Skin Aging: Causes

The skin is subject to intrinsic (endogenous) influences and extrinsic (exogenous) aging factors of aging.

Intrinsic aging factors

Intrinsic (“internal”) skin aging or endogenous aging refers to the physiological, chronological aging of the skin. Factors of intrinsic skin aging are:

  • Genetic predisposition
  • Hormonal balance (hormonal changes with age: menopause/menopause in women, andropause/menopause in men, and somatopause/growth hormone deficiency).
  • Accumulation of replication errors during cell division.

Areas of skin that are marked only by this aging process are, for example, areas on the inside of the arms or in the gluteal region (buttock region). This time-aged skin usually has very fine wrinkles due to loss of water and elasticity. Behavioral causes

  • Consumption of stimulants
    • Alcohol (woman: > 20 g/day; man > 30 g/day).
    • Tobacco (smoking) – smoking increases oxidative stress and also leads to increased formation and activation of the enzyme MMP-1. The metabolites formed during collagen degradation have an inflammatory effect (inflammation-inducing) and thus in the sense of aging. Collagen degradation is measurable by the hydroxyproline serum concentration.
  • Psycho-social situation
    • Stress

Medication

  • Medications (e.g., corticoids, which cause aging skin – by decreasing the thickness of the skin – to age faster, i.e., the skin becomes parchment-like).

Extrinsic aging factors

Extrinsic (“external”) skin aging or exogenous aging is determined by the environmental factors to which the skin is exposed. It represents an acceleration of intrinsic skin aging by various factors: Factors of extrinsic skin aging are:

  • Ultraviolet light (UV-A and UV-B) – sun rays or corresponding artificial rays (solariums) accelerate the aging process of the skin – in this context we speak of photoaging (photoaging; light aging). UV-A radiation is predominantly responsible for extrinsic skin aging. This penetrates deeper into the skin. The reason is that it has a longer wavelength than UV-B radiation. This leads to the activation of transcription factors such as AP-1 with the consequence of an increase in activity of metalloproteinases* .
  • Cigarette smoke
  • Exposure to heat and cold

* All skin sections – epidermis (epidermis), corium (dermis) and subcutaneous fat tissue – age due to ultraviolet light. The UV rays release reactive oxygen species (ROS) – see also oxidative stress. This leads, among other things, to DNA strand breaks. Furthermore, so-called toxic photoproducts are formed, which lead to skin aging as well as to an increased risk of skin cancer. Furthermore, UV radiation triggers collagen degradation through proteolysis. Matrix metalloproteinases (MMPs) are responsible for this. Skin changes of endogenous or exogenous origin also differ externally. The wrinkles of exogenous skin aging are very deep because the loss of elasticity is immense. In addition, the skin looks leathery and has irregular pigmentation. Especially sun-exposed skin areas such as the face or hands age prematurely. At the molecular level, there are different processes that contribute to skin aging:

  • Reactive Oxygen Species (ROS) – These so-called reactive oxygen species are also known as free radicals and are culprits in the main aging process. ROS are produced by the exogenous factors mentioned above and cause the oxidation of proteins (albumen), phospholipids (cell membrane components) and DNA (genetic material). In order to permanently prevent damage, the organism has antioxidant protective mechanisms. If these mechanisms are overloaded, damage to the cells and the DNA will occur in spite of everything. For more information, see “Oxidative stress – free radicals”.
  • Matrix metalloproteinases – UV light induces the formation of these enzymes (enzymes are biocatalysts; cleave proteins/protein here), which contribute increasingly to the degradation of elastic fibers and collagen. This leads to loss of elasticity and the formation of wrinkles, the formation of which is particularly promoted, for example, by the constant use of the mimic facial muscles.
  • Reduction of water binding capacity – Aged skin dries out faster and promotes the formation of wrinkles.
  • Change in hormone balance – estrogens induce collagen synthesis and stimulate the formation of hyaluronic acid, which is an important water-binding component of the skin. With age, the hormone concentration decreases, as does the collagen content. Progesterone inhibits collagenases and thus collagen degradation. Testosterone leads to crossing over (cross-shaped collagen strands). This leads to the fact that the connective and fatty tissue gets its hold (anti-cellulite factor) – furthermore, testosterone also leads to the inhibition of collagenases (= inhibition of collagen degradation).

