BJD
R EV IE W AR TI C LE
The impact of stress on epidermal barrier function:
an evidence-based review
M. Maarouf iD ,1 C.L. Maarouf,2 G. Yosipovitch iD 3 and V.Y. Shi4
1
College of Medicine, University of Arizona, Tucson, AZ, U.S.A.
2
Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, U.S.A.
3
Department of Dermatology and Cutaneous Surgery, University of Miami, Miami, FL, U.S.A.
4
Department of Medicine, Division of Dermatology, University of Arizona, Tucson, AZ, U.S.A.
Correspondence
Vivian Y. Shi.
E-mail: vshi@email.arizona.edu
Accepted for publication
2 January 2019
Funding sources
None.
Conflicts of interest
V.Y.S. is a stock shareholder of Dermveda; has
served as a paid advisor for Sanofi, Novartis, Sun
Pharma, Pfizer, Menlo Therapeutics, GpSkin, the
National Eczema Association and Global Parents
for Eczema Research; is an investigator for AbbVie
and LEO Pharma; and has received research fund-
ing from the Foundation for Atopic Dermatitis and
Skin Active Scientific. G.Y. is an ad board member
of Menlo, Trevi, Sienna, Sanofi Regeneron, Gal-
derma, Novartis, Pfizer, UCB Pharma and Bayer;
is a consultant for Opko; and has received research
funding from Sun Pharma, Pfizer and Kiniksa.
DOI 10.1111/bjd.17605
© 2019 British Association of Dermatologists
British Journal of Dermatology
Summary
Background The epidermal barrier functions to limit skin infection and inflammation
by inhibiting irritant and immunogen invasion. Abundant evidence suggests that
psychological stress stemming from crowding, isolation, nicotine smoking, insom-
nia, mental arithmetic tasks, physical pain, real-life stressors (examinations and
marital strain) and lack of positive personality traits may impart both acute and
chronic epidermal dysfunction.
Objectives To review the relationship between stress and epidermal barrier dysfunction.
Methods A review of the PubMed and Embase databases was conducted to identify
all English-language case–control, cross-sectional and randomized control trials
that have reported the effect of stress on epidermal barrier function. The authors’
conclusions are based on the available evidence from 21 studies that met the
inclusion and exclusion criteria.
Results Psychological stressors upregulate the hypothalamic–pituitary–adrenal axis
to stimulate local and systemic stress hormone production. This ultimately leads
to aberrant barrier dysfunction, characterized by decreased epidermal lipid and
structural protein production, decreased stratum corneum hydration and
increased transepidermal water loss.
Conclusions This evidence-based review explores the adverse effects of psychologi-
cal stressors on epidermal barrier function. Future investigations using more real-
life stressors are needed to elucidate further their impact on skin physiology and
identify practical stress-relieving therapies that minimize and restore epidermal
barrier dysfunction, particularly in at-risk populations.
What’s already known about this topic?
• The literature reports the negative effect of stress on prolonged wound healing.
• Less is known about the relationship between stress and epidermal barrier dysfunc-
tion, a chronic, superficial wound involving the upper epidermal layers.
What does this study add?
• Psychological stressors impact epidermal barrier function by activating the hypothala-
mic–pituitary–adrenal axis to stimulate local and systemic stress hormone production.
• Stress hormones negatively affect the epidermal barrier by decreasing epidermal
lipids and structural proteins, decreasing stratum corneum hydration and increasing
transepidermal water loss.
• Identification of such stressors can promote stress-avoidance and stress-reduction
behaviours that protect epidermal barrier function and prevent certain dermatologi-
cal conditions.
British Journal of Dermatology (2019) 1
2 Impact of stress on epidermal barrier function, M. Maarouf et al.

Fig 1. The effect of stress and hypothalamic–pituitary–adrenal (HPA) axis activation on skin barrier function. Psychological stress increases
amygdala activity, which signals the hypothalamus to produce corticotropin-releasing factor (CRF). CRF activates CRF-1 in the anterior pituitary to
stimulate production of proopiomelanocortin-derived adrenocorticotropic hormone (ACTH). Within the skin, CRF stimulates proinflammatory
mediators: nuclear factor (NF)-jB, interleukin (IL)-1, IL-6 and tumour necrosis factor (TNF)-a. The HPA axis culminates in ACTH stimulating the
adrenal glands to produce and secrete cortisol and norepinephrine. Cortisol suppresses the proinflammatory cytokines IL-1 and TNF-a, resulting in
deficient cutaneous repair. Increased glucocorticoid production following psychological stress also decreases the expression of antimicrobial
peptides in the epidermis. Such downregulation increases susceptibility to infection by microbes. Norepinephrine, released by the adrenal medulla,
inhibits epidermal proliferation and reduces blood perfusion via a-adrenergic-induced vasoconstriction. TEWL, transepidermal water loss.

