Micronutrients in hair loss

Abstract

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.

Full text

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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
INTRODUCTION
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].
MATERIALS AND METHODS
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
included.
ABSTRACT
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: leoespinoza@hotmail.cl
Review Article

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RESULTS
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 defi 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

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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
supplementation
Iron Serum Ferritin >40 ng/l CTE
ATE
AA
AGA
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 defi ciency is corrected
Zinc Serum Zinc (Zn) >10,7 mmol/L TE
AA
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
Insuffi ciency: < 30 ng/mL
Defi ciency:
< 20 ng/mL
CTE
FPHL
AA
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
Defi ciency: Biotin urinary
excretion low 20ug/L or 25
ug/24 hours
No evidence of hair loss
association
No evidence for biotin supplementation for hair loss
treatment
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
concentration
Defi ciency
below 20 mcg/dL
Defi ciency: TE and hair
breakage
Overload: TE
In defi ciency: 200.000 IU, single dose monthly for 1-6
months
TE: telogen effl uvium, CTE: chronic telogen effl uvium, ATE: acute telogen effl uvium, AA: alopecia areata, AGA: androgenetic alopecia, FPHL: female pattern hair
loss
Table 2. Iron defi ciency and hair loss.
Author Type of Alopecia Type of Study Results
Hard S.
(1963)[16]
Diffuse
Hair
Loss
Cross-sectional,
followed by
prospective
cohort
100% regrowth in 18/96 (18.8%) non-anemic women with iron
defi ciency (measured by serum iron) and DH treated with oral
iron therapy
Rushton DH, Ramsay ID, James
KC, Norris MJ, Gilkes JJ.
(1990)[17]
Diffuse
Androgen dependent
alopecia
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.
(2002)[18]
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 signifi cantly lower in TE and FPHL
compared to control patients.
Olsen EA
2010[20]
CTE, FHPL Case control study There was no statistically signifi cant increase in the incidence
of iron defi ciency in premenopausal or postmenopausal
women with FPHL or CTE versus control patients
Kantor J, Kessler LJ, Brooks DG,
Cotsarelis G.
(2003)[14]
TE, AGA, AA, AU, AT Case control study Serum ferritin levels were signifi cantly lower in women with
AGA (37.3 ug/L) and AA (24.9 ug/L) compared to control
patients.
Boffa MJ, Wood P, Griffi ths CE
(1995)[21]
AA Cross sectional study No increased incidence of iron defi ciency in patients with AA
compared with general population.
Sinclair R
(2002)[22]
DTHL Prospective cohort study There is no clear association between low serum ferritin and
CTE
AGA: androgenetic alopecia; AA: alopecia areata; AT: alopecia totalis; AU: alopecia universalis; CTE: chronic telogen effl uvium; DA: diffuse alopecia; DH: diffuse
hair loss; DTHL: diffuse telogen hair loss; FPA, female pattern alopecia, DTE: diffuse telogen effl uvium

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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 defi 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

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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 defi 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,

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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 defi 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 defi 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
[79,80].
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].

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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 defi 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.
CONCLUSION
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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