Something very strange happens at puberty, when truckloads of hormones begin arriving by the day. Children who were sweet, helpful and good fun to be around, turn almost overnight into grunting creatures who wear nothing but black, lie in bed till noon and consume 5,000-calorie snacks (and still say they’re hungry). They preface every request for help, or an invitation to go somewhere with their parents and siblings, by ‘Do I have to?’; become the most completely self-centred, self-obsessed and selfish creatures on the planet – until they go to other people’s homes, in which case they are perfectly adorable. They are spotty, start – and I mean this kindly – to smell and grow out of everything they have in the space of a few months. Their boredom threshold plummets and they do not seem able to concentrate on anything for more than five minutes at a time. You begin to wonder whether your child is a changeling, swapped with your own by an alien from the Planet MTV while you weren’t looking.
Teenagers are trapped in limbo – neither children nor adults: an excruciating mix of vulnerability and potential, which by turns engages, inspires and alienates adults, where everything they do has a high-intensity feel about it. We know this because our own adolescent experience – our first kiss, the first time we fell in love, the rush of first-time driving – still burns brightly thirty or forty years on.
However there is a darker side too: soaring rates of serious accidents, illicit use of drugs or alcohol, risky sexual behaviour and its consequences, and the first signs of emotional disorders which may be lifelong. Teenagers seem to be the very embodiment of hormonal mayhem – or are they? This chapter investigates the truth about teenagers and hormones – and it’s not what you expect.
All Growed Up
Puberty is an extraordinary event and human beings are lucky in that they only have to go through it once, which is not the norm in the rest of the animal kingdom. Most animals do not become sexually active and then remain so, as we do, but confine their sexual activity to a single breeding season. This means pretty much starting from scratch every year – new plumage or antlers, a huge increase in testicle size, commencement of courtship behaviour, territory marking, even an increase in song repertoire if you are a songbird. All these events are orchestrated by hormones and preceded by a hormone rush, just like the one experienced by teenagers. If you look in your garden in the spring and see blue tits scrapping among themselves while singing their heads off, they’re hormonal.
Another aspect of human puberty is that all other animals, including great apes, go straight from juvenile to adult. In humans, however, there is a stage between the appearance of reproductive hormones and the prime reproductive age. Boys become fertile at around thirteen, while they are still puny and unappealing. Girls acquire a womanly shape at puberty, yet are relatively infertile for several years thereafter. The conjunction of top male specimen at around twenty and fully reproductive female at eighteen is reflected in the average age of first birth across all cultures of nineteen years of age.
Let’s look first at the hormonal changes that lead a child through and beyond puberty, into independence, physical maturity and the ability to reproduce. These stages unfold in an orderly and highly integrated way, and while the whole process can be delayed or advanced, it will still follow that same prescribed pattern. If there is puberty without growth, or the other way around, there is almost certainly something amiss in the hormone department.
There are three main hormonal elements to puberty. Alterations in the secretions of the adrenal gland, differences in secretions of the ovaries or testes and changes relating to growth hormone. These are all interlinked – for instance, increasing production of testosterone and oestrogen primes the pituitary gland to produce an increase in growth hormone.
The first hormone event which will lead to puberty is largely hidden from us. Between the ages of six and eight, the adrenal gland starts to step up secretion of androgens such as DHEA (dehydroepiandrosterone), which the body uses as construction material for the manufacture of other steroids. These androgens will stimulate the growth of sebaceous glands, which produce the skin-lubricating fluid sebum. This results in greasier skin and body odour and also primes hair follicles in those areas where pubic hair will later begin to grow. This is called adrenarche. Parents first notice this at their kids’ parties, when twenty sweaty seven year olds rampaging in a confined space (your sitting room) are noticeably whiffy in a way that they were not when younger. The increase in adrenal hormone levels continues steadily until they peak in the mid-twenties.
In adult men, and in women of reproductive age, the hypothalamus is constantly secreting pulsed doses of gonadotrophin releasing hormone (GnRH), which tells the pituitary to secrete hormones, which then act on ovary and testicle to produce the reproductive hormones which will ensure a supply of sperm and eggs. These hormones as we have seen also influence our behaviour profoundly, making us sexual beings. But in childhood, the hypothalamus does not secrete GnRH, and as a result there are not only minimal levels of reproductive hormones in children but little or no sexual behaviour either. It is as if there were a brake on the hypothalamus. True puberty starts when the brakes are taken off and the hypothalamus is permitted to begin the pulsed secretion of gonadotrophin releasing hormone. The pattern of this hormone secretion is more important than the total amount of hormone secreted. If, as in some medical conditions, GnRH is ‘on’ all the time, rather than being delivered in pulsed doses every ninety minutes or so, surprisingly, puberty will be delayed. GnRH tells the anterior pituitary to produce both follicle stimulating hormone (FSH) and luteinising hormone (LH). You may be more familiar with these hormones as the ones controlling your monthly cycles, but FSH and LH in men control production of sperm and male hormones. This is an illustration of the way in which a hormone can have radically different effects depending on the target organ or tissue.
