Skin Care
Basic Skin Care
Skin Profile
Aging
Skin and Aging
- Sagging Eyelids Risk
Sagging eyelids (hooded eyes or dermatochalasis) are a frequent concern in middle-aged and older adults. It happens due to a loss of elastic fibers and a disruption of the collagen network. Sagging eyelids are usually a cosmetic concern, although they can cause visual field loss, ocular or eyelid irritation. They may also be a cause of headaches due to forced brow elevation to increase the visual field. A recent study identified nearly 30 genetic variations associated with sagging eyelids. These variations are located in 6 different genetic regions that contain four genes TGIF1, SMYD3, ATP8A1, and PJA2. Interestingly, some of the identified genetic variations, including variation in the TGIF1 gene (an inducer of transforming growth factor β) have protective effects while others are associated with increased incidents of sagging eyelids.
- Collagen Breakdown
Collagen is a connective tissue protein that makes up around a quarter of all the protein found in the body. It helps support and strengthen bones, teeth, tendons, skin, and internal organs. In particular, it affects your skin elasticity. Skin elasticity is the skin's ability to stretch and revert to its original form without developing wrinkles and imperfections. It is determined by collagen that makes up to 75% of our skin. The smoothness, firmness, and elasticity of the skin depend on the balance between collagen synthesis and its breakdown. Levels of MMPs increase in the course of normal aging and exposure to environmental factors (UV radiation) and irritation. In addition, genetic variants also increase activity of MMPs contributing to accelerated loss of collagen and premature skin aging.
- Youthfulness
The research into genetics for younger looking skin has recently yielded results showing several genetic variations. Individuals with these genetic variations look years younger and their facial skin showed fewer signs of aging. These genes are not only important for outward appearance but are also necessary to study general anti-aging and longevity.
- Skin Glycation
Our bodies use glucose as its main source of fuel. If glucose is not metabolized properly, it can bind to skin’s collagen and elastin fibers forming abnormal cross-links. This leads to structural and functional tissue impairment which produces advanced glycation products (AGEs). This process, called glycation, is responsible in accelerated aging of the skin as it impairs skin’s ability to regenerate and self-repair. Glycation has been described as caramelization (hardening) of the skin from the inside out. The skin-damaging effects of glycation cause wrinkles, dryness, skin laxity. Scientific research identified several genetic variations in NAT2, GLO1, and AGER genes are associated with excessive glycation. A recent study found that the presence of slow NAT2 acetylator types correlates with higher levels of AGEs in their skin. Genetic variations in the glyoxalase 1 enzyme (GLO1) that protects cells from AGEs can lower their activity which leads to the build-up of AGEs. Another gene implicated in glycation and skin aging is AGER receptor. Binding of AGEs to AGER results in activation of collagen breakdown enzymes and the pro-inflammatory cytokines. In simpler terms, it leads to the breakdown of collagen in the skin prompting wrinkles and other complexities.
Environment
Skin and the Environment
- Skin Detoxification Impairment
Human skin maintains a sophisticated detoxification system by converting environmental toxins and reactive oxygen species (ROS) into water-soluble forms ( by a mechanism called conjugation) and pairing these products with glutathione. Glutathione is a master detoxifier produced naturally by the liver. It is also found in fruits, vegetables, and meats. Glutathione also plays a critical role in maintaining optimal levels of vitamins C and E. Genetic variations in several enzymes can lower glutathione activity compromising its detoxification capacity which then results in the accumulation of ROS. Insufficient ROS detoxification may result in cellular damage, and may contribute to skin inflammation and premature aging. This also increases the individual's susceptibility to environmental toxins (automobile emissions, allergens, and cigarette smoke)
- Dermal Sensitivity
Skin sensitivity is largely determined by the skin barrier function. This determines skin permeability and the prevention of the entry of harmful pathogens and toxins. In addition, a hyper-reactive immune response to allergens and deficiency in protection from environmental toxins can both contribute to overall skin sensitivity risk. In some cases, dermal sensitivity leads to atopic dermatitis, or eczema, which is in fact one of the most common skin conditions (with prevalence rates of up to 20% in children and 3% in adults in the developed world). Eczema is characterized by very dry skin, and a typical age-related distribution of inflammatory lesions that are frequently infected by bacteria and viruses. It is important to consult a dermatologist if you experience any of these symptoms. Your overall dermal sensitivity risk has been calculated using the results from a large genome-wide study where a number of genetic variants associated with increased risk of skin sensitivity were identified.
