ArticlePDF Available

Micronutrients in hair loss



Alopecia is a common dermatological complaint. Affected patients are often distressed and attempt to arrest the hair loss by taking various over the counter nutritional supplements containing vitamins and minerals. The evidence supporting their efficacy however is limited. Moreover, there are toxicity reports. We reviewed the literature about the normal levels and the daily dietary needs of the most common micronutrients, their role in the hair follicle cycle as well as their use in the hair loss treatment. 4 independent researchers reviewed a total of 119 papers, and 92 articles published in the English language within the last 30 years were included. Telogen effluvium and alopecia areata have been associated with lower iron, zinc and vitamin D levels. Androgenetic alopecia has been associated with lower iron and vitamin D levels. Both lower and increased vitamin A levels can result in telogen effluvium, but lower levels are associated also with hair breakage. Vitamin C insufficiency results in hair shaft abnormality (cork screw hairs). No data exist about hair loss associated with abnormal biotin levels. The role of micronutrients for the hair follicle function is not completely understood. Empiric treatments of hair loss with micronutrients without confirmed deficiencies have not shown utility.
Our Dermatology Online
© Our Dermatol Online 3.2018 320
How to cite this article: Ruiz-Tagle SA, Figueira MM, Vial V, Espinoza-Benavides L, Miteva M. Micronutrients in hair loss. Our Dermatol Online. 2018;9(3):320-328.
Submission: 12.12.2017; Acceptance: 03.02.2018
DOI: 10.7241/ourd.20183.25
Hair follicle cells have a high turnover and active
metabolism, requiring a good supply of nutrients and
energy. A caloric deprivation or deficiency of several
macro and micronutrients, such as proteins, minerals,
essential fatty acids, and vitamins, can lead to hair
loss [1]. Patients with hair loss, particularly with hair
shedding are often distressed by their condition and
attempt to arrest the shedding taking multivitamins,
minerals and herbal products. While considered
helpful by patients the consumption of these products
may not be supported by evidence [2,3]. Moreover,
reports exist of worsening of hair loss as well as liver
toxicity [4].
In order to assess the current evidence about the
role of micronutrients for hair loss and hair growth,
we reviewed the major database sources PubMed
and Medline by using the key words hair, hair loss,
alopecia, telogen effluvium and the names of most
common vitamins and minerals listed as ingredients
in the commercial “hair” and “hair and nails”
supplements. We reviewed the literature about the
normal levels and the daily dietary needs for optimal
hair growth of the most common micronutrients,
their role in the hair follicle cycle as well as their
use in the hair loss treatment. A total of 119 papers
were reviewed by 4 independent researchers, and 92
articles published in English language within the
last 30 years were selected for inclusion. All articles
were peer-reviewed with available full-text texts in
English or Spanish, providing primary data. Also data
from the World Health Organization (WHO) and
Institute of Medicine (US) about Dietary Reference
Intakes and Recommended Dietary Allowance were
Alopecia is a common dermatological complaint. Affected patients are often distressed and attempt to arrest the hair loss
by taking various over the counter nutritional supplements containing vitamins and minerals. The evidence supporting
their efficacy however is limited. Moreover, there are toxicity reports. We reviewed the literature about the normal levels
and the daily dietary needs of the most common micronutrients, their role in the hair follicle cycle as well as their use in
the hair loss treatment. 4 independent researchers reviewed a total of 119 papers, and 92 articles published in the English
language within the last 30 years were included. Telogen effluvium and alopecia areata have been associated with lower iron,
zinc and vitamin D levels. Androgenetic alopecia has been associated with lower iron and vitamin D levels. Both lower and
increased vitamin A levels can result in telogen effluvium, but lower levels are associated also with hair breakage. Vitamin
C insufficiency results in hair shaft abnormality (cork screw hairs). No data exist about hair loss associated with abnormal
biotin levels. The role of micronutrients for the hair follicle function is not completely understood. Empiric treatments of
hair loss with micronutrients without confirmed deficiencies have not shown utility.
Key words: Alopecia; Supplements; Vitamins; Iron
Micronutrients in hair loss
Micronutrients in hair loss
Susana A. Ruiz-Tagle1, Marcella M. Figueira2, Verónica Vial3,
Leonardo Espinoza-Benavides3, Maria Miteva4
1Dermatology Department, Hospital Militar de Santiago, Chile, 2Instituto Professor Fernando Figueira, Recife, Brasil,
3Universidad de los Andes Medical School, Santiago, Chile, 4University of Miami, USA
Corresponding author: Dr. Leonardo Espinoza-Benavides, E-mail:
Review Article
© Our Dermatol Online 3.2018 321
Our results are summarized in Table 1.
1. Iron
Iron participates in the structure of many molecules in
the body, such enzymes, cytochromes and transcription
factors, and is involved in many critical physiologic
processes. It is a catalyst in oxidation-reduction reactions
and can control DNA synthesis in dividing cells.
Serum ferritin is the standard test for assessing iron
stores because it is one of the most sensitive and
specific markers of iron deficiency. It is directly related
to intracellular ferritin and total iron reserves [5,6].
Normal levels
The Recommended Dietary Allowance (RDA) for men
of any age and for postmenopausal women is 8 mg/day;
and for premenopausal women is 18 mg/day.
A cut-off of 41 ng/L of the ferritin’s serum level has
sensitivity and specificity of 98% in detecting iron
deficiency [7]. Serum ferritin values < 12 ng/l suggest
absent iron stores and it is considered diagnostic for
iron deficiency anemia [8]. The proposed optimal
ferritin level for hair regrowth is 70 ng/L [7,9,10].
It must be considered that ferritin is an acute phase
protein, and in neoplasia, infections and inflammatory
diseases it may be falsely elevated despite of the low
iron reserve. C Reactive Protein levels or erythrocyte
sedimentation levels can be used in such cases to rule
out false negative results [11].
Causes of de ciency
Iron deficiency is the most common nutritional
deficiency in the world. Data from the Third National
Health and Nutrition Examination Survey (NHANES
III; 1999-2000) indicated that iron deficiency anemia
was present in 1 to 2 percent of adults. Iron deficiency
without anemia was found in 9-16% of females aged
12-49 years and it was two times higher in non-Hispanic
American women. The prevalence of iron deficiency in
males aged 16-69 years was 2% [12].
In premenopausal women, the most common causes of
iron deficiency anemia are menstrual loss and pregnancy,
whereas gastrointestinal blood loss and malabsorption
are most common in men and postmenopausal women
[6]. Also, borderline iron deficient diets such as
vegetarian and vegan diets are another common cause.
Good food sources of iron include red meat, egg yolks,
green leafy vegetables, lentils, and beans; however,
non-animal foods provide less bioavailable-ingested
iron. Iron is absorbed mainly in the epithelium of distal
duodenum and proximal jejunum [13].
Many patients with iron deficiency and even anemia
are asymptomatic. When present, clinical symptoms
include hair loss, cheilitis and koilonychia [9].
Iron and hair
Currently, the role of iron on the hair follicle biology is
not completely understood and the exact mechanism
by which iron deficiency affects hair is also unclear.
It is believed that decreased iron bioavailability may
impair the proliferation of the follicular matrix cells.
Dividing cells require higher levels of ferritin. An
abnormal balance between cellular ferritin and free
iron has been suspected as a mechanism for abnormal
hair growth [14].
In 2008, Du et al. described iron-dependent genes in
the hair follicle bulge whose mutation causes high
levels of hepcidin, a liver protein that decreases iron
absorption [15]. In 1963, Hard first suggested the
role of iron as etiological factor in diffuse hair loss
in iron deficient non-anemic women [16]. Since
then various studies have evaluated the association;
most of them have addressed only women with non-
cicatricial alopecia. Data are contradictory and difficult
to compare due to discrepancy in the study designs,
the variables assessed and the population included
(Table 2). Kantor et al proposed the “Threshold
hypothesis”, stating that decreased iron stores can
lower the threshold to develop different type of alopecia
depending on the genetic predisposition and the family
history [14].
Treatment recommendation
The recommended oral daily dose for the treatment
of iron deficiency in adults is in the range of 150-
200 mg/day of elemental iron. It can be given by
mouth, under forms of ferrous sulfate, gluconate or
fumarate. Better bioavailability of elemental iron per
tablet is derived from the fumarates (33% of elemental
iron, versus 20% and 12% for sulfate and gluconate
respectively) [12], but there is no evidence that one
is more effective than the others. Sulfates are worst
tolerated as they can cause gastrointestinal upset and
constipation. The daily dose can be divided in order to
© Our Dermatol Online 3.2018 322
improve the tolerance and absorption.
