Symptoms of depression and difficulty initiating sleep from early adolescence to early adulthood: a longitudinal study

STUDY OBJECTIVES: To assess the direction of the relationship and degree of shared associations between symptoms of depression and difficulty initiating sleep (DIS) from early adolescence to early adulthood. DESIGN: Cross-sectional and longitudinal assessment of the symptoms of depression-DIS association from early adolescence (age 13 y) to early adulthood (age 23 y). SETTING: Hordaland, Norway. PARTICIPANTS: There were 1,105 individuals (55% male) who took part in the Norwegian Longitudinal Health Behaviour Study (NLHB) and participated at least once across seven data collection waves during the years 1990-2000. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Characteristic data were obtained during the first assessment. Symptoms of depression and instances of DIS were assessed during each data collection wave. Symptoms of depression and DIS were associated in all data waves, and one-step cross-lagged bivariate correlations were significant and comparatively high for both factors. Structural equation modelling indicated that DIS and symptoms of depression at wave 1 remain relatively stable across waves (all P < 0.001), and a significant and consistent unidirectional cross-lagged effect was noted running from symptoms of depression to DIS from early adolescence to early adulthood. DIS is only marginally and inconsistently associated with the lagged symptoms of depression score across waves. CONCLUSIONS: These results suggest that symptoms of depression established in early adolescence are a moderate predictor of difficulty initiating sleep (DIS) in early adulthood, whereas the reverse association of DIS predicting depression was not convincingly supported. These findings are in contrast to previous findings that suggest sleep problems as a risk factor for the later development of depression.

The extended Infant Feeding, Activity and Nutrition Trial (InFANT Extend) Program : a cluster-randomized controlled trial of an early intervention to prevent childhood obesity

BACKGROUND: Understanding how we can prevent childhood obesity in scalable and sustainable ways is imperative. Early RCT interventions focused on the first two years of life have shown promise however, differences in Body Mass Index between intervention and control groups diminish once the interventions cease. Innovative and cost-effective strategies seeking to continue to support parents to engender appropriate energy balance behaviours in young children need to be explored. METHODS/DESIGN: The Infant Feeding Activity and Nutrition Trial (InFANT) Extend Program builds on the early outcomes of the Melbourne InFANT Program. This cluster randomized controlled trial will test the efficacy of an extended (33 versus 15 month) and enhanced (use of web-based materials, and Facebook® engagement), version of the original Melbourne InFANT Program intervention in a new cohort. Outcomes at 36 months of age will be compared against the control group. DISCUSSION: This trial will provide important information regarding capacity and opportunities to maximize early childhood intervention effectiveness over the first three years of life. This study continues to build the evidence base regarding the design of cost-effective, scalable interventions to promote protective energy balance behaviors in early childhood, and in turn, promote improved child weight and health across the life course. TRIAL REGISTRATION: ACTRN12611000386932 . Registered 13 April 2011.

Cross-fostering reduces obesity induced by early exposure to monosodium glutamate in male rats

Maternal obesity programmes a range of metabolic disturbances for the offspring later in life. Moreover, environmental changes during the suckling period can influence offspring development. Because both periods significantly affect long-term metabolism, we aimed to study whether cross-fostering during the lactation period was sufficient to rescue a programmed obese phenotype in offspring induced by maternal obesity following monosodium L-glutamate (MSG) treatment. Obesity was induced in female Wistar rats by administering subcutaneous MSG (4 mg/g body weight) for the first 5 days of postnatal life. Control and obese female rats were mated in adulthood. The resultant pups were divided into control second generation (F2) (CTLF2), MSG-treated second generation (F2) (MSGF2), which suckled from their CTL and MSG biological dams, respectively, or CTLF2-CR, control offspring suckled by MSG dams and MSGF2-CR, MSG offspring suckled by CTL dams. At 120 days of age, fat tissue accumulation, lipid profile, hypothalamic leptin signalling, glucose tolerance, glucose-induced, and adrenergic inhibition of insulin secretion in isolated pancreatic islets were analysed. Maternal MSG-induced obesity led to an obese phenotype in male offspring, characterized by hyperinsulinaemia, hyperglycaemia, hyperleptinaemia, dyslipidaemia, and impaired leptin signalling, suggesting central leptin resistance, glucose intolerance, impaired glucose-stimulated, and adrenergic inhibition of insulin secretion. Cross-fostering normalized body weight, food intake, leptin signalling, lipid profiles, and insulinaemia, but not glucose homeostasis or insulin secretion from isolated pancreatic islets. Our findings suggest that alterations during the lactation period can mitigate the development of obesity and prevent the programming of adult diseases.