Age-Related Depletion of Skin Constituents

1. Aging

Aging is a physiologic mechanism that is marked by the deterioration of fertility- and survival-associated functions of the body. Aging or senescence encompasses all human beings as opposed to age-related dermatologic conditions which affect certain individuals. The process of aging is characterized by depletion of collagen and other proteins in the extracellular matrix of the dermis, decreased proliferation of cells in the basal layer of skin, the altered thickness of the epidermis, and increased degradation of matrix components. Exposure to ultraviolet-B radiation of the sun induces photodamage of the skin and further promotes the process of aging. (Zhang & Duan, 2018)

2. Molecular Mechanisms

The molecular mechanisms are discussed as follows. 

2.1 Reactive Oxygen Species and Oxidative Damage (AKA Free Radicals)

The reactive oxygen species include superoxide ion, hydrogen peroxide, and hydroxyl radical. These reactive oxygen species are produced in the mitochondria (Our cells micro energy generator) and tend to damage cellular structures such as proteins, nucleic acids, and cell membranes. During the onset of aging, enzymes that degrade these reactive oxygen species tend to have reduced activity and cause cellular stress and damage. This means that the strong free radical fighting enzymes that we use to have, have become weaker and fewer to neutralize free radicals accumulates, and, because of this, damaging free radicals accumulate within our skin and accelerates skin aging. Depletion of vitamins C and E also accelerates oxidative damage mediated by the reactive oxygen species. This means that if you do not replenish your skin’s vitamin C & E levels as you age, your skin aging will accelerate faster than if you maintain adequate levels of vitamin C & E. (Gilbert & Barresi, 2000)

2.2 Genetic Instability 

The genetic mutations accumulate accompanied by the accumulation of faulty proteins and enzymes. The efficacy of the DNA repair apparatus also declines with age, thus, promoting increased genetic mutations meaning, your skin ages faster as your DNA repair system wears out. (Gilbert & Barresi, 2000)

2.3 Telomere Shortening 

With repeated cycles of cell division, the telomeres at the end of each chromosome shorten. These telomeres are maintained by the enzyme telomerase. Shortening of telomere length limits the division of cells which marks the onset of aging. (Gilbert & Barresi, 2000)

2.4 Damage to Mitochondrial Genome 

The mitochondrial genome (our skins micro energy generator) is more susceptible to genetic mutations than the nuclear DNA. Mitochondrial gene mutations promote the synthesis of reactive oxygen species, and apoptosis, and reduce the synthesis of energy. The reactive oxygen species in turn damage the mitochondrial damage. (Gilbert & Barresi, 2000)

3. Age-Related Depletion of Skin Constituents

The phenomenon of aging is associated with the depletion of several components which are described as follows. 

3.1 Reduction in Growth Factors and Growth Hormone 

The insulin-like growth factor 1 (IGF-1) and growth hormone axis plays a crucial role in the growth and proliferation of body tissues. It is observed that the production and secretion of growth hormone decline with age, as elder adults, have a lower concentration of growth hormone as compared to younger adults. Studies suggest that levels of growth hormone decline at a rate of 14% per 10 years of an individual’s life. Along with the secretory rate, the half-life of growth hormone also declines with age. Aging is therefore known as a relatively deficient growth hormone state. (Sherlock & Toogood, 2007) Aging is also associated with a decline in epidermal growth factor levels. This leads to a concomitant decline in the proliferation of keratinocytes and promotes apoptosis of these cells, resulting in a reduced thickness of the stratum corneum and the epidermis. This means as our growth hormones decline, our skin becomes thinner. (Wang et al., 2020)

3.2 Reduction in Epidermal Lipids 

The epidermal permeability barrier comprises free fatty acids, cholesterol, and ceramides. These components are produced by the epidermal keratinocytes. As compared to the younger stratum corneum, the older stratum corneum exhibits a reduction of up to 30% in the total lipid content of the epidermis, owing to reduced synthesis of epidermal lipids. The decline in total lipid content is dominated by reduced cholesterol synthesis. Reduction in the total lipid content leads to dysfunction of the epidermal permeability barrier. Dermal aging is also associated with a rise in the skin pH. This alters the activity of enzymes that catalyze the processing of epidermal lipids and the development of extracellular multilamellar bilayers. Therefore, at higher skin pH, cosmetic formulations delay the recovery of the epidermal permeability barrier. This means that lotions and creams that are used by older adults should be manufactured with a higher pH than creams marketed to teens and younger adults. If older adults use pH neutral creams, lotions, pH neutral soaps or body washes, they will actually be impeding the recovery that the skin is trying to achieve. (Wang et al., 2020) 

3.3 Reduction in the Levels of Epidermal Permeability Barrier Proteins

At the onset of aging, the levels of structural epidermal permeability barrier proteins also decline. The proteins include filaggrin and loricrin. The reduction in the levels of these structural proteins is attributed to a decline in the calcium content of stratum granulosum. Defective proteins render the epidermal permeability barrier to be defective. (Wang et al., 2020) Loricrin and filaggrin are important constituents of the cornified envelope that forms the epidermal permeability barrier. These proteins are cross-linked to each other and with other members of the cornified envelope in the presence of calcium and the enzyme transglutaminase. An intact cornified envelope is crucial to the cutaneous integrity and barrier function of the skin. Aging is associated with a reduction in the levels of these proteins in the cornified envelope of the epidermis. (Rinnerthaler et al., 2013)

