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History of childhood and causation of health Are lives programmed?

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1 History of childhood and causation of health Are lives programmed?

2 What is a child? UN: 0-18 years And what is health??

3 WHO 1946: ’Health is a state of complete physical, mental and social well- being and not merely the absence of disease or infirmity’ (later added: ’ability to lead a socially and economically productive life’) Sigmund Freud: ’You have health if you are able to work and love’ Peter F Hjort: ’…Health is to master everyday’s demands’

4 Helse? Samme kategori ord som kjærlighet, lykke, kultur, bærekraftig Alle har et forhold til begrepene, ingen er enige om hvordan de skal defineres Hva lykke er? Det er å gå på en gressgrodd setervei i tynne, tynne sommerklær klø sine første myggestikk med doven ettertenksomhet og være meget ung og meget rik på uoppplevet kjærlighet (Inger Hagerup)

5 How can we measure health? Proxies (health indicators) MortalityMortalitet Morbidity Infant mortality (IMR) Life expectancy Under-5 mortality Birth weight Body height

6 All endpoints are proxies for what we call health

7 Quality of life model the different spheres(Lindstrøm, Allhardt) Global:macroenvironment, human rights Outer sphere:Socioeconomi Humen relations: Family, friends Personal: physical, mental, spiritual, activity, selfconfidence

8 What is mental health? (Meriam Webster): A state of emotional and psychological well-being in which an individual is able to use his or her cognitive and emotional capabilities, function in society, and meet the ordinary demands of everyday life”.

9 The three circles of social determinants of health Family Friends Neighbours Home Norms Expectations Community Area Local services Natural resources Pollution Local economy Schools Macrosocial influences Government Laws Economic system National priorities Welfare model Justice Equality

10 CHILD=child health indicators for life and development (EU) Demographic and socioeconomic determinants Health and disease (mortality, morbidity) Health determinants (positive,negative) Health policy

11 Children’s health and quality of life Global changes Technical changes Economical changes Societal changes Educational changes Population changes Life style changes Nutrition Changes in disease panorama ? ? ?? ? ?

12 What is epidemiology? Basicly: The study of the origin of diseases

13 Epidemiologiske undersøkelser dreier seg om undersøkelser av grupper av befolkningen, ikke av enkeltindivider Epidemiologi er grunnlaget for helseovervåkning og for å foreslå forebyggende tiltak i befolkningen

14 Eilert Sundt: Om dødeligheden i Norge (1855) …”der er intet blindt tilfælde (av dødsfall). Det lære vi, naar vi ikke alene saaledes med bevæget sind betragte de enkelte dødsfald, som kunne være inntruffet i den snevrere kreds, men tillige med sindigt overlæg samle en større mengde erfaringer ved at tælle alle de dødsfald, som i et længere tidsrum ere intrufne i i en by, en egn eller i et helt land.”

15 Helsediktet fra Salerno - ca e.Kr. Om årsakene til sykdom: Årsakene til øresting: Sno, byld, sult, støt og hete, flere ting er nevnt som grunn til øresting. Samme skade kan det gjøre at folk skriker i ens øre. Årsakene til sukkersyke: Er nyrene tørre, og sterkt opphetes, vil du få diabetes; også elskov, hopping og kappløp gjør sitt, og at en har slitt.

16 Hvordan skal vi måle sykdom eller helse? Forekomst (antall tilfeller, andel) må ha en teller (antall tilfeller) og en nevner (hele befolkningen, deler av befolkningen, aldersgrupper, osv. Vi må ha en kilde for å få frem tallene: register (dødsregisteret, kreftregisteret hvor alle tilfeller blir meldt), eller vi må gjøre spesielle undersøkelser, surveys

17 Examples (mortality) Number of deaths per inhabitants Infant mortality (IMR): number of deaths in first year of life per 1000 live born Deaths per inhabitants in a county Deaths per 1000 among people in certain employments Number of deaths per of a specific diagnose(cause specific mortality) Target population, everyone ”at risk” must be stated.

