OUR BIRTHDAY suit is in many ways the, original “amazing technicolour dreamcoat”. Far more versatile than any clothing yet devised, skin keeps out the rain and the germs, protects us from the sun and helps to keep our bodies at the right temperature. What’s more, it monitors its own state of repair with pain receptors that alert us to any burns or cuts, and then makes good any damage. And it has its own police force of immune cells, which keep watch for intruders and rogue cells. Skin is also a biochemical factory, churning out vitamin D and hormones. It even sprouts decorative hair and useful fingernails, and exudes odours that dogs at least find attractive. Without it, life as we know it would be impossible.
A coat of hair
Our iced cake
Advertisement
HUMANS are equipped with this talented tissue thanks to the evolutionary ingenuity of our animal ancestors. The first of these to leave the sea and venture onto the harsh world of dry land were equipped with and protected by their scaly outer coverings – our precursor skin. Mammalian skin, with its highly distinctive tufts or coats of hair, first appeared about 150 million years ago.
If someone had invented skin, they would be hailed as one of the great designers of all time. For its physical structure – a bit like a two-layered cake with icing – is beautifully suited to its job. The outermost of the two main layers of the cake is called the epidermis. This consists of cells known as keratinocytes, so named because they produce a family of fibrous proteins known as keratin, after keratos, the Greek word for horn (see Diagram). Supplies of this protein, organised into tough filaments, are particularly plentiful in the thick layers of epidermis that protect our palms and the soles of our feet – parts of our body that are subject to strong friction and shearing forces. Keratinocytes are versatile cells, they are also responsible for our keratin-rich fingernails, toenails and hair – and the horns, hoofs, claws and feathers of other creatures.
The epidermis is topped with a waterproof layer – the stratum corneum made up of dead keratinocytes, which are sometimes graphically described as cells that make so much keratin they eventually choke themselves to death with it. This inert layer of keratin-rich corpses – the icing on the layer cake – keeps us from losing too much of the water in our bodies to the outside world, and also protects us from absorbing many potentially damaging chemicals. But it is continually being sloughed off through everyday wear and tear, and so needs to be constantly renewed. To fulfil this role, keratinocytes produced in the deepest region of the epidermis gradually migrate upwards, destined to take their place among the dead on the outer reaches of the skin. Every month, give or take a few days, we shed our entire skin surface.
“Scrubs”, cosmetics that contain a mild abrasive, remove the stratum corneum. This exposes the under-lying living cells, making the skin look fresh and glistening and feel rather tender. Some antiwrinkie creams containing alpha-hydroxy acids work in a similar way. You can simulate this effect on a patch of skin by sticking on, then stripping off, a piece of Sellotape; for the best result, this needs to be done several times, but take care – the procedure may leave the skin in immediate danger of infection, as it seems to be the dryness of the normal skin surface that discourages bacteria and other microscopic invaders. Skin creams containing a derivative of vitamin A called Retin-A also appear to help eradicate minor skin wrinkles by encouraging the growth of epidermal cells, but this substance can also leave the skin unable to tolerate strong sunlight.
Wear and tear
Durable stuff
GENERALLY our skin fits us well, though it may begin to sag with age, so there must be something controlling epidermal cells to prevent them from proliferating inappropriately. In diseases such as psoriasis, this control seems to break down: too many of the cells are produced and then shed, leaving unsightly, flaking red patches. In Britain alone, at least 2 million people suffer from this debilitating condition. The underlying cause is still unclear, but research suggests that the skin’s wound-repair mechanism is switched on at the wrong time.
Skin is strong yet elastic thanks to the dermis – a thicker layer of skin cells that lies beneath the continually renewed epidermis, and forms the cake’s bottom layer. Dermis is made up of a tightly interwoven meshwork of strong and elastic protein fibres. Most are members of a family of proteins called collagen, interlaced with another group known as elastin. These fibres are embedded in a complex gel of sugarlike molecules known as glycosaminoglycans. The dermis is designed both to adapt to bodily movements and to resist mechanical damage, so its texture varies – it is thin and flexible over our joints but very thick and tough on the back. After the keratins, the collagens – the durable stuff of leather – are the leading skin proteins.
A fighting force
Some common itches
RUNNING through this meshwork of connective tissue are blood vessels, lymph vessels and nerve endings, as well as the collagen- and elastin-producing cells, the fibroblasts. The rich blood supply provides nutrients and energy to both the dermis and epidermis, while specialised nerve endings enable us to feel pain, heat, cold and the surfaces or substances we touch. The immune system appears in the guise of histamine-releasing mast cells – vanguards of the inflammatory response against any of the invaders or irritants notorious for their role in skin allergies. (Hay fever sufferers take antihistamine drugs to block the action of these cells.)
