Till to date the single most studied and proved cause for Premature Greying Hair is Oxidative Stress due to Free Radicals. Duvik contains the more than sufficient amount of antioxidants to combat this condition.

Things to Note:

One study out of 24 studies that are published in American and British journals concluded the fact that the mediclinical findings of premature greying of hair is Genetics, Autoimmune diseases, Low serum ferritin levels, Beta carotene, thyroid disease, low levels of Vit B12, and certain enzymes. It’s recommended that Duvik and Griz should be start simultaneously, in order to combat the utmost valued regime. As Griz contains Folate, Beta carotene, selenium, certain anti-oxidants and enzymes. One of the most important thing is that Griz alone treatment is effective only in new hair that will be grown after 12 weeks but Duvik can change the color of already premature greying hair.

Side Effect:

Generally None

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Biomarker of Oxidative Stress in Premature Hair Graying at Young Age

Dwi Rita Anggraini1*, Lita Feriyawati1, Mega Sari Sitorus1, Milahayati Daulay 2
1 Department of Anatomy, Faculty of Medicine, Universitas Sumatera Utara, Medan, Indonesia;
2 Department of Physiology, Faculty of Medicine, Universitas Sumatera Utara, Medan, Indonesia

Abstract

BACKGROUND: Gray hair is a physiological process of aging that occurs in everyone. Premature hair graying (PHG) is the term when early hair gray at an unusual age. The causes of PHG are multifactorial, genetic, nutritional, and environmental, including oxidative stress.

Free radicals caused interference with cellular responses that cause direct damage to various proteins and DNA in the long term. The body’s defense mechanisms likely antioxidant enzymes, including catalase, glutathione peroxidase (GPx), and superoxide dismutase (SOD) was activated against free radicals.

AIM: We aimed to evaluate markers of oxidative stress and associated with severe graying at young age.

MATERIALS AND METHODS: We recruited consecutive 40 respondents with PHG and healthy controls, male sex and aged <25 years. The severe graying was graded with total of gray hair. The serum samples were collected to detect oxidative stress markers through malondialdehyde (MDA), SOD, catalase, and GPx measurement with enzyme-linked immunosorbent assay.

RESULTS: Serum MDA concentration was higher but not significantly (p > 0.05), while serum SOD, catalase, and GPx level, indicators of antioxidant were significantly lower (p < 0.001, p = 0.017 and p < 0.001, respectively) in PHG compared to controls. The correlation between oxidative stress and graying severity was not significant (p > 0.05), but the association between onset and severity of graying was significant (p < 0.001).

CONCLUSIONS: Respondents with PHG had increased of pro-oxidants and decreased of antioxidants compared than controls. The severity of graying is equivalent to the level of oxidative stress.

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Premature Graying as a Consequence of Compromised Antioxidant Activity in Hair Bulb Melanocytes and Their Precursors

PLOS ONE | www.plosone.org
April 2014 | Volume 9 | Issue 4 | e93589
Ying Shi, Long-FeiLuo, Xiao-Ming Liu, Qiong Zhou, Shi-ZhengXu, Tie-Chi Lei* Department of Dermatology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China

Abstract:

Intricate coordinated mechanisms that govern the synchrony of hair growth and melanin synthesis remain largely unclear.

These two events can be uncoupled in prematurely gray hair, probably due to oxidative insults that lead to the death of oxidative stress-sensitive melanocytes. In this study, we examined the gene expression profiles of middle (bulge) and lower (hair bulb) segments that had been micro-dissected from unpigmented and from normally pigmented hair follicles from thsame donors using quantitative real-time RT-PCR (qPCR) arrays.

We found a significant down-regulation of melanogenesisrelatedgenes (TYR, TYRP1, MITF, PAX3, POMC) in unpigmented hair bulbs and of marker genes typical for melanocyte precursor cells (PAX3, SOX10, DCT) in unpigmented mid-segments compared with their pigmented analogues. qPCR, western blotting and spin trapping assays revealed that catalase protein expression and hydroxyl radical scavenging activities are strongly repressed in unpigmented hair follicles.

These data provide the first clear evidence that compromised antioxidant activity in gray hair follicles simultaneously affects mature hair bulb melanocytes and their immature precursorcells in the bulge region.

