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A low-glycemic-load diet improves symptoms in acne vulgaris patients: A randomized controlled trial

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Although the pathogenesis of acne is currently unknown, recent epidemiologic studies of non-Westernized populations suggest that dietary factors, including the glycemic load, may be involved. The objective was to determine whether a low-glycemic-load diet improves acne lesion counts in young males. Forty-three male acne patients aged 15-25 y were recruited for a 12-wk, parallel design, dietary intervention incorporating investigator-blinded dermatology assessments. The experimental treatment was a low-glycemic-load diet composed of 25% energy from protein and 45% from low-glycemic-index carbohydrates. In contrast, the control situation emphasized carbohydrate-dense foods without reference to the glycemic index. Acne lesion counts and severity were assessed during monthly visits, and insulin sensitivity (using the homeostasis model assessment) was measured at baseline and 12 wk. At 12 wk, mean (+/-SEM) total lesion counts had decreased more (P=0.03) in the low-glycemic-load group (-23.5 +/- 3.9) than in the control group (-12.0 +/- 3.5). The experimental diet also resulted in a greater reduction in weight (-2.9 +/- 0.8 compared with 0.5 +/- 0.3 kg; P<0.001) and body mass index (in kg/m(2); -0.92 +/- 0.25 compared with 0.01 +/- 0.11; P=0.001) and a greater improvement in insulin sensitivity (-0.22 +/- 0.12 compared with 0.47 +/- 0.31; P=0.026) than did the control diet. The improvement in acne and insulin sensitivity after a low-glycemic-load diet suggests that nutrition-related lifestyle factors may play a role in the pathogenesis of acne. However, further studies are needed to isolate the independent effects of weight loss and dietary intervention and to further elucidate the underlying pathophysiologic mechanisms.
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A low-glycemic-load diet improves symptoms in acne vulgaris
patients: a randomized controlled trial
13
Robyn N Smith, Neil J Mann, Anna Braue, Henna Ma¨kela¨inen, and George A.Varigos
ABSTRACT
Background: Although the pathogenesis of acne is currently un-
known, recent epidemiologic studies of non-Westernized popula-
tions suggest that dietary factors, including the glycemic load, may
be involved.
Objective: The objective was to determine whether a low-glycemic-
load diet improves acne lesion counts in young males.
Design: Forty-three male acne patients aged 15-25 y were recruited
for a 12-wk, parallel design, dietary intervention incorporating
investigator-blinded dermatology assessments. The experimental
treatment was a low-glycemic-load diet composed of 25% energy
from protein and 45% from low-glycemic-index carbohydrates. In
contrast, the control situation emphasized carbohydrate-dense foods
without reference to the glycemic index. Acne lesion counts and
severity were assessed during monthly visits, and insulin sensitivity
(using the homeostasis model assessment) was measured at baseline
and 12 wk.
Results: At 12 wk, mean (SEM) total lesion counts had decreased
more (P ҃ 0.03) in the low-glycemic-load group (Ҁ23.5 3.9) than
in the control group (Ҁ12.0 3.5). The experimental diet also
resulted in a greater reduction in weight (Ҁ2.9 0.8 compared with
0.5 0.3 kg; P 0.001) and body mass index (in kg/m
2
; Ҁ0.92
0.25 compared with 0.01 0.11; P ҃ 0.001) and a greater improve-
ment in insulin sensitivity (Ҁ0.22 0.12 compared with 0.47
0.31; P ҃ 0.026) than did the control diet.
Conclusion: The improvement in acne and insulin sensitivity after
a low-glycemic-load diet suggests that nutrition-related lifestyle fac-
tors may play a role in the pathogenesis of acne. However, further
studies are needed to isolate the independent effects of weight loss
and dietary intervention and to further elucidate the underlying
pathophysiologic mechanisms. Am J Clin Nutr 2007;86:
107–15.
KEY WORDS Acne, glycemic index, glycemic load, insulin
resistance, hyperinsulinemia
INTRODUCTION
Acne is a common and complex skin disease that affects in-
dividuals of all ages. In Western populations, acne is estimated to
affect 79 –95% of the adolescent population, 40 –54% of indi-
viduals older than 25 y, and 12% of women and 3% of men by
middle age (1). In contrast, acne remains rare in non-Westernized
societies such as the Inuit (2), Okinawan Islanders (3), Ache
hunter-gatherers, and Kitavan Islanders (1). Although familial
and ethnic factors are implicated in acne prevalence, this obser-
vation is complicated by the finding that incidence rates of acne
have increased with the adoption of Western lifestyles (2). These
observations suggest that lifestyle factors, including diet, may be
involved in acne pathogenesis.
Historically, much debate has surrounded the subject of diet in
the management of acne. In the 1930s, acne was considered to be
a disease of disturbed carbohydrate metabolism because early
work suggested that impaired glucose tolerance occurred in acne
patients (4). On the basis of these observations and the anecdotal
impressions of physicians, patients were often discouraged from
eating excessive amounts of carbohydrates and high-sugar foods
(5, 6). The diet and acne connection finally fell from favor in
1969 when a clinical study found no exacerbation of acne lesions
in a group that ingested a chocolate bar compared with a group
that ingested a placebo bar (7). Although it is the most widely
cited reference dissociating diet and acne, this study has been
criticized for a number of design flaws, including the similar
nutrient composition of the placebo and the chocolate bar (8 –10).
Recently, there has been a reappraisal of the diet and acne
connection because of a greater understanding of how diet may
affect endocrine factors involved in acne (1, 10). Of interest is the
concept of the glycemic index (GI)—a system of classifying the
glycemic response of carbohydrates. Because the GI can only be
used to compare foods of equal carbohydrate content, the glyce-
mic load was later developed to characterize the glycemic effect
of whole meals or diets (GI ҂ available dietary carbohydrate).
