Lifetime stressor exposure is associated with greater rewarding effects of stress-related eating.

Acute stressors tend to shift preferences toward comfort foods, yet they do not ubiquitously increase the amount of food consumed. Moreover, although many individuals eat more under stress, others eat less or show no change. Although the precise mechanisms explaining this variability in stress-related eating are unknown, they may be driven by individual differences in the rewarding effects of comfort eating, which are enhanced by greater lifetime stressor exposure. To investigate this possibility, we examined whether differences in lifetime stressor exposure predicted reductions in negative affect following snacking (i.e., negative reinforcement) and if this effect was specific to stress-related snacking or snacking in general. Participants were 26 women (23% non-White) between 20 and 45 years old (M = 31), with a mean body mass index of 26, who completed three laboratory visits. Participants completed an assessment of lifetime stressor exposure (i.e., STRAIN) on the first visit and, on two subsequent laboratory visits in counterbalanced order, were given snacks after an acute social stress task (i.e., TSST) or rest period. Greater lifetime stressor exposure was related to greater post-ingestive decreases in negative affect following the acute social stressor but not following the rest period. If stress-related eating is more comforting for women with greater lifetime stressors and contributes to a stronger stress-eating association, then this may inform obesity-related clinical treatments that target behaviors and cognitions related to reward-based learning.

Lifetime stressor exposure, eating expectancy, and acute social stress-related eating behavior: A pre-registered study of the emotional eating cycle.

Eating behaviors in response to acute stressors are highly variable: whereas many individuals eat more following stressors, others eat less or show no change in food consumption. Understanding factors that predict individual differences in eating behaviors may help elucidate the psychosocial mechanisms underlying obesity, yet few experimental studies on this topic have been conducted to date. To address this issue, we conducted the present pre-registered study, where we investigated how lifetime stressor exposure moderates the extent to which eating expectancies enhance the learned association between stress-induced negative affect and snack intake. Participants were 44 women (30% non-White) between 18 and 50 years old (M = 27.9), with a mean body mass index of 25.6, who completed assessments of lifetime stressor exposure, eating behaviors, and eating expectancies (eating helps manage negative affect); in a subsequent visit, they were given snacks after an acute social stress task (TSST). The moderated moderation model (PROCESS model 3) yielded a significant three-way interaction. When eating expectancies were high, acute social stress-induced negative affect predicted greater M&M intake for women with very high total lifetime stressor exposure but less M&M intake for women with fewer lifetime stressors. These data thus highlight how lifetime stressor exposure interacts with eating expectancies and acute stress-induced negative affect to predict eating behavior. Replications in larger samples may help explain variability in stress-eating as well as how lifetime stressors contribute to obesity.

Self-reported emotional eaters consume more food under stress if they experience heightened stress reactivity and emotional relief from stress upon eating.

Group data means from individuals who self-assess as emotional eaters do not reliably show increased food intake in response to stress or negative emotions. This inconsistency in predictive validity of self-reported emotional eating (EE) could be attributable to unconsidered moderation of the relationship between self-reported EE and behavioral measures of EE. Greater emotional relief from stress by eating may provide enhanced negative reinforcement and promote future EE in response to stress as a form of self-medication. Thus, we predicted that greater emotional relief from stress by eating (decrease in negative affect from stress to post-eating) would moderate the extent to which heightened stress reactivity (measured by systolic blood pressure, SBP) moderates the relationship between self-reported EE and food intake post-stress. We also hypothesized that self-reported EE would not predict greater food consumption on the rest day. 43 undergraduate women completed online assessments of eating behaviors. Participants were given snacks to eat after a mental stress task (TSST) or rest period on separate days in counterbalanced order. Our prediction was supported, as the moderated moderation model (PROCESS model 3) was highly significant on the stress day. Self-reported EE predicted increased food intake post-stress only under conditions of high stress reactivity and high emotional relief. On the rest day, self-reported EE predicted greater snack food intake only when SBP was high. This conditional increased intake substantiates stress as a promoter of snack food consumption for women with greater EE. Overall, our findings identified factors that may distinguish the subset of self-reported emotional eaters who are more likely to display EE behaviors in a laboratory setting, yet further studies are needed to directly test whether negative reinforcement via emotional relief from stress by eating drives enhanced EE following stress.

