Purpose

Comfort eating is a prevalent behavior. Prior research shows that comfort eating is associated with reduced stress responses and increased metabolic risk across adolescence, young adulthood, and middle adulthood. The purpose of the current research was to test if comfort eating prospectively predicted all-cause mortality in older adulthood.

Method

The US Health and Retirement Study is an ongoing, nationally representative, longitudinal study of older adults. The final sample for the present study (N = 1445) included participants randomly selected to report how often they comfort ate. Comfort eating data were collected in 2008 and all-cause mortality data were collected in 2014. Participants also reported how often they consumed high-fat/sugar food as well as their height and weight in 2008.

Results

For each 1-unit increase in comfort eating, the expected odds of all-cause mortality (n = 255 deceased) decreased by 14%, OR = 0.86, p = 0.048, 95% CI [0.74, 0.99]. This analysis statistically accounted for other predictors of mortality in the sample including age, biological sex, race, highest educational degree attained, moderate and vigorous exercise, smoking, and cumulative illness. High-fat/sugar intake did not mediate (or diminish) the association but body mass index did.

Conclusion

Comfort eating-irrespective of consuming high-fat/sugar food-may be associated with reduced mortality in older adults because it may promote greater body mass, and greater body mass is associated with lower risk of mortality in nationally representative samples. Interventionists might consider both beneficial and detrimental aspects of comfort eating across the lifespan.

Theoretically driven smartphone-delivered behavioral interventions that target mechanisms underlying eating behavior are lacking. In this study, we administered a 28-day self-paced smartphone-delivered intervention rooted in an operant conditioning theoretical framework that targets craving-related eating using mindful eating practices. At pre-intervention and 1-month post-intervention, we assessed food cravings among adult overweight or obese women (N = 104; M age = 46.2 ± 14.1 years; M BMI = 31.5 ± 4.5) using ecological momentary assessment via text message (SMS), self-reported eating behavior (e.g., trait food craving), and in-person weight. Seventy-eight participants (75.0%) completed the intervention within 7 months ('all completers'), and of these, 64 completed the intervention within 3 months ('timely completers'). Participants experienced significant reductions in craving-related eating (40.21% reduction; p < .001) and self-reported overeating behavior (trait food craving, p < .001; other measures ps < .01). Reductions in trait food craving were significantly correlated with weight loss for timely completers (r = .30, p = .020), this pattern of results was also evident in all completers (r = .22, p = .065). Taken together, results suggest that smartphone-delivered mindful eating training targeting craving-related eating may (1) target behavior that impacts a relative metabolic pathway, and (2) represent a low-burden and highly disseminable method to reduce problematic overeating among overweight individuals. ClinicalTrials.gov registration: NCT02694731.

[This corrects the article DOI: 10.1371/journal.pone.0216541.].

Protein and peptide oligomers are thought to play important roles in the pathogenesis of a number of neurodegenerative diseases. For this reason, considerable effort has been devoted to understanding the oligomerization process and to determining structure-activity relationships among the many types of oligomers that have been described. We discuss here a method for producing pure populations of amyloid β-protein (Aβ) of specific sizes using the most pathologic form of the peptide, Aβ42. This work was necessitated because Aβ oligomerization produces oligomers of many different sizes that are non-covalently associated, which means that dissociation or further assembly may occur. These characteristics preclude rigorous structure-activity determinations. In studies of Aβ40, we have used the method of photo-induced cross-linking of unmodified proteins (PICUP) to produce zero-length carbon-carbon bonds among the monomers comprising each oligomer, thus stabilizing the oligomers. We then isolated pure populations of oligomers by fractionating the oligomers by size using SDS-PAGE and then extracting each population from the stained gel bands. Although this procedure worked well with the shorter Aβ40 peptide, we found that a significant percentage of Aβ42 oligomers had not been stabilized. Here, we discuss a new method capable of yielding stable Aβ42 oligomers of sizes from dimer through dodecamer.

Evidence suggests that amyloid β-protein (Aβ) oligomers may be seminal pathogenic agents in Alzheimer's disease (AD). If so, developing oligomer-targeted therapeutics requires an understanding of oligomer structure. This has been difficult due to the instability of these non-covalently associated Aβ assemblies. We previously used rapid, zero-length, in situ chemical cross-linking to stabilize oligomers of Aβ40. These enabled us to isolate pure, stable populations of dimers, trimers, and tetramers and to determine their structure-activity relationships. However, equivalent methods applied to Aβ42 did not produce stable oligomers. We report here that the use of an Aβ42 homologue, [F10, Y42]Aβ42, coupled with sequential denaturation/dissociation and gel electrophoresis procedures, provides the means to produce highly pure, stable populations of oligomers of sizes ranging from dimer through dodecamer that are suitable for structure-activity relationship determination.

