Acne vulgaris, the most common form of acne, is an inflammatory disease of the sebaceous (oil secreting) glands and hair follicles of the skin. It is characterized by comedones (blackheads) , papules (pimples), and pustules (blisters). (1)
Causes
(a) Many factors can cause acne. Research has centered on hormonal dysfunction and oversecretion of sebum as possible primary causes.(2) A diet high in fat can contribute to acne vulgaris. Acne is associated with oily skin due to an excess of sebum, the fatty secretion of the sebaceous glands. Eating fat increases sebum production.(3,4)
(c) One new theory is that a deficiency of pantothenic acid may play a role in some cases.(5)
At Risk
This disease is most common in adolescence. Acne activity is primarily dependent on the genetic sensitivity of the hair follicle and oil gland to androgenic (male) hormones circulating in the blood stream.
Prevention and Management
General:
Most teenage acne will clear as the follicles mature and become less sensitive to the hormone induced changes, however in some, it will persist well into adulthood, especially those with strong genetic tendencies toward acne. The most important method of prevention is to keep the skin clean and free from dirt and oil.(6)
Nutritional Influences:
A low-fat, high-fiber, nutrient-dense diet adequate in vitamins and minerals and low in sugar, refined and convenience foods should be consumed. In one experimental study, patients experienced a rapid clearing of acne following supplementation with one ounce of bran cereal daily.(7) More studies are needed to determine if a high fiber diet is useful in treating acne.
Blood zinc levels are often lower in people who suffer from acne.(8)
Studies have shown that selenium is beneficial for treating acne pustules, possibly because one of the functions of selenium is to help fight infections. Patients with low RBC glutathione peroxidase levels and pustular acne responded best to selenium supplementation.(9)
Vitamin E works closely with selenium. Syndromes caused by selenium deficiency overlap those caused by a vitamin E deficiency; because of the close relationship, vitamin E and selenium are often combined to make treatment more effective.(10)
Vitamin A and its synthetic derivatives appear to be beneficial; high doses are needed, however. Because of the potential for toxicity, vitamin A and vitamin A derivatives should be used only under medical supervision.
Vitamin E affects the biologic utilization of vitamin A. The absorption of vitamin A is markedly impaired in vitamin E deficient animals.(11,12)
Excess supplementation of iodine may cause or exacerbate acneiform eruptions.(13) Kelp as a dietary supplement (14) or fast foods (15) may contain sufficient iodine for this adverse effect.
A deficiency of omega-6 essential fatty acids in the pilosebaceous epithelium might account for follicular hyperkeratosis in acne.(16)
Abstracts
Kremer JM, Bigaouette J. Nutrient intake of patients with rheumatoid arthritis is deficient in pyridoxine, zinc, copper, and magnesium. J Rheumatol 1996 Jun;23(6):990-4. OBJECTIVE: To determine nutrient intake of patients with active rheumatoid arthritis and compare it with the typical American diet (TAD) and the recommended dietary allowance (RDA). METHODS: 41 patients with active RA recorded a detailed dietary history. Information collected was analyzed for nutrient intake of energy, fats, protein, carbohydrate, vitamins and minerals, which were then statistically compared with the TAD and the RDA. RESULTS: Both men and women ingested significantly less energy from carbohydrates [women 47.4% (6.4) vs 55% RDA. p = 0.0001: men = 48.9% (7.4). p = 0.025] and more energy from fat [women = 36.8% (4.5) vs 30% RDA. p = 0.001 and men = 35.2% (5.9) p = 0.02]. Women ingested significantly more saturated and mono-unsaturated fat than the RDA (p = 0.02 and p = 0.04 respectively) while men ingested significantly less polyunsaturated fat (PUFA) (p = 0.0001). Both groups took in less fiber (p = 0.0001). Deficient dietary intake of pyridoxine was observed vs the RDA for both sexes (men and women p = 0.0001). Deficient folate intake was seen vs the TAD for men (p = 0.02) with a deficient trend in women (p = 0.06). Zinc and magnesium intake was deficient vs the RDA in both sexes (p values < or =" 0.001)" p =" 0.004" p =" 0.02">Leung LH. Pantothenic acid deficiency as the pathogenesis of acne vulgaris. Med Hypotheses 1995 Jun;44(6):490-2. For years, the pathogenesis of acne vulgaris has been known to be strongly influenced by hormonal factors. However, the exact role of and the interrelationship among the various hormones in question have not been well elucidated. Here, I wish to suggest a radically different theory for its pathogenesis and relate its basic pathology to a deficiency in pantothenic acid, a vitamin hitherto not known to cause any deficiency syndrome in humans. Hence, the effect of hormonal factors in this disease entity becomes secondary to that of the availability of pantothenic acid. A complete cure of this condition is effected by a very liberal replacement therapy with the vitamin.
References
(1) Diseases. 2nd ed. Springhouse (PA):Springhouse Corporation. 1997. p 1173.
(2) Diseases. 2nd ed. Springhouse (PA):Springhouse Corporation. 1997. p 1173.
(3) Rosenberg EW, Kirk BS. Acne diet reconsidered. Arch Dermatol 1981;117:193-95.
(4) Klurfeld DM. The Diet and Acne. Archives of Dermatology 1983;119(4):276.
(5) Leung LH. Pantothenic acid deficiency as the pathogenesis of acne vulgaris. Med Hypotheses 1995 Jun;44(6):490-2
(6) Somer E. The Essential Guide to Vitamins and Minerals. New York:HarperPerennial. 1992.
(7) Putzier E. Dermatomycoses and an antifungal diet. Wiener Medizinische Wochenschrift 1989 Aug 31;139(15-16): 379-80.
(8) Pohit J et al. Zinc status of acne vulgaris patients. J Appl Nutr 1985;37(1):18-25.
(9) Michaelsson G, Edqvist L. Erythrocyte glutathione peroxidase activity in acne vulgaris and the effect of selenium and vitamin E treatment. Acta Derm Venereol (Stockh) 1984;64(1):9-14.
(10) Michaelsson G, Edqvist L. Erythrocyte glutathione peroxidase activity. in acne vulgaris and the effect of selenium and vitamin E treatment. Acta Derm Venereol (Stockh) 1984;64(1):9-14.
(11) Ames SR. Factors affecting absorption, transport and storage of vitamin A. Am J Clin Nutr 1969;22:934.
(12) Ayers S Jr, Mihan R. Acne vulgaris and lipid peroxidation: New concepts in pathogenesis and treatment. Int J Dermatol 1978;17:305.
(13) Hitch JM. Acneiform eruptions induced by drugs and chemicals. JAMA 1967;200:879-80.
(14) Fischer AA. Contact Dermatitis. 3rd ed. Philadelphia:Lea and Febiger;1986. p 593.
(15) How nutritious are fast-foods? Consum Rep 1975;40:278-81.
(16) Downing DT et al. Essential fatty acids and acne vulgaris. J Am Acad Dermatol 1986;14:221-25.
Source
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