Is Hair Loss Caused by Skull Expansion???

[wookster]

:dunno:

Big Head, Bald Head - Is Hair Loss Caused by Skull Expansion?

A new study suggests that people who agonize over hair loss (known as androgenetic alopecia) might have their big heads to blame. A UK researcher has determined that men and women whose skull bones keep growing during adulthood are far more likely to develop male and female pattern baldness.

The Medical Hypotheses journal reports a possible breakthrough in our understanding of androgenetic alopecia which could one day lead to an alopecia cure.



In his article, he explains how both male and female thinning hair and baldness involves the continued growth of the skull bones that lie directly under the scalp where hair loss develops. This bone growth is called skull expansion.

Skull expansion seems to have finally solved certain mysteries that have been baffling hair loss boffins for years. These include why the same shape (or pattern) of hair loss will always develop in men with extreme baldness. Severe hair loss at the front (frontal baldness) and crown of the head will leave just a small horseshoe shaped area of hair growing at the back and sides. Skull expansion explains why this happens - something the current theory for hair loss cannot do.

Another mystery involves the male sex hormone dihydrotestosterone (DHT). Male pattern baldness has been linked to DHT, but this hormone also causes body and facial hair to grow at puberty. Skull expansion explains how DHT is connected to both hair loss and hair growth.

If this theory for androgenetic alopecia by skull expansion is confirmed, it could lead to a total redirection of genetic research, affect future treatment methods and might eventually lead to an alopecia cure.

 

[Boondock]

I don't buy it:

--- Some men don't lose their hair in the normal pattern

--- It doesn't explain why transplanted hair remains firm

--- It's possible that male pattern baldness may be correlated with increase in skull size, without one causing the other.

 

[wookster]

I don't buy it:

--- Some men don't lose their hair in the normal pattern

--- It doesn't explain why transplanted hair remains firm

--- It's possible that male pattern baldness may be correlated with increase in skull size, without one causing the other.

Let me assume the role of Devil's advocate here since I don't necessarily agree with the hypothesis but what the heck... :woot: Transplated hair does not always remain firm even though I assume it does grow robustly in most of the case histories of hair trnasplantation... :dunno:

http://www.sciencedirect.com/scienc...serid=10&md5=9a580c7c3aed3870e1448f73fb5dafb9

The bones of the human skull continue to grow during adulthood and observations made of those with Androgenetic Alopecia suggest that such growth may be responsible for the development of this condition. Studies of human cranial anatomy indicate that frontal and parietal bone growth can account for the development of the male pattern baldness (male pattern baldness) profile and the variations that can occur in the rate and location of hair loss. Steroid hormones such as DHT promote facial and body hair growth. Logically, this suggests that DHT should stimulate hair growth within the male pattern baldness region and not hair loss. However, DHT also has an anabolic effect on bone formation, and it is hypothesised that this stimulation of bone growth will overwhelm the hair growth promoting effects of DHT. Androgen receptor sites, 5-alpha-reductase (5?-R) and DHT have all been associated with Androgenetic Alopecia, but they also exist within numerous types of bone cells. DHT will stimulate the proliferation of osteoblast cells and the formation of new bone.

Verification of this hypothesis would imply that DHT is primarily involved with Androgenetic Alopecia through its stimulation of the skull expansion process rather than through interaction with individual follicles. Also, increased androgen receptor gene expression, 5?-R activity and subsequent production of DHT within the male pattern baldness region of balding individuals, may simply represent the body’s attempt to compensate for the skull expansion expression of hair follicle miniaturisation. Furthermore, it suggests that male pattern baldness region follicles are not individually programmed for hair loss. A redirection of genetic research towards the identification of those genes responsible for skull shape and development would be appropriate, and may reveal the genetic connection to Androgenetic Alopecia including its paternal link.

 

[Boondock]

Pfft...I know you don't really believe in this either.

It just leaves too much unexplained. How come some folks start balding in their 30s? Are their skulls suddenly expanding? Are diffuse thinners just ballooning their skulls all over the place?

It's also quite a dispiriting thought, when you think about it. How do we solve hair loss now? Clamp our skulls down from age 16? (don't try that anyone, by the way).

