In the context of common complex disease, we assert that epigenetic concepts could inform: (1) updates in health risk information that could improve the motivational potency of health communications, (2) the development of new approaches to targeted and tailored interventions, and (3) novel measures of intervention impact. In this section, we expand on these points, offering several examples of how epigenetics might inform the future of health promotion research (Table 1
Epigenetic discovery health promotion research innovation and translation
Individual variation in whether risk exposures negatively influence gene expression
Improving motivational potency of health communications
Evaluating relative benefit of validating beliefs about individual variability in extent of harm produced by risk behaviors on motivation
Intervention adherence can prompt measurable gene expression
Intervention targeting and tailoring
Comparative effectiveness of targeting relapse prevention approach based on gene expression profile following intervention participation
New technology to measure epigenetic processes (e.g., methylation) in saliva and blood samples
Novel biomarkers of intervention impact
Evaluate intervention adherence on gene expression in randomized effectiveness trials
Improving motivational potency of health communications
Messaging is a key element of health promotion interventions with the challenge being how to frame health risk information in ways that motivate behavior change (Gallagher & Updegraff, 2012
). New understandings of epigenetic processes have been suggested for use to update public health messages about health risks in ways that might enhance both their credibility and persuasiveness (Loi et al., 2013
). For example, it is common to hear that the public is confused and frustrated by contradictory research findings related to risk exposures and health (e.g., alcohol intake is beneficial or harmful for some but not all health outcomes). Moreover, public health recommendations to limit risk behaviors can be inconsistent with direct experience—individuals are observed to stay healthy despite engaging in risk behaviors such as cigarette smoking or poor diet. This apparent lack of coherence in explanations could lead the public to question the validity of health recommendations (Cameron et al., 2012
). There is strong conceptual support that the public’s explanations (or mental models) for individual differences in the health effects of exposures (e.g., poor diet, cigarette smoking) can influence their health behavior (Bostrom et al., 1992
; Cameron et al., 2012
Additionally, when asked about the causes of common health conditions, the public is likely to suggest health behaviors and genetics as key factors. Environmental exposures are less likely to be suggested, particularly by majority populations and those not
living in social disadvantage (Robert & Booske, 2011
). Thus many of those targeted by public health messages have limited imaginations for the role of social environment on health (Robert & Booske, 2011
), and generally low literacy regarding how genes and environment interact
to influence health outcomes (Condit & Shen, 2011
). An example relevant to epigenetics is that some genetic susceptibility factors only become important in the presence of an environmental exposure. Given the large and persistent health disparities associated with social- and community-level exposures, improved understanding of genome responsivity to the environment could serve as a bridge linking social environment exposures to health outcomes, decrease victim blaming and galvanize public support for social environmental solutions to public health problems (Thayer & Kuzawa, 2011
Health communications also could incorporate epigenetic concepts to explain how exposures such as lifestyle habits and the social environment can influence individuals differently. For example, descriptions of how accumulating exposures can turn genes on and off and influence health outcomes could be used to illustrate the need to make healthy lifestyle choices. Communications to increase understanding of environmental responsivity and life stages when risk might be heightened could be developed and evaluated to increase the salience of adopting risk reduction during those developmental stages. Explanations that validate beliefs about individual variability in response to risky lifestyle behaviors could be compared to general messages that recommend benefits for all, with regard to their relative influence on risk perceptions, motivation to reduce risk and behavior changes.
Among the many challenges these communication approaches will face is how to leverage mental models of individual variation in health outcomes while maintaining motivation and personal efficacy that risk reduction is needed and achievable. Communication strategies such as metaphors concerning environmental responsivity could be developed and rigorously evaluated for their effectiveness in reducing target audiences’ likelihood of ascribing a deterministic role to genetics (Cameron et al., 2012
; Parrott & Smith, 2014
). These principles will undoubtedly include conceptualizing ways that concepts relevant to epigenetics (e.g., risk uncertainty) can be applied to increase the motivational relevance and other constructs key to effective communications (Fischhoff & Davis, 2014
). However an important caveat is that such communications will not have sufficient potency to promote behavior change (Hollands et al., 2016
). Thus, research, guided by social and behavioral conceptual models, will be needed to evaluate whether these communication updates add value to evidence-based behavioral intervention approaches.
Intervention targeting and tailoring
Emerging understandings of variation in epigenetic response also could be used to customize health promotion interventions. Consider the work of Crujeiras et al. (2013
) that evaluated the association of epigenetic changes in specific genes with appetite control among men who had participated in a standard weight loss intervention (30 % calorie restriction goal). Compared to non-regainers, weight regainers (those who regained greater than 10 % of weight lost) were more likely to have genes involved in stimulating appetite turned on (i.e., lower total methylation at loci) and to have genes associated with appetite suppression turned off. These post-intervention epigenetic responses to weight loss could be used to tailor or target weight maintenance strategies to these groups. For example, interventions could emphasize prolonged ongoing support for those at highest risk and compare the value of these approaches to standard weight maintenance approaches.
