Premature Graying Of Hair Research Articles

Delving into diversity: Exploring different risk factors of premature greying of hair.

Dear Madam, Hair is said to grey prematurely when a minimum of five grey hairs occur before the age of 20 in Caucasians, 25 in Asians and 30 in Africans1. Some authors propose using 25 years as a cut-off for people in the South Asian subcontinent. Also, there's no universal grading system for premature greying of hair (PGH). This letter addresses the various evolving risk factors for PGH in young adults worldwide. PGH may be familial or genetically influenced, traveling in an Autosomal Dominant pattern. A positive family history, in particular the paternal history is the most powerful risk factor2. PGH is also linked to nutritional deficiencies including vitamins (especially B12) and minerals. For example in one study, significantly lower levels of serum calcium, ferritin, vitamin B12, and high HDL were observed in patients3. T3 and T4 act on hair follicles to cause melanogenesis and their deficiency is therefore associated with PGH, alopecia, and changes in hair morphology. Another study found notably reduced levels of copper in cases (PGH) as compared to the control group. This study, however, did not observe lower levels of zinc or iron among the affected population. A separate case-control study concerning the association of epidemiological and biochemical factors with PGH reported that a significantly higher percentage of individuals with premature greying had atopic diathesis, led sedentary lifestyles, had family histories of the condition, smoked, and had reported higher levels of perceived stress compared to controls. Though, interestingly enough, regular application of hair oil seemed to confer a safeguarding effect against premature greying. Upon further review of the literature, it became apparent that both BMI and exposure to sunlight emerged as substantial predictors of PGH. Despite the prescription of various vitamins and minerals like biotin, calcium pantothenate, zinc, copper, and selenium (all of which have been recognized as risk factors), the outcomes have been disappointing. Calcium pantothenate is frequently recommended for premature greying of hair (PGH)4. This highlights an existing knowledge gap concerning the precise causative risk factors, necessitating further investigation for a comprehensive understanding and improved management of individuals experiencing premature greying of hair.

Prevalence and Predictors of Premature Graying of Hair Before the Age of 30: A Cross-Sectional Study in SaudiArabia.

Graying is an inherent and unavoidable consequence of the aging process, impacting individuals of all genders. There are limited studies in Saudi Arabia that have examined the prevalence and predictors of premature graying of hair (PGH). This study aims to explore the prevalence and predictors of PGH before the age of 30 among the population of Saudi Arabia. This is a cross-sectional online survey that was conducted between July 2023 and February 2024 in Saudi Arabia. Binary logistic regression analysis was used to identify risk factors of having gray hair before the age of 30. A total of 1193 participants were involved in this study. A significant portion of respondents reported having gray hair before the age of 30 (55.9%). The younger population (younger than 44 years), smokers, and those who have comorbidities, have anxiety, have depression, have a family history of gray hair before the age of 30 years, have a dry scalp, suffer from vitamin or mineral deficiencies, have hair loss due to immune diseases (such as alopecia), and use minoxidil or rosemary for hair loss were more likely to have gray hair before the age of 30 years (p < 0.05). This study highlighted the high prevalence rate and associated predictors of PGH in Saudi Arabia. Identified predictors include genetic, health, and lifestyle factors. Healthcare professionals and decision makers are advised to promote the awareness of the general public on its risk factors to enhance the prevention of PGH. Public health initiatives include campaigns on smoking cessation, healthy nutrition, and mental health.

