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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.
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© 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.
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... Provitamin A, or beta-carotene, is obtained through consumption of plants and nuts. 1 Dermatologic manifestations of vitamin A deficiency include ichthyosis, fragile hair, and telogen effluvium. 2 There is no upper intake level for beta-carotene; 1 however, over-supplementation with preformed vitamin A can result in telogen effluvium in addition to other systemic symptoms, such as hepatotoxicity. 1 Therefore, it is important to consider which formulation of vitamin A is being ingested. ...
... Zinc is also crucial to proper immune cell function and response. 2 As an essential element, zinc must be supplied to the human body through diet. ...
... One symptom of severe zinc deficiency is alopecia, with hair regrowth after supplementation. 1 Yet, the exact role of zinc in hair health is still unknown. 2 El-Esawy et al. compared serum zinc levels in male patients with androgenetic alopecia (n = 60) to healthy controls (n = 60). 15 Serum zinc was significantly lower in patients with androgenetic alopecia compared to controls. ...
UNSTRUCTURED Oral supplements are a growing industry, garnering the attention of patients and medical professionals alike. The marketplace for oral supplements is flooded with a wide range of products offering broad availability and convenience, and supported by a spectrum of customer testimonials. Currently, these supplements are regulated as foods rather than drugs, under the governance of the Food and Drug Administration (FDA). The “food” classification allows these products to become available to customers without proof of meeting the efficacy and safety standards required of pharmaceuticals to enter the marketplace. In line with the surge in popularity of oral supplements, patients are increasingly looking to these medical alternatives as a method to alleviate and potentially treat their atopic dermatitis (AD). To ensure physicians are providing the best care options in the treatment of AD, it is paramount that they understand the utility, safety, and knowledge gaps associated with each type of dietary supplement. Currently, there are research gaps related to the lack of clinical trials investigating dietary supplements, and the fact that existing studies are largely limited to in-vitro or animal-based studies. We undertook a literature review designed to objectively identify the effectiveness of oral supplements in the treatment of patients with AD. With the exception of Vitamin B12, magnesium, and apple cider vinegar, this review does not address the efficacy of topical formulations in AD.
... Provitamin A, or beta-carotene, is obtained through consumption of plants and nuts. 1 Dermatologic manifestations of vitamin A deficiency include ichthyosis, fragile hair, and telogen effluvium. 2 There is no upper intake level for beta-carotene; 1 however, over-supplementation with preformed vitamin A can result in telogen effluvium in addition to other systemic symptoms, such as hepatotoxicity. 1 Therefore, it is important to consider which formulation of vitamin A is being ingested. ...
... Zinc is also crucial to proper immune cell function and response. 2 As an essential element, zinc must be supplied to the human body through diet. ...
... One symptom of severe zinc deficiency is alopecia, with hair regrowth after supplementation. 1 Yet, the exact role of zinc in hair health is still unknown. 2 El-Esawy et al. compared serum zinc levels in male patients with androgenetic alopecia (n = 60) to healthy controls (n = 60). 15 Serum zinc was significantly lower in patients with androgenetic alopecia compared to controls. ...
... 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. ...
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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.
... In general, the mechanism of hair nutrition is based on the appropriate flow of micronutrients and proper levels of energy supply to all types of cells involved so that the phases of the hair life cycle, anagen, catagen and telogen, are triggered and run properly [17]. Hair, with the leading role of the hair follicle as the transporter in the process, needs a wide range of nutrients: proteins, fatty acids, and minerals [18]. Nutrient deficiencies interrupt hair growth and regrowth cycles [19]. ...
