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Higher levels of protective parenting are associated with better young adult health: exploration of mediation through epigenetic influences on pro-inflammatory processes.

Beach SR, Lei MK, Brody GH, Dogan MV, Philibert RA - Front Psychol (2015)

Bottom Line: Supporting expectations, in a sample of 398 African American youth residing in rural Georgia, followed from age 11 to age 19, parenting at ages 11-13 was associated with youth reports of better health at age 19.We found that parenting was associated with changes in TNF methylation as well as with changes in cell-type composition.The current research suggests the potential value of examining the health-related effects of parenting in late childhood and early adolescence.

View Article: PubMed Central - PubMed

Affiliation: Center for Family Research, University of Georgia , Athens, GA, USA.

ABSTRACT
The current investigation was designed to examine the association of parenting during late childhood and early adolescence, a time of rapid physical development, with biological propensity for inflammation. Based on life course theory, it was hypothesized that parenting during this period of rapid growth and development would be associated with biological outcomes and self-reported health assessed in young adulthood. It was expected that association of parenting with health would be mediated either by effects on methylation of a key inflammatory factor, Tumor necrosis factor (TNF), or else by association with a pro-inflammatory shift in the distribution of mononuclear blood cells. Supporting expectations, in a sample of 398 African American youth residing in rural Georgia, followed from age 11 to age 19, parenting at ages 11-13 was associated with youth reports of better health at age 19. We found that parenting was associated with changes in TNF methylation as well as with changes in cell-type composition. However, whereas methylation of TNF was a significant mediator of the association of parenting with young adult health, variation in mononuclear white blood cell types was not a significant mediator of the association of parenting with young adult health. The current research suggests the potential value of examining the health-related effects of parenting in late childhood and early adolescence. Further examination of protection against pro-inflammatory tendencies conferred by parenting appears warranted.

No MeSH data available.


Related in: MedlinePlus

The conceptual model showing two potential biological, indirect pathways from protective parenting to self-reported young adult poor health. (1) A positive efffect (+) on level of methylation of TNF, and (2) a negative effect (–) on activation of monocytes reflecting greater innate immune system activation, with each associated in turn with young adult health.
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Figure 1: The conceptual model showing two potential biological, indirect pathways from protective parenting to self-reported young adult poor health. (1) A positive efffect (+) on level of methylation of TNF, and (2) a negative effect (–) on activation of monocytes reflecting greater innate immune system activation, with each associated in turn with young adult health.

Mentions: The two different types of potential effects on early programming of pro-inflammatory responses (Gluckman et al., 2005; Rickard and Lummaa, 2007) suggest the need to examine two indirect pathways in models examining potential biological mechanisms of influence from parenting to later health outcomes. With regard to epigenetic change of inflammation related genes, we focus on methylation of TNF due to the central role of TNF-α in inflammatory processes. All cells involved in inflammation have receptors for TNF-α and are activated by it to facilitate further inflammation. This positive feedback quickly amplifies the acute phase inflammatory response, making TNF an attractive focus of empirical attention. With regard to cell-type variation, we examine variation in concentration of cell-types in lymphocyte pellets to identify variation that may reflect relatively greater responsiveness of the innate vs. the acquired immune system. The resulting general model is portrayed in Figure 1. To the extent that the significant indirect effects (IE) suggested in the figure are identified, they focus theoretical attention on biological mechanisms potentially conferring long-lasting effects of protective parenting on health. Accordingly, we examine the hypothesis that protective parenting during childhood and early adolescence will be associated with self-reported health in young adulthood, leading to a negative (-) association and that inflammatory mechanisms in the form of differences in TNF methylation and cell-type variation will account for some or all of this association. In the process of examining three main hypotheses, we also examine three measurement hypotheses:


Higher levels of protective parenting are associated with better young adult health: exploration of mediation through epigenetic influences on pro-inflammatory processes.

Beach SR, Lei MK, Brody GH, Dogan MV, Philibert RA - Front Psychol (2015)

The conceptual model showing two potential biological, indirect pathways from protective parenting to self-reported young adult poor health. (1) A positive efffect (+) on level of methylation of TNF, and (2) a negative effect (–) on activation of monocytes reflecting greater innate immune system activation, with each associated in turn with young adult health.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4446530&req=5

Figure 1: The conceptual model showing two potential biological, indirect pathways from protective parenting to self-reported young adult poor health. (1) A positive efffect (+) on level of methylation of TNF, and (2) a negative effect (–) on activation of monocytes reflecting greater innate immune system activation, with each associated in turn with young adult health.
Mentions: The two different types of potential effects on early programming of pro-inflammatory responses (Gluckman et al., 2005; Rickard and Lummaa, 2007) suggest the need to examine two indirect pathways in models examining potential biological mechanisms of influence from parenting to later health outcomes. With regard to epigenetic change of inflammation related genes, we focus on methylation of TNF due to the central role of TNF-α in inflammatory processes. All cells involved in inflammation have receptors for TNF-α and are activated by it to facilitate further inflammation. This positive feedback quickly amplifies the acute phase inflammatory response, making TNF an attractive focus of empirical attention. With regard to cell-type variation, we examine variation in concentration of cell-types in lymphocyte pellets to identify variation that may reflect relatively greater responsiveness of the innate vs. the acquired immune system. The resulting general model is portrayed in Figure 1. To the extent that the significant indirect effects (IE) suggested in the figure are identified, they focus theoretical attention on biological mechanisms potentially conferring long-lasting effects of protective parenting on health. Accordingly, we examine the hypothesis that protective parenting during childhood and early adolescence will be associated with self-reported health in young adulthood, leading to a negative (-) association and that inflammatory mechanisms in the form of differences in TNF methylation and cell-type variation will account for some or all of this association. In the process of examining three main hypotheses, we also examine three measurement hypotheses:

Bottom Line: Supporting expectations, in a sample of 398 African American youth residing in rural Georgia, followed from age 11 to age 19, parenting at ages 11-13 was associated with youth reports of better health at age 19.We found that parenting was associated with changes in TNF methylation as well as with changes in cell-type composition.The current research suggests the potential value of examining the health-related effects of parenting in late childhood and early adolescence.

View Article: PubMed Central - PubMed

Affiliation: Center for Family Research, University of Georgia , Athens, GA, USA.

ABSTRACT
The current investigation was designed to examine the association of parenting during late childhood and early adolescence, a time of rapid physical development, with biological propensity for inflammation. Based on life course theory, it was hypothesized that parenting during this period of rapid growth and development would be associated with biological outcomes and self-reported health assessed in young adulthood. It was expected that association of parenting with health would be mediated either by effects on methylation of a key inflammatory factor, Tumor necrosis factor (TNF), or else by association with a pro-inflammatory shift in the distribution of mononuclear blood cells. Supporting expectations, in a sample of 398 African American youth residing in rural Georgia, followed from age 11 to age 19, parenting at ages 11-13 was associated with youth reports of better health at age 19. We found that parenting was associated with changes in TNF methylation as well as with changes in cell-type composition. However, whereas methylation of TNF was a significant mediator of the association of parenting with young adult health, variation in mononuclear white blood cell types was not a significant mediator of the association of parenting with young adult health. The current research suggests the potential value of examining the health-related effects of parenting in late childhood and early adolescence. Further examination of protection against pro-inflammatory tendencies conferred by parenting appears warranted.

No MeSH data available.


Related in: MedlinePlus