Cordain et al (1) postulated that high-glycemic-load diets may be
a significant contributor to the high prevalence of acne seen in
Western countries. The authors speculate that the frequent con-
sumption of high-GI carbohydrates may repeatedly expose ad-
olescents to acute hyperinsulinemia. Hyperinsulinemia has been
implicated in acne pathophysiology because of its association
with increased androgen bioavailability and free concentrations
of insulin-like growth factor I (IGF-I) (10, 11). Therefore, we
1
From the School of Applied Sciences, RMIT University, Melbourne,
Australia (RNS and NJM); the Australian Technology Network, Centre for
Metabolic Fitness(NJM); theDepartment ofDermatology, Royal Melbourne
Hospital, Parkville, Australia (AB and GAV); the Department of Biochem-
istry and Food Chemistry, Turku University, Turku, Finland (HM); and the
Department of Dermatology, Royal Children’s Hospital, Parkville, Australia
(GAV).
2
Supported by a research grant from Meat and Livestock Australia.
3
Address reprint requests to RN Smith, School of Applied Sciences,
RMIT University, GPO Box 2476V, Melbourne, Victoria, Australia, 3001.
E-mail: robyn.smith@rmit.edu.au.
Received September 20, 2006.
Accepted for publication February 9, 2007.
107Am J Clin Nutr 2007;86:107–15. Printed in USA. © 2007 American Society for Nutrition
by guest on June 1, 2013ajcn.nutrition.orgDownloaded from
hypothesized that low-glycemic-load dietary interventions may
have a therapeutic effect on acne based on the beneficial endo-
crine effects of these diets. Consequently, the aim of this prelim-
inary study was to investigate the efficacy of a low-glycemic-
load diet in reducing the severity of acne symptoms.
SUBJECTS AND METHODS
Subjects
Males with facial acne were recruited through posted fliers at
the RMIT University (Melbourne, Australia) and newspaper ad-
vertisements. Informed consent was obtained from each partic-
ipant or guardian (if aged 18 y), and the study was conducted
at RMIT University after obtaining approval from the RMIT
Human Ethics committee. This study included only male partic-
ipants aged 15-25 y with mild-to-moderate facial acne. Partici-
pants were required to have had acne for 6 mo before recruit-
ment. Individuals were excluded if they were currently taking
medications known to affect acne or glucose metabolism. Addi-
tionally, a washout period of 6 mo was required for subjects who
had previously taken oral retinoids or 2 mo for subjects who had
taken oral antibiotics or topical antibacterial or retinoid agents.
Study design
It was calculated that 19 subjects per group would provide
80% power (at the 2-sided 5% level) to detect a difference of 20%
in the reduction of acne lesions between groups, assuming an SD
of 22%. To compensate for subject withdrawal, 54 subjects were
enrolled in the study.
Eligible participants were recruited between June 2003 and
June 2004. Approximately 2–3 wk after recruitment, participants
attended their baseline appointment and were randomly assigned
to either the low-glycemic-load (LGL) or the control group
(Figure 1). Randomization was carried out by computer gener-
ated random numbers, and allocation to groups was performed by
a third party.
This study was designed as a parallel dietary intervention
study with investigator-blinded dermatology assessments. Top-
ical therapy, in the form of a noncomedogenic cleanser, was
standardized for both groups, and facial acne was scored at
monthly visits (weeks 0, 4, 8, and 12) at the academic research
clinic. On all visits, height and weight were measured. All sub-
jects were weighed in light clothes, and body mass index (BMI)
was calculated as weight (kg)/height squared (m). At baseline
and 12-wk, a venous blood sample was taken after an overnight
fast, and an oral glucose insulin sensitivity (OGIS) test was
performed in a subgroup of participants from the LGL and con-
trol groups.
The primary endpoints of the study were changes in inflam-
matory lesion counts (papules, pustules, and nodules) and total
lesion counts (inflammatory lesions and noninflammatory le-
sions) after 12 wk. Secondary endpoints included changes in
anthropometric measures and insulin sensitivity indexes.
Dietary intervention
Participants were informed that the study’s intent was to com-
pare the dietary carbohydrate to protein ratio and were not in-
formed of the study’s true intent. The LGL diet was achieved by
modifying the amount and type of carbohydrate. The LGL group
was instructed to substitute high-GI foods with foods higher in
protein (eg, lean meat, poultry, or fish) or with foods with a lower
GI (eg, whole-grain bread, pasta, and fruit). Some staple foods
were supplied, and the participants were urged to consume these
or similar foods daily. Each participant received individualized
dietary plans that were isocalorically matched with their baseline
diet as determined from 7-d weighed and measured food records.
The recommended LGL diet consisted of 25% of energy from
protein, 45% from low-GI carbohydrates, and 30% energy from
fats. In contrast, the control group received carbohydrate-dense
staples and were instructed to eat these or similar foods daily. The
foods provided had moderate-to-high GI values and were typical
of their normal diet as evidenced from 7-d weighed and measured
food records. The control group was not informed about the GI,
FIGURE 1. Recruitment to completion of participants after 12 wk (t
0
҃ baseline, t
12
҃ 12 wk).
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but were urged to include carbohydrates as a regular part of their
diet. All participants were instructed on how to use food scales
and to keep foods records. During the study period, nutrient
intakes were calculated from 3-d weighed and measured food
records each month by using Australia-specific dietary analysis
software (FOODWORKS; Xyris Software, Highgate Hill, Aus-
tralia). Dietary compliance was monitored via regular telephone
interviews, assessments of daily glycemic load, and 24-h urine
samples (weeks 0 and 12) for an assessment of urea excretion
relative to urinary creatinine as a marker of protein intake.
