Posts Tagged ‘Hormones’

Trace elements content and hormonal profiles in women with androgenetic alopecia

Thursday, May 12th, 2011

J Trace Elem Med Biol. 2010 Dec 15.
Trace elements content and hormonal profiles in women with androgenetic alopecia.
Skalnaya MG, Tkachev VP.

Russian Society of Trace Elements in Medicine, Zemlyanoy Val str., 46, Moscow 105064, Russia; ANO “Centre for Biotic Medicine”, Zemlyanoy Val str., 46, Moscow 105064, Russia.

It is well-known that some trace element imbalances play a significant role in the pathomechanism of many forms of alopecia. Androgenetic alopecia, however, is a specific local sensitivity of hair follicle receptors to androgens.

In a clinical and laboratory study, 153 women with androgenetic alopecia (AGA) and 32 control women were examined. In AGA patients telogen hair and vellus hair (miniaturization, D<30μm) significantly differed in frontal and parietal hair comparison with occipital area (20±0.9% vs. 12±0.5% and 33±0.9% vs. 12±0.6% respectively).

In the AGA group levels of androstenedione and dihydrotestosterone were higher than in the control group. Hair elemental content, analyzed by ICP-MS, demonstrated a lowered Cu and Zn content in the frontal area in comparison to the occipital area. It is important to note, that the AGA patients with elevated levels of androstenedione and dihydrotestosterone presented an increased Cu content and decreased Mn, Se, Zn contents in the occipital area of scalp. The occipital level of Cu positively correlated with the concentration of free testosterone in the serum.

A negative correlation between the Zn content in the occipital area and the dehydroepiandrosterone level in the blood was found.

Unfortunately, a routine treatment course of AGA patients, including topical inhibitor of 5-alpha-reductase and minoxidil, had no effect on the Cu hair content in occipital and frontal areas.

However, there were positive changes in the morphological structure and other trace element contents. These data led us to hypothesize a key role of Cu metabolism disturbances in the AGA onset, development of AGA, and potential pharmaceutical targets for the treatment of AGA.

Evidence of increased DNA methylation of the androgen receptor gene in occipital hair follicles from men with androgenetic alopecia

Monday, May 9th, 2011

Br J Dermatol. 2011 Mar 24. doi: 10.1111/j.1365-2133.2011.10335.x. [Epub ahead of print]

Evidence of increased DNA methylation of the androgen receptor gene in occipital hair follicles from men with androgenetic alopecia.

Cobb JE, Wong NC, Yip LW, Martinick J, Bosnich R, Sinclair RD, Craig JM, Saffery R, Harrap SB, Ellis JA.

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Department of Physiology, University of Melbourne, Victoria Australia 3010 Developmental Epigenetics, Murdoch Childrens Research Institute, Flemington Road, Parkville, Victoria Australia 3052 Department of Dermatology, St Vincent’s Hospital, Victoria Australia 3065 New Hair Clinic, 627 Chapel Street, South Yarra, Victoria Australia 3141 National Hair Institute, 104 Canterbury Road, Middle Park, Victoria Australia 3206 Environmental and Genetic Epidemiology

In order to compare and clarify the underlying hormonal basis, a study was conducted in 12 young women (ages 14-33) and 12 young men (ages 18-30) with AGA (Sawaya and Price, 1997). Androgen receptor, type I and type II 5x-reductase, and cytochrome p-450 aromatase, were measured in hair follicles from scalp biopsies of these young subjects. Both young women and young men had higher levels of type I and type II 5x-reductase and androgen receptors in frontal hair follicles compared to occipital hair follicles; however, the levels in women were approximately half the levels in men (Sawaya and Price, 1997). At the same time, young women had much higher levels of cytochrome p-450 aromatase in frontal follicles than men who had minimal aromatase, and women had even higher aromatase levels in occipital follicles. The differences in aromatase, which is capable of converting testosterone to estradiol, are particularly notable. The findings of this study suggest that the milder expression of AGA in women may in part be the result of lower levels of 5x-reductase and androgen receptors in frontal follicles of women compared to levels in men; additionally, higher levels of aromatase in women may result in increased local formation of estradiol from testosterone, and less formation of 5x-reductase products such as DHT.

The Patterned Baldness Multifactorial Model: Hormonal-Immune Interactions

Monday, January 3rd, 2011

During research into male pattern baldness, so called androgenic alopecia, I found an abstract of a study published in April of 1999 that talked about AGA and the “sensitivity to the male sex hormones” relating to the androgen metabolism model. This abstract went further and mentioned a lesser-known model referred to as the “multifactorial model”.

