A different interpretation of the increased use of interventions is that women have evolved to be worse at childbirth and that there are more complications now than there used to be. French obstetrician Michel Odent argues that since the use of artificial oxytocin during labour and childbirth, our natural oxytocin system (on which childbirth, placenta expulsion, attachment and breastfeeding relies heavily) has been very much underused in the last several decades. In accordance with recent advances in epigenetics and evolution theory, this underuse might result in the oxytocin system not working as well anymore in subsequent generations (see Box 21). But even if this were to be true, current statistics of 85% intervention-free births in some settings (which include high-risk births) still mean that C-section rates of up to 50% and induction rates of 20-30% are not at all justified. Moreover, if our current overuse of oxytocin-based interventions really has the power to mess with our ability as a species to give birth, breastfeed, love, and function socially and sexually, this would be a very strong argument to not use artificial oxytocin, unless absolutely necessary. By no means should this theory be used to justify more interventions.
Epigenetics and the evolution of our oxytocin system
Epigenetics is the study of external or environmental factors that turn genes on and off and affect how cells read genes. Epigenetics explains why identical twins, who, by definition, have the exact same DNA, do not look (nor behave) completely identically. After all, during their development (both before and especially after birth), there were certain (perhaps subtle) differences in experience and environment that turned some genes on or off in one twin and not in the other. In the nature versus nurture debate, gene expression is the way that the environment influences nature. Therefore, during certain critical periods, the environment (nurture) is at least as important as the actual genetic code (nature) in terms of outcome. Experimental psychologist Bruce Hood compares genes with books in a library. If the library is the full genome, then the genes (books) can be read to build the proteins that make up our body and define how it works. Epigenetic processes act like moving a book out of reach or blocking access to it by putting some furniture in front of it so the information can’t be read anymore. For each gene there is a critical period (or perhaps several) after which the gene is either turned on or off and once the critical period is over, this ‘setting’ can no longer be changed. One of those critical periods is early life. In recent years researchers have shown that, for example, nutrition in early life (maternal diet while pregnant and neonatal diet) affects gene expression and thus the susceptibility to several diseases in adulthood. It is thought that epigenetics is one of the mechanisms responsible for the fact that breastfed children have lower incidences of several acute and chronic diseases.
Epigenetic inheritance and the primal period
Epigenetic markers (the epigenome) may be transmitted from generation to generation, thereby providing a much faster mechanism of evolution than Neo-Darwinian evolution. The latter is an extremely slow and gradual process by which small changes in DNA that provide an evolutionary advantage accumulate over long periods. In epigenetics there are no changes in the actual DNA, and despite its inheritability, the epigenetic markers may reverse back when the environment during the critical period is different. The mechanism believed to be responsible for most epigenetic inheritance in humans is the environment of the womb influencing persistent gene expression in the foetus. For women who breastfeed their children, breastmilk may also be a source of transfer of epigenetic markers. In summary: the primal period (as defined by French obstetrician Michel Odent as the period of foetal life, perinatal period and year following birth) is a major critical period, not only in terms of environment influencing gene expression, but also for transferral of epigenetic markers from mother to child.
The oxytocin system
In historic times and from an evolutionary perspective, our species’ survival depended heavily on the proper workings of our oxytocin system. Michel Odent refers to it as a physiological system to emphasize “its capacity to secrete oxytocin, to use it as a neuromodulator, to store it in the posterior pituitary gland, to release it in a pulsatile effective way, and to develop receptors”. If any part of our oxytocin system was faulty, we wouldn’t be able to go into labour, give birth and expulse the placenta and we wouldn’t be able to breastfeed. A faulty oxytocin system would mean that women would lose their babies and/or would die in childbirth. Since neither women nor their offspring would survive, the faulty genetic or epigenetic marker would not be passed on and would disappear from the population. This is what happened before the advent of obstetrics and formula. In recent times however, our species survival no longer depends on our physiological oxytocin system. If labour doesn’t come on naturally, we induce it. In many hospital settings, the expulsion of the placenta no longer relies on our own secretion of oxytocin, but is helped along by drugs. If labour really takes too long, we perform a C-section. If we can’t or choose not to breastfeed, we give our baby formula. And most mothers who chose to breastfeed only do this for a few months before changing to formula, opposed to the years of breastfeeding that were customary among our ancestors and are still common in certain parts of the world and among a minority of mothers in the Western world. It is not only possible to go through the whole process of giving birth and raising a child without relying on our own oxytocin system, it is now becoming the norm rather than the exception in the developed world. This means that a less than optimal oxytocin system is likely to be present in an ever-growing population of mothers and their children, as the oxytocin system is shown to be influenced by epigenetic processes, the markers of which can be inherited during the primal period.
