The Ancient Egyptians knew all about skincare. Scrolls dating back 3,500 years describe elaborate routines to keep the face soft and smooth, the body gently perfumed. If disease and imperfections threatened to spoil the day – and they certainly did in 1550BC – there were treatments on hand for most common ailments: wrinkles and moles, eczema and itches, boils, stings and bites.
How helpful the ancient therapies were is hard to ascertain. But as with the peddling of modern skincare products, it’s not clear how much that mattered. Wax, olive oil and fresh milk would swiftly banish wrinkles, one scroll asserts, with the afflicted instructed to “See to it!” Unsightly mole? Try berries, grain, honey and leaves crushed in water that has been used to wash the phallus. An itchy neck? A smear of chopped-up bat will “heal it at once”. But what about that annoying crocodile bite? Slap a lump of meat on it, declares the Ebers papyrus, one of the world’s oldest known medical works.
The advice can make the eyes ache from rolling, but there was sense in some of the ancient strategies. Many recipes drew on natural antiseptics, such as garlic and onions; moisturising olive oil and aloe vera; and anti-inflammatory compounds, including salicin from willow. Before mocking the physicians of old, we should consider what scientists three millennia hence might make of today’s creams, balms, emulsions and serums, the Botox, tucks and peels.
Plenty remains unknown about skin, but for all the outstanding mysteries, researchers have nailed down some fundamentals of what it does, how it works, the transformation with age and how diseases arise.
Rather than a mere casing for the body, doctors consider the skin a complex, vital organ. It is famously the largest organ in the body, the size of a single bedsheet and three times heavier than the brain. It is our frontline defence against the outside world with all its sharp edges and germs, sunlight and pollution. It ensures we don’t get too hot or too cold, or absorb or lose too much water. It’s our tactile connection to the world, a sensory surface that surrounds us. It is a display that’s used to assess us in an instant: our heritage, age, health, emotions. The skin is far from a lifeless surface: zoom in and you’ll find it teeming with bacteria, viruses and fungi, not to mention minuscule, transparent mites that mate on our faces as we sleep.
The complexity of the skin begins with its structure. It has three main layers: the outer epidermis or top layer, the dermis or middle layer, and the bottom layer, the fatty hypodermis. The epidermis itself is a multi-layered tissue, thick on the palms and soles of the feet, but incredibly thin on the eyelids – all the better for blinking with. There is no blood supply to the epidermis: the outer surface is a flexible sheath of hardened and dead cells that keeps water, germs and pollution at bay. The dead cells are constantly replenished from below. The fresh supply replaces the 40,000 or so skin cells the body sheds each day, meaning you have new skin every month.
Among other cells in the epidermis are the melanocytes. These make melanin, the pigment that give skin its colour. When exposed to the sun, melanocytes ramp up their melanin production. This darkens the skin and protects against damaging ultraviolet light in the sun’s rays. Expose the skin to too much sunlight and over time, DNA damage can build up in melanocytes and lead to melanoma skin cancer. There is a balance to be had though: getting some sun is a must. Skin cells deep in the epidermis need sunlight to produce vitamin D, which is important for healthy bones, teeth and muscles. For most people, the skin provides plenty of vitamin D in the spring and summer, but from October to April, health officials recommend a daily 10µg supplement.
The epidermis is anchored to the dermis. This is the thickest of the skin’s three layers and makes up about 90% of the organ. The dermis is held together by collagen, a protein that gives skin its strength and resilience. It’s also rich in elastin, another protein that makes it stretchy and able to spring back into shape. A thin but extensive network of blood vessels in the dermis provides nutrients to the epidermis. It also controls how much heat is conserved or lost by the body: too cold and the blood vessels constrict, too hot and they dilate, allowing more blood to the skin’s surface where it releases heat.
Some of the skin’s most important components are embedded in the dermis: hair follicles, sebaceous and sweat glands. There are also nerve endings that allow us to sense hot and cold, rough and smooth, pleasure and pain. A typical adult has about five million hair follicles rooted in the dermis. They are found all over the body, except for the lips, the palms of the hands and the soles of the feet.