6483 Diaphyseal Medullary Stenosis With Malignant Fibrous Histiocytoma: A Rare Skeletal Dysplasia/Sarcoma Syndrome

Abstract Disclosure: A. Grover: None. C.R. Ferreira: None. R.I. Gafni: None. S. Jumani: None. M.T. Collins: None. K.L. Roszko: None. I.R. Hartley: None. Introduction: Diaphyseal medullary stenosis with malignant fibrous histiocytoma (DMS-MFH) is a rare autosomal dominant syndrome associated with pathologic fractures, myopathy, premature hair graying, and aggressive osteosarcomas. DMS-MFH has been linked to genetic variants in the methylthioadenosine phosphorylase (MTAP) gene, which encodes an enzyme in the methionine salvage and polyamine synthesis pathway. This pathway is implicated in other skeletal fragility disorders, such as Snyder-Robinson syndrome, suggesting a still undefined role of this pathway in bone biology. We describe a kindred with DMS-MFH and identify diagnostic challenges. Case: A 53-year-old perimenopausal woman presented with four fragility fractures over one year. Relevant history included premature hair graying, esophageal strictures, and nephrolithiasis. The patient’s bone formation markers were slightly elevated; bone resorption markers were within reference range. Her only osteoporosis risk factor was perimenopausal status. Bone series showed a diffuse heterogeneous appearance of the long bones with a mixed lytic/sclerotic appearance. DEXA scan revealed osteopenia. Family history was significant for 2 sons with aggressive osteosarcomas diagnosed in their late teens; one died at age 20. The other son is currently 39-years-old with recurrent osteosarcomas in three different limbs. The family also has a multigenerational history of severe bone fragility, muscle weakness, and premature hair graying. The patient, her living son, and his father underwent genome sequencing that identified a variant in MTAP (c.885A&amp;gt;G; p.(R295=)) in the patient and son. This variant was previously reported in three other families with DMS-MFH and has been shown to alter splicing. Notably, commercial genetic testing did not report this as a relevant variant, and diagnosis required independent analysis of the raw sequence data. Based on these findings, the patient and her son were diagnosed with DMS-MFH. Given the bone fragility with elevated bone turnover markers we treated the patient with yearly zoledronic acid infusions with no subsequent fractures. Surveillance for osteosarcoma is also being performed with annual whole-body MRI. Conclusion: DMS-MFH has been reported in only five families to date. The sixth family described here has clinical characteristics similar to the other kindreds. Due to high risk of aggressive osteosarcoma, timely diagnosis is imperative to decrease morbidity and mortality. Commercial genome sequencing may miss this diagnosis, so targeted genetic testing should be pursued. As more cases are identified, characterization of affected families may enhance our understanding of the natural history of the disease and guide surveillance and treatment strategies. Presentation: 6/2/2024

Adequate Nutrition and Premature Hair Graying: A Review of Literature

Adequate Nutrition and Premature Hair Graying: A Review of Literature

The possibilities of correction of premature greying of hair and involutive hair changes

The review highlights the available published data on the etiopathogenesis of early graying, hair involution and restoration methods. Early graying of hair is defined as settlement before the age of 20 in Caucasians, before the age of 25 in Asians and before the age of 30 in Africans. In etiopathogenesis, an imbalance between oxidative stress and the antioxidant system is considered as the leading mechanism, a significant role is played by genetic predisposition, hormonal disorders of the thyroid gland, acute stress; the causes may also be deficiency of vitamin B12, copper, iron. Currently, the active molecule palmitoyl tetrapeptide-20 is used to prevent pigment loss and restore it. The endocannabinoid system in the hair follicle is also considered as a target for stimulation during the restoration of hair growth.

A case study of Duchenne muscular dystrophy caused by Alu element insertion in DMD gene and analysis of its gray-hair symptoms.

Duchenne muscular dystrophy (DMD) is a severe X-linked recessive genetic disorder caused by mutations in the DMD gene, which leads to a deficiency of the dystrophin protein. The main mutation types of this gene include exon deletions and duplications, point mutations, and insertions. These mutations disrupt the normal expression of dystrophin, ultimately leading to the disease. In this study, we reported a case of DMD caused by an insertion mutation in exon 59 (E59) of the DMD gene. The affected child exhibited significant abnormalities in related biochemical markers, early symptoms of DMD, and multiple gray hair. His mother and sister were carriers with slightly abnormal biochemical markers. The mother had mild clinical symptoms, while the sister had no clinical symptoms. Other family members were genetically and physically normal. Sequencing and sequence alignment revealed that the inserted fragment was an Alu element from the AluYa5 subfamily. This insertion produced two stop codons and a polyadenylate (polyA) tail. To understand the impact of this insertion on the DMD gene and its association with clinical symptoms, exonic splicing enhancer (ESE) prediction indicated that the insertion did not affect the splicing of E59. Therefore, we speculated that the insertion sequence would be present in the mRNA sequence of the DMD gene. The two stop codons and polyA tail likely terminate translation, preventing the production of functional dystrophin protein, which may be the mechanism leading to DMD. In addition to typical DMD symptoms, the child also exhibited premature graying of hair. This study reports, for the first time, a case of DMD caused by the insertion of an Alu element into the coding region of the DMD gene. This finding provides clues for studying gene mutations induced by Alu sequence insertion and expands the understanding of DMD gene mutations.