In boys, LH secretion stimulates the production of testosterone by cells in the testes. LH too is secreted in pulsed doses. At first, there is a very clear daily pattern, with peak production occurring during sleep, especially between midnight and 8 a.m. As puberty progresses, LH is also secreted during the day. The production of testosterone mirrors that of LH, being at first, greatest at night. Simultaneously, levels of the substances that keep testosterone under lock and key in the bloodstream – sex hormone binding globulins – decrease, thus making even more testosterone available, fifty times more than was experienced before puberty. That’s some hormone rush. The earliest visible sign of sexual development in boys is enlargement of the testicles. The penis also begins to lengthen in early puberty, and later thickens.
In girls, the first sign of changes in gonadotrophin secretion are seen in levels of FSH, rather than luteinising hormone (which is the one that prompts ovulation). The effect of FSH is to stimulate the growth of follicles in the ovary which begin to produce oestrogen. It also ups the activity of an enzyme, aromatase, which converts androgens to oestrogens. Before puberty, pulses of LH occur at night. These are irregular, but as time passes they become progressively larger and more regular. Just as with boys, LH is then secreted during the day too. The secretion of LH at night is not linked to darkness but to dreaming (REM) sleep. This can be demonstrated very easily. If you blindfold a teenager during the day, so that they experience darkness but are not asleep, there is no alteration in the amount of LH secreted. If, however, sleeping periods are switched, so that normal sleep takes place during the day and activity occurs throughout the night, LH secretion will then also take place during the day, coinciding with dreaming sleep. Oestrogens are also pulsed. Peak secretion of oestrogens in teenage girls is between 6 and 10 in the morning. These rhythms of secretion disappear once ovulation is established.
The time between onset of these GnRH pulses and the first period in girls is relatively short. But having a period for the first time does not mean that the girl is fertile. Regular cycling may take three years to establish and although sporadic periods occur they are frequently associated with anovular cycles (in which no egg is released). This may be the source of that well-known old wives’ tale about not getting pregnant the first time you do it. If there are teenagers reading this book, your mantra should be you can get pregnant at any time of your cycle, in any position. I have never understood why it is that the tune should suddenly change at thirty-five when you are told that you can only get pregnant during your fertile period. More likely to – yes, but definitely not ‘only’. Be warned.
Once oestrogens and testosterone begin to be produced, it is their impact on body form which provides the most dramatic expression of adolescence. Oestrogen stimulates growth of the womb and breast but also determines the shape of the female figure by some judicious rearranging of the deposition of fat. In boys, the consequence of testosterone is also to sculpt the body, increasing lean body mass and shaping features as well as promoting body hair and beard growth. Oestrogen and testosterone also promote fusion at the end of the long bones, which will eventually signal the termination of their period of rapid growth.
Acne is common in both sexes during adolescence. Mothers tell their teenagers that their spots are the result of eating too much chocolate or fatty food. Not enough fresh air (as in, you’ve been in your room too long) is also proffered as a cause. Actually it’s the fault of your hormones, not your diet. There is an abnormal response in the skin to normal levels of testosterone in the blood. This has a profound effect on appearance for some unlucky people. The response is self-limiting and goes away with time, but there is no way of predicting how long it will take – it can be a couple of years or decades. It may leave deep, pitted scarring. Adolescents, although the most likely sufferers, aren’t the only ones to get acne. It is often reported, for the first time, by women in their thirties. Typically, they also report a highly stressed lifestyle. In this case, stress causes an increase in the level of male hormones, bringing back teenage spots.
Growth
In the last chapter we established that the growth of babies in the womb is not wholly dependent on growth hormone and that nutrition is an important factor. However, increasingly growth hormone – as you would expect from its name – does dictate and coordinate growth in the baby, promoting increases in bone, soft tissue and organ size. A tiny baby has no growth hormone receptors in its tissues, but these begin to appear when it is about seven months of age and it is at this age that GH begins its effect.
Height is one of the most heritable body factors and if you come from a tall family, the odds are that you too will be tall. Smaller parents are likely to have less tall children – still perfectly proportioned, just built on a smaller scale. Your eventual height is influenced by many different things: whether or not your mother smoked during pregnancy, her nutrition in pregnancy, whether you got enough to eat as a child, whether you were seriously ill or emotionally deprived, stressed or abused, what illnesses you had, to name but a few.
Season also affects growth – which is mediated through the hormone of sleep, melatonin – both in children and in babies before birth. A large study of over a million Danish babies showed that those babies born in April were on average 2.2 mm taller than those born in December. This confirms earlier work from Austria showing a height variation of up to 6 mm depending on month of birth, with once again the tallest children being born in the spring.
