Primal Health Research


“Primal Health Research” explores correlations between the ‘primal period’ (from conception until the first birthday) and health in later life. In the book “Primal Health”(first edition 1986)1 we predicted a new generation of research confirming that our health is shaped during the primal period. In order to prepare for a renewed understanding of health and diseases, a simplified vocabulary was proposed(see glossary.) Today the point is not to anticipate a phenomenon, but to observe its development and to draw preliminary conclusions. From 1993 onwards, our quarterly newsletter did just that. Since 1998 a computerized database is a necessity.

It is not possible to identify the studies which belong to this new framework through the usual scientific and medical networks, because they are unrelated according to the current classifications. For example it would take a long time – without appropriate keywords – to find out that a pregnancy disease such as pre-eclampsia has been studied in relation to health conditions as diverse as prostate cancer, breast cancer, schizophrenia, mental retardation and cerebral palsy.


SuniIn July 1982 I was invited to speak in Oxford at a conference organized by the McCarrison Society. My presentation, entitled ‘Childbirth and the diseases of civilization’, was a plea for a new kind of research to test the hypothesis that our health is to a great extent shaped at the very beginning of our life. We already had theoretical reasons to suppose that the sudden increased incidence of certain pathological conditions might be related to new powerful ways to interfere with the physiological processes in the perinatal period. At this conference I met Niko Tinbergen, one of the Nobel Prize winners in 1973 as a founder of ethology. He was the pioneer I was looking for since he had explored the risks for autism in relation to how the child was born. The correspondence we had afterwards encouraged me to prepare a book about the concept of health and what makes human beings more or less healthy.

This is how in 1986 I published the first edition of ‘Primal Health’1 Then we could predict that the spectacular advances in computer sciences would facilitate the new generation of research we were waiting for. It would become suddenly easier to explore correlations between what happens at the beginning of our life and what will happen later on in terms of health and personality traits.

I was convinced that we had to prepare for this new generation of research, first by adapting our vocabulary. I had to give a definition of ‘the beginning of our life’. The period of human development when the basic adaptive systems – those involved in what we commonly call health – reach their maturity was called ‘primal period’: it includes fetal life, the perinatal period, and the year following birth. I also underlined the need for a simple term in order to get rid of the artificial and obsolete separations between the nervous system, the immune system and the endocrine system. I suggested the term ‘primal adaptive system’ when referring to this network: a way to avoid awkward terms such as ‘psycho-neuro-immuno-endocrinologic system’. Health is how well our primal adaptive system works. ‘Primal health’ is the basic state of health in which we are at the end of the primal period; after that we can take advantage and cultivate this basic state of health. ‘Primal health research’ is this new framework of studies exploring correlations between what happens during the primal period and what will happen later on in life

After the publication of ‘Primal Health’, the next step was to create in 1987 the ‘Primal Health Research Centre’, based in London. Apart from occasional studies we can do by ourselves, our objective is to compile in the medical and scientific literature all studies that belong to the framework of primal health research. An explosion of such studies started in the late 1980s. First I was just collecting and classifying printed articles. It is around 1990 that variants of the hypotheses included in “Primal Health” appeared in the mainstream medical literature. The “fetal origins of disease hypothesis” was inspired by the countless studies published by the “Barker group”, a team of British epidemiologists based in Southampton. It became the “fetal/infant origins of disease hypothesis” in the mid-1990s2. There are obvious similarities between the “studies testing the fetal/infant origins of disease hypothesis” and “Primal Health Research”. One of the main differences is that our key word is “health” instead of “disease”. This gives an opportunity to stress that my first preoccupation has been to understand the genesis of a good health, while the “Barker hypothesis” leads to focus on the origins of a small number of specific illnesses, particularly metabolic and cardiovascular pathological conditions3. Improving our understanding of health may appear more fruitful than studying the origins of particular diseases.

In 1993 I was asked to prepare a second edition of ‘Primal Health’. I thought it was impossible to update a book about such a fast evolving field of research. It was more relevant to launch a quarterly newsletter to provide updated information to a small core of supporters who had already understood the importance of this new generation of research. Thus the first issue of the ‘Primal Health Research Newsletter’ was published in summer 1993: the topic was: ‘can drug addiction start at birth?’ Since that time another issue of the newsletter has been published every three months. Each issue can be presented as an essay on one particular subject in relation to Primal Health Research. Our essays are reproduced in the Journal of prenatal & perinatal psychology and Health and also in the website of APPPAH, the Association for prenatal & perinatal psychology and Health (visit Some of these essays have been modified in order to be included in the objective of this website is to convince anyone that prenatal ecology is the most vital aspect of human ecology, and that the period inside the womb is the life period with the highest adaptability and vulnerability to environmental factors.