Epidermis

Aging of the epidermis (epidermis) Here, aging leads to differentiation disorders of keratinocytes (horn-forming cells), leading to parakeratosis and roughness of the skin in old age. Skin aging is accompanied by a decrease in vitamin D synthesis and vitamin D concentration in the skin. Furthermore, aging leads to the decrease of melanocytes (pigment cells of the skin). These are cells loaded with melanin, which are responsible for skin color. The stimulation of melanocytes is equally dependent on UV radiation and stress. Both lead to the release of the hormone ACTH, which stimulates the melanocyte-stimulating hormone (MSH) and thus stimulates pigment formation. Age spots can thus be triggered by both exogenous (UV light) and endogenous influences (stress). Skin aging also causes a decrease in Langerhans cells. The latter are antigen-presenting cells of the skin. They have an important function in the immune defense – for example against bacteria and viruses. Influence of hormones Estrogens have an anabolic effect on the epidermis, i.e. stimulate the activity of the stratum germinativum (germ layer). The effect of estrogens occurs via the induction of IGF-1 in the skin. IGF-1 receptors can be detected in the stratum basale (basal layer) and stratum spinosum (prickle cell layer). Furthermore, estrogens stimulate the release of histamine (tissue hormone) from mast cells. Furthermore, estrogens (estradiol) have an influence on the size and melanin content of melanocytes, i.e. they have a stimulating effect: It is known that estrogens – for example present in a contraceptive (birth control pill) or produced in increased amounts during pregnancy – can lead to hyperpigmentation chloasma (melasma) on the face. Progestins can also contribute to this to a small extent. Estrogens have antioxidant protection for the skin by scavenging radicals. Testosterone has a stimulating effect on keratinocytes via a keratinocyte-growth factor, leading to an increase in keratin content. Vitamin D3 and thyroxine jointly influence keratinocyte proliferation. Langerhans cells – antigen-presenting cells of the skin – are under the influence of progesterone.

Dermis – connective tissue

Aging of connective tissue: decrease in the thickness of the corium (dermis), as well as fibroblasts and mast cells. Particularly pronounced is the decrease in elastic fibers in the corium, which are important for wrinkle-free skin. The UVB rays cause the elastic fibers to be thinned and destroyed – as a result, there is a breakdown of the elastica cross-linking and destruction of the collagen matrix. Matrix metalloproteinases (MMPs) are responsible for this. These aging processes are intensified by endogenous, i.e. intrinsic, factors. Influence of hormones Matrix metalloproteinases (MMPs) are inhibited by progesterone and testosterone. Estrogens (estradiol) stimulate collagen synthesis and also have a positive effect on elastin. The important thing is not collagen synthesis (new collagen formation), but the balance between formation and degradation. Caution. An increased estradiol dose leads to an increased activity of collagenases! Furthermore, estrogens stimulate the synthesis of hyaluronic acid, which is an important component of glycosaminoglycans (GAG). Glycosaminoglycans are divided into the following groups:

  • Hyaluronic acid
  • Chondroitin sulfate
  • Heparan sulfate
  • Keratan sulfate

Glycosaminoglycans serve to stabilize the skin by storing water. Thus, they are a reflection of the freshness of the skin.

Sebaceous glands

Aging of sebaceous glands Sebaceous gland function depends on sex hormones – androgens and estrogens. Their functionality decreases to half in old age compared to young people.Influence of hormones The cause of aging is intrinsic factors as well as the decreasing secretion of sex hormones (estrogens, testosterone) as well as growth hormones (STH, IGF-1).

Etiology (causes)

Biographic causes

  • Age – increasing age; young skin is more elastic. Biological skin aging begins in women between the ages of 25 and 30, and in men from the age of 35. Approximately from the age of 40, the first age-related skin changes become visible.
  • Occupations – occupational groups with occupational contact with chemicals and UV-A and UV-B radiation exposure.

Behavioral causes

  • Nutrition
    • Inadequate macro- and micronutrient supply (nutrients and vital substances) – see micronutrient therapy.
  • Consumption of stimulants
    • Alcohol
    • Tobacco (smoking) – increases oxidative stress and leads to increased formation and activation of the enzyme MMP-1 leads (matrix metalloproteinase), which stimulates collagen degradation.
  • Psycho-social situation
    • Stress

Causes related to disease

Medication

  • Corticoids – cause skin atrophy (thinning of the skin).

X-rays

  • Irradiations for tumor diseases

Environmental pollution – intoxications (poisonings).

  • For example, occupational contact with chemicals
  • UV-A and UV-B rays accelerate skin aging (photoaging).