 

[wookster]

:shock:

http://www.fbi.gov/hq/lab/fsc/backissu/july2001/milner.htm

Despite man's best efforts, the outward facial appearance associated with increasing age is unstoppable. As part of this change, there is a continuous alteration of the morphological properties of soft tissue structures and their composition, especially in relation to the extracellular matrix, which serves as tissue scaffolding. The possibility that progressive change to underlying bone tissue may accompany that seen in soft tissues has received much attention in the literature during the past 50 years and has been comprehensively reviewed by Behrents (1984). Histological alteration of bone architecture is known to occur with a disorganization of the highly ordered Haversian system, a reduced number of resident osteocytes, and a reduced overall bone mass and density. Nevertheless, bone remains a highly dynamic tissue with active remodeling occurring through old age. Beyond the fourth decade, this remodeling process has been shown to occur in a differential pattern within anatomically defined areas to produce gross changes in shape at the macroscopic level. This has been described for many long bones of the skeleton where an overall increase in width and length of the shaft results from endosteal bone resorption and preferential periosteal apposition. In essence, these dimensional changes can be regarded as growth.

 

[Bryan]

Come on, wookster, are you going to keep promoting this stupid garbage every few months?? You're wasting perfectly good bandwidth on this site with this childish prattle.

 

[wookster]

Come on, wookster, are you going to keep promoting this stupid garbage every few months?? You're wasting perfectly good bandwidth on this site with this childish prattle.

:salut: :gay2: :salut:

I don't recall ever making a previous post specifically about the skull expansion theory.

I don't see male pattern baldness as being due to the process of evolution through natural selection but it appears to be more associated with an unhealthy pathological condition.

 

[Bryan]

I don't recall ever making a previous post specifically about the skull expansion theory.

Are you SURE about that? I've seen that theory mentioned a few times in the past, and YOU are the one I generally tend to associate with these goof-ball theories of balding!

I don't see male pattern baldness as being due to the process of evolution through natural selection but it appears to be more associated with an unhealthy pathological condition.

And what would that "pathological condition" be?

 

[wookster]

I don't see male pattern baldness as being due to the process of evolution through natural selection but it appears to be more associated with an unhealthy pathological condition.

And what would that "pathological condition" be?

That is still an unsolved variable at the present time :woot:

 

[Tyler_Durden]

This bloke spent 7 years on this study?

 

[Bryan]

And what would that "pathological condition" be?

That is still an unsolved variable at the present time :woot:

So you didn't have anything specific in mind when you wrote that, you were just speaking off the top of your head? :jackit:

 

[wookster]

And what would that "pathological condition" be?

That is still an unsolved variable at the present time :woot:

So you didn't have anything specific in mind when you wrote that, you were just speaking off the top of your head? :jackit:

I don't appreciate your attempts at trying to force me into a corner there buddy :thumbdown2:

There appears to be evidence that skull morphology does change with age. How does that relate to Foote's theory of male pattern baldness? Like I said, that is still an unsolved variable at this time :dunno:

 

[OverMachoGrande]

Maybe skull expansion is caused by high levels of IGF-1, which is know to correlate with hair loss.

 

[Bryan]

I don't appreciate your attempts at trying to force me into a corner there buddy :thumbdown2:

Then I suggest that you not engage in wild-*** speculation.

 

[barcafan]

ooooohhh a challenge made by bryan, let's see if the challengee responds

 

[wookster]

I recall reading studies posted by Bryan about balding human hair follicles
re-enlarging? after being transplanted to the backs of immunodeficient mice?

If that is true then human balding follicles could be more constricted by the scalpal terrain than by any internal genetic mechanism within the follicles themselves. :woot:

 

[wookster]

Brain growth and baldness, is there a connection?

:bravo:

http://www.hairlosstalk.com/interact/viewtopic.php?f=11&t=51153

A primate-specific acceleration in the evolution of the caspase-dependent apoptosis pathway


Programmed cell death, or apoptosis, plays an essential role in mammalian development, especially the development of the nervous system. Here, we systematically examine the molecular evolution of the mammalian intrinsic apoptosis program. We divided the program into its several constituent pathways and examined the evolution of each pathway in diverse mammalian taxa spanning primates, rodents and carnivores. We observed that genes involved in the caspase-dependent apoptosis pathway stood out in several ways. First, these genes display an accelerated rate of protein sequence evolution in primates relative to rodents or carnivores. Secondly, this acceleration is most pronounced along the lineage leading to humans, and it is associated with signatures of positive selection. Finally, several genes in this pathway, including APAF1, CASP9 and CASP3, have been shown to be associated with dramatic defects in neuronal cell number and brain size when mutated in mice. These observations suggest the possibility that evolutionary changes in the caspase-dependent apoptosis pathway may have contributed to brain evolution in primates and humans. Our results also lend further support to the hypothesis that genes regulating brain size during development might have played a particularly important role in transforming brain size during evolution.