Crucially, the mother manages to switch off some of the paternal genes involved in growth during pregnancy – which means that a 5′ woman can have a 6′ 6″ man’s baby without the baby’s feet bursting out of the womb. It’s the same mechanism that allows Great Danes to impregnate spaniels, but the mother spaniel not to expire in the process.
Adolescence is marked by a huge surge in growth hormone production. It starts soon after the initiation of gonadotrophin releasing hormone secretion. The relationship between these two hormones is an indirect one, however, involving oestrogen. The idea that a female hormone is driving growth in boys as well as girls is counterintuitive at first, but it explains much about the gender differences in growth and why girls grow earlier and faster than boys: it’s because they have oestrogens which pump up production of growth hormone. In boys, the enzyme aromatase converts testosterone to oestrogen. That this is key to growth is shown by those rare cases in which children have gene mutations affecting either aromatase or oestrogen receptors, whose growth patterns are radically altered.
The secretion of growth hormone is carefully timetabled in a pattern that persists through puberty. Growth hormone is released principally at night during sleep, in short bursts every one to two hours during the deep sleep phase. So when your mum says, if you don’t go to bed now you won’t grow up to be big and strong, she’s right. If the onset of sleep is delayed, so is the onset of growth hormone release. Children who are deprived of sleep are smaller than they should be.
It is apparent to all that there are big gender differences in growth hormone during puberty. These accounted for my own misery at school. I was 5′ 10″ at twelve, which was to be my final height. Forced to do ballroom dancing lessons with boys of the same age from a nearby boys’ school, I found myself towering over them by what appeared to be several feet. As we whirled about, they missed the overhead beams in the centuries-old building in Winchester which passed for a dance hall, whereas I did not. After two hideously embarrassing lessons, I was excused all further dancing duties. One of my former dancing partners is now six inches taller than me (and still as poor on the dancefloor as he was then). Thank God my mother smoked forty cigarettes a day during pregnancy, or else I would have been 6′ 3″.
Before the onset of the teenage growth spurt, boys grow very slightly faster than girls, but girls’ growth spurt starts about two years before that of boys between twelve and fourteen. For some four years, girls are on average taller than boys. But by adulthood, men are on average 14 cm taller than women. This difference is almost entirely due to what happens at puberty – boys grow on average for two years longer after puberty, with an intense growth spurt occurring between the ages of fourteen and sixteen. Both sexes have a pubertal growth spurt of roughly six years, but girls reach maximum growth velocity early in puberty, about a year after the appearance of breast development. Boys don’t reach their maximal height velocity until mid puberty. It is the combination of a longer growth period with a greater average yearly rate of growth that allows men to be taller than women.
During early puberty, limbs elongate first, leading to that funny coltish look of teenagers. Then the trunk begins to change, and then whoosh, suddenly they are beanpoles. When girls begin their periods, their growth slows down dramatically, with on average, only a further 5 cm of height being added. Because testosterone is such a potent anabolic steroid, boys acquire a dramatic increase in body mass index (BMI) from 16 to 21, almost all of which is down to the increase in the amount of lean tissue. The BMI of girls also increases, but in their case, the rise in BMI is largely down to an increase in body fat of about 11 kg. This might appear appalling to teenage girls, who seem to have a horror of fat, but it is the fat content of their bodies which determines their ability to have babies.
More growth hormone doesn’t necessarily make you taller. You might think that all basketball players have hormone problems, since their average height now approaches 7′. Actually, they are simply constitutionally tall and have the same growth hormone levels as someone with constitutional short stature – what some people rather disparagingly call small normals. Excess growth hormone before a child has stopped growing is called gigantism. Excess growth hormone after growth has stopped, in adulthood, does not result in further height gain but in enlargement of the bones of jaw, hands and feet, a condition called acromegaly. One of the effects of growth hormone is on facial structure, turning the round soft faces of children into the more sculpted features of adults.
About one in 5,000 children is growth hormone deficient, with the condition being more common in boys than in girls – although this may simply be that small girls are less likely to be brought to a doctor’s attention than small boys. There are many causes of deficiency, which include head injuries, tumours or radiotherapy affecting the pituitary gland. A child can be growth hormone deficient, or multiple-hormone deficient, lacking other hormones such as oestrogen or thyroid hormones. Certain medical conditions are also associated with short stature, such as chronic kidney disease, the chromosome disorder, Turner’s Syndrome, and the genetic disease Prader Willi Syndrome in which short stature is also associated with obesity and learning difficulties.
Growth hormone used to be extracted, rather gruesomely, from pituitary glands collected from cadavers. There were always concerns about potential infection of those treated with cadaver-derived pituitary products and this was heightened even before the BSE crisis, when it became apparent that new variant Creutzfeldt Jakob disease (CJD) could be transmitted from one person to another through growth hormone preparations. The use of cadaver-derived products is now banned in most of Europe and in the US. For the last decade, all growth hormone has been produced using recombinant technology, which uses cells genetically engineered to secrete a particular product, a method of production now used for almost all hormones. It is safe, clean and provides hormones free from impurities. However, it is very costly indeed – about £20,000 for a year’s treatment of one child. For 90 per cent of GH-deficient children, it increases rate of growth and increases final height to within the lower end of the normal range, preventing dwarfism (the fate of such children in the past).