Recalled and momentary virtual portions created of snacks predict actual intake under laboratory stress condition.

Virtual portion tasks have been used to predict food intake in healthy individuals, severity of illness in individuals with anorexia nervosa, and weight loss in bariatric surgery patients. Whether portion creation in response to a recalled interpersonal stress ("recalled stress portions") could be used as a proxy for ad lib intake, after a stressor, remains untested, and the mechanism supporting this relationship is unclear. The present study's goals were: 1) to validate virtual portion tasks as proxies for actual food intake in a stressful context and 2) to test a causal pathway in which these virtual stress portions predict ad lib intake after stress. We proposed that this relationship is mediated by virtual portions created the moment after laboratory stress or rest manipulation (momentary portions), and before the participant actually ate food. At screening, 29 healthy undergraduate white women created virtual portions of eight snacks (apples, olives, potato chips, pretzels, caramel popcorn, milk chocolate) that they typically eat and also portions they recall eating in response to a stressful interpersonal situation. In addition, after a Trier Social Stress Test, or a rest period, on separate days in counterbalanced order, participants created 'momentary' virtual portions of the same snacks presented during screening, and then were given potato chips, mini golden Oreos, and M&Ms to eat. Recalled stress (b = 0.07 ± 0.02, p = 0.003), and momentary stress (b = 0.12 ± 0.02, p = 0.00001), portions of milk chocolate accounted for 29% and 51%, respectively, of the variance in ad lib stress intake of M&Ms. Typical (b = 0.15 ± 0.07, p = 0.03), and momentary rest (b = 0.21 ± 0.06, p = 0.002), portions of chips accounted for 16% and 31%, respectively, of the variance in ad lib rest intake of chips. The causal pathway from recalled stress portion to ad lib stress snack intake was completely mediated by momentary stress portion for milk chocolate and M&Ms (ß = 0.04 ± 0.02, z = 2.4, p = 0.0154). These findings illustrate the planning and recall components of eating in response to stress, but not necessarily under rest conditions. This recalled stress virtual portion paradigm has clinical and research value in that it can detect those who overconsume in response to stress.

Negative affect is associated with increased stress-eating for women with high perceived life stress.

Perceived life stress (PLS) and cognitive restraint are associated with increased comfort food intake under stress and lead to weight gain and obesity, but the mechanisms by which they do so remain unclear. Stress and negative affect (NA) are associated with increased reward-driven comfort food intake as a means to 'feel better', particularly for individuals with higher PLS and cognitive restraint. Thus, we propose that PLS and cognitive restraint increase stress-eating by strengthening the relationship between stress-induced NA and comfort food intake. Upon comfort eating, individuals with higher PLS show greater reductions in the negative consequences of stress (e.g. NA). The rewarding effects of this 'emotional relief' may promote future stress-induced comfort eating, but this has yet to be examined. Thus, we investigate the pathways by which PLS or cognitive restraint increase snack intake under stress by proposing that 1) stress-induced NA is a stronger predictor of increased snack intake for women with greater PLS and cognitive restraint, and 2) greater PLS will be associated with greater reductions in NA upon snacking under stress (i.e. emotional relief). Forty-three healthy women were given snacks (chips, golden oreos, and M&Ms) to eat after a Trier Social Stress Test or rest period on separate days in counterbalanced order. Following linear regression analyses, we determined that stress-induced NA predicted more snack intake for women with higher PLS, and that higher PLS was associated with heightened emotional relief upon snacking under stress. Future studies are needed to directly assess whether greater emotional relief following stress-eating reinforces the learned association between stress-induced NA and intake, and ultimately explains greater stress-eating and obesity in women with higher PLS. This work may lead clinicians to focus on NA in the treatment of obesity-and stress-related illnesses for women with higher PLS.

Physiological responses to acute stress and the drive to eat: The impact of perceived life stress.

