Finnish researchers looked at the risks of having asthma and allergic diseases among adults aged 31 (in a population born in 1966). It appeared that those born by caesarean had a risk of having asthma multiplied by 3.23 compared with those born by the vaginal route.(2) On the other hand, the risks of having allergic diseases such as hay fever or eczema, or the risks of having an allergic tendency detected by skin tests, were not increased. The same team looked at the risks of having asthma in childhood, at age seven.(3) They found that birth complications in general, and caesarean births in particular, were risk factors. Another Finnish team linked data from the 1987 National Birth Register with data from several health registers to obtain information on asthma. This study, involving nearly 60 000 children, confirmed that the risks of having asthma in childhood were increased among those born by caesarean.(4) A Danish study also found that a caesarean birth is a risk factor for asthma, but not for allergic rhinitis,(5) while a British study confirmed that there are no increased risks for allergies following a caesarean birth.(6)

When trying to interpret such convergent findings, I cannot help thinking of the well-documented fact that respiratory problems of the newborn baby are significantly more frequent after a scheduled ‘non-labour’ caesarean than after a birth by the vaginal route or a caesarean during labour. Unfortunately none of these studies found in our data bank compared ‘labour caesareans’ and ‘non-labour caesareans’. Today we are in a position to understand that the fetus is supposed to participate in the initiation of labour. One of the probable ways is by giving a signal, which is the release in the amniotic fluid of a substance indicating that its lungs are mature. Furthermore it seems that hormones released by mother and baby during the birth process can give a last touch to the maturation of the lungs.(7) It is therefore easy to anticipate that babies born by non-labour caesarean are more at risk of respiratory difficulties not only immediately after birth, but also later on in life(8) It is noticeable that a caesarean birth appears as a risk factor for asthma as a respiratory disease, but not as an allergic disease.

While a caesarean birth is not a significant risk factor for allergic diseases properly speaking (those classified as ‘atopic’, such as hay fever, allergic rhinitis and eczema), it might increase the risk of food allergy. According to a Norwegian study, caesarean born children of allergic mothers are at high risk of being allergic to eggs, fish and nuts.(9)

At a time when about one million Americans, several millions Chinese, and many others are born every year ‘from above’, one can wonder why the keyword caesarean, compared with many other key-words, does not lead us to a greater number of entries. The first obvious reason is that ‘Primal Health Research’ is a new discipline that has difficulties at establishing itself, since scientists are human beings who had not been genetically programmed to think long-term. It is significant that all papers relating caesarean and asthma have been published after the dawn of the twenty first century. Another reason is that most research protocols exploring risk factors in the period surrounding birth use imprecise concepts such as ‘birth complications’ or ‘birth optimality’(scores measuring how a person was born compared with what is considered optimal). The results of this group of studies suggest that the way we are born has life-long consequences, but do not provide details about the effects of specific deviations from the physiological model.

In the current obstetrical context, we need answers to such urgent questions as: ‘What are the long-term effects of being born by ‘non-labour caesarean’. It seems that researchers have not realized that today a great part of humanity is already born by ‘non-labour caesarean’. There are many reasons to contrast ‘in-labour’ and ‘non-labour’ caesareans. A non-labour caesarean implies that the fetus has not participated in the initiation of labour. Today we are in a position to explain that the fetus is able to send signals when he (she) is ready to be born. For example, when the baby’s lungs have reached a certain degree of maturation, they can release in the amniotic fluid factors that will activate the system of prostaglandins.
The medical literature cannot yet satisfy the curiosity of those who think long-term. For example once I stumbled on a study of children whose mothers were depressed three months after giving birth; at age eleven, these children were more likely to exhibit violent behaviours, including fighting at school and using weapons during fights. My first reaction was to wonder if there is an increased risk of postnatal depression after caesarean. Not only is it difficult to find more than a couple of studies suggesting that after an emergency caesarean section the risk of maternal depression is increased (multiplied by seven according to an Australian study),(10) but it is impossible - until now - to find a study focusing on the risks after a non-labour caesarean.