Now, however, thanks to biotechnology, there is an unlimited, safe supply of growth hormone and the possibility of using GH to promote growth in non-growth hormone deficient short children has become a reality. To do this for those children with Turner’s Syndrome or other non-GH medical problems affecting height is one thing, but there has been an increasing demand for growth hormone for normal healthy children, especially boys, who are just a bit short, especially for boys. What growth hormone won’t do is make you grow beyond your height potential, so it may be of limited value, with a very small gain in height for rather too great a risk. Also, at what point do you decide that a child is likely to be short and when should you stop giving growth hormone? The answers are not clear, and nor are the side effects fully understood, yet one in five prescriptions for GH is still for ‘idiopathic’ height problems – in other words, for children that are healthy but destined to be smaller than average. In the US, there is even more pressure on physicians to prescribe GH. This is the first of many examples you will encounter in this book of hormones prescribed for lifestyle reasons.
So, there are three groups of hormone changes affecting teenagers: those to adrenal hormones, sex hormones and growth hormones. But there are also more subtle changes occurring in other hormone systems. For instance, the regulation of the stress hormone cortisol undergoes modifications during puberty. Cortisol stimulates the appetite and drives the extraordinary phenomenon that is teenage fridge-raiding and carbohydrate consumption. So far, though, I have not uncovered any research which indicates why they also consistently leave the empty packets behind them in the fridge. This is adaptive (the raiding, not the empty packets) in that fuel is required for growth and an increase in appetite ensures that they get it. There are also alterations in oxytocin, the hormone of bonding.
Teenage Behaviour
Teenagers get a rush from intensity, excitement and arousal: loud music, big dippers, horror movies, etc. In some teenagers this thrill-seeking and quest for novelty is subtle and easily managed. In others, their behaviour is more extreme and can get out of control. This is reflected in the statistics for teenage deaths, three quarters of which result from accident or misadventure.
Romeo and Juliet is the classic story of the way in which teenagers lose the ability to think logically or behave rationally. It is a story of adolescent love, in which passionate feelings accelerate at top speed and the motivation to be together transcends all else. Shakespeare gives Juliet’s age as thirteen and the entire action, from first meeting to death, takes just four days. One day into their relationship, this girl and boy are already well on their way to spurning family, danger and public outrage, driven by emotional intensity. They act as if being together is more important than life itself. If they were adults, the psychiatrists would have had them sectioned by Day 2, never mind by Day 4.
It is tempting to believe – indeed, it has always been assumed – that such behaviour is entirely hormone driven. After all, aren’t teenagers hormones on wheels? Having just read how hormones change during puberty, it does seem logical. However, links between hormone levels and poor behaviour in teenagers are either weak or non-existent. Certainly, high levels of hormones in teenage boys are not associated with emotional problems, and the evidence suggests that those with peak levels of sex hormones, whom you might expect to have the most emotional disturbance, are likely to be perfectly normal.
The changes that kick-start puberty – the release of gonadotrophin releasing hormone – begin in the brain, in the hypothalamus, which implies that the initial driver for the changes of puberty runs ahead of the hormonal system. Therefore it is likely to be the maturation of the brain that is behind the hormone level increases, and not the other way around.
It is particularly interesting to see the effects on the brain when hormones begin surging through the blood system. Hormones can directly affect only those brain cells which have the right receptors – for instance, neurons that produce the neurotransmitter serotonin (high levels of which result in feelings of calm and well-being) have oestrogen receptors, which means that rising levels of oestrogen have effects on mood and arousal via these receptors. There are also plenty of testosterone receptors in the brain too, meaning that the brain hears testosterone loud and clear and this affects behaviour.
A good example of the interactions between hormone and behaviour is seen in sleep. As every parent knows, teenagers find it very hard to get out of bed in the morning and to go to bed at night. Compare this with what they were like as five year olds, when you had trouble keeping them in bed beyond 6 in the morning. Actually this isn’t just your teenagers being difficult, for a subtle biological shift in sleep patterns occurs during puberty. Once again, it’s partly adaptive in that teenagers need more sleep for growth. There is an increased drive for sleepiness. But there is also an increase in the level of melatonin, the hormone of sleep, which is released only at night. One of the effects of this is similar to having gone through several time zones on a transatlantic flight. Hence the classic teen school-holiday pattern of sleeping from 2 a.m. until noon.
Come term time, the teenage body is in disarray as it is forced by a 7 a.m. wake-up call – while still on Planet MTV time – to gather itself together, even though it thinks it’s 4 in the morning. These jetlagged teenagers have come around by the end of the week to parental time zone hours, only to wreck themselves with another bout of 2 a.m. to noon sleeping at the weekend. Many become chronically sleep deprived, with all the implications for behaviour that that implies – irritability, unable to concentrate, with poor attention span – which are inevitably reflected in their school performance.