Assessment of Serum Ischemia Modified Albumin Level and Erectile Functions in Individuals with Premature Greying of Hair

Assessment of Serum Ischemia Modified Albumin Level and Erectile Functions in Individuals with Premature Greying of Hair

Deciphering potential causative factors for undiagnosed Waardenburg syndrome through multi-data integration

BackgroundWaardenburg syndrome (WS) is a rare genetic disorder mainly characterized by hearing loss and pigmentary abnormalities. Currently, seven causative genes have been identified for WS, but clinical genetic testing results show that 38.9% of WS patients remain molecularly unexplained. In this study, we performed multi-data integration analysis through protein-protein interaction and phenotype-similarity to comprehensively decipher the potential causative factors of undiagnosed WS. In addition, we explored the association between genotypes and phenotypes in WS with the manually collected 443 cases from published literature.ResultsWe predicted two possible WS pathogenic genes (KIT, CHD7) through multi-data integration analysis, which were further supported by gene expression profiles in single cells and phenotypes in gene knockout mouse. We also predicted twenty, seven, and five potential WS pathogenic variations in gene PAX3, MITF, and SOX10, respectively. Genotype-phenotype association analysis showed that white forelock and telecanthus were dominantly present in patients with PAX3 variants; skin freckles and premature graying of hair were more frequently observed in cases with MITF variants; while aganglionic megacolon and constipation occurred more often in those with SOX10 variants. Patients with variations of PAX3 and MITF were more likely to have synophrys and broad nasal root. Iris pigmentary abnormality was more common in patients with variations of PAX3 and SOX10. Moreover, we found that patients with variants of SOX10 had a higher risk of suffering from auditory system diseases and nervous system diseases, which were closely associated with the high expression abundance of SOX10 in ear tissues and brain tissues.ConclusionsOur study provides new insights into the potential causative factors of WS and an alternative way to explore clinically undiagnosed cases, which will promote clinical diagnosis and genetic counseling. However, the two potential disease-causing genes (KIT, CHD7) and 32 potential pathogenic variants (PAX3: 20, MITF: 7, SOX10: 5) predicted by multi-data integration in this study are all computational predictions and need to be further verified through experiments in follow-up research.

SASH1 S519N Variant Links Skin Hyperpigmentation and Premature Hair Graying to Dysfunction of Melanocyte Lineage

A better understanding of human melanocyte (MC) and MC stem cell biology is essential for treating MC-related diseases. This study employed an inherited pigmentation disorder carrying the SASH1S519N variant in a Hispanic family to investigate SASH1 function in the MC lineage and the underlying mechanism for this disorder. We used a multidisciplinary approach, including clinical examinations, human cell assays, yeast 2-hybrid screening, and biochemical techniques. Results linked early hair graying to the SASH1S519N variant, a previously unrecognized clinical phenotype in hyperpigmentation disorders. Invitro, we identified SASH1 as a regulator in MC stem cell maintenance and discovered that TNKS2 is crucial for SASH1's role. In addition, the S519N variant is located in one of multiple tankyrase-binding motifs and alters the binding kinetics and affinity of the interaction. In summary, this disorder links both gain and loss of pigmentation in the same individual, hinting to accelerated aging in human MC stem cells. The findings offer insights into the roles of SASH1 and TNKS2 in MC stem cell maintenance and the molecular mechanisms of pigmentation disorders. We propose that a comprehensive clinical evaluation of patients with MC-related disorders should include an assessment and history of hair pigmentation loss.

Fractal Pattern in the Premature Graying of Hair: A Case Report

Fractal Pattern in the Premature Graying of Hair: A Case Report

Anti-aging mechanism and effect of treatment with raw and wine-steamed Polygonatum sibiricum on D-galactose-induced aging in mice by inhibiting oxidative stress and modulating gut microbiota.

