My International Women’s Day post: A gender for parenting
It’s International Women’s Day again! Last year I griped about the career prospect inequalities for women and I am pleased to say that although it’s not exactly “all change at the top”, I think that the world is waking up to women in the workplace and the agenda for change here has started rolling into place. So this year, I am moving the gender agenda on…
A few months ago I attended a fascinating talk on the impact of post-natal depression in mothers on their children. As you can probably already guess, the impact is not just for the duration of the mother’s depression, but due to the massive development of the baby’s brain in the first year of life in response to its environment, problems in its “environment” (which is largely provided by the baby’s primary carer) can be life-long. For mothers to get depression (or worse still, psychosis) at this time is crippling as not only does it affect them for the duration of their illness, but can impact the child LIFE-LONG. I don’t think any other mental illness can have such a profound effect.
The talk went into much detail about the observed negative outcomes in children and the mechanisms that led to these outcomes. In brief, lack of love, warmth, responsive parenting, talking and interacting with babies in “motherese” lead to abnormal or insufficient normal brain connections in the baby (motherese is the repetitive and sing-song baby-like voice that mothers adopt when talking to babies that is infinitely nauseating to non-parents – isn’t it darling? Yeees-it is! Yeees –it is!). Many clinical trials have been undertaken to treat post-natal depression to prevent these negative outcomes in children, such as cognitive behavioural therapy (CBT) and anti-depressant medication, but all with marginal effects. Really interesting stuff that I am sure I will blog about in more detail another time.
A PhD student had done some interesting work around the ability of depressed mothers to differentiate between a distressed cry and a non-distressed cry from various recordings of a baby crying. Depressed mothers can typically not differentiate the cries and find all cries aversive. Interestingly though, depressed mothers that had been musically-trained (played grade 4 or above piano) continued to be able to distinguish a distress cry from a non-distressed cry from her baby presumably because of their superior ear in differentiating musicality in sounds. This led to the suggestion that training in music may be protective in some way for the negative impact of maternal depression as these mothers preserved the ability to identify distress in their babies. Someone suggested teaching mothers the piano in pregnancy.
When questions went to the floor, other people suggested a blast of oxytocin nasal spray. Oxytocin is the “mothering” hormone released in pregnancy and during breast feeding and given to apes has been found to increase “maternal behaviour”.
Tentatively, I put up my hand. From the back of the hall (I have not yet escaped my student-style sitting at the back of packed lecture theatre habits) I wait my turn to be picked. “Umm – wouldn’t it just be easier to ask the dads to step up and do the parenting bit?”
It struck me as obvious that if the best anti-depressants were contra-indicated in breast feeding, and available anti-depressants were not achieving good enough effects and CBT was taking too long to treat mothers, that one should look not to new and under-developed drugs like oxytocin or expensive and frankly bizarre suggestions of NHS funded piano lessons for mothers to “cure” the mother; but to additional support that could take over the “warmth, love, responsive parenting, engagement and social interaction” with the baby. The clue was in the term “parenting”. Dads are parents too.
What amazed me was the response.
Maybe I had asked a silly question. Maybe there were already piles of research, unread by me; that excluded fathers from nurturing a baby. There was an awkward silence as if I had breached some sort of sacred unspoken code of conduct. There followed mutterings from the row of my esteemed male colleagues sitting in the front row. I imagined that they were saying “Trust her (rampant feminist implied) to bring this up!”
The speaker responded to my question thus (as verbatim as I can remember but cannot be vouched to be word for word): “Yes, but people don’t respond well to being told to do things, and of course there is already a large role for fathers to support their wives. Often fathers are at work and are not available to do this.”
I wondered if I had time travelled to the 1960s.
Can it be that in the 21st century, my esteemed, brilliant, talented, caring profession is still stuck in a time-warp? Decades after my predecessors saddled mothers with terms such as “Refrigerator mother”, “Schizophrenogenic mother”, “Good-enough mother”, “Tell me about your mother” and volumes on the paramount importance of maternal bonding and maternal attachment – can it be that we have not moved on from the primeval importance of mothers to babies? I am not disputing Bowlby here; I agree that attachment is vital. My dispute is with the gender requirement. Why can’t fathers bond and attach to their children – particularly if the mother is down or out?
My view on the issue is this:
Parental bonding and responsive parenting to babies is vital.
Biology provides some mothers with an advantage over fathers for bonding through pregnancy, birth and breast-feeding hormones. This hormonally driven advantage is lost once mothers stop breast feeding. In the UK, less than 1% of mothers last to 6 months of breast feeding. The hormones do not make mothers “better” at bonding, but makes them “desire” to bond and care for their young – kick starting the supposed “maternal instinct”. If there is a strong “desire” to parent, maternity hormones are completely unnecessary, which is why mothers who adopt babies are still perfectly wonderful mothers without having exposure to any maternity hormones. Believe me when I say that it was not oxytocin that told me that if my baby is crying I should pick her up, and if my baby is crying and her nappy stinks that I should change the nappy. That’s just common sense and I don’t need hormones for that.
