Mediating effect of coping dispositions on the association between trauma and gastrointestinal symptoms.

Inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) are two gastrointestinal (GI) conditions known to be exacerbated by traumatic life experiences. One way in which these experiences might influence individuals' susceptibility to GI pathology, is by reducing their ability to deal with adversities effectively and predisposing them to passive coping styles that leave them vulnerable to the somatic effects of trauma. To validate this hypothesis, the present cross-sectional study assessed the mediating effect of coping dispositions on the association between trauma and GI disease activity in an adult sample of 189 bowel patients (94 IBD, 95 IBS) and 92 controls. Results confirmed that GI patients exhibit significantly more cumulative trauma, pervasive feelings of uncontrollability and passive coping strategies than controls. Moreover, the use of passive coping styles was positively associated with the accumulation of trauma and the expression of GI symptoms. Using hierarchical regression and mediation analyses, we found support for the sequential model postulating passive coping styles as (partial) mediators of trauma-induced (GI) disease manifestations. Specifically, out of all coping styles associated with cumulative trauma, behavioural disengagement most powerfully mediated the effect of trauma on GI symptom severity, accounting for 12% (IBD) to 14% (IBS) of its total effect. A somewhat smaller mediating role was observed for social support coping, the reduced reliance on which explained 7% (IBS) to 10% (IBD) of trauma's total effect. Finally, neuroticism acted as a channel through which past traumatization affected subjects' proneness to behavioural disengagement and, consequently, their GI disease activity.

The Impact of Psychotrauma and Emotional Stress Vulnerability on Physical and Mental Functioning of Patients with Inflammatory Bowel Disease.

Inflammatory bowel disease (IBD) is a chronic health condition thought to be influenced by personal life experiences and emotional stress sensitivity (neuroticism). In the present study, we examined the impact of cumulative trauma experiences and trait neuroticism (as a measure for emotional stress vulnerability) on physical and mental functioning of n = 211 patients diagnosed with IBD (112 Crohn's disease, 99 ulcerative colitis). All patients were assessed for self-reported trauma histories, emotional stress vulnerability, clinical disease activity, functional gastrointestinal (GI) symptoms, and quality of life. Results showed that patients with severe IBD activity have endured significantly more interpersonal trauma and victimization than those with quiescent IBD. Moreover, cumulative trauma was found to exert an indirect (neuroticism-mediated) effect on patients' symptom complexity, with trauma and neuroticism conjointly explaining 16-21% of the variance in gastrointestinal and 35% of the variance in mental symptoms. Upon correction for condition (using a small group of available controls, n = 51), the predictive capacity of trauma and neuroticism increased further, with both predictors now explaining 31% of the somatic-and almost 50% of the mental symptom heterogeneity. In terms of trauma type, victimization (domestic violence and intimate abuse) proved the best predictor of cross-sample symptom variability and the only trauma profile with a consistent direct and indirect (neuroticism-mediated) effect on patients' mental (QoL) and physical fitness. Results are consistent with the growing body of evidence linking experiential vulnerability factors (trauma and neuroticism) and associated feelings of personal ineffectiveness, helplessness, and uncontrollability to interindividual differences in (GI) disease activity and quality of life.

Impact of the COVID-19 pandemic on inflammatory bowel disease: The role of emotional stress and social isolation.

Inflammatory bowel disease (IBD) is a chronic health condition exacerbated by negative emotional stress experiences. In the current study, we examined whether the outbreak of the COVID-19 pandemic coincided with an increase in stress experiences and accordingly an aggravation of disease activity in IBD patients. Sixty-three IBD patients (30 Crohn's disease or CD, 33 ulcerative colitis) completed an online survey during the COVID-19-related lockdown, assessing clinical disease activity, disease-related quality of life, presence of functional gastrointestinal symptoms, social isolation and stress experiences. Scores were then compared to pre-lockdown baseline screening. The pandemic yielded a significant baseline-to-lockdown increase in emotional stress and social isolation. Stress increments, particularly those occasioned by interpersonal tension and excessive interpersonal proximity, were associated with a worsening of functional gastrointestinal symptoms. Exacerbations of loneliness coincided with an escalation of CD activity, functional gastrointestinal symptoms and a decline in subjective health. Lastly, COVID-19 anxiety was significantly related to CD symptom severity and social dysfunction. The findings show that shifts in IBD expression are closely linked to changes in emotional stress experiences and interpersonal relatedness. As such, they contribute to a better understanding of inter-individual differences in IBD progression and provide leads for therapeutic interventions.

