Skincare expert Jasmina Vico talks us through the science of skin
How your skin works
The three main layers of the skin are the epidermis, dermis and subcutaneous fat. The main responsibilities of the dermis are sweating, helping you feel things, growing hair, making oil and bringing blood to your skin. It is made of a complex arrangement of extracellular matrix proteins including collagen and elastin, which provides elasticity.Fibroblasts are a major source of matrix proteins and the tissue inhibitors of metalloproteinases, which control the extracellular matrix (ECM) turnover and remodelling.
How it ages
As we age, the ECM loses its integrity as the protein structures become fragmented. Fibroblasts lose their ECM connections as enzymes slowly degrade the protein networks. This leads to a change in fibroblast shape, severely affecting the cells' function. Protein production by fibroblasts is reduced, contributing further to the breakdown of the ECM network.
This vicious circle causes a significant reduction in elasticity and a loss of skin tone. Whilst the cause of this remains uncertain, scientists are predicting that it could be due to a combination of oxidative stress damage to the DNA, cell senescence, and chronic inflammation. However, the dermis is not the only culprit at play.
Causes of ageing
We’re all exposed to various natural factors that contribute to the loss of elasticity and ECM integrity as we age, and sun exposure makes it much worse. Fibroblasts do not react directly with UV light but rather scientists believe that the epidermis might be responding to UV exposure by releasing chemicals that diffuse into the dermis and lead to enzyme release in dermal fibroblasts. This interchange is thought to result in wrinkles – the sign of UV-induced skin ageing. However, recent research has shown that a third player is adding to the signs of skin ageing actively too.
As we age, the fat layer below our skin shrinks. Additionally to this, a connection between UV light and fat has recently been found. A new type of fat depot in the deep dermis was discovered that can penetrate the upper dermis, which is well within reach of UV light. These fat cells can also respond to chemicals released by cells in the epidermis. In response to chronic UV damage, these fat cells die and are replaced by scar tissue. While we know that protection from UV light can slow down skin damage and therefore soften the ageing, there’s still no cure to this altogether.
Why cells can't repair themselves
Our body is made of cells. We have trillion of them, and they’re organized into different tissues that make up our organs. Cells divide themselves to produce new ones for the growth and repiar of body tissue, and they can divide about 50%-70% in our lifetime. Once they are exposed to the damage, cells division stops. In the nucleus of each cell, the DNA molecule is packaged into thread-like structures called chromosomes. Each chromosome is made up of DNA tightly coiled many times around proteins called histones that support its structure.
Chromosomes are protected by caps at the end of each strand of DNA called telomeres. However, telomeres get shorter each time a cell copies itself and once telomeres get too short to do their job it causes cells to age and stop functioning properly. We inherit the DNA that determines the initial length of telomeres from our parents. However, stress also plays a key factor – the more stressed you are, the more you age as with stress people’s telomeres become shorter. Our body’s natural response to stress is to go into fight or flight mode. Stress hormone cortisol increases, heart rate, blood pressure and more. High levels of cortisol increase cell damage through oxidative stress.
How skin ages throughout our life
Skin is soft, thin and immature. Even though the skin is constantly renewing itself during this period, it is also extremely sensitive and remembers everything which is one of many reasons why sun protection is crucial especially during this time.
The teen years can be filled with skin problems. As hormonal levels rise, our skin reacts and pimples or acne can be the result of this. Those with dry skin are a little bit better off, as these ageing changes are less noticeable. Strong sun exposure, squeezing acne, and too little sleep are habits that also damage the skin.
As this period hits, many have overcome the dreadful period of pubescence and everything that comes along with it. However, the skin has remembered everything that was done to pubescent skin and might have been damaged long-term.
The real changes become apparent from the age of 25 years old. The production of collagen and elastin now starts to slow down and pigmentation starts to come to the fore. Now it is prevention that matters most and should be prioritised, as opposed to curing the damage.
Due to the quantity of hyaluronic acid decreasing as well as subcutaneous fat, blood vessels, defective collage and elastin, pigmentation and wrinkles appear. All the changes in the skin now really start to show and come to the surface the most. However, there are two different types of wrinkes to differentiate: static and dynamic wrinkles. Static wrinkles show due to the changes inside the skin, while dynamic wrinkles appear because of constant muscular activity.
With menopause approaching, the skin changes itself once again and the dermis and epidermis become thinner – yet at the same time the skin becomes more stable. Nonetheless, there are no cosmetics that can completely undo the years and make it be young again. Now more than ever, sun and other skin damages would leave deep wrinkles and pigmentations on the skin and make it look older.
The skin looks very hardened with low elasticity and large numbers of deep wrinkles. Even though there is nothing that will fully counteract wrinkles or other skin damage, it’s useful to understand the origin of it and whether it is due to an environmental aspect or not, as it is never too late to avoid further skin damage.