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 Table of Contents  
Year : 2015  |  Volume : 2  |  Issue : 2  |  Page : 73-75

Premature graying of hair: The voids and tiffs

1 Skinnocence: The Skin Clinic and Research Centre, Gurgaon, Haryana, India
2 Department of Dermatology and STD, MAMC-LN Hospital, New Delhi, India

Date of Web Publication29-Dec-2015

Correspondence Address:
Sidharth Sonthalia
Skinnocence: The Skin Clinic and Research Centre, C-2246 (Ground Floor), “Suhridaya“, Block-C, Sushant Lok-1, Gurgaon - 122 009, Haryana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2349-5847.172774

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How to cite this article:
Sonthalia S, Sarkar R. Premature graying of hair: The voids and tiffs. Pigment Int 2015;2:73-5

How to cite this URL:
Sonthalia S, Sarkar R. Premature graying of hair: The voids and tiffs. Pigment Int [serial online] 2015 [cited 2022 Dec 5];2:73-5. Available from: https://www.pigmentinternational.com/text.asp?2015/2/2/73/172774

  Introduction Top

The color, thickness and other attributes of hair have a colossal bearing on one's physical appearance and self-esteem. Graying of hair, or “canities” is a physiological phenomenon; essentially a part of chronological aging. The term premature hair graying (PHG) or premature canities is used when graying begins before the “usual” age of onset. Hair is said to gray prematurely when it occurs before the age of 20 in Caucasians, 25 in Asians and 30 in Africans.[1],[2] Although, a similar cut-off has not been clearly defined for Indians per se, 20 years has been arbitrarily accepted in the study by Bhat et al.[3] In recent times, the banality of this innocuous disorder has been capsized, especially in ethnic groups with predominantly dark-colored hair, including Indian population. Premature canities has a significant recusant impact on the self-esteem and sociocultural acceptance of the affected individual.

Our current notion about the provenance of PHG revolves around a robust genetic component with a speculated autosomal dominant pattern of inheritance, with additional role of various acquired and environmental factors.[2] Premature canities occur more commonly as an isolated genetically inherited condition without any underlying pathology. It has been suggested that PHG may reflect a genetically regulated early exhaustion of the melanocyte reservoir's seeding potential or a defect in cell activation/migration, compounded by environmental factors, inflammation, or psychological stress.[4] Other than specific premature aging syndromes, its association has been reported with auto-immune disorders such as hypo- or hyper-thyroidism, atopic diathesis, pernicious anemia; nutritional deficiencies like chronic protein loss and deficiency of iron and copper; and HIV infection, cystic fibrosis, and Hodgkin's lymphoma.[4] Other causes implicated include stress, smoking, drugs like chloroquine, and application of topical agents such as dithranol and resorcin. A newfangled interest in the role of oxidative damage in the incitement of premature graying is transpiring. Premature canities may be a sequel to the inability of body's anti-oxidant systems to cope with the excessive oxidative stress resulting from both the endogenous reactive oxygen species generated during melanin synthesis and the additional load of extrinsic oxidative stress generated by ultraviolet radiation, pollution, and stressful conditions, culminating into melanocyte damage.[4],[5]

PHG is increasingly identified as an independent risk factor for systemic conditions, especially coronary artery disease (CAD).[6] It's suggested association with low bone density and osteopenia needs further validation. The prevention and treatment of PHG remains far from satisfactory, with inconsistent and nonreproducible results seen with all attempted therapies. These include oral p-aminobenzoic acid, calcium pantothenate with/without gray hair avulsion, brewer's yeast, multi-vitamin supplements, and use of hair dyes.

With this brief review, a void regarding many aspects of this intriguing condition is clearly sensed.

  Lack of Indian Data Top

First and foremost, there is a lack of epidemiological and clinical data on PHG from the Indian subcontinent. An evidence-based cut-off for defining PHG in the Indian context remains elusive. The only Indian study published to date by Bhat et al. included only 35 subjects (cases plus controls), all being students younger than 20 years.[3] PHG was arbitrarily defined as the presence of at least 5 gray hair fibers. Thus, till now, no study has evaluated the age of onset of premature canities in Indian population. The cut-off for “premature” graying for Indians should be based on the outcome of properly planned studies involving cohort with a broader age range, rather than being taken arbitrarily.

  Mode of Inheritance Top

Although an autosomal dominant mode of inheritance has been speculated for PHG, it has not been affirmed.[2] Since a strong family history seems to be the most important determinant of this condition, elaborate pedigree charting of at least first-, second-, and third-degree relatives should be undertaken to establish explicitly the mode of inheritance.

  Study Sample Size and Discernment of Etiopathogenesis Top

Future studies should be case–controlled with larger sample size. Statistical evaluation of established, as well as plausible associated conditions, needs to be undertaken, and the role of factors like micronutrient deficiency, oxidative stress, and other tenable causes need to be explored for better understanding of the etiopathogenesis.

  Scoring System for Premature Hair Graying Top

There is a strong need of a universally acceptable, objective and reproducible scoring system to quantify the degree, severity and progression of PHG. It will be helpful in ascertaining the relation of canities and a suspected etiological factor and also serve as a benchmark for the appraisal of the efficacy of therapeutic modalities. Such a score should be circumspect, incorporating different areas of the scalp with objective measurement of extent or amount of graying in every area. The scalp could be divided into different zones and the amount of graying in each zone may be calculated as the percentage of gray hair present over a defined unit area, e.g., 1 or 2 cm 2. This unit area may be selected from a representative portion of each zone, e.g., areas showing maximum graying in that zone. In addition, the scoring system should ideally interpolate a rubric of appraising the progression, retardation, or reversal of graying over time.