Concomitant treatment with ascorbic acid, 500-
1000 mg per day and L-Lysine 1000 mg per day, may
also enhance the absorption [18]. It is recommended to
repeat ferritin tests at 3 months interval and continue
the oral iron therapy for 3-6 months after the iron
deficiency is corrected [6,7,11].
2. Zinc
Zinc is an essential trace mineral that participates in
Table. 1 Micronutrients in hair loss association and treatment
Nutritient Laboratory test Normal level Hair loss association Recommended
Iron Serum Ferritin >40 ng/l CTE
150-200 mg/day of elemental iron. Ferritin tests at 3
months interval and continue oral iron therapy for 3-6
months after the iron de ciency is corrected
Zinc Serum Zinc (Zn) >10,7 mmol/L TE
50 mg Zn Gluconate daily for 12 weeks or 5 mg/kg/
day Zn Sulphate for 3 months
Vitamin D Serum 25(OH) D2 >30 ng/mL
Insuf ciency: < 30 ng/mL
De ciency:
< 20 ng/mL
50,000 IU once a week for 1-3 months. Maintenance
dose of 800-2000 IU to avoid recurrences
Biotin Urinary excretion of
biotin/organic acids
and Carboxylase
activity in peripheral
blood lymphocytes
De ciency: Biotin urinary
excretion low 20ug/L or 25
ug/24 hours
No evidence of hair loss
No evidence for biotin supplementation for hair loss
Vitamin C Serum vitamin C >11mmol/L or 0,6-2.0 mg/dL Cork screw hairs 300-1000 mg daily of oral vitamin C for 1 month
Vitamin A Serum Retinol
De ciency
below 20 mcg/dL
De ciency: TE and hair
Overload: TE
In de ciency: 200.000 IU, single dose monthly for 1-6
TE: telogen ef uvium, CTE: chronic telogen ef uvium, ATE: acute telogen ef uvium, AA: alopecia areata, AGA: androgenetic alopecia, FPHL: female pattern hair
Table 2. Iron de ciency and hair loss.
Author Type of Alopecia Type of Study Results
Hard S.
followed by
100% regrowth in 18/96 (18.8%) non-anemic women with iron
de ciency (measured by serum iron) and DH treated with oral
iron therapy
Rushton DH, Ramsay ID, James
KC, Norris MJ, Gilkes JJ.
Androgen dependent
Case control study 72% of 50 premenopausal women with DA had serum ferritin
levels less than 40 mg/L.
Rushton DH, Norris MJ, Dover R,
Busuttil N.
CTE Cross-sectional study 65% of 200 healthy women with increased hair shedding had
ferritin levels less than 70 ug/L.
Rasheed H
(2013) [19]
TE, FPHL Prospective case control study Serum ferritin levels were signi cantly lower in TE and FPHL
compared to control patients.
Olsen EA
CTE, FHPL Case control study There was no statistically signi cant increase in the incidence
of iron de ciency in premenopausal or postmenopausal
women with FPHL or CTE versus control patients
Kantor J, Kessler LJ, Brooks DG,
Cotsarelis G.
TE, AGA, AA, AU, AT Case control study Serum ferritin levels were signi cantly lower in women with
AGA (37.3 ug/L) and AA (24.9 ug/L) compared to control
Boffa MJ, Wood P, Grif ths CE
AA Cross sectional study No increased incidence of iron de ciency in patients with AA
compared with general population.
Sinclair R
DTHL Prospective cohort study There is no clear association between low serum ferritin and
AGA: androgenetic alopecia; AA: alopecia areata; AT: alopecia totalis; AU: alopecia universalis; CTE: chronic telogen ef uvium; DA: diffuse alopecia; DH: diffuse
hair loss; DTHL: diffuse telogen hair loss; FPA, female pattern alopecia, DTE: diffuse telogen ef uvium
© Our Dermatol Online 3.2018 323
the structure and function of proteins, such as enzymes,
transcription factors, hormonal receptor sites, and
biologic membranes throughout the body. It is also
involved in signal transduction, gene expression, and
plays a regulatory role in apoptosis [23]. Zinc is crucial
for the proper function of lymphocytes, neutrophils and
Natural Killer cells in the immune response, as well as
for the skin barrier [24].
Serum or plasma zinc level is the standard test for
assessing zinc status [25].
Normal levels
RDA for zinc is 11 mg and 8 mg per day for men and
women respectively [26]. The lower limit of normal
(morning) fasting plasma zinc has been set at 10.7
mmol/L (700 mg/L) [27].
Causes of de ciency
Severe zinc deficiency has been documented in patients
on parenteral feeding without adequate zinc intake and
in cases of acrodermatitis enteropathica, an inherited
disorder of zinc absorption caused by a mutation in a
zinc transporter [28].
Acquired zinc deficiency can also be caused
by insufficient uptake from food, intestinal
malabsorption syndromes or pregnancy. Long-term
alcohol consumption is associated with impaired
zinc absorption and increased urinary zinc excretion
[21]. Avoidance of red meat by young women can
be a cause of concomitant iron and zinc deficiency
[29]. The first source of zinc from diet is red meat;
other good sources are beans, nuts, crab and lobster.
Phytates present in cereals and legumes inhibit the
zinc absorption [30].
Cutaneous manifestations present as impaired wound
healing and an increased susceptibility to infections,
paronychia, periorificial dermatitis, diffuse alopecia
[31], and hair color and texture changes [25].
Zinc and hair
The exact role of zinc in the function of the hair follicle
is unclear. Zinc has been considered a hair growth
modulator and immunomodulator because the DNA
polymerase is zinc dependent and zinc acts in multiple
aspects of T-lymphocyte activation, signal transduction
and cellular apoptosis [24,32]. Zinc deficiency has
been related to alopecia areata [33-36], and telogen
effluvium [35,37].
Some studies have found lower zinc serum levels
in patients with alopecia areata comparing with
controls. It has also been shown in alopecia areata
that the disease duration, severity and resistance
to therapies are correlated inversely with low serum
zinc levels [38].
Treatment recommendations
There is scarce evidence on the proper zinc
supplementation and the therapeutic response in
alopecia areata. Zinc Gluconate dosed as 50 mg daily
for 12 weeksproduced regrowth in 15 patients with
alopecia areata who had low serum zinc level. Positive
therapeutic effects were observed in 9 out of 15 patients
(66.7%) although this was not statistically significant
[33]. The most recent and the only double blind, cross
over study used Zinc Sulphate in a dose of 5 mg/kg/
day for 3 months in patients with alopecia areata which
resulted in hair regrowth for 60% of the group receiving
treatment [34].
Zinc can be supplemented using several forms such
as zinc gluconate, zinc sulfate and zinc acetate with
different elemental zinc contribution [39]. There are
no data about the differences in the efficacy.
3. Vitamin D
Vitamin D is a fat-soluble vitamin belonging to the
family of steroid hormones that plays an important role
in the calcium homeostasis and musculoskeletal health.
Vitamin D consists of 2 bioequivalent forms,
Ergocalciferol (vitamin D2) and Cholecalciferol
(vitamin D3). The main source in the body is the
endogenous synthesis in the skin as a result of the action
of ultraviolet B radiation on 7-dehydrocholesterol,
which results in the formation of vitamin D3. The
skin is the only organ capable of synthesizing and
activating Vitamin D, in addition to expressing its
receptor [40].
Vitamin D can be obtained exogenously from few
foods like fatty fish, fish liver oil, egg yolk and some
mushrooms. Ingested and cutaneous produced vitamin
D needs 2 hydroxylation steps, first in the liver, turning
into Calcidiol or 25-hydroxyvitamin D, and then in the
kidneys to turn into its active metabolite, Calcitriol or
1,25- (OH) 2 D [41].
The most stable form of the vitamin D in the serum is
25 hydroxyvitamin D or 25(OH) D, which is routinely
© Our Dermatol Online 3.2018 324
measured to assess the vitamin D status. Besides being
the predominant circulating form, it also has a longer
half-life [42].
Normal levels
The optimal 25(OH)D serum level is 30 ng/ml
(75nmol/L) [43,44]. In 2003, the World Health
Organization (WHO) defined vitamin D insufficiency
as serum 25(OH) D below 20 ng/ml [45]. Other
authors define Vitamin D deficiency as serum 25 (OH)
D less than 20 ng/ml and insufficiency below 30 ng/
ml [46,47].