Some mothers lack this advantage over fathers (having low levels of hormones or being unresponsive to hormones) and have no “maternal instinct” and are uninterested in babies (in the same way that many men lack the “aggressive instinct” that they are supposedly stereotyped to possess). Many men possess a “nurturing instinct”, in the same way that many women possess an “aggressive instinct”.
Some mothers get post-natal depression and are completely incapable or are severely handicapped in bonding and responsive parenting.
The conclusion should therefore be that fathers who have a strong desire to bond and care for their babies are no worse parents than mothers. Once mothers have stopped breast-feeding, they and their husbands are equally placed biologically to provide the love, care and nurture that is required to support a baby’s development. If a mother has post-natal depression or is uninterested or incapable of parenting for whatever reason, than the father is better placed to provide the love, care and support (provided he is not also disinterested or depressed), and particularly if he is warm and loving.
And yet, no one is shouting this from the rooftops, because there is no evidence to support this.
Just piles and piles of research on the bad outcomes for babies raised by mothers with problems.
Why is that?
Because in the past, it was the mother’s role to nurture babies and look after children. The body of evidence regarding mothers has built up over time. People writing research proposals and funding bodies granting money for research want to see an evidence base for the work that researchers they fund are building on. There is very little that has been done on fathers as the main carers for babies because up until the last few decades, this just happened so rarely. Even today, the vast majority of funded research in the parenting area relates to looking at mothers and their children. There is no evidence that fathers can care for babies, but equally, there is no evidence that they can’t. There remain large personal and societal incentives for many people and organisations NOT to produce research and data that may support equality in parenting capability. Yet, anecdotally, the gay dads that I have met (both personally and professionally) have largely been fantastically capable of love, warmth and responsive parenting and I am just sad for the many children whose lives are inordinately altered by mothers with post-natal depression where fathers have not stepped in.
The next stage in gender equality is surely to evaluate if the skewed evidence that we have been fed by parenting researchers who lived through a different society is scientifically relevant going forward, and to generate new evidence on parenting; where parenting is not just a proxy for “mothering”. My profession should be at the fore front of this, advocating for this research to take place and stamping out the gender bias in parenting. For if going forwards we are moving towards equality within the workplace (which we are), are we as child psychiatrists going to hinder this progression by continuing the rhetoric of hanging the responsibility of childcare on to aspirant mothers, or are we going to apathetically hang back and allow governments to enact it’s solution: to hand childcare over to the state? I believe we should speak with one loud voice for parental responsibility for parenting. Both parents in concert where possible and gender being irrelevant.
I am reminded of Harlow’s controversial primate experiments. The baby monkey chose to lay with the wire frame dummy covered in faux fur that gave it warmth and comfort, rather than the wire frame monkey that gave it milk. It is love that matters not mammary glands, and I am confident in my assertion that mothers and fathers are equally capable of that.
How anxiety in pregnancy can lead to anxious children
This is the last of the How to improve your child’s success before they are even born series. See Part 1, Part 2 and Part 3. OK, its pretty heavy going on the science, but if you really want to understand anxiety then its worth a read.
Most people are aware that stress and anxiety are not good for pregnant mothers. Even in 400 B.C., Hippocrates espoused the influence of emotions on pregnancy outcomes, leading to a plethora of literary dramas old and new where stress has caused the leading lady to miscarry or go into premature labour. More recently though, following Barker’s theories of foetal adaptation to the mother’s womb environment (see my post How to improve your child’s success before they are even born: Part 3), scientists have found that a mother’s anxiety in pregnancy can influence psychological and behavioural outcomes of her developing foetus over and above those caused by premature delivery. There is now a well-established literature base linking mother’s anxiety in pregnancy to several psychological and psychiatric outcomes in children, including: anxiety, attention deficit hyperactivity disorder (ADHD), cognitive problems, changes in temperament, aggression, conduct problems and even schizophrenia (Beydoun & Saftlas, 2008; Talge et al. 2007; Van den Bergh et al., 2005).
Animals stressed in pregnancy give birth to anxious baby animals
The first evidence for this came from animal studies. Researchers found that rats and monkeys exposed to stress in pregnancy produced offspring that had long-term difficulties with attention, motor behaviour, aggression, memory and showed “hyper-vigilant behaviour” (Van den Bergh et al., 2005). Hyper-vigilant behaviour in animals is a proxy for human anxiety. It incorporates being alert to potential threat with corresponding changes in body systems to prepare to respond to threat. Think about how you would have felt travelling to work on the underground the day after the 7/7 London bombings of 2005, and this is probably a good picture of human “hyper-vigilant” state. Darting eyes on the look-out for suspicious bags with no owner, or people with over-sized back packs, slight tension in muscles, slightly increased heart rate and breathing rate, a little bit more perspiration than usual and if someone were to pop a balloon behind you, you’d probably have been ready to run. Hyper-vigilance is a good thing if you are in a stressful situation. It has served me well on many a walk home from the night-bus stop. If you are continually hyper-vigilant or hyper-vigilant in non-threatening situations like social situations or on aeroplanes; it can be very problematic and is called “anxiety”.