Polygonatum sibiricum (PS) is a traditional Chinese medicine (TCM) first recorded in Mingyi Bielu. The book documents that PS can nourish five internal organs, be taken for a long time, relax the body and prolong lifespan. Presently, PS is widely used in TCM to prevent premature graying of hair. Based on TCM theory and clinical trials, the wine steaming processed product from PS provides a better effect. However, no published study has elucidated the anti-aging mechanism. The study aim was to investigate the anti-aging mechanism of PS and its wine steaming processed product in mice, specifically focusing on the effect of D-galactose (D-gal) surrounding the intestinal flora and the Kelch-like ECH-associated protein 1-nuclear factor erythroid 2-related factor 2-antioxidant response elements (Keap1/Nrf2/ARE) pathway. The chemical components in Raw PS (RPS) and Wine-steamed PS (WPS) were identified by ultra-performance liquid chromatography-hybrid quadrupole-Orbitrap high-resolution mass spectrometry (UPLC-Q-Orbitrap HRMS). An aging model using Kunming mice was established through intraperitoneally injected D-gal. Concentrations of RPS and WPS at 5, 10, or 15g/kg/day levels were administered intragastrically, respectively. The body weight, liver and spleen indexes, superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and malondialdehyde (MDA) activities in serum and brain tissue were recorded. Hematoxylin and eosin (HE) stained brain tissue was histopathologically examined. The expressions of Keap1, Nrf2 and heme oxygenase 1 (HO-1) in the brain tissue at the mRNA and protein levels were respectively detected by reverse transcription-polymerase chain reaction (RT-PCR) and western blot (WB). Moreover, an Illumina Hiseq platform was used for 16S ribosomal RNA (16S rRNA) high-throughput sequencing to evaluate the proportions of intestinal flora in aging mice. The proportions of saccharides, flavonoids, and triterpene acids were different between RPS and WPS. In the aging model mice, WPS outperformed RPS in improving body weight and mental state by increasing the spleen index, SOD and GSH-PX activities, decreasing the liver index and MDA activities, and restoring the histopathological morphology in D-gal-induced aging mice. At the mRNA levels, RPS and WPS significantly reduced the expression of Keap1 and increased the expressions of Nrf2 and HO-1. The trend in protein expressions was similar to that of the mRNA results, and WPS had a stronger effect than RPS. Fecal microbiota analysis showed that RPS and WPS restored intestinal microbiota proportions to normal levels. The results demonstrated that PS and its WPS had a positive effect in relieving oxidative stress in aging mice. WPS outperformed RPS, which might be related to the activation of the Keap1/Nrf2/ARE pathway and regulation of intestinal flora.

Vitiligo Causes and Treatment: A Review

Vitiligo is a chronic autoimmune disorder characterized by patches of skin losing pigment due to the destruction of melanocytes, the cells responsible for producing pigment. The condition can affect people of all ages and ethnicities, with symptoms including milky-white patches on the skin, premature graying of hair, and color loss in mucous membranes like the mouth or nose. Among the main causes of vitiligo are; Autoimmune Response: Vitiligo is primarily an autoimmune disease where the immune system mistakenly attacks melanocytes, leading to depigmentation. Factors like family history, genetic predisposition, and immune system disorders contribute to its development, Triggers: Events such as sunburn, emotional distress, or exposure to certain chemicals can trigger or exacerbate vitiligo. The treatment options are; Medications: Treatments include light therapy (phototherapy), oral medications like psoralen combined with UVA light (PUVA), and depigmentation therapy using monobenzone to match skin tones Surgery: Surgical options are available for some cases of vitiligo and Psychological Support: Counseling and mental health services can help individuals cope with the emotional impact of vitiligo, in conclusion, v is a multifaceted skin condition lacking a conclusive remedy, many types of vitiligo, but the most common one is Non-segmental Vitiligo (NSV), honmental and genetic are the most important causes of vitiligo. Important symptoms of vitiligo are; depigmented patches, hair discoloration, sensitivity to sunlight, treatment of vitiligo have many approach, among them are; topical Corticosteroids, phototherapy and Cosmetic Camouflage.