Eczema, also known as dermatitis is an inflammatory disease of the epidermis and upper dermis that causes severe itching. It is very common, and can be caused by contact with irritating chemicals or with substances that can provoke an allergic reaction. Dandruff is in reality only a mild form of dermatitis, which stimulates the shedding of dead cells from the stratum corneum.
The dermis is also home to a variety of other peculiar but, by and large, useful structures which we investigate below: the sebaceous or grease-producing glands, sweat glands and hair follicles.
Scattered about in the dermis, especially on our face, upper back and chest, are tiny grease-producing glands called sebaceous glands. Attached to hair shafts, these glands churn out a thick, greasy liquid known as sebum. They start doing this at puberty, when a person reaches the age of between about 10 and 13 years. Look at a baby’s nose: you won’t see all those big, grease-producing pores that pit an adult’s.
Every attempt to find a function for these glands has failed. Sebum offers no protection against sunlight, water loss or bacteria, nor does it smell much. It seems tailor-made to do just one thing: cause acne.
Acne is a disease of the sebaceous gland’s duct, or tubular passages to the skin’s surface; and it strikes when a high output of sebum leads to a blockage of the duct. Black heads are signs of a partial blockage – their dark centre is not dirt but the skin pigment, melanin. In mild cases of acne, the duct becomes completely blocked, producing a whitehead. In severe acne, the sebum breaks through the duct’s wall to inflame the surrounding cells. Sebum can do this because it is rich in fats known as triglycerides, which skin bacteria readily break down to produce irritating chemicals, called free fatty acids. These fatty acids act as detergents, breaking down cell membranes to cause inflammation. It is this process that starts the spot, not an invasion of bacteria (see Diagram).
Mark of puberty?
Keeping a cool body
TERENCE KEALY, a biologist at the University of Cambridge, argues that sebaceous glands have actually evolved to cause acne. He reasons that spots on the skin act as a marker of puberty, a signal that an individual has reached sexual maturity. His explanation is certainly plausible, for the sex hormones that surge out of our ovaries and testicles at puberty, trigger the production of sebum, which may lead to acne. Androgens, the steroid hormones more prevalent in men than in women, apparently play a major role, which may explain why boys often suffer the worst outbreaks. Yet there turns out to be no clear link between an individual’s androgen levels and the severity of his or her acne. People with bad acne do not have “abnormal” hormone levels; for some unknown reason, their skin is simply more sensitive than other people’s to these chemical messengers. Researchers do know, however, that stress worsens acne.
Unfortunately, there is not much that can be done to treat the condition. Powerful drugs can stop the proliferation of sebum-producing cells, but they have serious side effects and can cause birth defects, so scientists are trying to find better treatments. Meanwhile, research on acne has established one cheering fact: eating chocolate or fatty foods definitely does not make it worse. Moderate exposure to sunlight can help to reduce acne, because the sun’s ultraviolet radiation inhibits the proliferation of inflammation-causing cells. Topical treatments with antibiotic creams can help a bit, by suppressing the bacteria that break the sebum down into free fatty acids. But the only really good news is that acne goes away as you get older – though nobody yet understands why.
Skin is equipped with two sorts of sweat-producing glands. One type, the eccrine glands, appear all over the body but are very numerous on the forehead, soles of the feet and palms of the hand, where some 620 tiny glands are crammed into every square centimetre of skin. The perspiration that they produce is 99 per cent water, which ensures that it cools the body as it evaporates. Body temperature could rise to lethal levels were anything to block these glands. In the James Bond film Goldfinger the murder of the villain’s assistant by coating her all over in gold paint was no Hollywood fantasy, but a real possibility.
Wise travellers
Fight or flight
WHEN our body temperature rises, after physical exertion or in hot weather, our skin is noticeably sweaty; but most of the time we do not notice the small amounts of fluid that continually escape from our bodies in this way – about half a litre per day per adult. The rate at which the body loses water through the eccrine glands may increase tenfold in severe heat, but it also rises, albeit less dramatically, when we are in a dry, low-humidity environment such as an aeroplane. For this reason, wise travellers drink lots of water rather than dehydrating alcoholic drinks, especially on long-haul flights.
The second type of sweat gland, the apocrine gland, is concentrated in the armpits and the groin and develops at puberty. These glands secrete a milky liquid that is much thicker than ordinary, watery sweat from the eccrine glands. Sensitive to the “fight or flight” hormone, adrenaline, they produce particularly copious amounts when we are nervous or stressed. This milky secretion has no odour at first, but bacteria on the skin’s surface soon break down the secretion to produce, in both men and women, a complex mix of volatile steroids and fatty acids. This chemical cocktail gives off musky or peppery odours – one of which resembles a sexual attractant produced by randy male pigs. Deodorants work by temporarily turning off the apocrine glands and by suppressing the growth of bacteria in the armpit.
