Tiffany Ju

Consumption After a Diet Violation: Disinhibition or Compensation?

Previous research, restricted to the laboratory, has found that restrained eaters overeat after they violate their diet. However, there has been no evidence showing that this same process occurs outside the lab. We hypothesized that outside of this artificial setting, restrained eaters would be able to control their eating. In Study 1, 127 participants reported hourly on their diet violations and eating over 2 days. In Study 2, 89 participants tracked their intake for 8 days, and 50 of these participants consumed a milk shake (a diet violation) on Day 7, as part of an ostensibly unrelated study. As hypothesized, dieters did not overeat following violations of their diet in either study. These findings are in contrast with those of previous lab studies and dispel the widely held belief that diet violations lead to overeating in everyday life.

Consumption After a Diet Violation

Previous research, restricted to the laboratory, has found that restrained eaters overeat after they violate their diet. However, there has been no evidence showing that this same process occurs outside the lab. We hypothesized that outside of this artificial setting, restrained eaters would be able to control their eating. In Study 1, 127 participants reported hourly on their diet violations and eating over 2 days. In Study 2, 89 participants tracked their intake for 8 days, and 50 of these participants consumed a milk shake (a diet violation) on Day 7, as part of an ostensibly unrelated study. As hypothesized, dieters did not overeat following violations of their diet in either study. These findings are in contrast with those of previous lab studies and dispel the widely held belief that diet violations lead to overeating in everyday life.

Resilience is decreased in irritable bowel syndrome and associated with symptoms and cortisol response

Irritable bowel syndrome (IBS) is a stress‐sensitive disorder associated with early adverse life events (EALs) and a dysregulated hypothalamic‐pituitary‐adrenal (HPA) axis. Resilience is the ability to recover and adapt positively to stress but has not been well studied in IBS. The aims of this study are to compare resilience in IBS and healthy controls (HCs) and to assess its relationships with IBS symptom severity, quality of life (QOL), EALs, and HPA axis response.

Surgically induced changes in gut microbiome and hedonic eating as related to weight loss: Preliminary findings in obese women undergoing bariatric surgery.

Objective Weight loss surgery results in significant changes in the anatomy, function, and intraluminal environment of the gastrointestinal tract affecting the gut microbiome. Although bariatric surgery results in sustained weight loss, decreased appetite, and hedonic eating, it is unknown whether the surgery-induced alterations in gut microbiota play a role in the observed changes in hedonic eating. We explored the following hypotheses: (1) laparoscopic sleeve gastrectomy (LSG) results in changes in gut microbial composition; (2) alterations in gut microbiota are related to weight loss; (3) alterations in gut microbiome are associated with changes in appetite and hedonic eating. Methods Eight obese women underwent LSG. Their body mass index, body fat mass, food intake, hunger, hedonic eating scores, and stool samples were obtained at baseline and 1-month postsurgery. 16S ribosomal RNA gene sequencing was performed on stool samples. DESeq2 changes in microbial abundance. Multilevel-sparse partial least squares discriminant analysis was applied to genus-level abundance for discriminative microbial signatures. Results LSG resulted in significant reductions in body mass index, food intake, and hedonic eating. A microbial signature composed of five bacterial genera discriminated between pre- and postsurgery status. Several bacterial genera were significantly associated with weight loss (Bilophila, q = 3E-05; Faecalibacterium q = 4E-05), lower appetite (Enterococcus, q = 3E-05), and reduced hedonic eating (Akkermansia, q = .037) after surgery. Conclusions In this preliminary analysis, changes in gut microbial abundance discriminated between pre- and postoperative status. Alterations in gut microbiome were significantly associated with weight loss and with reduced hedonic eating after surgery; however, a larger sample is needed to confirm these findings.

Corticotropin-releasing hormone receptor 1 (CRH-R1) polymorphisms are associated with irritable bowel syndrome and acoustic startle response