In animals it is easy to experiment and find out what is happening, you can wire animals up to measure muscle tension, heart rates and perspiration fairly unobtrusively. Even better, you can take blood samples and measure the levels of “stress hormone” cortisol. By doing these experiments, scientists have been studying the various effects of maternal stress on animal offspring and among several suspected effects, they have found pretty conclusively that in animals stress in pregnancy causes changes in the development of the foetal stress regulation system, the Hypothalamic-Pituitary-Axis (HPA) re-setting it to be on heightened alert.
How does the body deal with stress? What goes wrong to cause anxiety? – an analogy
What is the HPA-axis? The HPA axis is a collection of parts of the body that communicate by hormones to regulate certain bodily responses, including the stress response. In its function to regulate stress-response, it works pretty much like the emergency fire service. When you see a fire, you pick up the phone and dial 999. This puts you through to a national call centre, where you are asked which emergency service you would like. Once they realise that it is the fire service you need, they contact the regional fire control centre which contacts your local fire brigade which sends out an engine to where you are. The firemen hopefully put out the fire and call back the fire brigade centre to report that the job is done, which then feeds this information back regionally so that the case can be closed. Alternatively, if the fire has gotten out of hand, they can report regionally or nationally depending on the extent of the fire to request more engines to help.
The hypothalamus (a region in the brain) is the national call centre. When the eyes see threat, they alert the hypothalamus. This lets the brain’s pituitary gland, (regional fire control centre) know that there is a threat and a stress response is required. The pituitary communicates with the kidneys (local fire brigade), which then provides the stress response: the steroid hormone cortisol (fire engine). The fire engine goes out to sort the problem. Cortisol does this by going to the heart and making it pump harder, it goes to the lungs and makes it breathe quicker, it goes to the sweat glands and makes them produce sweat, it goes to the muscles and makes them tense and ready for action. All so that you can either fight or flee the threat.
If a city undergoes a heat wave and there is an increased propensity to fires starting and burning out of control. The fire service would probably request more resources on standby and be on heightened alert to send out more engines. More engines than needed might be sent out to small fires to ensure that they did not catch and turn into large fires. This is precautionary and helpful in the short term, but is an over-reaction if continued long term, beyond the time of realistic threat. The same thing happens to our body’s emergency response system. If there is a history of heightened stress, the body responds by increasing the base level of cortisol in the blood stream and increasing the amount of cortisol released in response to stress. This is not a problem if there is continued threat, but if the situation calms down and the body does not down regulate its stress-response system, the result is persistent anxiety.
In animals at least, it has been shown that the animals themselves do not need to have been exposed to stress for their bodies to be placed on heightened alert, they merely have to be exposed to their mother’s heightened alert system in the womb. Thus in animal experiments, giving pregnant mothers injections of cortisol equivalent substances can cause their children to have higher base levels of cortisol and heightened cortisol response when they are born and with continued effect into adult life (Van den Bergh et al., 2005). These animals went on to display a range of long-term behavioural and cognitive impairments. This can be thought of as part of Barker’s hypothesized foetal programming whereby the foetus exposed to high levels of maternal stress hormone predicts a hostile environment and prepares itself by adapting its HPA-axis to best cope with impending fight for survival. Where the resulting environment is actually not that stressful; the HPA-axis is now not working properly and leads to a range of problems.
Who cares about animals? What about humans?
Stressing humans to study anxiety is rather unethical. Shockingly, it used to be allowed and “Little Albert” is a classic case in psychology literature. Little Albert was a 9 month old boy who was not afraid of rats and was given a rat to play with. A dastardly psychologist John B. Watson wanted to see if it was possible to cause a phobia of rats. Every time little Albert touched the rat, a man stood behind him and banged a piece of metal with a hammer making a loud noise scaring little Albert. Needless to say, after a while of this, Albert became afraid of rats and stopped going near them, proving it is possible to induce a phobia. No wonder experimental psychology has a bad name!
These days, we are thankfully not allowed to do such things, but it does mean that extrapolating work from animal studies into humans is harder. We have to rely on stress that occurs naturally in the lives of pregnant women rather than purposefully causing stress in order to study its effects on offspring. Natural and man-made disasters have been used to study the effects of anxiety in pregnancy.
Studies of children who were in the womb of mothers affected by 9/11 showed that these children were born with lower birth weights even though they were born at term, compared to children conceived following 9/11 (Berkowitz et al., 2003). Infants whose mothers were pregnant during the 1998 Canadian ice storm that led to electricity and water shortages for up to 5 weeks scored lower on mental development indices and tests of language development compared to other children, even after taking into account birth complications, birth weight, prematurity and post-natal depression (La Plante et al., 2004).
It is not just extreme stress such as a national disaster that can cause effects. Studies have also used questionnaires asking pregnant mothers about their levels of stress at varying times in their pregnancy and then studied their children at varying ages from newborn to adolescence. In general the link between maternal stress and impaired offspring outcome is borne out, sometimes even with a direct dose-response effect (Beydoun & Saftlas, 2008; Talge et al. 2007; Van den Bergh et al., 2005). Results from different studies vary as each study is different in terms of the stress they are measuring (some studies ask for work stress, bereavement, marital stress, criticism from partners, or just how anxious you feel), the time in pregnancy the stress occurs (studies vary in studying stress in the first, second or third trimester), and the outcome and age of children they are studying (some studies look at language and development in the first year, others look at ADHD symptoms in childhood and yet others look for anxiety and conduct problems in adolescence). Despite this, the majority consensus of all the studies is that there is a significant negative effect of maternal pre-natal anxiety which can have lasting effect. In this way, it is not just your DNA that is biologically influencing your child’s outcome, but environment, via biological mechanisms.This is epigenetics, the new buzz in child psychiatry research.
