Acne and diet: Truth or myth?

Adilson Costa, MD
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In this article, we discuss the newest concepts regarding the relationship between acne and diet.

Possibly the most influential component in this relationship is sebum. We also discuss in depth the

factors that could be present in a high glycemic index diet and the secondary hyperinsulinemia pattern

that follows. For example, a diet-based hyperinsulinemic condition associated with the secondary

presence of insulin-like growth factor 1 (IGF-1) may induce the synthesis of androgens in various body

tissues which, remarkably, also induce the production of sebum. 1,2

Acne and the modern pattern of food consumption

Acne is not related to obesity,3,4 but with Westernization of the diet. The absence of acne in natives

from Kitava and Papua New Guinea, and the Ache people of Paraguay, was attributed to their diet,

which is substantially based on a lower glycemic index. 5 The same characteristic is noted in Inuit

people.6 Rural residents of Kenya, Zambia and Bantu present with less acne than their descendents

who migrated to the USA.7-9

The frequent consumption of carbohydrates - the "Western diet" - which means a high glycemic index,

may repeatedly expose adolescents to acute hyperinsulinemia. Acute hyperinsulinemia influences

follicular epithelial growth and keratinization, as well as sebaceous secretion mediated by bovine

androgens.5

Nutrition as an accelerator of sexual maturity and acne break-out factor

The improvement in people's diets has been associated with precocious sexual maturity. For example,

adolescent females with a low glycemic index diet present with a delay in menarche. 10 In 1970, the

first menarche occurred at about 12 years of age whereas, in 1835, it occurred at approximately age

16 years.11 In addition, the more serious cases of comedones prevail in girls with precocious menarche

and high dihydroepiandrosterone levels.12 The predominance and prognosis of acne are also correlated

with sexual maturity.

Hyperinsulinemia, through food intake, stimulates androgen synthesis, which in turn stimulates
sebaceous production. Moreover, hyperinsulinemia increases the synthesis of IGF‐1 and decreases

insulin‐like growth factor‐binding protein‐3 (IGFBP‐3). The high serum levels of both these proteins
play a direct role in the proliferation of keratinocytes and apoptosis, which culminates in the

hyperproliferation of keratinocytes.13 IGF-1 appears to mediate comedo-associated factors such as

androgens, growth hormones and glucocorticoids. These endogenous androgens increase the serum

levels of IGF-1 and vice-versa, thus causing an increase in sebum production. 14,15

Food that could worsen acne

Milk

Despite its low glycemic index, milk paradoxically induces an increase in IGF-1 levels, an effect that is

particularly pronounced with skimmed milk intake, which causes a break-out and/or worsening of

acne.14,15 Furthermore, milk contains estrogen, progesterone, androgen precursors and 5α-reductase-

dependent steroids, which are implicated in comedogenesis. 16

Milk also contains other bioactive molecules that act in the pilosebaceous unit, such as glucocorticoids,

transforming growth factor-beta, hormone peptides similar to thyrotropins, and opiaceous compounds.

It is speculated that the processing of skimmed milk increases either the bioavailability of such

bioactive molecules or their interaction with binding proteins; whey proteins, especially α-

lactoalbumin, are added to the formula of skimmed and low-fat milk, and appear to play an important

role in comedogenesis.14,15 Milk is also rich is iodine, which can stimulate the appearance of acne;

iodine contained in milk results from supplementation of the animal's diet and the use of iodine-based

solutions in milking equipment.17

Fatty-acid-based food

It has been suggested by recent evidence that monounsaturated fatty acids stimulate morphological

changes in the sebaceous glands - changes which are not seen with saturated fatty acids. 18

Monounsaturated fatty acids are largely composed of sapienic acid, which comes from the delta-6

desaturase of palmitic acid, a saturated fatty acid.19 Delta-6 desaturase and the resulting accumulation

of sapienic acid in sebum appear to be important factors in sebaceous lipogenesis. 20 Rats with delta-9

desaturase deficiency, which is equivalent to delta-6 desaturase in humans, have hypoplasia of the

sebaceous glands.21

In a 3-month study by Costa et al,22 in which a dietary supplement of 3 g of essential fatty acids

(linoleic, linolenic and gamma-linolenic acids) was given daily, a reduction in the size of the sebaceous

glands was observed. An intake of polyunsaturated fatty acids (omega-6 and omega-3) modulates the
inflammatory response.23 The typical Western diet maintains a relatively higher concentration of

omega-6, compared with omega-3, because of the predominance of omega-6 in most vegetable oils

and foods processed with such oils.23 The supplemental intake of omega-3 fatty acids suppresses

interleukin (IL)-1-beta,24,25 IL-1-alpha,24-27 tumor necrosis factor-alpha,24-27 IL-6,25-27 and IL-8.27 The

suppression of IL-1-alpha by an omega-3-rich diet may positively influence the differentiation of

corneocytes by preventing or diminishing the hypercornification that occurs during

microcomedogenesis.24 Examples of foods rich in omega-3 include whole grains, fresh fruits and

vegetables, fish, olive oil, garlic, as well as moderate wine consumption; examples of foods rich in

omega-6 are meat, evening primrose oil, borage oil, and black currant seed oil. 28

Zinc and vitamin A

Michaëlsson et al29 observed that blood levels of both retinol-binding protein and zinc are low in

patients with severe acne. Moreover, diets low in zinc may worsen or activate acne, especially in those

with pustular reactions; this is verified by various reports of acne exacerbation by administration of a

parenteral low-zinc diet.30

Chocolate

Chocolate has long been incriminated as an aggravating factor in acne. Patients often refer to the

break-out of pustules a few days after chocolate intake. 31 

In 1969, a preliminary study concluded that there was no evidence linking chocolate intake to acne.

However, according to Cordain,1 this early study was not accurate because the placebo group received

a chocolate-like bar with high concentrations of substances that predispose to hyperglycemia and

insulinemia.

In recent nutritional studies, an increase in postprandial insulinemia has been observed in young

adults after a chocolate-based diet.32 This may result from the fact that chocolate is rich in biologically

active compounds (eg, caffeine, theobromine, and serotonin), which increase secretion of insulin and

its peripheral resistance.33,34 Additionally, milk contains amino acids (eg, arginine, leucine, and

phenylalanine) that produce insulin when combined with carbohydrates. 35,36

Conclusions
The association between diet and acne has, at the present time, been well evaluated. Importantly,

evidence shows that acne is not as prevalent in non-Western societies, but that its prevalence can be

increased upon the adoption of a Western diet. This goes against the claim that ethnic factors are the

only ones to be implicated in its etiology, and reinforces the idea of a relationship between acne and

diet.

According to scientific arguments provided in this article, it is possible to envisage that foods rich in

fatty acids, mainly those rich in omega-3, as well as a diet based on a low glycemic index, can protect

sebaceous glands against mechanisms that lead to clinical acne manifestations.

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