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W pracy przedstawiono mechanizm łysienia androgenowego u mężczyzn ( male androgenetic alopecia – MAGA) z uwzględnieniem roli enzymu 5-α-reduktazy, która odpowiada za konwersję testosteronu, najważniejszego hormonu męskiego, do jego aktywnej formy – dihydrotestosteronu (DHT). Opisane zostały konsekwencje pobudzenia przez DHT receptorów androgenowych ( androgen receptors – ARs), zlokalizowanych w chromosomie X komórek linii brodawkowej ( dermal papilla cells – DPCs). Powoduje to transkrypcję genów uruchamianą przez androgeny, zostaje zaburzone odżywianie mieszka włosowego, ale przede wszystkim przyspieszeniu ulega moment zakończenia anagenu i przejścia do fazy katagenu. Przedstawiono również, w jaki sposób enzym ten może być poddawany działaniu molekuł pełniących funkcję jego inhibitorów. Ponadto zaprezentowano uzasadnienie dla prowadzenia bardziej dogłębnych badań poświęconych mechanizmom działania, w których ekstrakty palmy sabałowej ( Serenoa repens ) wywołują efekt inhibicji 5-α-reduktazy. Dodatkowo w pracy został zawarty postulat na rzecz rozpoznawania i pomiaru substancji aktywnych znajdujących się w ekstraktach palmy sabałowej, w tym dwóch najbardziej obiecujących związków fitosterolowych – stigmasterolu i β-sitosterolu – ze względu na udowodnioną już aktywność inhibitorową w stosunku do 5-α-reduktazy w ekstraktach z surowców pochodzących z innych gatunków roślin. W ramach postulatu na rzecz pogłębienia badań zwrócono uwagę na konieczność oceny wpływu stosowania ekstraktów z palmy sabałowej na cykl życia włosów, cykl życia mieszka włosowego, różne czynniki wzrostu i angiogenezę, a także aktywność układu immunologicznego czy stres oksydacyjny. Inne obszary obserwacji działania ekstraktów z palmy sabałowej mogłyby obejmować ich zastosowanie w terapiach w połączeniu z innymi ekstraktami roślinnymi lub środkami terapii, np. z osoczem bogatopłytkowym czy osoczem bogatym w fibrynę.
... Biotin and biotin metabolites affect transcription of genes encoding cytokines, oncogenes, glucose metabolism and cellular homeostasis [49]. Hair follicles grow when the internal cellular environment has been corrected to achieve redox balance, energy generation, and repair of cellular damage and regulation of cellular function to meet the high metabolic demand [50]. Nutrients with one carbon metabolism, vitamins, B12, B6, folate, riboflavin, methionine, choline, betaine and bioactive compounds like retinoic acid, resveratrol, curcumin, sulforaphane and tea polyphenols modulate epigenetic patterns by regulating universal methyl donor and enzymes that catalyze DNA methylation and histone modifications [39,25]. ...
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Background: To understand the scientific mechanism of hair loss caused by non-androgenic factors and the importance of nutrients in prevention, reversal of damage and restoration of hair growth, without the use of anti-androgens. Methodology: A total of 100 patients, 62 male and 38 female, who presented with Androgenetic Alopecia (AGA), Male Pattern Hair Loss (MPHL) and Female Pattern Hair Loss (FPHL), were included in the study. Early hair loss grades and patients with associated medical conditions were excluded. All patients were evaluated for DHT, DHEAS, SHBG, free testosterone, scalp trichoscopy, global photography and hair fall. The cause for initiation of hair fall was inquired and noted. All patients were treated with a low dose once in three days nutritional supplement combinations of Antioxidant, Calcium, vitamin D3 on day 1. Iron, folic acid, vitamin C, vitamin E on day 2 and amino acids with B-complex, biotin and omega 3 on day 3. The cycle repeated every 3 days for 4 months. Clinical progress was recorded every 2 months, hair fall was recorded every month. Results: Levels of DHT, DHEAS, SHBG, free testosterone, in all the men and women were within normal limits. Hair loss commenced due to restricted eating, stress, lack of sleep, pollution, smoking, alcohol, late nights, circadian rhythm, poor scalp hygiene etc. but was now presenting as AGA or pattern hair loss. Peri pilar trichoscopic signs were seen only in the early months of commencement of hair loss and not after 3-4 months of progress. Focal atrichia was more common than expected. With the nutritional supplements, hair fall was controlled within 4 weeks–6 weeks. The average improvement in density in women at 4 months was 20% and the improvement in caliber was 25%. While in men the average improvement in density at 4 months was 24% and improvement in caliber was 18%, without use of minoxidil or finasteride. Conclusion: All alopecias commence with simple hair fall triggered by non-androgenic factors. These factors act by generation of ROS leading to cellular dysfunction from damage to DNA and metabolism. The ROS also sensatise androgen receptors and pathways making the cells sensitive to normal androgens. The ROS can be neutralized, deranged metabolism and DNA damage can be repaired with restoration of cellular function, with combinations of nutritional supplements resulting in hair growth without the use of anti-androgens.
... Most of the time, it isverydifficult to distinguish the cause for hair loss from one another. A clinical data, laboratoryfindings, physical examination, Dermoscopy, and some cases biopsy may be needed for a definitivediagnosis [1][2][3]. In this study,scalp dermoscopy is done to differentiate between different causes of diffuse alopecias in females. ...