In the late 1990s the spectacular advances in information technology and the fast development of primal health research led us to create a database available on the web. Today access to the Primal Health Research Database is free. We need this database because it is difficult to identify – among thousands of scientific and medical journals – studies that belong to this new framework: they are unrelated according to the current classifications. For example it would take a long time to find out that a pregnancy disease such as pre-eclampsia has been studied in relation to health conditions as diverse as prostate cancer, breast cancer, hypertension, asthma, allergic rhinitis, diabetes type 1, body size, age at menarche, behavior disorder, schizophrenia, mental retardation and cerebral palsy. After the Primal Health Research Database was established, I accepted to re-publish the book ‘Primal Health’ without any alteration of the original text. We just added an introduction to the second edition.2 This new edition was a useful document to evaluate the progress of primal health research within two decades. The original 1986 chapter ‘Research in Primal Health’ was followed by only 15 references!

One of the possible functions of our database is to train ourselves to think long-term. Human beings have not been programmed for long-term thinking. For millions of years our tropical ancestors consumed the food they could find from day to day in their environment, either by collecting shellfish and small fish in shallow water, by gathering plants and fruits, or by scavenging and hunting. After the comparatively recent advent of agriculture and animal breeding, they had to increase their capacity to anticipate. They were obliged to think at least in terms of seasons. Today we have at our disposal such powerful technologies that we must suddenly learn to think in terms of decades and centuries.

The sudden emergence in the scientific literature of the phrase ‘gene expression’ as a frequent keyword has suddenly assigned to our database an unexpected important new function.

Today the database contains hundreds of studies that have been published in authoritative medical and scientific journals. We offer a list of keywords and a list of authors in order to facilitate access to the relevant references and abstracts. In all fields of medicine and health sciences there are already studies that belong to the framework of primal health research. The advantage of our database is to offer an overview of hundreds of studies and to draw conclusions. Only such an overview can support our primary hypothesis that our health (including our capacity to love) is shaped during the primal period. Primal Health Research leads to a new understanding of the word ‘health’.

1. Odent M. Primal Health. Century Hutchinson. London 1986 (paperback 1987).
2. Odent M. Primal Health. 2nd edition. Clairview Books. Forest Row (UK) 2002.
3. Gluckman PD, Hanson MA, Cooper C, Thornburg KL. Effect of In Utero and Early-Life Conditions on Adult Health and
Disease. NEJM 2008; 359: 61-73.


The recent emergence in the scientific literature of ‘gene expression’ as a frequent keyword has suddenly assigned an unexpected new function to our database.

Apart from purely genetic diseases such as Down syndrome, cystic fibrosis, colour blindness, haemophilia, phenylketonuria, Huntington’s chorea, sickle-cell disease, or Turner syndrome, it is now well-accepted that both genetic and environmental factors are at the origin of most pathological conditions and personality traits.

Until recently, it was commonplace to contrast genetic and environmental factors. There have been endless discussions about the relative contributions of these two factors. Such discussions led in particular to twin and adoption studies, in order to disentangle the effects of genes versus environment. Today many geneticists aim to identify genes involved in the predisposition towards specific diseases while epidemiologists look for environmental risk factors. The dialogue has always been difficult between those who tend to exaggerate the genetic factors and those who tend to minimize them. We are still under the indirect influence of the obsolete Nature versus Culture debates based on narrow preconceived ideas. The view that humans acquire all, or almost all, their traits from “nurture” was known as tabula rasa. The opposite view was the basis for philosophical movements such as ‘Nativism’ and ‘Innatism’.

Today the concept of ‘gene expression’ is a turning point regarding our understanding of the origin of pathological conditions and personality traits. We are now in a position to explain that some of our genes express themselves, while others become silenced; of course they still exist and they will reappear within the next generation. Gene expression is the process by which inheritable information from a gene, such as a DNA sequence, is made into a functional gene product, such as a protein or RNA. It has been demonstrated that methylation of DNA is a common method of gene silencing.


Gene expression is to a great extent dependent on environmental factors during the primal period. We must constantly keep this important point in mind. That is why, in the current scientific context, the first questions related to disease causation are not about the identification of the genes involved or the relative roles of genetic and environmental factors. The questions are about the timing. They concern the critical periods for genes-environment interaction. This is why the Primal Health Research Database is suddenly assigned an unexpected new function. The database has become a unique tool to provide some clues about the critical period for the genesis of states of health, pathological conditions, and personality traits. It can even contribute to an unprecedented classification of health conditions according to their critical period for genes-environment interaction.