Calculation of dietary glycemic index and glycemic load
Daily dietary glycemic index and glycemic load were calcu-
lated from diet records. The dietary GI was calculated as (GI for
food item ҂ proportion of total carbohydrate contributed by
item), and the glycemic load was calculated as (GI for food
item ҂ its carbohydrate content in grams/100). The GI values
used had glucose as the reference food and were taken from
reference tables (12) and from Sydney University’s GI website
(13). If a food from Australia was not available, the GI was
estimated by using similar foods of known value.
Standardized topical lotion
All participants were provided with a topical cleanser
(Cetaphil gentle skin cleanser; Galderma, Frenchs Forrest, Aus-
tralia) and advised to use it in place of their normal wash, soap,
or cleanser. The subjects began using the topical wash 2 wk
before baseline and were asked to maintain a standard level of use
during the trial.
Dermatology assessment
Scaling of the acne was performed by a dermatology registrar
who was blinded to the group assignment of the participants. The
registrar assessed facial acne occurrence and severity only using
a modified Cunliffe-Leeds lesion count technique (14). To en-
sure that all acne lesions were counted, located, and graded by
size and severity, lesions were mapped by placing a transparent
plastic film with a laser-printed grid gently against the skin.
Facial anatomical landmarks, such as the ear, chin, and tip of the
nose, were used to ensure consistency between assessments.
Each side of the face was assessed separately. Where necessary,
the registrar palpated the skin to determine the lesion type. To
maintain the reproducibility of this procedure, one physician
performed all the dermatology assessments. A small group of
volunteers (n ҃ 4) was counted 1-wk apart to evaluate the re-
producibility by the same physician (9.5% CV).
Laboratory analyses
Code-labeled serum samples were stored at Ҁ80 °C for anal-
ysis after the study by an independent laboratory. Baseline and
12-wk samples for each participant were included in the same
assay run to avoid interassay variability. Serum insulin was mea-
sured by using a commercially available microparticle enzyme
immunoassay (Abbott Laboratories, Tokyo, Japan; intraassay
CV: 4.0%). Capillary blood glucose was measured on the day of
testing with a Glucose 201ѿ analyzer (HemoCue, Sweden; in-
traassay CV: 1.6%).
Insulin sensitivity measures
The homeostasis model assessment of insulin resistance
(HOMA-IR) was calculated as fasting glucose (mmol/L) ҂ fast-
ing insulin (
U/mL)/22.5 (15). We also used the model-derived
formula proposed by Mari et al (16) to calculate the OGIS index
from a 2-h oral-glucose-tolerance test. This formula was calcu-
lated by using 6 fixed-rate constants: oral glucose dose (75 g);
body surface area; glucose concentrations (mg/dL) at 0, 90, and
120 min; and insulin concentrations (
U/mL) at 0 and 90 min. In
the present study, some participants were unable to complete the
2-h test because of scheduling interference (eg, school and work
commitments). Consequently, the OGIS data presented are for
only 18 subjects in the LGL group and for 17 subjects in the
control group.
Statistical analysis
All statistical analyses were performed with the use of SPSS
11.0 for WINDOWS (SPSS Inc, Chicago, IL). Baseline charac-
teristics were analyzed for between-group significance with a
Mann-Whitney U test or an independent-sample t test, depending
on whether or not the data were normally distributed. Repeated-
measures analysis of variance was used to analyze dietary and
acne (lesion count) data and to explore the effects of time, treat-
ment, and an interaction of these 2 factors. We compared changes
in lesion counts using repeated-measures analysis of log-
transformed data at each follow-up visit with baseline lesion
counts as the covariate. P values 0.05 were considered signif-
icant. Analysis of covariance (ANCOVA) was used to test for
overall treatment differences at 12 wk, with baseline data as the
covariate. Secondary analyses were performed with adjustment
for changes in BMI.
The primary clinical outcome (changes in lesion counts at 12
wk) was analyzed by using an intention-to-treat model for all
randomized subjects with the use of the last measurement carried
forward for all missing data.
Bivariate linear regression analysis was also conducted, pool-
ing data from both groups, to explore relations between dietary
variables and acne improvement.
RESULTS
Subjects
Forty-three subjects completed the study per protocol (Figure 1).
Seven participants did not complete the study (5 in the control
and 2 in the LGL group), and 4 were removed from data set
(2 began taking acne medications and 2 were noncompliant).
Baseline characteristics of the subjects are shown in Table 1.
Dietary intakes
Dietary intakes of the LGL and control groups at baseline and
during the trial period is shown in Table 2. No significant group
differences were observed in any of the dietary variables at base-
line. During the trial period, dietary glycemic load decreased
significantly in the LGL group compared with the control group,
and this change was achieved by a reduction in carbohydrate
intake and by the consumption of low-GI foods (as indicated by
a reduction in the calculated dietary GI). Protein intake increased
in the LGL group and decreased slightly in the control group,
which indicates that some carbohydrates were replaced with
A LOW-GLYCEMIC-LOAD DIET AND ACNE VULGARIS 109
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foods higher in protein. This observation was substantiated by
a 15.4% increase in the ratio of urinary urea to creatinine at
12 wk for the LGL group compared with a 12.3% decrease for the
control group (P ҃ 0.009), which indicated good dietary com-
pliance.
Study outcomes
As shown in Figure 2, both the LGL and control groups
showed reductions in inflammatory and total lesion counts from
0 to 12 wk. Repeated-measures analysis that used baseline counts
as the covariate indicated an overall difference between the LGL
and control groups (main effect of group), but no significant
change over time (main effect of time) or difference in the time
course between the groups (group ҂ time interaction) was ob-
served. At 12 wk, the LGL group had a greater reduction in the
mean number of total and inflammatory lesions than did the con-
trol group (Table 3). Examples of acne improvement in the LGL
group are shown in Figure 3. The mean number of total lesions
fell by 23.5 (51%) in the LGL group and by 12.0 (31%) in the
control group (P ҃ 0.03). Inflammatory lesion counts fell by 17.0
(45%) in the LGL group and by 7.4 (23%) in the control group (P
҃ 0.02). The results at 12 wk were also materially unchanged by
an intention-to-treat analysis.