Interesting finer details
The theory regarding differences in timing effects is that this relates to timing of brain development. Throughout pregnancy the developing foetal brain goes from a neural tube to a baby’s brain which is a complicated journey. Different parts of the brain are forming throughout the 40 weeks, and the effects of insult to the brain at a particular period in pregnancy will depend on the part of the brain that is forming at that time. So for instance, a brain insult (such as anxiety) occurring at the time that the language centres in the brain are forming may lead to language deficits down the line. It is known that the links between pre-natal anxiety and schizophrenia are related only to stress that occurs in the first trimester (Khashan et al., 2008), whilst maternal anxiety experienced in the third trimester is more likely to cause offspring anxiety (O’Connor et al., 2002). Even more interestingly, there appear to be differential effects depending on the gender of the developing foetus, females more likely to develop anxiety, males more likely to be affected by attention, cognitive problems and aggressive tendencies! There is strong evidence for this in animal models and supportive evidence for this from human studies (Glover 2011; Glover & Hill, 2012)
The reason for these different gender outcomes has been thought about from an evolutionary perspective. Historically the female role in species survival in animals and humans has been to bear children and look after them, the male role has been to protect and provide resources. Different skills are required for these different roles. Thus, in a hostile environment, it pays for the mother to be fertile to ensure succession and hyper-vigilant to prey and threat. It pays for the father to go and explore new territory for food and shelter, to take risks to achieve this and to be aggressive enough to fight others for territory and food. In this context, the effect of stress in generating anxiety in females and cognitive impairment and aggression in males can be understood. Hey, in an Armageddon situation I think we would all want rough and tough Bruce Willis at our side not intellectual Stephen Fry.
In animal models it has also been found that stressed out female rats reach sexual maturity earlier, are sexually active earlier, have more offspring but invest less time in the care of each (Meaney, 2007). We have to remember we are talking about rats here, but in humans there is evidence that a harsh early environment (poverty, neglect, abuse) can lead to precocious puberty. You can draw any other rat-human parallels yourself.
The astute amongst you, might be complaining that this is all hogwash and that so many things might be confounding the picture. A confounder is something that can be related to both the purported cause and the outcome. The main ones affecting our current scenario are things like poverty, post-natal depression and maternal educational level. One could argue that a deprived, uneducated mother prone to depression is more likely to experience stress during pregnancy and more likely to have difficulty raising children, thereby causing the psychological deficits seen in their offspring in childhood and adolescence. In animal studies, this is easy to exclude, the new born pups or monkeys are cross fostered so that the mother stressed in pregnancy is replaced once the baby is born by an unstressed mother. Results remain. It is not possible to do this with humans.
In the majority of human studies, known and suspected confounders (social class, post-natal depression, maternal education to name a few) were measured and significant results remained even when these confounders were taken into account. What about the effect of genetics? It is possible to argue that a mother genetically predisposed to anxiety is likely to be anxious in pregnancy and to pass on anxiety genes thereby causing offspring to be anxious. You can see how hard it is to prove anything in science, yet clever research designs continue to come up to try and get to the answers. In a master-stroke of research design now possible due to the frequency of in-vitro fertilisation, Rice (2010) compared, in a cohort of IVF children, the association between prenatal stress and child outcome in those who were genetically related to the mother with those who were not (i.e. receiving egg donation). They found there was an association between mother’s stress in pregnancy and child’s symptoms of anxiety and conduct disorder even in the unrelated mothers.
How does this relate to you and me?
So, how to prevent anxiety in pregnancy? For me, I was smug reaching pregnancy having achieved a stable, loving relationship, stable financial and employment situation and having lived child-free life to the full. I felt I was ready to face pregnancy and motherhood in the best position that I could be in to avoid anxiety. There would have been nothing to stop a loved one being run over by a bus or being faced with infertility problems or illness but, at least the readily controllable variables were answered for.
Things can’t always go as planned though! Typical of most pregnant ladies, the thought of a new bald addition to the family somehow provokes the mental image of bald addition being placed into a beautiful, white cot with pressed linen sheets in a light and bright nursery attached to a south-facing home with wooden floors, modern furniture and period features. Hence in the first trimester of pregnancy Banker and I embarked on a 10 month process of flat hunting, flat offers, flat rejections, flat offer accepted, flat exchange of contracts, flat completion delay, eviction from rental and 2 weeks of homelessness, worldly goods in storage and 2 week enforced holiday in France to avoid sleeping on the street, flat completion, moving in, moving out, flat total remodelling and renovation, all of which no doubt sent the cortisol flying through my placenta!
