You probably have canities! No, it's not an STD or dental problem.

Guys checking their hair pre-party

Canities is the fancy word for premature greying of the hair, and most people have some amount of greying, from very sparse, to fairly widespread.

The color, density, and styling of hair have a colossal bearing on one’s self-esteem, especially in today’s times where a person’s first impression may turn out to his or her last impression. However, increased longevity of human life means that we spend an increasing proportion of our lives sporting signs of aging on our scalp. The most dramatic age-related change in hair is the onset of hair graying or canities, which is the gradual age-dependent dilution of hair color to gray or white, also known assenile canities (canities (L.), canus, hoary, gray). The graying of hair occurs due to an admixture of normally pigmented, hypomelanotic, and amelanotic melanosomes. White hair is the endpoint of graying. The age of onset of senile canities appears to be genetically controlled and inheritable. The average age for Caucasians is mid-30s; for Asians, late-30s; and for Africans, mid-40s. A good rule of thumb is that by 50 years of age, 50% of people have 50% gray hair. [1]

The darker the hair color, the more noticeable early graying will be. Particular hair colors are associated with some ethnic groups. The Fischer–Saller scale, named after Eugen Fischer and Karl Saller, is used to determine the shades of hair color [Table 2]. [2] Majority of the human population (80–90%) fall into the U to Y category (dark brown/black hair) of this scale.

WHAT HAPPENS DURING PHYSIOLOGICAL AGING (CANITIES)?

The type of hair fiber keeps on changing with age. Neonates... have unpigmented lanugo hair while adults have short (mostly pigmented) vellus hair or fine pigmented intermediate hair and long terminal hair shafts. Similarly, surface morphology also shows variation with age, particularly with the reduction in the cuticular scale size. The synthetic capacity of hair bulb melanocytes is maximum during youth. An average scalp hair follicle usually receives 7 ± 15 melanocyte replacements from an outer root sheath reservoir to the hair bulb, which occurs in the first 45 years preceding the onset of gray hair.[4]  Different theories have been suggested for the age-related gradual loss of pigmentation. This includes exhaustion of enzymes involved in melanogenesis, impaired deoxyribonucleic acid (DNA) synthesis, loss of telomerase, loss of antioxidant mechanisms, and anti-apoptotic signals. Table 3 shows various changes that take place in a white hair bulb during canities.[5] The net result is that fewer melanosomes are incorporated into cortical keratinocytes of the hair shaft. Cessation of pigment production by melanocytes in the hair matrix area surrounding the dermal papilla is a slow process resulting in slow outgrowth of graying hair at the pace of normal hair growth. All hair bulbs do not decrease pigment incorporation in the growing hair at the same time giving “salt and pepper pattern”to the scalp hair.

It has been observed that hair graying pattern depends on gender, age of onset, and smoking habits, with smokers having higher chances of having canities.[6] Temporal area is involved in males first while in females, it is the frontal area. Age of onset also affects the area of involvement; parietal and occipital areas are involved in patients of young age while frontal area is involved in late onset group.[6]

WHY DOES PREMATURE CANITIES OCCUR?

Premature canities is a common cause of referral to dermatologists. It occurs most commonly without any underlying pathology, but is said to be inherited in an autosomal dominant manner. It is different from poliosis which is circumscribed hypomelanosis of hair. The diseases associated with poliosis are given in Table 4. The pathogenesis of premature canities has not yet been clearly elucidated.[7] A hypothesis that pH and cysteine level of melanosomes play critical roles in determining the course of mixed melanosomes leading to dark, light, or red hair phenotype has been proposed because of the diversity of human hair pigmentation.[8] The role of pH in controlling mixed melanogenesis has attracted much attention as it is seen that tyrosinase activity is progressively suspended by lowering the pH, with a shift to more pheomelanin phenotype.[8-11] Concentration of cysteine in melanosomesis another control point in mixed melanogenesis.[7] Chemical hair straightening is done by alkaline disruption of the disulphide bonds in the cortex of the hair shaft. It causes considerable damage to the hair because of the pH (9–12) of the chemicals leaving the hair dry and fragile. In a questionnaire-based study, Shetty et al. reported that 22% of the cases experienced graying of hair also.[8,12] There is definitely a role of trace metal ions in hair pigmentation. Copper ions are required by tyrosinase at its active center; thus, it is likely that copper ions in melanocytes are necessary to maintain normal color.[7] Fatemi Naieni et al. compared the mean copper concentration in patients with PHG and controls and found lower mean serum copper concentration in the cases.
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Data suggest that oxidative stress can also play a major role in the premature aging of skin and hair.[5] This theory has been widely accepted these days. Reactive oxygen species (ROS) or free radicals, generated by a variety of internal and environmental factors may result in direct damage to various cellular structural membranes, lipids, proteins, and DNA. To combat these free radicals, our body has endogenous defense mechanisms such as antioxidative enzymes which include superoxide dismutase, catalase, glutathione peroxidase as well as non-enzymatic antioxidative molecules like vitamin E, vitamin C, glutathione, and ubiquinone. The production of these endogenous defense mechanisms decreases while that of free radical increases, resulting in aging.[5]

APPROACH TO MANAGEMENT OF PREMATURE CANITIES

...Recent experimental work indicates that cinnamidopropyltrimonium chloride, a quaternized UV absorber, delivered from a shampoo system, is suitable for photo protection of hair, while simultaneously providing an additional conditional benefit on hair,[23] Solid lipid nanoparticles have been developed as novel carriers of UV blockers for use on skin and hair, offering photoprotection on their own too by reacting and scattering ultraviolet radiation (UVR).[ 24]

Recent advances in the management of aging hair and scalp are anti-aging compounds. Shampoos are largely ineffective as anti-aging agents due to water dilution and short contact time, and antioxidants such as vitamin C and E in these preparations protect fatty substances in the shampoo from oxidation, and not the hair.

— Portions excerpted from Sehrawat M, Sinha S, Meena N, Sharma PK. Biology of hair pigmentation and its role in premature canities. Pigment Int 2017;4:7-12.
tinyurl.com/y59sopwa

HERE'S A NEW SOLUTION TO PREMATURE CANITIES

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