The human skin is composed of multiple layers. The outermost layer, the epidermis, acts as the skin’s barrier to protect the body from the environment and external factors.
Deeper down is the dermis containing collagen, elastin fibres and fibroblasts. Collagen and elastin form the structure of the dermis making it tight and plump.
Fibroblasts are special cells that synthesize collagen and elastin. The subcutis is the deepest layer of the skin, composed primarily of fat.
Over 75% of young skin is made of collagen.
With age, the ability to replenish collagen decreases.
The density of collagen and elastin in the dermis declines, hence the structure and elasticity of the skin degrades, causing it to become thinner and more rigid. The fall in collagen also results in the loss of hyaluronic acid. This reduces the moisture, suppleness and elasticity of the skin.
The diminished elasticity of the skin reduces its ability to retain its shape and it does not conform as closely to the contours of the face.
The skin appears looser and sags. Lines and furrows emerge to enable movement. Gravity then pulls on the skin, all leading to sagging eyelids, bags under the eyes, and jowls.
The solution is Pure GOLD COLLAGEN®. The active ingredients reach the dermis from the inside, to re-activate collagen formation.
Skin ageing mechanism
Skin ageing is a complex biological process which affects several constituents of the skin and hence its appearance. There are two primary skin-ageing mechanisms, intrinsic and extrinsic [1-2]. Genetic variations are thought to be the main cause of intrinsic ageing, determining slow tissue degeneration, which result as the time passes, “the biological clock”. Extrinsic ageing instead is caused by environmental factors and in particular by sun exposure, also known as photo-ageing.
Both intrinsic and extrinsic ageing act simultaneously and are associated with phenotypic changes in the skin (i.e. wrinkle formation). However, deep inside in the dermis, fibrillar collagens, elastin fibres and hyaluronic acid, which are the major components of the extracellular matrix, undergo different structural and functional changes. Collagen and elastin are long-life proteins and hence are pre-disposed to intrinsic molecular aging. While the half-life* of many proteins is measured in hours, collagen and elastin have half-life measured in years [1]. As a consequence these fibres accumulate damage over time and this decreases their ability to function correctly. Intrinsically aged skin is generally characterised by dermal atrophy with reduced density of collagen fibres, elastin and hyaluronic acid. (Figure below, modified from reference [1]).
Structural changes in the dermis are more severe when the skin is both intrinsically old and photo-aged [1]. Extrinsically aged skin is characterised by degradation and alteration of collagen fibres and the accumulation of disorganised elastin proteins throughout the dermis, process also known as elastosis (Figure below, modified from reference [1]). Evidence indicates that the activation of matrix metalloproteinases play a major role in the pathogenesis of photoaging [3]. Metalloproteinases can be induced by UVA and UVB [4] and show proteolytic activity that results in the degradation of collagen and elastin fibres. As a result, the collagen density decreases each year with faster rate in photo-exposed skin [2]. Extrinsically aged skin is characterised by several clinical manifestation including leathery appearance, increased wrinkle formation, reduced recoil capacity, increased fragility of the skin and altered colour pigmentation.
* The half life is a prediction of the time it takes for half of the amount of a protein to be degraded.
1. E.C. Naylor, Maturitas, 2011, 69, 249-256
2. Baumann, J Pathol, 2007; 211: 241–251
3. El-Domyati M, Exp. Dermatology, 2002, 11: 398–405.
4. M. Berneburg, Photodermatol Photoimmunol Photomed 2000; 16: 239–244