PHYSICOCHEMICAL AND PHYTOCHEMICAL ANALYSIS OF HERBO-MINERAL HAIR DYE FOR PREMATURE HAIR GRAYING

Background: Premature Hair Graying (PHG/ Canities) is the burning problem of today’s society. Despite extensive research, the treatment for PHG is still unsatisfactory. Ayurveda considers Palitya (premature hair graying) as an ailment of vitiated Pitta dosha (deranged functional factor of the body responsible for digestion and metabolism). Ayurveda therapeutics can provide the natural solution to this problem without adverse effects and also can prevent the recurrence. Objective: In present research work, attempts are made to formulate unique, safe and effective herbomineral hair dye (Keshranjak yog) an Ayurvedic formulation. The prepared formulation is also evaluated for its efficiency through various organoleptic, phytochemical and physicochemical parameters. Results: The pH of prepared herbomineral hair dye was found to be 6 which is close to neutral; to suit the requirements of different scalp and hair types. Total phenolic content (8.1%±0.7), total flavonoid content (6±1.2) of prepared sample were found to be acceptable and within limit. Conclusion: The dyeing effect of the developed dye may be attributed to keshya (good for hair), Kesharanjak (hair coloring) properties according to Ayurveda and presence of tannins, phenols as per pharmaceutics. Nowadays natural remedies are widely accepted as they are safer with minimal side effects as compared to the chemical hair dye. Kesharanjak yog may provide vital nourishment to the scalp skin and can color the hair in an utmost gentle manner. Due to nontoxic nature can act as public healthcare product.

A phytochemical and comparative study to assess the efficacy of Kaidarya (Murraya koenigii (L.) Sprengel) siddha taila plus Kaidarya vati and Kaidarya vati in Akala palitya.

An urgent concern for the younger population is premature hair greying. Regardless of gender, it naturally occurs in the fourth decade, although these days, it strikes in the early twenties as well. According to Ayurveda, faulty eating habits, physical strain, psychological issues, environmental variables, and changes in lifestyle are chief reasons which leads to impaired digestion and Pitta dosha [associated with fire and water element] vitiation, particularly reduced production of Bhrajaka Pitta [biological pigment], which mostly leads to hair colour loss. Current study was phytochemical, comparative, interventional clinical study done to evaluate the efficacy of Kaidarya [Murraya koenigii (L.) Sprengel] siddha taila plus Kaidarya vati and Kaidarya vati alone in Akala palitya. Here, Group A patients were allotted to Kaidarya siddha taila plus kaidarya vati treatment whereas Group B patients were assigned with kaidarya vati alone. The sample was 84 but total enrolled subjects were 95 with respect to dropout rate. The paired t-test was used to analyse the data from Group A and Group B both before and after treatment. A noteworthy distinction was noted between the mean values obtained prior to and following therapy. An independent t-test was used to compare the results between Groups A and B. A significant difference in Akala palitya was found between Groups A and B. Group A's [Kaidarya siddha taila plus Kaidarya vati] mean difference score is higher than Group B's [Kaidraya vati]. Therefore, effect of Kaidarya siddha taila plus kaidarya vati is more than Kaidarya vati in the management of Akala palitya [premature greying of hair].

Premature Graying of Hair

Premature Graying of hair (PGH) is a common and psychologically distressing condition of the hair. It is seen as being aggravated by various triggering factors. But the pathogenesis and the treatment options are still under study and limited. Thus, proper and extensive research seems to be needed.

A study of biochemical factors and knowledge, attitude, and practice in patients with premature graying of hair

A study of biochemical factors and knowledge, attitude, and practice in patients with premature graying of hair

White horses - non-coding sequences drive premature hair greying and predisposition to melanoma.

The Grey allele in horses is causing premature hair greying and susceptibility to melanoma. The causal mutation is a 4.6 kb tandem duplication in intron 6 of the Syntaxin 17 gene. A recent study demonstrated that the most common allele at the Grey locus (G3) involves three tandem copies of this sequence, whilst a more rare allele (G2) has two tandem copies and the wild-type allele (G1) only one copy. The G3 allele is causing fast greying and high incidence of skin melanoma, whereas the G2 allele is causing slow greying and no obvious increase in melanoma incidence. Further somatic copy number expansion has been documented in melanoma tissue from Grey horses. Functional studies showed that this intronic sequence acts as a weak melanocyte-specific enhancer that becomes substantially stronger by the copy number expansion. The Grey mutation is associated with upregulated expression of both Syntaxin 17 and the neighbouring NR4A3 gene in Grey horse melanomas. It is still an open question which of these genes is most important for the phenotypic effects or if causality is due to the combined effect of upregulation of both genes. Interestingly, RNAseq data in the Human Protein Atlas give support for a possible role of NR4A3 because it is particularly upregulated in human skin cancer, and it belongs to a cluster of genes associated with skin cancer and melanin biosynthesis. The Grey mutation and its association with melanoma provide a possibility to study the path to tumour development in numerous Grey horses carrying exactly the same predisposing mutation.