The stress-eating relationship is mediated by the release of cortisol from the hypothalamic pituitary adrenal (HPA) axis. Variability in stress-induced eating, and consequently, obesity, may be explained in part by individual differences in chronic stress, which disrupts the regulatory effects of the HPA axis on stress-induced eating. A greater understanding of the physiological mechanisms by which chronic stress affects acute stress-induced eating is critical in order to inform efforts to prevent and treat obesity. The current study examined the relationship between physiological responses to acute stress (cortisol and cardiovascular factors) and the drive to eat (ratings of hunger and desire to eat) in female undergraduates with high and low perceived life stress. Participants (n = 64) rated their perceived life stress in an online screening and, on a separate visit, rated their drive to eat before and after a mental stress task. The present report focused on only participants in the lowest (n = 16) and highest (n = 14) quartiles of perceived life stress. Women with high perceived life stress showed greater stress-induced cortisol responses, but no significant changes in blood pressure or heart rate. The heightened cortisol responses were not associated with hunger and desire to eat, but the cardiovascular responses were positively associated with the drive to eat. Women with low perceived life stress showed no relationships between physiological stress markers and the drive to eat. These results suggest that the cortisol stress response is dissociated from the drive to eat in chronically stressed women, although due to the small sample size the data should be regarded as preliminary. Further studies are needed to explore how cortisol and cardiovascular reactivity affect stress-induced eating.

The impact of chronic stress on the predictors of acute stress-induced eating in women.

Chronic stress is associated with palatable food intake and thus, the development of obesity. This may be due to chronic stress disrupting the regulatory effects of the hypothalamic pituitary adrenal (HPA) axis on stress-induced eating. Thus, the primary objective of the current study was to investigate how chronic stress (CS) and cortisol stress reactivity affect eating behaviors following acute stress. Exploratory analyses also sought to determine the distinct psychophysiological factors driving acute stress-induced eating in women with high versus low CS. Women with high (n = 21) and low (n = 14) perceived CS were subjected to the Trier Social Stress task and a rest period on two separate days in order to assess HPA axis and subjective psychological responses to acute stress. Following either stress or rest, participants portioned and consumed snack foods. Women displaying high cortisol reactivity to acute stress ate a smaller percentage of the food they poured than low cortisol reactors, but only in the low CS group. Additionally, stress-induced eating behaviors were associated with cortisol stress reactivity, depressive symptoms, and hunger for women with low CS, but only with a reduction in negative affect for women with high CS. Results indicated that chronic stress may disrupt HPA axis regulation of acute stress-induced consummatory behavior in favor of affective regulation. Replication in women across the weight spectrum may yield a greater understanding of how chronic stress affects the mechanisms underlying acute stress-induced eating, and inform prevention and treatment efforts for conditions related to stress and obesity.

Stress-induced eating in women with binge-eating disorder and obesity.

The purpose of the current study was to investigate stress-induced eating in women with binge-eating disorder (BED) and obesity. Three groups of women [obese with BED (n=9); obese non-BED (n=11); and normal weight (NW) non-BED (n=12)], rated their levels of hunger and psychological distress before and after completing the Trier Social Stress Test, followed by food anticipation and then consumption of their preferred snack food. We differentiated between the motivational and hedonic components of eating by measuring the amount of food participants poured into a serving bowl compared to the amount consumed. Stress did not affect poured and consumed calories differently between groups. Across all subjects, calories poured and consumed were positively correlated with post-stress hunger, but calories poured was positively correlated with post-stress anxiety and negative affect. These results indicate that stress-related psychological factors may be more strongly associated with the motivational drive to eat (i.e. amount poured) rather than the hedonic aspects of eating (i.e. amount consumed) for women in general. Exploratory correlation analyses per subgroup suggest that post-stress hunger was positively associated with calories poured and consumed in both non-BED groups. In the obese BED group, calories consumed was negatively associated with dietary restraint and, although not significantly, positively associated with stress-induced changes in anxiety.These findings suggest that stress-induced snacking in obese BED women may be influenced by psychological factors more so than homeostatic hunger mechanisms. After controlling for dietary restraint and negative affect, the NW non-BED women ate a greater percentage of the food they poured than both obese groups, suggesting that obesity may be associated with a heightened motivational drive to eat coupled with a reduction in hedonic pleasure from eating post-stress. Further studies that incorporate novel approaches to measuring the motivational versus hedonic aspects of stress-induced eating may expose nuanced eating behaviors that differentiate BED and obesity. If confirmed, our findings would support prevention and treatment strategies that target subsets of women based on obesity and BED status.

