diet and acne (review, Arbor Nutrition)

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Study 1: Low GI diet as treatment for acne

A new Australian trial has used a low glycaemic load (GL) diet as a

treatment to reduce acne.

Method: Single blind controlled clinical trial on 43 young men (15-25

years) with acne who were placed on either a low GL diet (25% energy

from protein, 45% from low glycaemic index (GI) carbohydrates, dietary

glycaemic load=101) or a conventional control diet (emphasising

CHO-dense foods with no reference to their GI, dietary glycaemic

load=174) for 12 weeks. Assessment of acne was made by researchers who

were blinded as to which diet the subject was on. A sub-set of 31

subjects had sebum analysis.

Results: The low GL subjects had significantly fewer acne lesions at the

end of the trial than controls. They consumed less energy (p=0.06) and

had greater weight loss, lower free androgen index (p= 0.04), increased

insulin-like growth factor binding protein-1 (p=0.001), less

self-reported skin oiliness (p=0.013). The fall in lesion count was

correlated with the significantly (p=0.007) higher ratio of saturated to

monounsaturated fat in sebum in the low vs control GL group (r = 0.39,

p=0.03). See Graph in Acrobat version.

Refs.: Am J Clin Nutr. 2007 Jul;86(1):107-15. and J Dermatol Sci. 2008

Apr;50(1):41-52.

Study 2: Milk and acne prevalence

An newly reported American study has compared milk consumption with acne

prevalence in boys.

Method: Observational prospective cohort study on 4,273 young boys whose

diet was analysed on three occasions over 3 years, and self-reported

their acne status a year later, at which stage they were teenagers.

Results: Adjusted multivariate prevalence ratios for acne were higher in

those who consumed more skim but not other types of milk. See Table.

Ref.: J Am Acad Dermatol. 2008 May;58(5):787-93

COMMENTARY

For many years the conventional wisdom dispensed by physicians on the

relationship between diet and acne vulgaris has been that there is none

(ref.1, 2). In a recent study, the fact that nearly a half of a group of

final year medical students believed that diet was an important factor

in acne was held to be an unfortunate misconception " likely to

perpetuate misinformation in the community " (ref.3).

The `expert view' from doctors is in stark contrast to what their

patients think. Many studies have shown that the average person is under

the distinct impression that diet can indeed affect acne, particularly

fatty foods and chocolate (ref.4-6).

A careful look into this question reveals something rather fascinating -

that although medical textbooks in earlier days strongly supported the

idea of `acne diets', for the last 50 years this has completely reversed

(ref.7, 8). Yet experts' current confidence that there is nothing to the

diet-acne story is itself based on almost no evidence (ref.2, 9).

The fact is that the most commonly cited evidence in support of the

`modern' view is a single randomised clinical trial, conducted nearly 40

years ago. This trial found no increase in acne prevalence after 4 weeks

of eating chocolate vs control candy bars on top of normal diet

(ref.10). That it was a small study involving subjects with a high

baseline acne prevalence and that both control and active candy bars

were equally high in fat and sugar (both groups had significantly

increased sebum production during the treatment phase) may have escaped

the attention of many of those who have subsequently cited it.

Since then the subject appears to have been dropped from researchers'

agenda altogether. A review of over 1,500 controlled trials on acne

found that less than half a percent even mentioned diet (ref.11).

Amongst the few research papers that have addressed the topic was a

short trial of acne patients in 1978 which failed to find benefit from

eliminating foods for which they had a positive skin prick allergy test

(ref.12). In 2002 Cordain et al. reported the fascinating fact that acne

was completely absent in two spectacularly non-westernised societies and

wondered if it might therefore be considered a `disease of

civilisation'. They speculated that acne could be partly due to the

impact of higher glycaemic load on insulin levels (ref.13). Until now

that is where the subject has been left to rest.

The findings of new Study 2 linking milk intake with acne prevalence are

an interesting addition to this scant research literature. The authors -

from the renowned `Harvard group' of nutritional epidemiologists -

earlier published the results from the girls in this teenage cohort,

which were of similar nature, but applied to total, whole and low fat

milks (ref.14).

Their data is prospective, but does not prove that it is a causal link.

If the connection does indeed turn out to be causal, one could consider

any number of factors related to milk intake, including its fat content,

proteins, hormones and many other constituents. There is not much in the

current literature to guide us to any one conclusion. What we can say is

that the pathology of acne is too complex to lend itself to any of

simplistic explanations, such as acne being `caused by' an excess of

dietary fat.

In that context, the findings of New Study 1 are particularly

interesting. This well conducted randomised clinical trial from

Australia explored Cordain's hypothesis that acne may be related to

dietary glycaemic load. The researchers found that ome fairly modest

dietary switches from higher to lower GI foods can significantly

benefit acne sufferers. This was achieved in a group of young men whose

acne, although categorised as mild to moderate in grade, was certainly

enough to impact the self-esteem of the typical self-conscious young

adult.

The authors attempted to identify a mechanism related to hormonal

changes and insulin metabolism. The role of insulin-like growth factors

may be of importance (ref.15), and whilst this trial found no

significant change in IGF-1 levels, it did report an increase in

IGF-binding protein from low GI diet that could have resulted from

improved insulin sensitivity. Although not yet conclusive, such work may

also help throw light on the role of diet in other hormone-related

disorders which feature acne, such as polycystic ovary syndrome

(ref.16).

New Study 2 is not a large trial and clearly more such work will be

needed. However, it represents a good start in the right direction. Acne

is a matter of everyday clinical concern to primary care physicians and

their adolescent patients, and questions about diet in relation to acne

are commonplace.

ly, one has to conclude that the advice doctors have been giving

such patients over many decades has been based on little more than

assumption. Perhaps " we don't know " would have been a better response.

We are not sure that this is quite what was intended in the American

Academy of Dermatology's latest guidelines for acne management where

they state: " no evidence exists on the role of diet in acne " (ref.17).

In any case, the new research means that that conclusion is no longer

accurate.

Clinicians must make up their own mind if results of such preliminary

nature warrant suggesting to their acne patients that they `have a go'

at a lower GL diet. Our own view is that this is not a hard dietary

change to make, is unlikely to cause harm, and offers at least some

chance of a benefit.

References:

1. Semin Cutan Med Surg. 2005 Jun;24(2):84-91.

2. J Am Acad Dermatol. 2005 Feb;52(2):360-2.

3. Australas J Dermatol. 2001 May;42(2):98-101.

4. J Am Acad Dermatol. 2001 Mar;44(3):439-45.

5. Clin Dermatol. 2004 Sep-Oct;22(5):387-93.

6. West Afr J Med. 2004 Jan-Mar;23(1):85-7.

7. Arch Dermatol. 2002 Dec;138(12):1591-2.

8. Eyre and Spottiswoode, London 1939.

9. Fam Pract. 2005 Feb;22(1):62-70.

10. JAMA. 1969 Dec 15;210(11):2071-4.

11. J Am Acad Dermatol. 2002 Aug;47(2):231-40.

12. Dermatologica. 1978;157(5):294-5.

13. Arch Dermatol. 2002 Dec;138(12):1584-90.

14. Dermatol Online J. 2006 May 30;12(4):1.

15. Clin Dermatol. 2008 Jan-Feb;26(1):93-6.

16. Nutr Clin Pract. 2008 Feb;23(1):63-71.

17. J Am Acad Dermatol. 2007 Apr;56(4):651-63.

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Communications PTL 2008

S. Kalman PhD, RD, CCRC, FACN

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