Causes of de ciency
Conditions associated with vitamin D deficiency are
malnutrition, intestinal malabsorption, especially
affecting the proximal small intestine, obesity and some
paraneoplasic syndromes [42]. Vitamin D deficiency in
healthy adults has been estimated to affect up to 30%
of the population [48-50].
Among the risk factors are dark skin, very low sunlight
exposure, atmospheric pollution, and multiple
within short interval pregnancies, vegetarian diet and
some medications such anticonvulsants, rifampicin,
antiretroviral agents and corticosteroids [51].
Vitamin D and hair
The action of 1,25- (OH) 2 D is mediated by its binding
to the Vitamin D receptor (VDR) which is a member
of the nuclear receptor superfamily. VDR distribution
on the body is not restricted to organs involved in
calcium and bone metabolism but also in the cells of
the immune system [42], and in appendageal structures
such as the hair follicles [52].
In the hair follicle, the VDR is expressed in the
mesodermal dermal papilla cells and the epidermal
keratinocytes depending on the stage of the hair cycle.
VDR expression in the hair follicle is increased during
late anagen and catagen, correlating with proliferation
and differentiation of the keratinocytes in preparation
for the new hair cycle [53]. Lack of VDR in the
keratinocytes as opposed to the dermal papilla would
cause its dissociation from hair bulb by the end of
catagen, leading to defective initiating of subsequent
anagen phase [41,54]. VDR therefore exerts a regulatory
role on the hair cycle, independent of the vitamin D
binding [55].
Patients with mutations in the VDR, such as hereditary
vitamin D-resistant rickets (Vitamin D-dependent
rickets type IIA) have normal hair at birth due to the
normal hair cycle in the fetus; however, they develop
alopecia totalis between 1 to 3 months of age, after the
first hair is shed [56,57].
It has been shown among 80 women with chronic
telogen effluvium and female pattern of hair loss that
the serum vitamin D level was significantly lower
compared to controls [18].
A significant lower serum 25 (OH) D level (below
20 ng/ml) were observed in patients with alopecia areata
compared with a healthy control group [49, 58-60].
Disease severity in alopecia areata is inversely correlated
with the serum levels of vitamin D [49].
Treatment recommendations
People with normal serum level of 25(OH) D are
advised to take a supplement containing 800 IU of
vitamin D per day to maintain a normal level [40,47].
D2 (ergocalciferol) and D3 (cholecalciferol) are
available as dietary supplements. Both seem to be
effective in preventing or treating vitamin D deficiency.
The longer half-life of D3 suggests that less frequent
dosing may be needed. Supplements of vitamins D2
and D3 should be taken with a meal containing fat to
ensure maximum absorption [61].
There are no accepted guidelines for treating vitamin
D deficiency and insufficiency. A recent review
recommends the use of vitamin D3 over vitamin
D2 [62]. One time dose of vitamin D3 of at least
300,000 IU is most effective in improving vitamin D
status for up of 3 months. However, the most widely
used mode of supplementation is an average weekly
dose of 50,000 IU (cholecalciferol) for 1-3 months,
depending on the severity of Vitamin D deficiency.
A maintenance daily dose of 800 to 2000 IU or more will
be needekd to avoid recurrent deficiency [40,52,61].
Vitamin D topical analogues have been tested in mice
with congenital alopecia with positive response [63]. In
human studies, topical calcitriol has shown to prevent
alopecia induced by chemotherapy agents (paclitaxel
and cyclophosphamide) [56].
4. Biotin
Biotin is an essential nutrient; a water-soluble vitamin
classified as a B-complex vitamin. Biotin serves as a
coenzyme for carboxylation reactions on fatty acids,
© Our Dermatol Online 3.2018 325
aminoacids and glucose metabolism and has an
essential role in gene regulation [64,65].
The main source of biotin is the diet; it is widely
distributed in foods like egg yolk, cereals and vegetables.
Evidence suggests that dietary biotin is 100%
bioavailable. It is also synthetized by normal intestinal
microflora, but it is unknown how much this source
contributes to the biotin status [66].
To achieve its active form and to be absorbed in
the intestine, biotin is subjected to a proteolysis.
Biotinidase is a critical enzyme in this process. There
are hereditary disorders of biotinidase deficiency that
can be detected with a newborn screening [66].
Normal levels
There is no conclusive data on validated markers for
assessing the biotin status. Measuring urinary excretion
of biotin and organic acids such 3- Hydroxyisovaleric and
quantifying biotinylated carboxylases in lymphocytes
have been utilized. The latter has shown to be the most
reliable marker [67]. A low plasma biotin concentration
is not a sensitive indicator of inadequate biotin intake.
Deficiency of Biotin has been defined as urinary
excretion less than 20ug/L or 25 ug/24 hours [68]. The
adequate intake (AI) for biotin is 30 μg/d in men and
women [69].
Causes of de ciency
Real biotin deficiency can be observed only in rare
and specific conditions: a diet that contains raw
egg whites, patients receiving parenteral nutrition
without biotin supplementation, and treatments with
anticonvulsants such primidone, and carbamazepine
[70,71]. Cutaneous findings include severe dermatitis,
dry skin, seborrheic dermatitis, fungal infections,
macular rash, fine and brittle hair and hair loss [54].
Biotin and hair
There is no evidence regarding direct effect of biotin
on the hair follicle development and cycle. There is
no data that biotin is related to hair disorders either.
Treatment recommendations
There are no published data supporting the evidence
that biotin supplements can be an effective treatment
of hair loss.
5. Vitamin C
Vitamin C is a water-soluble vitamin and an essential
micronutrient. It is a potent antioxidant and is required
for the biosynthesis of collagen, specifically procollagen
triple helix and also is needed in the synthesis of
catecholamines [72]. It also plays an important role
in immune function and modulates iron absorption,
transport, and storage [73].
Normal levels
Recommended daily intake in adults is 90 mg in men
and 75 mg in women [69].
Measuring the plasma vitamin C levels assesses the
vitamin C status. Normal plasma level is in the range
of 0,4- 0,9 mg/dL. Vitamin C deficiency is defined as
plasma level less than 0,2 mg/dL [74].
Causes of de ciency
According to NAHNES 2003-2004, 7.1% of the total
population suffers from vitamin C deficiency, with the
smokers being at the most risk. The principal cause of
deficiency is the minimal consumption of fruits and
vegetables [75]. The clinical presentation of Vitamin
C deficiency is scurvy, with skin manifestations due
to decreased and altered collagen production [76,77].
Vitamin C and hair
Vitamin C promotes hair shaft elongation in cultured
human hair follicles and triggers hair growth in mice
by progression from telogen to anagen. This has been
achieved by increasing the Insulin Growth Factor 1
(IGF1) production in the dermal papilla cells [78].
Treatment recommendations
The recommended treatment for Vitamin C deficiency
is 300-1000 mg daily of oral vitamin C for 1 month
6. Vitamin A
Vitamin A is a fat-soluble vitamin. There are two main
forms of vitamin A: 1) retinoids or preformed vitamin A
and 2) carotenoids or provitamin A. Retinoids are the
active form. The common food sources for retinoids
are animal derived food (eggs, chicken, fish, and meat).
Leafy greens, orange and yellow vegetables and nuts
are good sources of carotenoids. Vitamin A has a role
in growth, vision, epithelial differentiation, immune
function and reproduction. The most common
symptom of vitamin A deficiency is xerophthalmia
with night blindness [81].
© Our Dermatol Online 3.2018 326
Normal levels
The retinol RDA for adults is 3,000 IU for men and
2,300 IU for women [18]. Serum retinol concentration
is the most common method used to evaluate vitamin
A status. Other methods such as dose response tests and
isotope dilution assays attempt to evaluate liver reserves
of vitamin A but are not feasible on daily basis.81
Vitamin A deficiency is defined as retinol serum level
below 20μ/dL [83].
Causes of de ciency
Vitamin A deficiency is rare in developed nations but
remains a concern in developing countries, particularly
in areas with poor nutrition. Several factors such as
malnutrition and fat malabsorption can lead to vitamin
A deficiency. Hypervitaminosis A is seen with long-term
supplementation and oral retinoid treatments [84].
