BJD

R E V I E W A RT I C L E British Journal of Dermatology

Epidemiology of acne vulgaris

K. Bhate and H.C. Williams
Centre of Evidence Based Dermatology, University of Nottingham, Room A103, King’s Meadow Campus, Lenton Lane, Nottingham NG7 2NR, U.K.

Summary

Correspondence Despite acne being an almost universal condition in younger people, relatively
Ketaki Bhate. little is known about its epidemiology. We sought to review what is known
E-mail: ketaki.bhate@nottingham.ac.uk about the distribution and causes of acne by conducting a systematic review of
relevant epidemiological studies. We searched Medline and Embase to the end
Accepted for publication
31 October 2012 of November 2011. The role of Propionibacterium acnes in pathogenesis is unclear:
antibiotics have a direct antimicrobial as well as an anti-inflammatory effect.
Funding sources Moderate-to-severe acne affects around 20% of young people and severity corre-
None. lates with pubertal maturity. Acne may be presenting at a younger age because
of earlier puberty. It is unclear if ethnicity is truly associated with acne. Black
Conflicts of interest
individuals are more prone to postinflammatory hyperpigmentation and specific
None declared.
subtypes such as ‘pomade acne’. Acne persists into the 20s and 30s in around
DOI 10.1111/bjd.12149 64% and 43% of individuals, respectively. The heritability of acne is almost
80% in first-degree relatives. Acne occurs earlier and is more severe in those
with a positive family history. Suicidal ideation is more common in those
with severe compared with mild acne. In the U.S.A., the cost of acne is over
3 billion dollars per year in terms of treatment and loss of productivity. A
systematic review in 2005 found no clear evidence of dietary components
increasing acne risk. One small randomized controlled trial showed that low
glycaemic index (GI) diets can lower acne severity. A possible association
between dairy food intake and acne requires closer scrutiny. Natural sunlight or
poor hygiene are not associated. The association between smoking and acne is
probably due to confounding. Validated core outcomes in future studies will
help in combining future evidence.

The clinical and histological features of acne, a chronic inflam-
matory disease of the pilosebaceous unit, are well described.1
Acne lesions are typically classified as noninflammatory (open
and closed comedones) or inflammatory (papules and pus-
tules). Seborrhoea, or grease production, is also a feature.2
Scarring is often present following inflammation3 as illustrated
in Figure 1. The pathophysiological events occurring in acne
are also relatively well studied. Lesions start when keratino-
cytes lining the hair follicle desquamate creating a microcome-
done. At puberty increased sebum production creates an
environment that can sustain the colonization of Propionibacteri-
um acnes. As P. acnes proliferates, inflammatory and chemotactic
mediators are produced, which in turn drive inflammatory
processes.4
Despite advances in understanding the pathophysiology of
acne, much less appears to have been written about its epide-
miology, which is strange considering that acne is almost
universal in teenage years. Epidemiology not only describes
the burden of disease in terms of incidence, prevalence and
variations according to age, sex, social class, ethnic group and
geography, but also has the potential to identify specific risk
factors for disease occurrence or progression, which may be
amenable to manipulation. Discovery of risk factors or factors
that exacerbate existing disease could lead to appropriate pri-
mary or secondary preventative measures and treatments,
which in turn could lead to population benefits in terms of
health and reduced expenditure on relatively ineffective treat-
ments. Epidemiology is also concerned with natural history
and progression.5,6
This article seeks to provide a comprehensive review on the
epidemiology of acne vulgaris. The epidemiology of other
forms of acne – acne rosacea, infantile acne and acne inversa
(hidradenitis suppurativa) – are not discussed in this review.7–9
We begin with an overview of the descriptive epidemiology
of acne vulgaris including incidence, prevalence, severity,
morbidity, economics and financial implications, demograph-
ics and natural history. We then move on to possible causative
factors, which in turn lead into possible prevention strategies.