Correction: The effect of information content on acceptance of cultured meat in a tasting context.

[This corrects the article DOI: 10.1371/journal.pone.0231176.].

Effects of high and low sucrose-containing beverages on blood glucose and hypoglycemic-like symptoms.

BACKGROUND AND AIMS: There is this intriguing but not yet well-explored suggestion that highly absorbable sucrose-sweetened drinks might exacerbate hunger by promoting temporal hypoglycemia-like responses already in non-diabetic healthy individuals. This might provide a possible additional explanatory mechanism for previous reported associations between consumption of sugar-sweetened drinks and body weight gain. The current study involves two separate and independently conducted human experiments exploring the effects of two different single-doses of sugar-sweetened beverages on temporal blood glucose nadir and possible related behavioral hypoglycemic-like symptoms in healthy participants. METHODS: By way of two separately conducted between-subjects experiments, effects of 1) a low (29 g) sugar-containing beverage compared to a sweetened zero-energy drink and a milk drink (experiment-1) or 2) a high (80 g) sugar-sweetened beverage compared to a zero-energy and a non-sweetened colored water drink (experiment-2) were measured on changes in blood glucose, behavioral hypoglycemia, appetite and mood. RESULTS: Experiment-1: The 29 g sucrose containing beverage caused a high (37%) glycemic increase and a smaller response (15%) to the milk drink, which both peaked 30 min after consumption, whereas the sweetened zero-energy drink had very little effect on blood glucose. Regardless of the different magnitude of peak glycemic responses, both the sugar and milk drinks rather equally caused blood glucose concentrations to return to normal and stable baseline values 90 min later. There were no (different) effects of the beverages on behavioral hypoglycemic-like symptoms, appetite or mood. Experiment-2: the 80 g sucrose containing beverage caused a large (72%) glycemic peak response at +30 min after consumption, whereas neither the sweetened zero-energy nor the non-sweetened colored water drink had any meaningful effect on blood glucose. After intake of the 80 g sugar beverage, blood glucose concentrations remained elevated (13%) at +120 min and returned to lower baseline values in the direction of hypoglycemia levels at +165 min. There were no (differential) effects of the beverages on behavioral hypoglycemic symptoms, appetite or mood. CONCLUSIONS: The current findings indicate that instead of a low (29 g) sugar-containing beverage, a high (80 g) sugar-containing beverage caused blood glucose concentrations to fall below baseline values almost reaching hypoglycemia levels at the end of measurements. There were no hypoglycemic-like behavioral symptoms including changes in appetite or mood: at least not at end of measurements +165 min after consumption. Since this might include that in particular consumption of high-glycemic index drinks could still promote symptoms in the longer run, further research is needed to explore possible hypoglycemic-like effects of high dosages of sugar-sweetened beverages across more extended/delayed time measurements.

The effect of information content on acceptance of cultured meat in a tasting context.

