International Journal of Cosmetic Science, 2002, 24, 17^23
Causes of hair loss and the developments
in hair rejuvenation
D. H. Rushton, M. J. Norris, R. Dovery and Nina Busuttilz

School of Pharmacy & Biomedical Sciences, University of Portsmouth, Portsmouth, Hants PO12DT,
yImperial Cancer Research Fund, Lincoln's Inn Field, LondonWC2A 3PX, and zBio-Scienti¢c Ltd,
24 Harmont House, 20 Harley Street, LondonW1G 9PJ, UK
Received 8 July 2001, Accepted12 July 2001
Keywords: androgenetic alopecia, chronic telogen e¥uvium, common balding, ¢nasteride, Florisene1,
hair loss, hair shedding, hair treatments, male pattern balding, Propecia1, Regaine1
Synopsis
Hair is considered to be a major component of an
individual's general appearance. The psychological
impact of hair loss results in a measurably detrimen-
tal change in self-esteem and is associated with
images of reduced worth. It is not surprising that
both men and women ¢nd hair loss a stressful experi-
ence. Genetic hair loss is the major problem a¡ecting
men and by the age of 50, up to 50% will be a¡ected.
Initial attempts to regenerate the lost hair have
centred on applying a topical solution of between
2% to 5% minoxidil; however, the results proved dis-
appointing. Recently, ¢nasteride, a type II 5a reduc-
tase inhibitor has been found to regrow a noticeable
amount of hair in about 40% of balding men. Further
developments in treatments have lead to the use of a
dual type I and type II inhibitor where 90% of those
treated regrow a noticeable amount of hair. In
women the major cause of hair loss before the age of
50 is nutritional, with 30% a¡ected. Increased and
persistent hair shedding (chronic telogen e¥uvium)
and reduced hair volume are the principle changes
occurring. The main cause appears to be depleted
iron stores, compromised by a suboptimal intake of
the essential amino acid L -lysine. Correction of these
imbalances stops the excessive hair loss and returns
the hair back to its former glory. However, it can take
many months to redress the situation.
Correspondence: Dr D Hugh Rushton, 24 Harmont House,
20 Harley Street, London W1G 9PJ, U.K. E-mail: rushton@
btinternet.com
ß 2002 Blackwell Science Ltd
ReÂsumeÂ
Les cheveux sont considërës comme ëtant une com-
posante majeure de l'aspect gënëral d'un individu.
L'impact psychologique de la perte des cheveux con-
duit a© une diminution mesurable de l'estime de soi et
s'associe a© des images de contexte nëgatif. Il n'est pas
surprenant que les hommes comme les femmes
ressentent la perte de cheveux comme une expëri-
ence stressante. La perte gënëtique des cheveux est
le proble©me principal qui touche les hommes et
autour de l'aªge de 50 ans, jusqu'a© 50% seront con-
cernës. Les premie©res tentatives de rëgënëration des
cheveux perdus se sont focalisëes sur l'application
topique d'une solution comprenant entre 2% et 5%
de minoxidil; cependant, les rësultats se sont avërës
dëcevants. Rëcemment, le ¢nastëride, un inhibiteur
de la 5a-rëductase de type II s'est avërë permettre la
repousse d'une quantitë signi¢cative de cheveux chez
environ 40% des hommes dëgarnis. Les dëveloppe-
ments ultërieurs des traitements ont conduit a© l'utili-
sation d'un inhibiteur associant type I et type II pour
lequel 90% des personnes traitëes constatent une
repousse signi¢cative des cheveux. Chez les femmes
la cause principale de la perte des cheveux avant
l'aªge de 50 ans est d'origine nutritionnelle, avec 30%
de la population a¡ectëe. Une perte de cheveux per-
sistante et croissante (telogen e¥uvium chronique)
et un volume des cheveux rëduit sont les principaux
e¡ets qui se produisent. La cause principale semble
eªtre des rëserves de fer ëpuisëes, associëes a© une prise
insu¤sante de l'acide aminë essentiel L-lysine.
La correction de ces dësëquilibres stoppe la perte
17
Hair loss and rejuvenation
excessive de cheveux et rend aux cheveux leur ëclat
d'antan. Cependant, plusieurs mois peuvent eªtre
nëcessaires pour redresser la situation.
Introduction
Hair is considered to be a major component of an indi-
vidual's general appearance. Throughout history,
and in most (although not all) civilizations, scalp hair
has been associated with positive signals such as
beauty and power. Baldness or hair loss on the other
