Antisocial behaviours from a primal health research perspective

As human beings we are endowed with gregarious tendencies. Like most other primates we need to live in groups. Since we are also endowed with the capacity to communicate in sophisticated ways, particularly through language, we create cultural milieus. Cultural milieus prescribe and proscribe behaviour, that is, what people should do and should not do given their social surroundings and circumstances. Norms are established, with at least some degree of consensus, that are enforced through social sanctions.

Because antisocial behaviour is contrary to the standards of the particular society, this framework is imprecise. Furthermore, there are many degrees of deviation from what is considered normal, and there are many sorts of deviations. In other words, the gregarious tendencies are unequal between the members of a given human group.

The Primal Health Research perspective will help us to overcome such difficulties and to include diverse personality traits, behaviours, and diseases under the same umbrella. When studying antisocial behaviours, the conventional barriers between medicine, criminology and the study of personality traits become blurred, even misleading. Nevertheless, they serve as reference points. We’ll first consider deviations that are usually studied within the framework of psychiatry.

Deviations usually classified as pathological.

- Schizophrenia

Schizophrenia is a productive keyword when exploring the Primal Health Data Bank. Increasing and converging evidence suggests that cerebral anomalies in this condition develop pre- and perinatally. An accumulation of data published after 1990 points to the conclusion that the pathogenesis of schizophrenia is a chapter of ‘womb ecology’.

The first clues provided by data concern head circumference at birth. “Pre-schizophrenic” newborn babies have a disproportionately smaller head circumference (in relation to body length) than controls.(1) Low birth weight and length, as well as low placental weight, are also risk factors.(2) Furthermore, the frequent minor physical anomalies (particularly anomalies of the mouth in males) associated with schizophrenia are obvious consequences of prenatal developmental defects.(3)

Studies of schizophrenia after prenatal exposure to famine are highly convincing. Those who spent the first half of their fetal life during the Dutch famine of winter 1944-1945 were at increased risk of becoming schizophrenic.(4) Rates of adult schizophrenia following prenatal exposure to the Chinese famine of 1959-1961 confirmed the Dutch data.(5)

Among diseases in pregnancy, we must give particular importance to influenza, which has been widely studied as a risk factor.(6,7) (Only one study failed to detect a correlation between schizophrenia and influenza prevalence during prenatal life).(8) Serologic evidence of prenatal influenza in the etiology of schizophrenia confirms the epidemiological data.(9) The existence of maternal influenza in pregnancy as a risk factor for schizophrenia can help interpret the numerous studies relating the keywords ‘seasonality of birth’ and ‘schizophrenia’. It is already known that in the Northern hemisphere there is a significant excess of winter/spring births among schizophrenic patients.(10,11) This is confirmed by an overview of the medical literature.(12 to 31) It appears also that the quarterly birth distribution of patients with schizophrenia is reversed in the Southern hemisphere, (13,14,22,28) and that season-of-birth effects are difficult to demonstrate in tropical and equatorial countries.(21,24,29) A relationship between maternal antibodies to toxoplasmosis and the risk of schizophrenia and other disorders of the schizophrenia spectrum in offspring has also been demonstrated.(32)

The most common pregnancy complications emerge as risk factors. A study covering all psychiatric hospital admissions and all hospital births in Scotland identified obstetric records of people born 1971-74 who were subsequently admitted to hospital with a diagnosis of schizophrenia, and then compared their standardised obstetric records with those of matched controls. There were 115 schizophrenic and control pairs involved. The former showed a highly significant excess of pregnancy complications. In particular, there was a significant excess of pre-eclampsia (10 versus 2).(33) All Swedish children born during 1973-79 were involved in a study linking data from the Swedish Birth Register with data from the Swedish Inpatient Register. Among boys whose mothers suffered bleeding during late pregnancy, the risk was multiplied by four.(34)

Drugs to treat diseases in pregnancy may cause more harm than the disease itself. A Danish study of 7999 individuals and 116 cases of schizophrenia found a significant association between second-trimester exposure to analgesics and increased risk of schizophrenia.(35) In a previous study of 7,866 individuals and 84 cases of schizophrenia, the same team of researchers had found that drugs prescribed to treat hypertension (particularly diuretics) in the third trimester conferred a 4.01-fold elevated risk.(36)

