Niacinamide SOS (save our skin): Why we love this awesome vitamin...

Niacinamide, aka Vitamin B3 (or its active equivalent, Nicotinic acid) is a literal powerhouse, and one of our most highly esteemed ingredients, offering a myriad of skin benefits as well as general health benefits. It is an essential component of all living cells, necessary for protein, carbohydrate and fat metabolism, but most importantly for energy production, owing to its role as precursor to electron-chain energy transporter NAD+.

Numerous peer-reviewed studies over the last few decades have revealed it’s multitude of skin benefits such as brightening the skin, reducing fine lines and wrinkles, and soothing properties, as well as enhancing the skin’s barrier and rebalancing microbiota. Due to its versatility and ability to help with a near exhaustive list of skin concerns, as well as the wealth of scientific evidence supporting it’s clinical efficacy, it should come as no surprise that Niacinamide is a popular choice in the cosmetic field.

Gift that keeps on giving. Benefits of Niacinamide for the Skin:
Niacinamide continues to be the subject of ongoing extensive research, with novel advantages and revelations regarding its mechanism of action being consistently unveiled. Below some of the major benefits of Niacinamide are outlined, as well as some intriguing new findings.

Niacinamide in topical preparations has been demonstrated in several in-vivo investigations to diminish hyperpigmentation and promote skin tone uniformity. A study involving Asian women revealed a 73% reduction in pigmented area following an 8-week application of a 5% Niacinamide moisturiser. Similarly, a study involving Hispanic women illustrated comparable outcomes in pigmentation mitigation between a 4% Niacinamide formulation and a 4% hydroquinone formulation after an 8-week period, with decreased melanin levels observed in skin biopsies subsequent to Niacinamide application.

•  Improves skin texture, making it smoother and more even.
• Helps balance skin microbiota, particularly in rosacea and acne prone skin.
• Hydrates the skin by improving the skin's barrier function, leading to better hydration.
• Reduces inflammation via it’s anti-inflammatory action, making it effective in reducing redness and irritation.
• Minimizes pores giving the skin a more refined look.
• Brightens the skin and improves overall radiance.
• Reduces hyperpigmentation and helps fade dark spots resulting in a more even skin tone.
• Protects against environmental damage owing to it’s antioxidant properties, protecting the skin from environmental stressors such as pollution and UV rays.
• Boosts collagen production and aids in improving skin elasticity and reducing the appearance of fine lines and wrinkles.
• Soothes sensitive and reactive skin, reducing redness and discomfort.
• Regulates oil production making it beneficial for those with oily or combination skin types.

Overall, Niacinamide is a fantastic ingredient to incorporate into your skincare routine, and we use it in many of our formulations, including our Plumping Cream, Firming Eye Cream and Brightening Facial Serum. Whether you have acne-prone or sensitive skin, aging concerns, or just want to improve your skin's overall health, we think Niacinamide can help you!

References

1. Gehring, W (2004) Nicotinic Acid/Niacinamide and the Skin. J Cosmet Dermatol 3:88-93
2. Cosmetic Ingredient Review (2005) Final Report of the Safety Assessment of Niacinamide and Niacin. Int J Toxicol 24:1-31.
3. Matts, PJ et al. (2002) A Review of the Range of Effects of Niacinamide in Human Skin. IFSCC Magazine 5:285-289.
4. Mi, T. et al. (2018). Niacinamide and 12-hydroxystearic acid prevented benzo(a)pyrene and squalene peroxides induced hyperpigmentation in skin equivalent. Exp Dermatol 28:742-746
5. Hakozaki, T et al. (2002) The Effect of Niacinamide on Reducing Cutaneous Pigmentation and Suppression of Melanosome Transfer. Brit J Dermatol 147:20-31.
6. Navarrete-Solis, J et al. (2011) A Double-Blind, Randomized Clinical Trial of Niacina-mide 4% versus Hydroquinone 4% in the Treatment of Melasma. Dermatol Res Pract 2011: 379173
7. Bissett, DL et al. (2003) Topical Niacinamide Provides Skin Aging Appearance Benefits while Enhancing Barrier Function. J Clin Dermatol 32S:9-18.
8. Tanno, O et al. (2000) Nicotinamide increases biosynthesis of ceramides as well as other stratum corneum lipids to improve the epidermal permeability barrier. Br J Dermatol 143:524-531.
9. Mathapathi, MS et al. (2017) Niacinamide Leave-on Formulation Provides Long lasting Protection Against Bacteria In Vivo. Exp Dermatol 26:827-829.
10. Khodaeiani, E et al. (2013) Topical 4% Nicotinamide vs. 1% Clindamycin in Moderate
    Inflammatory Acne Vulgaris. Int J Dermatol 52:999-1004.
11. Draelos, ZD et al. (2006) The Effect of 2% Niacinamide on Facial Sebum Production. J Cosmet Laser Ther 8:96-100.