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International Journal of Cosmetic Science
Volume 37, Issue S2 p. 25-30
The impact of oxidative stress on hair
R. M. Trüeb
17 November 2015

Abstract:

Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to detoxify the reactive intermediates or to repair the resulting damage. Reactive oxygen species or free radicals are highly reactive molecules that can directly damage lipids, proteins, and DNA. They are generated by a multitude of endogenous and environmental challenges, while the body possesses endogenous defense mechanisms. With age, production of free radicals increases, while the endogenous defense mechanisms decrease. This imbalance leads to progressive damage of cellular structures, presumably resulting in the aging phenotype. While the role of oxidative stress has been widely discussed in skin aging, little focus has been placed on its impact on hair condition. Moreover, most literature on age-related hair changes focuses on alopecia, but it is equally important that the hair fibers that emerge from the scalp exhibit significant age-related changes that have equal impact on the overall cosmetic properties of hair. Sources of oxidative stress with impact on the pre-emerging fiber include: oxidative metabolism, smoking, UVR, and inflammation from microbial, pollutant, or irritant origins. Sources of oxidative stress with impact on the post-emerging fiber include: UVR (enhanced by copper), chemical insults, and oxidized scalp lipids. The role of the dermatologist is recognition and treatment of pre- and post-emerging factors for lifetime scalp and hair health.

Introduction

Hair care, colour and style play an important role in people's physical appearance and self-perception. Hair defines an individual's gender, age, sexual attitude and social status.

Differences in the appearance of hair (hair condition) are due to factors from within, that is type of hair produced by a follicle, and due to factors from without, that is the type of hair care and cosmetics practiced by the individual.

Table 1. Factors with effect on the condition of the hair fibre
Factors from within	Factors from without
Genetics Sex Age General health status Nutritional status As they relate to each other	Hair weathering Exposure to ultraviolet radiation (UVR) Hair care habits Hair treatments (chemical, physical) Scalp condition

The science of hair care not only addresses the aesthetic problem of the condition of hair, in terms of hair quality and colour, but also the biological problems underlying its derangements, in terms of microscopic, biochemical and molecular changes.

Whereas the role of oxidative stress has been widely discussed in relation to the appearance of skin, in comparison, little focus has been placed on its role in impacting scalp health and hair condition.

Oxidative stress

Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to detoxify the reactive intermediates or to repair the resulting damage.

The free radical theory of ageing as originally proposed by Harman as early as 1956 states that organisms/organs age because cells accumulate free radical damage over time. Today, it is one of the most widely accepted theories used to explain mechanisms underlying the ageing process, including the hair follicle. Free radicals are highly reactive molecules with unpaired electrons that can directly damage various cellular structural membranes, lipids, proteins and DNA. The damaging effects of these reactive oxygen species are induced internally during normal metabolism and externally through exposure to various oxidative stresses from the environment.

The body possesses endogenous defence mechanisms, such as anti-oxidative enzymes (superoxide dismutase, catalase, glutathione peroxidase) and non-enzymatic anti-oxidative molecules (vitamin E, vitamin C, glutathione, ubiquinone), protecting it from free radicals by reducing and neutralizing them. With age, the production of free radicals increases, whereas the endogenous defence mechanisms decrease. This imbalance leads to the progressive damage of cellular structures, presumably resulting in the ageing phenotype.

Sources of oxidative stress with impact on the condition of hair

Most literature on age-related hair changes focuses on alopecia, but it is equally important that the hair fibres that emerge from the scalp exhibit significant age-related changes that have an equal impact on the overall cosmetic properties of the hair. It is these changes that are ultimately experienced by subjects that have retained their hair as they age. Traditionally, the study of hair ageing has focused on two main streams of interest: on one hand, the aesthetic problem of ageing hair and its management, in other words everything that happens outside the skin; on the other hand, the biological problem of ageing hair, in terms of microscopic, biochemical (hormonal, enzymatic) and molecular changes within the hair follicle in the depth of the skin 7, 8. Rather, the condition of the hair fibre should be viewed as the result of a combination of pre-emerging and of post-emerging factors. Sources of oxidative stress with impact on the pre-emerging fibre include oxidative metabolism, smoking, UVR and inflammation from microbial, pollutant or irritant origins. Sources of oxidative stress with impact on the post-emerging fibre include UVR, chemical insults and oxidized scalp lipids (Fig. 1).

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Figure 1: Sources of oxidative stress with impact on the condition of the hair fibre.