The risk of schizophrenia in relation to intrauterine pollution, particularly pollution with heavy metals, is a new and promising avenue for research. Lead levels of stored blood samples were collected from expectant California mothers between 1959 and 1966. A comparison was made between 44 women whose children went on to develop schizophrenia and 75 mothers whose children did not. Children of mothers whose blood topped 150 micrograms of lead per litre were twice as likely to develop schizophrenia as those whose blood levels were below this threshold.(37)

In spite of methodological difficulties, it has been possible to demonstrate that certain maternal emotional states in pregnancy are risk factors. In a Finnish study, data were collected prospectively in a cohort of 11,017 individuals born in 1966. In the sixth or seventh month of pregnancy mothers were asked whether the pregnancy was wanted, mistimed but wanted, or unwanted. Schizophrenia diagnoses were obtained from the Finnish hospital discharge register. The risk of later schizophrenia among unwanted children was raised compared with wanted or mistimed children even after adjustmenst for socio-demographics, pregnancy and perinatal variables (risk multiplied by 2.4).(38)

Animal experiments can help interpret epidemiological studies. Prenatal lesions of the hippocampi of rats apparently remain silent until adult life when there is an abnormally dramatic response to stress and challenge from amphetamines.(39) It seems highly probable, when taking animal experiments into account, that a developmental defect of the hippocampus during fetal life is one of the main components of the chain of events that lead to schizophrenia.

Several studies detected such risk factors in the perinatal period as fetal distress during labour, abnormal presentations and ‘complicated’ c-sections, while they could not detect any association between obstetric complications and family history of schizophrenia.(40, 41) In fact, the inclusion of multiple variables suggests that these complications may be partly secondary to earlier events. However, we must keep in mind that, in animal models, dopaminergic systems appear to be particularly vulnerable to a wide range of perinatal insults(42), and that schizophrenia is associated with alterations of dopaminergic functions.

It is noticeable that most studies could not find any protective effect of breastfeeding.(43) However, according to an Italian study, breast milk might postpone the onset of the illness without reducing the risk.(44) We must pay special attention to a Danish study involving 6841 individuals of whom 1671 had been breastfed for two weeks or less (early weaning) and 5170 had been breastfed longer. Breastfeeding for two weeks only (or no breastfeeding at all) was associated with elevated risk of schizophrenia.(45) When comparing this study with others, it appears that the protective effect of breastfeeding appears only if the cut-off for early weaning is two weeks instead of one month. This study tends to confirm that the risks of schizophrenia are established during an early phase of development that ends soon after birth.

The study of schizophrenia from a primal health research perspective is an ideal opportunity to illustrate the importance of timing when considering the effects of gene-environment interactions on human development. Epidemiological studies reveal a great diversity of environmental factors that can increase the risks of schizophrenia. However, the timing of an insult is more important than its nature. The fact that maternal-fetal blood incompatibility also appears as a risk factor confirms that the chain of events leading to schizophrenia starts at an early phase of development.(46)

- Autism

Autism is also considered a pathological deviation from the usual gregarious human tendencies. An accumulation of data (included in the Primal Health Research Data Bank) suggests that the timing of the gene-environment interactions is different for autism than for schizophrenia. Several authoritative studies indicate the paramount importance of what happened at birth in the genesis of the different autistic spectrum disorders.

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. An ethologist familiar with the observation of animal behaviour, he researched the non-verbal behaviour of autistic children in particular. As a "field ethologist" he studied the children in their home environment. Not only did he offer detailed descriptions of his observations, but he also listed factors that predispose to autism or can exaggerate the symptoms(47). These factors in the perinatal period included: induction of labour, "deep forceps" delivery, birth under anaesthesia, and resuscitation at birth. We must also save from oblivion a report by Ryoko Hattori, a psychiatrist from Kumamoto, Japan.(48) She evaluated the risks of becoming autistic according to the place of birth, such as a certain hospital where children were significantly more at risk. In that particular hospital, the routine was to induce labour a week before the expected date of birth and to administer a complex mixture of sedatives, anaesthesia agents and analgesics during labour.