18 Two types of epidemiological studies Descriptive Descriptions of prevaence of illness(disease) in a population (group) – nothing about causes Analytical Try to look for causal factors

19 Typer av epidemiologiske undersøkelser Hypotesegenererende pasient serier av pasienter tverrsnittsstudier av befolkningen Hypotesetesting Observerende: pasient-kontroll (case-control) cohort Eksperimentelle Randomiserte(RTC)

20 Måling av sykelighet Forekomst/prevalens egner seg vesentlig for tilstander som er noenlunde stabile gjennom en tid (kroniske?). Uttrykkes i antall tilfelle per (for eksempel) av målpopulasjonen For noen sykdommer er dette et uegnet mål, for eksempel ved akutte infeksjonssykdommer. Da kan vi måle insidens: antall nye tilfeller per

21 Letalitet Det er også hensiktsmessig å kjenne uttrykket letalitet, som er antall døde per antall som er blitt syke

22 Lif expectancy at birth, Norway life time, years

23 Cohort Studies – definition (R.Doll) ”…the delineation of a group of persons who are distinguished in some specific way from the majority of the population and observation of them long enough to allow any unusual morbidity or mortality to be recognised”.

24 ”Case control” Compare exposure (risk factors) for people with a known endpoint (disease) with a control group without the disease The Norwegian Mother and Child Cohort Study studies cases and controls from the same set of data (”nested case control” )

25 Kohortdesignets fordeler: Man undersøker eksponeringsforhold (potensielle årsaksfaktorer) før utfallet er kjent

26 Assosiasjon mellom eksponering (risiko) og utfall (sykdom) RisikoSykdom (a) 25(b) - 20(c) 145(d ) Odds ratio= a x d/b x c

27 Association is not equivalent to causality! Criteria for associations= causes (Bradford-Hill): strength consistency specificity time sequence biological gradient (dose/response) plausibility coherence experimental proof analogy

28 Hvor kan vi hente data fra? Utfallsdata (sykdom,død): Registre (døds-,kreft-,fødsels-,diabetes-,pasi-entutskrivnings-) Helseundersøkelser (statens h.u.,CONOR, SSB, helsestasjonsdata, meldepliktige sykdommer) Spesielle undersøkelser (surveys)

29 Hvor kan vi hente eksponeringsdata? Eksempler: Kommunedata (luft,vann etc) Trafikketaten (trafikktetthet etc) Spesielle spørreundersøkelser til enkeltindivider Spesielle målinger (forurensning, støy etc) Biologiske prøver SSB (sosioøkonomi etc)

30 ER SYKDOMMEN ARVELIG? Design i genetisk epidemiologi Tvilling- og adopsjonsstudier Segregasjonsstudier Koplingsanalyse ”Vanlig epidemiologisk design”: Ved samspill mellom arv og miljø, behandler man de genetiske faktorene som en vanlig risikofaktor. NB: de aller fleste sykdommer er styrt av mange gener, og av miljøpåvirkning!

31 Intervensjonsstudier Virker et tiltak? Randomiserte forsøk= RCT (randomized control trials Ofte vanskelig design! Alltid ved legemiddelutprøving

32 ”Økologisk” (Ecological) design Her sammenlignes hele grupper, ikke knyttet opp mot enkeltindivider, eksempel er fra Forsdahl studie av hjerte-kar dødsfall i Finnmark

33 New indicator for child health (Student, Croatia): ”The proportion of children that smile to you when you meet them”

34

35 Health and Illness in Norwegian Childhood through 100 years- from Poverty to Wealth Rannveig Nordhagen Norwegian Institute of Public Health Oslo, Norway

36 Ord om barn og barndom Barnets innebygde mål er å bli voksen, før dette eksisterer det bare som en mulighet, et potensial (Aristoteles) Barndommens historie er et langt mareritt, som vi bare langsomt holder på å våkne opp fra (Lloyd de Mause, am. psykoaanalytiker)

37 Scenario 1900: Population 2,2 mill Emigration : Infant mortality : boys: 105,5/1 000,girls: 92/1000 Important diseases: Infections (Tbc) Life expectancy: 0 år: 51,5 5 år: 55,5 20 år: 44,04

38 2007 Folkemengde: Innvandrere: 8% (i 2060: 19-27%) Spedbarnsdødelighet: 3 per 1000 Viktigste sykdommer: Hjerte-kar sykdommer, kreft (kroniske lidelser) Forventet gjenstående levetid (ved 0 år) Kvinner: > 82 år, menn: 78 år

39 Chr Krohg: Fighting for existence

40 Helene Scherfbeck

41 Spedbarnsdødeligheten E.Munch: Fostermothers in court ”Angel mothers”: Fostermothers who starved the children to death

42 Infant mortality in Norway per

43 IMR and U5MR per in some selected countries in 1960 and 2003

44 Life expectancy at birth, Norway life time, years

45 Tbc mortality, Norway, , age years BCG Chemotherapy Mortality per

46 Mortality of tbc per

47 Causes of infant mortality, Norway 2002 All 3.5/ per 1000 Per : Birth/perinatal complications: 153 Malformations: 108 SIDS 31