No one knows why we have these smell-producing glands, but the general view is that they are probably a vestige of our distant evolutionary past. Humans probably do not produce true pheromones, chemical substances releasing odours that, in some species, act as “releasers” of rigid behaviour patterns. For example, during the mating season female moths release pheromones that cause males to fly automatically towards them. In contrast, humans learn to experience body odours as socially significant, and most people can correctly guess the sex of an individual from a mere whiff of his or her armpit odour.
Although the skin protects us from many of the physical and chemical onslaughts of a hostile environment, it is not a perfect barrier, and some chemicals can get through. This permeability can be used to our advantage, as when doctors prescribe nicotine “skin patches” for people trying to stop smoking. But often, undesirable chemicals are inadvertently absorbed. Spill some industrial solvents or pesticides on your bare hands and the chemicals may be absorbed so quickly that they are virtually impossible to wash off.
Skin care
Body at risk
IF A potentially toxic chemical such as a pesticide or a dry cleaning solvent reaches the epidermis it might cause dermatitis, acne or even, in time, skin cancer. If it reaches as far down as the dermis, the toxic chemical may enter the bloodstream and circulate round the body, leaving widespread damage in its wake. Now that we realise just how permeable the skin can be, governments around the world are tightening regulations on the use and storage of chemicals to minimise workers and consumers’ exposure to them. Fragrances added to soaps, washing powders, perfumes or aftershaves may be readily absorbed, and lead to an allergic response. Even some “natural” fragrances extracted from plants for use in aromatherapy oils contain chemicals that, given internally at high doses, cause cancer in laboratory rats. Unfortunately, no one knows whether any of these substances might prove harmful to people when massaged into the skin.
Emergency repairs
How skin heals
SUPERFICIAL damage that harms only the epidermis heals quickly, leaving no scar. In a child, the healing of minor grazes can happen in a day or two as their keratinocytes multiply rapidly, but this process slows with age. If the damage extends into the dermis, however, a scar will form.
Damage to the skin sets off a remarkable cascade of cellular activity, starting with the flooding of the wound with blood and the formation of a clot. Cellular messengers released as a result of this in turn stimulate the migration of more immune cells and fibroblasts to the site. The immune cells kill invading microbes, while the fibroblasts proliferate to form a temporary plug, or scab, which helps keep out any infection. Gradually, as the wound heals the entire structure of the skin becomes rebuilt (see Diagram).
People who suffer extensive burns are left vulnerable to infection and water loss, and in these cases skin grafts can literally save their lives. Surgeons can remove the epidermis and part of the dermis from a volunteer’s inner high, leg, upper arm or forearm, and leave the donor site to heal naturally. If the entire dermis is removed, for example by severe grazing or burning, the site must be surgically closed. Skin grafts from one person to another will only “take”, however, if immune “markers” on skin cells are closely matched. This code of markers is called the human leucocyte antigen or HLA system. Only identical twins have perfectly matching HLA systems.
1: Mammalian exclusive and versatile hair
HAIR comes in two main sorts – the soft, fine hair on the forearm, for instance, is called vellus hair while the coarser stuff that grows on our heads is called terminal hair. The so-called “unwanted” hair that grows on women’s faces arises when some vellus hair turns into terminal hair. The baldness that affects many men as they age is the result of the converse process, the transformation of terminal hair into vellus hair. Some people worry that they are too hairy or not hairy enough, but everyone has more or less the same amount of hair on their body; it is simply less obvious in fair-haired individuals.
For the most part, hair is made up of modified, dead keratinocytes – the only living part is the hair’s root, or follicle, which is buried in the dermis. In mammals, hair grows in cycles, although merino sheep bred to produce hair all the time are a notable exception. Typically, over a period of two years, individual hair follicles go through a period of rapid growth followed by a resting phase; then they are shed, as a new hair begins to form underneath.
The longer the growing phase on any particular part of the body, the longer the hair produced. The active phase in scalp and beard follicles may last between three and six years, but is a matter of only weeks or months elsewhere on the body. The hair on our heads grows about a third of a millimetre a day, or about 1 centimetre a month. This is slow compared to the rate at which wool grows on wensleydale sheep; this has been clocked at more than a millimetre per day.
This pattern of programmed replacement normally happens at random across the scalp, so hair loss is not obvious. But men who go bald lose terminal hairs in patches which fail to regrow as coarse terminal hair. Research aimed at understanding what switches hair follicles on or off may eventually lead to a cure for baldness and other sorts of disruption to the normal cycle of hair growth. Hair loss during chemotherapy is a particular problem: many cancer patients say that going bald is one of the worst things about the treatment.