Among the three recent large and authoritative studies of autism from a Primal Health Research perspective, the Australian one will convince anyone that the main risk factors occur in the perinatal period.(49) 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 of 1313 controls. No differences in gestational age at birth (including the proportion of 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 importance 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.(50) 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.(51) In addition, we must consider data indicating that perinatal factors may play a lesser role in autism in ‘high-functioning’ individuals compared with studies of autism associated with severe retardation(52), as well as data suggesting that anesthesia during labour is a risk factor for the development of dyskinesia among autistic children.(53)

Although the risk factors for autism seem to occur mostly in the perinatal period, we must keep in mind the association of autism with fetal valproate syndrome (anti-epileptic medication)(54) and with thalidomide embryopathy.(55)

- Attention Deficit Hyperactivity Disorder (ADHD)

ADHD is also considered a pathological deviation from the norms. Children with this condition cannot socialise like others. An overview of the studies introduced by the key word ‘ADHD’ suggests the main risk factors occur during fetal life. The best-documented risk factors are low birthweight(56,57), premature birth(58), smoking in pregnancy(59,60,61), alcohol and drugs in pregnancy(59), maternal iodine deficiency(62), and also the degree of anxiety of the mother, particularly between 12 and 22 weeks gestation.(63)

In fact, all mental diseases interfere with the process of socialisation, including maniac depressive psychosis, which has not yet been widely studied from a primal health research perspective.

- Deviations usually classified as criminal behaviour.

When exploring the Primal Health Research Data Base, the keyword ‘criminality’ leads to research indicating the importance of prenatal factors. Two Finnish studies suggest that certain maternal emotional states in pregnancy are risk factors. In one of these studies the authors identified 167 children whose fathers had died before they were born.(64) Also identified were 168 children whose fathers had died during the children's first year of life. Then the medical records of all 335 of these children were followed for 35 years. Most of the fathers had died during the Second World War when cigarettes and alcohol were severely rationed, if they were obtainable at all. In both groups, the parents were of comparable age and from comparable social classes. All the children grew up fatherless. However, only those who lost their father while in the womb were at increased risk of criminality (plus alcoholism and mental diseases). The results of this study suggest that the emotional state of the mother during pregnancy has more long-term effects on the child than during the year following birth. The other Finnish study researched 12,059 children born in 1966 and followed to the end of 1998.(65) The pregnant mothers were asked at the antenatal clinic if they felt themselves to be depressed. The Finnish Ministry of Justice provided information on criminal offences for all descendants. For male children of prenatally depressed mothers there was a significant increase in criminality.

Smoking in pregnancy is a well documented risk factor for criminality.(66) In one study(67), involving a cohort of 4169 male and 3943 female subjects born between 1959 and 1961, a dose-response relationship was found between the amount of maternal prenatal smoking and criminal arrest in male and female subjects.

More than 4000 male subjects born in the same hospital in Copenhagen were followed up until age 18(68) and then assessed again at the age of 34.(69) The authors looked in particular at the interaction between birth complications and early maternal rejection. The main risk factor found in these studies for being a violent criminal is the association of birth complications with early maternal rejection. Early maternal rejection by itself is not a risk factor. We can conclude once more that very early influences are implicated in violent criminality.

At the crossroads between psychiatry, criminality and psychology

‘Antisocial personality disorder’ refers to individuals with a lack of regard for the moral or legal standards of the local culture, and who exhibit a marked inability to get along with others or abide by societal rules. They may be termed psychopaths or sociopaths. Many eventually end up in prison or die by violence or in accidents caused by risk-taking.

We must bear in mind that psychiatrists themselves are not in unanimous agreement on the existence, content, and diagnosis of antisocial personality disorders. In spite of these difficulties, the keyword ‘antisocial personality disorder’ leads to epidemiological studies that are within the framework of Primal Health Research. The largest study looked at the consequences of the blockade of food supplies in the Netherlands during the winter of 1944-1945. The participants were 100,543 Dutch men born in large urban areas in 1944-1946 who were given psychiatric examinations for military induction at age 18 years.(70) They were classified by the degree and timing of their prenatal nutritional deficiency based on their date and place of birth. Men exposed to severe maternal nutritional deficiency during the first and/or second trimesters of their fetal life exhibited increased risk for antisocial personality disorder. Third-trimester exposure to severe nutritional deficiency and prenatal exposure to moderate nutritional deficiency were not associated with increased risk.

The eccentrics and the geniuses

Certain deviations from the typical human gregarious tendencies are classified as personality traits. Among these deviations we must mention the case of the eccentrics and the geniuses. Most highly-creative, legendary geniuses had unusual, eccentric personalities and manifested many schizotypal traits. Isaac Newton never married and lived most of his life alone. Albert Einstein had poor grooming and hygiene and well-documented interpersonal deficiencies. Bertrand Russell had been an aloof, lonely, and somewhat insecure child, before leading an unstable adult life.