hand has a negative attribute [1].
The psychological impact of hair loss results in
a measurably detrimental change in self-esteem
and is associated with images of reduced worth
[2, 3]. It is not surprising that both men and
women with genetic hair loss ¢nd it a stressful experi-
ence. An Egyptian papyrus over 4000 years old
records the anxieties prompted by premature
hair loss at that time [4].The study by Cash [3] showed
that balding men had less body image satisfaction
and su¡ered from preoccupation, stress and even
distress, which was more marked in those who
were younger, single, and had hair loss which was
more extensive or of earlier onset. Similar ¢ndings
have been observed in women with alopecia areata
(loss of hair in patches), totalis/universalis (complete
loss of scalp/body hair), genetic hair loss and
increased hair shedding (chronic telogen e¥uvium,
CTE).
Even in conditions such as CTE where a complete
recovery can be expected, the distress caused by the
loss of hair can have a profound e¡ect upon an indivi-
dual's self-con¢dence and quality of life. This can
result in the su¡erer seeking help from unscrupulous
organizations who sell useless and ine¡ective lotions
and potions for large sums of money.
Signi¢cant amounts of time and money are
devoted to hair care, $2.2 billion in the USA and $3.3
billion in Europe (source, Procter & Gamble, UK),
with an estimated $1 billion spent on trying to pre-
vent or treat hair loss, yet none of the causes of hair
loss is life threatening.
Classifying hair loss in men
Male pattern hair loss, also known as androgenic,
androgen-dependent or androgenetic alopecia is the
most common type of hair loss in men [5, 6]. Over
40 years ago, Hamilton ¢rst described and categor-
ized the progressive pattern of hair loss in men, and
a modi¢ed version is still in use today [6]. In some
18
D. Hugh Rushton et al.
men (5%, D. H. Rushton, unpublished data), a di¡use
pattern of loss similar to that seen in women prevails
[7].
Pathology
Androgenetic alopecia occurs in a characteristic
pattern and the changes can be summarized as
follows. Initially, a reduction in the percentage of
hair follicles in the anagen growth phase occurs,
resulting in a reduction in the length of hair grown.
This aspect can be speci¢cally evaluated in genetic
hair loss by determining the percentage of telogen
(resting) hair less than 3 cm in length, within the
a¡ected area [8]. As the genetically orchestrated
changes emerge there is an increase in the propor-
tion of vellus hair (hair <40 mm in diameter being
<3 cm in length), followed by a reduction in hair
density [8].
The expression of androgenetic alopecia requires a
genetic predisposition as well as postpubertal levels
of circulating testosterone or one of its metabolites.
It is now known that men with male balding have an
increased capacity to convert testosterone to dihy-
drotestosterone [9] via increased activity of the
enzyme responsible for this conversion,5a reductase
[10]. There are two 5a reductase enzymes (Type I
and Type II); both are present in the scalp [11] but
the role they play is still unknown. Furthermore, it is
not yet clear whether the genetic and hormonal basis
is the same in men and women.
Treatment options
Historically, the treatment of hair loss has involved a
great deal of quackery and charlatanism. The ¢rst
real scienti¢c e¡ort at hair regeneration occurred
with the drug minoxidil. Initially developed to treat
hypertension, its hair growth properties were soon
recognized and a 2% topical solution developed and
approved in the USA in1988 as the ¢rst product clini-
cally proven to stimulate hair growth (Rogaine1
USA, Regaine1 UK). At the present time it is still
unclear precisely how minoxidil produces hyper-
trichosis (stimulates hair growth), which is not
necessarily the same as preventing or reversing the
expression of genetic hair loss. Rushton et al. demon-
strated the lack of e¤cacy of minoxidil in a¡ecting
the genetic expression in 1989 [12], a ¢nding con-
¢rmed recently by Price & Menefee [13]. Furthermore,
over the past 10 years of use, patients have often
been dissatis¢ed with statistically signi¢cant, but
ß 2002 International Journal of Cosmetic Science, 24, 17^23
Hair loss and rejuvenation D. Hugh Rushton et al.