Disruption of epidermal barrier function threatens the body’s
innate defence by increasing transcutaneous evaporative water
loss and entry of microbes, immunogens and toxic substances.
Psychological stress is a well-recognized instigator and aggra-
vator of inflammatory dermatoses associated with barrier dys-
function,1–6 even in healthy individuals.7 The American
Psychological Association describes psychological stress as any
uncomfortable ‘emotional experience accompanied by pre-
dictable biochemical, physiological, and behavioral changes’.1
Psychological stress and adverse health behaviours pro-
foundly disrupt neurocutaneous physiology. The right pre-
frontal cortex dominates stress response8,9 by stimulating the
neuroendocrine and autonomic nervous systems in the medial
hypothalamus.10 Mental stress profoundly disturbs the homeo-
static permeability barrier through the hypothalamic–
pituitary–adrenal (HPA) axis. The skin adapts to stressors
through coordination with the HPA axis. Psychological stress
increases amygdala activity, which signals the hypothalamus to
produce corticotropin-releasing factor (CRF).11,12 CRF acti-
vates CRF receptor type 1 in the anterior pituitary to increase
proopiomelanocortin-derived adrenocorticotropic hormone
(ACTH) production, which in turn stimulates cortisol secre-
tion from the adrenals.13 Cortisol functions as an immunosup-
pressant to counteract the effect of stressors. Furthermore,
stress activates the sympathetic nervous system to increase
norepinephrine and epinephrine release to inhibit fibroblast
growth and proliferation, impairing cutaneous healing
(Fig. 1).14
The skin is often referred to as the ‘peripheral brain’ as it
contains CRF, CRF-1 and proopiomelanocortin, and the
machinery used to synthesize ACTH and metabolize local cor-
ticosteroids. CRF stimulates the same proinflammatory media-
tors [nuclear factor-jB, interleukin (IL)-1, IL-6 and tumour
necrosis factor (TNF)-a] that are upregulated when the skin is
invaded by pathogens. In addition to hormonal influences,
stress disrupts barrier function by triggering neurogenic
inflammation.15 Stress-induced nerve growth factors stimulate
release of sensory neuropeptides,16 such as nerve growth fac-
tor, peripheral CRF, substance P and calcitonin gene-related
peptide, leading to mast cell degranulation and inflammatory

British Journal of Dermatology (2019) © 2019 British Association of Dermatologists


barrier breakdown.17 The resultant itch, pain, vasomotor insta-
bility and oedema fuel the itch–scratch cycle. These inflamma-
tory responses are carefully regulated by CRF’s concomitant
upregulation of anti-inflammatory proopiomelanocortin pep-
tides and corticosteroids.13
The body responds to barrier damage by increasing lipid
synthesis and corticosteroid and proinflammatory cytokine
expression.18,19 Paradoxically, cortisol can transiently suppress
production of the proinflammatory cytokines IL-1 and TNF-a,
resulting in deficient cutaneous repair.20 Increased glucocorti-
coid production following psychological stress decreases
antimicrobial peptide expression, increasing susceptibility to
microbial infection (Fig. 1).21
Homeostasis of a semipermeable layer is reliant on lamellar
body lipids, such as ceramides, free fatty acids and cholesterol,
within the stratum granulosum–stratum corneum interface.22
These components are hydrophobic molecules that limit
transepidermal water loss (TEWL). Conversely, within the epi-
dermis, natural moisturizing factors, composed of hydrophilic
substances such as urea, lactate and amino acids, help to retain
water, hydrating the skin.23 Additionally, a mildly acidic acid
mantle with appropriate epidermal and sebaceous lipid pro-
duction is important for proper barrier function and repair.24
Aberrance of any component can delay skin barrier recovery,
as measured by the return of barrier indices to baseline values
following disruption (i.e. TEWL ≤ 20 g m 2 h 1).
