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Acne is a disease of civilization. It did not exist in the paleolithic era or in traditional societies. This suggests that the disease is predominately environmental, not genetic or hormonal.

Acne and lipid peroxidation

Your skin has sebaceous glands which secrete sebum (the oily substance on your face) to moisturize your face However, sometimes the sebum on your face degrades into other chemical products in a process known as "oxidation." This is the same process as the rusting of iron or the browning of an apple. In other words, the sebum in your face is chemically degraded to a different product. This resulting product is known as lipid peroxides.

The lipid peroxides causes inflammation of your skin (inflammation is the body's response to irritants and injury, producing redness, heat, pain and swelling (lipid peroxides in themselves are irritants)). Both the lipid peroxides themselves and the accompanying inflammation causes acne. The article shows that antioxidants could prevent acne. Antioxidants prevent the oxidation of substances, including sebum. So the more antioxidants you supplement, the less your sebum would be turned into lipid peroxides, resulting in less acne. The article shows how antioxidants in its oral and topical forms, including a vitamin C precursor, zinc, vitamin E, vitamin A, niacinamide and lactoferrin (a dairy-based glycoprotein) reduces acne. Here are some quotes from the article:

An emerging candidate is the stable vitamin C precursor, sodium ascorbyl phosphate (SAP), an agent which has been shown to reduce sebum oxidation products by up to 40%. A preliminary open-label study involving 60 acne patients used 5% SAP (applied twice daily) and showed superior efficacy and tolerance after 12 weeks vs. 5% benzoyl peroxide (BP) [108]. It was also reported in a second open-label study that 5% SAP was more effective than 1% clindamycin in the overall and inflammatory lesion counts after 12 weeks [109]. This was followed up recently by randomized double-blind intervention studies. The first showed that 5% SAP reduced inflammatory acne lesions 49% after 8 weeks, a result that was slightly enhanced by the co-administration of SAP and 0.2% retinol. The combination reduced inflammatory lesions by 63% over the same period [110]. The most recent study showed that 61% of patients treated with 5% SAP lotion showed improvement in the Investigator's Global Assessment Score (IGAS) and 71% improved as measured by the Subjects' Global Assessment Score (SGAS). These results were in contrast with the group receiving the placebo vehicle lotion where the reports were 38% improvement via IGAS and 52% via the SGAS at the end of the 12-week study [111].

Green tea is a source of plant-based antioxidants, particularly the catechins which are well known to prevent local and systemic declines in SOD and GSH-Px activity, as well as attenuating lipid peroxidation [112,113]. A recent clinical study has reported value of a topical (2%) green tea lotion in mild-to-moderate acne. The open-label study showed that twice-daily application of the green tea lotion reduced total lesion count by 58% after 6 weeks [114]. A similar study using a 2% tea (unspecified type of tea) lotion found that it was more effective than 5% zinc sulfate topical preparation in reduction of acne lesions after 8 weeks [115]. It should be pointed out that there are multiple mechanisms whereby green tea may be therapeutic in acne - anti-inflammatory activity, anti-microbial activity against P. acnes, and a potential ability to reduce sebum production via 5-α-reductase inhibition [116,117]. In any case, the antioxidant activity of green tea and its catechins warrant further investigation.

Additional support for the use of topical antioxidants is found in a recent open-label trial of the antioxidant agent fullerene. It has been reported that fullerene, a spherical carbon molecule with a unique cage structure capable of acting as a sponge to free radicals, has antioxidant activity several hundred times higher than vitamin-based antioxidants. In particular, fullerene can protect against lipid peroxidation. A 1% fullerene gel applied twice daily reduced the number of inflammatory lesions by 38% during the 8-week investigation. While small (n = 11) and without a placebo control, this pilot investigation in adults with acne suggests potential value of fullerene as a topical antioxidant therapy [118].

