Skin ageing is a process that has led to the creation of countless products and treatments. It’s a natural consequence of our skin’s ageing process- but can be dramatically accelerated by sunlight.
Photoageing, i.e., skin ageing via sunlight, is the most significant cause of skin ageing in humans. How does it happen, though? What is the mechanism behind sunlight leading to the formation of a wrinkle in our skin?
This blog post is the first of our series of in-depth articles that aim to give you a deeper understanding of a subject- in this case, photoageing. We’re about to take a deep dive into the processes that lead to photoageing, and the mechanisms that allow us to also prevent it from occurring.
Understanding Our Skin
The skin consists of three layers. There’s the epidermis (the outermost layer), the dermis (the middle layer) and, finally, the hypodermis (the deepest layer).
The outermost layer of our skin serves as a barrier between the environment and our bodies.
It may be the part we are most familiar with but is only a few millimetres thick – the thickness ranges from approximately 0.5 mm (on our eyelids) to a maximum of 4 mm (on the soles of our feet).
Despite being incredibly thin, the epidermis has a complex structure consisting of five distinct layers (which can have layers within themselves). New cells are constantly made in the lower layers, moving to the surface about every four weeks, where they harden into dead cells (in the uppermost layers) and are then shed, either when rubbed or intentionally exfoliated.
Apart from the cells that enable us to perceive touch, fight invading pathogens and produce proteins (the most common type of cells), the epidermis also plays host to melanocytes. These are cells that store melanin, a pigment that gives our skin its colour.
Melanin is one of our body’s naturally evolved defences against the sun’s UV rays – something we will be getting further into later on.
The dermis lies just under the epidermis. This is where you would find nerve fibres, blood vessels, sweat glands, sebaceous glands and hair follicles.
Its largest component, however, is the extracellular matrix (ECM)- a dense, three-dimensional network that’s composed of a mesh of fibrous proteins like collagen and elastin.
Collagen is the most abundant protein in the ECM (and, in fact, in the human body). The fibres it forms provide structural support to the ECM and its components, effectively contributing to the overall structure and elasticity of our skin.
This layer of the skin is unaffected by photoaging but is still worth mentioning to give you an overall picture of the skin’s layers.
It’s known as the hypodermis (also as the subcutaneous layer or subcutis) and is mostly made up of fat and connective tissue, along with larger blood vessels, lymph vessels, sweat glands, sebaceous glands and nerves. This layer merges with the dermis in folds that form tiny cavities filled with fat and water. The fat provides insulation to help regulate body temperature and acts as a shock absorber, protecting bones and joints from blows or bumps.
How the Sun’s UV Rays Affect our Skin
Sunlight contains UV radiation, of which there are three types:
UV-A rays: These rays have the lowest energy in the UV spectrum, but are the most prevalent form of UV radiation reaching the Earth’s surface. They penetrate through the epidermis and reach our skin’s dermis, playing a major role in skin ageing and wrinkling.
UV-B rays: Although more intense than UV-A rays, UV-B rays don’t penetrate as deeply into our skin’s layers. They tend to damage the more superficial layers of our epidermis. They do have one redeeming effect in the epidermis, though: they form vitamin D3, which is essential for our health.UV-C rays: The most intense form of UV radiation, UV-C rays could be incredibly damaging to us but are thankfully blocked by the earth’s ozone layer.
UV-A and UV-B rays cause skin ageing through a few different processes:
UV-A rays lead to the formation of ‘free radicals’ in our skin. These unstable molecules are the main perpetuators of photoageing. They tend to attach themselves to proteins, such as collagen, and other cellular structures, leading to structural and functional damage.
Since UV-B rays are more intense, they can make their way directly into our cells, causing damage on a cellular level. Our cells respond to UV-B damage by:
i. Increasing the production of our skin pigment melanin (which leads to a tan or darkening of skin)
ii. Initiating apoptosis, or cell death, for cells that are damaged beyond repair, leading to a typical sunburn
iii. Starting a cascade of inflammatory processes
…which brings us to –
Cells in various layers of our skin release ‘cytokines’, which are chemicals that, when exposed to chronic UV radiation, promote inflammation.