Parents are not much help here. Urging their offspring to go to bed means that they go to their rooms at bedtime only to surf the net, text their mates and watch late-night TV because they find it impossible to sleep – just as we adults would if we were jet-lagged. So the hormone involvement is relatively modest; it is the knock-on effect of changes in behaviour that wreak the havoc.
Teenagers and Sex
The behaviour that is entirely hormone-driven in teenage boys is their sexual appetite. They go from thinking girls are silly, soppy creatures in pink, to being completely girl-obsessed. It is said that teenage boys think about sex every seven seconds. As little as that? For boys, adolescence is one long wankfest. Teenagers can ejaculate and have another erection barely minutes later. Compare this to men in their fifties, where the recovery time, or refractory period (as it is called), may be several hours. For teenage boys the mere sight of a woman is enough to engender an erection, whereas forty years on it will require manual stimulation of the penis to prompt an erection, no matter how erotic the situation. As puberty brings more testosterone with every new dawn, so boys become ever more sexually rampant. In early puberty they are puny, smaller than girls and rather unattractive to them. Their greatest hope of actually finding a girl that is willing (in their dreams), lies not in their testosterone-supercharged sex drive, which girls in general find rather unattractive in its lack of subtlety, but in the changes that testosterone makes to their bodies, in fashioning a broader, more muscular, leaner adult from the body of a child. It takes several years for boys to learn to live with their testosterone, and gradually those inappropriately timed erections and sexual obessions begin to calm down.
This period of rampant hormones but still puny bodies is an important learning period. In general, teenage boys of this age are roundly rejected by girls, despite their boasts to each other, but one day those carefully honed chat-up lines will have the desired effect.
Oestrogen is only one of the hormones involved in sexual response in women, as we saw in the previous chapter, and human females are covert about their sexuality, not advertising when they are fertile. Girls are not therefore as overwhelmed by their sexuality as boys. Nevertheless they are beginning to preen and become sexual beings. This can be very disturbing if they are younger than the age at which society considers sexual activity acceptable, and it is also a cause for alarm, for their brain is still that of a child, with a marked immaturity and specifically an inability to understand the consequences of risk.
Baby Adults or Adult Babies?
The thing that is really irritating about teenagers (and by now you will have guessed that I have two teenage boys) is that one moment their behaviour is that of adults, while the next it is that of a not-very-bright three year old, or possibly, a retarded chimp. Or an amoeba. Going from captaining a rugby side, for instance, where their increased strength and agility, not to mention mature social skills, are fully deployed, to kicking a rugby ball in the sitting room … and being astonished when their mother goes into orbit because the ball has just smashed a picture. The rapid oscillation between child and adult is one of the hallmarks of the teenager.
In fact teenage brains are going through a process of maturation and it is this maturation which many now believe is responsible for much of the behaviour that we classically attribute to hormones. These changes are actually entirely independent of hormones and are a function of age, which is illustrated by those children who, for various medical reasons, do not go through puberty and yet are cognitively normal.
It has been discovered only very recently that there are two main features of brain maturation that happen to coincide with puberty. Previously it was believed that the brain was pretty well set by adolescence but in the last couple of years, and to everyone’s surprise, it has been realized that maturation is not completed until late teens or even early twenties. One feature is that myelin, a sort of fatty insulating material, is added to axons, the main transmission lines of the nervous system, which has the effect of speeding up messages. The other feature is a pruning of nerve connections, the synapses, in the pre-frontal cortex. This area of the brain is responsible for what is called executive action, which is a shopping list of the things that teenagers lack – such as goal-setting, priority-setting, planning, organization and impulse-inhibition. During childhood, for reasons that are not clear, a tangle of nerve cells sprout in this brain area, which lies behind the eyes, but during puberty these areas of increased synaptic density are then reduced by about half, presumably to increase efficiency.
These changes in the adolescent brain primarily affect motivation and emotion, which manifest themselves as mood swings, conflict with authority and risk-taking. For example, it is not just testosterone that drives risk-taking, but the inability of the immature brain to assess risk properly that gets teenagers into trouble.
The remodelling of the cortex helps explain another feature of teenagers: their astonishing level of self-centredness. For a while, as their brain is undergoing changes, they find it hard to recognize other people’s emotions. This has been demonstrated in a number of research studies: if you show teenagers pictures of faces, they will be some 20 per cent less accurate in gauging the emotions depicted, and don’t re-acquire this ability until they are eighteen or so. This makes them socially inept, unable to read social situations – or in parental language, a nightmare. They seem unable to read the signs, are unaware when they are treading on thin ice with their behaviour, and furthermore have no appreciation of parental feelings or of the impact of what they are doing on those around them. Teenagers exist in a universe of one.