Shampoos contain varying amounts of detergent designed to dissolve general grime, as well as products of the skin such as sebum, sweat and layers of dry skin (which, when over-abundant, forms the notorious dandruff). Too much detergent, however, can dry out the hair, making it brittle and dull-looking. The shine of healthy hair is caused by light reflected from the hair’s cuticle or outer layer. The smoother, straighter and less damaged the hair, the more light it reflects. Hair conditioners act much like fabric conditioners, by helping to smooth the hair’s rough outer cuticle, but some can make fine hair look lank and limp.
2: Sun, skin and some serious risks
RELAXING in the sunshine can be wonderful, and good for you too. Skin exposed to sunlight manufactures vitamin D, which is vital for healthy bones. But too much of a good thing can be dangerous. Sunburn can seem to be just a temporary inconvenience, but it can cause long-term damage to your looks and your health.
The colour of our skin is mainly due to a brown pigment called melanin, which occurs in the epidermis. This pigment – a protein – is produced as granules in epidermal cells called melanocytes, and is then shared with the surrounding keratinocytes. The total number of melanocytes – and there are between 1000 and 2000 of them per square centimetre of skin – is much the same for all of us regardless of our skin colouring. Melanocytes in darker-skinned people are more active, and make more and bigger melanin granules (melanosomes) than do those in paler-skinned individuals. Darker skin is much less susceptible to the harmful effects of sunlight.
Each of us can be classed into a “skin type” ranging from type I to VI, depending on how readily we burn and tan. Those with the lightest skins and red or auburn hair may always burn and never tan, while those with the darkest skins burn only after intense and prolonged exposure to ultraviolet light from the Sun or from sunbeds. People born with truly white skin and flaxen hair have inherited a condition known as albinism. Their skin cannot make melanin, and they suffer terrible damage from solar radiation if not protected from it.
Ultraviolet radiation produced by the Sun is divided into three bands – UV-A, UV-B, and UV-C. UV-C has the most energy, and so is the most harmful, but fortunately the ozone layer prevents it from reaching the Earth’s surface. The ozone layer also mops up some of the next most energetic and dangerous band, UV-B, but enough gets through to put sunbathers at risk (see Diagram). Some scientists fear that the damage to the ozone layer caused by chlorofluorocarbons (CFCs) will let more UV-B through to the Earth’s surface, resulting in much greater damage to the skin.
A suntan is the skin’s attempt to shield itself from the Sun’s harmful rays; skin colour darkens as the upper layers of skin step up production of the protective pigment melanin. But the skin’s in-built sunscreen is not effective enough to prevent damage altogether, especially in light-coloured individuals, and the greater the cumulative exposure to sunlight, the greater the risk of one day developing skin cancer. It is important to protect youthful skin from damage, as time spent in the sun in our first 18 years of life probably accounts for as much as 70 per cent of our lifetime exposure.
Ultraviolet light from the Sun may cause skin cancer directly, by damaging the DNA of a skin cell to create a rogue mutant that eventually multiplies out of control. Solar radiation can also damage the skin’s ability to defend itself against such rogue cells. In a healthy, protected epidermis, Langerhans cells detect and destroy viruses and damaged cells that could otherwise go on to cause cancer.
Malignant melanoma – a tumour of the melanocytes – is a virulent form of skin cancer that quickly spreads from an innocent-looking mole to become life-threatening, if not treated early on. The number of Britons dying from this disease is now doubling every 10 years, as people spend more holidays in the sun. Another form of skin cancer – a slow-growing cancer of the basal cells of the epidermis, called basal cell carcinoma – usually develops only in people aged 50 or more in Britain. But in hot, sunny Australia, where it has become very common, people in their thirties are now developing this form of cancer.
Humans probably evolved in Africa, with dark skins to protect them from the intense sunlight typical of latitudes near the equator. As groups of early humans migrated to higher latitudes, they lost some of their protective melanin and became paler, probably so their skins could still produce enough vitamin D, even in the weaker sunlight. The genes controlling skin colour are still unknown, but probably at least four different genes play a role. Some of these genes create subtle variations in skin colour depending on small changes in the length and degree of folding of the melanin molecules, or how the melanin clumps. Modern genetics has shown that skin colour genes do not demarcate human “races”; in other words, a person’s skin colour does not reveal anything predictable about what other genes they possess.
- ҹ1000y skin: the Facts, by Rona MacKie (Oxford University Press, 1992). The Sun and Your Skin, by Ronald Marks (Macdonald Optima, London, 1988). Molecular Aspects of Dermatology, edited by Graham Priestley (John Wiley, Chichester, 1993). The Imperial Cancer Research Fund produces teaching packs and work booklets for teachers and students on skin cancer and how to prevent it. Copies can be obtained by sending a stamped addressed envelope to “Skin Cancer”, PR Department, ICRF, P.O. Box 123, Lincoln’s Inn Fields, London, WC2A 3PX. This literature is free but donations are welcomed.