Parents' psychological stress over time may affect children's cortisol at age 8.

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. RESULTS: Instead of increasing, cortisol levels significantly decreased. Repeated measures GLM indicated a significant relation between higher parenting stress at child age 1 and at age 8, and elevated cortisol levels. A t-test indicated that cortisol levels after the blood draw were significantly higher in children whose parents reported a serious life event at age 8. CONCLUSION: Parenting stress could be a relevant factor for children's adjustment of the HPA axis with long-term effects and leave children more vulnerable to experiences of stress.

Parent perceptions of child sleep: a study of 10,000 Swedish children.

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. RESULTS: The population trends were towards improved sleep with increasing age. Individual sleep patterns show some stability. Reports of frequent night wakings and low sleep quality (LSQ) were strongly associated with each other within and between the age groups (odds ratio [OR] 2.8-60.2, p < 0.001). Perception of poor child sleep was influenced by child temperament at ages 1 and 3 (OR 2.2-4.4, p < 0.001), foreign origin at age 1 (OR 2.1-2.3, p < 0.001), and to some extent, parents' age and education at ages 1-3 (OR 1.4-2.1, p < 0.05 or stronger), but not by single parent status or infant night feedings. Reporting multiple or unspecific causes of night wakings was associated with reporting LSQ (OR 1.8-4.7, p < 0.05 or stronger). CONCLUSION: With increasing age, fewer wakings, improved sleep quality and a more uniform sleep schedule seem normal. However, frequent wakings and low quality sleep at early ages seem surprisingly stable. A difficult temperament and foreign origin were associated with lower quality sleep and more frequent wakings in early ages, whereas being a single parent was not. Finally, night feeding does not seem to condition children to frequent wakings.

Psychological stress and obesity.

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. These variables were summarized in cross-sectional and longitudinal composite measures of psychological stress. Logistic regression models were used to calculate odds ratios for childhood obesity for psychological stress. RESULTS: A total of 4.2% of the children were obese according to age-adjusted international standards. Children from families that reported stress in at least 2 of the 4 domains assessed had significantly higher adjusted odds ratios (OR) for obesity, both cross-sectionally (OR, 2.1; 95% CI, 1.3-3.5; P < .01) and longitudinally (OR, 2.6; 95% CI, 1.3-5.4, P < .01). CONCLUSION: Psychological stress in the family may be a contributing factor for childhood obesity. This finding underscores how important it is to give children with obesity and their families psychological and social support in addition to recommendations about changing life style.

Psychological stress and the risk of diabetes-related autoimmunity: a review article.

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. Ten retrospective case-control studies were found. Nine studies showed a positive association between stress and development/onset of T1D in children, adolescents or adults. One study did not find an association between stress and development/onset of T1D. An association between stress and diabetes-related autoimmunity was found at 1 and 2-3 years of age in a large epidemiological study of the general population. The hypothesis that psychological stress (via beta cell stress or direct influence on the immune system) may contribute to the induction or progression of diabetes-related autoimmunity has gained some strong initial support, but is in need of further empirical verification. It seems much clearer that stress can precipitate manifest T1D, although the biological mechanisms are still not known.

Mothers' experiences of serious life events increase the risk of diabetes-related autoimmunity in their children.

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., irrespective of genetic risk for type 1 diabetes) whether mothers' experiences of serious life events, such as divorce and violence, were associated with diabetes-related autoimmunity in their children at age 2.5 years. RESEARCH DESIGN AND METHODS: The study cohort was comprised of the first 5,986 consecutive children and their families from the prospective population-based All Babies in Southeast Sweden project for whom 2.5-year study data were available. Data were drawn from parental questionnaires that included questions about experiences of serious life events and the blood samples taken from the children when the children were age 2.5 years. The blood samples were analyzed for diabetes-related autoantibodies against tyrosine phosphatase and GAD. RESULTS: Mothers' experiences of divorce (odds ratio 3.6, 95% CI 1.4-9.6, P < 0.05) and violence (2.9, 1.0-7.8, P < 0.05) were associated with diabetes-related autoimmunity in the children, independent of a family history of type 1 diabetes. CONCLUSIONS: The results support the beta-cell stress hypothesis and suggest that maternal experiences of serious life events such as divorce and violence seem to be involved in the induction or progression of diabetes-related autoimmunity in children at age 2.5 years, independent of family history of type 1 diabetes.

Psychological stress may induce diabetes-related autoimmunity in infancy.

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. RESEARCH DESIGN AND METHODS: The first 4,400 consecutive 1-year-old children from a large prospective population-based project participated in the study. Parents completed questionnaires at birth and at 1 year, including various measures of psychosocial stress (e.g., parenting stress) and sociodemographic background. Blood samples drawn from the children at 1 year were analyzed for type 1 diabetes-associated autoantibodies toward tyrosine phosphatase and GAD. Antibodies toward tetanus toxoid were used as non-diabetes-related control antibodies. RESULTS: Psychosocial factors, i.e., high parenting stress (odds ratio 1.8 [95% CI 1.2-2.9], P < 0.01), experiences of a serious life event (2.3 [1.3-4.0], P < 0.01), foreign origin of the mother (2.1 [1.3-3.3], P < 0.001), and low paternal education (1.6 [1.1-2.3], P < 0.01) were associated with diabetes-related autoimmunity in the child, independent of family history of diabetes. CONCLUSIONS: Psychological stress, measured as psychosocial strain in the family, seems to be involved in the induction, or progression, of diabetes-related autoimmunity in the child during the 1st year of life.

Psychosocial correlates of parenting stress, lack of support and lack of confidence/security.

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. Mothers lacking social support or confidence/security exhibited significantly higher stress. Although parenting stress is a complex phenomenon certain risk factors can be emphasized, such as sleep problems which appear more important than child health problems. These risk factors can be used both in efforts to prevent stress and in studies of stress effects.

Mothers' attachment insecurity and diabetes-related autoantibodies in their infants.

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. The proportion of children with insecure mothers was larger, but not significantly so, in the autoantibody-positive group than in the negative group. If an association exists between maternal attachment insecurity and diabetes-related autoimmunity during infancy, it does not appear to be strong.

Could parenting stress and lack of support/confidence function as mediating mechanisms between certain environmental factors and the development of autoimmunity in children?: a study within ABIS.

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. Disparate factors of social, environmental, and medical character have been associated with the onset of type 1 diabetes or with the autoimmune process leading to the disease-for instance, parental age, maternal infections, delivery mood, need for neonatal intensive care, and low socioeconomic status. Our results, based on the analyses of 4337 nonselected newborn children and their mothers, show that all these risk factors were also associated with psychological mechanisms (defined as lack of social support/confidence and high parenting stress). These results support the hypothesis of psychological mechanisms as mediating variables between a number of disparate risk factors and the development of type 1 diabetes.