Positive parenting, parenting stress, and child self-regulation patterns differ across maternal demographic risk.

We examined relations between positive parenting, parenting stress, and children's regulatory abilities across infancy and early childhood. First-time mothers and their infants (N = 682) were recruited prenatally. Mothers belonged to one of three potential demographic risk groups: adolescent mothers (AM), adult low-educated mothers (LEM), and adult high-educated mothers (HEM). Parent-child interactions were observed in the home and scored for positive parenting (at 4, 8, and 18 months) and child self-regulation (at 4, 8, 18, and 30 months). Parenting stress was measured by questionnaire at 6, 12, and 24 months. A multigroup cross-lagged panel model indicated different patterns of effects for adolescent and adult mothers: for AM, positive parenting and parenting stress were related early in infancy, but no relations emerged with regulation until 18 months. For LEM, parenting related to regulation only at later ages, and for HEM, positive parenting, parenting stress, and regulation were associated early in the infant's life but not later. Differing patterns of influence indicate, perhaps, the importance of considering demographic risk and timing of parenting in childhood in relation to child regulatory outcomes. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Indirect effects of parental physical discipline on child literacy through child externalizing and internalizing problems: A longitudinal mediation.

Data from the Early Childhood Longitudinal Study (ECLS-K; N = 6,420; 67.9% White/non-Hispanic, 15% Hispanic, 13% Black/non-Hispanic, 2% Asian, 3% Native American/Alaska Native; 25% of parents' income <$25,000, 25% = $25,001 to $45,000, 29% = $45,001 to $75,000, 20% = $75,001 or greater) were used to test structural equation models in which child externalizing or internalizing problems mediate the relation between parental physical discipline and child literacy development over time. Results show that parents' physical discipline in Kindergarten was associated with lower literacy levels in 8th grade and slower growth in literacy development from K-8. Additionally, parents' physical discipline during Kindergarten predicted more externalizing symptoms 1 year later, which in turn predicted lower literacy skills in eighth grade (partial mediation detected) and lower growth rates in literacy skills over time (complete mediation detected). Overall, parents' physical discipline administered during their child's kindergarten year may have cascading detrimental impacts on child literacy development through externalizing problem behaviors. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

A Ketogenic Diet Extends Longevity and Healthspan in Adult Mice.

Calorie restriction, without malnutrition, has been shown to increase lifespan and is associated with a shift away from glycolysis toward beta-oxidation. The objective of this study was to mimic this metabolic shift using low-carbohydrate diets and to determine the influence of these diets on longevity and healthspan in mice. C57BL/6 mice were assigned to a ketogenic, low-carbohydrate, or control diet at 12 months of age and were either allowed to live their natural lifespan or tested for physiological function after 1 or 14 months of dietary intervention. The ketogenic diet (KD) significantly increased median lifespan and survival compared to controls. In aged mice, only those consuming a KD displayed preservation of physiological function. The KD increased protein acetylation levels and regulated mTORC1 signaling in a tissue-dependent manner. This study demonstrates that a KD extends longevity and healthspan in mice.

The Influence of Dietary Fat Source on Life Span in Calorie Restricted Mice.

Calorie restriction (CR) without malnutrition extends life span in several animal models. It has been proposed that a decrease in the amount of polyunsaturated fatty acids (PUFAs), and especially n-3 fatty acids, in membrane phospholipids may contribute to life span extension with CR. Phospholipid PUFAs are sensitive to dietary fatty acid composition, and thus, the purpose of this study was to determine the influence of dietary lipids on life span in CR mice. C57BL/6J mice were assigned to four groups (a 5% CR control group and three 40% CR groups) and fed diets with soybean oil (high in n-6 PUFAs), fish oil (high in n-3 PUFAs), or lard (high in saturated and monounsaturated fatty acids) as the primary lipid source. Life span was increased (p < .05) in all CR groups compared to the Control mice. Life span was also increased (p < .05) in the CR lard mice compared to animals consuming either the CR fish or soybean oil diets. These results indicate that dietary lipid composition can influence life span in mice on CR, and suggest that a diet containing a low proportion of PUFAs and high proportion of monounsaturated and saturated fats may maximize life span in animals maintained on CR.

The influence of Shc proteins on life span in mice.

The signaling molecule p66Shc is often described as a longevity protein. This conclusion is based on a single life span study that used a small number of mice. The purpose of the present studies was to measure life span in a sufficient number of mice to determine if longevity is altered in mice with decreased Shc levels (ShcKO). Studies were completed at UC Davis and the European Institute of Oncology (EIO). At UC Davis, male C57BL/6J WT and ShcKO mice were fed 5% or 40% calorie-restricted (CR) diets. In the 5% CR group, there was no difference in survival curves between genotypes. There was also no difference between genotypes in prevalence of neoplasms or other measures of end-of-life pathology. At 40% calorie restriction group, 70th percentile survival was increased in ShcKO, while there were no differences between genotypes in median or subsequent life span measures. At EIO, there was no increase in life span in ShcKO male or female mice on C57BL/6J, 129Sv, or hybrid C57BL/6J-129Sv backgrounds. These studies indicate that p66Shc is not a longevity protein. However, additional studies are needed to determine the extent to which Shc proteins may influence the onset and severity of specific age-related diseases.