The LGL group also showed significant reductions in weight
(P ҃쏝0.001), BMI (P ҃ 0.001) and HOMA-IR (P ҃ 0.026) when
compared with the control group. The change in HOMA correlated
with the change in OGIS index (r ҃Ҁ0.36, P ҃ 0.035), with both
models suggesting a trend for improved insulin sensitivity in
the LGL group and a trend for increasing insulin resistance in the
control group. Statistical adjustment of study endpoints for the
change in BMI was found to alter the outcome for HOMA-IR
(P ҃ 0.10) and total lesion counts (P ҃ 0.07), but not inflammatory
TABLE 1
Subject characteristics at baseline by dietary group
1
Variable
LGL group
(n ҃ 23)
Control group
(n ҃ 20) P
2
Ethnicity (n)
White 20 17 0.60
Asian 3 3
Age (y) 18.2 0.5
3
18.5 0.5 0.76
Body weight (kg) 73.5 2.5 73.3 3.3 0.90
BMI (kg/m
2
) 22.9 0.6 22.5 0.7 0.34
Total lesion count 40.6 5.0 34.9 4.3 0.40
Inflammatory lesion count 31.9 3.9 28.4 3.6 0.72
OGIS (mL m
Ҁ2
min
Ҁ1
)
4
481 9 503 9 0.12
HOMA-IR 1.6 0.2 1.5 0.2 0.88
1
OGIS, oral glucose insulin sensitivity; HOMA-IR, homeostasis model
assessment of insulin resistance; LGL, low glycemic load.
2
Corresponds with an independent-sample t test or Mann-Whitney U
test for means and the Fisher’s exact test for ethnicity.
3
x SEM (all such values).
4
n ҃ 18 for the LGL group and n ҃ 17 for the control group.
TABLE 2
Dietary intakes of low-glycemic-load (LGL) and control groups at baseline and during the trial period
Variable
LGL group
(n ҃ 23)
Control group
(n ҃ 20)
P
1
Group Time Group ҂ time interaction
Energy (kJ/d) 0.15 0.09 0.100
Baseline
2
10 625 572
3
10 540 546
Trial period
4
9320 460 10 620 494
Dietary glycemic index 0.001 0.001 0.001
Baseline 57.5 1.0 57.2 0.8
Trial period 43.2 0.8 56.4 0.8
Dietary glycemic load 0.001 0.001 0.001
Baseline 174.7 9.1 181.5 11.5
Trial period 101.5 6.1 174.3 10.7
Carbohydrate (% of total energy) 0.013 0.195 0.001
Baseline 50.2 1.1 48.2 1.2
Trial period 44.1 1.3 50.1 1.2
Protein (% total energy) 0.001 0.001 0.001
Baseline 16.3 0.6 17.5 0.9
Trial period 22.7 0.8 17.4 0.8
Total fat (% total energy) 0.84 0.74 0.45
Baseline 32.5 1.1 31.8 1.2
Trial period 31.5 0.9 31.4 1.2
Saturated fat (% total energy) 0.002 0.001 0.001
Baseline 13.5 0.6 12.9 0.7
Trial period 9.0 0.4 13.0 0.9
Fiber (g/d) 0.002 0.001 0.001
Baseline 25.3 1.8 25.2 2.1
Trial period 36.9 2.0 25.2 2.0
1
Repeated-measures ANOVA was done to incorporate data from all time points and to evaluate the differences between the LGL and the control groups
(main effect of group), the change over time (main effect of time), and the differences in the time course between the 2 groups (group ҂ time interaction).
2
An independent-sample t test showed no significant differences between the LGL and the control groups for any of the listed dietary variables at baseline.
3
x SE (all such values).
4
Means of data collected at 4, 8, and 12 wk.
110 SMITH ET AL
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counts (P ҃ 0.04). However, we found no significant interaction
effect of dietary treatment and the change in BMI on acne lesion
counts.
Dietary variables as predictors of acne improvement
Dietary correlates with acne improvement include reductions
in glycemic load (r ҃ 0.49, P ҃ 0.001), dietary GI (r ҃ 0.30,
P ҃ 0.05), carbohydrate intake (r ҃ 0.46, P ҃ 0.002), percentage
saturated fat (r ҃ 0.36, P ҃ 0.019), and total energy intake (r ҃
0.40, P ҃ 0.010). These relations are shown in Figure 4.
DISCUSSION
This study was the first randomized controlled intervention to
examine the influence of dietary glycemic load on the clinical
assessment of acne. After adjustment for differences in acne
severity at baseline, we found that the LGL group had greater
overall reduction in total and inflammatory lesion counts than did
the control group. Analysis of the primary endpoint data also
showed that the differences between groups remained significant
after an intention-to-treat model was used. However, we found
no significant effect of time on acne, possibly because acne is a
FIGURE 2. Mean (SEM) percentage changes from baseline in inflammatory acne lesion counts and in total acne lesion counts in the low-glycemic-load
group (solid line; n ҃ 23) and the control group (dashed line; n ҃ 20) at each visit. Repeated-measures ANOVA was performed by incorporating the absolute
data (log transformed) from each follow-up visit, with baseline counts as the covariate.
A LOW-GLYCEMIC-LOAD DIET AND ACNE VULGARIS 111
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dynamic condition in which both spontaneous improvements
and flares can occur over time.