3.4 Reduced Sebum Production by Sebaceous Glands

Similar to other structures in the skin, the sebaceous glands (our skin oil glands) also demonstrate altered activity during the onset of aging. The average production of sebum (skin oil) by the sebaceous glands declines during the later decades of life leading to a reduction in the levels of surface sebum (surface oil), marked by reduced formation of squalene and wax esters in the skin. Reduction in the synthesis of sebum is associated with a reduction in the synthesis of androgens as a person grows older. (Pochi et al., 1979)

3.4 Reduction of Coenzyme Q10

Coenzyme Q10 is involved in electron transfer and protects against oxidative damage. The onset of aging and other dermatologic conditions is characterized by the intracellular deficiency of coenzyme Q10. Coenzyme Q10 is a lipophilic antioxidant that prevents oxidative damage to DNA and mitochondria (our skin’s micro energy generator). The significance of the role of coenzyme Q10 in aging is demonstrated by the improvement of senescence grading scores upon coenzyme Q10 supplementation. (Yan et al., 2006)

3.6 Reduced Melanin Synthesis

The senescent melanocytes are characterized by hypomelanosis which is the reduced production of melanin. This is due to the downregulation of MITF, TRP-1, and TRP-2 as well as due to decreased degradation of melanosomes owing to reduced autophagy in skin aging. Skin hypopigmentation is also associated with oxidative stress owing to mitochondrial redox imbalances. Accumulation of reactive oxygen species further damages the melanocytes. (Lee, 2021)

3.7 Reduced Sweat Production

Aging is also characterized by the altered function of the thermoregulatory mechanisms. A reduction in the secretion of sweat glands is observed in older individuals. This leads to increased thermal strain and inefficient heat loss during warm weather. (Smith et al., 2013) 

3.8 Reduced Collagen Production

Collagen depletion, exacerbated by photodamage, is the key feature of dermal aging. Exposure to ultraviolet radiation upregulates the expression of matrix metalloproteases which catalyze the degradation of collagen. Aging is associated with alterations in the function of fibroblasts, usually mediated by free radicals and resultant oxidative damage to these cells. Aging is also characterized by impaired expression and the production of antioxidant enzymes. (Varani et al., 2006)

Our Products 

Our product range comprises soaps and creams that are suitable for every skin type especially aged skin and skin disorders such as psoriasis, eczema, dermatitis and actinic keratosis. The ingredients have skin nourishing and rejuvenating properties that help improve dermatologic conditions and combat aging and associated skin changes. The ingredients in our products restore the levels of depleted components of the skin and enhance the overall appearance of the skin. We provide you with a scientific review of our ingredients on the “Ingredients Studies” page and full-length scientific articles on all of our ingredients is located on our “Article” page.

The collagen-building peptide complex comprises synthetic peptides that stimulate the production of collagen, restoring the normal levels of collagen in the dermal matrix and improving the appearance of wrinkles and fine lines. The formulation of our cream & lotion products enhances the total lipid content of the skin and strengthens the epidermal permeability barrier. This reduced transepidermal water loss and improves the overall skin integrity. 


Gilbert, S. F., & Barresi, M. (2000). Developmental biology, ed. Sunderland (MA): Sinauer

Lee, A. Y. (2021). Skin Pigmentation Abnormalities and Their Possible Relationship with Skin Aging. Int J Mol Sci, 22(7). 

Pochi, P. E., Strauss, J. S., & Downing, D. T. (1979). Age-related changes in sebaceous gland activity. J Invest Dermatol, 73(1), 108-111. 

Rinnerthaler, M., Duschl, J., Steinbacher, P., Salzmann, M., Bischof, J., Schuller, M., Wimmer, H., Peer, T., Bauer, J. W., & Richter, K. (2013). Age-related changes in the composition of the cornified envelope in human skin. Exp Dermatol, 22(5), 329-335. 

Sherlock, M., & Toogood, A. A. (2007). Aging and the growth hormone/insulin-like growth factor-I axis. Pituitary, 10(2), 189-203. 

Smith, C. J., Alexander, L. M., & Kenney, W. L. (2013). Nonuniform, age-related decrements in regional sweating and skin blood flow. Am J Physiol Regul Integr Comp Physiol, 305(8), R877-885. 

Varani, J., Dame, M. K., Rittie, L., Fligiel, S. E., Kang, S., Fisher, G. J., & Voorhees, J. J. (2006). Decreased collagen production in chronologically aged skin: roles of age-dependent alteration in fibroblast function and defective mechanical stimulation. Am J Pathol, 168(6), 1861-1868. 

Wang, Z., Man, M. Q., Li, T., Elias, P. M., & Mauro, T. M. (2020). Aging-associated alterations in epidermal function and their clinical significance. Aging (Albany NY), 12(6), 5551-5565. 

Yan, J., Fujii, K., Yao, J., Kishida, H., Hosoe, K., Sawashita, J., Takeda, T., Mori, M., & Higuchi, K. (2006). Reduced coenzyme Q10 supplementation decelerates senescence in SAMP1 mice. Exp Gerontol, 41(2), 130-140. 

Zhang, S., & Duan, E. (2018). Fighting against Skin Aging: The Way from Bench to Bedside. Cell Transplant, 27(5), 729-738. 

Shopping Cart