In 2006, Brosschot, Gerin, and Thayer introduced the perseverative cognition hypothesis (PCH), which suggested that worry and/or repetitive thinking may lead to disease by prolonging stress-related physiological activation by amplifying short-term responses, delaying recovery, or reactivating responses after a stressor has been experienced. In the last decade, a number of important reviews and papers have been published clearly demonstrating that perseverative cognition is associated with somatic outcomes (e.g., Brosschot et al., 2005; Verkuil et al., 2010; O'Connor et al., 2013; Ottaviani et al., 2015).

More specifically, the PCH proposes that worry, rumination and related thought processes are not only psychological phenomena but can also impact on physical health. It is argued that perseverative cognition (PC)—the cognitive representation of past stressful events or feared future events—mediates the relationship between stress and physical disease as, when stressors are perseverated upon in thought, the damaging physiological activation associated with stress is also protracted, thus increasing susceptibility to stress-related ill-health. The hypothesis states that, in such instances where the physical stressor is absent, the cognitive representation alone can induce a physiological stress response, which, when prolonged, increases the likelihood of stress-related diseases. In this sense, the direct relationship between stress and disease is intensified when a stressor is subject to thought.

Since the PCH was proposed, a substantial amount of evidence has been identified which supports the main tenets of the theory. In one of the first reviews published, Verkuil et al. (2010) presented convincing research evidence of a link between the prolonged physiological activation associated with PC and somatic health outcomes. More recently, Ottaviani et al. (2015) conducted a comprehensive meta-analysis to synthesize the physiological concomitants of PC in healthy participants. These authors concluded that there was clear evidence that PC affects cardiovascular, autonomic, and endocrine nervous system pathways consistent with a pathogenic route to long-term disease outcomes. Specifically, they found higher levels of heart rate, blood pressure, and cortisol activity and lower heart rate variability during PC or related to trait PC.

However, despite the accumulating evidence for a direct pathway from PC to disease outcomes, we were interested in exploring the existence of an additional indirect pathway via health behaviors. In the broader stress literature, it is well-established that stress can affect health indirectly, through the modification of health behaviors (Rod et al., 2009; O'Connor and Conner, 2011). Stress induced modifications of habitual health behaviors such as food choice and eating behavior have been shown to be particularly important in understanding physical disease risk (Steptoe et al., 1998; O'Connor et al., 2008). Recent findings have confirmed that stress is frequently associated with increased unhealthy food intake in laboratory-based and naturalistic studies (e.g., Adam and Epel, 2007; O'Connor et al., 2008; Dallman, 2010; Van Strien et al., 2012).

For example, in a 28-day diary study, O'Connor et al. (2008) showed that daily stressors were associated with increased consumption of high fat and high sugar between-meal snack foods and with a reduction in main meals and vegetable consumption. Moreover, evidence is beginning to emerge showing associations between rumination and the consumption of unhealthy foods such as cakes, crisps, and confectionary (e.g., Cropley et al., 2012). Therefore, it remains possible that PC might also amplify, prolong, and reactivate the same physiological and psychological processes that account for the negative effects of stress on eating behavior.

Other studies have provided evidence of a relationship between stress and increased alcohol consumption, which has been identified as a significant risk factor for chronic disease (Rehm et al., 2009). For example, in a daily diary study, Grzywacz and Almeida (2008) reported that participants were more likely to binge drink on days when they experienced more severe stressors. Similarly, in an experimental study, a blunted cortisol response to a laboratory stressor was associated with greater post-stressor alcohol consumption (Pratt and Davidson, 2009). Corbin et al. (2013) suggest that alcohol may be used to deal with negative emotion when alternative coping strategies are not available. In the sample of college students they surveyed, stress levels were positively associated with drinking to cope, and drinking problems. Moreover, those who reported drinking to cope drank more heavily. Again, similar to eating behavior, data are emerging showing that measures of (negative work) rumination are associated with more alcohol consumption on workdays (Frone, 2015).

Nevertheless, taking the above findings together, it is surprising how little research has explicitly explored the relationship between measures of PC and health behaviors. In addition, it is important to distinguish between health promoting and health risk behaviors. Health-promoting behaviors are health-enhancing behaviors which individuals are encouraged to perform more to protect their health; whereas health risk behaviors are health-damaging behaviors which individuals are encouraged to perform less. Given that PC exacerbates the relationship between the experience of stress and the physiological response, it is also possible that, as the experience of the stressor is prolonged by worry, or ruminative processes, so too may be its detrimental impact on different types of health behaviors. For example, PC might be more strongly associated with health risk behaviors such as alcohol consumption, smoking, and high fat food intake compared to health promoting behaviors such a physical exercise, given the former may be strategies to help alleviate rumination, and worry. Furthermore, over time, PC-induced increases in health risk behaviors and decreases in health promoting behaviors are likely to influence pathogenic pathways to long-term disease outcomes. Figure 1 represents the original model proposed by Brosschot et al. (2006) with an additional route to the pathogenic disease state via poorer health behaviors (e.g., higher levels of alcohol, tobacco and unhealthy food consumption, and lower physical activity levels and lower consumption of healthy foods). In this conceptualization, we theorize that rumination about past stressful events or worry about feared future events will mediate the effects of stressors on health behaviors (particularly those previously shown to be influenced by stress), which will have negative consequences for health outcomes and disease processes. Therefore, the primary aim of the current review and meta-analysis was to quantify the existing evidence relating any measure of PC to health behaviors.