It has nothing to do with hormones, but let me say a word about addiction. One of the reasons why we get hooked on tobacco for example, is that we tried it as an adolescent. The teenage brain gets a bigger bang from nicotine than an adult one does. The same is true of alcohol and drugs too. This intense reward increases the likelihood of addiction. Indeed, one of the strongest predictors of alcoholism is the age of first initiation. It’s a deadly combination – increased likelihood of addiction coupled with poor assessment of risk.
Testosterone (Again)
Research shows that the No. 1 risk factor in homicide is maleness, and the second is youth. Teenage boys are primarily the violent ones, rather than girls. Boys have testosterone, girls don’t. Surely this must implicate testosterone as a cause of violence?
First, there is no consistent relationship between normal circulating testosterone levels and violence in teenagers. In fact some studies have shown a negative association. You could turn the question around and ask whether testosterone levels are linked to popularity and respect by peers in teenagers. I suspect there would be a greater likelihood of finding such a correlation as many studies have shown high levels of testosterone and leadership to be linked.
Being split up from your best mate is a peril of adolescence. ‘They’re a bad influence on you’ is the general gist of parental or teacher wisdom on this one. Actually, one hypothesis is that teenage boys pick up cues from the environment and use them to determine ‘normal’ behaviour. This is illustrated by recent work from the Medical Research Council (MRC) unit at the Institute of Psychiatry, which shows that it is not testosterone levels that determine your waywardness as a teenager but the people you hang with. Keep the company of bad boys and you will take your behaviour cue from them. Hang out with sober sorts and your behaviour will be like theirs. Testosterone levels are related to leadership in boys with non-deviant peers and to aggression in those with deviant mates. I say this despite the ignominy of proving Mrs Glass, form teacher of Year 9, right.
What boys are concerned with, if not always consciously, is status. Much of the driver for male behaviour is that women, with whom teenage boys are obsessed, find power and status irresistible in a man. Lower status men find themselves ignored by women who consistently prefer partners who can impress them. So impress they must if they are to secure their ideal woman. On one level, this is classic boy meets girl stuff, but make no mistake it is underpinned by a specific and very powerful biological drive, for the right choice of mate is essential if you are to transmit your genes to the next generation.
If levels of testosterone are not closely linked to teenage violence, what is? Deprivation in childhood. The theory – and there is a wealth of literature on this subject – is that if low status males are to avoid the road to genetic nothingness (the words of neuroscientist Steven Pinker), they may have to adopt aggressive, high-risk strategies. If you’ve got nothing, you have nothing to lose through your behaviour. Certainly in humans, both violence and risk-taking behaviour show a pronounced social gradient, being lowest in the highest social classes and highest in the lowest ones. This is surely not what you would expect if testosterone were the only driver of violence.
Respect is everything in deprived communities and a great deal of violence is initiated by perceived slights to status. As Sir Michael Marmot, the distinguished epidemiologist, points out in his book The Status Syndrome, we are shaped by evolution to seek status. Professors don’t kill each other when jockeying for position in being given grants, although they frequently knife with words and bludgeon with faint praise in a poisonously competitive atmosphere – and in any case, the law is rather touchy about murder. But if you are at the bottom of the heap, with every chance of spending time in prison, with those closest to you living fractured, short lives, and with no chance of taking a place in mainstream society, how long are you likely to spend in weighing up the result of your actions before lashing out, or even murdering someone? How much more likely, then, is this to be the case for teenagers, as adolescence is the period in life when the brain’s ability to fully consider the implications of action is seriously compromised?
The hormone link to high-risk choices is likely not to be testosterone, at least not initially, but the stress hormone cortisol. Stress during early life raises cortisol levels, so increasing behavioural problems (such as hyperactivity). These tend to make children more aggressive, less affiliative and more likely to perceive others as threatening. Stress either in pregnancy or in early life permanently resets the stress response of the child, so that there is an increased reaction to stress – known as hyperarousal. A stressed child, when meeting someone new (even in a familiar environment), will withdraw and refuse to make eye contact, rather than chat happily. This increased stress response plays out in reduced life expectancy because cortisol affects almost every body system. It is also closely linked with depressive illness.
So testosterone plays a part here only after the fact. Aggression and stress raise testosterone levels. Aggression and stress also reinforce each other at the biological level. Animal work reported in the journal Behavioural Neuroscience in October 2004 suggests that there is a fast feedback loop between stress hormones and the hypothalamus, which allows aggressive behaviour to escalate.
Testosterone in Adults
Let me digress briefly from the teenage years. Whilst testosterone is not necessarily a marker for violent behaviour in teenagers, in adulthood, high testosterone levels are strongly linked to criminality, with those committing the most violent crimes, and especially the ones that cause most trouble and confrontation within prison, tending to be those that have the highest testosterone levels.
Testosterone in humans is about dominance, not aggression: most men assert their dominance without recourse to violence. For instance, in a series of studies examining the links between testosterone and brief social encounters, people with high testosterone displayed a more forward and businesslike manner, and were those people most likely to impress on first encounter. Lock men away in a closed environment, and the one that is most dominant is likely to have the highest testosterone level. In fact anti-social acts are often not violent, but just attempts to dominate figures of authority (teachers, policemen etc).