There are many reasons to go beyond the keyword ‘caesarean’ when exploring the database. Since the modern safe caesarean has the capacity to reduce the incidence of long and difficult labours by the vaginal route, in particular operative deliveries (forceps and even ventouse), we have to look at all studies detecting risk factors in the perinatal period in general and compare the benefits and risks of different deviations from the physiological model.

An overview of the bank leads us to notice that when researchers explore the background of people who have expressed some sort of “impaired capacity to love” - either love of oneself or love of others - they always detect risk factors at birth. “Impaired capacity to love” is a convenient term to underline the links between all these conditions. It includes self-destructive behaviour. That is why I present Primal Health Research as a discipline that participates in the “scientification of love”.(11) Furthermore when researchers find risk factors in the period surrounding birth, it is always about a very important issue specific to our time – either a condition which can be defined as an ‘impaired capacity to love’ or a clear-cut medical condition such as asthma.

Here are typical examples of conditions I classify in the framework of ‘impaired capacity to love’: juvenile violent criminality, suicides, drug addiction, anorexia nervosa and autism. All of them have been studied from a Primal Health Research perspective.
Autism can be taken as an example to illustrate the sort of research that has already been done, and also to call attention on the need for a new generation of studies. Autism is undoubtedly topical. It can be presented as an impaired capacity to love. My interest in autism started in 1982, when I met Niko Tinbergen, one of the founders of ethology, who shared the Nobel prize with Konrad Lorenz and Karl Von Frisch in 1973. As an ethologist familiar with the observation of animal behaviour, he studied in particular the non-verbal behaviour of autistic children. As a "field ethologist" he studied the children in their home environment. Not only could he offer detailed descriptions of his observations, but at the same time he listed factors which predispose to autism or which can exaggerate the symptoms(12).

He found such factors evident in the period surrounding birth: induction of labour, "deep forceps" delivery, birth under anaesthesia, and resuscitation at birth. Interestingly this pioneer introduced the variable ‘labour induction’. When I met him he was exploring possible links between difficulty in establishing eye-to-eye contact among autistic children and the absence of eye-to-eye contact between mother and baby at birth. The work of Tinbergen (and his wife) represents the first attempt to explore autism from a "primal health research" perspective.

It is probably because I met Niko Tinbergen that I read with special attention, in June 1991, a report by Ryoko Hattori, a psychiatrist from Kumamoto, Japan.(13) She evaluated the risks of becoming autistic according to the place of birth. She found that children born in a certain hospital were significantly more at risk of becoming autistic. In that particular hospital the routine was to induce labour a week before the expected date of birth and to use a complex mixture of sedatives, anaesthesia agents and analgesics during labour. This study could not dissociate the effects of labour induction and the effects of drugs used during labour.

We had to wait until 2002 for a large-scale study to be published in the medical literature.(14) The researchers had at their disposal the recorded data from the Swedish nationwide Birth Register regarding all Swedish children born during a period of 20 years (from 1974 until1993). They also had at their disposal data regarding 408 children (321 boys and 87 girls) diagnosed as autistic after being discharged from a hospital from 1987 through 1994 (diagnosis according to strict criteria). For each case five matched controls were selected, resulting in a control sample of 2040 infants. The risk of autism was significantly associated with caesarean delivery, a 5-minute Apgar score below 7 (in other words: baby not in good shape at birth), maternal birth outside Europe and North America, bleeding in pregnancy, daily smoking in early pregnancy, being small for gestational age, and congenital malformations. Unfortunately the authors could not dissociate scheduled caesareans and caesareans during labour. Also, the variable ‘labour induction’ could not be taken into account, because it did not appear in the National Birth Register until 1991, as I learnt from personal correspondence with one of the authors.