The negative effect of stress on delayed wound healing of
deep dermal lacerations and injuries is widely reported. Less
attention has been paid to the negative association of stress
with epidermal barrier dysfunction, a chronic, superficial and
microscopic wound involving only the stratum granulosum
and stratum corneum. Herein we review evidence that sup-
ports psychological stress-associated disruption of proper epi-
dermal barrier function and repair mechanisms. Such
understanding will shed light on the long-standing question
of whether stressors influence behaviour that subsequently
causes pathology, or rather if underlying pathology impairs
the epidermal response to stress.
Materials and methods
A review of the PubMed and Embase databases was completed
in November 2018 by three research personnel to identify
studies reporting the effect of stress on epidermal barrier func-
tion. Search terms included ‘stress’ AND ‘epidermal barrier
function’ OR ‘skin barrier recovery’ OR ‘transepidermal water
loss’, ‘epidermal barrier proteins’, OR ‘epidermal barrier
lipids’, OR ‘natural moisturizing factor’, OR ‘sebum’ OR ‘der-
mal microvascular flow’. Case–control studies, cross-sectional
studies and randomized control trials published in the English
language between January 2000 and November 2018 that
identified the impact of stress on epidermal barrier function
through measures of TEWL, histology and serum markers
were included. Review articles, conference abstracts, letters to
the editor, in vitro studies; and studies containing patients with
underlying medical or dermatological conditions, nonmammal
© 2019 British Association of Dermatologists
Impact of stress on epidermal barrier function, M. Maarouf et al. 3
models, mechanical-stress-induced models, stress-reduction
models and wound healing models were excluded. Twenty-
one studies are reviewed herein (Fig. 2, Table S1; see Sup-
porting Information).
Environmental stress
Crowding and isolation
The physical environment impacts dermatological health, and
changing surroundings causes additional psychological stress.25
Mouse crowding is extensively used to model mental stress.
Stressed mice exposed to 7 days of cage crowding (40 mice
per cage) develop exfoliation with increased wrinkling, com-
pared with mice in a controlled environment (five mice per
cage). Increased TEWL and decreased stratum corneum hydra-
tion were detected within 2 and 4 days after crowing, respec-
tively. Microscopically, stressed mice developed epidermal
hyperplasia and vasodilation, with significantly decreased cera-
mide and pyrrolidonecarboxylic acid levels. Transdermal pene-
tration of indomethacin and nicotinic acid amide was
significantly enhanced, suggesting a weakened and more per-
meable barrier.26
In a separate study, mice under crowding conditions devel-
oped significant epidermal thickness and proliferative activity,
decreased corneocyte size and cutaneous blood perfusion.
These changes were most apparent in the cages with the high-
est numbers of mice. Crowding significantly increased serum
epinephrine and dopamine levels, and decreased skin-surface
lipids. Conversely, isolation (one mouse per cage) also
increased norepinephrine levels and cutaneous blood perfusion
rate and delayed skin barrier recovery. Topical application of
carpronium chloride (a parasympathetic stimulator) to over-
crowded mice reversed stress-induced elevation of serum
stress hormones, including corticosterone, norepinephrine and
epinephrine, and significantly improved skin blood perfusion
and skin barrier recovery rate. A study evaluating psychologi-
cal stress in 23 individuals confined in a facility for 2 weeks
noted increased IL-1b, TEWL and sebum sampling on forearm
and cheek than obtained before and after completion of the
study, suggesting that isolation may also represent a unique
form of environmental stress that induces epidermal barrier
function changes.27 Isolation stress may have wide implica-
tions, particularly for elderly individuals, who already have
baseline barrier dysfunction.28
Relocation from familiar environments is commonly stress
inducing. Cage transfer induced barrier stress characterized by
immediate TEWL increase, with recovery observed after 1 day
and reaching near baseline levels by day 3 in mice. Intraperi-
toneal pretreatment with chlorpromazine (an antipsychotic
sedative) reduced stressor-induced skin barrier recovery delay,
suggesting that psychological stress was the basis for the
altered barrier. Not surprisingly, systemic corticosterone
administration delayed skin barrier recovery in a dose-depen-
dent manner, while topical corticosterone prevented skin bar-
rier recovery delay, further confirming that topical
British Journal of Dermatology (2019)
4 Impact of stress on epidermal barrier function, M. Maarouf et al.
Fig 2. PRISMA flow diagram.