Social Support Attenuates Physiological Stress Responses and Experimental Pain Sensitivity to Cold Pressor Pain.

BACKGROUND: Social support improves health and has been shown to attenuate stress and pain. The precise characteristics of social support responsible for these effects, however, remain elusive. PURPOSE: The purpose of this study is to examine the relative efficacy of social support versus a neutral non-verbal social presence to attenuate stress and pain. METHODS: Seventy-six participants provided pain ratings and task assessments during a cold pressor task (CPT) in one of three conditions: verbal social support, neutral non-support, or alone. Reactivity to the CPT was assessed via cardiovascular measures, cortisol, and subjective ratings. RESULTS: Participants receiving social support showed attenuated blood pressure, heart rate, and cortisol reactivity, as well as reduced pain ratings, task difficulty, tension, and effort compared to neutral non-support and alone conditions. CONCLUSIONS: Social support, not the mere presence of another individual, attenuated stress and pain during a CPT. Given the negative health consequences of stress and pain, clinical studies incorporating social support into medical procedures and treatments are warranted.

Binge eating disorder and obesity: preliminary evidence for distinct cardiovascular and psychological phenotypes.

This study investigated cardiovascular functioning, mood, and eating-related psychological factors at rest and in response to mental stress in three groups of women: 1) Obese women with binge eating disorder (BED; n=9); 2) obese non-BED women (n=15); and 3) normal weight (NW) non-BED women (n=15). Compared to both obese and NW non-BED women, obese women with BED showed heightened overall blood pressure and reported greater depression symptoms, perceived stress, and eating-related psychopathology. Additionally, obese women with BED reported greater overall negative affect and state anxiety compared to obese non-BED women. The heart rate response to stress was blunted in the obese BED group compared to the other groups, but this effect was no longer significant after controlling for baseline differences in depression. Correlational analyses revealed a positive association between stress-induced changes in hunger and cardiovascular measures only in obese women with BED. Longitudinal studies are needed to determine if stress dysregulation and stress-induced increases in hunger contribute to the onset and/or maintenance of BED. In particular, studies utilizing an additional NW BED control group are warranted in order to further examine the impact of BED above and beyond the impact of obesity on psychophysiological functioning and to inform the growing literature regarding stress-related factors that distinguish the BED and obesity phenotypes.

Menstrual mood disorders are associated with blunted sympathetic reactivity to stress.

OBJECTIVE: Few studies have directly compared women with a menstrually related mood disorder (MRMD) with women who have suffered from depression for stress reactivity phenotypes. It is unclear whether blunted responses to stress in women with a MRMD reflect a unique phenotype of MRMDs or may be explained by a history of depression. METHODS: We assessed cardiovascular reactivity to stress in four groups: 1) Women with a MRMD without a history of depression (n=37); 2) women with a MRMD plus a history of depression (n=26); 3) women without a MRMD and without a history of depression (n=43); and 4) women without a MRMD but with a history of depression (n=20). RESULTS: Women with a MRMD showed blunted myocardial (heart rate and cardiac index) reactivity to mental stress compared to non-MRMD women, irrespective of histories of depression. Hypo-reactivity to stress predicted greater premenstrual symptom severity in the entire sample. Women with a MRMD showed blunted norepinephrine and diastolic blood pressure stress reactivity relative to women with no MRMD, but only when no history of depression was present. Both MRMD women and women with depression histories reported greater negative subjective responses to stress relative to their non-MRMD and never depressed counterparts. CONCLUSION: Our findings support the assertion that a blunted stress reactivity profile represents a unique phenotype of MRMDs and also underscore the importance of psychiatric histories to stress reactivity. Furthermore, our results emphasize the clinical relevance of myocardial hypo-reactivity to stress, since it predicts heightened premenstrual symptom severity.