Table I Within-group comparison (mean  SE) for hair densities and percent of hair in the anagen growth phase from men
using topical 2% minoxidil (n ˆ 15)

Time (months) 0 12 P-value


Total Hair Density (THD) 195  16 199  13 NS
(Range) (78±303) (97±283)

Useful Hair Density (UHD) 73  14 69  12 NS
(Range) (0±177) (0±160)
Anagen % 56.8  4.88 59.2  4.97 yNS
(Range) (13.5±84.3) (12.1±84.7)

THD ˆ All hair per cm2.

UHD ˆ Hair longer than 3 cm per cm2.

Student's t-test (paired samples).
yWilcoxon Signed Rank-test (paired samples).

Table II Within-group comparison (mean SE) for hair densities and percent of hair in the anagen growth phase from men
taking ¢nasteride (1.25 mg d 1) (n ˆ 15)

Time (months) 0 12 P-value


Total Hair Density (THD) 229  12 242  10 ˆ0.06
(Range) (156±293) (182±310)

Useful Hair Density (UHD) 134  12 145  15 NS
(Range) (46±226) (45±224)
Anagen % 68.5  2.60 78.6  3.10 y<0.01
(Range) (48.1±88.4) (58.0±98.6)

THD ˆ All hair per cm2.

UHD ˆ Hair longer than 3 cm per cm2.

Student's t-test (paired samples).
yWilcoxon Signed Rank-test (paired samples).

Table III Within-group comparison (mean  SE) for hair densities and percent of hair in the anagen growth phase from 25
men taking ¢nasteride (1.25 mg d 1), a Type II 5a reductase inhibitor (5-AR) and using a topical Type I 5-AR inhibitor

Dual 5-AR Inhibitor

Time (months) 0 12 P-value


Total Hair Density (THD) 214  18 251  17 <0.0001
(Range) (83±467) (117±468)

Useful Hair Density (UHD) 111  14 155  17 <0.001
(Range) (27±264) (24±381)
Anagen % 66.8  2.6 72.0  2.6 y<0.01
(Range) (40.3±91.8) (53.1±95.7)

THD ˆ All hair per cm2.

UHD ˆ Hair longer than 3 cm per cm2.

Student's t-test (paired samples).
yWilcoxon Signed Rank-test (paired samples).