Cultured meat, in particular beef, is an emerging food technology potentially challenged by issues of consumer acceptance. To understand drivers of consumer acceptance as well as sensory perception of cultured meat, we investigated the effect of information content on participants' acceptance of cultured meat in a tasting context. Hundred ninety-three citizens from the Netherlands participated, divided across three age and sex-matched groups which each received information on either societal benefits, personal benefits or information on the quality and taste of cultured meat. They filled out a questionnaire and tasted two pieces of hamburger, labeled 'conventional' or 'cultured', although both pieces were in fact conventional. Sensory analysis of both hamburgers was performed. We observed that provision of information and the tasting experience increased acceptance of cultured meat and that information on personal benefits of cultured meat increased acceptance more than information on quality and taste but not than societal benefits of cultured meat. Previous awareness of cultured meat was the best predictor of its acceptance. In contrast to previous studies, sex and social economic status were not associated with different acceptance rates. Surprisingly, 58% of the respondents were willing to pay a premium for cultured meat of, on average, 37% above the price of regular meat. All participants tasted the 'cultured' hamburger and evaluated its taste to be better than the conventional one in spite of the absence of an objective difference. This is the first acceptance study of cultured meat where participants were offered to eat and evaluate meat that was labeled 'cultured'. We conclude that having positive information importantly improves acceptance and willingness to taste and that the specific content of the information is of subordinate importance. Awareness of cultured meat is the best predictor of acceptance.

The serotonin transporter gene-linked polymorphic region (5-HTTLPR) and the sleep-promoting effects of tryptophan: A randomized placebo-controlled crossover study.

BACKGROUND: The low-expressive short (S) allele of a functional polymorphism (5-HTTLPR) within the serotonin (5-hydroxytriptamine; 5-HT) transporter gene (SLC6A4) has been associated with a reduced functioning of the brain 5-HT system relative to the long (L) allele. As a consequence, the S-allele is found to predispose individuals to a higher risk of sleep quality reduction and clinical insomnia. AIMS: The present study investigated whether subchronic pre-sleep tryptophan administration could compensate for this predisposition by improving sleep in 5-HTTLPR S-allele carriers. METHODS: In a double-blind placebo-controlled crossover design a sample of homozygous 5-HTTLPR S-allele (n = 47) and L-allele (n = 51) carriers were assessed for subjective (sleep diary) and objective (actigraphy) sleep during a treatment protocol consisting of 1 week of placebo (1000 mg/day) and 1 week of tryptophan administration (1000 mg/day). RESULTS: The results support the sleep-promoting effects of tryptophan. Tryptophan improved objective sleep efficiency and objective wake after sleep onset irrespective of allelic variation. There was a marginally significant improvement of subjective sleep quality in the 5-HTTLPR S-allele group but not in the L-allele group following tryptophan relative to placebo intake. In contrast, a significantly poorer sleep quality in the S-allele as opposed to the L-allele group in the placebo condition was not observed in the tryptophan condition. CONCLUSIONS: Tryptophan augmentation promises to be a valuable treatment strategy for sleep impairments related to genetic deficiencies in 5-HT functioning.

The involvement of sleep in the relationship between the serotonin transporter gene-linked polymorphic region (5-HTTLPR) and depression: A systematic review.

BACKGROUND: Recent meta-analyses stimulate an ongoing debate whether 5-HTTLPR modulates the risk for depression including a more pronounced association between stress and depression in the short (S) allele relative to the long (L) allele. Elucidating the pathways by which 5-HTTLPR contributes to depression could resolve this controversy. Insomnia independently contributes to the onset and course of negative affective symptoms and, hence, represents one of the primary risk factors for depression. To evaluate the relevance of this relationship for the interaction between 5-HTTLPR and stress in depression, the present review investigated the moderating influence of 5-HTTLPR on the relationship between stress and sleep quality as well as on the relationship between sleep and affective symptomatology. METHODS: A systematic search was performed in the PubMed and PsycINFO databases to include a complete outline of studies investigating the relationships of interest. RESULTS: Results of the included articles reveal that the 5-HTTLPR S-allele relative to the L-allele increases the risk for stress-related sleep quality reductions and promotes the negative affective consequences of inadequate sleep. LIMITATIONS: The apparent involvement of sleep in the association between 5-HTTLPR and depression remains to be more directly (empirically) examined and studies exploring the influence of 5-HTTLPR on sleep quality produced inconsistent results. CONCLUSIONS: The reviewed findings support the involvement of sleep in the interaction between 5-HTTLPR and stress in depression. This could have important implications for the inconsistent findings characterizing this field of research and may provide valuable insight into the pathophysiological mechanisms underlying genetic contributions to depression.