Individual scoring systems have been used in previous epidemiological and investigative studies on PHG. In the Indian study by Bhat et al., a scale format was used: With presence of <50, 50–100, and more than 100 gray hair classified as mild, moderate and severe graying respectively.[3] Subjective scores have been employed in two Korean studies.[7],[8] Severity of PHG was graded by subjects themselves based on their estimate of the extent of graying. In the randomized double blind placebo-controlled interventional study by Jo et al., a modified phototrichogram was used in which macro photographs of a 1 cm 2 circular area, 2 cm from the vertex, were taken at baseline and follow-up visits.[9] In addition, different colors were used to mark the pigmented hair, existing gray hair, and new gray hair for easier comparison. The hair whitening score used by Kocaman et al., defined according to the percentage of white hair present, was conducted on older individuals to evaluate the cardiovascular risk, and thus seems impractical for individuals younger than 20 years with PHG.[6] The overt fallacies of the above mentioned scoring systems include: Lack of standardization and reproducibility, use of random cut-offs, and lack of area-wise assessment of the scalp. The subjective scores dependent on subjects' self-reported estimation of graying suffer from the drawbacks of one's focus on preferentially scoring the severity of a more concerning scalp area, and the inter-individual variation emanating from the difficulty in thoroughly examining one's own scalp. In our opinion, trichoscopy-based scoring may be instrumental for objective evaluation of PHG and merits consideration for future studies and trials.

  The Impact of Premature Hair Graying on Quality of Life Top

Skin and hair disorders are unique in terms of the dichotomy of the patient's perception of his condition and the dermatologist's concerns for the same. Hair disorders like androgenetic alopecia and alopecia areata are well-known to be associated with a significant negative impact on quality of life (QoL). The paramount role of hair color in the self-esteem of an individual and sociocultural synergy becomes more germane for adolescents and young adults, the population that constitutes the majority of patients with PHG. The recent increase in the number of patients seeking consultation for PHG corroborates with this issue. Youngsters with PHG often complain of embarrassment, anxiety, altered mood and even depression due to their hair color. However, to the best of our knowledge, there is no published literature evaluating the QoL in such patients. Thus, assessment of the impact of PHG on the QoL of patients should be undertaken in future studies.

  Exploring New Therapies Top

Oral Polypodium leucotomos, a fern extract with strong photoprotective and anti-oxidant properties may also provide some sun-protection for the graying hair.[10] The use of 0.5–5% topical melitane (acetyl hexapeptide-1, a biomimetic peptide agonist of α-melanocyte stimulating hormone) for 4–6 months is being promoted to stimulate hair pigmentation and reverse hair graying. However, published evidence is lacking and needs to be generated in randomized placebo-controlled trials. The role of herbal extracts such as Pueraria lobata, although established in a cohort of 35–65 years-old Korean women, needs further confirmation in men, individuals of different ethnicity, and younger population.[9]

  Conclusion Top

With increasing number of individuals seeking medical help for PHG, it has become imperative to assess our current understanding of this peculiar disorder and fill these voids and sort out the tiffs.

  References Top

Trüeb RM. Pharmacologic interventions in aging hair. Clin Interv Aging 2006;1:121-9.  Back to cited text no. 1
Tobin DJ, Paus R. Graying: Gerontobiology of the hair follicle pigmentary unit. Exp Gerontol 2001;36:29-54.  Back to cited text no. 2
Bhat RM, Sharma R, Pinto AC, Dandekeri S, Martis J. Epidemiological and investigative study of premature graying of hair in higher secondary and pre-university school children. Int J Trichology 2013;5:17-21.  Back to cited text no. 3
Pandhi D, Khanna D. Premature graying of hair. Indian J Dermatol Venereol Leprol 2013;79:641-53.  Back to cited text no. 4
[PUBMED]  Medknow Journal  
Trüeb RM. Oxidative stress in ageing of hair. Int J Trichology 2009;1:6-14.  Back to cited text no. 5
Kocaman SA, Çetin M, Durakoglugil ME, Erdogan T, Çanga A, Çiçek Y, et al. The degree of premature hair graying as an independent risk marker for coronary artery disease: A predictor of biological age rather than chronological age. Anadolu Kardiyol Derg 2012;12:457-63.  Back to cited text no. 6
Jo SJ, Paik SH, Choi JW, Lee JH, Cho S, Kim KH, et al. Hair graying pattern depends on gender, onset age and smoking habits. Acta Derm Venereol 2012;92:160-1.  Back to cited text no. 7
Shin H, Ryu HH, Yoon J, Jo S, Jang S, Choi M, et al. Association of premature hair graying with family history, smoking, and obesity: A cross-sectional study. J Am Acad Dermatol 2015;72:321-7.  Back to cited text no. 8
Jo SJ, Shin H, Paik SH, Na SJ, Jin Y, Park WS, et al. Efficacy and safety of pueraria lobata extract in gray hair prevention: A randomized, double-blind, placebo-controlled study. Ann Dermatol 2013;25:218-22.  Back to cited text no. 9
Middelkamp-Hup MA, Pathak MA, Parrado C, Goukassian D, Rius-Díaz F, Mihm MC,et al. Oral Polypodium leucotomos extract decreases ultraviolet-induced damage of human skin. J Am Acad Dermatol 2004;51:910-8.  Back to cited text no. 10

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Lack of Indian Data
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