A new phase was reached in our understanding of the risk factors for autism after the publication of an important Australian study that dissociated non-labour caesarean and in-labour caesarean, and that looked at labour induction.(15) This study included the 481 subjects born in Western Australia between 1980 and 1995 and considered autistic (in the framework of ‘autism spectrum disorder’). These subjects were compared with 1313 controls, and also with their 481 non-autistic siblings. By comparing with the controls, it appeared that among those born by non-labour caesarean the risks were multiplied by 2.05 (this was statistically significant) and among those born by emergency caesarean they were multiplied by 1.57 (statistically significant). Epidural anaesthesia, a delayed first breath, and an Apgar score below 7 were other risk factors. By comparing with the siblings, labour induction, delayed first breath, and Apgar score below 7 also were significant factors. There was also a tendency to more caesareans, but the difference was not statistically significant. It is noticeable that the duration of fetal life (and the rate of premature baby), birth weight in relation to the time spent in the womb, the rates of pre-eclampsia, head circumference and length at birth were the same in both groups. That there was no difference regarding the effects of pre-birth environment factors leads to give a greater importance to the in-labour intrauterine environment.

Other studies – all of them much smaller than the main Swedish one - have evaluated the rates of birth complications among autistic children by using different scores of ‘optimality’. It also appears from these studies that children with what is called today ‘autistic spectrum disorders’ have higher rates of birth complications. Is there a cause and effect relationship? Once more the concept of ‘labour induction’ does not appear in the protocols and results of such studies, and scheduled caesareans are not dissociated from caesareans during labour.(16,17,18,19)
There is food for thought in the results of a study suggesting that the symptoms of autism appear after an unusual pattern of brain growth with a sudden change after birth. During the year following birth there is a sudden and excessive increase in brain size.(18) We must keep in mind that the perinatal period is a period of re-organization of brain development. We must also give importance to the results of studies suggesting that children with autistic disorders show alterations in their oxytocin system…in the way they release their ‘hormones of love’.(20) From that point of view, the period surrounding birth can also be presented as a phase of re-organization.

From a cul-de-sac to an avenue

These studies looking at the long term consequences of how we are born have usually been shunned by the medical community and the media, despite their publication in authoritative medical and scientific journals, and although they explore highly topical conditions. Most of them have not been replicated, even by the original investigators, and they are rarely quoted after publication.

Because I have personally met the authors of several of these studies, I can offer some comments about this family of research. I came to the conclusion that research can be politically incorrect. Most researchers looking at how people were born have faced extreme bureaucratic difficulties. It may be that they are shaking the very foundations of our societies, insofar as the birth process has always been ritually disturbed. It may be also that very few people have developed their capacity to think long-term and are ready to perceive the importance of this developing field of research, which is a new branch of epidemiology. I recently coined the term ‘cul-de-sac epidemiology’ when referring to these studies.(21) This term contrasts with ‘circular epidemiology’ which has been used in order to describe a common and regrettable tendency to constantly repeat the same studies, even when there is no doubt about the results.

Several rules are apparent from an overview of this new generation of research. One of them is the 'wait-for-puberty' rule. It appears from animal experiments that often the consequences of early events - such as drugs used during labour or brain lesions at the time of birth - cannot be detected until puberty. This leads to a comparison with human health conditions (e.g. schizophrenia, drug addiction, anorexia, etc.) that cannot be recognised before puberty although risk factors are found during fetal life or the perinatal period. The 'wait-for-puberty' rule leads to caution when interpreting the results of studies with a follow-up shorter than 15 years. It leads to anticipate that there is a future for a new branch of medicine, specialized in the diseases of adolescents.

The new generation of research we are expecting will try to provide answers to questions of the future. Some of the new questions will be inspired by observations and experiments among mammals whose life span is much shorter than ours. For example, today, 90% of the ‘English bulldogs’ are born by scheduled caesarean. In addition, the English bulldog male’s lack of stamina does not allow successful mating, so that artificial insemination is needed. If there is a link between these two facts, we must at least raise questions about the possible particularities of genital sexuality of a human population born by scheduled caesarean.