In this model, “hormones affect the hair follicle in a way that causes it to be perceived as a foreign body by the immune system, which then mounts an attack.” [15] This study suggests hormonal/immune interactions. The immune system is usually looked at in cases of Alopecia Areata but not AGA. The topic of Alopecia Areata is beyond the scope of this paper.

The author believes further research is needed to better determine the extent of hormonal/immune interactions on MPB.

The above was written on July 22, 2010

The Patterned Baldness Non Androgen-Dependent Model

Monday, January 3rd, 2011

More recently, on May of 2010, a study published by the Royal Hallamshire Hospital in the UK titled “Female pattern hair loss in complete androgen insensitivity syndrome” showed a puzzling finding, namely that women with complete insensitivity to androgens still exhibited AGA.

This is stated clearly in this quote: “We describe female pattern hair loss occurring in a patient with complete androgen insensitivity syndrome suggesting that mechanisms other than direct androgen action contribute to this common form of hair loss in women”. [30]

This study shows that other factors besides androgens and androgen metabolism maybe at play here.

The above was written on July 23, 2010

The Patterned Baldness Estrogen Metabolism Model

Monday, January 3rd, 2011

An abstract of a study published in October of 2006 titled “The hair follicle as an estrogen target and source” argues that estrogen also alters hair growth by binding to estrogen receptors (ER’s) and that estrogen alters androgen metabolism (AM) in the follicle. [25]

The study team, expressed their view aptly when the said: “that the time has come to pay estrogen-mediated signaling the full attention it deserves in future endocrinological therapy of common hair growth disorders.”

During the research for this paper, the author found a few references discussing the importance of the ratio between estrogen and androgen in AGA cases.

The above was written on July 23, 2010

Dermal Papilla Androgen Sensitivity, Androgen Receptors & Methylation

Thursday, December 30th, 2010

Due to the understanding of male pattern baldness as Androgenic Alopecia (i.e. as an androgen-dependent process), many studies have focused on androgen metabolism (AM) in the body and how androgens effect hair.  Studies have shown that “all dermal papilla cells from androgen-sensitive sites contain low capacity, high affinity androgen receptors.” [18]

The dermal papilla (DP), at the base of the hair follicle, has androgen receptors (AR’s) that androgens from the blood bind to. In androgen-sensitive follicles, the androgens are synthesized and diffused over small distances; this induces changes in neighboring cells (like keratinocytes cells) in what is known as “paracrine interactions”. The diffusible proteins are called paracrine factors. [18]

When beard and scalp cells were incubated in androgens, androgens stimulated the cells’ ability to triggered mitosis (cell division) in beard cells but not in scalp cells. The interesting outcome here was that incubation with androgens had the exact opposite effect on scalp cells; these (scalp) cells’ mitogenic capacity was inhibited. [18]

Androgen-sensitive follicles are not simply targeted and affected by androgens; they are actually involved in androgen metabolism (AM) and can convert androgens using steroid-producing (steroidogenic) enzymes, also known as intrafollicular steroidogenic enzymes. [25]

A 2004 study shed more light on specific processes that shorten the hair cycle (that occur within the DP). According to the study, the three processes are as follows: “(1) the conversion of testosterone to DHT by type II 5-alpha-reductase; (2) the synthesis of TGF-beta2 in dermal papilla cells; and (3) the activation of the intrinsic caspase network.” [6]

The research seems to indicate AM activity at the DP of the hair follicle, amongst other interactions is not fully understood yet. Some of the known intrafollicular steroidogenic enzymes found in the DP are: Steroid Sulfatase (STS), 17beta-hydroxysteroid dehydrogenases (17b-HSD), 3beta-hydroxysteroid dehydrogenases (3b-HSD)  and type 1 and 2 5alpha-reductase (type 1 and type 2 5alpha-R). Type 2 5-alpha-reductase has been the target of a number of studies that showed it to accelerate the conversion of free testosterone into DHT. [10] [11] [12] [24] [25] [28] [31]

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Free Testosterone

Thursday, December 30th, 2010

The levels of free testosterone (free T) and the type 2 5alpha-reductase enzyme in serum has been the target of research; there seems to exist a strong coloration between the levels of available free testosterone in serum of the human body and baldness. [21] [23]

A 1997 study found that “several strong associations also were found between hormone levels and hair patterning.” This study found that “men with vertex and frontal baldness had higher levels of free T”. [2]

It is also known that both 5alpha-reductase enzymes types 1 and 2 convert testosterone (T) to dihydrotestosterone (DHT) as mentioned earlier, [4] particularly type 2.

Do Women Get Patterned Hair Loss?