corticosteroids can reverse barrier damage caused by systemic
stress hormones.29
Health behaviours
Smoking and nicotine
Cigarette smoking has notorious effects on the skin, including
retarding innate immune responses,30,31 delaying cutaneous
wound healing32,33 and increasing dermal matrix metallopro-
teinase-8 levels, which causes wrinkling and skin ageing.33
Nicotinic acetylcholine receptor (nAChR) stimulation by stress-
ful situations is known to regulate the late stages of epidermal
differentiation. Interestingly, topical application of a-bungaro-
toxin (an nAChR antagonist) reversed insomnia-induced barrier
permeability dysfunction and recovery.34
Nicotine appears to impair epidermal barrier function by
regulating barrier protein expression. Topical nicotine or
a-bungarotoxin increased filaggrin monomers in both mice
skin and a human EpiDerm model, likely secondary to
British Journal of Dermatology (2019)
increased epidermal protease activity. In mice, nicotine addi-
tionally decreased involucrin and loricrin levels, whereas a-
bungarotoxin increased involucrin and loricrin levels. In Epi-
Derm, both nicotine and a-bungarotoxin treatment caused
premature involucrin production, suggesting an aberrant
assembly of the cornified envelope. It appears that a-bungaro-
toxin in mice is useful in recovering stress-induced permeabil-
ity defects, with concurrent proliferation of envelope proteins
that strengthen epidermal barrier function. However, transla-
tion to the EpiDerm model did not result in similar findings,
and the utility of an nAChR antagonist in human skin deserves
further investigation.34
In a case–control study involving 99 volunteers, smokers
and nonsmokers had no difference in epidermal barrier func-
tion, measured by baseline TEWL, skin pH and stratum cor-
neum hydration, and mean number of tape strips needed to
induce stratum corneum damage. Skin barrier recovery
strongly correlated with the extent of cigarette consumption.
Additionally, skin barrier recovery following acute smoking
abstinence was worse in heavy smokers (≥ 20 cigarettes per
© 2019 British Association of Dermatologists

day) than in light-to-moderate smokers (< 20 cigarettes per
day). Smoking cessation appears to be psychologically chal-
lenging while negatively impacting barrier recovery. Addition-
ally, heavy, but perhaps not light-to-moderate, cigarette
smoking can severely compromise epidermal barrier home-
ostasis.35
Sleep and circadian rhythm
Sleep disturbance is closely associated with depression, anxiety
and mania.36 Several studies have demonstrated that skin bar-
rier biophysical parameters fluctuate on a circadian timeline.
Stimulation of the suprachiasmatic nucleus by light initiates
neuroendocrine signals, resulting in the release of cortisol by
adrenal glands and melatonin by the anterior pituitary gland.
Both hormones increase inflammatory cell activity and cyclin
levels, with a concomitant decrease in anti-inflammatory
cytokines (Fig. 1). Low nocturnal sebum production and high
TEWL in the afternoon result in xeroderma that likely con-
tributes to nocturnal pruritus, which only further propagates
the itch–scratch cycle.37
Nocturnal itch causes insomniac psychological stress in
patients with chronic inflammatory dermatoses.38 Insomniac
psychological stress, or psychological stress derived from sleep
deprivation, by continuous light and loud noise for 42 h in
mice led to significant alteration of skin barrier recovery kinet-
ics compared with control mice. Tape stripping showed signif-
icant alteration of stratum corneum integrity, with
compromised TEWL of deeper layers.39 While insomniac psy-
chological stress did not significantly affect epidermal thick-
ness, markers of keratinocyte proliferation declined by 25%.