ß 2002 International Journal of Cosmetic Science, 24, 17^23 19

Hair loss and rejuvenation
cosmetically insigni¢cant, increases in hair counts,
leading to poor compliance with the twice-daily
topical application. A 5% variant is now available in
some countries but, as with 2% minoxidil, the loss of
hair continues unabated [13].
Recently, ¢nasteride, a type II 5a reductase inhibi-
tor (5-AR), has been licensed in the USA and around
the world, including the UK, under the name of Pro-
pecia1. Results from clinical trials claim signi¢cant
increases in hair count in men with male pattern hair
loss treated with ¢nasteride for12 months compared
to placebo [14].
Employing the unit area trichogram, a quantita-
tive and validated method of hair evaluation [12],
data from subjects treated with topical minoxidil
(Table I), ¢nasteride (Table II) and ¢nasteride to-
gether with a topical type I 5-AR inhibitor are pre-
sented in Table III.
Results
Minoxidil was ine¡ective in preventing further
expression of the underlying genetic hair loss.
Although anyone using minoxidil will have more,
¢ner hair than they would have had, had they not
used it, progression of their genetic hair loss will con-
tinue. In ¢nasteride-only treated subjects around
40% of individuals reported a noticeable increase in
hair growth as de¢ned as an increase obvious to
themselves, their partner or their hairdresser. Objec-
tive changes, i.e., hair longer than 3 cm per cm2,
(Useful Hair Density, UHD) occurred in ¢nasteride
(but not minoxidil) treated subjects and amounted
to a mean increase of11 UHD hairs. In comparison to
these preparations, over 80% of men treated with
the dual type I and II 5-AR inhibitor reported a
noticeable increase with a signi¢cant mean increase
of 44 UHD hairs per cm2. In both the ¢nasteride and
¢nasteride; ‡ a topical type I 5-AR inhibitor (but in
the minoxidil) treated subjects, a signi¢cant increase
(P < 0.01) in the number of hairs in the anagen
growth phase occurred.
Classifying hair loss in women
Whereas androgenetic alopecia is the most common
type of hair loss in men, in women it appears to a¡ect
less than 10% of premenopausal women (D. H.
Rushton, unpublished data). When it does occur, a
di¡use loss of hair a¡ecting the frontal-vertex area
with the sparing of a narrow (1 cm) band of denser
hair in the frontal hairline is observed. Ludwig [7]
20
D. Hugh Rushton et al.
was the ¢rst to described the pattern of hair loss in
women. Reduced hair density also occurs in
hypothyroidism [15] and a¡ects around 2% of preme-
nopausal women; however, it is signi¢cantly more
prevalent after the menopause.
Another problem that a¡ects women is a delay in
the initiation of the new hair cycle, a so-called lag
phase e¡ect, where the hair does not re-enter the
growth phase (anagen) when it should. Often the
delay may last for several months during which time
the resting telogen hair is lost from the scalp leaving
an empty hair follicle [16]. However, the most com-
mon cause of hair loss in women is CTE, which a¡ects
30% of females in the UK (D. H. Rushton & M. J. Norris,
unpublished data).
Pathology
In women, androgenetic alopecia occurs in a charac-
teristic pattern where there is a progressive loss of
hair from just behind the front hair line. There is a
reduction in hair density (hair per cm2) but the hair
that remains is relatively normal in appearance [17].
In the vast majority of a¡ected women there is no
increase in circulating androgens, which has raised
questions about whether or not this type of di¡use
loss is really androgen-mediated. There is some sup-
port for this because not all those treated with anti-
androgens respond, suggesting that the genetic and
hormonal basis may not be the same in men and
women. Compounding matters, increased hair shed-
ding is a complicating feature, with 70% having a
suboptimal nutritional status (see below) [18].
The most frequent hair problem in premenopausal
women is increased hair shedding. This is where
there is a relative change in the proportion of growing
(anagen) to resting (telogen) hair. In most cases, the
excessive shedding has been present for at least
6 months [19].Where the problem persists there is a
reduction in hair volume, or less hair to clip up or tie
back in the ponytail. This condition is known as
chronic telogen e¥uvium (CTE) and studies have
shown that in 95% of such cases CTE arises from a
nutritional imbalance involving the essential amino
acid L -lysine and iron (D. H. Rushton et al., unpub-
lished data) ¢ndings con¢rmed in two recent
studies [20, 21].
Treatment options
Treatment for genetic hair loss in women has been
available since the late 1970s. The most e¡ective
ß 2002 International Journal of Cosmetic Science, 24, 17^23
Hair loss and rejuvenation