Effects of 5-HTTLPR genotype and cognitive rumination on long-term cortisol reactivity measured in human hair.

Ample experimental and associative studies have shown that carrying two short (S) alleles of the serotonin transporter gene (5-HTTLPR) contributes to an increased vulnerability for stress and related affective disorders. Recent findings indicate that this relationship might become even more profound when also possessing a negative ruminative (stress-related) thinking style. However, previous studies on the relationship among 5-HTTLPR, stress, and stress-responsiveness almost exclusively measured salivary cortisol concentrations during exposure to a single acute (laboratory) stressor. Measuring cortisol concentrations over longer periods of time might better reflect (chronic) Gene by biological (HPA) stress responsiveness associations. In recent years, the strategy to assess hair cortisol concentration (HCC) has been established as a more reliable marker for chronic HPA activations. The current study explored associations between 3-months accumulated HCC and the tendency to ruminate about negative events in 27 S/S and 27 L/L 5-HTTLPR-carriers (screened from a large n = 827 DNA database). Hierarchical regression (including moderation) analyses revealed clear significant interactions between Genotype and Rumination (p < 0.01, f2=0.26); indicating greatest accumulation of HCC in high ruminating S/S-allele carriers. These findings implicate that the combined possession of a genetic (S-allele 5-HTTLPR) and cognitive (Rumination) stress-vulnerability might meaningfully increases long-term stress responsiveness; most likely due to increased daily (chronic) stress experiences. Lay summary The current study investigated whether the combined possession of a biological (genetic) and cognitive (negative thinking pattern) stress vulnerability may lead to a greater vulnerability to experience daily stress. This hypothesis was confirmed as a higher accumulation of the cortisol stress hormone was found over the past 3 months in scalp hair of participants that carried both vulnerability factors in combination.

The serotonin transporter polymorphism (5-HTTLPR) and cortisol stress responsiveness: preliminary evidence for a modulating role for sleep quality.

The short (S) allele of a functional polymorphism (5-HTTLPR) within the promoter region of the serotonin transporter gene (SLC6A4) is found to predispose the risk for stress-related affective disorders relative to the long (L) allele. Evidence suggests that elevated stress reactivity of the hypothalamic-pituitary-adrenal (HPA) axis might underlie this association although there is little understanding about the origin of inconsistent findings. Since inadequate sleep is commonly known to promote HPA stress reactivity, it might well play an important modulating role. The present study tested this hypothesis by investigating whether sleep quality moderates the relationship between 5-HTTLPR and cortisol stress responsiveness. From a large 5-HTTLPR database (n = 771), a sample of healthy male and female participants homozygous for either the 5-HTTLPR S-allele (n = 25) or L-allele (n = 25) were assessed for sleep quality and salivary cortisol secretion during acute laboratory stress. Diminished sleep quality was found to exclusively potentiate cortisol stress reactivity in the homozygous L-allele genotype. Accounting for this 5-HTTLPR-dependent influence enhanced the predictive value of 5-HTTLPR on cortisol stress responsiveness, revealing greater HPA reactivity in S-allele relative to L-allele carriers. Current findings suggest that variations in sleep quality may serve as a confounding factor in the search for genetic differences in stress sensitivity and related affective disorders.

Does stress influence sleep patterns, food intake, weight gain, abdominal obesity and weight loss interventions and vice versa?

Decades of research have reported only weak associations between the intakes of specific foods or drinks and weight gain and obesity. Randomized controlled dietary intervention trials have only shown very modest effects of changes in nutrient intake and diet composition on body weight in obese subjects. This review summarizes the scientific evidence on the role mental stress (either in or not in association with impaired sleep) may play in poor sleep, enhanced appetite, cravings and decreased motivation for physical activity. All these factors contribute to weight gain and obesity, possibly via decreasing the efficacy of weight loss interventions. We also review evidence for the role that lifestyle and stress management may play in achieving weight loss in stress-vulnerable individuals with overweight.