Health promotion-related conceptual frameworks could be helpful for specifying individual and group-level exposures most germane for targeted or tailored interventions. Antonucci et al. (2014
), for example, conceptualize accumulating exposures over a life span as a “convoy”. In considering the role of supportive others, they suggest that individuals acquire a convoy of relationships that move with them throughout the life course and change qualitatively over time. Linking this concept with epigenetic mechanisms suggests that health risks, and the success of health promotion interventions might be influenced by shifts in qualities of this convoy of support at windows of heightened responsivity. In considering which exposures are critical the researcher could pose questions such as what convoys of health behaviors, social support, or built environment exposures were occurring at responsivity milestones and have they changed detrimentally or beneficially over the life course? As well, such an approach could be used to identify those with exposure risk profiles and tailor or target interventions accordingly.
Such interventions might target groups who share “exposures” that occurred at important developmental junctures of high epigenetic responsivity (Mitchell et al., 2013
). For example, intrauterine exposures have been shown to prompt epigenetic effects on neuroendocrine response and to be associated with increased likelihood of childhood and adult-onset obesity (El Hajj et al., 2014
). Thus, obesity prevention interventions could be targeted to children born to obese mothers. Individually tailored interventions also could be evaluated as a motivational tool via personalized feedback to mothers regarding their child’s prenatal exposure. Integrating these approaches to leverage mother’s motivation to protect their children may be a particularly promising communication approach (Koehly et al., 2015
). Each of these approaches have support from communication theory that they might increase the motivational relevance of health behaviors and prompt more thorough information processing than generic public health messages (Griffin et al., 1999
Novel measures of intervention impact
Understandings of epigenetics also could suggest new biomarkers that are more sensitive to intervention adherence and illuminate the processes through which interventions do or do not influence health outcomes. Too often large well-designed intervention trials that are based on strong conceptual models show null results, that is, no benefit of the intervention over comparison groups. Often intervention effectiveness is based on self-reported outcomes. Many researchers have raised concerns that the very act of completing repeated survey assessments could prompt behavior change among participants in comparison conditions or that responses reflect the heightened social desirability of reporting behavior change (DeMaio, 1985
). Together, these factors may undermine the validity of self-reports, even when using rigorous behavioral assessments, and mask the benefits of health promotion interventions.
Health promotion research has a long tradition of using biomarkers (e.g., saliva samples) to validate self-reported behavior change where possible and to minimize related threats to validity when evaluating intervention effectiveness. Similarly epigenetic methylation processes could be assessed to indicate whether self-reported intervention adherence is concordant with physiological processes that might improve intervention adherence (e.g., release of dopamine associated with improved mood) or benefits of sustained behavior change (e.g., changes in gene expression associated with inflammation processes). These new approaches could give evidence of whether improvements in self-reported initiation and maintenance of behavior change deemed statistically insignificant are in fact concordant with physiological responses that suggest health benefit of intervention participation. It is possible that interventions shown to produce small improvements in health habits relative to a comparison group bring physiological benefits that are currently not being measured.
Bryan and colleagues are among the few research teams that evaluated the effect of participating in health promotion interventions and its association with epigenetic processes (Bryan et al., 2013
). Their preliminary findings with 64 participants who participated in a 12-month exercise intervention gives insight into the link between physical activity and breast cancer. Self-reported physical activity based on the frequently used physical activity record (PAR) was associated with epigenetic modifications involved in turning off genes that prevent the cell proliferation that gives rise to malignant breast tumors. These epigenetic changes could be added as indicators of intervention benefit. Similarly, Ronn and colleagues assessed genome wide methylation in the adipose tissue of sedentary men before and after their participation in a 6-month exercise intervention (Ronn et al., 2013
). The investigators analyzed abdominal adipose biopsies from men before and 48 h after their last exercise session. Results indicated a comprehensive increase in methylation (turning genes off) in all regions suggesting a more metabolically active adipose tissue after intervention participation.
In each of these instances, the health promotion researcher hypothesizes and tests, for example, whether adherence to a behavior change intervention is associated with methylation (appropriately turning genes off or on) that may be biologically beneficial for the health outcome of interest or influenced by intervention participation. Additionally, these approaches could enable evaluation of whether the intervention group or some subgroup of individuals based on intervention adherence level or convoy characteristics (e.g., life course social support or stress) show patterns of methylation consistent with a conceptual model or hypothesis. Thus, methylation patterns offer a measure of epigenetic modifications that may be more sensitive to intervention effectiveness.