Zinc and nicotinamide are both nutrients which support antioxidant pathways [119,120], and preliminary clinical trials show value in topical application. Zinc is well known to enhance efficacy of topical antibiotics, while a 4% nicotinamide gel has been shown to outperform 1% clindamycin gel when applied twice daily for 12 weeks (82% vs. 68% improvement respectively) [121]. There are a limited number of small studies indicating value of oral zinc in acne, the most recent showing that 30 mg of zinc gluconate reduces total inflammatory lesion count by 57% after two months [122]. In the open-label Nicomide Improvement in Clinical Outcomes Study (NICOS) an oral nutrient combination (750 mg nicotinamide, 25 mg zinc, 1.5 mg copper, 500 mcg folic acid) taken daily for eight weeks appeared to be effective and well tolerated. After four weeks 79% of the subjects demonstrated at least moderate improvement, and the addition of oral antibiotic therapy to one subgroup (51 of the total n of 198) did not provide any additional clinical benefit [123].

An oral multi-nutrient antioxidant agent has been the subject of a recent 12-week preliminary trial involving 48 patients with acne. The antioxidant capsule was taken tid for a daily total of 45 mg zinc, 180 mg vitamin C, 18 mg mixed carotenoids, 45 IU d-alpha-tocopherol acetate and 390 mcg of chromium. Significant improvements were noted in physician evaluations after 8 weeks, and after 12 weeks 79% of the patients were found to have an 80% or more improvement. As this was an open-label study, broad conclusions cannot be made concerning the outcome. It is interesting to note, however, that the clinical benefits did not appear until 2 to 3 months after internal consumption of the agent [124]. This implies that the use of internal agents may take time. Indeed oral vitamin E consumption can take weeks before sebum levels are significantly elevated [125]. The addition of mixed carotenoids, presumably inclusive of lycopene, is theoretically sound. Lycopene can reduce lipid peroxidation and it can support SOD and GSH-Px activity [126,127]. Related carotenoids such as lutein and zeaxanthin are also of potential value since they can reduce lipid peroxidation in the skin [128]. It could be speculated that another lipophilic antioxidant, co-enzyme Q10, found in skin surface lipids, would be of therapeutic value [129].

Lactoferrin, a dairy-based glycoprotein with strong antioxidant activity [130,131], has also been the subject of a recent clinical trial in acne. In a 12-week double-blind, placebo-controlled study, the oral consumption of 200 mg of lactoferrin reduced total lesion count by 23% over placebo. The inflammatory lesion count declined by over 38% during the course of the three months. In support of the total lesion reduction, the severity of acne according to the Leeds Acne Grading System declined 20% compared with placebo [132].

Acne and histamine intolerance

Histamine is suggested to cause acne. There is anecdotal evidence of people clearing their skin up after avoiding canned, dried and fermented foods (foods that are high in histamine content). Also anti-histamines are used to treat acne.

Cream may have additives like like carrageenan and polysorbate 80. Carrageenan is pro-inflammatory and polysorbate 80 causes a histamine release.

Conventional milk is another anecdotal cause of acne. Conventional milk may have added vitamins, and these vitamins may be bound to polysorbate 80 as an emulsifier. One person experienced that switching to raw milk with no added vitamins, his face has cleared up. But when reintroducing conventional milk, his acne flared back.

Vitamin A and acne

Ray Peat suggests that acne could be cured by vitamin A. Anecdotal evidence suggests that large doses of vitamin A from supplements or liver subsides their acne.[1][2]

From Kligman et al. (1981).[1]

Oral vitamin A (retinol) is generally not considered useful in the treatment of acne vulgaris. We conducted a study which showed that retinol was indeed ineffective at the usual doses of 50,000 to 100,000 IU daily. Retinol was highly efficacious in doses of 300,000 units for women and 400,000 to 500,000 units for men, toxicity was slight and limited mainly to skin (xerosis) and mucous membranes (cheilitis). The danger of hypervitaminosis A in this dosage range has been exaggerated. Retinol is a valuable drug for treating stubborn, severely inflammatory acne vulgaris. It is administered until the disease is brought under control, usually within three to four months. Then the dosage is progressively reduced relying on conventional drugs to keep the disease in abeyance.


  1. Kligman, A. M., Mills, O. H., Leyden, J. J., Gross, P. R., Allen, H. B., & Rudolph, R. I. (1981). Oral vitamin A in acne vulgaris Preliminary report. International journal of dermatology, 20(4), 278-285.