“The densest, hairiest part of the body is the nose,” says Prof Des Tobin, a dermatological scientist at University College Dublin. “Because it has grown the least since you were a baby.”
Most sebaceous glands are attached to hair follicles and produce an oily substance called sebum. This keeps the skin soft and smooth, provides added waterproofing, and keeps bacterial and fungal growth in check. The three million sweat glands cool the body by producing up to two litres of water an hour, which removes heat as it evaporates. With nerves wired in, the entire exterior of the human body is transformed into a sensory surface. You can bend the finest hair by one degree and know that you’ve been touched. “The sensory receptors in the skin are a symphony of nerve endings,” says Nina Jablonski, professor emeritus of anthropology at Penn State University and author of Skin: A Natural History. “What we recognise now is that caring touch in early development is extremely important and the importance of touch never goes away.”
Beneath the dermis is the hypodermis, or subcutaneous tissue, a layer of fat and connective tissue. This final layer of skin cushions and binds to muscles and bones, carries nerves and blood vessels from the skin into the body and as insulation helps maintain a stable body temperature.
As a purely physical barrier, the skin defends against bacteria, viruses, fungi and other infectious organisms. The defence is bolstered by an extraordinary array of protective substances and immune responses that are built into the skin. Secretions from the sweat and sebaceous glands combine to form a thin, acidic film on the epidermis that limits which microbes can grow there. Sweat contributes a substance called dermcidin, which kills a range of bacteria. Sebum, meanwhile, contains other antimicrobials such as lauric and sapienic acids.
The skin even possesses its own immune system. Keratinoctyes, the main skin cells in the epidermis, recognise both pathogens and flesh damage. Once triggered, they kickstart the inflammatory response, calling in white blood cells to fight infection and mop up cellular debris. Keratinocytes muck in, releasing antimicrobials such as beta-defensin and cathelicidin. Other cells in the epidermis are actively on the look out for would-be invaders. Langerhans cells, for example, can reach between other cells in the epidermis in search of germs. When they spot an infection, they marshal the skin’s T-cells which attack the intruders. The average adult can draw on about a million T-cells per square centimetre of skin to tackle local infections. Yet more cells in the dermis have similar defensive duties.
Despite the skin’s hostility to microbes, it is teeming with life. The skin has its own extensive microbiome – a rich community of bacteria, viruses, fungi and other microbes – that make their home on the hard epidermis. Researchers estimate that tens of thousands, and perhaps several million, bacteria colonise each square centimetre of skin, making the skin second only to the gut in terms of sheer density of bacteria. The science of the skin’s microbiome is still in its infancy, but different populations thrive in different parts – the oily face, the moist groin and armpits, the dry palms and forearms – and the inhabitants are often beneficial. Resident microbes serve up nutrients, crowd out bad bugs, and help the immune system tell friendly bugs from foes. About 90% of people have microscopic mites called Demodex folliculorum nestling in their pores. They feed on sebum and emerge at night to mate on our faces and nipples.
Perhaps the most remarkable property of skin is its ability to repair. Graze your knee and, if you are healthy, a carefully choreographed process honed through evolutionary history swings into action. The first priority is to prevent further blood loss, says Prof Mat Hardman, chair of wound healing at Hull York Medical School and the University of Hull. Blood vessels that are damaged in the wound constrict to stem the flow, while platelets in blood that has seeped into the wound clump together on a net of fibrin protein. The resulting clot is a temporary patch.
With the bleeding under control, the skin turns red as immune cells pour in from the circulation. These clean the wound of germs and debris. At this point, you can often see clear fluid on and around the wound. For the next stage, skin cells in the epidermis spread under the dried clot, turning it pink. New blood vessels form deeper in the skin and cells in the dermis start churning out fresh collagen, a scaffold to strengthen the repair. Finally, the collagen is “remodelled” to resemble the structure of normal skin. The entire process can take years to complete, but in a few months the scar should be as strong as the skin before the injury.