Thursday, December 30th, 2010

Yes. It could be referred to as female pattern baldness, patterned baldness, diffused baldness, female baldness, or even as male pattern baldness (MPB)

Thirteen percent (13%) of pre-menopausal women are thought to experience some symptoms of patterned baldness, this number climbs up to 75% of women experiencing patterned baldness after the age of 65. [13]   Hair loss is increasing in both men and women, men in their early twenties are now experiencing MPB.

In my personal experience, I see many women, including ones in their twenties and thirties with thin hair and bald spots. In many cases when a metabolic issue exists hair loss is more likely to occur.

In women, the hair loss progresses as a diffused thinning of hair all over the top areas and crown of the head (i.e. parietal region). [5] [13] In this case, this hair loss is either referred to as male-pattern baldness, or as female-pattern baldness. [13]

I have heard of women who were very effected emotionally when their physicians told them they had “male pattern baldness” (because her doctor viewed it is a male-hormone dependent condition).

If this indeed was pure a male hormone issue then why are women experiencing hair loss at younger ages and more often? More importantly, how are some able to stop it using diet and nutrition, lifestyle and topical treatments?

I believe the use of the term male pattern baldness to describe any female hair loss is inappropriate.

Edited: 12/29/2010

Is Self Diagnosis of MPB Possible?

Wednesday, December 29th, 2010

Can a man diagnose himself of having MPB?

Yes! In men, male pattern baldness (MPB) or Androgenic Alopecia (AGA) can be identified and defined visually. The use of the Hamilton Norwood Classification scale or other scales aids in this process and offers a more accurate classification.

Let me repeat: Self diagnosis for MPB is possible. I diagnosed myself, I then went to see the family doctor and asked him “what’s happening to my hair” he answered “male pattern baldness”. Don’t take my word for it, a study published in December, 2004 entitled “Validity of self reported male balding patterns in epidemiological studies” examined and compared the accuracy and reliability of the assessment of balding patterns when conducted by “trained observers” verses assessments of balding patterns conducted by “men” who are experiencing the balding themselves.

In this study, the trained observers and “men” used a classification system known as the “Hamilton-Norwood classification system” (shown below). This study found while it was best to have a trained observer assess the balding pattern, it found that “men’s self evaluation is accurate enough to ensure reliability and validity of results.” In other words, a man should be able to assess his own hair loss pattern using this scale reliably. [*1]

How to identify?

MPB causes a gradual thinning of the hair on the scalp, following a certain pattern. With MPB, the hair line either recedes uniformly from the forehead (this is known as frontal hair loss or frontal balding) or it recedes in a manner that follows an “M” shape (known as vertex hair loss). Vertex hair loss is also accompanied by hair loss at the crown or back of the head. [21] [23]

Both patterns could progress to partial baldness that leave hair around the sides of the head (resembling a “U” shape) or even to total baldness. The Hamilton Norwood scale is used by researchers and individuals to access or quantify their baldness pattern. [21] [23]

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Should the Term “Androgenic Alopecia” Be Used? (Research History)

Wednesday, December 29th, 2010

About 60 years ago Hamilton made an important observation when he noticed that castrated men did not have AGA. He concluded that hair growth on the scalp was androgen-dependent.

Despite androgens causing hair loss in many men, androgens are actually crucial as they are responsible for the development of puberty; they also aid in, if not cause, male maturation, growth of muscles and the appearance of other sexual characteristics in young humans. [25]

Androgens, such as testosterone (T) and dihydrotestosterone (DHT), have been identified by researchers to be the main regulators of hair growth. Androgens contribute to the changing of vellus (tiny, un-pigmented) hairs into terminal (thicker) hair follicles. [18]

Paradoxically, androgens are also are often thought of as the main culprit behind male pattern baldness.

Androgens in the scalp of adults with androgen-dependent hair follicles seem to have two undesirable effects. The first being that they shorten the anagen phase (long growth phase). [6]

A study published in November 2002 further explained that the follicles experience a “transformation from long growth (anagen) and short rest (telogen) cycles, to long rest and short growth cycles.”  [3]

The second effect always accompanies the first and maybe the manifestation of it. This effect is manifested as the gradual changing of (thick) terminal hair follicles to (thinner) vellus hair (due to the reduction of the cellular hair matrix volume). This change in thickness has been referred to as a “progressive miniaturisation of the follicle.”[3] [5] [18] [23]

In summary, androgens shorten the long growth cycle (anagen phase) and cause follicles to enter into the resting cycle (telogen phase) faster and remain in that phase longer; this results in finer and finer hair. This process  is what we’ve identified as, or termed, AGA.

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