Effective Home Remedies For Skin Pigmentation
Vitiligo is a pigmentary disorder resulting in pale patches on the skin due to the loss of melanocytes. Interestingly, one study has found a higher frequency of the R160W MC1R allele in controls than in vitiligo patients,409 leading the authors to suggest that the R160W allele is protective against vitiligo. The suggested explanation for this protective function is due to the R160W substitution resulting in an epitope with lower antigenicity, thus protecting the carrier melanocytes against the autoimmune processes thought to be linked to vitiligo.409 However, this is speculative as the causes of vitiligo are not fully understood, and further research into both vitiligo and the association of particular MC1R variant alleles with this disease is needed to determine if there is any real link between MC1R and vitiligo, and if so what the molecular mechanisms underlying this link might be.
Because VZV becomes latent in cranial nerve, dorsal root, and autonomic ganglia along the entire neuroaxis, the virus can manifest anywhere on the body. Typically, the activated virus causes a prodrome consisting of skin sensitivity and mild-to-severe radicular pain, and after five days, a rash appears. The pain is associated with itching and dysesthesia. As with HSV-1, VZV infection decreases sensation in the affected dermatome, yet the affected skin is exquisitely sensitive to touch. The rash may continue to produce pustules that lead to crusting and ulceration. In many affected patients, healing is delayed beyond two weeks and is accompanied by increased skin pigmentation and scarring. Lesions can erupt outside the affected dermatome but rarely cross the midline and are not clinically significant. Distribution of 10 or more lesions outside a single dermatome suggests early evidence of viral dissemination. The term zoster sine herpete is used to describe VZV that is reactivated...
First, within a long evolutionary sense, various regional differences in the biological attributes of human populations have arisen as a result of natural selection pressures exerted by local environments on human biology. In this sense, environment acts as a determinant of the local human genotype. Many examples are well known in the anthropological and biomedical literature. They include (i) variation in skin pigmentation, which (especially in today's world in which there has been considerable redistribution of regional populations over recent centuries) contributes to variations in local population risks of skin cancer and vitamin D insufficiency (ii) various enzymatic polymorphisms which are associated with altered risks of various diseases (e.g. the N-acetylation pathway enzymes, various of the cytochrome P450 oxidative enzymes, the activity of alcohol dehydrogenase, and lactase activity) many of which such polymorphisms are presumed to reflect the allele-selecting impacts of...
Clinically the patient presents with truncal obesity, moon face, hypertension, diabetes, abdominal striae, acne and a buffalo hump, and experiences profound weakness. Pituitary ACTH-producing tumours tend also to produce skin pigmentation as ACTH has a similar molecular structure to melanocyte-stimulating hormone (MSH). Because patients have a tendency to bruise easily with delicate skin which is easily damaged, and have an increased risk of infection, post-operative problems are increased.
Populations that have arisen in low latitudes with high UV intensity have darker pigmentation than populations from higher latitudes. In black African skin, melanosomes are large, individual, and numerous, while in lighter skin-types, the melanosomes are smaller, less dense, and clustered in membrane-bound groups.29-32 The high amounts of eumelanin as well as the numerous large melanosomes within deeply pigmented African skin provide better protection from UV-induced DNA damage, filtering twice as much UVB as white skin.33 Skin pigmentation and photosensitivity have been categorized into the Fitzpatrick skin types I-VI, where I is fair skin that burns and never tans, and VI is very dark and never burns.34 However, it has been suggested that the eumelanin pheomelanin content of hair may be a more accurate measurement of UV sensitivity.35
Definition Various regionally limited congenital alterations of skin pigmentation or skin color are referred to as birthmarks. They may not be observed at birth, but usually they are obvious by several months of age. They can be due to the presence of an increased number of superficial lymph or blood vessels, increased pigment in the epidermis, aberrant tissue present in the skin, or pigment variation in the dermis.
Epidemiology of macular degeneration AMD has a multifactorial (or complex) etiology with contributions from a combination of environmental and genetic factors and a strong age effect. The prevalence of AMD increases dramatically with age, although the prevalence cited in various reports is highly dependent on the definition used for AMD. Overall, AMD increases from less than 1 to 2 at 50 years of age to as high as 15 at 90 years old. It has been suggested that increased skin pigmentation tends to protect from AMD, and this correlates to lower prevalence of AMD in African derived populations than Caucasians in some, but not all, studies. Various other risk factors may predispose to AMD including systemic hypertension and atherosclerosis, as well as cigarette smoking. Both photo-oxidation and inflammation have been suggested as possible pathogenic mechanisms for AMD, although the precise mechanism through which these result in disease has not been delineated.
Skin pigmentation due to melanin is a highly heritable trait, and skin color was once used to determine the zygosity of twins. Twin studies of a sample of 134 Australian twins give a heritability of 0.83 for skin color measured at 685nm at the inner forearm (Clark et al., 1981). Values for more UVR-exposed sites such as the forehead are much lower and can be accounted for purely by environmental factors. This initially surprising result reflects large variation in UVR exposure and needs to be taken in context. Pigmentation is of two sorts constitutive and facultative, the former referring to colour in the absence of UVR and the latter, color in response to UVR. In practice, the upper inner forearm receives UVR (as does even the buttock, a site that is to be preferred in such studies) and it seems likely that the figure quoted of 0.83 is likely to be an underestimate. Similarly, the lower heritability quoted for sun-exposed skin needs to be interpreted in the light of high ambient...
There is mounting evidence that MC1R plays a role in DNA repair, perhaps via multiple signaling pathways. A loss of activation of these DNA repair pathways in melanocytes expressing reduced function MC1R alleles would explain the link between MC1R variants and melanoma, independent of skin pigmentation phenotype.