Vitamin A and hair
There is genetic evidence that the alfa retinoid
nuclear receptor forms a dimer with Vitamin D
receptor and plays a major role in controlling hair
cycling [85]. Retinoids play a crucial role for the
anagen initiation, and depletion of vitamin A
results in epidermal interfollicular hyperplasia with
keratinocyte hyperproliferation and aberrant terminal
differentiation, accompanied by an inflammatory
reaction of the skin [86].
Vitamin A deficiency causes ichthyosis-like skin
changes and is often associated with telogen effluvium
and fragility of the hair [87,88].
Iatrogenic retinoid-induced hair loss is frequently
observed in clinical practice. It has been shown that
retinoids can inhibit hair shaft formation during
anagen and induce premature catagen [89]. Telogen
effluvium can occur with isotretinoin therapy (mostly
in doses over 0.5 mg/kg/24 h)[90]. This generally occurs
after 3 to 8 weeks of treatment and stops 6 to 8 weeks
after stopping it. However, telogen effluvium is more
common with acitretin treatment in doses of 25 mg
or more daily [91]. Isotretinoin - associated telogen
effluvium may also be attributed to an effect on the
biotinidase activity [90,92].
Treatment recommendations
In vitamin A deficiency, a single dose of 200,000 IU
is given by mouth every 4-6 months [82]. Telogen
effluvium in the course of systemic isotretinoin
treatment has a benign reversible nature and usually
requires no treatment.
Our results show that the role of micronutrients for
the hair follicle function and the mechanisms by which
deficiency could lead to hair loss are not completely
understood. Empiric treatments of hair loss conditions
without confirmed deficiencies have not shown utility.
1. Finner AM. Nutrition and hair: de ciencies and supplements.
Dermatol Clin. 2013;31:167–7.
2. Reuter J, Merfort I, Schempp CM. Botanicals in dermatology: an
evidence-based review. Am J Clin Dermatol. 2010;11:247–67.
3. Bandaranayake I, Mirmirani P. Hair loss remedies--separating fact
from ction. Cutis. 2004;73:107–14.
4. Fernández J, Navascués C, Albines G, Franco L, Pipa M, Rodríguez
M. Three cases of liver toxicity with a dietary supplement intended
to stop hair loss. Rev Esp Enfermedades Dig Organo Soc Esp Patol
Dig. 2014;106:552–5.
5. Beutler E, Felitti V, Ho NJ, Gelbart T. Relationship of body iron
stores to levels of serum ferritin, serum iron, unsaturated iron
binding capacity and transferrin saturation in patients with iron
storage disease. Acta Haematol. 2002;107:145–9.
6. Goddard AF, James MW, McIntyre AS, Scott BB, British Society
of Gastroenterology. Guidelines for the management of iron
de ciency anaemia. Gut. 2011;60:1309–16.
7. St Pierre SA, Vercellotti GM, Donovan JC, Hordinsky MK. Iron
de ciency and diffuse nonscarring scalp alopecia in women: more
pieces to the puzzle. J Am Acad Dermatol. 2010;63:1070–6.
8. Thomas DW, Hinchliffe RF, Briggs C, Macdougall IC, Littlewood T,
Cavill I, et al. Guideline for the laboratory diagnosis of functional
iron de ciency. Br J Haematol. 2013;161:639–48.
9. Trost LB, Bergfeld WF, Calogeras E. The diagnosis and treatment
of iron de ciency and its potential relationship to hair loss. J Am
Acad Dermatol. 2006;54:824–44.
10. Rushton DH, Dover R, Norris MJ, Gilkes JJH. Iron and hair loss
in women; what is de ciency? This is the real question! J Am Acad
Dermatol. 2007;56:518–9; author reply 519.
11. Elston DM. Commentary: Iron de ciency and hair loss: problems
with measurement of iron. J Am Acad Dermatol. 2010;63:1077–82.
12. Centers for Disease Control and Prevention. Iron de ciency-US,
1999-2000 Morb Mortal Wkly Rep. 2002;51:897–9.
13. Gulec S, Anderson GJ, Collins JF. Mechanistic and regulatory
aspects of intestinal iron absorption. Am J Physiol Gastrointest
Liver Physiol. 2014;307:G397–409.
14. Kantor J, Kessler LJ, Brooks DG, Cotsarelis G. Decreased serum
ferritin is associated with alopecia in women. J Invest Dermatol.
15. Du X, She E, Gelbart T, Truksa J, Lee P, Xia Y, et al. The serine
protease TMPRSS6 is required to sense iron de ciency. Science.
16. Hård S. Non-anemic iron de ciency as an etiological factor in
diffuse loss of hair of the scalp in women. Acta Derm Venereo.
17. Rushton DH, Ramsay ID, James KC, Norris MJ, Gilkes JJ.
Biochemical and trichological characterization of diffuse alopecia
in women. Br J Dermatol. 1990;123:187–97.
18. Rasheed H, Mahgoub D, Hegazy R, El-Komy M, Abdel Hay R,
Hamid MA, et al. Serum ferritin and vitamin d in female hair loss:
do they play a role? Skin Pharmacol Physiol. 2013;26:101–7.
19. Rushton DH, Norris MJ, Dover R, Busuttil N. Causes of hair
loss and the developments in hair rejuvenation. Int J Cosmet Sci.
© Our Dermatol Online 3.2018 327
20. Olsen EA, Reed KB, Cacchio PB, Caudill L. Iron de ciency in
female pattern hair loss, chronic telogen ef uvium, and control
groups. J Am Acad Dermatol. 2010;63:991–9.
21. Boffa MJ, Wood P, Grif ths CE. Iron status of patients with
alopecia areata. Br J Dermatol. 1995;132:662–4.
22. Sinclair R. There is no clear association between low serum ferritin
and chronic diffuse telogen hair loss. Br J Dermatol. 2002;147:982–
23. Hambidge KM, Krebs NF. Zinc de ciency: a special challenge.
J Nutr. 2007;137:1101–5.
24. Shankar AH, Prasad AS. Zinc and immune function: the
biological basis of altered resistance to infection. Am J Clin Nutr.
1998;68(2 Suppl):447S-63S.
25. Maverakis E, Fung MA, Lynch PJ, Draznin M, Michael DJ, Ruben
B, et al. Acrodermatitis enteropathica and an overview of zinc
metabolism. J Am Acad Dermatol. 2007;56:116–24.
26. Institute of Medicine (US) Panel on Micronutrients. Dietary
Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron,
Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel,
Silicon, Vanadium, and Zinc [Internet]. Washington (DC): National
Academies Press (US); 2001 [cited 2015 Oct 15]. Available from:
27. Maret W, Sandstead HH. Zinc requirements and the risks and
bene ts of zinc supplementation. J Trace Elem Med Biol Organ
Soc Miner Trace Elem GMS. 2006;20:3–18.
28. Küry S, Dréno B, Bézieau S, Giraudet S, Khar M, Kamoun R, et
al. Identi cation of SLC39A4, a gene involved in acrodermatitis
enteropathica. Nat Genet. 2002;31:239–40.
29. Hunt JR. Bioavailability of iron, zinc, and other trace minerals from
vegetarian diets. Am J Clin Nutr. 2003;78(3 Suppl):633S-9S.
30. Organization WH, Nutrition WEC on TE in H. Trace elements in
human nutrition : report of a WHO expert committee [meeting
held in Geneva from 9 to 17 April 1973]. 1973 [cited 2015 Dec 29];
Available from:
31. Kumar P, Lal NR, Mondal AK, Mondal A, Gharami RC, Maiti A.
Zinc and skin: a brief summary. Dermatol Online J. 2012;18:1.
32. Plonka PM, Handjiski B, Popik M, Michalczyk D, Paus R. Zinc
as an ambivalent but potent modulator of murine hair growth in
vivo- preliminary observations. Exp Dermatol. 2005;14:844–53.
33. Park H, Kim CW, Kim SS, Park CW. The therapeutic effect and
the changed serum zinc level after zinc supplementation in alopecia
areata patients who had a low serum zinc level. Ann Dermatol.
34. Sharquie KE, Noaimi AA, Shwail ER. Oral zinc sulphate in
treatment of alopecia areata. J Clin Exp Dermatol Res. 2012;3:150
35. Kil MS, Kim CW, Kim SS. Analysis of serum zinc and copper
concentrations in hair loss. Ann Dermatol. 2013;25:405–9.
36. Bhat YJ, Manzoor S, Khan AR, Qayoom S. Trace element levels in
alopecia areata. Indian J Dermatol Venereol Leprol. 2009;75:29–31.