Testosterone levels also alter with stress. Professor James Dabbs of Georgia State University is the leading authority in this field, and has focused his research on male children and adults, lawyers and criminals, sportsmen and even politicians using saliva to test testosterone levels. His work on sportsmen is particularly interesting. For two hours after a competition, testosterone levels in the winners are elevated, while those of the losers are reduced. If the winner feels that he was lucky or didn’t really deserve to win, the rise in testosterone is less marked. During a study of football fans who watched Brazil beat Italy in the 1994 World Cup, testosterone was increased significantly post-match in Brazilian fans. Guess who won the match? The point is that testosterone levels rise and fall with experience of success or failure and even with anticipation of those things. In general, testosterone rises following aggression but is not a cause of aggression per se.
Dabbs also studied some women prisoners, showing that high testosterone levels are related to criminal violence and aggressive dominance, rather than being a uniquely male hormone. In the next chapter, we will see that women have testosterone too – quite a bit of it.
Hormone Determinism
Professor Dabbs claims that innate levels of testosterone can predict your future effectively. White-collar workers have lower testosterone than blue-collar workers; actors and football players have higher levels than vicars. This opens up a number of possibilities: could teenagers be tested and then steered towards those professions most suited to their testosterone levels – or could those with lower levels even be given supplements? To be honest, I’m not that convinced by this work, which seems like hormone determinism to me. Hormones are just part of what you are and there’s more to human life than the endocrine system, magnificent though it is.
Stress and Depression
Major depression often becomes apparent for the first time in adolescence. Although it may be triggered by a life event (bereavement, family break-up) it is more likely to happen to those who are already genetically susceptible. Depression is twice as likely in teenage girls than in boys, a pattern which will endure for life. This poses the question, could it be attributed to the ovarian steroids unleashed in puberty?
During adolescence, reproductive hormones make girls more sensitive to the effects of stress. In addition, this occurs at a time when the stress response is changing, with more cortisol being produced. Although the basic level of cortisol secretion does not vary across the menstrual cycle, women become more sensitive to it, particularly during the luteal phase, which is the second, post-ovulation, half of their cycle. As I explain elsewhere, high levels of cortisol are a feature of depressive illness. Many researchers suggest that society’s view of women affects self-esteem and creates feelings of worthlessness, which is why more women have depressive illness. I’m not convinced by this as a reason for this high rate of depression in women. Since sex hormones have an effect on mood when women are on the pill, when they are taking the progestogen element of HRT and in the second half of their cycle, a biological explanation seems rather more plausible, with hormones the most likely culprits.
Puberty
In the UK, 95 per cent of girls will have menstruated by fifteen, and 50 per cent by the age of twelve and a half. The age at which normal puberty occurs is heavily influenced by genes. If your mother started her periods early, probably you will too. Ethnicity is also important – with blacks starting before whites, and whites before Asians, as a vastly generalized rule. Periods are actually quite a late event of puberty in girls, but their start (called the menarche) is a convenient and well-defined marker, which is often used as an indicator of puberty, even though the process has actually begun some years before. Environment is also very influential. If you have experienced serious illness as a small child, or you have been very short of food, puberty will be delayed. Extra hormones are not necessarily required in these situations. A team from Israel found recently that supplementing a child’s diet, particularly with Vitamin A and iron, was as effective as hormonal therapy.
What is the trigger for puberty? In girls, it is associated with a critical body mass, or rather a critical percentage of body fat. And when leptin, a hormone that is produced by fat, was discovered a decade ago, everyone thought that they had discovered the puberty ‘on’ switch. Certainly, children (boys and girls) who have no leptin because of a rare gene defect do not go through puberty, but will do so if given leptin. There is a gender difference in leptin secretion: it rises throughout puberty in girls, but not in boys. However, since fat mass steadily increases during this time in girls (and decreases in boys) and leptin is produced by fat, this isn’t surprising. Leptin and the initiation of puberty is the subject of intense study at the moment, but early indications are that it is not the ‘on’ trigger as was originally thought. Instead it is thought to have a permissive role. In other words, when the noise from leptin is loud enough, something, previously held in check, is allowed to happen, which then cranks up the hypothalamus to let loose the gonadotrophin releasing hormone. Whatever the trigger, which could well be initiated in the brain itself, as suggested earlier, the hypothalamus goes through a change – from not responding to oestrogen with a surge of luteinising hormone which will prompt ovulation, to doing precisely that.
IS PUBERTY GETTING EARLIER?