Histories of major depression and premenstrual dysphoric disorder: Evidence for phenotypic differences.

This study examined unique versus shared stress and pain-related phenotypes associated with premenstrual dysphoric disorder (PMDD) and prior major depressive disorder (MDD). Sympathetic nervous system (SNS) and hypothalamic-pituitary-adrenal (HPA)-axis measures were assessed at rest and during mental stress, as well as sensitivity to cold pressor and tourniquet ischemic pain tasks in four groups of women: (1) non-PMDD with no prior MDD (N=18); (2) non-PMDD with prior MDD (N=9); (3) PMDD with no prior MDD (N=17); (4) PMDD with prior MDD (N=10). PMDD women showed blunted SNS responses to stress compared to non-PMDD women, irrespective of prior MDD; while women with prior MDD showed exaggerated diastolic blood pressure responses to stress versus never depressed women, irrespective of PMDD. However, only in women with histories of MDD did PMDD women have lower cortisol concentrations than non-PMDD women, and only in non-PMDD women was MDD associated with reduced cold pressor pain sensitivity. These results suggest both unique phenotypic differences between women with PMDD and those with a history of MDD, but also indicate that histories of MDD may have special relevance for PMDD.

Central processing of noxious somatic stimuli in patients with irritable bowel syndrome compared with healthy controls.

OBJECTIVE: To compare a central analgesic mechanism known as diffuse noxious inhibitory controls (DNIC) using somatic test stimuli and somatic conditioning stimuli, (CS) in irritable bowel syndrome (IBS) patients and healthy controls. METHODS: Participants were 48 premenopausal females (27 with IBS), mean age of 29 years. The phasic heat test stimulus (peak temperature, 50 degrees C) was applied to the left palm. The DNIC effect, which measured reductions in average pain ratings (APR) during counter irritation (submersion of the participant's right hand in painful 12 degrees C circulating water) compared with baseline, was compared between groups. In addition, a second, counterbalanced, CS protocol (right hand submerged in nonpainful 32 degrees C circulating water) was performed. Differences in APR between the 2 counterirritation protocols were compared between groups to control for nonspecific effects known to influence DNIC. Psychologic measures and cardiovascular reactivity were also assessed. RESULTS: IBS patients demonstrated smaller DNIC than controls (P=0.011, repeated measures analysis of variance), and greater state-anxiety, depression, catastrophizing, and anger-out expression (P<0.05). Group differences in DNIC were enhanced after controlling for nonspecific effects occurring during the nonpainful CS, and for psychologic measures (P=0.001, repeated measures analysis of covariance). There were no group differences in age, cardiovascular reactivity, APR, or pain ratings for the 12 degrees C CS. DISCUSSION: These data demonstrate deficient DNIC in IBS. This is the first study to adequately control for alternative explanations of pain reduction during counterirritation. Only by controlling for nonspecific effects can evidence of deficient DNIC be attributed to dysregulation in endogenous analgesic mechanisms.

Menstrual cycle phase does not influence gender differences in experimental pain sensitivity.

Influence of menstrual cycle phase on experimental pain sensitivity in women and on gender differences in pain sensitivity was examined in 48 men and 49 women in response to cold pressor, heat, and ischemic pain. Each woman was tested at three points in their menstrual cycle in randomized order, the early follicular, late follicular, and luteal phases, while men were also tested three times, controlling for number of days between test sessions. Cycle phase was confirmed via serum hormone levels. As expected, women were significantly more sensitive to cold pain (p<.01), to heat pain (p<.0001), and to ischemic pain (p<.01) than men. However, pain perception during each task was not influenced by the menstrual cycle in women, nor did the menstrual cycle influence the magnitude of the gender differences in pain sensitivity. These results indicate that although women are more sensitive to a variety of noxious stimuli than men, menstrual cycle phase does not appear to moderate those differences in healthy men and women.