REFERENCES 

1. Landry J, et al. The silencing protein SIR2 and its homologs are NAD-dependent protein deacetylases. Proc Natl Acad Sci USA. 2000;97:5807–5811. 
2. Schmeisser K, et al. Role of sirtuins in lifespan regulation is linked to methylation of nicotinamide. Nat Chem Biol. 2013;9:693–700.
3. Vaziri H, et al. hSIR2SIRT1 functions as an NAD-dependent p53 deacetylase. Cell. 2001;107:149–159.
4. Du J, et al. Sirt5 is a NAD-dependent protein lysine demalonylase and desuccinylase. Science. 2011;334:806–809. 
5. Feldman JL, et al. Kinetic and structural basis for acyl-group selectivity and NAD dependence in sirtuin-catalyzed deacylation. Biochemistry. 2015;54:3037–3050. 
6. Bitterman KJ, Anderson RM, Cohen HY, Latorre-Esteves M, Sinclair DA. Inhibition of silencing and accelerated aging by nicotinamide, a putative negative regulator of yeast sir2 and human SIRT1. J Biol Chem. 2002;277:45099–45107. 
7. Kraus D, et al. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature. 2014;508:258–262. 
8. Anderson RM, Bitterman KJ, Wood JG, Medvedik O, Sinclair DA. Nicotinamide and PNC1 govern lifespan extension by calorie restriction in Saccharomyces cerevisiae. Nature. 2003;423:181–185. 
9. Anderson RM, et al. Manipulation of a nuclear NAD+ salvage pathway delays aging without altering steady-state NAD+ levels. J Biol Chem. 2002;277:18881–18890. 
10. Camacho-Pereira J, et al. CD38 dictates age-related NAD decline and mitochondrial dysfunction through an SIRT3-dependent mechanism. Cell Metab. 2016;23:1127–1139. 
11. Braidy N, et al. Age related changes in NAD+ metabolism oxidative stress and Sirt1 activity in Wistar rats. PLoS ONE. 2011;6:e19194.
12. Gomes AP, et al. Declining NAD+ induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging. Cell. 2013;155:1624–1638. 
13. Gong B, et al. Nicotinamide riboside restores cognition through an upregulation of proliferator-activated receptor-gamma coactivator 1α regulated beta-secretase 1 degradation and mitochondrial gene expression in Alzheimer’s mouse models. Neurobiol Aging. 2013;34:1581–1588. 
14. Zhang H, et al. NAD+ repletion improves mitochondrial and stem cell function and enhances life span in mice. Science. 2016;352:1436–1443. 
15. Escande C, et al. Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. Diabetes. 2013;62:1084–1093. 
16. Haffner CD, et al. Discovery, synthesis, and biological evaluation of thiazoloquin(az)olin(on)es as potent CD38 inhibitors. J Med Chem. 2015;58:3548–3571. 
17. Mouchiroud L, Houtkooper RH, Auwerx J. NAD+ metabolism: a therapeutic target for age-related metabolic disease. Crit Rev Biochem Mol Biol. 2013;48:397–408. A thorough review outlining the potential mechanisms and roles of NAD in metabolism and disease. 
18. Canto C, et al. The NAD+ precursor nicotinamide riboside enhances oxidative metabolism and protects against high-fat diet-induced obesity. Cell Metab. 2012;15:838–847. 
19. Khan NA, et al. Effective treatment of mitochondrial myopathy by nicotinamide riboside, a vitamin B3. EMBO Mol Med. 2014;6:721–731. 
20. Yoshino J, Mills KF, Yoon MJ, Imai S. Nicotinamide mononucleotide, a key NAD+ intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice. Cell Metab. 2011;14:528–536. 
21. Tummala KS, et al. Inhibition of de novo NAD+ synthesis by oncogenic URI causes liver tumorigenesis through DNA damage. Cancer Cell. 2014;26:826–839. 
22. Scheibye-Knudsen M, et al. A high-fat diet and NAD+ activate Sirt1 to rescue premature aging in cockayne syndrome. Cell Metab. 2014;20:840–855. 
23. Brown KD, et al. Activation of SIRT3 by the NAD+ precursor nicotinamide riboside protects from noise-induced hearing loss. Cell Metab. 2014;20:1059–1068. 
24. Yang H, et al. Nutrient-sensitive mitochondrial NAD+ levels dictate cell survival. Cell. 2007;130:1095–1107. 
25. Lin SJ, Defossez PA, Guarente L. Requirement of NAD and SIR2 for life-span extension by calorie restriction in Saccharomyces cerevisiae. Science. 2000;289:2126–2128.