Pre-emerging factors: oxidative stress in ageing of hair From a clinician's perspective, age-dependent progressive loss of hair quality and quantity occurs in fundamentally three different settings: as a symptom of one of the rare premature ageing syndromes (progerias), as a result of androgenetic alopecia, and with onset of senescence (senescent alopecia). The premature ageing syndromes are exceedingly rare; nevertheless, their study has given insights into the roles of telomeres, mitochondrial function, human growth hormone and insulin-like growth factor 1 (IGF-1) for the growth and ageing of hair. Androgenetic alopecia and senescent alopecia share the features of decrease in the number of anagen follicles and hair diameter, resulting in age-dependent progressive thinning of hair, which is why they have long not been considered as different entities by some experts, with considerable overlap further obscuring the delineation from each other. Nevertheless, they differ in age of onset (early vs. lat), distribution (patterned vs. diffuse) and pathophysiologic factors (increased vs. decreased 5-alpha-reductase activity).

Senescent alopecia

Ultimately, a study comparing androgenetic alopecia and senescent alopecia using microarray analysis demonstrated significant differences in the gene expression patterns, further corroborating that they in fact represent different entities:9 In androgenetic alopecia, genes required for anagen onset, epithelial signal to dermal papilla, hair shaft differentiation and anagen maintenance were downregulated, and genes for catagen and telogen induction and maintenance were upregulated; whereas in senescent alopecia, genes involved in epithelial signal to dermal papilla, actin cytoskeleton and mitochondrial function were down-regulated, while oxidative stress and inflammatory response genes were up-regulated.

More recently, Nishimura et al. 10 found mouse hair follicles to age through defective renewal of hair follicle stem cells becoming incomplete with ageing. Whereas the evidence was originally provided for follicular melanocyte stem cells, Nishimura found mouse hair follicles to age much in the same manner. Hair production is fuelled by stem cells, which transition between cyclical bouts of rest and activity. Aged hair follicle stem cells exhibit enhanced resting and abbreviated growth phases and are delayed in response to tissue-regenerating cues. Ultimately, aged hair follicle stem cells are poor at initiating proliferation and show diminished self-renewing capacity upon extensive use. Ageing-related loss of hair follicle stem cell marker expression starts well before hair follicles have shortened. Using genomic instability syndromes and exposure to ionizing radiation as models, Nishimura proposed an accumulation of DNA damage to be involved in the ageing process (oral communication on the occasion of 7th World Congress for Hair Research, 4–6 May 2013, Edinburgh, Scotland).

Androgenetic alopecia

Androgenetic alopecia is understood to represent a genetically determined, androgen-induced, and age-dependent, progressive shortening of anagen duration with successive hair cycles. The net result is a decreased number of hairs in anagen, and progressive follicular miniaturization, with increased shedding of short-lived telogen hairs, whereas the affected hair follicles produce shorter and finer hairs that cover the scalp poorly. Of the hormones that affect hair growth, the most studied are the androgens:11 It is assumed that the genetically predisposed hair follicles are the target for androgen-stimulated hair follicle miniaturization. Studies have shown increased levels of androgen receptor (AR) in dermal papilla cells (DPCs) of frontal hairs compared with occipital hairs, and increased activity of 5-alpha-reductase, an enzyme important in converting testosterone to the more potent androgen dihydrotestosterone (DHT), in balding areas compared with non-balding areas of the scalp. These studies support the idea that increased levels of DHT interact with increased expression of AR in dermal papilla cells to cause the release of inhibitory factors that result in changes in the hair follicle, ultimately leading to terminal-to-vellus hair transformation.

As androgenetic alopecia involves a process of premature termination of anagen associated with premature entry into catagen, the molecular controls of the anagen–catagen transformation of the hair cycle are critical: Catagen has been suggested to occur as a consequence of decreased expression of anagen maintaining factors, such as IGF-1, basic fibroblast growth factor and vascular endothelial growth factor, and increased expression of cytokines promoting apoptosis, such as transforming growth factor-beta 1, interleukin-1-alpha and tumour necrosis factor-alpha 12.

The diagnosis and treatment of androgenetic alopecia are relatively straightforward with the hair growth promoting agent minoxidil and the selective 5-alpha-reductase type II inhibitor finasteride having best evidence levels for therapeutic use 13. Nevertheless, the limited success rate of treatment with minoxidil and finasteride means that further pathogenic pathways must be taken into account.

Cigarette smoke

Whereas cigarette smoking-related premature skin ageing has attracted the attention of the medical community since the 1960s, it is only in 1996 that Mosley and Gibbs14 originally reported a relationship between smoking, baldness in men and premature grey hair. Eventually, a population-based cross-sectional survey among Asian men 40 years or older showed statistically significant positive associations between severity of androgenetic alopecia and smoking status, current cigarette smoking of 20 cigarettes or more per day, and smoking intensity. The odds ratio of early-onset history for androgenetic alopecia grades increased in a dose–response pattern. Moreover, risk for moderate or severe androgenetic increased for family history of first-degree and second-degree relatives, as well as for paternal relatives 15.