The link between “genius and insanity” has been widely studied since the nineteenth century, after Cesare Lumbroso, an Italian psychiatrist, published his book “l’uomo di genio” in 1864, and Francis Galto had published “Hereditary Genius” in 1869. The personality traits of geniuses might simply be written off as unimportant details, but for the fact that their family history indicates strong connections between genius and schizophrenia. J.L. Karlsson, a psychiatrist in Iceland, looked into the genetic relationship between schizophrenia and creativity, by examining the relatives of individuals listed in Iceland’s Who’s Who. He reported that the relatives of these successful people suffered an increased rate of schizophrenia.(71) It is noticeable that James Joyce’s daughter was schizophrenic, and the family pedigree of Bertrand Russell was loaded with schizophrenic people: his uncle William was “insane”; his aunt Agatha was delusional; his son John was diagnosed with schizophrenia and his granddaughter Helen also suffered from schizophrenia and committed suicide by setting fire to herself. As well, Albert Einstein’s son by his first marriage suffered from schizophrenia. The son of John Nash, the gifted schizophrenic mathematician and Nobel Laureate in Economics, suffers from schizophrenia too. A few schizophrenic individuals, but many first-, second- or third-degree relatives, who share part of the schizophrenic genome, are some of the most creative individuals around. The close relationship between madness and creativity led David Horrobin to assume that “schizophrenia shaped humanity”.(72)

For obvious reasons, it is difficult to study imprecise concepts such as social behaviours and creativity from a Primal Health Research perspective. It will probably be easier, in the near future, to improve our understanding of the gene-environment interactions, particularly during fetal life. We are learning today that in some cases a parent’s gene is silenced in one organ and that can be the brain. This is why the concept of imprinted genes might help us to interpret the relationship between antisocial behaviours, schizophrenia, and creativity.

I tried in the past to review the primal period of famous geniuses such as Galilée, Newton, Pascal, Darwin, and Einstein. It is noticeable that these highly-creative people were born premature and before the age of intensive care units. It is likely that their survival was due to an exceptionally loving, vigilant and stimulating environment that exposed them to a great variety of sensory stimulations at an age when others are still in the womb. During a critical phase of development the gene-environment interactions occurred in unusual conditions.

Is there a link between prematurity and creativity?(73) Who will study sociability and creativity in relation to “Kangaroo care”?

