Youthful looking skin is the result of a delicate balance maintained through different mechanisms that either stimulate certain actions or moderate others. The loss of this balance causes the appearance of skin aging signs. Our patented technology enables an equilibrium among the various mechanisms and slows skin aging.
Skin hydration, which depends on both water diffusion and retention from the deepest parts of the skin, is considerably reduced with aging. Since water binds to protein and is essential to support proper enzymatic reactions, a loss of hydration leads to altered structural and mechanical properties of the skin. The stratum corneum (SC) dries out causing skin flaking, reducing skin flexibility, and precipitating wrinkle formation.
Moisturizes for a smoother and more supple younger looking skin
Poor hydration alters the barrier function of the skin with aging, leaving it more vulnerable to external and internal stress. Permeability barrier disruption is associated with skin irritation and inflammation, in part through the recruitment of inflammatory cells that generate reactive free radicals, as well as inflammatory lipids and cytokines.
Relieves itching due to dry skin
A major feature of aged skin is the progressive disorganization of the ECM within the dermis that generates wrinkles and sagging. Dermal ECM is made up of collagen, elastin, proteoglycans, and GAGs that together establish the structural integrity of the skin. In the dermis, ECM components are produced by fibroblasts to form a tridimensional network that, in return, provides support and anchorage for cells. Proper attachment of dermal fibroblasts to the ECM promotes cell functions, including migration, proliferation, and differentiation. Thus, not surprisingly, any modification in the dermal ECM tridimensional network contributes to skin aging by affecting the biomechanical properties of the skin.
Strengthens the skin and prevent skin sagging
Importantly, oxidative stress affects the functioning of mitochondria which are in every cell, including epidermal keratinocytes and dermal fibroblasts. Mitochondria couple cellular respiration with energy production to form adenosine triphosphate (ATP) that supports cellular metabolism. Accumulation of ROS damage with aging alters mitochondrial integrity. Old mitochondria produce less ATP, causing an energy crisis that, at the skin level, translates into a dull complexion.
Assures a constant and sufficient energy contribution to the cells, allowing their metabolism to be more active and reactive in their functions
Oxygen supplementation to the skin is assured in two complementary ways, internally and externally. Within the body, blood carries oxygen that is delivered to cells via diffusion, following its release from the hemoglobin content of red cells. There are no blood vessels present within the epidermis. As a consequence, oxygen has to diffuse from the small vessels that irrigate the dermis to the upper layers. Unfortunately, dermal capillaries become more fragile with age and oxygen diffuses less efficiently from the deeper layers to the upper layers of the skin. From external sources, oxygen is absorbed through cellular respiration which is influenced by cellular metabolism and the quality of ambient air. Over time, urban living can contribute to poor oxygenation of the skin cells, thus negatively affecting the complexion of the skin.
Allows the cells to breathe better, bringing the skin a more luminous and radiant tone
The mmaintenance of the ECM relies on a delicate balance between production and degradation of its components. Both mechanisms are altered with aging, a phenomenon amplified by sun exposure, cigarette smoke, and urban pollution. The dermis of aged skin contains a decreased number of fibroblasts with a reduced capacity to produce collagen and elastin fibers. Reduced collagen and elastin is associated with a loss of skin firmness and resilience.
Protects the Extracellular Matrix and its constituents like collagen and elastin fibers
The skin, being exposed to the external world, has developed immune functions assumed primarily by Langerhans cells in the epidermis. These cells act as sentinels to alert the immune system to the presence of pathogens and other foreign materials. Not surprisingly, the immune functions of the skin are altered with aging and sun exposure. Langerhans cells are depleted from the epidermis, and those remaining become less efficient in their protective role. The consequences are increased skin susceptibility to infections and skin cancer.
Brings a better protection against external aggressions to promote healthy looking skin
Skin cohesion and exchanges
One of the most striking manifestations of skin aging, as revealed by histological techniques, is a flattening at the dermal-epidermal junction (DEJ) with loss of the dermal papillae. The latter structures form villosities that facilitate nutritional exchanges and metabolic byproducts evacuation between the dermis and the epidermis. Their disappearance with aging contributes to slow down epidermal cell turnover. The DEJ is a structure of major importance for skin cohesion, since it anchors the epidermis to the underlying dermis. This zone is constituted by various types of anchoring fibrils such as fibronectins, laminins, and collagen IV & VII. Their decrease expression with age weakens skin structure and contributes to wrinkle formation.