 2012 The Authors

474 BJD  2012 British Association of Dermatologists 2013 168, pp474–485

Fig 1. Moderate inflammatory acne accompanied by scarring.
Search methods
We searched the Medline database (in process and other non-
indexed citations and Ovid Medline 1946–present) and Em-
base from 1974 until the end of November 2011.
Additionally, NHS evidence, a collection of filtered resources
for the U.K. National Health Service, was searched. Our search
strategy involved several separate searches for each section,
combining the terms acne vulgaris with: epidemiology, aetiol-
ogy, cause, prevalence, incidence, cost, pharmacoeconomics,
socioeconomic, social, natural history, race, ethnicity, morbid-
ity, quality of life, geography, family size, severity, excoria-
tion, obesity, overweight, pathogenesis, washing, sweat,
cleanse, sun, sunlight, light, diet, dairy, milk, glycaemic ⁄gly-
cemic index (GI), GI, high GI, chocolate, hygiene, smoking,
prevention, climate, environment, infection, Propionibacterium ac-
nes, stress, picking, chloracne, drugs and medicine. The func-
tion of truncation in the Ovid search engine to expand upon
suffixes was employed. In order to make the search as wide as
possible, additional limits such as study type were not applied.
There were no prespecified criteria for study inclusion or
exclusion and there was no time limit to which studies
included in this review dated back to. Additional articles were
identified from citations retrieved from electronic biblio-
graphic searching. Our aim was to provide a review that cov-
ered all aspects of what could be considered as acne
epidemiology in one succinct article. We did not prespecify
any particular study type given the wide scope of this review.
Although we comment on the quality of evidence for key in-
dividual studies, we did not undertake any formal grading of
the quality of evidence given the large diversity of study types.
 2012 The Authors
BJD  2012 British Association of Dermatologists 2013 168, pp474–485
Epidemiology of acne vulgaris, K. Bhate and H.C. Williams 475
Similarly, we did not attempt any meta-analysis given the vari-
ation in study design and outcomes, although we have
attempted to provide summative descriptive comments for
each aspect of the field. Meta-analysis was also compromised
by the high degree of variability in the outcome measures
employed by our included studies, including photonumeric
scores, lesion counts and patient-assessed scores, many of
which have not been tested for reliability or validity as has
been highlighted elsewhere.10
How common is acne?
A degree of acne affects nearly all people between the ages of
15 and 17 years11–13 and in 15–20% of young people, acne is
moderate to severe.11,14,15 Prevalence rates of acne by age16
and 1996 census data estimated that 40–50 million U.S. indi-
viduals have acne, with an 85% prevalence rate in those aged
12–24 years.17 A study by Lucky et al.18 found that the sever-
ity of acne in boys correlated with pubertal maturation and
that 50% of 10- and 11-year-old boys had more than 10 com-
edones. Another study by the same team showed that 78% of
girls between aged 8 and 12 years had acne.19 Of note, the
severity of acne increased with advancing maturity and prepu-
bertal girls with severe acne had notably higher dehydroepi-
androsterone sulphate levels.18,19 Acne consistently represents
the top three most prevalent skin conditions in the general
population as found in large studies in the U.K., France and
the U.S.A.20–22
How long does acne last?
Acne begins in the early teens with the onset of facial sebum
production and facial comedones followed by inflammatory le-
sions.14,23 Acne can occur in prepubertal children but this is
usually noninflammatory in nature as children have not yet
begun production of sebum, which provides the correct envi-
ronment to host P. acnes.24 Around 20% of neonates have an
acneiform eruption but this usually resolves by 3 months.25
One Danish study has shown that the average age at onset of
puberty in boys has dropped from 11Æ92 to 11Æ66 years over a
15-year period.26 Friedlander et al.24 postulated that this youn-
ger age of puberty was the reason for the observation that
younger patients between the ages of 8 and 11 were present-
ing with acne in their clinics. Acne is a chronic disease and
can persist, in some cases, into adulthood,27–29 for unclear rea-
sons.30 A German population study found 64% of those aged
20–29 years and 43% of those between 30 and 39 years had
visible acne31 and another study of 2000 adults found that 3%
of men and 5% of women still had a degree of acne between
the ages of 40 and 49.32 Sequential prevalence studies showing
that acne decreases with age are not as strong as cohort studies
that document natural history of acne over time in the same
individuals. Self-reported acne studies are unreliable.33 We
found few high-quality cohort studies of acne, which may be
because studies of this nature are often difficult to conduct par-
ticularly due to the widespread availability of acne therapy.
476 Epidemiology of acne vulgaris, K. Bhate and H.C. Williams
Additionally, the definition of acne and its severity has varied
so much over time that it is difficult to compare and collate
the results of different studies. A validated and universal out-
come measure needs to be employed for future studies.10 Pre-
dictors of acne severity include family members with acne and
the early onset of comedonal acne.14,34 Longitudinal studies in
the natural history of acne are required, in particular with a
view to identifying risk factors for severe disease. It is
unknown whether or not prepubertal treatment can alter P.
