Publications by authors named "Anneli Sepa"

Objective: To examine possible relations between parents' psychological stress and children's saliva cortisol levels in connection with a mild stressor (drawing a blood sample).

Method: Parenting stress and serious life events at birth, age 1, age 2, age 5, and age 8 were assessed. Eighty-two paired saliva samples collected from their 8-year-old children just before and 30 min after blood was drawn were analyzed.

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Aim: To gather normative data on parent-reported child sleep and investigate what influences it.

Methods: Subjective sleep report data on night wakings, sleep quality, bedtime and risetime were gathered from parents of around 10,000 children from birth to age 5 in a cohort questionnaire study. The data were analysed for trends, and sleep measures were compared with background factors such as child temperament, foreign origin, family situation, parents' age and education and night feedings.

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Objective: To examine whether there is a relationship between psychological stress in the family and obesity in 5- to 6-year-old children.

Study Design: A total of 7443 Swedish families reported on psychological stress across 4 domains as part of the prospective All Babies in Southeast Sweden-project (ABIS). Domains assessed included serious life events, parenting stress, lack of social support, and parental worries.

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The beta cell stress hypothesis suggests that any phenomenon that induces insulin resistance, and thereby extra pressure on the beta cells, should be regarded as a risk factor for type 1 diabetes (T1D). Psychological stress decreases insulin sensitivity and increases insulin resistance and may hence be important in the development/onset of T1D. The aim of the current review article was to evaluate existing empirical evidence concerning an association between psychological stress and development/onset of T1D as well as diabetes-related autoimmunity.

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Objective: Stressful life events have been shown to constitute a risk factor for type 1 diabetes during childhood. Our aim was to investigate in the general child population (i.e.

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Psychological stress may, via hormonal levels, increase insulin resistance. The aim of this study was to investigate whether mothers' attachment insecurity is associated with the induction or progression of diabetes-related autoimmunity in early childhood. Adult attachment interviews were conducted with 18 mothers of infants who were positive, and 32 mothers of infants who were negative, for glutamic acid decarboxylase, selected from ABIS, a large prospective population-based project.

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Objective: In retrospective studies, a number of disparate environmental factors (including experiences of serious life events) have been proposed as trigger mechanisms for type 1 diabetes or the autoimmune process behind the disease. Psychosocial stress in families may affect children negatively due to a link to hormonal levels and nervous signals that in turn influence both insulin sensitivity/insulin need and the immune system. Our aim was to investigate whether psychological stress, measured as psychosocial strain in families, is associated with diabetes-related autoimmunity during infancy.

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The purpose of the current study was to identify important correlates of parenting stress, frequently conceptualized as a mediator of suboptimal family function, and of social support and confidence/security, often regarded as buffers. Potential correlates of these concepts were assessed in questionnaires at delivery and at one year, in a sample of 16,000 families in Sweden. Predictors (1) of parenting stress were parental dissatisfaction and poor child sleeping patterns; (2) of lack of support included lack of confidence/security, parents born abroad, single motherhood, and maternal health problems; and (3) of lack of confidence/security were lack of support and serious life events.

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Despite extensive research, the etiology of type 1 diabetes is still to a large extent unknown. We would like to propose psychoimmunology as one possible pathway. Psychological mechanisms are directly linked to hormonal and nervous signals, which increase the need for insulin and affect the immune system.

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