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British Journal of Dermatology


Epidemiology of acne vulgaris

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

Ketaki Bhate.

Accepted for publication

31 October 2012

Funding sources

Conicts of interest
None declared.
DOI 10.1111/bjd.12149

Despite acne being an almost universal condition in younger people, relatively

little is known about its epidemiology. We sought to review what is known
about the distribution and causes of acne by conducting a systematic review of
relevant epidemiological studies. We searched Medline and Embase to the end
of November 2011. The role of Propionibacterium acnes in pathogenesis is unclear:
antibiotics have a direct antimicrobial as well as an anti-inflammatory effect.
Moderate-to-severe acne affects around 20% of young people and severity correlates 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
individuals are more prone to postinflammatory hyperpigmentation and specific
subtypes such as pomade acne. Acne persists into the 20s and 30s in around
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 inflammatory disease of the pilosebaceous unit, are well described.1
Acne lesions are typically classified as noninflammatory (open
and closed comedones) or inflammatory (papules and pustules). 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 keratinocytes lining the hair follicle desquamate creating a microcomedone. At puberty increased sebum production creates an
environment that can sustain the colonization of Propionibacterium acnes. As P. acnes proliferates, inflammatory and chemotactic
mediators are produced, which in turn drive inflammatory
Despite advances in understanding the pathophysiology of
acne, much less appears to have been written about its epidemiology, 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 primary or secondary preventative measures and treatments,
which in turn could lead to population benefits in terms of
health and reduced expenditure on relatively ineffective treatments. 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.79
We begin with an overview of the descriptive epidemiology
of acne vulgaris including incidence, prevalence, severity,
morbidity, economics and financial implications, demographics and natural history. We then move on to possible causative
factors, which in turn lead into possible prevention strategies.

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Epidemiology of acne vulgaris, K. Bhate and H.C. Williams 475

Similarly, we did not attempt any meta-analysis given the variation 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?

Fig 1. Moderate inflammatory acne accompanied by scarring.

Search methods
We searched the Medline database (in process and other nonindexed citations and Ovid Medline 1946present) and Embase 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, aetiology, cause, prevalence, incidence, cost, pharmacoeconomics,
socioeconomic, social, natural history, race, ethnicity, morbidity, quality of life, geography, family size, severity, excoriation, obesity, overweight, pathogenesis, washing, sweat,
cleanse, sun, sunlight, light, diet, dairy, milk, glycaemic glycemic index (GI), GI, high GI, chocolate, hygiene, smoking,
prevention, climate, environment, infection, Propionibacterium acnes, stress, picking, chloracne, drugs and medicine. The function 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 bibliographic searching. Our aim was to provide a review that covered 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 individual studies, we did not undertake any formal grading of
the quality of evidence given the large diversity of study types.
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A degree of acne affects nearly all people between the ages of

15 and 17 years1113 and in 1520% of young people, acne is
moderate to severe.11,14,15 Prevalence rates of acne by age16
and 1996 census data estimated that 4050 million U.S. individuals have acne, with an 85% prevalence rate in those aged
1224 years.17 A study by Lucky et al.18 found that the severity of acne in boys correlated with pubertal maturation and
that 50% of 10- and 11-year-old boys had more than 10 comedones. 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 prepubertal girls with severe acne had notably higher dehydroepiandrosterone 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.2022

How long does acne last?

Acne begins in the early teens with the onset of facial sebum
production and facial comedones followed by inflammatory lesions.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 environment 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 1192 to 1166 years over a
15-year period.26 Friedlander et al.24 postulated that this younger age of puberty was the reason for the observation that
younger patients between the ages of 8 and 11 were presenting with acne in their clinics. Acne is a chronic disease and
can persist, in some cases, into adulthood,2729 for unclear reasons.30 A German population study found 64% of those aged
2029 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 particularly 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 outcome measure needs to be employed for future studies.10 Predictors 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 ideation. Female subjects score worse than males in the Dermatology Life Quality Index and acne quality of life self-assessment
score, and impact upon quality of life is associated with
longer acne duration.3840 Depression and anxiety are often
seen more in female subjects.4043 The medias 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 ideation and substantial acne to have a threefold increase compared 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 psychological 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 correlation.49,50 The presence of acne lowers the perception of overall 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 socioeconomic background were referred less to dermatologists
than those of a higher socioeconomic background and, additionally, 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 productivity.57 The presence of acne has been reported to have a
negative effect upon work school performance.58 Unemployment 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-

sidered in this study.56 Anger can also be associated with

skin-related quality of life59 as well as emotional and behavioural difficulties.60 Such psychosocial effects must be considered by the healthcare professional treating a patient with
acne. Although there is no definitive study on the socioeconomics of acne, it is likely, given data in the literature so far,
that acne does have a significant impact upon the socioeconomic potential of populations.