acnes colonization and therefore subsequent inflammatory acne.
Acne vulgaris and its association with self-consciousness,
anxiety in social interaction, dissatisfaction with appearance
and overall impaired quality of life is well reported.11,35,36 A
recent review of studies by Dunn et al.37 concluded that acne
can negatively affect quality of life, self-esteem and mood,
and increase the risk of anxiety, depression and suicidal idea-
tion. Female subjects score worse than males in the Dermatol-
ogy Life Quality Index and acne quality of life self-assessment
score, and impact upon quality of life is associated with
longer acne duration.38–40 Depression and anxiety are often
seen more in female subjects.40–43 The media’s portrayal of
flawless skin as an ideal is in part a culprit of psychological
morbidity in females.44 Halvorsen et al.45 in a well-conducted
questionnaire-based cross-sectional survey found suicidal idea-
tion and substantial acne to have a threefold increase com-
pared with mild acne in male subjects. Magin et al.46 on the
other hand, in a prospective cohort study in 244 subjects,
found no correlation between acne and acne severity and psy-
chological or psychiatric morbidity, although the study would
have benefited from longer follow-up. An association with
low attachment to friends and not thriving at school has also
been noted.45 Quality of life does not always correlate with
acne severity,47,48 although some surveys have noted a correl-
ation.49,50 The presence of acne lowers the perception of over-
all health,51 and teasing and bullying is also a significant cause
of morbidity.52
Socioeconomic impact
A large cohort study in Canada found that those of low socio-
economic background were referred less to dermatologists
than those of a higher socioeconomic background and, add-
itionally, those in rural areas were referred less than those
based in urban areas.53 Interestingly, a cross-sectional study
from Saudi Arabia found acne to be more prevalent in high
socioeconomic classes.54 A Texan study of adolescents with a
low socioeconomic background found those with acne
reported lower self-esteem.55 Studies have shown that patients
with acne have a higher rate of unemployment than matched
controls.56 In the U.S.A., over 3 billion dollars per year is lost
in the direct and indirect costs of treatment and loss of pro-
ductivity.57 The presence of acne has been reported to have a
negative effect upon work ⁄school performance.58 Unemploy-
ment rates were compared in 625 patients with acne and 625
controls and were higher in the group of patients with acne,
although social status and academic background were not con-
BJD  2012 British Association of Dermatologists 2013 168, pp474–485
sidered in this study.56 Anger can also be associated with
skin-related quality of life59 as well as emotional and behavio-
ural difficulties.60 Such psychosocial effects must be consid-
ered by the healthcare professional treating a patient with
acne. Although there is no definitive study on the socioeco-
nomics of acne, it is likely, given data in the literature so far,
that acne does have a significant impact upon the socioeco-
nomic potential of populations.
Genetics
The risk factors and genes associated with acne prognosis
remain unclear.61 A large study of Chinese undergraduates
found acne to have a 78% heritability in first-degree rela-
tives15 and other population-based studies have concurred.34
Acne occurs earlier and is more severe in those with a positive
family history.34,61 Several retrospective twin studies have
found a possible genetic basis with familial clustering.62–66
More recently, a prospective twin study comparing monozy-
gotic and dizygotic twins found that acne severity was geneti-
cally determined, although the low power of the study could
not rule out the influence of additional environmental fac-
tors.67 Twin studies in acne are summarized in Table 1 and
highlight the need for a further large, twin-based prospective
study and subsequent further molecular genetic analyses.
Ethnicity
Frequency in different ethnic groups
In 1908, Fox68 reported that 7Æ4% (163 ⁄2200) of caucasian
patients and 4Æ6% (101 ⁄2200) of black patients had acne vul-
garis. Hazen69 in 1914 found a similar frequency of acne in
2000 outpatient visits of black patients when compared with
2000 caucasian patients (8Æ4% and 9%, respectively). Such
clinic-based studies are not a good method of making infer-
ences about population characteristics as the estimates could
reflect selection bias in those attending or differences in diag-
nostic perception.
Conversely, Cheng et al.70 found that on a scale of ‘never’,
‘rarely’, ‘sometimes’, ‘often’ and ‘always’, white individuals
have an increased risk of developing acne frequency compared
with nonwhites, particularly black subjects (n = 1214). Given
this was a questionnaire-based study it is also susceptible to
selection bias. There have been many other similar studies,
some finding acne between black and white individuals to be
similar in prevalence ⁄incidence and others finding a slight dis-
crepancy. There are relatively few comparative surveys
between ethnic groups, studies in the literature tending to
conclude that acne is one of the more common skin condi-
tions in the ethnic group under review.71,72 Freyre et al.73
conducted a cross-sectional study in Peru of 2214 subjects
aged between 12 and 18 years who were either Mestizo,
Indian or white. They found the prevalence of acne in Indians
was significantly less (27Æ97%) than in Mestizos (43Æ08%) or
whites (44Æ47%). Again, there is an element of selection bias
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 Table 1 Twin studies in acne vulgaris