Over the last century, the age at first period has dramatically decreased. It is likely that menarche for girls in the nineteenth century was around seventeen because of poor health and nutritional factors, such as, crucially, lack of access to fresh foods in winter. Victorian novels are full of young girls complaining of ‘green sickness’ or ‘chlorosis’. Today we would call this iron-deficient anaemia and lack of iron is one of the factors that can help delay puberty. Between the mid-nineteenth and the mid-twentieth century, age at first period went down from seventeen to fourteen in the US and the better developed European countries. Today, US figures are 12.9 in white Americans and 12.7 in black Americans. Across the world today, the average age at menarche varies enormously, with those girls living in underprivileged conditions in China and Senegal (two countries where studies have been carried out) still experiencing their first period at an average age of sixteen. Interestingly, there is a North–South gradient, which has existed for at least a century, with higher ages at menarche in Scandinavia, for example, than in France. The trend towards lower menarche seems to have bottomed out with Britain, Sweden and Belgium seeing a small increase in menarchal age, while it is still declining in Denmark, France and Finland.
One of the problems of these statistics is the different markers that are used to express age at puberty. I have already mentioned age at first period, which is a relatively late indicator, but another, which is frequently used, is B2 or thelarche, which describes when breast development first appears. This precedes menarche and is not always easy to assess, particularly in children who are obese, and there is quite a variation between assessors’ estimates – something which makes you suspicious about the reliability of the data. This age seems to be diminishing fairly dramatically in the US, and is now 8.4 for white girls and 9.5 in black Americans. There is no such trend in Europe. Precocious puberty is defined in Europe as less than eight, for breast development and less than nine for the parallel testicular development in boys. But in the US, the age limit has now been reset to under seven in Caucasian girls and six in African Americans – for breast development. Onset of periods seems to have halted at an older age and is showing no sign of further decrease. What is interesting is that the time between onset of periods and regular cycling seems to be increasing, from 1.9 to three years.
Precocious puberty is twenty times more common in girls than in boys, and in 90 per cent of them there is no obvious cause. In boys, less than 10 per cent of cases have no identifiable cause and most have some underlying problem such as pituitary tumours. There is also a phenomenon in which children adopted from developing countries and then raised in a more affluent environment have an increased incidence of early puberty. In a study from Belgium, there was an eighty-fold increase in incidence of sexual precocity in children adopted from abroad, compared to native Belgian children. It is surprising, however, that no such reports come from the US, where physicians are as attuned to the problem, and where over 100,000 children have been adopted, over the last decade, often from very deprived circumstances.
Diets that have a high fat rather than high vegetable matter content are associated with early onset of periods, and diets high in phytoestrogens (natural oestrogen-like chemicals found in plants) with a later onset. This might be especially relevant for children adopted from deprived countries where plant oestrogens are a large part of the diet. There has also been a big decrease in the amount of exercise taken by children over the last fifty years: those in developed countries are more likely to be in front of the TV than out exercising. Increasing fat levels may be sending out a louder leptin signal, earlier than before, as a result, while those in developing countries may be involved in hard physical work by puberty, which is likely to decrease their body fat. It seems highly likely then that early puberty is the result of lifestyle factors, although this is not the view of some activists who feel that early puberty reflects exposure to ubiquitous chemicals in the modern environment.
DECREASING AGE OF PUBERTY – AN EFFECT OF CHEMICALS?
Although precocious puberty in girls is widespread in the USA, particularly among African Americans, there is no such phenomenon in western Europe. There is no suggestion that boys are affected either, in the US or in Europe. You would also expect – if there really was a problem caused by chemicals – there to be disturbance of other secondary sexual characteristics, such as inappropriate body hair or disturbances of growth, particularly those affecting the timing of the changes seen in the growing zone at the ends of long bones, which signal the end of growth. These have not been seen. In the Belgian study of children adopted from abroad, it is suggested that the children, who all had detectable levels of DDT, were exposed to it in their home country, and that it exerted an inhibitory effect on the pituitary, and that interrupted exposure caused precocious puberty on emigration. This seems to me like a conclusion looking for data which simply isn’t there. DDT is still used to control mosquitoes in some developing countries, where death from malaria is common and feared, and it would be a surprise if residues were not found in children. But to call the DDT causal is stretching the evidence. If this is truly the case, it is odd that a similar effect hasn’t been found amongst the 100,000 children adopted into the USA from other countries over the last decade, or indeed in Britain. The major changes in nutrition, lifestyle and body fat are much more likely to be the cause than endocrine disrupting chemicals.
Teenage Genius
This chapter has contained a rather gloomy picture of the adolescent brain. Can I redress the balance and close by saying that teenagers are also our salvation. Their brains are more open to ideas, they are more amenable to change and are less set in their ways because they come without the baggage of experience that binds creative thought so tightly. I don’t think it is an accident that teenagers are behind some of the world’s great discoveries, particularly in technology. An example of what I mean is Ada, Countess of Lovelace, muse to Charles Babbage, he of the difference engine and father of computing. It was seventeen-year-old Ada, the daughter of the poet Lord Byron, who saw the potential of Babbage’s invention, predicting that it could be used to manipulate figures and symbols. That’s a teenager’s insight for you.