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 relatives15 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.6266
More recently, a prospective twin study comparing monozygotic and dizygotic twins found that acne severity was genetically determined, although the low power of the study could
not rule out the influence of additional environmental factors.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.

Frequency in different ethnic groups
In 1908, Fox68 reported that 74% (163 2200) of caucasian
patients and 46% (101 2200) of black patients had acne vulgaris. Hazen69 in 1914 found a similar frequency of acne in
2000 outpatient visits of black patients when compared with
2000 caucasian patients (84% and 9%, respectively). Such
clinic-based studies are not a good method of making inferences about population characteristics as the estimates could
reflect selection bias in those attending or differences in diagnostic 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 discrepancy. 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 conditions 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 (2797%) than in Mestizos (4308%) or
whites (4447%). Again, there is an element of selection bias
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et al.65

et al.62

Evans et al.67
Women and men. Unclear if
they had pre-existing acne

Random sample of 347 twin

births registered at selected
(main) obstetric hospitals.
200 pairs randomly
selected: 52% female, 60%
monozygotic, 40%
dizygotic. Age 1426 years
All women. With and
without acne vulgaris

Identical twins: 5 male,

15 female. Nonidentical
same sex twins: 12 male,
8 female. Age 1218 years

63% of the twins female,

37% male

115 twin pairs studied.

Unclear male to female ratio


458 monozygotic
twins, 1099
dizygotic twins
778 twin pairs.
Unclear proportions
of monozygotic
vs. dizygotic

200 pairs,
monozygotic and

40 pairs of twins:
20 identical,
20 nonidentical
(?mono and

6 twin pairs had acne, 2

were monozygotic and
4 were dizygotic
930 pairs of twins: 342
monozygotic, 345
dizygotic, 243 unknown

Sample size

Inheritance = agreement in monozygotic agreement in dizygotic 1 agreement in dizygotic.

of serum
and acne



et al.64




Table 1 Twin studies in acne vulgaris

Genetic factors explained significant

proportions of acne variance contributing
to 3197% of phenotypic appearance

81% of acne variation attributed to genetic


19% of twins had diagnosis of acne. Ratio

of observed to expected: 4 in monozygotic
males, 23 in dizygotic males, 42 in
monozygotic females, 17 in dizygotic
The incidence of acne in nonidentical and
identical twin groups was similar 16 20
in each group. Identical twins had the
same rates of sebum excretion but
different degrees of acne severity;
nonidentical twins had different rates of
sebum excretion and acne grades. Authors
suggested sebum excretion is under genetic
control and the development of clinical
lesions is modified by environment
Concordance: 98% in monozygotic and
55% in dizygotic. Inheritance 95%.a
Prevalence of family history was associated
with severity of acne

There is a genetic component to acne

Main findings

Environmental factors such as

antiacne medication not taken
into account

Of retrospective design

Unblinded assessment. Does not

measure any environmental factors
(including diet or therapy) that are
likely to be shared by twins at
those ages

No mention of antiacne therapy.