They essentially signal our bodies to bring cells from the immune system to the site of injury (in this case, sites of UV exposure), to repair damage and protect against further damage. However, an excessive number of cytokines can lead to localised inflammation, which can create breaks in the ECM and damage our skin’s collagen.
Both cellular damage and inflammation lead to the production of a family of proteins called matrixmetalloproteinases (MMP), whose job it is to break down and remodel the extracellular matrix. This involves breaking down the collagen and elastin proteins in the matrix, along with inhibiting the production of collagen in our skin.
Given that collagen makes up a large part of our extracellular matrix, their effects begin to affect the structure and elasticity of our skin. Although this takes place within the dermis, the break in the skin’s structure will even affect the integrity of the upper layers of the epidermis, gradually forming visible fine lines and wrinkles on the surface.
And that’s basically the process that leads to photoageing.
Our bodies have evolved innovative ways to protect against this damage –
The melanin produced by melanocytes has the ability to absorb UV radiation, thereby protecting cells from damage. In addition to damaging the skin, excess UV radiation can also deplete vitamins in our body and higher amounts of melanin were an evolutionary advantage – and the reason why populations that have historically lived close to the equator have darker skin.
Our skin has a complex system of antioxidants that help neutralise free radicals and protect against UV-induced damage. This system consists of two broad categories of antioxidants:
i. Enzymatic antioxidants: These are enzymes produced by our bodies that neutralise harmful free radicals formed by various factors, including UV radiation.
ii. Non-enzymatic antioxidants: Antioxidants such as vitamin C, vitamin E, coenzyme Q10 and glutathione are found in the dermis and epidermis. These form a part of our skin’s innate antioxidant defence, neutralising the free radicals formed when UV-rays start damaging our skin, by physically interacting with them and making them less reactive.
Another important family of antioxidants in the context of our skin are carotenoids, which include vitamin A (beta-carotene), lycopene, lutein and zeaxanthin. These compounds are preferential UV absorbers, meaning that they absorb UV radiation and protect our skin from damage. While glutathione and coenzyme Q10 are made by our bodies, we obtain vitamins and carotenoids from the food we eat.
Photoageing and a host of other diseases that can result from overexposure to sunlight begin to take place when these inherent defences of our body are overwhelmed.
Luckily, there are a number of very simple strategies to minimise the effects of photoageing that are entirely in our control. These include:
When used correctly, sunscreen can prevent sun damage and photoageing. It works by forming a barrier on the epidermis that absorbs UV rays. Inorganic compounds such as zinc oxide and titanium dioxide (commonly remembered as the white paint-like substance sportspersons would use in the 1980s and 90s) form a physical coat on the skin that prevents UV-rays from coming in contact with the skin’s surface. Certain organic compounds are also very effective sunscreens. These compounds have complex structures that absorb UV rays.
The strength of a sunscreen is measured by its SPF (Sun Protection Factor), a measure of the fraction of radiation that will reach the skin. An SPF 15 protects against 93% of UV-B rays, SPF 50 protects against 97%. There’s no sunscreen that offers 100% protection.
A higher SPF doesn’t necessarily guarantee better protection from photoageing, as the ‘SPF’ normally accounts for the quantity of UV-B rays that are blocked, not UV-A. Using a broad-spectrum sunscreen that explicitly protects against UV-A rays as well (which would be mentioned on the packaging) is an easy way to ensure that your skin is receiving the best protection possible.
A final point to remember while using sunscreen is to follow its instructions for application frequency and quantity of use. SPF is measured at a dose of 2 mg of sunscreen per square centimetre of skin; using less sunscreen than recommended may not offer sufficient protection.
Eating an antioxidant-rich diet
Eating a wide variety of fruits and vegetables ensures that we receive a healthy mix of antioxidants of different kinds, that together replenish and contribute to our skin’s innate system of antioxidants mentioned earlier.
The advantage of dietary antioxidants is that they tend to build up in our skin; as long as our diet includes foods (or supplements) that contain them, they will continue to offer protection from UV rays.
Exposure to the sun is not just unavoidable, it’s essential- but photoageing can be minimised by a few simple steps, including through food we eat. The nutrients in our food, as always, demonstrate their remarkable effects, right down to maintaining the health of our skin and preventing the formation of a wrinkle.