Few well-controlled dietary studies have examined the effect
of diet on acne. Fulton et al (7), in a crossover single-blind study,
found no effect of chocolate on acne when compared with a
placebo bar. However, a later examination of the ingredients in
the placebo bar indicated that the fatty acid composition and
sugar contents were virtually identical to that found in the choc-
olate (8). Anderson examined the effect of the daily consumption
of chocolate, milk, or nuts and found no effect on acne (17).
However, this study has also been criticized for its small sample
size, short follow-up, and lack of control (18). Chiu et al (19)
showed, in university students, an association between worsen-
ing diet quality and exacerbation ofacne during a preexamination
period. However, stress was found to be the main contributing
factor, and diet was assessed by using a nonquantitative, self-
assessed measure of diet quality. Recently, a retrospective eval-
uation of dietary intake showed a positive association between
milk intake and physician-diagnosed severe acne (20). However,
the authors admit that this association may have been affected by
the imprecision inherent in the measurement of dietary intakes
via dietary recall.
High-glycemic-load diets have recently been implicated in
acne etiology because of their ability to increase the insulin
demand and other factors associated with insulin resistance (eg,
hyperphagia, elevated nonesterified fatty acids, and obesity)
(11). Clinical and experimental evidence suggests that insulin
may increase androgen production and affect, through its influ-
ence on steroidogenic enzymes (21), gonadotrophin releasing
hormone secretion (22) and sex hormone– binding globulin pro-
duction (23–25). Additionally, insulin has been shown to de-
crease a binding protein for IGF-I, which may facilitate the effect
of IGF-I on cell proliferation (26). Overall, these events may
influence 1 or more of the 4 underlying causes of acne: 1) in-
creased proliferation of basal keratinocytes within the piloseba-
ceous duct, 2) abnormal desquamation of follicular corneocytes,
3) androgen-mediated increases in sebum production, and 4)
colonization and inflammation of the comedo by Propionibac-
terium acnes (11).
The role of insulin in acne development is also supported by
the high prevalence of acne in women with polycystic ovary
syndrome (PCOS), a condition associated with insulin resis-
tance, hyperinsulinemia, and hyperandogenism (27). Insulin re-
sistance is believed to be the underlying disturbance in PCOS,
because it generally precedes and gives rise to the cluster of
endocrine abnormalities that characterize PCOS (elevated an-
drogen and IGF-I concentrations and low sex hormone– binding
globulin; 28). Treatments for PCOS now include oral hypogly-
cemic agents, which improve insulin sensitivity, restore fertility,
and alleviate acne (29).
Our study also suggests that changes in acne may be closely
related to changes in insulin sensitivity, because we observed a
positive effect of the LGL diet on insulin sensitivity compared
with the control diet. However, the improvement in insulin sen-
sitivity may be attributable not only to the reduction in glycemic
load (30), but also to the reduction in body mass. The participants
in the LGL group lost weight despite receiving dietary advice to
maintain their baseline energy intake. This may have been due to
the dual effect of added protein and low-GI foods, because both
influence hunger and satiety. Feeding studies have shown that
low-GI foods increase satiety, delay hunger, and decrease food
intake when compared with high-GI foods (31, 32). Similar ef-
fects on satiety have been reported for high-protein meals com-
pared with isocaloric high-carbohydrate or high-fat meals (33).
Therefore, the combined effect of low-GI foods and added pro-
tein may have reduced ad libitum food intake, which made it
difficult for our participants to maintain the energy density of their
baseline diets. This observation is supported by previous studies that
showed ad libitum LGL diets to reduce energy intake without the
need for an externally imposed energy restriction (34, 35).
Because the participants in the LGL group lost weight, we
cannot preclude a role for the change in BMI in the overall
treatment effect. When we statistically adjusted the data for
changes in BMI, the effect of the LGL diet on total lesion counts
and HOMA-IR was lost. This suggests that the therapeutic effect
may be a factor of the weight loss or simply that weight loss is
another manifestation of an LGL diet. Apart from women with
PCOS, little evidence suggests an association between acne se-
verity and body weight. Aizawa and Niimura (36) showed mild
peripheral insulin resistance in female acne sufferers that was not
associated with obesity or menstrual irregularities. In contrast,
Bourne and Jacobs (29) showed that adult men with acne were
TABLE 3
Absolute mean differences from baseline to 12 wk in outcome variables by dietary group
1
Variable LGL group Control group P
2
Per protocol analysis
Total count Ҁ23.5 3.9 [23]
3
Ҁ12.0 3.5 [20] 0.03
Inflammatory count Ҁ17.0 3.1 [23] Ҁ7.4 2.5 [20] 0.02
Weight (kg) Ҁ2.9 0.8 [23] 0.5 0.3 [20] 0.001
BMI (kg/m
2
)
Ҁ0.92 0.25 [23] 0.01 0.11 [20] 0.001
HOMA-IR
4
Ҁ0.22 0.12 [23] 0.47 0.31 [20] 0.026
OGIS (mL m
Ҁ2
min
Ҁ1
)
12.7 7.9 [18] Ҁ18.3 9.9 [17] 0.08
Intention-to-treat analysis
Total count Ҁ22.0 3.5 [27] Ҁ10.9 2.9 [27] 0.02
Inflammatory count Ҁ16.2 2.9 [27] Ҁ5.6 2.5 [27] 0.01
1
HOMA-IR, homeostasis model assessment of insulin resistance; OGIS, oral glucose insulin sensitivity index.
2
By ANCOVA for between-group comparison with baseline as a covariate.
3
x SEM; n in brackets (all such values).
4
Values are nonparametrically distributed. ANCOVA was performed on log-transformed data.