Background: Diffuse alopecia in females is a common complaint and still a major challenge in the practice of dermatology. Female androgenetic alopecia (FAGA), chronictelogen effluvium (CTE), and diffuse alopecia areata(AA) are its three main causes for diffuse hair loss. It is often difficult one from the other and clinical data, physical examination, biochemical tests, dermoscopy, and some cases biopsy may be needed for a definitive diagnosis.In this study, scalp dermoscopy as a main tool used to differentiate between different causes of hair loss and definitive role of dermoscopy in the treatment follow up. Objectives: Our aim is to evaluate and determine dermoscopic findings of different causes of diffuse alopecia that can be used as the clinical indicator of the disease. Another aim is to study the correlation of haemoglobin, S. ferritin and TSH levels in different causes of diffuse alopecia in females. Methods: Total50 patients were enrolled for this prospective study and was conducted for a period of 6 months. Detailed history, Clinical examination, Dermoscopic evaluation, complete hemogam, S. ferritin and Thyroid profile was done. Results: Most of them (66%) were between age group 18 to 30. Out of total cases 31 cases were TE, 9 cases were FAGA, 7 cases of diffuse Alopecia. Dermoscopic findings seen were yellow dots in 41 patients, thinning of hair in 33 patients, vellus hairs in 14 patients, peripilar sign in 12 patients, hair diameter diversity more than 20 % (HDD) in 8 patients, exclamation mark hair in 7 patients, honey comb pigment pattern and loss of follicles in 3 patients each. Conclusion: In TE cases most common dermoscopic findings were Yellow Dots, In FPHL most common and specific finding was HDD > 20%. A thorough dermascopic evaluation and follow up is must for different patterns of hair loss among females.
... Folic acid is the synthetic form of folate, a type of B vitamin. 26,27 ...
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Background: Oral supplementation with some amino acids (like methionine, taurine, and cysteine) could be useful in subjects with hair loss conditions such as androgenic alopecia (AGA or FAGA) or telogen effluvium (TE). Hydrolysed collagen (HC) oral supplementation has demonstrated to have beneficial effects on nail and skin health and could improve hair growth. A food supplement in tablet formulation containing hydrolysed fish-origin collagen (300 mg/dose), taurine, cysteine, methionine, iron, and selenium has been recently available. To date no controlled data are available regarding the clinical efficacy of this product as adjuvant to hair loss specific treatments in these clinical conditions. Study aims: To evaluate and compare the efficacy and tolerability of an oral supplementation based on HC and amino acids in subjects with hair loss due to AGA/FAGA or chronic TE in combination with drug treatments in comparison with drug treatments alone. Methods and subjects: In a prospective, 12-week, randomized, assessor-blinded controlled trial 83 subjects (mean age 41 ± 16 years; 26 men and 57 women) were enrolled in the study. Fifty-nine subjects suffered from AGA/FAGA (Hamilton I-VA, Ludwig I-1, II-2) and 24 from chronic TE. Subjects were randomized to oral supplementation (1 tablet day) in combination with the specify drug treatment decided by the investigator according to the type of hair loss (AGA/FAGA or TE) (Group A; N = 48) or to specific drugs treatment only (Group B; N = 35). The main outcome of the trial was the clinical efficacy evaluation using a 7-point global assessment score (GAS) (from +3: Much Improved to -3 Much worsened; with score 0 representing no modification). The GAS score was evaluated using standardized photographs by an investigator unaware of the treatment groups at week 6 and at week 12. A secondary outcome was the evaluation of acceptability of the treatment regimen using a 10-point evaluation score. Results: Seventy-six participants (91.6%) completed the 12-week study period. The GAS score at week 6 was 0.5 ± 0.2 in group A and 0.0 ± 0.1 in Group B (p < 0.05; Mann-Whitney). At week 12 the GAS score in Group A was statistically significant higher in comparison with Group B (1.67 ± 0.16 and 0.66 ± 0.20, p < 0.001; Mann-Whitney test). A higher percentage of Group A subjects achieved a GAS score of ≥2 in comparison with group B (50% vs. 23%). The oral supplement was generally well tolerated. Conclusion: An oral supplement containing hydrolysed fish-origin collagen, taurine, cysteine, methionine, iron, and selenium has demonstrated to improve the clinical efficacy of specific anti-hair loss treatments in subjects with AGA/FAGA or chronic TE.
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.
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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.
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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.
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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.