 2012 The Authors

Study Design Participants Sample size Main findings Limitations
66
Niermann Retrospective 115 twin pairs studied. 6 twin pairs had acne, 2 There is a genetic component to acne Incomplete reporting. Unclear where
case-note Unclear male to female ratio were monozygotic and the conclusions come from in the
analysis 4 were dizygotic results
Friedman63 Retrospective 63% of the twins female, 930 pairs of twins: 342 19% of twins had diagnosis of acne. Ratio Incomplete reporting and limited
case-note 37% male monozygotic, 345 of observed to expected: 4 in monozygotic discussion. Retrospective
analysis dizygotic, 243 unknown males, 2Æ3 in dizygotic males, 4Æ2 in
zygosity monozygotic females, 1Æ7 in dizygotic
females
Walton Measurement Identical twins: 5 male, 40 pairs of twins: The incidence of acne in nonidentical and No mention of antiacne therapy.
et al.64 of serum 15 female. Nonidentical 20 identical, identical twin groups was similar – 16 ⁄ 20 Small sample size. Unblinded
excretion same sex twins: 12 male, 20 nonidentical in each group. Identical twins had the assessment. Reporting of methods
and acne 8 female. Age 12–18 years (?mono and same rates of sebum excretion but limited. Results open to
grades dizygotic) different degrees of acne severity; misinterpretation
nonidentical twins had different rates of
sebum excretion and acne grades. Authors