Here biology and scientific literature come to the rescue again. Thankfully, like all natural miracles, the pregnant body seems to do all it can to protect itself and its prize. It is well known that in the third trimester of pregnancy and for a period post-natally the body dumbs itself right down (Henry & Rendell, 2007). Having for many years prized myself on my amazing memory and lauded it over my husband who seems to have been born with the happy disposition of the forgetful, I became just the same. Misplacing things left, right and centre, but instead of fretting and panicking, just sitting back and saying “Ah, sod it”. During my last week at work, I merrily typed away at a patient’s report only to re-read it to find that it was gobbledegook! Evolutionarily this dumbing down particularly affecting memory impairment is likely to protect against the harmful effects of third trimester anxiety, as well as to help block out the trauma of childbirth so that we become willing victims for another round!
Further, there was a caveat in the maternal anxiety literature! In a review of the literature, Vivette Glover (2011), a fellow North West London resident, describes studies selecting only well-off middle to upper class women in stable circumstances. They found that in this group mild stress in pregnancy had a beneficial influence on child outcome with better mental and physical development of the children and a similar trend for IQ. The suggestion is that in this group of women, a small amount of pre-natal stress may actually enhance foetal brain development. This inverted-U shaped dose-response effect is typical of anxiety and you will be familiar with the idea that a small amount of anxiety helps you sharpen your attention to perform on stage or in an exam, but too much anxiety can cripple your efforts. If Big Sis wins the Nobel Prize, I’ll be remembering to send a bottle of bubbly to my builders for the aptly timed “mild” stress!
References and Influences:
Beydoun H, Saftlas AF. Physical and mental health outcomes of prenatal maternal stress in human and animal studies: a review of recent evidence (2008). Paediatric and Perinatal Epidemiology, 22, 438–466.
Talge, N.M., Neal, C., Glover, V. and the Early Stress, Translational Research and Prevention Science Network: Fetal and Neonatal Experience on Child and Adolescent Mental Health (2007). Antenatal maternal stress and long-term effects on child neurodevelopment: how and why? Journal of Child Psychology and Psychiatry, 48, 245–261.
Van den Bergh, B.R.H., Mulder, E.J.H., Mennesa, M. & Glover, V. (2005). Antenatal maternal anxiety and stress and the neurobehavioural development of the fetus and child: links and possible mechanisms. A review. Neuroscience and Biobehavioral Reviews, 29, 237–258.
Berkowitz, G.S., Wolff, M.S., Janevic, T.M., Holzman,I.R., Yehuda, R., & Landrigan, P.J. (2003). The World Trade Center disaster and intrauterine growth restriction. Journal of the American Medical Association, 290, 595–596.
LaPlante, D. P., Barr, R.G., Brunet, A., Du Fort, G.G., Meaney, M.J., Saucier, J.F., Zelazo, P.R., & King, S. (2004). Stress during pregnancy affects general intellectual and language functioning in human toddlers. Pediatric Research, 56, 400–410.
Khashan, A.S., Abel, K.M., McNamee, R., Pedersen, M.G.,Webb, R.T., Baker, P.N., et al. (2008). Higher risk of offspring schizophrenia following antenatal maternal exposure to severe adverse life events. Archives of General Psychiatry, 65, 146–152.
O’Connor, T.G., Heron, J., Golding, J., Beveridge, M., & Glover, V. (2002b). Maternal antenatal anxiety and children’s behavioural/emotional problems at 4 years. Report from the Avon Longitudinal Study of Parents and Children. British Journal of Psychiatry, 180, 502–508.
Glover, V. (2011). Annual Research Review: Prenatal stress and the origins of psychopathology: an evolutionary perspective. Journal of Child Psychology and Psychiatry 52, p 356–367.
Glover, V. & Hill, J. (2012). Sex differences in the programming effects of prenatal stress on psychopathology and stress responses: An evolutionary perspective. Physiology & Behavior 106 (2012) 736–740.
Meaney, M.J. (2007). Environmental programming of phenotypic diversity in female reproductive strategies. Advances in Genetics, 59, 173–215.
Rice, F., Harold, G.T., Boivin, J., van den Bree, M., Hay, D.F., & Thapar, A. (2010). The links between prenatal stress and offspring development and psychopathology: Disentangling environmental and inherited influences. Psychological Medicine, 40, 335–345.
Henry, J.D. & Rendell, P.G. (2007). A review of the impact of pregnancy on memory function. Journal of clinical and experimental neuropsychology, 29 (8), 793–803.
 Interestingly, there appears to be an evolutionarily hard-wired biological predisposition to phobia development to things which are traditionally harmful. Thus, it is easy to induce a phobia for things like rodents, snakes and spiders but very difficult to induce a phobia to cars, guns and knives which are more likely to be a threat in the modern age.
 A dose-response effect is an effect whereby the greater dose of something purported to cause a particular effect, will cause a greater effect. For example, if sun exposure is linked to tanned skin, a dose response effect would mean that more sun exposure leads to a deeper tan. Finding a dose-response effect is good (but not necessarily definitive) evidence that a causal link exists.
How smoke exposure in pregnancy can cause aggressive kids
This is part 3 of the “How to improve the success of your kids before they are even born” blog series. See Part 1 and Part 2.