- Pollution Defense Impairment
Air pollution is the cause of increased signs of aging, dark spots, and inflammation. The Chinese Dermatologist Association has found that those living in highly polluted areas (i.e. big cities) age 10 times faster than those who live in the countryside. Two important enzymes, EPHX1 and NQO1, protect our bodies from systemic absorption of highly reactive foreign chemicals (epoxides and quinones) from within the epidermis (most superficial layer of our skin). Biotransformation enzyme, EPHX1, plays a critical part in preventing the absorption of epoxides by catalyzing them into a less reactive, water-soluble form. Similarly, NQO1 converts coenzyme Q10 (ubiquinone) to its reduced form, ubiquinol, which then scavenges free radicals in the mitochondria and skin lipid membrane. Genetic variants in the EPHX1 gene cause epoxide hydrolase deficiency while SNPs in the NQO1 gene slow down production of ubiquinol. Individuals who have reduced levels of these two enzymes have significantly diminished skin defense from environmental toxins.
- Contact Skin Sensitivity
Contact skin sensitivities (contact allergy) are becoming more prevalent around the world. One of the most common types is the allergic reaction to nickel or other metals.The rise of contact allergy can be due to increased exposure to nickel in the environment as it is found in everyday items (jewelry, belt buckles, watch straps, metal zips, bra hooks, buttons, pocket knives, lipstick holders etc). Recent studies have identified genetic variations which are associated with the presence of nickel and other metal sensitivity.
- Skin Barrier Sensitivity
Our skin barrier serves a crucial, protective function for the skin by preventing entry of harmful microbes, toxins, and allergens while maintaining proper skin hydration. Skin barrier function is performed primarily in the outermost layer of the epidermis called the Stratum Corneum (SC). Stratum Corneum is also responsible for thermoregulation and innate immunity. Genetic variations in the Flaggirin (FLG) gene may cause skin barrier defects increasing its permeability and promoting skin sensitivity and irritation. In more extreme cases, genetic variations in the FLG gene are also associated with eczema and allergies. In up to 10% persons of European ancestry, parts of the FLG gene are deleted. As a result, this has strongly predisposed those people to eczema, asthma, and other severe allergies.Variations in the FLG gene may be the cause of sensitive or hypersensitive skin. People with a sensitive skin barrier are also three times more likely to suffer from a peanut allergy.
the Sun
Skin and the Sun
- Facial Pigmented Spots
Facial pigmented spots (solar lentigines and seborrheic keratosis) are a common feature of aging skin and are usually a result of sun exposure. With age, the repeated UV exposure causes melanin, a compound responsible for pigmentation as well as protecting the skin, to cluster or clump together. These clumps form an area of hyperpigmentation.Pigmented age spots develop earlier and are more pronounced in Asian than in Caucasian skin (as a result of SLC45A2). While there are some similarities in manifestation of pigmented spots in different populations (determined by the MC1R, ASIP, IRF4, BNC2 genes), there are also ethnic differences.
- Photoaging
Skin photoaging is defined as premature aging of the skin due to sun exposure (UV radiation). UV radiation causes DNA damage, oxidative stress, and disrupts normal architecture of skin connective tissue that impairs skin function. Clinical data suggests that extrinsic skin aging parameters have a strong genetic basis. Studies have identified genetic variations in STXBP5L and FBXO40 genes. This was determined by careful analysis of age, smoking history, hormonal status, body-mass index, hair color at age 20,estimated sun exposure, and intensity. Another recent study also found that the MC1R gene, which is responsible for producing pale skin and red hair, is also linked to the susceptibility for increased photoaging.
- Poor Tanning Ability
Tanning is the physiologically stimulated response to ultraviolet (UV) radiation in sunlight. UV exposure increases the production of eumelanin(one of the types of melanin) that darkens the skin in an attempt to protect it from damage. Ability of skin to tan is variable and is determined by genetics. Many genes are involved in the production of melanin which is the substance that gives skin, hair, and eyes their color. Large studies identified a number of genetic variants in the key pigmentation genes that are associated with tanning phenotype. Variants in the tyrosinase (TYR) gene encode skin color. MC1R gene is strongly associated with red hair, freckling and sun sensitivity: nearly all people with red hair have genetic variants in the MC1R gene, and hence diminished ability to tan. Similarly, genetic variants of OCA2 gene are responsible for the production of light colored eyes and light skin tones in East Asia. People with a number of genetic variants in the pigmentary genes tend to have lighter eye color, fair skin, and diminished ability to tan.
- Sensitivity to Sun
Humans vary over 1000-fold in their sensitivity to the harmful effects of ultraviolet radiation. Skin pigmentation, tanning ability and sensitivity to sun have high heritability. Several large-scale studies identified genetic variations that affect our skin sensitivity and tendency to get sun burns. The main determinants of sensitivity to sun are skin pigmentation genes (ASIP, TYR, MC1R, and OCA2) that are also associated with poor tanning. In addition, skin DNA repair genes are strongly associated with tendency to sun burns, and increased risk of melanoma. Interestingly, the DNA repair genes (NTM, ERCC1) have no association in either direction with tanning ability. This implies that there is a pigmentation-independent mechanism underlying sunburn reaction.