Variations in Heritability of Cortisol Reactivity to Stress as a Function of Early Familial Adversity Among 19-Month-Old Twins

Ouellet‐Morin, Isabelle; Boivin, Michel; Dionne, Ginette; Lupien, Sonia J.; Arsenault, Louise; Barr, Ronald G.; Pérusse, Daniel; Tremblay, Richard E.

doi:10.1001/archgenpsychiatry.2007.27

Cited by 116 publications

(76 citation statements)

References 106 publications

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“…It has been shown that genetic factors (e.g., the serotonin transporter gene 5-HTTLPR, and FKBP5 which is associated with GR responsiveness) may in part determine who is at risk to develop psychopathology after being exposed to childhood abuse (see Caspi et al, 2003;Kendler et al, 2005;Binder et al, 2008). Interestingly, some of these same genes also appear to be associated with alterations in HPA-axis reactivity after stress exposure (Binder et al, 2008;McCormack et al, 2009; see also Ouellet-Morin et al, 2008). When investigated in combination with other risk and protective factors (i.e., social support, and exposure to adult negative and positive life events), gene Â environment studies on HPA-axis reactivity might help to identify the more vulnerable vs resilient individuals in the face of early life stress.…”

Section: Discussionmentioning

confidence: 99%

The role of childhood abuse in HPA-axis reactivity in Social Anxiety Disorder: A pilot study

Elzinga

Spinhoven

Berretty

et al. 2010

Biological Psychology

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Section: Discussionmentioning

confidence: 99%

The role of childhood abuse in HPA-axis reactivity in Social Anxiety Disorder: A pilot study

Elzinga

Spinhoven

Berretty

et al. 2010

Biological Psychology

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“…21 Traditionally, genetic predispositions were thought to play a major role in determining stress reactivity, but more recent data suggest that previous experiences also play an important role. 22 Stress reactivity, much like brain development itself, results from a complex, dynamic interaction between genes (nature) and the environment (nurture) over time. Neural pathways activated in response to frequent environmental stimuli are strengthened over time.…”

Section: Measuring Adversity: the Physiologic Stress Responsementioning

confidence: 99%

Home Visiting and the Biology of Toxic Stress: Opportunities to Address Early Childhood Adversity

Garner

2013

Pediatrics

149

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Home visiting is an important mechanism for minimizing the lifelong effects of early childhood adversity. To do so, it must be informed by the biology of early brain and child development. Advances in neuroscience, epigenetics, and the physiology of stress are revealing the biological mechanisms underlying well-established associations between early childhood adversity and suboptimal life-course trajectories. Left unchecked, mediators of physiologic stress become toxic, alter both genome and brain, and lead to a vicious cycle of chronic stress. This so-called "toxic stress" results a wide array of behavioral attempts to blunt the stress response, a process known as "behavioral allostasis." Although behaviors like smoking, overeating, promiscuity, and substance abuse decrease stress transiently, over time they become maladaptive and result in the unhealthy lifestyles and noncommunicable diseases that are the leading causes of morbidity and mortality. The biology of toxic stress and the concept of behavioral allostasis shed new light on the developmental origins of lifelong disease and highlight opportunities for early intervention and prevention. Future efforts to minimize the effects of childhood adversity should focus on expanding the capacity of caregivers and communities to promote (1) the safe, stable, and nurturing relationships that buffer toxic stress, and (2) the rudimentary but foundational social-emotional, language, and cognitive skills needed to develop healthy, adaptive coping skills. Building these critical caregiver and community capacities will require a public health approach with unprecedented levels of collaboration and coordination between the healthcare, childcare, early education, early intervention, and home visiting sectors. Pediatrics 2013;132:S65-S73

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“…Twin cohorts offer considerable potential for studying diet-genotype interactions and global impact of genomic variation in response to diet despite not being used extensively in nutrigenetics [9,28,49]. Studies include quantification of specific diet-gene interactions in identical and fraternal twins [e.g.…”

Section: Twin Studiesmentioning

confidence: 99%

The challenges for molecular nutrition research 1: linking genotype to healthy nutrition

Williams¹,

Ordovas

Lairon

et al. 2008

Genes Nutr

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Nutrition science finds itself at a major crossroad. On the one hand we can continue the current path, which has resulted in some substantial advances, but also many conflicting messages which impair the trust of the general population, especially those who are motivated to improve their health through diet. The other road is uncharted and is being built over the many exciting new developments in life sciences. This new era of nutrition recognizes the complex relation between the health of the individual, its genome, and the life-long dietary exposure, and has lead to the realisation that nutrition is essentially a gene-environment interaction science. This review on the relation between genotype, diet and health is the first of a series dealing with the major challenges in molecular nutrition, analyzing the foundations of nutrition research. With the unravelling of the human genome and the linking of its variability to a multitude of phenotypes from ''healthy'' to an enormously complex range of predispositions, the dietary modulation of these propensities has become an area of active research. Classical genetic approaches applied so far in medical genetics have steered away from incorporating dietary effects in their models and paradoxically, most genetic studies analyzing diet-associated phenotypes and diseases simply ignore diet. Yet, a modest but increasing number of studies are accounting for diet as a modulator of genetic associations. These range from observational cohorts to intervention studies with prospectively selected genotypes. New statistical and All authors are member of The European Nutrigenomics Organisation (http://www.nugo.org). bioinformatics approaches are becoming available to aid in design and evaluation of these studies. This review discusses the various approaches used and provides concrete recommendations for future research. C. M. Williams (&)Hugh

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Variations in Heritability of Cortisol Reactivity to Stress as a Function of Early Familial Adversity Among 19-Month-Old Twins

Abstract: This pattern of differing genetic and environmental contributions according to familial adversity suggests that, early in life, high familial adversity may have a programming developmental effect on cortisol reactivity.

Cited by 116 publications

References 106 publications

The role of childhood abuse in HPA-axis reactivity in Social Anxiety Disorder: A pilot study

The role of childhood abuse in HPA-axis reactivity in Social Anxiety Disorder: A pilot study

Home Visiting and the Biology of Toxic Stress: Opportunities to Address Early Childhood Adversity

The challenges for molecular nutrition research 1: linking genotype to healthy nutrition

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