A secondary aim of the current review and meta-analysis was to establish whether different types of PC had a differential impact on health behaviors. As outlined above, PC is an umbrella term which encompasses repetitive, negative thought processes related to the experience of a stressor. This term was developed as it was thought that disparate concepts such as rumination and worry were either too narrowly or too broadly defined to allow for a model which linked negative, repetitive thought, and somatic health (Verkuil et al., 2010). Indeed, there has been recent debate about whether rumination and worry ought to be considered separately or collapsed into a single phenomenal category (cf., Ottaviani et al., 2015). Nevertheless, the most widely researched of these thought processes are depressive rumination and worry (Verkuil et al., 2010). Nolen-Hoeksema et al. (2008) described rumination as “thinking perseveratively about one's feelings and problems” (p. 400) regardless of thought content (positive or negative). However, although ruminative thoughts can be positive, within the PCH, PC only encompasses negative thoughts (Verkuil et al., 2010).

Moreover, there is good agreement that rumination is best conceptualized as having two components: brooding and reflection (Treynor et al., 2003). Brooding is described as a passive and judgemental form of rumination, whereas reflection is more contemplative with a focus on problem-solving. Treynor et al. (2003) provided evidence that brooding is the more maladaptive component of rumination as brooding predicted symptoms of depression one year later, whereas, although reflection predicted current depression, it predicted lower levels of depression over time. Reflection is thus considered to be a somewhat adaptive component of rumination.

Whereas rumination has been shown to be associated with depression, worry is a central aspect of anxiety disorders, and particularly generalized anxiety disorder (Borkovec and Inz, 1990). Borkovec et al. (1983) were the first research group to aim to define and categorize the process of worrying and to distinguish it from related processes such as anxiety, fear, and mental problem-solving. Borkovec et al. (1983) defined worry as “a chain of thoughts and images, negatively affect-laden, and relatively uncontrollable. The worry process represents an attempt to engage in mental problem-solving on an issue whose outcome is uncertain but contains the possibility of one or more negative outcomes. Consequently, worry relates closely to fear processes” (p. 10). Therefore, within the PCH, worry is viewed as worry about feared events (or stressors) in the future.

To summarize, the primary aim of the current review was to systematically review empirical studies which have investigated the relationship between any type of PC and any health behavior outcome. As the PCH aimed to model how stress-related thinking may impact on health outcomes in otherwise healthy populations, the aim here was also to review studies involving physically and mentally healthy participants. It was hypothesized that higher levels of PC would be associated with more health risk behaviors (defined as those behaviors which, if performed, would hinder health) and less health promoting behaviors (defined as those behaviors which, if performed, would benefit health). The secondary aim was to explore whether different types of PC (rumination and worry) had differential effects on health behaviors.

The main findings of this systematic review and meta-analysis are that increases in PC are associated with increases in health risk behaviors (substance use, alcohol consumption, unhealthy eating, and smoking) that are driven primarily through rumination. In contrast, measures of worry and reflection were not associated with health behaviors. These results are important for a number of reasons. First, they provide partial support for our hypothesis that in Brosschot et al.'s (2006) original PCH, there may be scope for an additional route to pathogenic disease via poorer health behaviors. In this conceptualization, we theorize that rumination about past stressful events will mediate the effects of stressors on health behaviors (particularly those previously shown to be influenced by stress), which will have negative consequences for health outcomes and disease processes.