The influence of sleep on human hypothalamic-pituitary-adrenal (HPA) axis reactivity: A systematic review.

Inadequate sleep is highly prevalent and known to decline both physical- and mental health. Literature suggests that altered functioning of the hypothalamic-pituitary-adrenal (HPA) axis might underlie this association. This assumption is mainly based on changes in basal neuroendocrine activity and it is of equal importance to elucidate whether sleep may also influence HPA stress responsiveness. The present review provides a complete outline of recent human studies that have investigated how different aspects of sleep influence cortisol reactivity to laboratory stress. From the available data it can be concluded that both objective and subjective decrements in sleep quality potentiate the stress reactivity of the HPA axis. On the contrary, normal variations in sleep duration do not seem to influence cortisol stress responsiveness whereas excessive daytime sleepiness is associated with a blunting of the cortisol response. Given its well-established health consequences, sensitization of the HPA axis might well be a crucial component linking inadequate sleep to stress-related pathology.

Mind wandering during attention performance: Effects of ADHD-inattention symptomatology, negative mood, ruminative response style and working memory capacity.

OBJECTIVE: In adulthood, depressive mood is often comorbid with ADHD, but its role in ADHD-inattentiveness and especially relations with mind wandering remains to be elucidated. This study investigated the effects of laboratory-induced dysphoric mood on task-unrelated mind wandering and its consequences on cognitive task performance in college students with high (n = 46) or low (n = 44) ADHD-Inattention symptomatology and Hyperactivity/Impulsivity symptoms in the normal range. METHODS: These non-clinical high/low ADHD-Inattention symptom groups underwent negative or positive mood induction after which mind wandering frequency was measured in a sustained attention (SART), and a reading task. Effects of ruminative response style and working memory capacity on mind wandering frequency were also investigated. RESULTS: Significantly higher frequencies of self -reported mind wandering in daily life, in the SART and reading task were reported in the ADHD-Inattention symptom group, with detrimental effects on text comprehension in the reading task. Induced dysphoric mood did specifically enhance the frequency of mind wandering in the ADHD-Inattention symptom group only during the SART, and was related to their higher self-reported intrusive ruminative response styles. Working memory capacity did not differ between high/low attention groups and did not influence any of the reported effects. CONCLUSIONS: These combined results suggest that in a non-clinical sample with high ADHD-inattention symptoms, dysphoric mood and a ruminative response style seem to be more important determinants of dysfunctional mind wandering than a failure in working memory capacity/executive control, and perhaps need other ways of remediation, like cognitive behavioral therapy or mindfulness training.

Gene by cognition interaction on stress-induced attention bias for food: Effects of 5-HTTLPR and ruminative thinking.

INTRODUCTION: Stress is often found to increase the preference and intake of high caloric foods. This effect is known as emotional eating and is influenced by cognitive as well as biological stress vulnerabilities. An S-allele of the 5-HTTLPR gene has been linked to decreased (brain) serotonin efficiency, leading to decreased stress resilience and increased risks for negative affect and eating related disturbances. Recently it has been proposed that a cognitive ruminative thinking style can further exacerbate the effect of this gene by prolonging the already increased stress response, thereby potentially increasing the risk of compensating by overeating high palatable foods. OBJECTIVE: This study was aimed at investigating whether there is an increased risk for emotional eating in high ruminative S/S-allele carriers reflected by an increased attention bias for high caloric foods during stress. METHODS: From a large (N=827) DNA database, participants (N=100) were selected based on genotype (S/S or L/L) and ruminative thinking style and performed an eye-tracking visual food-picture probe task before and after acute stress exposure. A significant Genotype x Rumination x Stress-interaction was found on attention bias for savory food; indicating that a stress-induced attention bias for specifically high-caloric foods is moderated by a gene x cognitive risk factor. CONCLUSION: Both a genetic (5-HTTLPR) and cognitive (ruminative thinking) stress vulnerability may mutually increase the risk for stress-related abnormal eating patterns.