Fights the look of wrinkles and reinforces cutaneous structure
Reactive oxygen species (ROS) are major contributors to skin aging. Derived from molecular oxygen, ROS can form from interaction of UV radiations with biological materials, as a by-product of cellular metabolism, or can be synthesized by immune cells as a defense mechanism against bacteria. ROS are molecules that have lost or gained an electron and electrons are not stable in odd numbers. Thus, in their quest for missing electrons, ROS take electrons from cellular and extracellular components in their surroundings. Importantly, ROS are responsible for alterations affecting the structure and function of lipids at the membrane of cells and of proteins within the extracellular matrix (ECM). The skin possesses natural antioxidant defenses under the form of superoxide dismutase (SOD) and catalase activities that can transform ROS into inoffensive molecules. Unfortunately, both activities decrease with age and sun exposure, leaving more free radicals responsible for cellular damages.
Reduces the appearance of aging and photoaging
In response to various stimuli (UVs, hormones, cytokines, etc.), melanocytes synthesize photoprotective melanin pigments and transfer them to keratinocytes where they accumulate, modulating skin pigmentation. Aged skin often exhibits irregular pigmentation, particularly in chronically sun-exposed areas where anarchical melanine production and accumulation is associated with the formation of lentigines (age-spots). Increased pigment production in lentigo has been associated with keratinization impairment, on a chronic inflammation background. The incidence of lentigo augments with age, affecting more than 90% of white people older than 50 years, making it a major cosmetic concern in an aging society.
Evens skin tone and reduces the appearance of age spots
Keratinization is the process by which the epidermis forms its outer protective layer, the stratum corneum (SC). Normal keratinization relies on a delicate balance between cell proliferation, differentiation, and desquamation. Keratin, a highly fibrous protein, is produced during the differentiation process and causes cell walls to harden, thus forming the SC. Aging is associated with reduced epidermal proliferation, rapid differentiation, and slower desquamation of the SC. Keratinocytes that remain in the skin longer tend to become more keratinized therefore the aged cell is more rigid and the aged skin more fragile.
Softens skin and restores suppleness
The ECM is rich in long-lived proteins. As such, these proteins are vulnerable to various post-translational modifications that tend to accumulate with time and UV exposure, affecting their structure and biological functions. Glycation is a good example of such a modification. Resulting from the non-enzymatic addition of sugars to proteins, glycation generates abnormal cross-linking between adjacent proteins. The process is accelerated in the presence of high glucose levels and free radicals. In the aging body, cross-links affecting glycated collagen and elastin fibers contribute to hardening and brittleness of the skin, and interferes with skin renewal.
Makes the skin less fragile, more supple and assures better cell renewal
Accumulation of ROS with aging may affect DNA, generating damages that prevent its exact replication during cell division or introducing mutations that precipitate the process of aging. It is estimated that thousands of DNA alterations rise in each cell daily. Fortunately, the skin has developed mechanisms to repair this damage. However, not surprisingly, the efficiency of these repair systems diminishes with time, a phenomenon associated with accelerate aging.
Prevents premature aging of the skin by preserving healthy cells
With aging, fragmentation of collagen and elastin fibers is increased through the activation of specific enzymes: matrix metalloproteinases (MMPs) for collagen, neutrophil elastase for elastin, and hyaluronidase for GAGs. Fragmentation of dermal ECM has important consequences. Fibroblasts cannot attach to fragmented collagen and are thus deprived of the level of mechanical tension required to maintain efficient collagen synthesis. These collapsed fibroblasts produce high levels of collagen-degrading enzymes, alimenting a self-perpetuating, deleterious cycle. Moreover, reduction in mechanical tension has been associated with increased levels of ROS production that accelerate the aging process and reduce the expression of anti-oxidant enzymes in the skin.
Improves skin elasticity and resiliency
Increased proteolytic activity with aging and the ECM fragments generated are potential triggers of inflammation. MMPs and elastase both facilitate the migration of inflammatory cells through their ability to proteolyse the ECM. Degradation of collagen and elastin also leads to the generation of fragments that further contribute to recruit inflammatory cells that, when activated, induce the release of additional proteolytic enzymes. In this aspect, skin aging can be viewed as a chronic inflammatory state.
Reduces skin redness and prevents skin inflammatory reactions
An increase in the release of pro-inflammatory mediators, proteolytic activity, and ROS ultimately affect skin microcirculation with aging. The three factors converge to alter the structure of dermal microcapillaries, causing vasodilatation and increased vessel permeability. As a consequence, plasmatic fluids tend to leak within the dermis generating edema and contributing to the formation of dark circle under the eyes. Vasodilatation is also associated with rosacea, a cosmetic concern in progression with aging.
Reduces the appearance of puffiness and dark circles while increasing overall draining of the tissues.