BJD  2012 British Association of Dermatologists 2013 168, pp474–485

suggested sebum excretion is under genetic
control and the development of clinical
lesions is modified by environment
Sobral-Filho Prospective Random sample of 347 twin 200 pairs, Concordance: 98% in monozygotic and Unblinded assessment. Does not
et al.65 transverse births registered at selected monozygotic and 55% in dizygotic. Inheritance 95%.a measure any environmental factors
study (‘main’) obstetric hospitals. dizygotic Prevalence of family history was associated (including diet or therapy) that are
200 pairs randomly with severity of acne likely to be shared by twins at
selected: 52% female, 60% those ages
monozygotic, 40%
dizygotic. Age 14–26 years
Bataille Cross-sectional All women. With and 458 monozygotic 81% of acne variation attributed to genetic Of retrospective design
et al.62 without acne vulgaris twins, 1099 factors
dizygotic twins
Evans et al.67 Prospective ⁄ Women and men. Unclear if 778 twin pairs. Genetic factors explained significant Environmental factors such as
longitudinal they had pre-existing acne Unclear proportions proportions of acne variance contributing antiacne medication not taken
of monozygotic to 31–97% of phenotypic appearance into account
vs. dizygotic
a
Inheritance = agreement in monozygotic – agreement in dizygotic ⁄ 1 – agreement in dizygotic.
Epidemiology of acne vulgaris, K. Bhate and H.C. Williams 477
478 Epidemiology of acne vulgaris, K. Bhate and H.C. Williams
in this study as the recruited schools were selected based on
large size and, in addition, there was only one single assessor.
Recently, a population-based, self-reported, cross-sectional
survey of 2895 people found the prevalence of acne to be
greater in African-Americans and Hispanics than in caucasians,
Asians and continental Indians.74 Limitation of recruitment to
female subjects only and to four cities makes interpretation of
these results difficult. Regardless, acne is seen as the most
common dermatological diagnosis in both black and white
subjects,75,76 and the current consensus with regard to man-
agement is that there is no difference between them.77
Pathophysiology in different ethnic groups
It is unclear whether, if there are any ethnic group differ-
ences, they can be explained by differences in pathophysi-
ology. A small case series of 60 women found a greater
density of P. acnes in black-skinned individuals.78 Studies into
sebaceous gland size and activity between black and white
subjects have been too small to be conclusive and several stud-
ies have been contradictory in terms of the conclusions drawn
from their results.79–81 Sebum production increases during
puberty and the onset of puberty is earlier in black individu-
als.18,82 Most studies to date have focused on caucasian and
black skin types and there are no such studies to our knowl-
edge in Asian or Hispanic patients for comparison.83
Special problems associated with specific ethnic groups
Postinflammatory hyperpigmentation or hyperpigmented ma-
cules are a common finding in darker skin types, which may be
due to the presence of polymorphonuclear cell infiltrates even
in noninflammatory lesions, for example, comedones.84,85
Keloid scarring is seen less frequently than hyperpigmentation
but is nonetheless a serious consequence of acne in darker
skin.77 The incidence of nodulocystic acne may be lower in
African-Americans compared with caucasians and Hispanics.77
There are specific subtypes of acne that have been described
in the literature, for example, pomade acne which is seen in
African-Americans. Pomade acne occurs at the hairline second-
ary to the use of pomade (containing high-melting hydrocar-
bons) and other hair products and consists of comedones and
small papules. Similarly, steroid acne can be caused by some
skin-lightening agents containing potent topical corticosteroids
used to lighten the skin or improve hyperpigmentation.77,83,86
Diet
Historically, dietary advice was commonplace as part of acne
therapy. Because early studies hinted that patients with acne
had impaired glucose tolerance and altered carbohydrate
metabolism, patients were advised to avoid excessive carbohy-
drate and sugary foods.87,88
In 1971 Anderson studied 27 students who consumed a
high-carbohydrate diet and found there were no flares in acne
over the study period. The lack of a control group and small
BJD  2012 British Association of Dermatologists 2013 168, pp474–485
sample size limits our interpretation of results.89 Nonetheless,
these findings, along with another study suggesting that high
chocolate intake does not worsen acne,90 resulted in quashing
the notion that diet was involved in acne pathogenesis and
was consequently removed from major textbooks of that time.
A concise systematic review by Magin et al.91 in 2005 of
seven studies, including one randomized controlled trial, con-
cluded that there was no clear, positive evidence that any die-
tary components increase acne risk.
The roles of iodine, vitamin A, antioxidants, omega-3 fatty
acids and fibre are not clear. Of note, however, there is some
evidence of benefit with high doses of oral zinc from double-
blind, randomized controlled trials.92,93
Care must be taken to separate those studies which evaluate
foods as a possible cause of acne occurrence as opposed to
foods which could influence severity or disease flares, as they
may not necessarily be the same. It is also important not to
discard dietary hypotheses in acne on the basis of absent or
poor evidence. Three dietary factors, chocolate, a high-GI diet
and dairy products are worthy of further discussion.
Glycaemic index
The GI quantifies the effect of ingested carbohydrates on blood
glucose levels and is calculated by a 2-h blood glucose
response curve after a 50-g carbohydrate load in 10 subjects.94
Glycaemic load is a function of the GI and portion size relating
to carbohydrates.95 The absence of acne in native non-West-
ernized people in Papua New Guinea and Paraguay have led to
the proposal that high glycaemic loads in the Western diet
could have a role in acne.96 Conversely, a questionnaire and
biochemical study found no significant differences in serum
glucose, insulin, leptin, GI or glycaemic load between patients
with acne and controls.97 In a single-blind, randomized con-
trolled trial of 43 men in which acne lesion counts and severity
were assessed monthly over a 12-week period, total lesion
counts decreased more in those on a low-glycaemic-load diet
compared with a control group who had consumed carbo-
hydrate-dense foods. Associated factors such as the weight loss
of participants and the fats and protein consumed needed fur-
ther delineation to establish what factors might have caused
the decreased lesion count, or if it was a combination of vari-
ous factors.98 As sebum is stimulated by androgens, a possible
mechanism for an association between a high-GI diet and acne
is that the hyperinsulinaemic state leads to increased androgen
along with insulin-like growth factor (IGF)-1 and altered reti-
noid signalling.95,99,100 This is an area worthy of further larger
trials with blinded outcome assessment.
Dairy
Robinson101 first described a possible role of dairy produce in
worsening acne after he studied the food diaries of 1925
patients. In 2005 Adebamowo et al.102, using a validated food
frequency questionnaire of over 47 000 women, found a
positive association between a history of acne and the intake
 2012 The Authors
 Epidemiology of acne vulgaris, K. Bhate and H.C. Williams 479