37. Abdel Aziz AM, Sh Hamed S, Gaballah MA. Possible Relationship
between Chronic Telogen Effluvium and Changes in Lead,
Cadmium, Zinc, and Iron Total Blood Levels in Females: A Case-
Control Study. Int J Trichology. 2015;7:100–6.
38. Abdel Fattah NSA, Atef MM, Al-Qaradaghi SMQ. Evaluation of
serum zinc level in patients with newly diagnosed and resistant
alopecia areata. Int J Dermatol. 2016;55:24-9.
39. Corbo MD, Lam J. Zinc de ciency and its management in the
pediatric population: a literature review and proposed etiologic
classi cation. J Am Acad Dermatol. 2013;69:616–24.e1.
40. Institute of Medicine (US) Committee to Review Dietary Reference
Intakes for Vitamin D and Calcium. Dietary Reference Intakes for
Calcium and Vitamin D [Internet]. Ross AC, Taylor CL, Yaktine
AL, Del Valle HB, editors. Washington (DC): National Academies
Press (US); 2011 [cited 2015 Oct 15]. Available from: http://www.
41. Bouillon R, Carmeliet G, Verlinden L, van Etten E, Verstuyf A,
Luderer HF, et al. Vitamin D and human health: lessons from
vitamin D receptor null mice. Endocr Rev. 2008;29:726–76.
42. Tsiaras WG, Weinstock MA. Factors in uencing vitamin D status.
Acta Derm Venereol. 2011;91:115–24.
43. Vieth R, Bischoff-Ferrari H, Boucher BJ, Dawson-Hughes B,
Garland CF, Heaney RP, et al. The urgent need to recommend an
intake of vitamin D that is effective. Am J Clin Nutr. 2007;85:649–
44. Weinstock MA, Moses AM. Skin cancer meets vitamin D: the way
forward for dermatology and public health. J Am Acad Dermatol.
45. WHO Scienti c Group on the Prevention and Management of
Osteoporosis (2000 : Geneva S. Prevention and management
of osteoporosis : report of a WHO scientific group. 2003
[cited 2015 Oct 15]; Available from:
46. Gallagher JC, Sai AJ. Vitamin D insuf ciency, de ciency, and bone
health. J Clin Endocrinol Metab. 2010;95:2630–3.
47. Holick MF. Vitamin D de ciency. N Engl J Med. 2007;357:266–81.
48. Mitchell DM, Henao MP, Finkelstein JS, Burnett-Bowie S-AM.
Prevalence and predictors of vitamin D de ciency in healthy
adults. Endocr Pract Off J Am Coll Endocrinol Am Assoc Clin
Endocrinol. 2012;18:914–23.
49. Aksu Cerman A, Sarikaya Solak S, Kivanc Altunay I. Vitamin D
de ciency in alopecia areata. Br J Dermatol. 2014;170:1299–304.
50. Yetley EA. Assessing the vitamin D status of the US population.
Am J Clin Nutr. 2008;88:558S-64S.
51. Pearce SHS, Cheetham TD. Diagnosis and management of vitamin
D de ciency. BMJ. 2010;340:b5664.
52. Płudowski P, Karczmarewicz E, Bayer M, Carter G, Chlebna-
Sokół D, Czech-Kowalska J, et al. Practical guidelines for the
supplementation of vitamin D and the treatment of de cits in
Central Europe - recommended vitamin D intakes in the general
population and groups at risk of vitamin D de ciency. Endokrynol
Pol. 2013;64:319–27.
53. Demay MB. The hair cycle and Vitamin D receptor. Arch Biochem
Biophys. 2012;523:19–21.
54. Demay MB, MacDonald PN, Skorija K, Dowd DR, Cianferotti
L, Cox M. Role of the vitamin D receptor in hair follicle biology.
J Steroid Biochem Mol Biol. 2007;103:344–6.
55. Bikle DD. Vitamin D metabolism and function in the skin. Mol
Cell Endocrinol. 2011;347:80–9.
56. Amor KT, Rashid RM, Mirmirani P. Does D matter? The role
of vitamin D in hair disorders and hair follicle cycling. Dermatol
Online J. 2010;16:3.
57. Bergman R, Schein-Goldshmid R, Hochberg Z, Ben-Izhak O,
Sprecher E. The alopecias associated with vitamin D-dependent
rickets type IIA and with hairless gene mutations: a comparative
clinical, histologic, and immunohistochemical study. Arch Dermatol.
58. Yilmaz N, Serarslan G, Gocke C. Vitamin D concentrations are
decreased in patients with alopecia areata. Vitam Trace Elem.
59. Mahamid M, Abu-Elhija O, Samamra M, Mahamid A, Nseir W.
Association between vitamin D levels and alopecia areata. Isr Med
Assoc J IMAJ. 2014;16:367–70.
60. D’ Ovidio R, Vessio M, d’ Ovidio FD. Reduced level of
25-hydroxyvitamin D in chronic/relapsing Alopecia Areata.
Dermatoendocrinol. 2013;5:271–3.
61. Kennel KA, Drake MT, Hurley DL. Vitamin D de ciency in adults:
when to test and how to treat. Mayo Clin Proc. 2010;85:752–7; quiz
62. Kearns MD, Alvarez JA, Tangpricha V. Large, single-dose, oral
vitamin d supplementation in adult populations: a systematic
review. Endocr Pract Off J Am Coll Endocrinol Am Assoc Clin
Endocrinol. 2014;20:341–51.
63. Vegesna V, O’Kelly J, Uskokovic M, Said J, Lemp N, Saitoh T,
et al. Vitamin D3 analogs stimulate hair growth in nude mice.
© Our Dermatol Online 3.2018 328
Endocrinology. 2002;143:4389–96.
64. Said HM. Biotin: the forgotten vitamin. Am J Clin Nutr.
65. Fernandez-Mejia C, Lazo-de-la-Vega-Monroy M-L. Biological
Effects of Pharmacological Concentrations of Biotin. J Evid-Based
Complement Altern Med. 2011;16:40–8.
66. Zempleni J, Kuroishi T. Biotin. Adv Nutr Bethesda Md. 2012;3:213–
67. Eng WK, Giraud D, Schlegel VL, Wang D, Lee BH, Zempleni J.
Identi cation and assessment of markers of biotin status in healthy
adults. Br J Nutr. 2013;110:321–9.
68. Sardesai V. Introduction to Clinical Nutrition, Third Edition. CRC
Press; 2011. 706 p.
69. Food and Nutrition Board, Institute of Medicine. Biotin. Dietary
Reference Intakes: Thiamin, Riboflavin, Niacin, Vitamin B6,
Vitamin B12, Pantothenic Acid, Biotin, and Choline. Washington,
DC: National Academy Press; 1998;374–89.
70. Kurowski HL, Gospe SM, Zeman FJ, Grivetti LE. Nutritional
factors and anticonvulsant therapies: effect on growth in children
with epilepsy. Am J Clin Nutr. 1993;58:858–61.
71. Said HM, Redha R, Nylander W. Biotin transport in the human
intestine: inhibition by anticonvulsant drugs. Am J Clin Nutr.
72. Li Y, Schellhorn HE. New developments and novel therapeutic
perspectives for vitamin C. J Nutr. 2007;137:2171–84.
73. Gershoff SN. Vitamin C (ascorbic acid): new roles, new
requirements? Nutr Rev. 1993;51:313–26.
74. Lor ia CM, Whelton PK, Caulfield LE, Szklo M, Klag MJ.
Agreement among indicators of vitamin C status. Am J Epidemiol.
75. Schleicher RL, Carroll MD, Ford ES, Lacher DA. Serum vitamin
C and the prevalence of vitamin C de ciency in the United States:
2003-2004 National Health and Nutrition Examination Survey
(NHANES). Am J Clin Nutr. 2009;90:1252–63.
76. Basavaraj KH, Seemanthini C, Rashmi R. Diet in dermatology:
present perspectives. Indian J Dermatol. 2010;55:205–10.
77. Hirschmann JV, Raugi GJ. Adult scurvy. J Am Acad Dermatol.
1999;41:895–906; quiz 907–10.
78. Kwack MH, Shin SH, Kim SR, Im SU, Han IS, Kim MK, et al.
l-Ascorbic acid 2-phosphate promotes elongation of hair shafts
via the secretion of insulin-like growth factor-1 from dermal
papilla cells through phosphatidylinositol 3-kinase. Br J Dermatol.