Michel Odent


  1. McNeil TF, Cantor–Graae E, Cardenal S. Prenatal cerebral development in individuals at genetic risk for psychosis: head size at birth in offspring of women with schizophrenia. Schizophr Res 1993 Jun;10(1):1–5
  2. Wahlbeck K, Forsen T, Osmond C, et al. Association of schizophrenia with low maternal body mass index, small size at birth, and thinness during childhood. Arch Gen Psychiatry 2001; 58(1): 48–52
  3. O’Callaghan E, Larkin C, Kinsella A, Waddington JL. Familial, obstetric, and other clinical correlates of minor physical anomalies in schizophrenia. Am J Psychiatry 1991 Apr;148(4):479–83
  4. Susser E, Neugebauer R. Schizophrenia after prenatal exposure to famine. Lancet 1995; 346
  5. St Clair D, Xu M, Wang P, et al. Rates of adult schizophrenia following prenatal exposure to the Chinese famine of 1959–1961. JAMA 2005; 294 (5): 557–62
  6. Mednick SA, Machon RA, Huttunen MO, Bonett D. Adult schizophrenia following prenatal exposure to an influenza epidemic. Arch Gen Psychiatry 1988 Feb;45(2):189–92
  7. Sham PC, O’Callaghan E, Takei N, et al. Schizophrenia following pre–natal exposure to influenza epidemics between 1939 and 1960. Br J Psychiatry. 1992 Apr;160:461–6
  8. Westergaard T, Mortensen PB, Pedersen CB, et al. Exposure to prenatal and childhood infections and the risk of schizophrenia: suggestions from a study of sibship characteristics and influenza prevalence. Arch Gen Psychiatry 1999 Nov;56(11):993–8
  9. Brown AS, Begg MD, Gravenstein S, et al. Serologic evidence of prenatal influenza in the etiology of schizophrenia. Arch Gen Psychiatry 2004 Aug;61(8):774–80
  10. Hare EH, Price JS. Mental disorder and season of birth: comparison of psychoses with neurosis. Br J Psychiatry. 1969 May;115(522):533–40
  11. Hare EH, Price JS, Slater E. Mental disorder and season of birth. Nature. 1973 Feb 16;241(5390):480.
  12. Davies G, Welham J, Chant D, Torrey EF, McGrath J. A systematic review and meta–analysis of Northern Hemisphere season of birth studies in schizophrenia. Schizophr Bull. 2003;29(3):587–93. Review
  13. McGrath JJ, Welham JL. Season of birth and schizophrenia: a systematic review and meta–analysis of data from the Southern Hemisphere. Schizophr Res. 1999 Feb 15;35(3):237–42.
  14. Berk M, Terre–Blanche MJ, Maude C, Lucas MD, Mendelsohn M, O'Neill–Kerr AJ. Season of birth and schizophrenia: southern hemisphere data. Aust N Z J Psychiatry. 1996 Apr;30(2):220–2.
  15. Messias E, Kirkpatrick B, Bromet E, Ross D, Buchanan RW, Carpenter WT Jr, Tek C, Kendler KS, Walsh D, Dollfus S. Summer birth and deficit schizophrenia: a pooled analysis from 6 countries. Arch Gen Psychiatry. 2004 Oct;61(10):985–9.
  16. Suvisaari JM, Haukka JK, Lonnqvist JK. Season of birth among patients with schizophrenia and their siblings: evidence for the procreational habits hypothesis. Am J Psychiatry. 2001 May;158(5):754–7.
  17. D'Amato T, Dalery J, Rochet T, Terra JL, Marie–Cardine M. Seasons of birth and psychiatry. A retrospective inpatients study] Encephale. 1991 Mar–Apr;17(2):67–71. French
  18. Messias E, Kirkpatrick B. Summer birth and deficit schizophrenia in the epidemiological catchment area study. J Nerv Ment Dis. 2001 Sep;189(9):608–12.
  19. Tatsumi M, Sasaki T, Iwanami A, Kosuga A, Tanabe Y, Kamijima K. Season of birth in Japanese patients with schizophrenia. Schizophr Res. 2002 Apr 1;54(3):213–8.
  20. Morgan VA, Jablensky AV, Castle DJ. Season of birth in schizophrenia and affective psychoses in Western Australia 1916–61
  21. Carrion–Baralt JR, Fuentes–Rivera Z, Schmeidler J, Silverman JM. A case–control study of the seasonality effects on schizophrenic births on a tropical island. Schizophr Res. 2004 Nov 1;71(1):145–53.
  22. McGrath J, Welham J, Pemberton M. Month of birth, hemisphere of birth and schizophrenia. Br J Psychiatry. 1995 Dec;167(6):783–5.
  23. Kirkpatrick B, Tek C, Allardyce J, Morrison G, McCreadie RG. Summer birth and deficit schizophrenia in Dumfries and Galloway, southwestern Scotland. Am J Psychiatry. 2002 Aug;159(8):1382–7.
  24. d'Amato T, Guillaud–Bataille JM, Rochet T, Jay M, Mercier C, Terra JL, Dalery J. No season–of–birth effect in schizophrenic patients from a tropical island in the Southern Hemisphere. Psychiatry Res. 1996 Mar 29;60(2–3):205–10.
