have an impact on the process somewhere, its in our best interest because we might be able to slow the process down. But we can't ignore the fact that androgen by itself is promoting loss.

lamka wrote:For me it is an extreme funny thread . After this series of photos had been uploaded I laughed so hard. Thanks you guys .

It depends what do you smoke. Organic tabaco or the one without any chemicals seems good to me. Also many times mentioned Gitanes without filter are good IMHO. I do not like this guy much but he talks about benefits of smoking + under the video there are interesting comments. It is worth reading. I have no hair loss(just dandruff), so I can not talk about effects of smoking to your body.
https://www.youtube.com/watch?v=ouTWt-80tdI

CS, would you post here your thoughts on smoking please ?

I rarely talk about this (have in the past), however due its controversial nature--after all the medical orthodox monopoly likes to create scapegoats for everything, all the while ignoring the real culprits, like mercury, aluminium, fluoride, glyphosate, etc.

Dr. William Campbell Douglass II wrote a nice book, which reveals more of a pro-smoking look, because it is beneficial.

You'll love the ad here: http://www.intbel.net/healthysmoke.html

In my older article here, I mentioned about how tobacco smoke does provide a source of B3 (Niacin), and it does have a positive benefit...it would explain why a significant percentage of smokers do not acquire Parkinson's or Alzheimer's.
http://www.immortalhair.org/apps/blog/show/1897941-prevent-neurological-diseases-with-a-controversial-mineral

I'm only down on smoking for the fact that it ages the skin. Hair wise, it's not negative. The research has failed to prove this, yet most assume it's bad.

http://waterfordwhispersnews.com/2014/02/02/charlie-sheen-found-alive-in-his-new-york-apartment-aged-48/

My grandfather on my fathers side was a avid tobacco smoker and never had heart disease or  Alzheimer's even though his father was effected by it, he was still bald as an egg though, which is what I was disagreeing about with lamka originally - that smoking doesn't prevents hair loss, as in the case of several of my family members.  I don't believe it's a negative for hair though as there are many smokers with hair.

father smokes a pack of day. been balding since 25, pretty close to bald since 40.

His brother doesn't, he's NW1.

I never touched a cigarette in my life and I'm receding at 21. Remember, things are never a result of just one factor, it's always many things in a complex interplay.

For what it's worth, my dad smoked 3 packs a day for30 years, he it 78 now and still has a juvenile hairline, little to no body hair, none on his chest or back.

Thank you so much CS. Nice post.

SlowMoe wrote:For what it's worth, my dad smoked 3 packs a day for30 years, he it 78 now and still has a juvenile hairline, little to no body hair, none on his chest or back.

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Hairy back is very bad sign. It usualy means hair loss. My dad have given up smoking and developed both - hair loss + some hair on his back.

Moderation is the key. The only one thing can not help you much. Smoking regular cigarettes is bad. Gitanes without filter, organic tabacco without filter is ok. I am glad that somebody see the benefits of tabacco smoking. Lifestyle + diet play role as well.

Here is research that shows negative effects of nicotine, however it's not the whole plant, just pure nicotine, so without the lithium and the other stuff is needed for the benefits. I think to some degree, the hormesis effect is a positive effect on digestion/motility.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3407298/

CS, did you post a comment that body hair is a good thing once? Im sure it was you.

Live forever wrote:CS, did you post a comment that body hair is a good thing once? Im sure it was you.

If there is sparse body hair, it's indicative of low IGF-1/growth hormone. It's needed to grow hair (scalp and body). However, if IGFBP-3 is too low, that can cause problems also.

http://www.ncbi.nlm.nih.gov/pubmed/10827403

Comp Biochem Physiol A Mol Integr Physiol. 2003 Sep;136(1):95-112.
Hyperinsulinemic diseases of civilization: more than just Syndrome X.
Cordain L, Eades MR, Eades MD.

Compensatory hyperinsulinemia stemming from peripheral insulin resistance is a well-recognized metabolic disturbance that is at the root cause of diseases and maladies of Syndrome X (hypertension, type 2 diabetes, dyslipidemia, coronary artery disease, obesity, abnormal glucose tolerance). Abnormalities of fibrinolysis and hyperuricemia also appear to be members of the cluster of illnesses comprising Syndrome X. Insulin is a well-established growth-promoting hormone, and recent evidence indicates that hyperinsulinemia causes a shift in a number of endocrine pathways that may favor unregulated tissue growth leading to additional illnesses. Specifically, hyperinsulinemia elevates serum concentrations of free insulin-like growth factor-1 (IGF-1) and androgens, while simultaneously reducing insulin-like growth factor-binding protein 3 (IGFBP-3) and sex hormone-binding globulin (SHBG). Since IGFBP-3 is a ligand for the nuclear retinoid X receptor alpha, insulin-mediated reductions in IGFBP-3 may also influence transcription of anti-proliferative genes normally activated by the body's endogenous retinoids. These endocrine shifts alter cellular proliferation and growth in a variety of tissues, the clinical course of which may promote acne, early menarche, certain epithelial cell carcinomas, increased stature, myopia, cutaneous papillomas (skin tags), acanthosis nigricans, polycystic ovary syndrome (PCOS) and male vertex balding. Consequently, these illnesses and conditions may, in part, have hyperinsulinemia at their root cause and therefore should be classified among the diseases of Syndrome X.

So, I have really sparse body hair. I have no chest, back or stomach hair. My face is JUST starting to fill in (hardly), but I'm only 23. Is this any indication to send me in a good direction?

There's too many things that could be influencing that.

Are you a taller guy?

I mention this because estrogen levels play a role in body hair growth and depending on the dose at puberty, sometimes guys can grow taller and not show a lot of body hair.

I'm tall with lots of body hair. What's that mean?

I shouldn't have given the impression that anything like this is something you can go "Yep, that's what's going on".

Height is very multi-factorial. A lot of different genes contribute to height. Do a search on Google scholar and you'll turn up a bunch of research on what contributes to height. Its beyond my knowledge though haha.

And body hair too. You've got too many factors to consider to really know for sure. How nice would it be if we could all do our own biopsies and see what was going on as individuals? Sheeeeeeit. That'll be the day.

Drawing on some generalities though, the same androgens contributing to hair loss promote body hair growth under normal physiological conditions. Body hair is the norm for a male. Having none suggests something different (not necessarily bad) is happening. Having a whole bunch suggests something different is going on. In the "typical" MPB profile, you've got lower levels of binding globulin so more free androgen and that'll often lead to an increase in body hair.