112 SMITH ET AL
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significantly heavier (5.6 kg) than men without acne. However,
the authors showed that this association was dependent on age,
because weight was not associated with acne in adolescents aged
15-19 y. Our data also showed a significant correlation between
acne lesion counts and BMI in males aged 18-25 y, but this was
not true for the subjects aged 18 y (data not shown). The reason
for this observation is unknown, but it is possible that the tran-
sient decline in insulin sensitivity that occurs with the progres-
sion through puberty may trigger acne in the younger population
(37, 38).
A few limitations of the study should be addressed. First, it is
possible that the topical application of the mild skin cleanser may
have contributed to the acne improvement through effects on the
epidermal barrier function (39). Because acne improved in the
control groupwithout any significant changesto their diet, apossible
direct effect of the cleanser should be considered. Second, because
of the nature of the LGL dietary intervention, we cannot solely
attribute the treatment effects to changes in glycemic load be-
cause other dietary factors (eg, zinc and vitamin A intake) may
mediate or confound the relation between diet and acne improve-
ment. Last, this study relied on self-reporting of dietary intakes.
Underreporting the quantity of food eaten is a known source of
measurement error when assessing adolescent diets (40).
To our knowledge, this is the first study to show a therapeutic
effect of dietary intervention on acne. After 12 wk, the LGL diet
was shown to significantly reduce acne lesion counts and improve
insulin sensitivity when compared with a high-glycemic-load diet.
Although we could not isolate the effect of the LGL diet from that of
FIGURE 3. Photographs of acne improvement in the low-glycemic-load group. A and B: subject A at baseline and 12 wk respectively; C and D: subject
B at baseline and 12 wk, respectively; and E and F: subject C at baseline and 12 wk, respectively.
A LOW-GLYCEMIC-LOAD DIET AND ACNE VULGARIS 113
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weight loss, these findings are consistent with earlier suggestions of
the association between hyperinsulinemia and acne. These ob-
servations will need to be substantiated and the underlying mech-
anisms determined in larger-scale studies.
The authors’ responsibilities were as follows—RNS, NJM, and AB: con-
tributed to the writing of this manuscript; RNS, AB, and HM: helped with the
data collection; RNS: responsible for the data analysis; and NJM and GAV:
provided significant advice and supervised the project. The sponsor of this
study, Meat and Livestock Australia, had no role in the data collection, data
analysis, data interpretation, or submission of this article for publication.
RNS received a postgraduate scholarship from MINTRAC (National Meat
Industry Training Council of Australia).
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Notice of duplicate publication
Smith RN, Mann NJ, Braue A, Ma¨kela¨inen H, Varigos GA. A low-glycemic-load diet improves symptoms in
acne vulgaris patients: a randomized controlled trial. Am J Clin Nutr 2007;86:107–15.
It has been brought to the attention of the Editor and Associate Editors of The American Journal of Clinical
Nutrition (AJCN) that the article noted above by Smith et al (Am J Clin Nutr 2007;86:107–15) substantially
duplicated an article by the same authors that was published in the Journal of the American Academy of
Dermatology (J Am Acad Dermatol 2007;57:247–56).
The article was submitted to the AJCN on 20 September 2006, accepted for publication on 9 February 2007, and
published in the July 2007 issue of the AJCN. The Journal of the American Academy of Dermatology received
the article on 16 October 2006, accepted it for publication on 9 January 2007, and published it online in the
Journal of the American Academy of Dermatology on 20 April 2007.
Duplicate publication violates the editorial policy of the American Society for Nutrition (ASN) as set forth in the
AJCN Information for Authors and as codified in the Authors’ Agreement signed by the authors. The Authors’
Agreement specifically states that “the Article and its scientific findings have not been previously published nor
submitted for publication elsewhere except in abstract form, and there is no offer or agreement for publication
pending.”
LETTERS TO THE EDITOR 251
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... Acne vulgaris is a chronic inflammatory disease of the pilosebaceous unit characterized by comedones, small bumps caused by follicular obstruction and sebaceous gland hyperplasia, and painful inflammatory lesions such as papules, pustules, and cysts [176][177][178]. Worldwide, it is the eighth most common disease, accounting for 0.29% of the global disease burden, and the second most common dermatologic disease [179,180]. ...
... It is thought to be a multifactorial disease caused by the oversecretion of sebum, the obstruction of the excretory ducts due to the abnormal desquamation of keratinocytes, and the proliferation and colonization of Cutibacterium acnes, which secretes proinflammatory mediators in the comedo [177,178]. In addition, a diet with a high glycemic index and a high level of milk protein plays an essential role in pathogenesis by increasing insulin signaling and insulin-like growth factor-1 (IGF-1), which inhibits the transcription factor that regulates mTORC1, Fox01. ...
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The gut microbiota (GM) comprises billions of microorganisms in the human gastrointestinal tract. This microbial community exerts numerous physiological functions. Prominent among these functions is the effect on host immunity through the uptake of nutrients that strengthen intestinal cells and cells involved in the immune response. The physiological functions of the GM are not limited to the gut, but bidirectional interactions between the gut microbiota and various extraintestinal organs have been identified. These interactions have been termed interorganic axes by several authors, among which the gut–brain, gut–skin, gut–lung, gut–heart, and gut–metabolism axes stand out. It has been shown that an organism is healthy or in homeostasis when the GM is in balance. However, altered GM or dysbiosis represents a critical factor in the pathogenesis of many local and systemic diseases. Therefore, probiotics intervene in this context, which, according to various published studies, allows balance to be maintained in the GM, leading to an individual’s good health.
... This finding has been demonstrated by several researchers who investigated the impact of the glycemic index of various diets and glycemic loads in individuals suffering from acne [27]. Smith et al. demonstrated that a low glycemic regimen for 12 weeks significantly reduced the serum IGF1 concentrations and alleviated acne disease [28]. A dietary change as a low glycemic regimen also booted the nuclear concentration of the factor forkhead box O1 (FOXO1), normalizing the transcription of acne-related genes. ...