  25. O'Callaghan E, Cotter D, Colgan K, Larkin C, Walsh D, Waddington JL. Confinement of winter birth excess in schizophrenia to the urban–born and its gender specificity. Br J Psychiatry. 1995 Jan;166(1):51–4
  26. Eagles JM, Hunter D, Geddes JR. Gender–specific changes since 1900 in the season–of–birth effect in schizophrenia. Br J Psychiatry. 1995 Oct;167(4):469–72
  27. O'Callaghan E, Gibson T, Colohan HA, Walshe D, Buckley P, Larkin C, Waddington JL Season of birth in schizophrenia. Evidence for confinement of an excess of winter births to patients without a family history of mental disorder. Br J Psychiatry. 1991 Jun;158:764–9.
  28. Kunugi H, Nanko S, Hayashi N, Saito K, Hirose T, Kazamatsuri H. Season of birth of schizophrenics in a recent Japanese sample. Psychiatry Clin Neurosci. 1997 Aug;51(4):213–6.
  29. Parker G, Mahendran R, Koh ES, Machin D. Season of birth in schizophrenia: no latitude at the equator. Br J Psychiatry. 2000 Jan;176:68–71.
  30. Davies G, Ahmad F, Chant D, Welham J, McGrath J. Seasonality of first admissions for schizophrenia in the Southern Hemisphere. Schizophr Res. 2000 Feb 14;41(3):457–62.
  31. Battle YL, Martin BC, Dorfman JH, Miller LS. Seasonality and infectious disease in schizophrenia: the birth hypothesis revisited. J Psychiatr Res. 1999 Nov–Dec;33(6):501–9.
  32. Brown AS, Schaefer CA, Quesenberry CPJr, et al. Maternal exposure to toxoplasmosis and risk of schizophrenia in adult offspring.Am J Psychiatry. 2005 Apr;162(4):767–73
  33. Kendell RE, Juszczak E, Cole SK. Obstetric complications and schizophrenia: a case control study based on standardised obstetric records. Br J Psychiatry. 1996 May;168(5):556–61
  34. Hultman CM, Sparen P, Takei N, et al. Prenatal and perinatal risk factors for schizophrenia, affective psychosis, and reactive psychosis of early onset: case–control study. BMJ 1999 Feb 13;318(7181):421–6
  35. Sorensen HJ, Mortensen FL, Reinisch JM, Mednick SA. Association between prenatal exposure to analgesics and risk of schizophrenia. Br J Psychiatry 2004 Nov;185:366–71
  36. Sorensen HJ, Mortensen FL, Reinisch JM, Mednick SA. Do hypertension and diuretic treatment in pregnancy increase the risk of schizophrenia in offspring? Am J Psychiatry 2003 Mar;160(3):464–8
  37. Opler MG, Brown AS, Graziano J, et al.. Prenatal lead exposure, delta–aminolevulinic acid, and schizophrenia. Environ Health Perspect 2004 Apr;112(5):548–52
  38. Myhrman A, Rantakallio P, Isohanni M, et al. Unwantedness of a pregnancy and schizophrenia in the child. Br J Psychiatry. 1996 Nov;169(5):637–40
  39. Lipska BK, Jaskiw GE, Weinberger DR. Postpubertal emergence of hyperresponsiveness to stress and to amphetamine after neonatal excitotoxic hippocampal damage: a potential animal model of schizophrenia. Neuropsychopharmacology. 1993 Aug;9(1):67–75
  40. O'Callaghan E, Gibson T, Colohan HA, et al. Risk of schizophrenia in adults born after obstetric complications and their association with early onset of illness: a controlled study. BMJ 1992 Nov 21;305(6864):1256–9
  41. Verdoux H, Geddes JR, Takei N, et al. Obstetric complications and age at onset in schizophrenia: an international collaborative meta–analysis of individual patient data. Am J Psychiatry 1997 Sep;154(9):1220–7
  42. Boksa P, El–Khodor BF. Birth insult interacts with stress at adulthood to alter dopaminergic function in animal models: possible implications for schizophrenia and other disorders. Neurosci Biobehav Rev. 2003 Jan–Mar;27(1–2):91–101
  43. Leask SJ, Done DJ, Crow TJ, et al. No association between breast–feeding and adult psychosis in two national birth cohorts. Br J Psychiatry 2000 Sep;177:218–21
  44. Amore M, Balista C, McCreadie RG. Can breast–feeding protect against schizophrenia? Case–control Study. Biol Neonate 2003;83(2):97–101
  45. Sorensen HJ, Mortensen FL, Reinisch JM, Mednick SA. Breastfeeding and risk of schizophrenia in the Copenhagen Perinatal Cohort. Acta Psychiatr Scand 2005 Jul;112(1):26–9
  46. Insel BJ, Brown AS, Bresnahan MA, et al. Maternal–fetal blood incompatibility and the risk of schizophrenia in offspring. Schizophr Res 2005 Dec 15;80(2–3):331–42
  47. Tinbergen N, Tinbergen A. Autistic children. Allen and Unwin. London 1983.
  48. Hattori R, et al. Autistic and developmental disorders after general anaesthetic delivery. Lancet 1991; 337: 1357–8.