Human evolution has favoured rapid healing over perfect healing, a compromise that’s clear when people suffer major burns. The skin that grows back is life-saving, but may be hairless and devoid of glands. But skin science is pointing to ways that such healing can be improved. If you wax a patch of skin, the wrenching out of hairs can kick follicles into their growth phase. This activates stem cells in the follicle which, evidence suggests, can stream into wounds and help the skin repair. In an ongoing clinical trial, Hardman is investigating whether waxing patients before surgery improves how well they heal. “In theory, it should apply to any kind of surgical procedure,” he says. “From an NHS perspective, this would be amazing because it doesn’t involve drugs.”
The skin, of course, changes with age. And as ever with skin, the mechanisms are complex. Scientists talk of intrinsic ageing and extrinsic ageing. Intrinsic ageing is the gradual weakening and deterioration of skin where genetics, heritage, hormone levels and certain diseases shape its appearance and performance. Extrinsic ageing is the impact of everything we throw at it: sunlight, diet, pollution, smoking, stress. Intrinsic ageing is slow and barely visible before the age of 60 or 70. Extrinsic ageing occurs much faster, manifesting decades earlier. “If you know anyone who’s a keen golfer or gardener, take a look at the skin on their backs. It will be beautiful, but the skin on their neck will look very different,” says Prof Rachel Watson, executive director at the Singaporean government’s A*Star Skin Research Labs. “That’s the difference between intrinsic and extrinsic ageing.”
Not all skin fares the same, however. Much of what scientists know about the organ is based on studies of Caucasians. Less is known about African and Asian skin, but it is clear that it ages differently. Watson, who left Manchester University for her post in Singapore, moved to help redress the balance and further research on Asian populations.
The general picture of skin ageing is a broad deterioration of everything involved. Skin cells in the epidermis become thinner. The proportion of pigment-producing melanocytes drops, making skin paler and translucent. The skin loses collagen and elastin that make it strong and elastic respectively, making it weaker and less supple. The fine blood vessels in the dermis break more easily, making older people more prone to bruising. The sebaceous glands produce less oil and fat in the underlying hypodermis disappears. Another crucial change is seen where the epidermis anchors to the dermis. In younger skin this interface is ridged, producing a 3D structure that forms a strong bond between the layers. With age, the ridges flatten out and the epidermis becomes less well tethered. “That’s why we see many more cuts or abrasions on the faces of older men who shave,” says Watson. “The epidermis and its junction with the underlying dermal tissue is much less robust.”
When sunlight meets skin, the effect is dramatic. Some light reflects off, but the rest is absorbed. Ultraviolet rays have the most impact. They can damage DNA and make cells release more enzymes that chop up and reshape collagen in the dermis. At the same time, UV-exposed cells churn out more stretchy elastin which, rather than helping, harms the skin because it’s not properly organised. The result is that UV ages the skin, amounting to perhaps 80% of visible ageing. “On the face, it’s a perfect storm,” says Watson. “You have all the changes that happen intrinsically and superimposed on that is the impact of sunlight, pollution, smoking, diet and the rest.”
White skin seems to fare worse than skin of colour. One reason is clear: black skin contains more melanin which protects against UV damage. But skin of colour is structurally more resistant too: the epidermis is thicker and more strongly anchored to the dermis which has more collagen and less elastin. “There’s a 40 to 50-year benefit from having darker skin,” says Watson.
Asian skin seems to lie somewhere between fair skin and skin of colour, but how ageing affects its resilience and pigmentation is the focus of ongoing research.
One upside of sunlight ageing the skin is there’s no mystery around how to prevent it. Avoiding peak sunshine hours, covering up, and wearing daily sunscreen that blocks UVA and UVB from April to September in the UK, will particularly help protect Caucasian skin. But scientists stress there is an urgent need to understand ageing in all skin colours.
According to Jablonski, we may never have paid so much attention to skin nor prized the unlined, dewy skin of youth so highly. “I am on the verge of my 70th birthday and I look like I’m on the verge of my 70th birthday. I wear makeup but I have wrinkles in abundance,” she says.
“I can afford, as a senior female professor, to say this is the way I look,” she adds. “But I’m not in a majority. Many people who have the means to prevent or obliterate the signs of ageing are taking advantage of it. They realise that an aged appearance can work against them.”