The mechanisms by which smoking accelerates hair loss have hypothesized to be multifactorial, including effect on microcirculation, direct (geno-) toxic effect, imbalance in the follicular protease/anti-protease systems involved in tissue remodelling in the course of the hair follicle cycle, inhibition of aromatase and hydroxylation of estradiol resulting in a relative hypo-oestrogenic state, and oxidative stress 16.

The fact that cigarette smoke-associated hair loss is of the androgenetic type indicates that genetic factors contribute. On the other hand, recent studies have focused on the role of oxidative stress: Naito et al.17 analysed the effect of the lipid peroxides on hair follicles and observed that the topical application of linoleinhydroperoxides, one of the lipid peroxides, leads to the early onset of the catagen phase in murine hair cycles. Furthermore, they found that lipid peroxides induced apoptosis of hair follicle cells. They also induced apoptosis in human epidermal keratinocytes by up-regulating apoptosis-related genes. These results indicate that lipid peroxides, which can cause free radicals, induce the apoptosis of hair follicle cells, and this is followed by early onset of the catagen phase.

Ultimately, Bahta et al.18 cultured DPCs from balding and non-balding scalp and demonstrated that balding DPCs grow slower in vitro than non-balding DPCs. Loss of proliferative capacity of balding DPCs was associated with changes in cell morphology, expression of senescence-associated beta-galactosidase, decreased expression of proliferating cell nuclear antigen and Bmi-1, upregulation of p16(INK4a)/pRb, and nuclear expression of markers of oxidative stress and DNA damage. The finding of premature senescence of balding DPC in vitro in association with expression of markers of oxidative stress and DNA damage suggests that balding DPCs are particularly sensitive to environmental stress.

Oxidative metabolism in greying

Hair greying is a natural age-associated feature. The hair-greying trait correlates closely with chronological ageing and occurs to varying degrees in all individuals. Although greying is understood as a loss of pigment in the shaft, its cellular and molecular origins are incompletely understood. Theories for the gradual loss of pigmentation include exhaustion of enzymes involved in melanogenesis, impaired DNA repair, loss of telomerase, anti-oxidant mechanisms and anti-apoptotic signals.

Greying is associated with evidence of reduction of active melanocytes, of tyrosinase activity and of melanosome transfer to hair follicle keratinocytes. Ultrastructural studies have shown not only that remaining melanocytes contain fewer melanosomes, but also that the residual melanosomes may be packaged within autophagolysosomes. This removal of melanosomes into autophagolysosomes suggests that they are defective, possibly with reactive melanin metabolites. This interpretation is supported by the observation that melanocytes in greying hair bulbs are frequently highly vacuolated, a common cellular response to increased oxidative stress 19.

The extraordinary melanogenic activity of pigmented bulbar melanocytes, continuing for up to 10 years in some hair follicles, is likely to generate large amounts of reactive oxygen species via the hydroxylation of tyrosine and the oxidation of DOPA to melanin. If not adequately removed by an efficient anti-oxidant system, an accumulation of these reactive oxidative species will generate significant oxidative stress. It is possible that the anti-oxidant system becomes impaired with age leading to damage to the melanocyte itself from its own melanogenesis-related oxidative stress. Wood et al.20 demonstrated for the first time that human white scalp hair shafts accumulate hydrogen peroxide (H2O2) in millimolar concentrations, and almost absent catalase and methionine sulfoxidereductase (MSR) protein expression in association with functional loss of methionine sulfoxide repair in the entire grey hair follicle. Accordingly, methionine sulfoxide formation of methionine residues (Met), including Met 374 in the active site of tyrosinase, the key enzyme in melanogenesis, limits enzyme functionality, which eventually leads to loss of hair colour.

Anecdotal evidence indicates that grey hair becomes coarser and less manageable than pigmented hair. Grey hair is said to often fail to hold a temporary or permanent set, and to be more resistant to incorporating artificial colour, both of which suggest changes to the underlying substructure of the hair fibre 21.

