363 Sensitive Skin Syndrome
populations around the world to evaluate the prevalence of SSS in the general population.5
Chen et al.’s meta-analysis—representing 18 countries and a total of 51,783 individuals—
showed around 71% of people self-reported SSS.6
Sensitive skin can impact all anatomic sites, including the face, scalp, and genital area.5,7
This can have a significant impact on an individual’s everyday social routine life. Often, the
individual must cope with other dermatologic disorders in addition to the SSS symptoms. An
individual with SSS must identify and avoid a wide variety of factors that can trigger their
symptoms. In turn, the manifestation of SSS symptoms can trigger psychological effects.
BIOPHYSIOLOGICAL CONTRIBUTORS OF SSS
Several physiological differences have been identified in individuals with SSS (Table I).
The epidermal layer of the skin in individuals with SSS has reduced barrier integrity due
to differences in lipid composition, with a decrease in ceramide and sphingolipid content.8
This results in increasing the potential penetration of irritants and insufficient protection of
nerve endings.5,8–10 Increased vascular reactivity has been observed in individuals with SSS,
resulting in more intense vascular reactions to irritants.11 Roussaki–Schulze and colleagues
reported that vascular reactions to methyl nicotinate in subjects with SSS was 75 times
higher compared with nonsensitive controls.12
Neurosensory dysfunction is another physiological element that contributes to SSS. Biopsies
from subjects with SSS demonstrated a decrease of peptidergic C-fiber density.14 These fibers
are involved in pain, itching, and temperature perception. Degeneration of these fibers
can induce hyper-reactivity of the remaining nerve endings, resulting in allodynia.11 An
additional neurosensory component is an increase in TRPV1. This is a nonselective cation
channel that responds to heat and low pH, and it is related to nociception, neurogenic
inflammation, and pruritus. TRPV-1 is also classically known as the capsaicin receptor.15,16
Based on self-reported SSS skin biopsies, Ehnis-Pérez et al. found TRPV1 is dramatically
upregulated in subjects with sensitive skin.15
Another important factor for individuals with SSS is that they may also suffer from other
comorbidities and/or additional disorders (Table II). Just like SSS, rosacea is more common
in individuals who are female with fair skin and hair, blue eyes, and lighter skin—that is,
Table I
Some Physiological Elements Contributing to SSS
Epidermal
5,8–10 Reduced barrier integrity
Decrease in ceramide and sphingolipid
Increased penetration of potential irritants
Decreased protection of nerve endings
Vascular
12,13 Increase in vascular activity
Intense vascular reaction to methyl nicotinate
Greater reactions to standard allergens
Lower alkali resistance
Neurosensorial
11,14–16 Decrease of intraepidermal nerve fiber density
Reduced peptidergic C-fiber density
Increase in transient receptor potential vanilloid-1 (TRPV1)

364 JOURNAL OF COSMETIC SCIENCE
phototypes I–III.17 In a genome-wide association study involving 22,952 subjects, Chang
and colleagues determined that rosacea is associated with several HLA alleles.18 This is in
line with the inflammatory nature of the syndrome. In a study involving 1,000 individuals
in Korea, 56.8% of whom had sensitive or very sensitive skin, Kim and colleagues found
that the group with SSS was more than 3 times more likely to suffer from acne, atopic
dermatitis, and facial blushing, and they were over 2 times more likely to suffer from
seborrheic dermatitis compared with the nonsensitive group.19 Brenaut and colleagues
found a similar result in an Indian population.20 In a study involving more than 3,000
individuals, subjects with SSS were 2–4 times more likely to report atopic dermatitis, acne,
psoriasis, vitiligo, rosacea, or contact dermatitis compared with the nonsensitive group.20
Sensitive skin has also been linked to sensitive eyes and eyelids, along with irritable bowel
syndrome.26,27 It is proposed that these conditions may be related to the neurosensory
dysfunctions identified in SSS (i.e., hyperexcitability of nerve endings, hyperactivation of
sensor proteins resulting from upregulation of TRP channels, and alterations in nerve fiber
density).26 The histological findings and clinical signs of small-fiber impairment with SSS
are similar to those experienced in small-fiber neuropathy.28
As part of a genome-wide association study, Farage et al. evaluated 23,426 subjects’ responses
and found that individuals with SSS reported other skin complaints—specifically, contact
dermatitis, freckles, atopic dermatitis, acne, and seborrheic dermatitis.25 These authors
found a connection between SSS and several specific loci also associated with genes for
rosacea, pigmentation, and skin cancer.25
OTHER HOST-RELATED FACTORS: AGING AND HORMONAL FLUCTUATIONS
Aging can be another physiologic factor in sensitive skin. As an individual ages, the skin
changes as it becomes thinner and drier, and it replaces itself at a slower rate.29 The elderly
skin is also more prone to higher permeability but a reduced elasticity, tensile strength,
vascularization, and cellularity.29 These physiological changes might lead one to conclude
that older skin is more susceptible to irritant effects and more likely to be sensitive. However,
clinical assessments using known irritant materials suggest that skin irritation susceptibility
generally decreases with age, as does the capacity to produce visible physiological signs of
dermatological irritation.9,29–32 Several studies have shown that the prevalence of SSS in older
Table II
Some Skin Comorbidities Associated with SSS
Comorbidity condition
Rosacea17,20,21
Acne19,20
Atopic dermatitis (eczema)5,19,20
Atopic22–24
Blushing19
Seborrheic dermatitis (dandruff)19,20,25
Psoriasis20
Vitiligo20
Contact dermatitis25
Freckles25
Sensitivity of the corneas and eyelids26
Irritable bowel syndrome26