Insomniac psychological stress also lowers structural lipid con-
tent by decreasing ceramide levels, and disrupts intercellular
cohesion by reducing desmoglein-1, corneodesmosomes and
intercorneocyte lamellar bodies.39
Topical administration of an epidermal lipid mixture
(cholesterol, free fatty acids and ceramides) accelerated skin
barrier recovery and reversed insomniac psychological
stress-induced barrier dysfunction, and further supports that
psychological stress causes barrier dysfunction. Intraperitoneal
injection of mifepristone (a glucocorticoid receptor antago-
nist) or antalarmin hydrochloride (a corticotropin-releasing
hormone receptor antagonist) 1 h prior to and 24 h following
insomniac psychological stress-induced stress in mice pre-
vented both structural and functional barrier breakdown, as
compared with a vehicle, suggesting that psychological stress
can prevent and reverse barrier damage.40
Mental and physical stress
Mental arithmetic tasks
Using near-infrared spectroscopy, Tanida et al. reported that
mental arithmetic tasks (consecutively subtracting two-digit
numbers from four-digit numbers as quickly as possible for
60 s) are associated with increased oxyhaemoglobin
© 2019 British Association of Dermatologists
Impact of stress on epidermal barrier function, M. Maarouf et al. 5
concentration in the bilateral prefrontal cortex. This activates
the HPA axis to secrete adrenal steroid hormones to stimulate
sebogenesis, providing a more hospitable environment for the
proliferation of Cutibacterium acnes.41 Oxyhaemoglobin concen-
tration in the bilateral prefrontal cortex positively correlates
with facial sebum levels and C. acnes load. Thus, stress response
system hyperactivation results in imbalance of skin barrier
homeostasis.41
Physical pain
Physical pain is a common human experience that imparts
acute and chronic psychological stress. When healthy
volunteers undergo a painful stimulus (3-min cold water
immersion), those who reported higher pain experienced sig-
nificantly faster skin barrier recovery, compared with individ-
uals who experienced lower pain. This unexpected response
is hypothesized to be due to the acute imposition of the
stressor. Furthermore, the higher-pain group, which had a
significantly faster skin barrier recovery rate, also had
increased norepinephrine, but not cortisol. The authors pro-
posed that this finding may be attributed to norepinephrine’s
ability to potentiate release of proinflammatory cytokines (i.e.
TNF-a and Toll-like receptor-2). Physical pain likely nega-
tively impacts barrier function through additional and alterna-
tive mechanisms stemming from both emotional and physical
stress.42
Mental and physical stress
Among healthy female participants who underwent induced
psychological stress, simulated job interview and 42-h sleep
deprivation, but not treadmill exercises (three consecutive
days, 1 h daily), skin barrier recovery was decreased signifi-
cantly. Interview was the only stressor that negatively affected
TEWL. Stratum corneum hydration was not significantly
affected by any of the stressors. Compared with baseline, all
three stressors significantly increased natural killer cell activi-
ties. Interview and sleep deprivation both significantly
increased plasma IL-1b, IL-10 and TNF-a levels. Interview
stress significantly increased plasma cortisol and nore-
pinephrine levels. Exercise stress significantly decreased cytoly-
tic and helper T-cell count. Additionally, increased IL-1b and
IL-10 negatively correlated with skin barrier recovery. None
of the three stressors induced measurable changes in plasma
ACTH or b-endorphin, which could be explained by their
short half-life.43
Stressor-induced elevation of TNF-a and IL-1 levels activates
sphingomyelinase, an enzyme vital to barrier repair, and thus
may play a compensatory and protective role.44 The authors
proposed that circulating and local pools of cytokine may have
an opposing action on barrier function recovery.43 That study
demonstrates that acute psychological stress and sleep depriva-
tion, but not exercise-induced physiological stress, appear to
impart skin barrier dysfunction, by increasing circulating
proinflammatory cytokines.45
British Journal of Dermatology (2019)
6 Impact of stress on epidermal barrier function, M. Maarouf et al.
When healthy athletes underwent endurance cardio exer-
cise, stratum corneum hydration and surface pH significantly
increased after exercise, while sebum content declined signifi-
cantly.46 In a separate study, stratum corneum hydration and
surface pH significantly increased after exercise, while sebum
content declined significantly. These skin biopsychical changes
can be attributed to increased sweat production, which deliv-
ers natural moisturizing factor to the stratum corneum, tem-
porarily improving epidermal barrier function. The differences
between the results in the two prior studies may be ‘dose
dependent’, as the participants in the latter study were athletes
who regularly exercised.47 Future studies should investigate
the effects of various exercises on epidermal barrier function
among athletes and people with active and sedentary lifestyles.
Academic and family stress
Among healthy medical, dental and pharmacy students, high-
stress periods (during final examinations) negatively correlated
with Profile of Mood States and Perceived Stress Scale and
were associated with significantly slower skin barrier recovery
rates compared with low-stress periods (following winter and
spring recess). Thus, the negative impact that stress poses on
epidermal barrier function can be alleviated upon stressor
removal.48
The postholiday period (1 month after the final exam) is
associated with significant TEWL increase and skin barrier
recovery delay compared with 3 weeks before the final exam.