In order to illustrate this new role of the primal health research database, we’ll explore the possible links between autism and anorexia nervosa, two conditions that, according to the data we have at our disposal, are to a great extent determined during the perinatal period. The mysterious increased prevalence of both diseases, concomitantly, is one of the reasons why we choose this example. It is well-accepted today that the increased prevalence in these two conditions is not simply resulting from improved diagnostic and greater public awareness.

Among the three recent large and authoritative studies of autism from a Primal Health Research perspective, the Australian study will convince anyone that the main risk factors occur in the perinatal period.1 The 465 subjects born in Western Australia between 1980 and 1995 and diagnosed with an autism spectrum disorder by 1999 were compared with the birth records of 481 siblings of the cases, and with 1313 controls. No differences in gestational age at birth (including premature infants), weight for gestational age, head circumference, or length were observed between cases and control subjects. Pre-eclampsia did not appear as a risk factor. These negative findings lend more credence to perinatal factors. Compared with their siblings, autism cases were more likely to have been induced, to have experienced fetal distress, and to be born with a low Apgar score. Compared with control subjects, they were more likely to be born after induction and to be born by elective or emergency c-section.

Similar conclusions can be drawn from a study involving all Swedish children born from 1974 to 1993. No association was found between autism and head circumference, maternal diabetes, being a twin, or season of birth, while c-section appeared to be a risk factor.2 This study could not consider labour induction as a possible risk factor, since this term did not appear in the Swedish birth registers until 1991. A recent report from Israel also found no prenatal differences between autistic children and controls, but the rates of birth complications were higher among the autistic population.3 We must add to these negative findings a series of studies exploring the possible links with different types of vaccinations in infancy. These, too, indirectly give weight to the perinatal factors. All epidemiological studies included in our database confirm that the risks of autism seem to be the same among children who did or did not receive MMR.4,5,6,7 They also seem to be the same among children who had or had not received a vaccine containing a mercury derivative.8 If we take into account that the risk of autism is not related to the mode of infant feeding (breast or bottle) we must conclude that the significant risk factors precede infancy.

We can draw similar conclusions from a large and authoritative Swedish study of risk factors for anorexia nervosa. The researchers had access to the birth records of all girls born in Sweden from 1973 to 1984,9 and of the 781 girls who had stayed in a Swedish hospital due to anorexia nervosa between age 10 and age 21. For each anorexic girl there were five controls (non-anorexic girls born in the same hospital during the same year). Apart from being born before 32 weeks gestation, the most significant risk factor for anorexia nervosa was a cephalohematoma at birth. Forceps and ventouse deliveries were also risk factors. An Italian retrospective study of subjects with eating disorders found that the risk of developing anorexia nervosa increased with the total number of obstetric complications. In addition, an increasing number of complications significantly anticipated the age of onset of anorexia nervosa.10

It appears from this Italian study that being shorter for gestational age significantly differentiates subjects with bulimia nervosa from those with anorexia nervosa. A study of smoking in pregnancy as a risk factor for bulimia nervosa also suggests that the concept of ‘eating disorder’ should be dismantled. Anorexia nervosa and bulimia nervosa should be studied separately. Not only can Primal Health Research establish links between pathological entities, but it can also dismantle of pre-existing entities.


The links suggested by the primal health research perspective between anorexia and bulimia prompt us to wonder what we can learn from other perspectives. This question inevitably leads to refer to clinical considerations mentioned by several teams of psychiatrists. Janet Treasure et al of the Institute of Psychiatry of King’s College hospital, in London, have emphasized the importance of autistic traits in anorexia nervosa.11 People with anorexia nervosa find it difficult to change self-set rules; they see the world in close-up detail, as if they were looking through a zoom lens, and risk getting constantly lost in the details.12 Christopher Gillbert and the team of the Department of Child and Adolescent Psychiatry at Goteborg University in Sweden, found that 23% of female patients with severe eating disorders had symptoms of the autism spectrum.13

The oxytocin system in both conditions offers another promising avenue of research. The first clues came from a study of midday blood samples from 29 autistic and 30 age-matched normal children.14 The autistic group had significantly lower blood oxytocin levels than the normal group. Oxytocin increased with age in the normal but not the autistic children. These results inspired an in-depth inquiry into the oxytocin system of autistic children. In recent years it has become clear that oxytocin can appear in the brain in several forms. There is the nonapeptide oxytocin (OT) and the ‘C-terminal extended peptides’, which are described together as OT-X. The OT-X represent intermediates of oxytocin synthesis that accumulate due to incomplete processing. Twenty-eight male children diagnosed with autistic disorder were compared with 31 age-matched non-psychiatric control children: there was a decrease in blood OT, an increase in OT-X and an increase in the ratio of OT-X/OT in the autistic sample, compared with control subjects.15 In other words, autistic children show deficits in the processing of oxytocin.