If folic acid is the Austin Powers of womb environment, then Dr Evil has got to be cigarette smoke. O.K., O.K., there are plenty of other bad guys obviously – thalidomide, heroin, alcohol. The reason I am casting cigarette smoke as the bad guy here is that whilst you have total control about exposure to the others, passive smoking is harder to control. The US Department of Health and Human Services (2006) estimated that more than 126 million non-smoking adults continue to be exposed to second-hand smoke in the US. Some of these millions are likely to be pregnant. Thank goodness for the U.K. law banning smoking in bars and restaurants. This was great for winter time, but having had both pregnancies through spring and summer, it was a real pain to anticipate a delightful al-fresco meal in the fresh air, only to find, given the laws prohibiting smokers from dining inside that all the outdoor tables at pubs and restaurants were over-run with smokers. Worse still, I found that friends would continue to light up in front of me in social situations when I was pregnant. Most of the time, I would alert them to smoking and pregnancy but this usually meant they moved a few paces away and tried to blow smoke in another direction with varying degrees of success. I’m not a smoking killjoy. I enjoyed cigarettes in my youth, and drinking in other people’s smoke used to bring back good memories, but when I became pregnant this changed and my mind would shout “TOXIN, TOXIN” if ever smoke touched my nasal hairs. Sometimes, not to cause a scene I just grinned and bore it, but images of damaged children would always run through my mind.
Most everyone knows that you shouldn’t smoke in pregnancy, but I’ll bet you didn’t know why? Studies have shown that there are over 4,000 chemicals in cigarette smoke and more than 40 of these are known to be linked with cancer (Thielen et al., 2008; US Department of Health and Human Services, 2010). Many of these chemicals, including nicotine, are able to cross the placenta into the foetus’s blood stream where, due to differing mother and baby physiology, concentrations can build up to higher levels in the foetus than in the mother (Lambers & Clark, 1996). Every time you have one, that’s two fags for the baby. There is evidence that links exposure to smoking in the womb to an increased risk of spontaneous abortion, pre-term delivery, and the baby going on to develop asthma, allergies, breathing problems and even cancer in later adult life. If you are a pregnancy smoker, you know all this and are as immune to this as being presented with a photo of a messed up smoker’s lung in the doctor’s surgery when they suggested you quit. What may influence you and what were my main concerns, were with the lesser known associations of smoking: with higher levels of aggression, conduct problems, attention problems, impulsivity, memory, speech and language and intelligence (Knopic 2012). It shouldn’t really sway you more, but put it this way, if your child develops cancer in adult life, it’s a long way off and is largely their problem to deal with. If your child is prone to aggression, that’s going to be your problem in a matter of months to years! If you did already know that, then I bet you didn’t know how cigarette smoke does this?
If you do then you are well ahead of the scientists! Scientists are still hard at work on this, but their current hypotheses surround the fascinating ideas around foetal programming and epigenetics. The theory of foetal programming is attributed to David Barker. David studied a group of mothers who were pregnant during the Dutch famine of 1944-1945 and followed up on the consequences of the children who were in utero during the famine. These mothers suffered malnutrition and stress, the children exposed to maternal starvation and stress were found to have lower birth-weight which is of no surprise. However, despite the end of the famine and a return to plentiful food supply, these children went on to have worse adult outcomes than children conceived just after the famine ended. These included cognitive deficits and higher likelihood of type 2 diabetes, heart problems and obesity. Barker’s theory is that there is a mechanism for Darwinian adaptation to environment occurring right there in our swollen abdomens that has probably been responsible for the success of our species. He postulated in the 1980s and 1990s that the developing foetus could take on information from the mother’s womb environment and use this to “forecast” the state of the environment into which it would be born. It is then able to prepare itself by adapting to be able to best survive the predicted environment (generate a predictive adaptive response); in much the same way that we might reach for the umbrella, coat and wellies on hearing a weather forecast for rain. Thus, if the developing foetus finds itself in an environment in which nutrients are scarce (such as the Dutch Famine) it thinks to itself “Bugger, I’m in for it when I get out, if my mother can’t find enough food to eat, there’ll be no damn food for me!” It therefore adapts (programmes) itself to be small and thrifty (conserve and use minimal resources) in order to be able to best survive the harsh environment it will face on birth.
Through this mechanism our ancestors lived to survive droughts and famines long enough to reproduce and eventually generate us. The foetuses that did not adapt themselves in this way would have died in infancy and childhood not being resourceful enough in their physiology to withstand periods of deprivation. The problem occurs if the forecast is wrong as adaptations made at these early stages of development are generally permanent. In the Dutch famine group, conditions improved after 1945 and food became plentiful again. The small and thrifty babies turned into children and adults that continued to store everything they ate and basically became more obese and prone to obesity related diseases, compared to children from similar backgrounds born just a year or so later. This is the fool in his heavy overcoat, wellies and umbrella at the beach in 30 degree heat cursing Michael Fish’s dodgy weather report.