 

[wookster]

:woot:

http://news.bbc.co.uk/1/hi/health/289781.stm

Brain growth linked to baldness

Revolutionary hair loss treatments could be on the way after skin specialists found a link between a brain cell growth protein and the rate at which hair falls out.

The German scientists found that by increasing the body's levels of brain growth proteins they also increased the rate at which hair falls out.

Restricting levels meant hair was shed at a slower rate.

The finding could lead to improved treatments to get rid of unwanted hair and for treating baldness, according to a report in New Scientist magazine.

[...]

Their earlier research showed that when mice lost hair, there was a high concentration of brain-derived neurotrophic factor (BDNF) and neurotrophin-4 (NT-4) around their follicles.

BDNF and NT-4 are two growth factors thought to be important in the development of brain cells.

The earlier research also showed that the genes that make the proteins are abnormally active at the same time.

Balding from birth

For the new study, the team genetically-engineered mice to produce excess quantities of both the factors.

They found that the mice shed their hair abnormally early.

In mice engineered to produce neither factor, hair took longer than normal to fall out.

"This is the first evidence that growth factors previously thought to be important for the development of brain cells are also important for the growth of hair follicles," Dr Paus told the magazine.

 

[wookster]

http://www.nature.com/jid/journal/v124/n4/abs/5602756a.html

"Control of Human Hair Growth by Neurotrophins: Brain-Derived Neurotrophic Factor Inhibits Hair Shaft Elongation, Induces Catagen, and Stimulates Follicular Transforming Growth Factor B2 Expression"

Well the question becomes how does all that extra BDNF circulate outside the the brain and into the scalp tissues :dunno:

 

[opeth88]

http://www.ncbi.nlm.nih.gov/pubmed/8853853

Division of Radiobiology, School of Medicine, University of Utah, Salt Lake City, USA.

Androgens are associated with the greater skeletal mass and size in men compared with women and have been used as anabolic agents promoting skeletal growth and mineral accretion in both sexes, but specific effects on growth and bone formation in the female skeleton are not well understood. The effects of 5 alpha-dihydrotestosterone (DHT) alone, and in combination with 17 beta-estradiol on bone and bone growth were studied in female ovariectomized (OVX) rats with established osteopenia. Eight weeks after OVX, rats were given 0.1 mg 17 beta-estradiol and/or 2.5 mg or 10 mg DHT administered by controlled-release pellets for 2 months. Body weights decreased with estrogen treatment but increased with DHT. Bone mineral density increased with the highest dose of DHT relative to OVX controls and the estrogen treated group. Dry and ashed bone weights and ash/dry weight ratios increased in the estrogen and DHT treated animals compared to the baseline OVX controls. Total bone calcium was greater with DHT and estrogen combined with DHT. The percent of calcium in the ash increased in all DHT treated groups. When normalized to final body weight, the total femur calcium content was significantly increased in the estrogen and estrogen with DHT groups, but not in the DHT groups compared with the baseline OVX and OVX control groups. The periosteal bone formation rates were increased with the high dose DHT alone and combined with estrogen. OVX rats had increased endochondral bone elongation rates relative to controls but this was decreased with estrogen treatment. DHT combined with estrogen increased endochondral growth rates relative to the estrogen treated group. Trabecular bone volume was decreased in all OVX groups relative to the base line group, but there were no significant effects observed with any treatments. Cancellous bone formation rates were suppressed with estrogen treatment but were partially reversed when combined with DHT. DHT treatments also increased most cancellous bone formation indices over OVX controls. While estrogen is known to preserve skeletal mass by reducing bone turnover, DHT increased skeletal mass by promoting bone growth and formation with concomitant increases in total body mass. DHT had greater effects on cortical bone and partially mitigated the suppressive effects of estrogen on bone growth and formation in the female skeleton.

Just thought I'd throw that in there. I am indeed, NOT an expert.