So why do we still care about our natural oxytocin system in this age of obstetrics and formula? One problem is that childbirth and breastfeeding are not the only processes that depend on oxytocin. A less than optimal oxytocin system can have far ranging repercussions on our ability to bond, love, feel empathy, and function socially and sexually. Research across species has shown that oxytocin plays a key role in attachment, social exploration, social recognition, and anxiety and stress-related behaviours. Research in 2015 indicates that our oxytocin system is involved in regulation of the fear response and that epigenetic modification of the oxytocin receptor gene may help explain why certain people are more susceptible or resilient to mental disease. It has been observed that part of the oxytocin system is impaired in mental disorders associated with social deficits: autism, borderline personality disorder and social anxiety disorder, all of which have been on the rise in the last decades. Another research article shows that the epigenetic regulation of the oxytocin receptor may be an important factor in the development of autism, which now affects between 1 in 300 to 1 in 100 people.
Autism and Attention Deficit Hyperactivity Disorder (ADHD)
At this point we cannot unequivocally prove that the underuse of our oxytocin system during labour, childbirth, afterbirth and infant feeding results in an impairment of our own and our children’s oxytocin system, but we can say that we know at least one of the mechanisms by which this would be possible: epigenetic regulation of the oxytocin receptor during the primal period. Moreover, there is mounting evidence that points towards long-term consequences of our modern way of birthing and infant feeding on processes that rely on oxytocin. Here are just a few examples considering autism and Attention Deficit Hyperactivity Disorder (ADHD).
- A 2013 research study found that labour induction or augmentation was associated with an increased risk of childhood diagnosis of an autism spectrum disorder.
- In a large 2004 Australian study perinatal conditions of a group of nearly 500 autistic people were compared to their non-autistic siblings. Results showed that the autistic group was more likely to have been induced and have experienced foetal distress at birth.
- A 2011 study showed that induction with artificial oxytocin was a risk factor for developing ADHD in childhood, as well as bipolar disorder and cognitive impairment .
- A 2013 research paper shows an association between lack of breastfeeding at 3 and 6 months of age and the diagnosis of ADHD between 6 and 12 years of age.
And the list goes on.
In this excerpt from my book on pregnancy and childbirth I explore Michel Odent’s hypothesis that our species has evolved to be worse at childbirth than earlier generations. The text includes interesting and scary research that shows a possible link between induction with artificial oxytocin (syntocinon or pitocin) and mental disorders such as autism, ADHD and borderline disorder.
Click here to read more excerpts of:
Making informed decisions on childbirth
One scientist’s international perspective
by Sofie Vantiers, Ph.D.
- Odent, M., Childbirth and the Evolution of Homo Sapiens. 2nd revised edition ed. 2014: Pinter & Martin Ltd. 160.
- Hood, B., Getting Under Your Skin, in The Domesticated Brain. 2014, Pelican. p. 224.
- Canani, R.B., et al., Epigenetic mechanisms elicited by nutrition in early life. Nutr Res Rev, 2011. 24(2): p. 198-205.
- Verduci, E., et al., Epigenetic effects of human breast milk. Nutrients, 2014. 6(4): p. 1711-24.
- Kumsta, R., et al., Epigenetic regulation of the oxytocin receptor gene: implications for behavioral neuroscience. Front Neurosci. 7: p. 83.
- Puglia, M.H., et al., Epigenetic modification of the oxytocin receptor gene influences the perception of anger and fear in the human brain. Proc Natl Acad Sci U S A. 112(11): p. 3308-13.
- Gregory, S.G., et al., Genomic and epigenetic evidence for oxytocin receptor deficiency in autism. BMC Med, 2009. 7: p. 62.
- Gregory, S.G., et al., Association of autism with induced or augmented childbirth in North Carolina Birth Record (1990-1998) and Education Research (1997-2007) databases. JAMA Pediatr. 167(10): p. 959-66.
- Glasson, E.J., et al., Perinatal factors and the development of autism: a population study. Arch Gen Psychiatry, 2004. 61(6): p. 618-27.
- Kurth, L. and R. Haussmann, Perinatal Pitocin as an early ADHD biomarker: neurodevelopmental risk? J Atten Disord. 15(5): p. 423-31.
- Freedman, D., Brown, A.S., Shen, L., Schaefer, C.A., Perinatal oxytocin increases the risk of offspring bipolar disorder and childhood cognitive impairment. J Affect Disord, 2015, 173: p. 65-72.
- Mimouni-Bloch, A., et al., Breastfeeding may protect from developing attention-deficit/hyperactivity disorder. Breastfeed Med, 2013. 8(4): p. 363-7.