How the foetus is able to use womb environment information to affect changes in its development is thought to be by epigenetic effects. In essence, epigenetics is the study of which sections of DNA gets expressed. In my analogy of DNA as a large manual for human construction, epigenetics is the study of the post-it notes put into the manual to instruct the builder which instructions to follow and which to ignore. Scientists have discovered several ways in which these post-it notes can be inserted, one of which is by a process called “DNA methylation”. Smoking has been shown to affect this process and others implicated in epigenetics which activate changes in the placenta (which can then affect the development of the foetus) and foetal development directly (Knopic, 2012). Epigenetic changes can also be inherited and can continue to influence at least 2 generations of descendants (at least in insects-Matthews & Philips 2010), thus what you do in pregnancy now may not only affect your children, but also your grandchildren!
A foetus exposed to high levels of toxins (like cigarette smoke) might prepare itself by bolstering its immune defences. On being born to a toxin free environment, the hypersensitive immune system gives rise to asthma and allergic reactions, which are essentially immune responses to normal everyday surroundings. It is harder to understand the adaptive nature of the psychological associations of prenatal exposure to cigarette smoking (aggression, impulsivity), but it makes sense that if toxins are part of what can be described as a “hostile” environment, that the newborn baby and subsequent child should be prepared to look out for danger and fight its way in the world. Aggression, hypervigilence and risk-taking behaviour would be beneficial traits to aid survival of a toddler in an Armageddon situation, but probably not so beneficial in a 3-bed semi in Barnes.
I went to a Justin Timberlake concert when I was pregnant with Big Sis and she came out ready to dance! Does that count?
US Department of Health and Human Services. (2006). The health consequences of involuntary exposure to tobacco smoke: A report of the surgeon general. Atlanta, GA: Centers for Disease Control and Prevention.
Thielen, A., Klus, H., & Muller, L. (2008). Tobacco smoke: unraveling a controversial subject. Experimental and Toxicologic Pathology, 60, 141–156.
US Department of Health and Human Services. (2010). A report of the surgeon general: How tobacco smoke causes disease: What it means to you. Atlanta, GA: Centers for Disease Control and Prevention.
Lambers, D. S., & Clark, K. E. (1996). The maternal and fetal physiologic effects of nicotine. Seminars in Perinatology, 20, 115–126.
Knopic, V.S., Maccani, M.A., Francazio, S. & McGeary, J.E. (2012). The epigenetics of maternal cigarette smoking during pregnancy and effects on child development. Development and Psychopathology 24 (2012), 1377–1390.
Matthews, S.G., & Phillips, D.I. (2010). Minireview: Transgenerational inheritance of the stress response: A new frontier in stress research. Endocrinology, 151, 7–13.
How to improve your child’s success before they are even born: Part 2
In part 1, I talked about genes. Now I will share my thoughts on the other major player: environment. Most people think of environment as the family you are born into and the community and school your child belongs to. Actually, that’s all window dressing compared to the environment that you are providing in your belly! Whilst you are chomping into bacon sarnies, struggling to pull up maternity jeans that won’t stay up and mapping out where all the pregnant-lady friendly toilets are on your route to and from work (thanks Premier Inn Belsize Park!), unbeknownst to you, you are already determining your child’s future.
The bad thing about medical training is that you are all too aware of what can go wrong. Pregnancy is generally viewed as a “magical” time; the miracle of new life being generated from within your body. Paediatric cardiologists however, will start wondering whether a congenital heart malformation is present in the foetal heart beat they are hearing, an orthopaedic surgeon might worry about detecting clubbed foot in the fuzzy ultrasound scan. From the view of the child psychiatrist, forget extra digits and cleft palates, it’s all about the brain and the mind. The good thing about having medical training is that you can spot the bullsh*t that is out there in terms of pregnancy health advice. A pregnant woman is like a goldmine. While women may feel guilty about spending money on themselves, parting with money for the benefit of their unborn baby is totally justifiable and guilt-free. It’s no wonder that the health food industry piles in on this market.
In a recent study in New Zealand (Jeffries, 2012) a researcher in true Ben Goldacre style went to 21 health food shops and 21 pharmacies and asked for advice on morning sickness and what she ought to take for nutritional supplementation for early pregnancy. The recommendations were noted and any endorsed products were bought and ingredients compared with official health guidelines. Only 23.8% of pharmacies and 4.8% of health food stores made recommendations for Kate Middleton style morning sickness in line with official guidelines and 66.7% of pharmacies and 33.3% of health food stores recommended buying products, often branded to target the pregnant mother market, which were contrary to guidelines. Almost 10% of pharmacies and double this number of health food stores gave advice on nutritional supplementation with the potential for vitamin A overdose! Pharmacies were good at recommending folic acid supplementation, but fewer than 50% of health food stores got this vital message across.
If you haven’t heard of the need for folic acid supplementation (400 micrograms a day) pre-pregnancy then there is a really big problem in the dissemination of this public health message. Like the ills of smoking and the benefits of sunscreen, there is little scientific dispute about the benefits of folic acid supplementation in pregnancy in the prevention of neural tube defect. What the hell is a neural tube? Well, once the egg and sperm unite to form one cell with a complete set of DNA, it starts to reproduce by dividing into two, spawning 2 then 4, then 8, then 16 cells. Pretty soon, you have a big blob of cells called a morula (named after a blackberry as that’s what it looks like). Once you have a big enough blob, cells start to differentiate into the precursors of body organs. At around 3 weeks of pregnancy, the cells which will form the brain initially form a 2 dimensional sheet which then curls around on itself to fuse into a 3 dimensional tube: the neural tube. This tube becomes your nervous system. One end of the tube will become the brain, the remainder, your spinal cord. As everything else “brain” is formed from this initial structure, problems at this stage can’t be glossed over or compensated for.
