Cosmeceutical Critique: NiacinamideDr. Leslie Baumann
Volume 33, Issue 8, Page 17 (August 2002)
Unlike many cosmeceutical ingredients, there is a great deal of research that supports the use of topical niacinamide. Studies have shown its usefulness in increasing synthesis of collagen and lipids, inhibiting the transfer of melanosomes, and decreasing inflammation. As a precursor to niacin, it may even play a role in preventing skin cancer.
Initially, the chemistry of niacinamide is confusing because of the complicated nomenclature; however, once one understands that niacinamide and niacin have several names, it becomes easier to understand. Niacin is also known as vitamin B3 or nicotinic acid. Niacinamide is also called nicotinamide. Most people shun the terms nicotinic acid and nicotinamide because they sound too much like nicotine.
Niacinamide is the physiologically active form of niacin and serves as a precursor to niacinamide adenine dinucleotide (NAD) and niacinamide adenine dinucleotide phosphate (NADP). NAD and NADP are very important for cellular energy production. In addition, NAD and its reduced form, NADH, act as coenzymes in more than 40 biochemical reactions. Niacin has long been known to be essential for healthy skin; deficiency causes pellagra. Niacinamide and niacin are not synthesized in the human body and therefore must be supplied externally, either through the diet or through topical application. Deficiency of niacin and niacinamide appears to play a role in the development of several types of cancer, including skin cancer. The presence of NAD is necessary to repair the DNA damage that occurs after sun exposure. In fact, research has shown that cells depleted of niacin develop genomic instability.
Oral supplementation with niacin has been shown to protect against the development of esophageal and stomach cancer (Genes Dev. 11:2347-58, 1997). Further, mice given oral niacin or topical niacinamide had a 70% decrease in UV-induced skin cancers and near-complete prevention of photoimmunosuppression (Nutr. Cancer 34:36-41, 1999). On the basis of this information, one can intuit that an adequate amount of biologically available NAD can help to reverse DNA damage, thereby preventing skin cancer and possibly aging of the skin.
Niacinamide has been used both topically and orally to treat inflammatory diseases for years. For example, oral niacin plus tetracycline for the treatment of bullous pemphigoid was described by Dr. M. Berk (Arch. Dermatol. 122:670-74, 1986). It has also been shown to decrease pruritus in a mouse model of atopic dermatitis, based on studies conducted at Kanebo Basic Research Laboratory in Japan. And Dr. Alan Shalita found topical niacinamide to be useful for the treatment of acne (Int. J. Dermatol. 34:434-37, 1995).
The mechanism by which niacinamide affects inflammation is unclear, but it has been shown to inhibit mast cell histamine release, neutrophil chemotaxis, and release of inflammatory mediators. It has also reduced the triglyceride and diglyceride content of sebum, resulting in less facial oil. Clinical trials have demonstrated the efficacy of topical niacinamide in treating inflammatory acne and rosacea in unrelated trials by Dr. Shalita, Dr. Zoe Draelos, and others.
Niacinamide has also been shown to increase biosynthesis of ceramides as well as other intercellular lipids in the stratum corneum (Br. J. Dermatol. 143:524-31, 2000). These lipids are very important in maintaining a functional skin barrier to prevent transepidermal water loss (TEWL). In fact, in vivo studies have demonstrated that topical niacinamide increases stratum corneum lipids, resulting in a decrease in TEWL and an increase in skin surface water content.
Clinically, niacinamide has been shown to significantly improve type I sensitive skin (associated with abnormal barrier function) by decreasing sensitivity and stinging. Improvement of the skin barrier may account for the increased skin smoothness and improved skin texture reported by patients using niacinamide-containing products.
Hyperpigmentation also seems to respond to topical niacinamide. In a poster presented at the 2001 annual meeting of the American Academy of Dermatology, niacinamide was shown to decrease melanosome transfer to keratinocytes. In addition, a poster at the 2002 annual meeting of the AAD demonstrated that moisturizers containing 2% and 5% concentrations of niacinamide resulted in a clinically detectable decrease in facial pigmentation.
Although oral niacin has been shown to be effective in reducing the incidence of skin cancer and probably has a beneficial effect on the skin, patients who take oral niacin long term to control hypertension tend to develop bothersome flushing. Because of this, topical products are more desirable.
Niacinamide does seem to be biologically available and absorbed when applied topically, as shown by a poster presented by John Oblong of Procter & Gamble Co., Cincinnati, at the AAD's 2001 annual meeting. This poster demonstrated that levels o
f NADPH, the reduced form of NADP, in aged human skin cells were increased when topical niacinamide was applied in vitro. Increased NADPH levels corresponded with an increase in the production of collagen, involucrin, filaggrin, and keratin.
There are now several companies that market topical products containing niacinamide. Three companies allowed me to use their data in the preparation of this column—Procter & Gamble, which includes niacinamide, panthenol, and vitamin A in its Olay Total Effects line; Niadyne Inc., which uses a patented form of niacin that it claims is more efficiently absorbed into the stratum corneum; and Naturally Clear, which markets several niacinamide products for acne.
DR. LESLIE S. BAUMANN is director of cosmetic dermatology at the University of Miami. To respond to this column, or to suggest topics for future columns, write to Dr. Baumann at our editorial offices or via e-mail at firstname.lastname@example.org.
© 2002 International Medical News Group. Published by Elsevier Inc. All rights reserved.