Race and histories of mood disorders modulate experimental pain tolerance in women.

UNLABELLED: Thirty-two African American and 23 non-Hispanic white women were compared for experimental pain threshold and tolerance to thermal, ischemic, and cold pressor pain. Approximately half of each group had prior mood disorders (17 African Americans, 13 non-Hispanic whites), though all were free of current mood disturbance. Women with prior mood disorders were less sensitive to ischemic pain than women with no prior mood disorders (P < .05), whereas African Americans were more sensitive to ischemic pain than non-Hispanic whites, though only at pain tolerance (P < .001). For cold pressor pain, the effects of race were only seen in women with prior mood disorders, since African Americans with prior mood disorders were more sensitive than non-Hispanic whites with prior mood disorders (P < .05). These results indicate that experimental pain sensitivity in women is influenced by both race and histories of mood disorders. PERSPECTIVE: We examined the association of race and histories of mood disorders with experimental pain sensitivity in an exclusively female sample. Our findings for racial differences in pain sensitivity may have implications for greater clinical pain in African American women. Persistent disturbance in pain modulatory mechanisms in women with a history of mood disorders may also have implications for the development of subsequent mood disturbances.

Associations of histories of depression and PMDD diagnosis with allopregnanolone concentrations following the oral administration of micronized progesterone.

Twenty-three women with premenstrual dysphoric disorder (PMDD) and 29 non-PMDD controls were compared for plasma progesterone (P) and its neuroactive steroid metabolite allopregnanolone (ALLO), as well as the ALLO/P ratio following the double-blind, placebo controlled administration of 300 mg oral micronized progesterone. Approximately half of each group had prior depression (DEP) (13 PMDD, 12 non-PMDD), though all were free of current depression. Progesterone and ALLO were sampled 160, 190, 225, and 255 min after progesterone administration. Changes over time in plasma concentrations and the ALLO/P ratio were assessed using area under the curve analyses. Women with prior DEP had lower ALLO levels (p=0.05) and marginally lower P levels (p<0.07) following progesterone administration compared to never depressed women, and this was especially evident in the non-PMDD women (p<0.01). PMDD women with no prior DEP had higher pre-progesterone ALLO/P ratios than all other groups (Ps<0.05) and higher ratios than the never depressed, non-PMDD women following oral progesterone (p<0.05). Results could not be accounted for by group differences in steroid hormone binding protein concentrations. For all women, progesterone administration was associated with increased confusion, fatigue, and with reduced confidence (Ps<0.01), even after controlling for placebo-associated mood change. These results suggest a persistent effect of prior DEP on P and ALLO concentrations following oral progesterone and that PMDD women, especially those with no prior DEP, may have alterations in the metabolic pathways underlying the conversion of P to ALLO.

Histories of depression, allopregnanolone responses to stress, and premenstrual symptoms in women.

Twenty-six women meeting DSM criteria for premenstrual dysphoric disorder (PMDD) and 39 non-PMDD controls were tested for allopregnanolone (ALLO) responses to mental stress. Approximately half of each group had a history of depression (DEP) (14 PMDD, 17 non-PMDD), though all were free of current psychiatric illness. ALLO was sampled in response to venipuncture stress, after an extended baseline, and again 30 and 60 min following the onset of mental stressors. All women with prior DEP, regardless of PMDD status, showed a blunted ALLO stress response at 30 and 60 min (p < 0.05), and also failed to show the expected decrease from venipuncture to baseline rest (p = 0.08) compared to women with no prior DEP. Women with prior DEP did not show the expected correlation between progesterone and ALLO (r = 0.16) that was seen in those with no prior DEP (r = 0.37, p < 0.05). ALLO levels at extended baseline and blunted ALLO reactivity predicted more severe premenstrual symptoms, but only in PMDD women with prior DEP (p values <0.05). These results suggest that a history of DEP is associated with a failure of ALLO to be appropriately responsive to challenge, with alterations in the conversion of progesterone to ALLO, and confirm prior reports linking ALLO to symptoms in PMDD, but only in PMDD women with histories of DEP.