In contrast to the findings of the aforementioned study, skin
barrier function did not significantly differ immediately after
and 3 weeks before the final examination.49 Such discrepan-
cies may be due to inherent differences in lifestyle and envi-
ronments. Psychological stress incurred following return from
holiday can negatively affect skin function. Stressor anticipa-
tion is similar to the phenomenon of increased depression and
suicide on Mondays following return to the work week.50
In healthy male medical students, exam blocks were associ-
ated with significantly higher salivary and stratum corneum
cortisol levels and TEWL increase compared with nonexam
periods. Exam psychological stress is also associated with sig-
nificantly increased levels of oral mucosal 11b-hydroxysteroid
dehydrogenase type I (11b-HSD1), a suprabasal epidermal
enzyme that catalyses the transformation of inactive cortisone
to active cortisol. Oral mucosal 11b-HSD1 levels significantly
correlated with stratum corneum cortisol levels and increased
TEWL.51 While the authors did not measure skin 11b-HSD1
expression, they hypothesized that increased 11b-HSD1
expression in the oral mucosa correlates with elevated cortisol
metabolism in the skin. Conversely, five clinically depressed
patients who were treated with 6 weeks of escitalopram, a
selective serotonin reuptake inhibitor, had significantly
improved stratum corneum hydration, and decreased stratum
corneum cortisol and 11b-HSD1 levels.51 Antidepressants
appear to modulate the HPA axis to restore barrier dysfunction
by reducing cutaneous cortisol and 11b-HSD1 expression.
British Journal of Dermatology (2019)
Social and marital stress
Social stress
In a randomized controlled trial by Robles, skin barrier
recovery was studied in 85 healthy participants who were
randomized to groups with either ‘no stress’ (read an article
in isolation), ‘stress’ (isolated preparation for the Trier Social
Stress Test: 5-min speech and 5-min mental arithmetic task
in front of an evaluative and harassing audience) or ‘stress +
support’ (preparation for Trier Social Stress Test with sup-
portive confederate).52 Compared with the ‘no stress’ group,
skin barrier recovery in the ‘stress’ and ‘stress + support’
groups was delayed by 10%, 2 h after skin disruption, with
increased salivary cortisol levels. There were no significant
differences reported between the ‘stress’ and ‘stress + sup-
port’ groups.52 This study further suggests that mental stress
delays epidermal barrier function recovery, which cannot be
mitigated by a simulated supportive confederate. This is in
contrast to the findings by Robinson et al., who investigated
skin barrier recovery among 72 healthy adults who com-
pleted relationship-building tasks and subsequent tape strip-
ping in pairs or alone.53 The ‘social closeness’ pair had
significantly more rapid skin barrier recovery than those who
underwent tape stripping alone, suggesting that social close-
ness during unfamiliar experiences may positively influence
skin barrier recovery.
Marital stress
Women undergoing marital separation had a similar barrier
disruption threshold to ‘happy’ age-matched controls, but
those who reported higher marital stress levels had signifi-
cantly longer TEWL recovery times.54 Couples therapy resulted
in clear differences in skin barrier recovery between men and
women. While greater attachment anxiety predicted signifi-
cantly faster skin barrier recovery among women, discussion
of attachment avoidance, such as comfortability with closeness
and intimacy, predicted slower skin barrier recovery. Con-
versely, skin barrier recovery in men was significantly slower
following discussion of attachment anxiety.55 While it is clear
that individuals respond to stressors uniquely, there appear to
be clear associations between stress-induced epidermal barrier
dysfunction and individual trait characteristics. Thus, tailored
and individualized stress support may be needed for optimal
cutaneous health among different cohorts.
Self-perceived personality traits
Despite studies reporting correlations between stress or unhap-
piness and epidermal barrier function changes, Benham argues
that skin barrier recovery is not associated with the Perceived
Stress Scale.56,57 In a case–control study utilizing a behavioural
survey, self-perceived stress did not significantly correlate with
skin barrier recovery among high-stress and low-stress
© 2019 British Association of Dermatologists

women.57 Although stress is an inherently subjective measure,
the self-reported stress described in that study may be limited
by recall bias.