Premature gray hair development in the interbrow region owing to the loss of maxillary first molars in young mice.

The exact sites of premature hair graying and whether tooth loss causes this condition remain unknown. In this study, we aimed to explore the effect of reduced mastication on premature hair graying. Maxillary first molars were extracted from young mice, and the mice were observed for 3 months, along with non-extraction control group mice. After 3 months, gray hair emerged in the interbrow region of mice in the tooth extraction group but not in the control group. The expression of tyrosinase-related protein-2 (TRP-2) mRNA was lower in the interbrow tissues of young mice without maxillary molars than in those with maxillary molars. Tooth loss leads to interbrow gray hair growth, possibly because of weakened trigeminal nerve input, suggesting that reduced mastication causes premature graying. Thus, prompt prosthetic treatment after molar loss is highly recommended.

Premature Graying of Hair: A Comprehensive Review and Recent Insights.

Hair symbolizes well-being and self-expression, with graying occurring naturally among different racial groups at varying ages. Premature graying has psychological and societal impacts, influencing self-esteem and quality of life. Gray hair usually advances gradually and is permanent, with occasional reports of natural repigmentation. Premature graying of hair (PMGH) results from a complex interplay of genetic, environmental, and cellular factors. Studies exploring links between gray hair and conditions such as osteopenia, hearing loss, smoking, obesity, dyslipidemia, and cardiovascular disease have yielded mixed results. Despite continuous research into the causes of gray hair, effective, evidence-based treatments are lacking and still need to be improved. Herein, we reviewed the causes, mechanisms, risk factors, psychosocial effects, and emerging therapies for PMGH.

Putrescine Upregulates Melanogenesis Through Modulation of MITF Transcription Factor in B16F1 Mouse Melanoma Cells.

Ageing is a biochemical, metabolic and genetic physiological phenomenon. The suppression of melanin biosynthesis, evident in the greying of the hair, is a hallmark of ageing resulting from translation failure, reduced enzyme activity and cellular senescence. Putrescine, the smallest member of the polyamine family and an organic chemical, is present in living mammalian cells and plays a crucial role in regulating skin melanogenesis. Therefore, the purpose of this study is to explore the effect of putrescine on the signalling pathways of melanogenesis in melanoma cells. Melanin production capacity of putrescine was analysed using a tyrosinase activity assay. To assess the cell viability of B16F1 cells exposed to putrescine, a tetrazolium dye MTT assay was performed. The effect of putrescine on melanin synthesis in the presence of H2O2 was evaluated using various in vitro assays in B16F1 cells. The effect of putrescine on melanin production in B16F1 cells was determined using a specific melanin production assay. Gene expression was analysed using real-time polymerase chain reaction (RT-PCR). Furthermore, the effect of putrescine on the expression of proteins related to melanin production in the cells treated with H2O2 was analysed by immunofluorescence and Western blot analysis. Putrescine increased tyrosinase activity and showed no cytotoxicity in B16F1 cells. In addition, putrescine effectively scavenged H2O2, as shown by the reduction of intracellular H2O2 amounts in 2',7'-dichlorofluorescin diacetate analysis, and promoted melanin production in living cells. The stimulation of melanogenesis by putrescine was attributed to the increased expression of Mitf, Tyr, Trp-1 and Trp-2 genes. Immunofluorescence assays revealed that putrescine enhanced the expression of proteins associated with melanogenesis and upregulated TYR, TRP-1 and TRP-2 via the microphthalmia-associated transcription factor (MITF) and increased the expression of methionine sulfoxide reductases A (MSRA) and B (MSRB) in the cells treated with H2O2, effectively promoting melanogenesis. These results suggest that putrescine can be used to stimulate melanin synthesis. This is the first study to investigate the effect of putrescine on the signalling pathways of melanogenesis in B16F1 melanoma cells. The results confirm that putrescine can promote melanogenesis through the expression of TYR, TRP-1 and TRP-2 via the MITF in cells treated with H2O2. Putrescine can be used exclusively as a cosmetic product to prevent premature greying of hair.