of skimmed milk. This study was, however, flawed because of

a high risk of recall bias and because confounding factors
were not fully taken into account. The same group then
undertook a 3-year prospective study of over 6000 girls aged
between 9 and 15 years. This study found a positive associa-
tion between the prevalence of acne and the consumption of
full-fat, skimmed and low-fat milk and no association with
nonmilk dairy foods, chocolate, pizza and French fries.103 It is
difficult to ascertain if milk was associated with the occurrence
of acne or whether it was associated with increased acne
severity. A similar study in boys found only a weak association
with skimmed milk and no association with milks of a higher
fat content.104 Again, the exact onset of acne was unknown.
All of the studies by Adebamowo et al. were limited because
acne occurrence was based on questionnaires rather than
blinded objective measurements. Additionally, the GI (a mea-
sure of carbohydrate on blood glucose over time) of skimmed
or nonfat milk is 4 and that of full-fat milk is 3,105 i.e. it may
be that the association could be explained by glycaemic load
rather than fat or dairy content per se. Another possibility is
that hormones such as the 5-a-reduced steroids, a-lactalbu-
min, testosterone precursors and IGF-1 (which stimulate the
synthesis of androgens) may still be present after the milk is
processed and the fat removed thereby going on to contribute
to acne pathogenesis.106–109 IGF-1 has been positively corre-
lated with acne.97 The evidence suggesting an association
between dairy food intake and acne is currently weak and
needs to be tested in an experimental fashion.
Chocolate
There is a well-recognized belief that chocolate causes or exac-
erbates acne, particularly among adolescents.110,111 There is,
however, limited evidence backing up such a claim. Two very
small earlier studies had such methodological shortcomings
that it was difficult to draw any conclusions89,112 (Table 2). In
1975 a single-blind, placebo-controlled, crossover trial in 65
male prisoners found there to be no difference in acne severity
between a chocolate-eating group and a chocolate-abstinent
group. This study also had major methodological flaws: meth-
ods of randomization were not described and blinding was
only partly described, and there was a high risk of bias as there
was no intention-to-treat analysis performed.89 More recently,
a small, nonrandomized, uncontrolled study of 10 people
found a significant increase in acneiform lesions upon con-
sumption of chocolate made up of 100% cocoa.113 The ques-
tion of whether chocolate worsens acne therefore remains
unanswered and there is much controversy and speculation
especially among adolescents who frequently turn to doctors
for advice. Such paucity of evidence highlights a clear need for
a well-designed, blinded, randomized, provocation trial.
Sunlight
Various authors have debated whether ultraviolet radiation or
visible light worsens, improves or has no effect upon acne
vulgaris. A systematic review of seven studies found no

Table 2 Interventional studies on chocolate and its effect upon acne

Sample
Study Design Participants size Main findings Limitations
Grant and Uncontrolled University 8 4 of 8 developed 5 new acne Small sample size. Uncontrolled.
Anderson112 provocation students. Mild lesions. Authors claimed not Incomplete reporting of
study to moderate significant but no statistics methods. Possibly too short
acne shown a follow-up time
Anderson89 Uncontrolled University Unknown One-third developed new Uncontrolled. No quantitative
provocation students with lesions having been given data, no statistics. Length of
study acne who six 39-g chocolate bars per follow-up not specified.
claimed that day for 1 week; milk, Follow-up duration may be
certain food peanuts and coca cola inadequate
exacerbated were also being tested
their acne
Fulton et al.90 Single blind, Male prisoners 65 No difference in acne Blinding and randomization
placebo- severity between the two methods not completely
controlled groups described, no intention-to-treat
crossover, analysis, just one observation in
randomized 4 weeks, the test period may
have been too long – could
tolerance have developed? The
high fat content of the placebo
bar may be acnegenic
Berman et al.113 Interventional, Men 10 Significant increase in the Small sample size. Uncontrolled,
uncontrolled. number of acne lesions no placebo group
100% chocolate on days 4 and 7
consumed