There have not been such in-depth inquiries into the oxytocin system of anorexic patients. However, it has been reported that the level of oxytocin in the cerebrospinal fluid of women with ‘restricting anorexia’ is significantly lower than the level of oxytocin in bulimic and control subjects.16 Such studies of the oxytocin system provide new reasons to dismantle the framework of ‘eating disorders’ while reinforcing the links between anorexia and autism. They offer interpretations of the perinatal period as critical in the origin of both conditions, since it is a time when the oxytocin system is highly-challenged, with a deep redistribution of the specific neuroreceptors. These are important considerations when the physiological processes in the perinatal period are routinely disturbed as happens these days.


Until now nosology – the naming and classification of diseases – was mostly based on descriptions of symptoms (e.g. scarlet fever), on altered functions (e.g., hyperthyroidism) or on altered organs (e.g., myocardial infarction). Today, the Primal Health Research Database makes possible a classification according to critical periods for genes-environment interaction. After studying in parallel anorexia nervosa and autism, one can reinforce the suggestions expressed by some psychiatrists that anorexia nervosa might be considered a female variant of the autistic spectrum. A plausible interpretation of why it is undoubtedly more female is that prenatal exposure to male hormones might protect against the expression of anorexia nervosa. Such an interpretation is suggested by a study of twins.17 Girls who have a twin brother were at low risk of anorexia nervosa, compared with girls who had a twin sister and with controls. This interpretation is reinforced by the negative results of genetic linkage analyses that could not detect any change on the X chromosome.18

With the fast development of primal health research we can anticipate that new nosological entities will appear while others will more or less fall away.


  1. Glemma EJ, Bower C, Petterson B, et al. Perinatal factors and the development of autism. Arch Gen Psychiatry 2004; 61: 618-27.
  2. Hultman C, Sparen P, Cnattingius S. Perinatal risk factors for infantile autism. Epidemiology 2002; 13: 417-23.
  3. Stein D, Weizman A, Ring A, Barak Y 2006. Obstetric complications in individuals diagnosed with autism and in healthy controls. Compr Psychiatry Jan-Feb;47(1):69-75.
  4. Taylor B, Miller E, et al. Autism and measles, mumps, and rubella vaccine: no epidemiological evidence for a causal association. Lancet 1999; 353: 2026-9.
  5. Kaye JA, Melero-Montes M, Jick H. Mumps, measles, and rubella vaccine and the incidence of autism recorded by general practitioners: a time trend analysis. BMJ 2001; 322: 460-3.
  6. Dales L, Hammer SJ, Smith NJ. Time trends in autism and in MMR immunization coverage in California. JAMA 2001; 285 (9): 1183-5.
  7. Madsen KM, Hviid A, et al. A population-based study of measles, mumps, and rubella vaccination and autism. N Engl J Med 2002; 347(19): 1474-5.
  8. Hviid A, Stellfeld M, Wohlfahrt J, Melbye M. Association between thimerosal-containing vaccine and autism. JAMA. 2003 Oct 1;290(13):1763-6.
  9. Cnattingius S, Hultman CM, Dahl M, Sparen P 1999 Very preterm birth, birth trauma and the risk of anorexia nervosa among girls. Arch Gen Psychiatry 56: 634-38.
  10. Favaro A, Tenconi E, Santonastaso P 2006 Perinatal factors and the risk of developing anorexia nervosa and bulimia nervosa. Arch Gen Psychiatry 63(1):82-8.
  11. Hambrook D, Tchanturia K, Schmidt U, Russell T, Treasure J. Empathy, systemizing, and autistic traits in anorexia nervosa: A pilot study. Br J Clin Psychol. 2008 Sep;47(Pt 3):335-9. Epub 2008 Jan 21.
  12. Southgate L, Tchanturia K, Treasure J. Information processing bias in anorexia nervosa. Psychiatry Res. 2008 Jun 23. (Epub ahead of print).
  13. Wentz E, Lacey JH, Waller G, Råstam M, Turk J, Gillberg C Childhood onset neuropsychiatric disorders in adult eating disorder patients. A pilot study. Eur Child Adolesc Psychiatry 2005 Dec;14(8):431-7.
  14. Modahl C, Green L, et al. Plasma oxytocin levels in autistic children. Biol Psychiatry 1998; 43 (4): 270-7.
  15. Green L, Fein D, et al. Oxytocin and autistic disorder: alterations in peptides forms. Biol Psychiatry 2001; 50 (8): 609-.
  16. Demitrack MA, Lesem MD, Listwak SJ, et al. CSF oxytocin in anorexia nervosa and bulimia nervosa: clinical and pathophysiologic considerations. Am J Psychiatry 1990 Jul;147(7):882-6.
  17. Culbert KM, Breedlove SM, Burt SA, Klump KL. Prenatal hormone exposure and risk for eating disorders: a comparison of opposite-sex and same-sex twins. Arch Gen Psychiatry. 2008 Mar;65(3):329-36.
  18. Devlin B, Bacanu SA, Klump KL et al. Linkage analysis of anorexia nervosa incorporating behavioral covariates. Hum Mol Genet. 2002 Mar 15;11(6):689-96.