Second, from a brain-body point of view, the current findings are important in the context of the development of allostatic load. McEwen (1998) introduced the concept of allostatic load to capture the wear and tear the body experiences as a result of repeated and prolonged adaption to environmental and psychosocial stressors. He proposed that the long-term impact of stress affects the body at cardiovascular, metabolic, neural, behavioral, and cellular levels. Similar to basic homeostatic systems such as body temperature, the HPA axis, the autonomic nervous system and the cardiovascular, metabolic and immune systems protect the body by adapting to internal and external stress. This is known as allostasis. However, if the activation of these systems (allostasis) is repeated and prolonged, allostatic load will be experienced in the form of increased stress hormone, immune cell, brain activity, and cardiovascular responses, ultimately, overtime leading to heightened risk of developing disease (McEwen, 1998, 2007). Numerous factors may contribute to the development of allostatic load including genes, early life experiences and disturbances of the sleep-wake cycle (McEwen, 2007). However, McEwen also argues that lifestyle choices such as alcohol consumption, diet, smoking, and exercise, that may be learned overtime (and triggered by PC), contribute to allostatic load by influencing the reactivity of the biological systems that release the physiological stress mediators (e.g., cortisol, adrenaline, blood pressure, heart rate, immune cells). In other words, environmental and psychosocial stressors give rise to PC, which in turn triggers maladaptive behavioral responses that may influence and exacerbate the prolonged stress response as conceptualized in the PCH, leading to increased risk of disease. Moreover, we also contend that the relationship between the prolonged stress response and health behaviors may be bi-directional (see Figure 1). Interestingly, in the short term, engaging in health risk behaviors such as comfort eating or alcohol consumption (triggered by stressors and then PC) may be perceived by individuals as beneficial, however, overtime these behaviors are likely to be damaging for health.

In addition to the PC-induced health behavior-prolonged stress response pathway, it is highly likely that PC-induced health risk behaviors will directly impact on pathogenic states such as changes in somatic health outcomes (see second dashed pathway in Figure 1). For example, for eating behavior, it is well established that stress (and possibly PC) contributes directly to diseases like cardiovascular disease and obesity risk to the extent that it produces deleterious changes in diet and helps maintain unhealthy eating behaviors (O'Connor et al., 2015). In terms of physical activity, a recent systematic review and meta-analysis, showed that greater time spent sedentary was linked to increased risk of diabetes, cardiovascular events, cardiovascular mortality, and all-cause mortality (Wilmot et al., 2012). Therefore, again the extent to which PC can disrupt habitual health behaviors such as exercise, eating behavior, alcohol consumption, and smoking, is likely to increase its direct effects on behavioral mediated changes in pathogenic states.

Nevertheless, we recognize that the current results ought to be considered preliminary at this stage precluding any firm conclusions. We are mindful that our analyses did not find evidence that worry about feared future events was associated with health behaviors. This is surprising given that worry has been identified as important in recent narrative reviews and meta-analyses in the context of the PCH (Verkuil et al., 2010; Ottaviani et al., 2015). A likely explanation for the absence of a significant effect here might be related to the heterogeneity of effect sizes across the studies and/or to do with the variability in types of worry measures utilized (e.g., health-related worry, cancer worry, trait worry, etc. as well as single-item vs. multi-item measures). Alternatively, this null finding may reflect that there are relatively few studies that have directly investigated the relationship between worry (and rumination) and health risk and health promoting behaviors. In many of the studies reviewed, exploring the relationship between worry (and rumination) has been of secondary interest. It might also be that worry, triggered by fear-appeals, has the capacity to promote some health behaviors, thereby, contributing to the observed mixed findings (Tannenbaum et al., 2015). We also acknowledge that limiting our search strategy to studies published from 1990 onwards may have resulted in our missing some important studies. However, we feel the potential impact of this approach is likely to be fairly minimal given that of the articles included in our review, none were published prior to 2003, suggesting few, if any, studies published prior to 1990 would have met our inclusion/exclusion criteria.

We hope the current findings will spur on PC researchers to include measures of health behaviors in their future studies and to adopt a myriad of different approaches to investigate the precise processes and mechanisms through which PC is linked to health behaviors in the context of the PCH. It is likely that these processes will differ dependent on the nature of the health behavior (i.e., health risk vs. health promoting, frequency of the behavior etc.) and in relation to the type of PC (rumination vs. worry; health-related worry vs. general worry etc.). Future research ought to attempt to replicate the current findings utilizing innovative techniques such as ecological momentary assessment, diary methods and time-lagged designs in combination with measures of the physiological concomitants of PC (Verkuil et al., 2012; Gartland et al., 2014). There is also scope to manipulate PC in carefully controlled laboratory studies in order to investigate whether changes in PC are associated with changes in health behaviors (such as food intake; cf., Newman et al., 2007).

In conclusion, this systematic review and meta-analysis showed that increases in PC are associated with increases in health risk behaviors (substance use, alcohol consumption, unhealthy eating, and smoking) that are driven primarily through rumination. These findings provide partial support for our hypothesis that in Brosschot et al.'s (2006) original PCH, there may be scope for an additional route to pathogenic disease via poorer health behaviors.

DO, FC, and AP conceived of the systematic review and meta-analysis. FC and LC conducted the data extraction and coding with input from AP and DO. AP and FC performed the meta-analysis. DO, AP, and FC drafted the manuscript. All authors approved the final version and agree to be accountable for this work.

FC is funded by an ESRC White Rose Training Centre Advanced Quantitative Methods Ph.D. studentship.