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University of Toronto Scarborough
Health Studies
R Song

Lecture 8: Nutrition, Growth, and Long-Term Consequences II March 12, 2011 Poverty, Child Health, and Behaviour  Besides growth and development, dietary quality affects: 1. Socialization/ interaction 2. Behaviour 3. Verbalization Behavioural/Intellectual Consequences  Reduced intellectual performance not only brain damage (due to under-nutrition), but also due to: 1. Reduced activity (less active) 2. Withdrawing from social environment and contact with peers (no energy to interact with others) 3. Extra care and coddling by mothers further hinders growth and independence (and reduced expectations of family and larger community); protected more (over protected) results in less socializing Poverty, Malnutrition, and Child Neglect  How adults interact and treat children with malnutrition Brazilian Favelas  During the 80s and 90s, large amount of people were poor; lived in areas known as “ghettos” (rural type of neighbourhoods)  "Infants are like birds", Biu once said, "here today, gone tomorrow. Alive or dead, it’s all the same to them. They don’t have that certain attachment to life of the older child". Scheper-Hughes 1991: 1144 o Not unusual statements from parents living in these conditions, with high rates of deaths in children Poverty in Brazil: Child Health Repercussions  Scheper-Hughes – poor Brazilian mothers only nurture those kids deemed to have higher chances of survival; others neglected; “mother love” is not universal  2 explanations for high infant mortality: 1. Synergism of nutrition and morbidity  Parental neglect  Reaction to the environment 2. Familial neglect; behaviours in reaction to high infant mortality  Like 18th century French peasants – who similarly viewed child death as deliverance from god (little grief)….. angelitos of Brazil Scheper-Hughes 1991, 1992  ‘A high expectancy of child death is a powerful shaper of maternal thinking and practice as evidenced, in particular, in delayed attachment to infants sometimes thought of as temporary household “visitors”’  Maternal attachment and bonding are delayed and much more gradual; develop only when baby shows its readiness to live (“become human”)  May be slow to personalize the infant, give it a name, or in Catholic countries like Brazil, to baptize it  Maternal care/love “shaped by overwhelming economic and cultural constraints”  Maternal “benign neglect”  “Ethoeugenic selective neglect” (Scheper-Hughes 1991) o Selective neglect of children who will not survive  “Passive infanticide” o Neglecting a child soon after birth Chronic Hunger and Culturally-Sanctioned Parental Neglect (Scheper-Hughes)  “Death Without Weeping” (1992)  Infant/child mortality in Brazilian favelas  Censuses count some things better than others o Death s are reported to authorities; not clear about how many child deaths occur  Infant mortality among poor: considered hardly worth documenting (cause of death often left blank…) Cultural Consequences of Child Malnutrition Quiz #1: What was not significant in the findings of favelas about mothers and infants? (in Scheper-Hughes article)? a) Mothers sometimes did not name children at birth b) High fertility was not the norms c) “Passive infanticide” was not uncommon d) Many infants death went unrecorded Long-term Consequences  Life History approach: focused on strategies from conception to maturity & death regarding growth, maintenance, reproduction  ‘‘Trade-offs occur when two traits compete for materials and energy within a single organism . . .’’ or, ‘‘. . .when selection for one trait decreases the value of a second trait’’ (Stearns, 1992: 223) (Bogin et al. 2007) Developmental Origins of Adult Disease  “Developmental Programming” Hypothesis: exposure to adverse environments during gestation results in a body that is smaller at birth and will be unhealthy in adulthood  These alterations in growth (resulting in low birth weight, short leg proportions to stature, etc.) have permanent maladaptive consequences that put individuals at risk for disease later in life, o i.e., heart disease, diabetes, other metabolic diseases  Ravelli et al. (1976) found elevated risk for adult obesity among those exposed to Dutch Famine of 1944–45 during first trimester of gestational growth  Short stature combined with a relatively high cormic index (short legs relative to total stature) – due to malnutrition, has been associated with: o Higher risk in adulthood for high cholesterol o Coronary heart disease o Impaired glucose and insulin regulation o Increased pulse pressure and systolic blood pressure o Higher fibrinogen levels (protein for clotting; a factor in cardiovascular disease) o Reduced human productivity and reproductive quality Developmental Origins of Adult Disease  “Predictive Adaptive Responses” (PAR) Hypothesis: small size at birth is the result of fetal development under some type of adversity o If that adversity is ameliorated after birth, then there may be a type of over-growth (compensation) under the relatively better conditions of post-natal life o Prediction being made by a fetus, can have consequences later in life  Gluckman and Hanson (2005) o At two levels of adaptation: 1. ‘‘Short-term adaptive responses for immediate survival’’ – which can be reversible, 2. ‘‘Predictive responses (of fetus) required to ensure postnatal survival to reproductive age’’ – where we see biological “trade- offs” that occur at the expense of maternal health quality and that of their offspring  e.g., rapid maturation and early reproduction, low quality offspring o Empirical evidence? - Does not support PAR hypothesis, but does support the DP Hypothesis Intergenerational Influences Hypothesis  Emanuel (1986) ‘‘. . . those factors, conditions, exposures and environments experienced by one generation that relate to the health, growth and development of the next generation.’’  Was proposed to account for the persistence of low birth weight across generations (e.g., Dutch women)  Both DP and PAR hypotheses account for intergenerational influences  Both recognize that poor quality of the intrauterine and early postnatal environment will result in fetus/infant metabolic and cardiac adjustments, possibly beneficial or harmful – metabolic and cardiac variations that influence the growth, development, and health of individuals for the rest of their life SES and Gradient Effect  In North America, these gradients are consistent by kindergarten age and are related to differential access, by SES, to “developmental priming mechanisms” for healthy child development: o Encouragement of exploration o Mentoring in basic skills o Celebration of developmental advances o Guided rehearsal and extension of new skills o Protection from inappropriate disapproval, teasing, or punishment o A rich and responsive language environment  Evidence from longitudinal studies shows that ECD and the socioeconomic and psychosocial environment of childhood are empirically linked to adult health status  Three different processes in which this occurs (Hertzman 1999): 1. Latent effects, by which the early life environment affects adult health independent of intervening experience 2. Pathway effects, through which the early life environment sets individuals onto life trajectories that in turn affect health status over time 3. Cumulative effects, whereby the intensity and duration of exposure to unfavorable environments adversely affects health status, according to a dose–response relationship  Association between low birth weight and cardiovascular disease in adulthood is evidence of a latent effect  Results from early childhood stimulation programs for disadvantaged children are consistent with a latent effect, given their effectiveness in improving adult well-being and competence through enrichment programs that are confined to the early years, and do not involve ongoing elements from school age to adulthood  Pathways model acknowledges that differences in early life environment may direct children onto different life courses (Hertzman 1999) o i.e.: stimulation, stability, and security
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