Low Local Estrone AlopeciaAlopecia caused by insufficient
local follicular estrone activity
Two essential intrafollicolar hormones regulate hair cycles:
diidrotestosterone ed estrone.
Diidrotestosterone reduces adenylcyclase activity so that the
follicle turns into catagen and the hair becomes telogen.
Estrone increases adenylcyclase activity, and thus maintains the
mitoses of the matrix, and the duration of the anagen. It also
activates the staminal cells in the early stages of the anagen
Today, it is usual to accept that male androgenetica alopecia
is associated with an increase in 5-alpha reductase activity which,
genetically, leads to higher levels of diidrotestosteron but this
has been studied mainly, if not exclusively, in males. The results
obtained have then been referred to women patients, which to my
mind is not appropriate and that is why there is talk of Female
Androgenetic Alopecia (FAGA). But to give a diagnosis of Androgenetic
Alopecia, there are two essential “sine qua non” conditions:
1) the condition must exist in at least one of the biological
2) there must be a significant quantity of androgen hormones.
Essentially, if a woman is bald for genetic reasons then her own
mother must be bald, and the baldness must not be due to Areata
Alopecia or Telogen Effluvium. In addition, we must remember that
androgen levels in a healthy woman are always much lower than
in a male. Also, in a male who is being treated with finasterid
or dutasterid DHT levels are approximately 10 times higher than
those in a healthy woman with alopecia consequently, for female
alopecia, “androgenetic” is by no means a good definition.
For this reason, in the 1970s and 1980s, to explain the development
of Androgenetic Alopecia in otherwise healthy women, reference
was made to “an increment in the metabolic use of testosterone
(T) and of its being converted cutaneously into diidrotestosterone
(DHT)” (Walter P. Ungher,). It was also thought that these
women had “a higher degree of follicular sensitivity (?)
to the effects of the androgens in the blood” (Thomsen 1979;
Mahoudeau; Bardin; Kirschner 1971 - 79). Another hypothesis was
that these women had low levels of Sex Hormone Binding Globulin
If we think that baldness process is caused by androgens, then
Androgenetic Alopecia would be present only in androgen sensitive
areas. In the scalp, these receptors have been found only in frontal
areas and in the crown, and not in temple and occipital areas.
Indeed, in males, androgenetic alopecia is present only in these
Female Alopecia also appears to be different from Male Alopecia
from a clinical point of view:
1) the pattern is centrifugal, and usually of Ludwig type;
2) in women, alopecia usually spreads to areas that are not sensitive
to androgens and involves zones that are not affected in Male
Androgenetic Alopecia, such as the nape;
3) follicular miniaturization is different. Initially, at least
there is no great loss in depth. It is more a question of thickness.
The hair shafts become thinner but remain long;
4) Women virtually never become really bald. Usually, it is a
question of hypotrichia;
5) 5-alpha reductase inhibitors seem to be practically ineffective
in women. At best, they have an almost negligible effect.
From therapeutic point of view high levels of estrogens (during
pregnancy, or in contraception) may have a beneficial effect in
many cases of female alopecia and estrogens, usually prescribed
with antiandrogens that are similar to progesterone, have been
used frequently, and have given good results. However, no clinical
trials have been undertaken to verify this.
With the exception of a few rare cases of anomalous surrenal or
ovarian hormonal production due to enzymatic defects, or to a
secreting tumor, in women alopecia is very different to that in
males, presumably because of the diverse metabolic and endocrinic
traits in the two sexes.
Female Ludwig Alopecia (FAGA) is, in my opinion, nearly always
the result of Telogen Effluvium or of low levels in follicular
estrone activity! Young women with thin, sparse hair in all parts
of the scalp (but especially in crown and frontal areas) whose
mothers are often in the same condition, but who have regular
menstrual periods, and normal fertility levels, without excessive
androgen, in which it is not possible to find clear proof of Telogen
Effluvium lead us to consider the possibility of genetic peripheral
resistance or of insufficiencies in the production of intrafollicular
estrone (deficit of 17 steroid oxydoreductase, aromatase, 3 alpha
reductase). These young females are suffering from hypotrichia
or alopecia due to local insufficient estrone!
All this is not only academic waffle! It has important therapeutic
5-alpha reductase inhibitors are ineffective in women because
they hit the wrong target by trying to inhibit the metabolism
of a hormone that is practically absent; whereas, a topical therapy
with estrone or 17 alpha estradiol may be effective in many cases.
When a woman is affected only at the top of the head, and has
a so-called “tonsure effect”, and especially if she
is losing hair at the temples and at the front of her head, then
we can say she has a Male Pattern Alopecia, MAGA, and we will
have to look for an androgen cause. On its own, a simple micropolycystic
ovary (which is not a real illness!) will never cause Male Pattern
Alopecia (MAGA), there has to be something more serius, such as
a real Policystic Ovary Syndrome, an ovarian or surrenalic androgen
secreting tumor, or a surrenalic enzymatic deficiency like a 21
We can therefore consider that real Androgenetic Alopecia is frequent
in men and rare in women and is caused by the conversion of the
testosterone into diidrotestosteron. Low Local Estrone Alopecia
is caused by local inadequate estrone activity, is frequent in
women and is rare (though possible) in men.