Eating dependence and weight gain; no human evidence for a 'sugar-addiction' model of overweight.

BACKGROUND AND AIMS: There is an increasing societal concern that consumption of specific foods such as sugar might become 'addictive' and, hence, promote weight gain. Claims about the addictiveness of sugar however are based largely on findings from few animal studies, whereas there is a lack of direct human evidence for symptoms of sugar-related substance dependence. The current study examined in a large sample of human participants whether foods mainly containing sugar in particular might cause 'addiction-like' problems that meet clinical DSM criteria for substance dependence, and, also whether in turn this relates to body weight and negative affectivity (depressed mood). METHODS: In a cross-sectional study, n = 1495 university students from a variety of faculties were assessed for DSM-related signs of food addiction for particular food categories (YFAS), and, also BMI and negative affectivity. RESULTS: Results revealed that from the total sample, 95% experienced at least one symptom of food dependence and 12.6% met the YFAS classification for 'food addiction' as related to DSM-IV criteria. The majority of respondents experienced these problems for combined high-fat savoury (30%) and high-fat sweet (25%) foods, whereas only a minority experienced such problems for low-fat/savoury (2%) and mainly sugar-containing foods (5%). Overweight correlated only with addictive-like problems for high-fat savoury and high-fat sweet foods (P < 0.0001), while this was not found for foods mainly containing sugar. CONCLUSION: The current findings indicate that sugary foods contribute minimally to 'food dependence' and increased risk of weight gain. Instead, they are consistent with the current scientific notion that food energy density, and the unique individual experience of eating, plays an important role in determining the reward value of food and promoting excessive energy intake.

Interaction between 5-HTTLPR genotype and cognitive stress vulnerability on sleep quality: effects of sub-chronic tryptophan administration.

BACKGROUND: Abundant evidence suggests that allelic variation in the serotonin transporter-linked polymorphic region (5-HTTLPR) influences susceptibility to stress and its affective consequences due to brain serotonergic vulnerability. Based on recent assumptions, the present study examined whether the 5-HTTLPR genotype may also interact with a vulnerability to chronic stress experience (conceptualized by trait neuroticism) in order to influence sleep quality and, additionally, whether this is influenced by brain serotonergic manipulations. METHODS: In a well-balanced experimental design, homozygous S-allele (n = 57) and L-allele (n = 54) genotypes with high and low chronic stress vulnerability (neuroticism) were first assessed for general past sleep quality during a month before onset of the experiment. Then subjects were assessed for sleep quality following 7 days of tryptophan (3.0g/day) or placebo intake. RESULTS: Although high neuroticism was significantly related to a higher frequency of stressful life events and daily hassles, it did not interact with the 5-HTTLPR genotype on general past sleep quality. However, as expected, a 7 day period of tryptophan administration was exclusively associated with better sleep quality scores in the S'/S' genotype with high trait neuroticism. CONCLUSIONS: Current findings suggest that 5-HTTLPR does not directly interact with stress vulnerability in order to influence sleep quality. Instead, based on current and previous findings, it is suggested that the S'/S' 5-HTTLPR genotype promotes the risk for stress-related sleep disturbances because of an increased susceptibility to the depressogenic consequences of stress. Accordingly, by way of reducing depressive symptomatology, tryptophan augmentation may particularly improve sleep quality in stress-vulnerable individuals carrying the 5-HTTLPR S-allele.

Gene × cognition interaction on stress-induced eating: effect of rumination.