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The association between acne and insulin resistance has not been investigated as thoroughly in males as it has been in women, despite the fact that in adult men, acne prevalence has grown. On the face, sebaceous glands produce and secrete sebum, which lubricates the skin and protects it from friction. Metformin, an insulin-sensitizing medication, may modify the association between acne vulgaris and insulin resistance (IR). Individuals with IR, metabolic syndrome or with impaired glucose tolerance are sometimes treated ‘off label’ with Metformin. In these conditions, IR may be a leading factor in the pathogenesis of acne, and in men, Metformin treatment may reduce the Global Acne Grading System (GAGS) score by enhancing insulin sensitivity. However, additional clinical studies are required to corroborate these assumptions.
... Diets with a high glycemic index (GI > 55) were associated with poor glycemic control, elevated levels of postprandial insulin and insulin-like growth factor 1 (IGF-1), whereas diets with a low glycemic index were found to decrease fasting IGF-1 levels [34]. Smith et al. demonstrated that a diet with a low glycemic index (GI < 50) decreased acne severity and the number of skin breakouts in teenagers with mild and moderate acne during a 10-week dietary intervention [35]. In the present study, the respondents were aware that foods with a high glycemic index can exert a negative effect on skin condition and aggravate acne, but very few participants limited their intake of such products. ...
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... The skimmed milk contains hormones and bioactive molecules, and it may have an acne stimulating effect due to androgens, progesterone, and insulin growth factor-1 (IGF-1) [116]. Western diets, which are typically high-glycemic-load (HGL) diets, can elevate IGF-1 and blood insulin levels chronically or acutely, which leads to increased sebum production and even acne [118]. There are positive correlations between acne severity and high glycemic load foods [64]. ...
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Skin is the largest organ in the human body, and the interplay between the environment factors and human skin leads to some skin diseases, such as acne, psoriasis, and atopic dermatitis. As the first line of human immune defense, skin plays significant roles in human health via preventing the invasion of pathogens that is heavily influenced by the skin microbiota. Despite being a challenging niche for microbes, human skin is colonized by diverse commensal microorganisms that shape the skin environment. The skin microbiota can affect human health, and its imbalance and dysbiosis contribute to the skin diseases. This review focuses on the advances in our understanding of skin microbiota and its interaction with human skin. Moreover, the potential roles of microbiota in skin health and diseases are described, and some key species are highlighted. The prevention, diagnosis and treatment strategies for microbe-related skin diseases, such as healthy diets, lifestyles, probiotics and prebiotics, are discussed. Strategies for modulation of skin microbiota using synthetic biology are discussed as an interesting venue for optimization of the skin-microbiota interactions. In summary, this review provides insights into human skin microbiota recovery, the interactions between human skin microbiota and diseases, and the strategies for engineering/rebuilding human skin microbiota.
... Similarly, the negative influence of confectionary is confirmed by the studies of other authors. A lot of studies indicated that the intake of available carbohydrate and glycemic load of diets is higher in individuals with acne than in those without [32], as well as that low-glycemic-load diets may lead to alleviating acne symptoms [33]. It is confirmed by the results of studies for specific products, including sugary products and sugary beverages [34]. ...
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Acne vulgaris is diagnosed in the majority of adolescents, decreasing their quality of life, while the diet may influence its aetiology in a gender-dependent manner. The aim of the study was to analyse associations between nutritional behaviours and acne-related quality of life in a population of Polish male adolescents. The study was conducted on a population of Polish secondary school adolescents (a studied sample of 925 adolescents), while the random quota sampling procedure of secondary schools was applied. To assess acne-related quality of life, the Acne Quality of Life (AQoL) Scale and Acne Disability Questionnaire (ADQ) were applied, while the Social Quality of Life (SOCQOL) Score and Cardiff Acne Disability Index (CADI) were calculated. To assess the diet, an Acne-specific Food Frequency Questionnaire (Acne-FFQ) was applied. Neither for the ADQ results, nor for the CADI calculated on the basis of ADQ, was there an association with dietary intake (p > 0.05). The results of the SOCQOL Score (calculated on the basis of AQoL) were positively correlated with the intake of fish (p = 0.0085; R = 0.1144), salty snacks (p = 0.0495; R = 0.0854), and non-chocolate confectionary (p = 0.0078; R = 0.1156). In a group of respondents declaring any acne-related quality of life problems in AQoL, while compared with those declaring no such problems, higher intakes of dairy beverages other than milk (p = 0.0063), white bread (p < 0.0001), other white cereal products (p < 0.0001), fast foods (p = 0.0006), salty snacks (p < 0.0001), chocolate confectionary (p < 0.0001), and other confectionary (p < 0.0001), but lower intake of wholegrain bread (p = 0.0084) were observed. It may be concluded that acne-related quality of life is associated with dietary intake in a population of Polish male adolescents. In the studied population, the most prominent influencing factors were salty snacks and non-chocolate confectionary, with both of them having a proacnegenic effect.
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Acne vulgaris is one of the commonest inflammatory skin diseases seen worldwide, affecting all ethnicities and races, with a peak prevalence between age 15 years and 20 years. The burden of this condition, and the resulting clinical and psychological sequelae, is substantial. The visual appearance of acne and its sequelae, including scarring and pigment changes, frequently results in psychological and social morbidity because of concerns about appearance. As understanding of the pathophysiology has evolved, approaches to achieving the optimal outcomes with effective treatment regimens continue to emerge. In the past few years, several novel therapeutics have been developed, including new agents aimed at reducing antimicrobial resistance and products with specific actions targeting retinoid receptors and androgen receptors. This Review considers the management approaches of an adolescent with acne vulgaris and reviews treatment options from the evidence base and international expert opinion. Approaches to selecting current treatments and novel and emerging treatment regimens are discussed.