48 Rate of low birthweight (< 2 500g) in the Nordic countries (NOMESCO 1997, %)

49 Rate ratio(RR) of children with social support at the age of 7 in relation to birthweight (Norway 1998)

50 Mortality of tbc, Norway, , age 0-4 years

51 ”Finsen-treatment” Hagavik hospital

52 Screening for tbc

53 Mortality rates and life expectancy (US) Infections Chronic Disease Life Expectancy Tarlov 1996

54 Vaccine Kari Kveim Lie 1997

55 ”The Oslo breakfeast”

56 Weight and hight screening

57 World war 2, : Food restrictions, undernutrition in towns Mean hight for different age groups of girls, Oslo from 1920 to GH Brundtland et al 1980

58 Relation between height at the age of 7, and unemployment at age Montgomery S et al. 1996

59 Parent reported overweight in Nordic children 1996,%

60 Chidren’s health and quality of life Global changes Technological changes Economical changes Societal changes Educational changes Changes in population Life style changes Nutritional changes Changes of disease pattern ? ? ?? ? ?

61 Infant mortality per live born, Norway,

62 Social class and infant mortality , England & Wales

63 Incidence of tye 1 diabetes in the Nordic countries , both sexes, 0-14 yrs

64 ”Binge drinking” and problems associated with use of alcohol, both sexes, yrs

65 Mortality 1-17 years. Norway 2002, per TotalInfectious diseases TumoursCongenital malformat

66 The child’s century? (essay by RB, Norwegian school boy, 1999) ”…the developing countries seem to mirror the industrial countries a century ago, which should mean that the development goes in the right direction - which I believe. With an increased effort towards the developing countries towards year 2 000, I think we rightly might call this century the children’s century.”

67 The greatest threats for children in (UNICEF): Wars AIDS/HIV infections Poverty

68 When are our lives determined?

69

70 Edvard Munch: Inheritance.

71 Why do we vaccinate against Rubella (German measels)?

72 Is this a clue??

73 Have we asked our questions at the right time?

74 Forsdahl/Bakketeig1991

75

76 Anders Forsdahl : …”whereas the weaker of the cohort die in infancy, the fit survive and carry with them a life-long vulnerability ”

77 Dødsårsaker, døde per , 2003

78 Standardised mortality ratios among men according to birthweight and weight at one year Barker 1991

79 Hazard ratios for coronary heart disease in adult life among Finnish men according to birthweight and weight at 12 months Bw (g)Hazard ratio (RR) ≤ > P value for trend0.006 Weight at 1 y (kg) ≤ > P value for trend<

80 Correlations of cause of death (SMRS) at ages years and IMR Barker 1986

81 Ethel Margaret Burnside, 17 yrs

82

83 A pet child has many names Forsdahl hypothesis?? Barker hypothesis? Fetal programming hypothesis? Fetal origins hypothesis?

84 The concept of biological (fetal) programming (Lucas): When an early stimulus or insult, operating at a critical or sensitive period (infetal life), results in a permanent or long-term change in the structure or function of the organism

85 Later programming hypothesis (Lucas 2): If the fetus experiences undernutrition in fetal life, the fetus adopts to this state, and if a later rapid overnutrition of the baby occurs, it can get out of balance- for instance what concerns the tolerance of glucose (insulin resistence- diabetes 2).

86 ”The growth accelaration hypothesis” (Singhal & Lucas 2004) Hypothesis about rapid growth very early in life

87 De viktigste assosiasjonene i de første Barker-studiene mellom fødselsvekt/vekt ved ett år: Hjerte-kar sykdommer,spesielt koronarlidelser Diabetes II Obstruktiv lungesykdom (KOLS) Risikofaktorer for hjerte-kar sykdommer: Hypertoni, koagulasjonsfaktorer, kolesterolnivå, overvekt Syndrom ”X”=diabetes2 +hypertoni+hyperlipidemi

88 Andre antropometriske mål ved fødselen som viser tilsvarende assosiasjoner: Abdominal omkrets Hodeomkrets Placental vekt/fødselsvekt Lengde Ponderal index =kg/m³ (lengde³) BMI =kg/m²(lengde²)

89 Low birthweight ”per se” is not the cause of later coronary disease, but what has happened in intrauterine life

90 Three hypotheses (P. Magnus) The environmental model: Exposures, i.e. those related to poverty, have effects of the growing fetus, later leading to adult disease Genetic confounder model: the association between birth weight and later disease (coronary) is completely causes by genes influencing both factors Environmental confounder model: Same background factors can influence both early and late phenotypes, example is smoking..