People often crave for high-caloric sweet foods when facing stress and this 'emotional eating' is a most important cause for weight gain and obesity. Eating under stress contrasts with the normally expected response of a loss of appetite, yet in spite of intensive research from neurobiological and cognitive disciplines we still do not know why stress or negative affect triggers overeating in so many of us. Since the prevalence of overweight and obesity still rises, the discovery of crucial risk factors is a most desirable goal of today's research on sub-optimal eating habits. This paper summarizes the most relevant current knowledge from the (human) literature regarding cognitive and biological vulnerabilities for stress-induced emotional eating. A (non-systematic) review of the most relevant studies reveals that most studies contemplate a rather one-directional way of focusing on either cognitive or biological factors, showing inconsistent results. The current paper elaborates and/or integrates these findings into a biological-cognitive interaction model in which a specific combination of genetic and cognitive vulnerabilities are thought to increase our bio-behavioral response to stress, critically increasing the rewarding value of pleasant foods and, hence, emotional eating.

Sucrose preload reduces snacking after mild mental stress in healthy participants as a function of 5-hydroxytryptamine transporter gene promoter polymorphism.

Brain serotonin (5-hydroxytryptamine, 5-HT) dysfunction is considered to promote food intake and eating-related disturbances, especially under stress or negative mood. Vulnerability for 5-HT disturbances is considered to be genetically determined, including a short (S) allele polymorphism in the serotonin transporter gene (5-HTTLPR) that is associated with lower serotonin function. Since 5-HT function may be slightly increased by carbohydrate consumption, S-allele 5-HTTLPR carriers in particular may benefit from a sugar-preload due to their enhanced 5-HT vulnerability. The aim of the current study was to investigate whether a sugar-containing preload may reduce appetite and energy intake after exposure to stress to induce negative mood, depending on genetic 5-HT vulnerability. From a population of 771 healthy young male and female genotyped college students 31 S/S carriers (8 males, 23 females) and 26 long allele (L/L) carriers (9 males, 17 females) (mean ± S.D. 22 ± 1.6 years; body mass index, BMI, 18-33 kg/m(2)) were monitored for changes in appetite and snacking behavior after stress exposure. Results revealed an increased energy intake after mild mental stress (negative mood) mainly for high-fat sweet foods, which was significantly greater in S/S carriers, and only in these genotypes this intake was significantly reduced by a sucrose-containing preload. Although alternative explanations are possible, it is suggested that S/S participants may have enhanced brain (hypothalamic) 5-HT responsiveness to food that makes them more susceptible to the beneficial satiation effects of a sucrose-preload as well as to the negative effects of mild mental stress on weight gain.

Effect of sub chronic tryptophan supplementation on stress-induced cortisol and appetite in subjects differing in 5-HTTLPR genotype and trait neuroticism.

Stress or negative effect often increases preference for, and intake of, palatable snack foods and this may be influenced by cognitive and genetic factors related to stress and 5-HT vulnerability. The short (S) compared to the long (L) allele of the 5-HT transporter linked polymorphic region (5-HTTLPR) has been associated (i) with decreased 5-HT transporter function and availability and hence, with 5-HT vulnerability, and (ii) with greater stress-responsiveness. Stress-proneness is furthermore promoted by cognitive stress-vulnerability, a key feature of trait neuroticism. Brain 5-HT function can be manipulated by dietary administration of its amino acid precursor tryptophan (Trp), and the beneficial effects of dietary Trp on stress experience and emotional eating may be greatest following repeated administration in both stress- and 5-HT-vulnerable subjects. The aim was to examine the influence of repeated Trp administration on stress responsiveness and emotional eating in homozygous 5-HTTLPR S-allele (N=60) and L-allele (N=58) carriers with high and low neuroticism. Following seven days of Trp or PLC intake, mood, cortisol and appetite were assessed before and after exposure to acute stress and snack intake and preference were measured post-stress. It was hypothesized that Trp would reduce stress experience and emotional eating particularly in S-allele carriers with high neuroticism. Results revealed Trp treatment caused a clear reduction in stress-induced cortisol levels in S/S-allele carriers exclusively, and prevented a stress-induced increase in appetite only in S/S-allele carriers with high trait neuroticism. The findings reveal an advantageous effect of sub chronic Trp treatment on stress experience and appetite depending on stress and (genetic) serotonergic vulnerability.