Table IV Biochemical results obtained in 200 apparently healthy women complaining of increased hair shedding and
reduced hair volume (chronic telogen e¥uvium)
Hb TIBC
(g dL 1) (lmol L 1)
Ref Range >12.0 45±70
Mean  SD 13.1  0.97 61.3  9.3
Median 13.2 61.2
% Below range 11 1.5
% Above range 0 17.5
yReference range from [18], S ˆ serum, TIBC ˆ total iron binding capacity.
approach uses an oral oestrogen in combination with
the anti-androgenic progestin, cyproterone acetate
(CPA) [22, 23]. This regimen has been shown to re-
generate around 30% more hair and prevent further
loss, where an androgenic component can be estab-
lished. In the USA spironolactone has been the princi-
ple active ingredient used to treat this problem but,
although it has fewer side-e¡ects, it is less e¡ective
[24]. Currently, the most e¡ective treatment for regen-
erating hair regrowth in women with genetic hair
loss is the use of oral anti-androgen therapy in combi-
nation with topical solutions containing 2^3% min-
oxidil; however, the nutrition status needs also to be
optimal to achieve the best results [23, 25]. Unfortu-
nately, anti-androgen therapy is associated with
changes similar to those seen with oral contra-
ceptives and not all women want to take oral medica-
tion. As around 80% of women exhibiting genetic
hair loss appear to have long periods of stability
where further hair loss is very limited, many elect to
do nothing. In such cases the use of topical 2% min-
oxidil (Regaine1/Rogaine1), together with ensuring
that the nutrition is optimized, results in a signi¢cant
increase in hair density [25].
The use of ¢nasteride (Propecia1) in the treatment
of female genetic hair loss has yet to be independently
evaluated.The only study published to date was spon-
sored by Merck Sharp & Dohme (the company that
makes ¢nasteride) in postmenopausal women. This
group of women may not be representative of the
balding process in premenopausal females [26]. Con-
sequently, until studies have been undertaken in
women under 50 years of age we do not know
whether ¢nasteride is as e¡ective in female genetic
hair loss as it is in men.We eagerly await the results
of ongoing studies in such women currently being
undertaken in the UK.
ß 2002 International Journal of Cosmetic Science, 24, 17^23
D. Hugh Rushton et al.
S-Ferritiny Vit B12 S-Folate S-Zinc
(ng mL 1) (pg mL 1) (nmol L 1) (lmol L 1)
40±400 200±1100 5±35 10.6±22.6
36.8  24.4 538  275 25.1  12.1 13.8  2.3
32 480 22 13.1
65 2 0.5 7
0 2.5 28.5 0
Chronic telogen e¥uvium (CTE)
The role of nutrition in hair growth is well estab-
lished in severe malnutrition, anaemia and anorexia
nervosa. However, in the absence of an underlying
pathology, nutritional e¡ects are poorly understood.
Investigating CTE in healthy women requires a di¡er-
ent approach. Data for various nutritional variables
obtained from 200 apparently healthy women com-
plaining of increased hair shedding are presented in
Table IV.
Depleted iron stores (as assessed by serum ferritin)
was the major and signi¢cant problem observed in
these women. Sixty-¢ve per cent failed to reach the
lower reference level for males (40 ng mL 1). More
signi¢cant was the fact that 95% had a serum ferritin
level below (70 ng mL 1), the 99% con¢dence limit
for iron staining in the bone marrow, the accepted
de¢nition of being iron replete [27].Total iron binding
capacity (TIBC) values not only re£ect the iron trans-
port status but are also indicative of protein insu¤-
ciency. In view of the low ferritin concentrations, it
was surprising to see 34.3% with TIBC levels in the
lower half of the reference range, indicating an ade-
quate iron status. Normally TIBC increases in
response to iron de¢ciency and these women would
have been expected to have TIBC levels in the upper
part of the normal range. However, TIBC levels are
reduced in protein malnutrition states, supporting
the view that a signi¢cant proportion of the women
with CTE had a suboptimal intake of ¢rst class pro-
tein and, in particular, the essential amino acid L -
lysine. The body can only get adequate bioavailable
amounts of L -lysine if meat and eggs are included in
the diet; those who eat little or no meat are at risk of
being de¢cient. Also of note was the ¢nding of a large
number of women (28.5%) with a raised serum folic
21
Hair loss and rejuvenation
Table V Within-group comparison (mean  SE) for the percent of hair in the telogen phase and serum ferritin concentration
obtained from 22 women taking an oral nutritional supplement (Florisene1) providing 72 mg of iron and1.5 g of the essential
amino acid L -lysine for 6 months
Time (months) 0 6
Hair in the telogen phase (%) 19.5  1.1
(Range) (8.5±28.9)
Serum ferritin values (ng mL 1) 33  4
(Range) (5±84)

