Diet and nutrition’s influence on acne vulgaris

In a recent study published in the journal Nutrients, researchers review existing publications to determine the role of nutrition in the development of acne vulgaris. To this end, the complex interaction of various factors was investigated to elucidate how diet influences biochemical markers, gene transcription related to sebaceous gland function, bacterial proliferation, and inflammation associated with acne.

Study: Impact of Diet and Nutrition in Patients with Acne Vulgaris. Image Credi: maxbelchenko / Shutterstock.com

What causes acne?

Acne vulgaris is a chronic inflammatory skin condition that primarily affects adolescents and young adults. It is 80-100% prevalent in individuals between 11 and 30 years of age, thereby affecting about 9% of the global population. The complex etiology of acne vulgaris involves genetic, hormonal, and environmental factors.

Acne presents with inflammatory and non-inflammatory lesions, such as papules, pustules, and comedones, with various clinical forms categorized by lesion severity. Microcalcifications are involved in lesion formation due to hormonal disturbances, sebum secretion, Cutibacterium acnes proliferation, and keratinization abnormalities.

Severe acne can lead to scarring and hyperpigmentation, thus significantly impacting the well-being and quality of life of affected individuals. Dietary influences on the development of acne are currently being explored, along with novel therapeutic approaches to alleviate symptoms and improve patient outcomes.

The role of food in the pathogenesis of acne vulgaris

A higher prevalence of acne is observed in Western populations than in non-Western populations due to dietary differences. Western diets, which are primarily characterized by low levels of long-chain omega-3 fatty acids and increased consumption of refined carbohydrates, dairy products, chocolate, and saturated fats, may exacerbate acne by promoting inflammation and altering metabolic cues.

More specifically, saturated fatty acids present in the Western diet induce inflammation through the expression of toll-like receptor 2 (TLR2)/ interleukin 1B (IL-1B) receptors, thereby leading to increased secretion of IL-17A and hyperproliferation of keratinocytes.

Diets with a high glycemic index (GI) and high dairy consumption are also associated with elevated levels of hormones involved in acne pathogenesis, such as insulin-like growth factor-1 (IGF-1) and insulin. Hyperinsulinemia, which results from high GI diets, stimulates IGF-1 synthesis in the liver and subsequently promotes sebaceous cell proliferation and lipogenesis. Insulin and IGF-1 lead to activation of the mammalian target of rapamycin complex 1 (mTORC1), which promotes sebaceous gland enlargement, lipid synthesis, and keratinocyte proliferation, contributing to acne development.

Abnormalities in the gut microbiome, which are induced by an abnormal diet, further exacerbate acne pathogenesis through dysregulation of the mTOR pathway and increased gut barrier permeability. Overall, diet plays a significant role in acne pathogenesis by influencing hormonal levels, inflammation, and gut microbiota composition.

Nutrients with possible adverse effects on acne

Milk and dairy products, particularly those high in whey protein and casein, have been associated with increased IGF-1 levels, which can lead to hyperinsulinemia and exacerbation of acne lesions. Cow’s milk also contains hormone precursors that can be converted into dihydrotestosterone (DHT), a potent inducer of acne. While conflicting data exist regarding the fat content of milk and its role in acne, it is suggested that hormones and bioactive molecules in milk are more significant contributors.

Chocolate consumption, especially dark chocolate, has been associated with the worsening of acne symptoms. The presence of saccharides in chocolate may induce insulin secretion and trigger signaling pathways that promote acne lesions. Cocoa ingredients can also increase the secretion of inflammatory cytokines, which may further aggravate acne.

Saturated and trans fatty acids from animal fats and hydrogenated plant fats have also been implicated in acne pathogenesis. These fats can stimulate pro-inflammatory cytokine production and activate signaling pathways like mTORC1, thus leading to increased sebum production and dermal inflammation.

Other dietary factors such as alcohol intake, excessive salt consumption, and high-GI foods like salty snacks, eggs, soft drinks, corn, candy, and high-gluten diets have also been associated with acne exacerbation.

Conclusions

Acne vulgaris significantly affects patients’ quality of life and well-being, thus highlighting the importance of understanding its contributing factors and implementing effective treatments. Previously, dietary factors were not widely recognized as significant contributors to acne; however, growing scientific evidence supports their role in its pathogenesis.

Dairy products, chocolate, and saturated fats have been identified as key dietary components that contribute to acne development. Other factors, such as alcohol, salted products, gluten, eggs, biscuits, corn, fruit, sweets, or soft drinks, may also exacerbate acne; however, further research is needed to confirm their impact.

Future studies should be designed meticulously to avoid limitations and provide accurate insights into the influence of diet on acne. Knowledge of dietary factors that negatively affect the development of acne will enable clinicians to offer appropriate recommendations and guidance, including elimination diets, to reduce acne lesions and enhance the quality of life for individuals with acne vulgaris.