79. Weinstein M, Babyn P, Zlotkin S. An orange a day keeps the doctor
away: scurvy in the year 2000. Pediatrics. 2001;108:E55.
80. Olmedo JM, Yiannias JA, Windgassen EB, Gornet MK. Scurvy: a
disease almost forgotten. Int J Dermatol. 2006;45:909–13.
81. Tanumihardjo SA. Biomarkers of vitamin A status: what do they
mean? In: World Health Organization. Report: Priorities in the
assessment of vitamin A and iron status in populations, Panama
City, Panama, 15–17 September 2010. Geneva, World Health
Organization, 2012.
82. World Health Organization. Vitamin A supplements: a guide to
their use in the treatment and prevention of vitamin A de ciency
and xerophthalmia, 2nd Edition (1997). Available at: http://
de ciency/9241545062/en/(Accessed on April 07, 2015)
83. De Pee S, Dary O. Biochemical indicators of vitamin A de ciency:
serum retinol and serum retinol binding protein. J Nutr.
2002 Sep;132(9 Suppl):2895S-901S.
84. Myhre AM, Carlsen MH, BMH, SK, Wold HL, Laake P, Blomhoff
R. Water-miscible, emulsified, and solid forms of retinol
supplements are more toxic than oil-based preparations. Am J Clin
Nutr. 2003;78:1152–9.
85. Haussler MR, Haussler CA, Jurutka PW, Thompson PD, Hsieh
JC, Remus LS, et al. The vitamin D hormone and its nuclear
receptor: molecular actions and disease states. J Endocrinol.
1997;154 Suppl: S57–73.
86. Li M, Chiba H, Warot X, Messaddeq N, Gérard C, Chambon P, et
al. RXR-alpha ablation in skin keratinocytes results in alopecia and
epidermal alterations. Dev Camb Engl. 2001;128:675–88.
87. Bleasel NR, Stapleton KM, Lee MS, Sullivan J. Vitamin A de ciency
phrynoderma: due to malabsorption and inadequate diet. J Am
Acad Dermatol. 1999;41(2 Pt 2):322–4.
88. Girard C, Dereure O, Blatière V, Guillot B, Bessis D. Vitamin a
de ciency phrynoderma associated with chronic giardiasis. Pediatr
Dermatol. 2006;23:346–9.
89. Foitzik K, Spexard T, Nakamura M, Halsner U, Paus R. Towards
dissecting the pathogenesis of retinoid-induced hair loss: all-trans
retinoic acid induces premature hair follicle regression (catagen) by
upregulation of transforming growth factor-beta2 in the dermal
papilla. J Invest Dermatol. 2005;124:1119–26.
90. Famenini S, Goh C. Evidence for supplemental treatments in
androgenetic alopecia. J Drugs Dermatol JDD. 2014;13:809–12.
91. Katz HI, Waalen J, Leach EE. Acitretin in psoriasis: an overview
of adverse effects. J Am Acad Dermatol. 1999;41(3 Pt 2):S7–12.
92. Schulpis KH, Georgala S, Papakonstantinou ED, Michas T,
Karikas GA. The effect of isotretinoin on biotinidase activity. Skin
Pharmacol Appl Skin Physiol. 1999;12:28–33.
Copyright by Susana A. Ruiz-Tagle, et al. This is an open access article
distributed under the terms of the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any
medium, provided the original author and source are credited.
Source of Support: Nil, Confl ict of Interest: None declared.
... The only two pathways we found with a lower expression in the AA group were related to ABC transporter and mineral absorption. These findings are in line with previous studies showing the impact of the modifications in the metabolism of micro and macronutrients on a further risk associated with the development of AA, through the Cosmetics 2022, 9, 55 6 of 13 dysregulation of immune cells and coenzyme-dependent enzyme function and imbalance in redox potential [76][77][78]. ...
... This confirms that the resident microbiota of the scalp can also affect its metabolic activity and macro and micronutrient supply. Many published studies reported the role of micronutrients in hair loss, including AA [76][77][78]. The impact of the microbiome on host metabolism is also pivotal because of the strict relation between metabolic and immunomodulatory pathways. ...
Full-text available
The continuous research advances in the microbiome field is changing clinicians’ points of view about the involvement of the microbiome in human health and disease, including autoimmune diseases such as alopecia areata (AA). Both gut and cutaneous dysbiosis have been considered to play roles in alopecia areata. A new approach is currently possible owing also to the use of omic techniques for studying the role of the microbiome in the disease by the deep understanding of microorganisms involved in the dysbiosis as well as of the pathways involved. These findings suggest the possibility to adopt a topical approach using either cosmetics or medical devices, to modulate or control, for example, the growth of overexpressed species using specific bacteriocins or postbiotics or with pH control. This will favour at the same time the growth of beneficial bacteria which, in turn, can impact positively both the structure of the scalp ecosystem on the host’s response to internal and external offenders. This approach, together with a “systemic” one, via oral supplementation, diet, or faecal transplantation, makes a reliable translation of microbiome research in clinical practice and should be taken into consideration every time alopecia areata is considered by a clinician.
... Folic acid is the synthetic form of folate, a type of B vitamin. 26,27 ...
... Ïîáóäîâàíà âåëèêîïàðàìåòðè÷íà ìîäåëü ó ï³äãðóïàõ íèçüêîãî òà âèñîêîãî ´åíåòè÷íîãî ðèçèêó çàáåçïå÷óº âàãîìå ï³ä´ðóíòÿ äëÿ ðîçðîáêè ñõåì ïåðñîíàë³çîâàíî¿ òåðàﳿ äàíîãî çàõâîðþâàííÿ [16,12 ]. Äåô³öèò çàë³çà òà öèíêó ïðè ÀÃÀ âèÿâëåíî ³ â ³íøèõ äîñë³äaeåííÿõ [39]. ...
Full-text available
Aim. To analyze modern scientific approaches to using the achievements of bioelementology in the diagnosis and treatment of various forms of alopecia. Identifying unresolved issues in this area of research. Materials and Methods. Literature search in MEDLINE, Embase, TOXNET databases, specialized journals and thesis papers depositories in Ukraine, Russia and Belarus. The references cited in the identified papers were used as well. The publications period used in the search was 2007-2020. Results and Discussion. The content analysis of scientific literature sources, which highlight the results of studies of homeostasis of trace elements and major elements in the human body, proves the validity of using the data obtained for the diagnosis, treatment and prevention of alopecia. Introduction of modern analytical methods made it possible to expand both qualitative and quantitative characteristics of the content of elements in hair, and then to substantiate the use of the elemental composition of hair as a medical diagnostic criterion. In addition, the analysis of hair for the content of trace elements and major elements is considered a potentially safe, non-invasive diagnostic tool; the samples do not require special equipment for storage and have no shelf life restrictions. At the present stage, an active search for the relationship between the elemental status of hair and alopecia of various origins is being carried out. It was established that all forms of alopecia are characterized by a disturbance of the homeostasis of iron, zinc, copper, and selenium. In addition, the researchers emphasize the importance of excess hair lead and cadmium in alopecia areata, of silicon in diffuse alopecia and androgenetic alopecia, and reduced levels of manganese in all forms of alopecia. The scientific community discusses the implementation of modern analytical methods to determine the elemental composition of biological fluids. The most promising are the methods of determining elements in the organs and human biological fluids using inductively coupled plasma-atomic emission and mass spectrometry. Trace elements and major elements play an important, but not entirely clear role in hair follicles normal development and immune cells function. These studies were mainly concerned with exploring of the cyclic accumulation of mast cells and macrophages in the perifollicular connective tissue. Accordingly, the dyscrasia can represent a modified risk factor, the assessment of which requires further in-depth studies. Conclusions. The content analysis of the published results of the studies of trace and major elements composition of hair showed that with alopecia areata there is a decrease in the content of S, Zn, Se, Mn, Mn, and Fe, and an excess of Pb, Cd, Ni, Cu, Al, Hg; diffuse forms of alopecia are characterized by a deficiency in the content of S, Fe, K, Ca, Zn, Cu, and Se; with androgenetic alopecia in women, there is a decrease in the content of Mn, Zn, Se, Mg, Fe, in men - a decrease in the levels of Zn, Cu, Mn, Mg, and Se; and an increase in the content of Cu and Cr. In order to correct alopecia of various origins, it is necessary to determine the quantitative ratio of trace elements and major elements in the hair and to systematize the results obtained in monitoring studies to establish their reference values in conditions of various geochemical locations.