Given the close interaction of melanin-transferring melanocytes with hair shaft-forming pre-cortical keratinocytes, it is conceivable that other functions of these cell types are affected by this activity. One possibility is that melanin transfer decreases keratinocyte turnover and increases keratinocyte terminal differentiation. Indeed, white beard hair has been shown to grow up to four times the rate of adjacent pigmented hair 22. In this way, ageing hair follicles may reprogramme their matrix keratinocytes to increase the production of medullary, rather than cortical, keratinocytes. In fact, the medulla is often enlarged and collapsed, forming a central cavity in grey and white hairs.

These observations underline the impact of pre-emerging factors on post-emerging properties of the hair fibre.

Post-emerging factors: oxidative stress from UVR and in dandruff

The ageing hair is increasingly sensitive to weathering, with increased cysteic acid residues and decreased cystine, and increased fibre reactivity to reducing and oxidizing agents. Moreover, ageing hair is more sensitive to UVR. Photochemical impairment of the hair includes degradation and loss of hair proteins as well as degradation of hair pigment. UV-B radiation is responsible for hair protein loss, and UV-A radiation is responsible for hair colour changes. Absorption of radiation in photosensitive amino acids of the hair and their photochemical degradation produces free radicals. They have adverse impact on hair proteins, especially keratin.

Hair weathering

Hair weathering is the progressive hair damage resulting from external factors, basically the ‘wear and tear’ from environment and cosmetic procedures that mainly affect the free end of the growing hair fibre: friction damage from combing and brushing, damage from excessive heat from a hair dryer or curling irons, structural and chemical damage from chemical treatment of hair, that is bleaching, colouring, perming and straightening, and finally effects of ultraviolet radiation or photoageing. Although all hair exhibits some degree of weathering, longer hair, subjected to repeated insults, inevitably shows more severe changes of weathering. Features of weathering include damaged cuticles, longitudinal fissures or split ends, and ultimately transverse fractures (trichorrhexisnodosa). These result from alterations in the ultrastructure, and physical and chemical properties of the hair fibre, that is mechanical abrasion of the cuticle, damage of the hair cortex with alterations of visco-elastic properties and tensile strength of the fibre, a depletion of specific amino acids.

Effects of UVR (photodamage)

Whereas the consequences of sustained ultraviolet UVR on unprotected skin are well appreciated, the effects of UVR on hair have not found the same attention in the scientific community 23. However, photodamage is well recognized to represent a common cause of poor hair condition.

Terrestrial solar UVR ranges from approximately 290–400 nm. UV-B (290–315 nm) reaches the upper dermis only, whereas UV-A (315–400 nm) penetration into the dermis increases with wavelength. With respect to the condition of the hair fibre, UVR has a dual effect, both on the pre- and on the post-emerging hair.

With respect to the effect of UVR exposure on the pre-emerging fibre, Camacho et al.24 originally reported a peculiar type of telogen effluvium following sunburn of the scalp with hairstyles that left areas of scalp uncovered during sun exposure. It has been proposed that the columns of the cells in the hair shaft act as a fibre-optic type system, transmitting UV light downward into the hair follicle 25. Morphologically, the keratinocytes within the hair shaft are arranged in compressed linear columns that resemble the coaxial bundles of commercial fibre-optic strands. Thus, hair follicular melanocytes located in the region of the hair matrix may function as UV biosensors and respond to photic inputs. Depending on the quantity of UVR exposure, it is conceivable that also photodamage may occur at this site, resulting in telogen effluvium. Mahé et al.26 proposed direct physicochemical stress from UVR to keratinocytes with production of radical oxygen species and release of proinflammatory cytokines resulting in injury of the putative site of follicular stem cells in the superficial portion of the hair follicle. Piérard-Franchimond et al.27 suggested that the production of porphyrins by Propionibacterium spp. in the pilosebaceous duct with photoactivation may lead to oxidative tissue injury and follicular microinflammation. All contribute to the evolution of alopecia, particularly androgenetic alopecia.