Student's t-test (paired samples).
yWilcoxon Signed Rank-test (paired samples).
acid level, suggesting excessive vitamin supplemen-
tation. On questioning, many were found to be taking
supplements in an attempt to stop their excessive hair
shedding!
Results
Correcting the iron and lysine imbalance with the
food supplement Florisene1 produced a signi¢cant
(39%, P < 0.001) reduction in the amount of hair
being shed. This corresponded with a signi¢cant
(P < 0.0001) increase in the mean serum ferritin
level from 33 ng mL 1 at baseline to 89 ng mL 1 after
6 months. However, it often took up to 24 months
for the full bene¢ts to materialize (Table V).
Conclusions
The demand for treatment of all forms of hair loss will
increase as the bene¢ts of medicine and science con-
tinue to provide e¡ective and targeted solutions to
hair problems.
Advances in treating genetic hair loss in men will
e¡ectively eliminate balding from those who want to
take treatment and for the ¢rst time a man will be able
to chose whether he will go bald.
Nutritionally induced hair loss has been identi¢ed
in women, and either a change in dietary habits or
taking the appropriate supplement will correct this
widespread problem.
There are, however, still problems for which we
have yet to unravel the underlying mechanism, but
the recognition that hair loss a¡ects the quality of life
for many of those a¡ected is now an important
acknowledged fact. Although none is life threaten-
ing, they do cause a great deal of distress. This will
drive the quest to address hair problems that are as
yet untreatable.
22
D. Hugh Rushton et al.
P-value
11.3  1.0 yP < 0.0001
(4.4±21.9)
89  11 
P < 0.0001
(27±211)
Acknowledgements
We would like to thank Drs Ian Ramsay, Jeremy Gilkes,
Andrew Messenger, Paul Cotterill and Walter Unger
for the medical supervision of the patients treated in
the ¢nasteride and minoxidil investigations.
References
1. Kingsley, D.H.The development and validation of a qual-
ity of life measure for the impact of androgen-depen-
dent alopecia. PhD Thesis, University of Portsmouth,
Portsmouth (1999).
2. Cash,T.F.Thepsychologyof physicalappearance.aesthe-
tics, attributes, and images. In: Body Images: Develop-
ment, Deviance and Change (T. F. Cash and T. Pruzinsky,
eds), pp.51^79. NewYork: Guilford Press (1990).
3. Cash,T.F. The psychological e¡ects of androgenetic alo-
pecia in men. J. Am. Acad. Dermatol. 26,926^931 (1992).
4. Giacometti, L. Facts legends and myths about the scalp
throughout history. Arch. Dermatol. 95,629^631 (1967).
5. Hamilton, J.B. Patterned loss of hair in man: types and
incidence. Ann. NYAcad. Sci. 53,708^728 (1951).
6. Norwood, O.T. Male pattern baldness: classi¢cation and
incidence. Southern Med. J. 68,1359^1370 (1975).
7. Ludwig, E. Classi¢cation of the types of androgenic alo-
pecia (common baldness) occurring in the female sex.
Br. J. Dermatol. 97, 247^254 (1977).
8. Rushton, D.H., Ramsay, I.D., Norris, M.J. and Gilkes,
J.J.H. Natural progression of male pattern baldness in
young men. Clin. Exp. Dermatol.16,188^192 (1991).
9. Bingham, K.D. and Shaw, D.A. The metabolism of
testosterone by human male scalp skin. J. Endocrinol.
57,111^121 (1973).
10. Schweikert, H.U. and Wilson, J.D. Regulation of human
hair growth by steroid hormones. I. Testosterone meta-
bolism in isolated hairs. J. Clin. Endocrinol. Metab. 38,
811^819 (1974).
11. Harris, G., Azzolina, B., Baginsky,W., et al. Identi¢cation