BACKGROUND Corticotropin-releasing hormone receptor 1 (CRH-R1) in the amygdala and the stria terminalis plays an important role in the activation of central stress circuits. Genetic factors may contribute to the hyperresponsiveness of these circuits in irritable bowel syndrome (IBS). AIMS To determine if CRH-R1 SNPs are associated with: (1) a diagnosis of IBS, (2) gastrointestinal (GI) symptoms, and (3) acoustic startle response (ASR) to threat, which is mediated by the amygdala via CRH. METHODS Three CRH-R1 SNPS (rs110402, rs242924, and rs7209436) were genotyped using salivary DNA from IBS and healthy control subjects (HCs). Eye blink ASR was obtained during safe (no shock), anticipation (abdominal shock may soon occur) and threat (abdominal shock likely) conditions in a subset of subjects. Associations between each SNP with IBS status, clinical traits and ASR were measured. RESULTS 235 IBS patients (mean age 37.5 yrs, 74% F) and 264 HCs (mean age 32.1 yrs, 70% F) were studied. Of these, 57 IBS and 41 HCs underwent the ASR protocol. The presence of IBS was associated with the major allele for all three CRH-R1 SNPs (p=0.009-0.025). Within IBS, the major allele for all three SNPs (p=0.017-0.065) was associated with GI symptom anxiety scores. Within subjects with at least one copy of the major allele for the CRH-R1 SNPs, IBS had significantly lower ASR compared to HCs during threat conditions (p=0.001-0.002). Within IBS, CRH-R1 SNPs were associated with a graded increase in ASR to threat (p=0.007-0.008). CONCLUSION These findings support that CRH-R1 contributes to the dysregulated stress responsiveness in IBS.

Sex Commonalities and Differences in Obesity-Related Alterations in Intrinsic Brain Activity and Connectivity: Obesity and Sex Influences on Brain Activity

This study aimed to characterize obesity‐related sex differences in the intrinsic activity and connectivity of the brains reward networks.

Differential Nociceptive Flexion Reflex Responses in Female Patients With Irritable Bowel Syndrome (IBS) and Healthy Female Controls

To examine mechanisms underlying the role of chronic stress in post-infectious irritable bowel syndrome (PI-IBS), we previously studied the effect of chronic stress and prior infectious colitis in the C. rodentium infected mouse (day 30 post infection), a model of human E. coli self-limiting colitis (NGM A:257,2010). Water avoidance stress (WAS; 1 hr on days 21-30 following infection) increased stress hormones (corticosterone and epinephrine), excitability of colonic nociceptive DRG neurons and colonic multi-unit afferent firing, compared to post-infected animals alone The current study examined pathways underlying this stress-post-infection effect using patch clamp recordings from Fast Blue labeled colonic DRG neurons to measure changes in excitability (rheobase (Rh) and/or increases in action potential discharge (APD)). At day 30, infection had resolved and histopathology was normal. However, tissue trypsin-like activity (>10 fold; p<0.01) and serine and cysteine proteases (~ 0.5-1 fold; p < 0.05) were elevated in unstressed post-infected animals. In patch clamp studies, excitability of neurons incubated in colonic tissue supernatants from unstressed post-infected mice was significantly inhibited by a global protease inhibitor (post-infected Rh = 61.5 +/7.5 pA vs. post-infected + inhibitor = 96.3 +/11.5 pA; p = 0.0162 and post-infected APD = 4.4 +/0.7 vs. post-infected + inhibitor 1.8 +/0.4; p = 0.007). In contrast, neuronal excitability with supernatants from uninfected WAS animals was not altered by the protease inhibitor and excitability did not differ between neurons exposed toWAS or control supernatants. Colonic histopathological scoring andWestern blots of tight junction proteins (occludin) were also not different between WAS and control groups. We therefore tested whether stress hormones could signal directly to DRG neurons. Labeled neurons were isolated using laser captured microdissection and corticosterone and β2 receptor mRNA identified by PCR. In patch clamp studies, colonic DRG neurons incubated in epinephrine (5 nM) and corticosterone (1 μM) were hyperexcitable compared to controls (epinephrine /corticosterone Rh = 48.6 +/10.9 pA vs control = 85.8 +/12.3 pA, p = 0.03 and epinephrine/corticosterone APD = 2.6 +/0.4 vs. control = 1.6 +/0.2; p = 0.04). Compared to controls, incubating neurons with protease activating receptor2 activating peptide (PAR2-AP; 30 μM) or WAS alone had no effect on Rh. However, WAS and PAR2-AP (30 μM) combined markedly decreased Rh (control + PAR2-AP = 85.8 +/12.3 pA vs. WAS + PAR2-AP 19.2 +/3.5 pA, p = 0.002). These data suggest tissue proteases and circulating stress hormones converge on DRG nociceptive neurons to increase sensory signaling from the colon. Moreover, this interaction enables sub-threshold levels of proteases to enhance peripheral sensory signaling.