With respect to the effect of UVR exposure on the post-emerging fibre, sunlight damage of the hair causes discoloration and irregular surface, reduced tensile strength and vulnerability towards additional environmental damage. Once the hair is exposed to sunlight, the light penetrates through several layers of the hair. UV-B can penetrate approximately 5 μm of thickness, mainly affecting the cuticle layer, whereas UV-A and visible light (VIS), which have longer wavelengths, penetrate the entire cuticle and influence the cortex as well. The cuticle layer surrounding the cortex, which protects the hair from environmental and chemical damage, is the most vulnerable to UVR-induced damage due to its external location. Among the various amino acids that constitute keratin, tryptophan, cysteine, tyrosine and hisitidine are particularly sensitive. Cysteine shows the most conspicuous alteration as it better absorbs 254–350 nm wavelength that matches with UV range. Cysteine is mainly damaged through breakdown of C-S fission. As concentration of cysteine is the highest level in hair cuticle, the photodegradation especially occurs in this region 28. Oxygen radicals created by UVR break down the disulphide bonds of structural units, forming carbonyl groups and new intra- and intermolecular cross-links that reduce structural integrity. The result is increased cuticle fragility, fibre porosity and surface roughness of the hair, as well as decreased mechanical strength, leading to further vulnerability of the hair to additional mechanical or chemical treatment. Ultimately, oxidative reactions caused by singlet oxygen occur more frequently in photodamaged hair 28.

Recently, Marsh et al.29 investigated the role of low levels of redox metals such as copper in accelerating damage to hair on exposure to UV irradiation. The methods used were proteomics to measure the protein damage via protein loss after different periods of exposure and mass spectroscopy methods to identify marker peptides that are specifically created by this type of damage. They identified for the first time in hair the role of exogenous copper in increasing UVR-induced damage in terms of both total protein degradation and increased formation of the marker peptide.

Dandruff

As skin cells die, a discrete amount of flaking is normal. The specific anatomic features of the scalp skin, such as the large number of terminal hair follicles and the enlarged epidermal surface due to numerous hair canals, contribute to a higher rate of exfoliation. Therefore, even a healthy scalp will develop some dandruff within 1 or 2 weeks if the hair is not washed.

Nevertheless, some people experience an exaggerated amount of flaking either chronically or as a result of certain triggers, which can also be accompanied by redness and irritation of the scalp. Pathologic dandruff results from accelerated proliferation of epidermal cells and thus increased exfoliation of variously large collections of abnormally keratinizing epidermal cells. The process results from focal inflammation of the scalp with parakeratosis, which causes abnormal exfoliation and an altered light refractive index of the keratinized cell aggregates. The clinical appearance of dandruff is determined by the size, adherence and light refractive characteristics of the flakes. Among the factors that lead to inflamed patches on the scalp are physical/chemical stimuli, microbial colonization, sebum production and composition.

The lipophilic yeast Malassezia spp. normally inhabits the scalp, making up about 45% of its resident microflora. In patients with dandruff, it is the predominant yeast type with about 75%. Modern classification and nomenclature of Malassezia spp. are based on DNA typing. The most common types found on the scalp are M. restricta and M. globosa, the latter of which in particular has a major role in the development of dandruff given its high level of lipase activity resulting in breakdown of sebum to free fatty acids that auto-oxidize to skin-irritating lipoperoxides 30.

Therefore, the mainstay for treatment of dandruff and preserving a healthy scalp is the use of anti-microbial shampoos that are effective in inhibiting Malassezia yeasts. Appropriate shampoo formulation allowing efficacy with short contact time and rinsing is equally important, as patients are compliant for only 30 s. Finally, the cosmetic aspects of shampoo-based therapy must be acceptable to patients and include a conditioning effect, or else compliance will be compromised.

Summary and conclusions

The science of hair care addresses not only the aesthetic problem of the condition of hair, in terms of hair quality and colour, but also the biological problems underlying its derangements, in terms of microscopic, biochemical and molecular changes. Whereas the role of oxidative stress has been widely discussed in relation to the skin, in comparison, little focus has been placed on its role for scalp health and hair condition. Moreover, the attention of the scientific community to age-related hair changes focuses on alopecia, and less so on the condition of the hair fibres that emerge from the scalp. Nevertheless, it is equally important that the hair fibres exhibit significant age-related changes with an additional impact on the overall cosmetic properties of hair.

There is increasing evidence for the impact of oxidative stress from within (endogenous) and from without (environmental) on the condition of hair.

Sources of oxidative stress with impact on the pre-emerging hair fibre include oxidative metabolism, smoking, UVR and inflammation from microbial, pollutant or irritant origins. Sources of oxidative stress with impact on the post-emerging fibre include UVR (enhanced by copper), chemical insults and oxidized scalp lipids.

The role of the dermatologist is in recognizing and treating the pre- and post-emerging factors for lifetime scalp and hair health in a polyhedral and patient-specific manner, including patient education on appropriate hair care (shampoo and conditioner), refraining from smoking, hair photoprotection, adequate nutrition, and effective treatment of hair (alopecia) and scalp conditions (dandruff) with the respective evidence-based pharmacologic and cosmetic agents.