Small sample size. Unblinded
assessment. Reporting of methods
limited. Results open to

Incomplete reporting. Unclear where

the conclusions come from in the
Incomplete reporting and limited
discussion. Retrospective


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 management is that there is no difference between them.77
Pathophysiology in different ethnic groups
It is unclear whether, if there are any ethnic group differences, they can be explained by differences in pathophysiology. 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 studies have been contradictory in terms of the conclusions drawn
from their results.7981 Sebum production increases during
puberty and the onset of puberty is earlier in black individuals.18,82 Most studies to date have focused on caucasian and
black skin types and there are no such studies to our knowledge in Asian or Hispanic patients for comparison.83
Special problems associated with specic ethnic groups
Postinflammatory hyperpigmentation or hyperpigmented macules 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 secondary to the use of pomade (containing high-melting hydrocarbons) 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

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 carbohydrate 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

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, concluded that there was no clear, positive evidence that any dietary 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 doubleblind, 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-Westernized 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 controlled 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 carbohydrate-dense foods. Associated factors such as the weight loss
of participants and the fats and protein consumed needed further delineation to establish what factors might have caused
the decreased lesion count, or if it was a combination of various 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 retinoid signalling.95,99,100 This is an area worthy of further larger
trials with blinded outcome assessment.
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
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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 association 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 measure 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-lactalbumin, 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.106109 IGF-1 has been positively correlated 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.

There is a well-recognized belief that chocolate causes or exacerbates 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: methods 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 consumption of chocolate made up of 100% cocoa.113 The question 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.

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





Main findings


Grant and




Fulton et al.90

Single blind,

students. Mild
to moderate
students with
acne who
claimed that
certain food
their acne
Male prisoners

4 of 8 developed 5 new acne

lesions. Authors claimed not
significant but no statistics
One-third developed new
lesions having been given
six 39-g chocolate bars per
day for 1 week; milk,
peanuts and coca cola
were also being tested

Small sample size. Uncontrolled.

Incomplete reporting of
methods. Possibly too short
a follow-up time
Uncontrolled. No quantitative
data, no statistics. Length of
follow-up not specified.
Follow-up duration may be


No difference in acne
severity between the two


Significant increase in the

number of acne lesions
on days 4 and 7

Blinding and randomization

methods not completely
described, no intention-to-treat
analysis, just one observation in
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
Small sample size. Uncontrolled,
no placebo group

Berman et al.113

100% chocolate



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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 therapeutic 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 trials, 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 difficult 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 therapeutic sun exposure.116

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 largescale, 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 possible 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. Clinicians are recommended to advise against smoking despite
some evidence suggesting it is beneficial with regard to acne.


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 (195) than in
individuals without acne (182), although the clinical significance 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 obesity 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

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 concluded 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 possible comedogenic effect of soaps on rabbit ear were not replicated 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, uncontrolled 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, randomized pilot study found no association between exerciseinduced 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.

Whether or not acne is caused by, exacerbated, improved,
cured, or is not associated with smoking remains controversial.31,125130 An earlier case series suggested an inverse relationship between acne and smoking, suggesting an antiinflammatory effect of a component found in cigarettes.125


Stress and picking

Stress is perceived to be a major trigger factor in exacerbating
acne vulgaris and this has been supported by early retrospective 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 predominantly questionnaire-based studies have similar findings.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
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Epidemiology of acne vulgaris, K. Bhate and H.C. Williams 481

expression of neuropeptides which may pose as a pathogenic

step in acne exacerbated or caused by stress.144 The association 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
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.

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 colonizer of the anaerobic lipid-rich environment, rather than a
primary pathogen.149151 A large, randomized controlled trial
comparing five antimicrobial regimens noted that clinical efficacy of oral antibiotics was less in those with resistant strains,
suggesting that antibiotics may work through a direct antimicrobial as well as anti-inflammatory effect. This is a concept
that the majority of experimental studies have supported,
although not all.152155 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 mechanisms in which P. acnes is directly involved in acne pathogenesis, 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 proinflammatory cytokines; however, the exact mechanism has not
been confirmed. Pathway targets have been used for experiments 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 concluded that P. acnes was unlikely to have an active role in the
development of inflammatory noninflammatory acne lesions.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 comedones and that their pilosebaceous units are under the control of
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BJD  2012 British Association of Dermatologists 2013 168, pp474485

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.

Despite many attempts at investigating the epidemiology of
acne, few studies have provided any clear answers. Observational studies, while useful at generating hypotheses, have
been generally limited by traditional drawbacks such as information bias, confounding, reverse causation and the lack of
suitable controls. Future observational studies need to distinguish between those factors that may be associated with the
first appearance of acne and those with an effect upon severity, 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. Additionally, 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.

Whats 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 development 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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