A complementary lesson

While browsing the data bank in order to learn about the possible long-term consequences of being caesarean born, we learn a complementary lesson. We cannot miss a group of studies that detected the possible harmful long-term effects of all sorts of difficult births by the vaginal route. Key words such as forceps, ventouse (or vacuum), cephalhaematoma or resuscitation open the way to such studies. Finally an overview of the bank provides new reasons to disturb the birth process as little as possible, and therefore new reasons to improve our understanding of the basic needs of women in labour. We might also conclude that one of the main functions of the safe modern caesarean should be to make obsolete such a tool as the forceps, which is in addition associated with the risks of serious damages of maternal tissues.(22) Are we going towards a simplified two options basic strategy: either a straightforward birth by the vaginal route, or a caesarean during labour, if possible before the stage of emergency?

References:

1 - Odent M. Primal Health. 1st edition Century-Hutchinson 1986. 2nd edition Clairview 2002.
2 - Xu B, Pekkanen J, Hartikainen AL, Jarvelin MR. Caesarean section and risk of asthma and allergy in adulthood. J allergy Clin Immunol 2001; 107 (4): 732-3.
3 - Xu B, Pekkanen J, Jarvelin MR. Obstetric complications and asthma in childhood. J Asthma 2000; 37(7): 589-94.
4 - Kero J, Gissler M, Gronlund MM, Kero P, Koskinen P, Hemminki E, Isolauri E. Mode of delivery and asthma -- is there a connection? Pediatr Res. 2002 Jul;52(1):6-11
5 - Bager P, Melbye M, Rostgaard K, Stabell Benn C, Westergaard T. Mode of delivery and risk of allergic rhinitis and asthma. J Allergy Clin Immunol 2003 Jan;111(1):51-6
6 - McKeever TM, Lewis SA, Smith C, Hubbard R. Mode of delivery and risk of developing allergic disease. J Allergy Clin Immunol 2002 May;109(5):800-2.
7 - Faxelius G, Hagnevik K, Lagercrantz H, Lundell B, Irestedt I. Catecholamine surge and lung function after delivery. Arch Dis Child 1983: 58 (4): 262-66.
8 - Hook B, Kiwi R, Amini SB, Fanoroff A, Hack M. Neonatal morbidity after elective repeat cesarean section and trial of labour. Pediatrics 1997; 100: 348-53.
9 - Eggesbo M, Botten G, Stigum H, et al. Is delivery by cesarean section a risk factor for food allergy? J Allergy Clin Immunol 2003; 112(2): 420-6.
10 - Hay D, Pawlby S, Angold A, et al. Pathways to violence in the children of mothers who were depressed postpartum. Dev Psychol 2003; 39: 1083-94.
11 – Odent M. The Scientification of Love. Free Association Books. London 1999 (2nd ed 2001)
12 - Tinbergen N, Tinbergen A. Autistic children. Allen and Unwin. London 1983.
13 - Hattori R, et al. Autistic and developmental disorders after general anaesthetic delivery. Lancet 1991; 337: 1357-8.
14 - Hultman C, Sparen P, Cnattingius S. Perinatal risk factors for infantile autism. Epidemiology 2002; 13: 417-23.
15 - Glemma EJ, Bower C, Petterson B, et al. Perinatal factors and the development of autism. Arch Gen Psychiatry 2004; 61: 618-27.
16 - Zwaigenbaum L, Szatmari P, et al. Pregnancy and birth complications in autism and liability to broader autism phenotype. J Am Acad Child Adolesc Psychiatry 2002; 41: 572-79.
17 - Lord C, Mulloy C, et al. Pre- and perinatal factors in high-functioning females and males with autism. J Autism Dev Disord 1991; 21 (2):197-209.
18 - Wilkerson DS, Volpe AG, et al. Perinatal complications as predictors of infant autism. Int J Neurosci 2002; 112 (9): 1085-98.
19 - Iuul-Dam N, Townsend J, Courchesne E. Prenatal, perinatal and neonatal factors in autism, pervasive developmental disorders, and the general population. Pediatrics 2001; 107 (4): E63.
20 - Courchesne E, Carper R, Akshoomoff N. Evidence of brain overgrowth in the first year of life in autism. JAMA 2003; 290: 337-44.
21 - Odent M. Between circular and cul-de-sac epidemiology. Lancet 2000; 355: 1371
22 – Odent M. The Caesarean. Free Associations Books. London 2004

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