Cortisol is a glucocorticoid hormone synthesized from cholesterol in the cortex of the adrenal gland. Cortisol has a variety of functions. It is known for its role in the body’s stress response. Cortisol also participates in the inflammatory response and regulation of metabolism. Glucocorticoids bind to both glucocorticoid receptors (GRs) and mineralocorticoid receptors (MRs). GRs exist in almost all tissues in the human body. MRs have a more restricted expression with the highest concentration in the kidneys. Both GRs and MRs are expressed in the dermis.

Research indicates that cortisol may have a relationship with collagen in the human body. This may point to a possible connection between stress and collagen-containing tissues such as skin and joints.

Collagen is the most abundant protein in the body and comprises much of the extracellular matrix. Supplementation with collagen has been shown to improve skin moisture and elasticity. Skin in the human body consists primarily of collagen type I. Collagen type I inhibition may be mediated by GR activation through the cortisol-mediated inhibition of the transforming growth factor-beta (TGF-β).

A recent study assessed collagen type I synthesis in the presence of cortisol. The study explored the gene and protein expression levels of collagen type I human dermal fibroblasts (HDFs) in the presence of three different concentrations of cortisol (1 nM, 10 nM, and 100 nM). The researchers reported that protein expression levels of procollagen type I were reduced in the presence of cortisol in a dose-dependent manner. This indicates that cortisol may inhibit collagen type I synthesis. The conclusion of the study indicates that GR is the main receptor type that is responsible for fibroblast changes in the presence of cortisol. 

The same study explores this relationship further by treating HDFs with cortisol and certain collagen peptides. The authors report that the presence of collagen peptides diminished the effect of cortisol-dependent reduction in procollagen type I. This suggests that at a cellular level, collagen peptides may modulate the effects of cortisol. In addition, while cortisol was shown to downregulate TGF-β expression, collagen peptides supported the recovery of the cortisol-mediated TGF-β signaling cascade. The authors postulate that collagen peptides may act as inhibitors to GR signaling. 

Supplementation with collagen peptides may support skin and joint health. This recent study also suggests that collagen peptides may also support skin health under conditions related to stress. Further exploration into the connection between collagen and cortisol may offer additional understandings of this relationship.

By Colleen Ambrose, ND, MAT