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Background: There is scarcity in literature about the reliability of salivary markers in acne vulgaris. Aims: The aims were to evaluate the insulin resistance (IR) and adipsin levels in serum and saliva in a sample of acne vulgaris patients; and to correlate IR and adipsin levels with the disease severity. Methods: This prospective case-control study included 60 acne vulgaris patients (patients Group), in addition, 60 apparently healthy individuals (control group). The severity of acne vulgaris was determined according to Global Acne Grading system (GAGS). Serum and salivary adipsin, fasting glucose, and fasting insulin levels were measured using ELISA kits. Results: Fasting glucose, fasting insulin, and homeostasis model assessment of insulin resistance (HOMA-IR) in patients group both in serum and saliva were elevated when compared with the control group. Serum and salivary levels of adipsin and Quantitative insulin sensitivity check index (QUIKI) in patients were decreased than the control group. Adipsin serum levels show significant negative correlations with all study variables except QUIKI with which the correlation was positive both in serum and saliva. There was a significant positive correlation between serum and salivary adipsin levels (r = 0.873, p < 0.00001) and serum and salivary fasting glucose (r = 1, p < 0.00001). Conclusion: Adipsin could be considered as a promising biomarker for acne vulgaris and its associated insulin resistance. Moreover, the salivary measurements may be considered as useful biomarkers in acne vulgaris patients, but more studies are still required.
Chapter
Dietary elimination of certain foods has been a long-standing strategy utilized by adolescents to try to improve their acne. Unfortunately, there is not enough research currently to support dietary modification as a cure for acne and no major dermatologic society includes dietary elimination in the guidelines for acne management. There is, however, newer research that demonstrates that a low glycemic diet and reduction of milk consumption may improve acne, though this must be balanced with the risks of removing foods from an adolescent’s diet that may be important for growth and development.
Article
About 50 million people in the United States have acne.¹ Acne affects 85% of all adolescents and about 12% of adult women.²,3 Acne is a chronic inflammatory condition presenting as comedones (blackheads and whiteheads), papules, pustules, and nodules. It is caused by androgen-induced sebum production, follicular hyperkeratinization, and colonization of the folliculosebaceous unit by the Proprionibacterium acnes bacterium.⁴ Follicles become impacted with sebum because of follicular keratinization and then become distended, forming comedones. Proprionibacterium acnes growth in the follicle results in cytokine release, causing inflammatory lesions.⁵ Although it is a benign condition, acne can have considerable morbidity, including pain and discomfort, permanent scarring, and depression and anxiety resulting in poor self-esteem.
Article
To test the widespread idea that chocolate is harmful in instances of acne vulgaris, 65 subjects with moderate acne ate either a bar containing ten times the amount of chocolate in a typical bar, or an identical-appearing bar which contained no chocolate. Counting of all the lesions on one side of the face before and after each ingestion period indicated no difference between the bars. Five normal subjects ingested two enriched chocolate bars daily for one month; this represented a daily addition of the diet of 1,200 calories, of which about half was vegetable fat. This excessive intake of chocolate and fat did not alter the composition or output of sebum. A review of studies purporting to show that diets high in carbohydrate or fat stimulate sebaceous secretion and adversely affect acne vulgaris indicates that these claims are unproved.
Background: Previous studies suggest possible associations between Western diet and acne. We examined data from the Nurses Health Study II to retrospectively evaluate whether intakes of dairy foods during high school were associated with physician-diagnosed severe teenage acne.
Article
For a textbook-perfect example of what happens to people when their eating habits change, consider the Canadian Eskimos. Few if any population groups have ever experienced such rapid changes in their way of living as the Eskimos.They offer compelling evidence of food s effect on growth and health. This is the third in a series about the nutritional diseases of civilization.
Article
The author describes changes in eating habits and type of foods consumed when the Eskimos gave up their previous nomadic existence to live in settlements. From 1 meal of high protein low fat and practically no carbohydrates with frequent nibbling the rest of the day on fish the Eskimo family in settlements gets 3 rich meals a day and seeminly endless sweet drinks candies and chocolates. More than half the total carbohydrates are consumed as refined sugar. In a series of test programs the author found that Eskimos have difficulty in keeping their blood sugar level stable after oral sugar loads while the white ma n does it easily. Some other new things observed in Eskimos are: 1) prenatal and postnatal growth acceleration to a significant degree and earlier onset of puberty which is directly attributable to increased sugar consumption without increased protein. 2) Increasing diabetes mellitus: in Alaska and Greenland it has gone up 3-fold during the last decade. 3) Increased atherosclerotic diseases; incidence of calcification of leg arteries among Eskimo men 40 to 69 years who had lived in settlements for more than 10 years was 5 times that of remote nomads. 4) Increased dental decay. 5) Significant increase in serum cholesterol and blood lipid levels with parallel increases of skinfold measurements especially in 18 to 40 year olds. 6) Increase in other "civilization diseases" like cholelithiasis gall bladder and acne vulgaris. Increased morbidity and mortality of infants may be related to increased bottled feeding and increased fertility to shortening of lactation due to the same reason.
Article
An account of the source, processing and composition of chocolate is presented. It is shown that chocolate liquor exhibits two exceptional dietary properties not possessed by any other food. Firstly, its lipid content of over 50% is uniquely stearie-rich and, secondly, it combines a high lipid content with a significant concentration of xanthine alkaloids. Prepared chocolate possesses a third unusual dietary property, the combination of a high lipid content with a high sugar content. The work of Fulton, Plewig and Kligman (1969) is reviewed and it is suggested that their conclusion, that chocolate did not affect the course of their acne patients, requires revision because their calculations did not make adequate allowance for the dietary properties of chocolate. A hypothetical mechanism is described by which the constituents of chocolate may possibly aggravate acne.