91 ”These diseases can best be focused on from a lifecycle perspective (Erikson 2006)

92 Pathways from early life to later health a)Programming Programming in intrauterine life - Later illness/health (latency model) b) Continuous life events Parents’ SES - Childrens SES Birth weight - Later illness

93 Foreslåtte mekanismer bark programmeringseffekten (Lucas) Cellulære mekanismer Ernæringsforholdene (miljøet) endrer genetisk ekspresjon permanent Ernæringsforholdene virker inn på (reduserer) fosterets cellemasse Seleksjon av kloner av gener Ernæringsforholdet endrer organstrukturen Ernæringsforholdene virker gjennom sensibilisering for hormoner

94 Regression models (Lucas 1999) - Early model: regression used simply to relate early size to later outcome - Combined model: includes both early and later size, obtained by adding later size to the early model - Interaction model: adds the interaction of early and later size to the combined model. The interaction terms is calculated as the product of early and later size - Late model: later size alone is related to outcome, which helps to interpret the relative importance of early and later size separately and together

95 The fetal hypothalamic-pituitary- adrenal axis (DM Sloboda) …Programming of the fetal HPA axis during development appears to play a central role in the link between fetal growth and long-term disease in adulthood. Prenatal programming of HPA axis function may increase the the risk of developing cardiovascular and metabolic disease.Cognitive and behavioural modifications have also associated with fetal programming and linked to alterations in HPA axis activity ….

96 Mor Far Barn

97 But what about genes?? Single gene conditions (2% of the population in a life perspective) Chromosome anomalies (Down) Multifactorial conditions

98 Antenatal maternal anxiety and depression and infant development and behaviour at 6 months Rannveig Nordhagen a Anne Inger Helmen Borge b a Norwegian Institute of Public Health, Oslo b Institute of Psychology, University of Oslo

99 Leonardo da Vinci: Woomb

100 The hypothesis of fetal ”programming” (Forsdahl/Barker/Lucas) The intrauterin environment afforded by the mother at a critical period of development may permanently ”program” the structure and physiology of her offspring, and have a lasting or lifelong significance, for instance on the brain development. Our hypothesis (slightly moderated from the title): Can the mother’s anxiety and depression in pregnancy affect the child’s behaviour at 6 months of age?

101 Rossetti: Ecce ancilla Domini (1850 )

102 The Norwegian Mother and Child Cohort Study An ongoing cohort study starting in pregnancy, basicly a questionnaire study,but biological samples (blood, urine) are collected. Linking to health registries may be performed (Birth, Death,Cancer etc). Aim: Recruitment of pregnant women, children, fathers. Status per : > women included

103 Study progress: 1992:Project planned 1995:Pilot project 1999:Project start at first hospital 2000:2 752 women recruited 2004: women recruited 2006:> women recruited The participation rate is < 50% of all invited women

104 Hospitals in Norway participating in the MoBa Study

105 Time of questionnaires: Q1:Week of pregnancy (ultrasound) Q2:Week 24 of pregnancy (nutrition) Q3:Week 30 of pregnancy Q4:6 months post partum Q5:18 months post partum Q6:Child 3 years Q7:Child 7 years Ca 100 Q in each questionnaire, and many subquestions Used in this study: Q1, Q3 and Q4 all reported by the mother

106 Included in this study: All mothers who had filled in Q1(week 17 in pregnancy), Q3 (week 30 in pregnancy) and Q4 (6 months post partum) Singleton births All together: women Some missing on single questions!

107 Variables used in this study Outcome variable: Problematic child at 6 months Measure: 10 Q mainly from Infant characteristic questionnaire (ICQ) (Bates et al.) Items: crying, soothability, easily upset, intensity of protest, easy to get along with, smiles, very demanding, require attention, easy to put to sleep)

108 Exposure variables Mother’s general anxiety and depression week 30 in pregnancy and 6 months pp (short version of symptom check list (SCL). 8 questions: 4 for anxiety, 4 for depression) ”Specific” anxiety (week 30): Fear of giving birth Worries about the baby’s health Covariates/confounders: Maternal factors: Anxiety/depression 6 months pp, mother’s education,mother’s age Child factors: sex of baby, birth weight E.Munch: Inheritance

109 Else Hagen: The Family

110 The results of this study cannot be published on the net, due to later scientific publication. Sorry!


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