and selective inhibition of an isozyme of the steroid
ß 2002 International Journal of Cosmetic Science, 24, 17^23
Hair loss and rejuvenation
5a-reductase in human scalp. Proc. Natl. Acad. Sci. USA.
89,10787^10791 (1992).
12. Rushton, D.H., Unger,W.P., Cotterill, P.C., et al. Quantita-
tive assessment of 2% topical minoxidil in the treatment
of male pattern baldness. Clin. Exp. Dermatol. 14, 40^
46 (1989).
13. Price, V.H. and Menefee, E. Quantitative estimation of
hair growth: comparative changes in weight and hair
count with 5% and 2% minoxidil, placebo and no treat-
ment. In: Hair research for the next millennium (D. J.Van
Neste and V. A. Randall, eds), pp. 67^71. Amsterdam:
Elsevier (1996).
14. Kaufman, K. Clinical studies on the e¡ects of oral ¢nas-
teride, a type II 5a-reductase inhibitor, on scalp hair in
men with male pattern baldness. In: Hair research for
the next millennium (D.J. Van Neste and V.A. Randall,
eds), pp.363^365. Amsterdam: Elsevier (1996).
15. James, K.C., Norris, M.J., Rushton, D.H., et al. The in£u-
ence of thyroid dysfunction on hair growth. J. Pharm.
Pharmacol. 39,64 (1987).
16. Courtois, M., Loussouarn, G., Hourseau, C. et al. Ageing
and hair cycles. Br. J. Dermatol.132,86^93 (1995).
17. Rushton, D.H., James, K.C. and Mortimer, C.H. The unit
area trichogram in the assessment of androgen-depen-
dent alopecia. Br. J. Dermatol.109, 429^437 (1983).
18. Rushton, D.H., Ramsay, I.D., James, K.C. et al. Biochem-
ical and trichological characterisation of di¡use alope-
cia in women. Br. J. Dermatol.123,187^197 (1990).
19. Rushton, D.H. Investigating and managing hair loss in
apparently healthy women. Can. J. Dermatol. 5, 455^
461 (1993).
20. Roberts, J.L. Examining the etiology of telogen e¥u-
vium in pre-and postmenopausal women: a chart
ß 2002 International Journal of Cosmetic Science, 24, 17^23
D. Hugh Rushton et al.
review study. Proceedings,Tri-Continental Hair Research
Meeting,Tokyo, Japan, Poster157 (2001).
21. Haycox, C.The incidence of depleted iron stores in North
American females presenting with hair loss. Proceed-
ings,Tri-Continental Hair Research Meeting,Tokyo, Japan,
Poster159 (2001).
22. Mortimer, C.H., Rushton, D.H. and James, K.C. E¡ective
medical treatment for common baldness in women.
Clin. Exp. Dermatol. 8,342^350 (1984).
23. Rushton, D.H. and Ramsay, I.D. The importance of ade-
quate serum ferritin levels during oral cyproterone
acetate and ethinyl oestradiol treatment of di¡use
androgen-dependent alopecia in women. Clin. Endocri-
nol. 36, 421^427 (1992).
24. Rushton, D.H., Futterweit, W., Kingsley, D.H., Kingsley,
P. and Norris, M.J. Quantitative assessment of spirono-
lactone treatment in women with di¡use androgen-
dependent alopecia. J. Soc. Cosmet. Chem. 42, 317^325
(1991).
25. Rushton, D.H. and Fenton, D.A. Quantitative evaluation
of topical 5% minoxidil in the treatment of di¡use
androgen-dependent alopecia in females. Br. J. Derma-
tol.127, 423 (1992).
26. Whiting, D.A., Waldstreicher, J., Sanchez, M. and Kauf-
man, K.D. Measuring reversal of hair miniaturization
in androgenetic alopecia by follicular counts in hori-
zontal sections of serial scalp biopsies: results of ¢nas-
teride 1 mg treatment of men and postmenopausal
women. J. Invest. Dermatol. Symp Proc. 4, 282^284
(1999).
27. Puolakka, J. Serum ferritin the evaluation of iron status
in young women. Acta. Obstet. Gynecol. Scand. Suppl.
95,35^41 (1980).
23