Imagine trying to make a rocket from a flat piece of cardboard. You roll the thing up then tape it along the seam. Now, if you run out of tape, and tape just the top and bottom, you have a gaping hole in the middle. If you tape one end, you have a gap at the other. It doesn’t matter what flashy cone nose you put on the rocket, its decoration or fancy tissue paper flames, the crux of the problem is you have a gaping big hole in your rocket, and that is essentially what a neural tube defect is, a gaping hole in your brain -spinal cord system. It happens in 1 in 1000 live births in the USA (NICHD 2012), but risk is massively reduced by having enough folic acid and vitamin B12 around at the time of neural tube formation. This happens at 3 weeks, often before people even know that they are pregnant, which means that unless you have been organised enough to be taking daily folic acid before conceiving, your child’s brain formation may have been determined before you even knew you could have the most significant impact.
In my mind, it’s not just to prevent a massive hole in my child’s brain; I am not very worried about a 1 in 1000 risk as this is pretty low. If my son were competing against 1000 other children for one place at that elite prep school, I wouldn’t really fancy his chances, so why worry about this level of risk? The reason I think folic acid is important is that I want to optimize brain development in my children as best I can. The majority of medical conditions are dimensional meaning that there is a continuum of damage or impairment from minor to major. Take a burn. You have a range of tissue damage from slight redness on the skin to a fourth degree burn where the burn has gone down through all layers of the skin into bone and muscle. When you have a fourth degree burn, it is without a doubt that other tissue will be damaged with lesser graded burns. What does this have to do with the neural tube? Well, the way I see it, a severe disorder like neural tube defect is your fourth degree burn. The risk of neural tube defect is low like for a fourth degree burn, but I don’t just want to prevent a fourth degree burn, I want to prevent any redness at all which in brain terms would mean any even mild problems with attention, irritability, emotional regulation, planning, memory or motor control. The risk of getting things sub-optimal at this stage of development may impact brain development even if it doesn’t result in a full-blown neural tube defect.
More recently research has headed this way. Spurred on by the well-known protective effects of folic acid on one brain development disorder, researchers (Suren 2013, Roth 2011) have conducted association studies using large cohorts (samples of over 85,000) of Norwegian mothers and babies and found associations between peri-conceptional folic acid supplementation and reduced levels of severe language delay at age 3 years and autistic spectrum disorder. Association studies can never confer causality or effect, but given that folic acid’s status in prevention of neural tube defects is pretty much established, any potential additional benefits are good extras. Thus, in my view, sod the dilemmas about private/ prep or state school, the biggest impact you can make on your child’s brain function is invest in folic acid pre-pregnancy! It doesn’t matter how much you spend on software down the line, invest in the best hardware you can from the outset: a Commodore 64 cannot keep up with the latest iPad; not just in computation, but in user-friendliness and performance across the board.
As soon as parenthood was on the agenda, I switched the contraceptive pill for the folic acid and vitamin B12 supplement, that way, the daily pill popping continued seamlessly and in the event of pregnancy I was covered. I carried on taking folic acid supplements throughout pregnancy, although the critical period is before conception and the first trimester. As soon as my pregnancy was suspected, I started popping multivitamin, iron and fish oil tablets as well. The evidence that these are required if you eat healthily throughout pregnancy is decidedly ropey as most people gain sufficient vitamins and minerals in their diet. What can I say; even I was susceptible to the powers of the nutrition supplement marketing moghuls! My one defence is that pregnancy did skew my dietary preferences towards voracious inhaling of vast quantities of Kentucky Fried Chicken, Walker’s Ready Salted and bacon butties so I probably did need the multivitamins.
Jeffries S, Healy B, Weatherall M, Beasley R, Shirtcliffe P. (2012) What risks do women face when seeking advice during pregnancy from pharmacies and natural health retailers? New Zealand Medical Journal. 125, 61-9
National Institute of Child Health and Human Development (2012). “How many people are affected by or are at risk for neural tube defects?”. Neural Tube Defects (NTD). U.S> National Institutes of Health. http://www.nichd.nih.gov/health/topics/ntds/conditioninfo/pages/risk.aspx
Suren, Roth, Bresnahan, Haugen, Hornig, Hirtz, Lie, Lipkin, Magnus, Reichborn-Kjennerud, Schjolberg, Davey Smith, Oyen, Susser &Stoltenberg. (2013). Association between maternal use of folic acid supplements and risk of autism spectrum disorders in children. Journal of the American Medical Association. 309, 570-7.
Roth, Magnus, Schjolberg, Stoltenberg, Suren, McKeague, Davey Smith, Reichborn-Kjennerud & Susser. (2011) Folic acid supplements in pregnancy and severe language delay in children. Journal of the American Medical Association. 306, 1566-73.