  49. Glasson EJ, Bower C, Petterson B, et al. Perinatal factors and the development of autism: a population study. Arch Gen Psychiatry 2004 Jun;61(6):618–27
  50. Hultman C, Sparen P, Cnattingius S. Perinatal risk factors for infantile autism. Epidemiology 2002; 13: 417–23.
  51. Stein D, Weizman A, Ring A, Barak Y. Obstetric complications in individuals diagnosed with autism and in healthy controls. Compr Psychiatry 2006 Jan–Feb;47(1):69–75.
  52. 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.
  53. Armenteros JL, Adams PB, et al. Haloperidol–related dyskinesias and pre– and perinatal complications in autistic children. Psychopharmacol Bull 1995; 31 (2): 363–9.
  54. Williams G, King J, Cunningham M, et al. Fetal valproate syndrome and autism: additional evidence of an association. Dev Med Child Neurol 2001 Mar;43(3):202–6.
  55. Stromland K, Nordin V, Miller M. Autism in thalidomide embryopathy: a population study. Dev Med Child Neurol 1994 Apr;36(4):351–6.
  56. Mick E, Biederman J, Prince J, et al. Impact of low birth weight on attention–deficit hyperactivity disorder. J Dev Behav Pediatr 2002 Feb;23(1):16–22
  57. Botting N, Powls, Cooke RW. Attention deficit hyperactivity disorders and other psychiatric outcomes in very low birthweight children at 12 years. J Child Psychol Psychiatry 1997 Nov;38(8):931–41
  58. Bhutta AT, Cleves MA, Casey PH, et al. Cognitive and behavioral outcomes of school–aged children who were born preterm: a meta–analysis. JAMA 2002 Aug 14;288(6):728–37
  59. Mick E, Biederman J, Faraone SV. Case–control study of attention–deficit hyperactivity disorder and maternal smoking, alcohol use, and drug use during pregnancy. J Am Acad Child Adoles Psychiatry 2002 Apr;41(4):378–85
  60. Milberger S, Biederman J, Faraone SV, et al. Further evidence of an association between attention–deficit/hyperactivity disorder and cigarette smoking. Findings from a high–risk sample of siblings. Am J Addict 1997 Summer;6(3):205–17
  61. Thapar A, Fowler T, Rice F, et al. Maternal smoking during pregnancy and attention deficit hyperactivity disorder symptoms in offspring. Am J Psychiatry 2003 Nov;160(11):1985–9
  62. Vermiglio F, Lo Presti VP, Moleti M, et al. Attention deficit and hyperactivity disorders in the offspring of mothers exposed to mild–moderate iodine deficiency: a possible novel iodine deficiency disorder in developed countries. J Clin Endocrinol Metab 2004 Dec;89(12):6054–60
  63. Van den Bergh BR, Marcoen A. High antenatal maternal anxiety is related to ADHD symptoms, externalizing problems, and anxiety in 8– and 9–year–olds. Child Dev 2004 Jul–Aug;75(4):1085–97
  64. Huttunen MO, Niskanen P. Prenatal loss of father and psychiatric disorders. Arch Gen Psychiatry 1978 Apr;35(4):429–31
  65. Maki P, Veijola J, Rasanen P, et al. Criminality in the offspring of antenatally depressed mothers: a 33–year follow–up of the Northern Finland 1966 Birth Cohort. J Affect Disord 2003 May;74(3):273–8
  66. Wakschlag LS, Pickett KE, Cook E, et al. Maternal smoking during pregnancy and severe antisocial behavior in offspring: a review. Am J Public Health 2002 Jun;92(6):966–74
  67. Brennan PA, Grekin FR, Mortensen EL, Mednick SA. Relationship of maternal smoking during pregnancy with criminal arrest and hospitalization for substance abuse in male and female adult offspring. Am J Psychiatry 2002 Jan;159(1):48–54
  68. Raine A, Brennan P, Mednick SA. Birth complications combined with early maternal rejection at age 1 year predispose to violent crime at age 18 years. Arch Gen Psychiatry 1994 Dec;51(12):984–8
  69. Raine A, Brennan P, Mednick SA. Interaction between birth complications and early maternal rejection in predisposing individuals to adult violence: specificity to serious, early–onset violence. Am J Psychiatry 1997 Sep;154(9):1265–71
  70. Neugebauer R, Hoek HW, Susser E. Prenatal exposure to wartime famine and development of antisocial personality disorder in early adulthood. JAMA 1999 Aug 4;282(5):455–62
  71. Nancy Andreasen. The Creating Brain. Dana Press 2005
  72. David Horrobin. The madness of Adam and Eve. Bantam Press 2001
  73. Odent M. Prématurité et Créativité. In: Un enfant…prématurément. Cahiers du nouveau–né 1983; 6: 177–180. Stock. Paris