... Moreover, modifications in the metabolism of micro-and macronutrients (Thompson et al., 2017;Gade et al., 2018;Ruiz-Tagle et al., 2018;Almohanna et al., 2019) play a pivotal role in the development of AA, and the resident microbiota can itself contribute to nutrient synthesis. As reported (Thompson et al., 2017), the pathophysiological mechanism through which sub-threshold levels of micronutrients might contribute to AA include the dysregulation of immune cell function, dysregulation of coenzyme-dependent enzyme function in DNA synthesis, and an imbalance between oxidant and antioxidant activity. ...
Full-text available
Involvement of the microbiome in many different scalp conditions has been investigated over the years. Studies on the role of the scalp microbiome in specific diseases, such as those involving hair growth alterations like non-cicatricial [androgenetic alopecia (AGA), alopecia areata (AA)] and cicatricial alopecia lichen planopilaris, are of major importance. In the present work, we highlighted the differences in microbial populations inhabiting the scalp of AA subjects and a healthy sample cohort by using an integrated approach relying on metagenomic targeted 16S sequencing analysis, urine metabolomics, and human marker gene expression. Significant differences in genera abundances (p < 0.05) were found in the hypodermis and especially the dermis layer. Based on 16S sequencing data, we explored the differences in predicted KEGG pathways and identified some significant differences in predicted pathways related to the AA pathologic condition such as flagellar, assembly, bacterial chemotaxis, mineral absorption, ABC transporters, cellular antigens, glycosaminoglycan degradation, lysosome, sphingolipid metabolism, cell division, protein digestion and absorption, and energy metabolism. All predicted pathways were significantly enhanced in AA samples compared to expression in healthy samples, with the exceptions of mineral absorption, and ABC transporters. We also determined the expression of TNF-α, FAS, KCNA3, NOD-2, and SOD-2 genes and explored the relationships between human gene expression levels and microbiome composition by Pearson's correlation analysis; here, significant correlations both positive (SOD vs. Staphylococcus, Candidatus Aquiluna) and negative (FAS and SOD2 vs. Anaerococcus, Neisseria, and Acinetobacter) were highlighted. Finally, we inspected volatile organic metabolite profiles in urinary samples and detected statistically significant differences (menthol, methanethiol, dihydrodehydro-beta-ionone, 2,5-dimethylfuran, 1,2,3,4, tetrahydro-1,5,7-trimethylnapthalene) when comparing AA and healthy subject groups. This multiple comparison approach highlighted potential traits associated with AA and their relationship with the microbiota inhabiting the scalp, opening up novel therapeutic interventions in such kind of hair growth disorders mainly by means of prebiotics, probiotics, and postbiotics.
... 5 Currently, there is no available information on the relationship between hair loss and abnormal biotin levels. 7 Biotin deficiency can affect the skin, immune system, and nervous system. 8 The dermatologic manifestations of its deficiency include hair loss and scaly, erythematous, eczematous periorificial lesions resembling those characteristic of zinc deficiency. ...
BACKGROUND: Biotin is popular in hair loss treatment supplements, although the frequency of its deficiency in patients with hair loss has not been established. OBJECTIVES: This work sought to assess the serum levels of biotin in patients with telogen effluvium. METHODS: This case-control study included 60 patients with telogen effluvium and 20 control subjects. Subjects who were on biotin therapy three months prior to the study and those reporting other causes of hair loss were excluded. The scalp of each patient was clinically and dermoscopically examined. Serum biotin levels were measured using enzyme-linked immunosorbent assay kits. RESULTS: Serum levels of biotin were optimal in patients and control groups with no significant difference between the groups. Insignificantly lower biotin levels in elderly patients, smokers, athletes, those with a history of recurrent infections, and women who were pregnant and/or lactating were observed. There was also an insignificant positive correlation between the serum level of biotin and patient age and an insignificant negative correlation between disease duration and patient body mass index. Serum biotin has a weak specificity and sensitivity in differentiating between cases and control subjects or between acute and chronic telogen effluvium. CONCLUSION: There was no significant difference in serum biotin levels between cases and controls or between those with acute or chronic telogen effluvium.
Background Vitamin D, a vitamin and hormone, plays an important role in dermatology and dermatotherapeutics, due to its anti-inflammatory and immunomodulatory properties, and regulation of keratinocyte differentiation and proliferation. It also affects the hair cycle, and its role in hair loss is under constant research. Objectives This review aims to give a brief overview of vitamin D biology within the hair follicle, role in the etiopathogenesis, and rationale for supplementation in various alopecias. Methods A PubMed literature search was performed to review relevant current literature and studies investigating the role of vitamin D in the etiopathogenesis, as a supplement and a potential therapeutic modality in hair loss. Results and Conclusion Vitamin D is intricately involved in various signaling pathways of growth and differentiation of hair follicles. Most studies show an inverse relationship between serum vitamin D levels and non-scarring alopecias such as telogen effluvium, androgenetic alopecia, alopecia areata, and trichotillomania. Vitamin D deficiency is also associated with scarring alopecia. However, conclusive studies to demonstrate the benefit of vitamin D administration in correcting hair loss and managing these conditions are lacking. Hence, further studies are needed before vitamin D can be routinely recommended as a treatment modality in these conditions.
Full-text available
The aim of the present study was to estimate the prevalence of telogen effluvium (TE) and to evaluate the efficacy of vitamin D in the treatment of this problem in women belonging to various cities of south Punjab, Pakistan. In the present study, 40 adult women suffering from the problem of TE were included. Each woman was treated with oral vitamin D3 (200,000 IU) therapy fortnightly and a total of 6 doses were given to each patient. After 15 d of the last dose, the condition of patients was assessed clinically. The mean age of female patients was 32.2±1.5 y, 42.5% of the patients between 21-30 y of age were found to be more frequently affected with TE compared to 35% females of 31-40 y of age. Results showed significant improvement in hair growth in young (r=0.457 p<0.003) women and in those, which do not use sunscreen (r=-0.331 p<0.037) but commonly utilize milk or milk protein (r=-0.311 p<0.051). Vitamin D3 therapy resulted in the improvement of the condition in 82.5% (p<0.001) patients of TE. The use of oral vitamin D3 (200,000 IU, fortnightly) for 3 mo resulted in significant improvement in hair regrowth in the patient of TE. Results showed improvement in hair growth in young women those do not use sunscreen but commonly utilize milk or milk protein.
Full-text available
Hair loss in women has been considered one of the most common problems faced the dermatologists. It is also considered a haunting problem for women because of the association of hair with femininity, beauty and personal strength, and thus can cause psychological problems for them. In Iraq, there was a little attention was advocated to determine the most type and prevalence of hair loss accurately and the associated causes. The aim of the study is to highlight the main physiological causes of hair loss for women in Basra Governorate, Southern Iraq. Given the important role that some hormones and nutrients play in addition to oxidative stress in influencing the appearance of hair loss disease in women. The study was conducted on volunteer patients that visiting the dermatology consultation unit in hospitals affiliated to the Basra Health Administration during the period from September 2019 to the beginning of January 2020. The study was applied on a random sample consisting of 67 women suffering from hair loss and another sample of 21 women as control volunteers sound for the purpose of comparison. The results of the current study have revealed a significant decrease in blood parameters (MCH-MCV-Hb) and a decrease in the level of iron in the patients group compared with the control group indicating the association of anemia with hair loss in women. The results showed a significant decrease in the concentration of zinc and vitamin D in the patients group compared with the control group. The results also showed a significant increase in the concentration of testosterone and a significant decrease in the level of estrogen and thyroid hormone T3 in the group of patients compared to the control group. Furthermore, the results presented a high level of (MDA) among the patients group compared to the control group, indicating that increased oxidative stress may cause hair loss in women.
Hair supplements are a vast and growing industry. Patients often turn to oral supplements to address hair concerns as they are easily accessible. There are numerous products on the market, many with thousands of reviews (both positive and negative). Nutritional supplements are regulated by the FDA as foods instead of drugs, meaning they do not have to prove their efficacy and safety before becoming available to consumers. While some oral supplements have strong evidence supporting their use for hair growth, many ingredients have not been tested in clinical trials, have only in vitro evidence for hair growth, or have only been tested in animals. Given these industry characteristics, it is important for dermatologists to be aware of the safety and utility of these ingredients to provide appropriate counseling to their patients. The goal of this review is to evaluate the efficacy of popular hair growth oral supplement ingredients and formulations. This review does not address the topical formulations of these ingredients and their effects on hair growth.