Positive affect is defined as the feelings that reflect a plea-
surable interaction with the environment, while negative affect
is defined as feelings that do not align with an agreeable situa-
tion. Such trait positivity or negativity defines the social
notion of personality traits.58 While it is impossible to com-
pare one individual’s subjective happiness with another’s, vol-
unteers with greater self-reported trait-positive affect had
significantly faster skin barrier recovery following a Trier
Social Stress Test and tape stripping than those with negative
affect.59 Such findings support trait-positive influence on skin
health as it affects other health outcomes, such as longevity,
decreased morbidity and the experience of pain.60 This may
be due to the likely health-promoting character of positive
affect-rich persons.
Stress reduction
Most research focuses on the impact of stressors on epidermal
barrier function, but few have examined the effect of stress-
reversal techniques to reduce cutaneous dysfunction. Because
stress is an inherent component of the human experience, and
prevention may not always be practical, it may be useful to
explore other stress-relieving modalities. Mindfulness and
meditation-based stress reduction have been shown to relieve
dermatological lesions.3 While stress reduction associated with
massage improves atopic dermatitis,61,62 the direct prophylac-
tic role in epidermal barrier function remains to be elucidated.
However, with the proven efficacy of relaxation and medita-
tion on reduction of dermatological conditions in mind,3 mul-
tiple investigators have evaluated the role of relaxation
modalities on repairing epidermal barrier function.
Guided relaxation maintains prophylactic and reparative
roles in epidermal barrier function recovery.63 Furthermore,
aromatherapy reduces sebum oxyhaemoglobin in the right
prefrontal cortex64 and stress-induced serum and salivary cor-
tisol response, and increases TEWL65 and skin barrier recov-
ery66 in both animal models and humans. While
aromatherapy is a popular stress-reducing experience67 to
repair epidermal barrier function,65 there have been multiple
reports of aerosolized oils exacerbating itch and contact der-
matitis.29,68 The potential of essential oils to induce airborne
dermatitis resulting in barrier disruption should be closely
scrutinized for its use in susceptible individuals who already
have an altered cutaneous barrier.
Stress reduction and subsequent improvement of skin bar-
rier recovery can result from persons who provide social sup-
port,53,55 which should encourage the role of support groups
among at-risk patients. Relationships with supportive involve-
ment are central to human life, and have a strong influence
on health. Additionally, strategic use of antidepressants can
improve skin conditions associated with barrier defects, such
as psoriasis, that have a profound effect on anxiety and
depression.69
© 2019 British Association of Dermatologists
Impact of stress on epidermal barrier function, M. Maarouf et al. 7
Discussion
Abundant evidence supports the adverse effects of stress on
epidermal barrier function, particularly among at-risk atopic,70
chronically ill and elderly populations with pre-existing aber-
rant, dry, itchy or fragile skin. Some of the data reviewed
herein examined mouse models of stress, which may not
accurately reflect events found in everyday human experience.
Conversely, in some cases, mouse studies are more controlled
than human studies due to an absence of variation in stressors
between individuals. For instance, crowding scenarios often
correspond to low socioeconomic status, which imparts addi-
tional stressors such as low nutritional value and less trait-
positive health promotion. Thus, a true challenge facing the
research community will be the investigation of psychological
stress in human models. Furthermore, there is inherent diffi-
culty with people reporting, quantifying and qualifying their
stress. Despite the presence of validated stress evaluation tools
such as the Stress Scale Score,56 human studies present recall
bias and subjectivity in the nature of qualifying stress.
The neurocutaneous axis, which mediates barrier dysfunc-
tion in chronic dermatoses, is not completely understood.
Future studies should explore parallel stress-mediating HPA
pathways and identify counterpathways that repair the aber-
rant skin barrier in atopic dermatitis, psoriasis, seborrhoeic
dermatitis, rosacea and acne. Attempts should be made to
study human volunteers under more realistic rather than simu-
lated stress conditions to evaluate better the true effect of psy-
chological stress on epidermal barrier function. Additionally,
identification of both fixed and modifiable psychological stress
triggers may reveal practical interventions for barrier healing.
Acknowledgments
We are grateful to Aleksi J. Hendricks for her critical review
of the manuscript.
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Supporting Information
Additional Supporting Information may be found in the online
version of this article at the publisher’s website:
Table S1 Summary of stress-induced skin changes.
British Journal of Dermatology (2019)