CLICK HERE to Search the Database by Keyword


In the book ‘Primal Health’ (1986) we proposed a simplified vocabulary in order to adapt to a new scientific context.

The primal period includes fetal life, perinatal period and early infancy (from conception until the first birthday).

Primal health research includes all studies exploring correlations between the primal period and health and behaviour later on in life.

The Primal adaptive system refers to the basic adaptive systems involved in what we commonly call health. The nervous system, the endocrine system, and the immune system should no longer be separated and should be understood as a whole (e.g. the brain is a gland, insulin is a neuromediator, lymphocytes can release endorphins, etc..). We need a simple term such as ‘primal adaptive system’ to replace complex phrases still used in the scientific literature, (e.g. ‘psychoneuroimmunoendocrinologic system’).

The ‘primal period’ may be presented as the period of maturation of the primal adaptive system. Health is how well the primal adaptive system works (it is not the absence of disease). At the end of the primal period we are in a basic state of health called ‘primal health’.

In order to clarify the meaning of ‘set point levels’ we proposed a comparison with a thermostat, which is set to a particular temperature at the beginning of the day.

BIOGRAPHY Michel Odent, MD

– Born in France in 1930.
– Medical studies at Paris University
– In charge of the surgical unit and the maternity unit at the Pithiviers state hospital (1962-1985).
– Founder of the Primal Health Research Centre (London).

– Introduced in the 1970s the concept of birthing pools in maternity hospitals. Author of the first article in the medical literature about the use of birthing pools (Odent M. Birth under water. Lancet 1983; i:1476-77).

– Introduced in the 1970s the concept of home-like birthing room in maternity hospitals (Jane Gillett. Childbirth in Pithiviers, France. Lancet 1979; i:894-96).

– Author of the first article in the medical literature about the initiation of lactation during the hour following birth (Odent M. The early expression of the rooting reflex. Proceedings of the 5th International Congress of Psychosomatic Obstetrics & Gynecology, Rome. London: Academic Press 1977: 1117-1119).

– Author of the first article applying the ‘Gate Control Theory of Pain’ to obstetrics (Odent M. La réflexotherapie lombaire. Nouvelle Presse Médicale 1975 (4):188)

– Founded the Primal Health Research Centre (London, UK). The objective is to test the assumption that human health is shaped during the ‘primal period’, which includes fetal life, perinatal period, and year following birth. (Michel Odent. Primal Health. London: Century Hutchinson, 1986)

– Created the Primal Health Research database, the only specialized database compiling studies that explore the long term consequences of what happened during the ‘Primal period’ (

– Created the website ‘’, in order to convince anyone that the most vital form of human ecology is prenatal ecology (concept already included in ‘Genèse de l’homme écologique’. Paris Epi 1979)

– Studies in progress to evaluate the effects of encouraging pregnant women to consume sea fish (Odent M, McMillan L, Kimmel T. Prenatal care and sea fish. European Journal of Obstetrics & Gynecology 1996 (68):49-51 and Odent M. Plea for a new generation of research in eclampsia. Clinical effectiveness in nursing 2006; 952: e232-e237)

– Author of 12 books in 22 languages. His 21st century books include ‘The Scientification of Love’, ‘The Farmer and the Obstetrician’, and ‘The Caesarean’. His 2008 book is entitled ‘The Functions of the orgasms: the highways to transcendence’.


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