Archive for the ‘Androgens’ Category

Study: Androgenetic alopecia in children: report of 20 cases.

Saturday, October 8th, 2011

Br J Dermatol. 2005 Mar;152(3):556-9.
Androgenetic alopecia in children: report of 20 cases.
Tosti A, Iorizzo M, Piraccini BM.
Source

Department of Dermatology, University of Bologna, Via Massarenti 1, 40138 Bologna, Italy. tosti@med.unibo.it
Abstract

Androgenetic alopecia (AGA) is the most common type of hair loss in adults. Although there are differences in the age at onset, the disease starts after puberty when enough testosterone is available to be transformed into dihydrotestosterone.

We report 20 prepubertal children with AGA, 12 girls and eight boys, age range 6-10 years, observed over the last 4 years. All had normal physical development. Clinical examination showed hair loss with thinning and widening of the central parting of the scalp, both in boys and girls. In eight cases frontal accentuation and breach of frontal hairline were also present. The clinical diagnosis was confirmed by pull test, trichogram and dermoscopy in all cases, and by scalp biopsy performed in six cases.

There was a strong family history of AGA in all patients. The onset of AGA is not expected to be seen in prepubertal patients without abnormal androgen levels. A common feature observed in our series of children with AGA was a strong genetic predisposition to the disease. Although the pathogenesis remains speculative, endocrine evaluation and a strict follow-up are strongly recommended.

PMID:
15787828
[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/15787828

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.

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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.

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.

Types of Alopecia and Overlap in their Causes

Sunday, January 2nd, 2011

Alopecia can strike anyone for any variety of reasons.  Even newborn babies can be born with this condition.  There are five most common types of hair loss, several other types of alopecia exist, the first five being the most common ones:

  • The most common form of baldness is a progressive hair thinning condition, so called Androgenic alopecia or male pattern baldness (MPB).
  • Female pattern baldness. The equivalent of MPB, and often is related to Polycystic Ovarian Syndrome (PCOS), malnutrition or wheat/gluten intolerance.
  • Alopecia areata, involves the loss of some of the hair from the head, Those with alopecia areata have scattered bald spots all over the head, or one large bald spot confined to one section of the head. It is known as “spot baldness”, it can result in hair loss ranging from just one location (Alopecia areata monolocularis) to every hair on the entire body (Alopecia areata universalis). Alopecia areata, is typically associated with sudden hair loss, sometimes related to trauma, or illness, stress, abusive hair styling such as tight braids and pony tails, wigs, hairpieces or chemicals used on the hair. Alopecia areata is an autoimmune disorder. *4
  • Alopecia totalis, involves the loss of all of the head hair, typically be characterized by the complete loss of hair on the head.  The shedding of normal hair will usually occur over a certain amount of time. The sufferers of alopecia totalis will sometime have a small amount of soft Lanugo hair left over after the normal hair has completely fallen out. *7
  • Alopecia universalis, which involves the loss of all of the hair from the head and the body, from the top of the head to the legs and feet including eye brows.  Alopecia universalis is the rarest condition of the five most common forms of alopecia. It is thought that alopecial universalis is an autoimmune condition. *5

The following are are thought of as being less common, these can be confused as female/male pattern baldness:

Traction alopecia is most commonly found in people with ponytails or cornrows who pull on their hair with excessive force.

Trichotillomania is the loss of hair caused by compulsive pulling and bending of the hairs. It tends to occur more in children than in adults. In this condition the hairs are not absent from the scalp but are broken. Where they break near the scalp they cause typical, short, “exclamation mark” hairs.

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The Genetic Link

Thursday, December 30th, 2010

Looking at research into Androgenic Alopecia (AGA) here’s what I found:

Hair follicles in different parts of the human body behave differently throughout the human lifespan. Beard growth is androgen-dependent, while hair sensitive to androgen experiences thinning as result of androgens. [25]

It seems androgens cause beard hair, armpit (axillary) hair and pubic hair follicles to enlarge while frontal and vertex scalp hair decrease is size. Others hair follicles like eyebrows and eyelashes don’t seem to change in size. [28]

Researchers in one study concluded this opposite impact of androgens on hair follicles of the beard and scalp was due “to differential gene expression within hair follicles”. [18] Another study stated the factors behind AGA “to be genetic predisposition coupled with the presence of sufficient circulating androgens” and “require the inheritance of several genes”. [3]

A study published in 2005 summarized the role of genetics with AGA by saying AGA is “androgen dependent, and genetic predisposition is the major requirement for the phenotype.”[9-] In other words, we can define AGA not only as androgen-dependent but also as a genetic condition.

Androgens would have no effect if it wasn’t for androgen receptors (AR’s). AR’s are what enables the human body to respond to androgens, and thus play a crucial role in male sexual development. Genetic variations in the AR gene are more common in men with an early onset of AGA.

German researchers named the androgen receptor gene as the cardinal prerequisite for balding.[9-] They concluded a certain variant of the androgen receptor is needed for AGA to develop. In the same year the results of this study were confirmed by other researchers.[10-]

This gene is recessive and a female would need two X chromosomes with the defect to show typical male pattern alopecia. Seeing that androgens and their interaction with the androgen receptor are the cause of AGA it seems logical that the androgen receptor gene plays an important part in its development.

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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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