Full-text available
Nowadays, the involvement of the microbiome in human health and many human diseases, including that strictly related to the scalphas been brought to the light. Indeed, more recently, authors highlighted the presence of a significant microbial shift both in nonscarring (Androgenetic alopecia and Alopecia areata) and scarring Alopecias. The advent of novel technologies together with the effort of many scientists in the microbiome field could provide in the nearest future a clearest framework about the strict relationship between human healthiness and symbiotic microorganism resident on different ecosystem of our body. In this view, the use of Omics approaches has to be considered as no longer negligible when studying the microbiome implication in human health and disease.
Full-text available
Introduction: Hair loss is a common and distressing problem that can affect both males and females of all ages. Chronic telogen effluvium (CTE) is idiopathic diffuse scalp hair shedding of at least 6 months duration. Hair loss can be one of the symptoms of metal toxicity. Lead (Pb) and cadmium (Cd) are highly toxic metals that can cause acute and chronic health problems in human. The aim of the present study is to determine if there is a relationship between these metals and CTE in women and if CTE is also associated with changes in zinc (Zn) or iron (Fe) blood levels. Materials and Methods: Pb, Cd, Fe and Zn total blood levels were determined in 40 female patients fulfilling the criteria of CTH and compared with total blood levels of same elements in 30 well-matched healthy women. Results: Quantitative analysis of total blood Fe, Zn, Pb and Cd revealed that there were no significant differences between patients and controls regarding Fe, Zn, and Pb. Yet, Cd level was significantly higher in patients than controls. In addition, Cd level showed significant positive correlation with the patient's body weight. Conclusion: Estimation of blood Pb and Cd levels can be important in cases of CTE as Cd toxicity can be the underlying hidden cause of such idiopathic condition.
Full-text available
Liver toxicity associated with herbal remedies and dietary supplements is an increasing concern. Several toxic hepatitis cases have been reported in the literature in association with products intended for weight loss where green tea extracts are an ingredient.Three hepatotoxicity cases are reported below in association with the use of Inneov masa capilar®, a dietary supplement intended to stop hair loss whose primary component is green tea catechins. In all of them, other potential causes of acute hepatitis were ruled out.We highlight the importance of awareness regarding these substances at history taking in order to identify and report hepatic adverse reactions secondary to apparently safe herbs as described in the present manuscript.
This article describes the information currently available in the National Nutrition Monitoring System that is relevant to assessing the vitamin D status of US population groups, the strengths and limitations of this information, and selected results of vitamin D nutritional status assessments. The National Health and Nutrition Examination Survey (NHANES) provides information on vitamin D intakes only from 1988 to 1994. NHANES collected information on supplement use and circulating 25-hydroxyvitamin D [25(OH)D] concentrations from 1988 through current surveys. The National Nutrient Database for Standard Reference started providing limited data on the vitamin D content of foods in 2002 and continues to update these values. The Food Label and Package Survey provides 2006–2007 label information on vitamin D fortification of marketed foods. Despite limitations in the available data and controversies about appropriate criteria for evaluating vitamin D status among population groups, we can make some useful comparisons of vitamin D status among life-stage groups. In general, males have higher vitamin D intakes and 25(OH)D concentrations than do females. Children tend to have higher vitamin D status than adults. The increasing use of multivitamin-mineral dietary supplements in younger to older adults is not associated with a corresponding increase in serum 25(OH)D concentrations. In general, leaner individuals have higher circulating concentrations of 25(OH)D and supplement use than do heavier individuals. Finally, non-Hispanic whites tend to have higher vitamin D status than do non-Hispanic blacks and Mexican Americans.
Botanical extracts and single compounds are increasingly used in cosmetics but also in over-the-counter drugs and food supplements. The focus of the present review is on controlled clinical trials with botanicals in the treatment of acne, inflammatory skin diseases, skin infections, UV-induced skin damage, skin cancer, alopecia, vitiligo, and wounds. Studies with botanical cosmetics and drugs are discussed, as well as studies with botanical food supplements. Experimental research on botanicals was considered to a limited extent when it seemed promising for clinical use in the near future. In acne therapy, Mahonia, tea tree oil, and Saccharomyces may have the potential to become standard treatments. Mahonia, Hypericum, Glycyrrhiza and some traditional Chinese medicines appear promising for atopic dermatitis. Some plant-derived substances like dithranol and methoxsalen (8-methoxypsoralen) [in combination with UVA] are already accepted as standard treatments in psoriasis; Mahonia and Capsicum (capsaicin) are the next candidates suggested by present evidence. Oral administration and topical application of antioxidant plant extracts (green and black tea, carotenoids, coffee, and many flavonoids from fruits and vegetables) can protect skin from UV-induced erythema, early aging, and irradiation-induced cancer. Hair loss and vitiligo are also traditional fields of application for botanicals. According to the number and quality of clinical trials with botanicals, the best evidence exists for the treatment of inflammatory skin diseases, i.e. atopic dermatitis and psoriasis. However, many more controlled clinical studies are needed to determine the efficacy and risks of plant-derived products in dermatology. Safety aspects, especially related to sensitization and photodermatitis, have to be taken into account. Therefore, clinicians should not only be informed of the beneficial effects but also the specific adverse effects of botanicals used for dermatologic disorders and cosmetic purposes.
Alopecia areata (AA) is a non-scarring, autoimmune, inflammatory hair loss disease. Zinc is a trace element involved in important functional activities of hair follicles. To evaluate serum zinc levels in patients with newly diagnosed and resistant lesions of AA in comparison to age- and sex-matched healthy controls. The present study included 100 subjects: 50 patients with AA divided into two equally distributed subgroups (25 patients with recent onset AA [subgroup 1] and 25 patients with resistant AA [subgroup 2]) and 50 age- and sex-matched healthy controls. Serum zinc levels were assessed in all subjects. Comparison of mean serum zinc levels was done between all patients and controls, between patients' subgroups as well as between patient's subgroup and controls. Correlations between serum zinc level and extent of AA and its duration were also done in all patients and each patient's subgroup. A significantly lower serum zinc level was found in patients with AA compared with controls and was significantly lower in patients with resistant AA compared to patients with newly diagnosed AA. Significant inverse correlations existed between serum zinc level, severity of AA, and disease duration in all patients as well as in patients with resistant AA. Lower serum zinc level existed in patients with AA and correlated inversely with disease duration, severity of AA, and its resistance to therapies. Therefore, assessment of serum zinc level in patients with AA appears useful as a marker of severity, disease duration, and resistance to therapies. Accordingly, zinc supplements may provide a therapeutic benefit. © 2015 The International Society of Dermatology.
Background: Alopecia areata (AA) is an autoimmune disease, based on the response to local and/or systemic corticosteroid treatment. The role of vitamin D in the pathogenesis of immune/autoimmune mediated diseases has been widely studied. Objectives: To investigate a possible association between serum 25-hydroxyvitamin D levels and alopecia areata. Methods: The study included 23 patients diagnosed with AA followed at our outpatient clinic during the period March 2010 to May 2011, as well as a control group matched for age and gender. All subjects underwent a complete work-up and medical examination, anthropometric measurements and laboratory tests. Laboratory tests included complete blood count, C-reactive protein (CRP), and vitamin D levels. Results: Mean CRP values were significantly higher in the AA group than the control group (1.1 +/- 0.7 mg/dl vs. 0.4 +/- 0.8 mg/ dl, P < 0.05). Vitamin D levels were significantly decreased in the AA group (11.32 +/- 10.18 ng/ml vs. 21.55 +/- 13.62 ng/ml in the control group, P < 0.05). Multivariate analysis showed that CRP (odds ratio 3.1, 95% confidence interval 2.6-4.2, P = 0.04) and serum vitamin D levels < 30 ng/ml (OR 2.3, 95% CI 2.2-3.1, P = 0.02) were associated with AA. Conclusions: We found a significant correlation between AA and vitamin D deficiency. Vitamin D deficiency can be a significant risk factor for AA occurrence.
Currently, topical minoxidil and finasteride are the only treatments that have been FDA approved for the treatment of female pattern hair loss and androgenetic alopecia. Given the incomplete efficacy and sife effect profile of these medications, some patients utilize alternative treatments to help improve this condition. In this review, we illustrate the scientific evidence underlying the efficacy of these alternative approaches, including biotin, caffeine, melatonin, a marine extract, and zinc. J Drugs Dermatol. 2014;13(7):809-812.