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BJD  2012 British Association of Dermatologists 2013 168, pp474–485
480 Epidemiology of acne vulgaris, K. Bhate and H.C. Williams
convincing evidence that natural sunlight improves acne.91
The manipulation of the electromagnetic spectrum into thera-
peutic benefit, however, has flooded the literature. A Cochrane
systematic review of clinical trials of light therapy published
up to 2008 found evidence for some benefit of light therapy,
in the short term at least, and therapy with blue, blue ⁄red or
infrared is of more benefit than yellow, red or green light.
Sample sizes were often small and of variable quality.114 The
increasing use of photodynamic therapy is also reported in tri-
als, again of variable quality, and while the short-term effects
are good they are limited by possible adverse effects.115 There
is limited evidence of natural sunlight and its effect upon acne
and this may be a result of such studies inherently being diffi-
cult to conduct. The use of light-based therapies may signify
evidence of sunlight being beneficial to acne sufferers, but the
risk of the development of skin cancers must be taken into
account and therefore care should be taken in advising thera-
peutic sun exposure.116
Hygiene
There is a common perception that poor levels of hygiene lead
to the development or exacerbation of acne vulgaris.117,118 A
comprehensive systematic review of 11 studies in 2005 con-
cluded that there is insufficient evidence that acne is caused
by, cured or exacerbated by washing,91 and there have been
no studies to our knowledge comparing no washing with
washing in patients with acne. Earlier observations of a possi-
ble comedogenic effect of soaps on rabbit ear were not repli-
cated in humans.119 An unblinded, randomized controlled
trial of 120 patients with acne reported less inflammatory
lesions in those using acidic soaps than those using alkaline
soaps.120 There is some evidence to suggest that medicated
washes may help acne, but the evidence is weak: one, uncon-
trolled study of 10 patients and another crossover trial of 41
patients which did not report methods of randomization or
assessment.121,122 More recently, a single-blind, randomized
controlled trial comparing washing the face with a mild
unmedicated cleanser once a day, twice a day and four times
a day found there was a statistically significant improvement
in lesion count in the twice-daily group with no worsening in
the four times-daily group.123 Some have suggested that sweat
can trigger or exacerbate acne;41 however, a single-blind, ran-
domized pilot study found no association between exercise-
induced sweat and truncal acne.124 The evidence does not
provide clear advice for or against washing as a means of
helping acne, and there is certainly no robust evidence that
acne is caused or propelled by a lack of hygiene.
Smoking
Whether or not acne is caused by, exacerbated, improved,
cured, or is not associated with smoking remains controver-
sial.31,125–130 An earlier case series suggested an inverse rela-
tionship between acne and smoking, suggesting an anti-
inflammatory effect of a component found in cigarettes.125
BJD  2012 British Association of Dermatologists 2013 168, pp474–485
Later, in 2001, a larger cross-sectional analysis of 896 young
people found a statistically significant correlation between acne
prevalence and the number of cigarettes smoked per day and
a dose-dependent relationship between consumption and
severity (not affected by age, sex or social class).31 A large-
scale, questionnaire study of 27 083 military men between
1983 and 2003 found the prevalence of acne to be lower in
active smokers, with a dose-dependent inverse relationship
between severe acne prevalence and cigarette consumption
from 21 cigarettes per day and higher.131 Although it is possi-
ble that smoking could ameliorate acne, further experimental
research in this area is unethical due to the harmful effects of
smoking. Further observational research is likely to perpetuate
previous problems in reporting bias and confounding. Clini-
cians are recommended to advise against smoking despite
some evidence suggesting it is beneficial with regard to acne.
Obesity
Relatively few studies have evaluated the possible relationship
between obesity and acne vulgaris. One study of 3000 patients
between the ages of 6 and 11 years found the mean body mass
index of patients with acne to be slightly higher (19Æ5) than in
individuals without acne (18Æ2), although the clinical signifi-
cance of such a small but statistically significant difference is
questionable.132 We have already commented on a randomized
controlled trial of a high-GI diet vs. a low-GI diet, which
found that in the participants on a low-GI diet the acne
improved. A confounding factor, however, was the associated
weight loss, which needs to be studied further. Acne and obes-
ity are often seen together in polycystic ovary syndrome
(PCOS), and studies have shown less acne in the obese patients
with PCOS than in nonobese patients with PCOS.133,134
Stress and picking
Stress is perceived to be a major trigger factor in exacerbating
acne vulgaris and this has been supported by early retrospect-
ive studies.28,135,136 An interventional study in biofeedback
training, relaxation training and stress reduction techniques
found that patients with acne had an improvement in severity
compared with their controls, and when relaxation techniques
were stopped, open and closed comedones recurred.137 A
cross-sectional study of sound design by Halvorsen et al.138
found an increase in mental distress with the severity of acne,
and stressful events such as university examinations have been
correlated with increased acne severity in a prospective study
of 22 patients, despite adjusting for confounding factors such
as lack of sleep and changes in diet.139 A recent Korean
questionnaire study found that 82% of patients believed that
stressful circumstances exacerbate acne.140 Other predomi-
nantly questionnaire-based studies have similar find-
ings.15,34,41,141,142 Another study also finding acne severity to
be greater in stressful examination situations using summer
holidays as a control found that there were no differences in
sebum production during stress.143 Stress induces the local
 2012 The Authors

expression of neuropeptides which may pose as a pathogenic
step in acne exacerbated or caused by stress.144 The associa-
tion between mental health problems as the result of acne
have been discussed elsewhere. A point to note is that there
have been relatively few studies examining stress as a possible
cause of acne or acne exacerbation; more studies have focused
on stress and mental health problems occurring as a result of
acne.
A very small, observational study showed that picking at
acne lesions worsened the inflammation and pustules.145 A
further study with the same group of 56 patients with acne
found that picking was more related to perfectionistic and
compulsive personality traits than acne severity.146 It is likely
that picking will ultimately affect the healing process and
increase the likelihood of scarring.
Infection
The exact role of bacteria such as P. acnes in the pathogenesis
of acne vulgaris is subject to much speculation. Propionibacterium
acnes was first implicated in acne pathogenesis in 1896 when
the microorganism found in acne lesions was thought to be
the main cause of acne; this was supported by another study
in 1909.147,148 Despite this, laboratory studies showed that
the number of P. acnes in the skin of patients with acne and
controls without acne was the same and there was no increase
in P. acnes number in severe acne vs. mild ⁄moderate acne,
prompting the suggestion that P. acnes was a secondary colo-
nizer of the anaerobic lipid-rich environment, rather than a
primary pathogen.149–151 A large, randomized controlled trial
comparing five antimicrobial regimens noted that clinical effi-
cacy of oral antibiotics was less in those with resistant strains,
suggesting that antibiotics may work through a direct antimi-
crobial as well as anti-inflammatory effect. This is a concept
that the majority of experimental studies have supported,
although not all.152–155 Similar bacterial resistance has been
seen in other studies as well,156,157 and in vitro experiments
have shown that resistance may be due to the formation of
biofilms.158 There have been several other postulated mecha-
nisms in which P. acnes is directly involved in acne pathogene-
sis, for example, the interaction of P. acnes and Toll-like
receptors involved in signalling of the innate and adaptive
immune response and the subsequent production of proin-
flammatory cytokines; however, the exact mechanism has not
been confirmed. Pathway targets have been used for experi-
ments into possible vaccine development.159,160 Conversely,
the authors of a recent literature review collating evidence of
P. acnes and it relationship to the pathogenesis of acne con-
cluded that P. acnes was unlikely to have an active role in the
development of inflammatory ⁄noninflammatory acne le-
sions.161 How and if P. acnes influences the development of
and perpetuation of acne lesions remains unclear at this stage.
Interestingly, acne is not described in other animals apart from
comedonal chin acne in cats and dogs, which is probably
another entity.162,163 Given that animals do develop comedo-
nes and that their pilosebaceous units are under the control of
 2012 The Authors
BJD  2012 British Association of Dermatologists 2013 168, pp474–485
Epidemiology of acne vulgaris, K. Bhate and H.C. Williams 481
testosterone, it is intriguing to wonder why humans are
unique in their propensity to develop acne – perhaps P. acnes
plays more of a role than an innocent bystander after all.
Conclusions
Despite many attempts at investigating the epidemiology of
acne, few studies have provided any clear answers. Observa-
tional studies, while useful at generating hypotheses, have
been generally limited by traditional drawbacks such as infor-
mation bias, confounding, reverse causation and the lack of
suitable controls. Future observational studies need to distin-
guish between those factors that may be associated with the
first appearance of acne and those with an effect upon sever-
ity, which would thereby influence treatment. The evidence of
dietary factors in acne requires closer examination in cohort
and experimental studies and the development of a universal
grading system is required to facilitate further meta-analytical
work in all aspects of acne epidemiological work. Addition-
ally, there is a paucity of longitudinal studies looking into the
natural history of acne and the various steps in the processes
leading to colonization with P. acnes. Such studies may identify
potential merit in the treatment of acne prepubertally with a
view to altering the natural history of P. acnes colonization and
subsequent inflammatory acne.
What’s already known about this topic?
• Acne is a common disease affecting all to a degree,
manifesting in adolescence with significant psychosocial
and socioeconomic consequences.
What does this study add?
• This review elucidates the risk factors for the develop-
ment of and severity of acne vulgaris leading to
improved understanding.
• We highlight the need for universal outcome measures
and important areas such as the natural history of acne
and relationship between foodstuffs and acne where
more high-quality studies would be valuable.
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