Objective

The prevalence of obesity has created a plethora of questionnaires characterizing psychological aspects of eating behavior, such as reward-related eating (RRE). The Reward-based Eating Drive questionnaires (RED-9, RED-13) broadly and deeply assess the RRE construct. However, large-sample research designs require shorter questionnaires that capture RRE quickly and precisely. This study sought to develop a brief, reliable, and valid version of the RED questionnaire.

Methods

All-subset correlation was used to find a subset that maximally associated with the full RED-13 in two separate samples. Results were validated in a third independent sample. Internal consistency, test-retest reliability, and ability to explain variance in external outcomes were also assessed.

Results

A five-item questionnaire (RED-X5) correlated strongly with RED-13 in the independent sample (r = 0.95). RED-X5 demonstrated high internal consistency (omega total ≥ 0.80) and 6-month test-retest reliability (r = 0.72). RED-X5 accurately reproduced known associations between RED-13 and BMI, diabetes status, and craving for sweet and savory foods. As a novel finding, RED questionnaires predicted laboratory intake of chips.

Conclusions

RED-X5 is a short, reliable, and valid measure of the RRE construct and can be readily implemented in large-sample research designs in which questionnaire space is limited.

CILK1 (ciliogenesis associated kinase 1)/ICK (intestinal cell kinase) is a highly conserved protein kinase that regulates primary cilia structure and function. CILK1 mutations cause a wide spectrum of human diseases collectively called ciliopathies. While several CILK1 heterozygous variants have been recently linked to juvenile myoclonic epilepsy (JME), it remains unclear whether these mutations cause seizures. Herein, we investigated whether mice harboring either a heterozygous null Cilk1 (Cilk1^+/-) mutation or a heterozygous loss-of-function Cilk1 mutation (Cilk1^R272Q/+) have epilepsy. We first evaluated the spontaneous seizure phenotype of Cilk1^+/- and Cilk1^R272Q/+ mice relative to wildtype littermates. We observed no electrographic differences among the three mouse genotypes during prolonged recordings. We also evaluated electrographic and behavioral responses of mice recovering from isoflurane anesthesia, an approach recently used to measure seizure-like activity. Again, we observed no electrographic or behavioral differences in control versus Cilk1^+/- and Cilk1^R272Q/+ mice upon isoflurane recovery. These results indicate that mice bearing a non-functional copy of Cilk1 fail to produce electrographic patterns resembling those of JME patients with a variant CILK1 copy. Our findings argue against CILK1 haploinsufficiency being the mechanism that links CILK1 variants to JME.

Animal models have shown that chronic stress increases cortisol, which contributes to overeating of highly palatable food, increased abdominal fat and lower cortisol reactivity. Few studies in humans have simultaneously examined these trajectories. We examined premenopausal women, either mothers of children with a diagnosis of an autism spectrum disorder (n = 92) or mothers of neurotypical children (n = 91). At baseline and 2-years, we assessed hair cortisol, metabolic health, and reward-based eating. We compared groups cross-sectionally and prospectively, accounting for BMI change. Caregivers, relative to controls, had lower cumulative hair cortisol at each time point, with no decreases over time. Caregivers also had stable levels of poor metabolic functioning and greater reward-based eating across both time points, and evidenced increased abdominal fat prospectively (all ps ≤.05), independent of change in BMI. This pattern of findings suggest that individuals under chronic stress, such as caregivers, would benefit from tailored interventions focusing on better regulation of stress and eating in tandem to prevent early onset of metabolic disease, regardless of weight status.

Objectives

When experiencing negative mood, people often eat to improve their mood. A learned association between mood and eating may cultivate frequent food cravings, detracting from health goals. Training in mindful eating may target this cycle of emotion-craving-eating by teaching individuals to manage urges when experiencing negative mood. We examined the impact of a mobile mindful eating intervention on the link between negative mood and food cravings among overweight women.

Methods

In a single-arm trial, participants (n = 64, M age = 46.1 years, M BMI = 31.5 kg/m²) completed ecological momentary assessments of negative mood and food cravings 3 times/day for 3 days pre- and post-intervention, as well as 1-month post-intervention. Using multilevel linear regression, we compared associations between negative mood and food craving strength at pre- vs. post-intervention (model 1) and post-intervention vs. 1-month follow-up (model 2).

Results

In model 1, negative mood interacted with time point (β =  - .20, SE = .09, p = .02, 95% CI [- .38, - .03]) to predict craving strength, indicating that the within-person association between negative mood and craving strength was significantly weaker at post-intervention (β = 0.18) relative to pre-intervention (β = 0.38). In model 2, negative mood did not interact with time point to predict craving strength (β = .13, SE = .09, p = .10, 95% CI - .03, .31]); the association did not significantly differ between post-intervention and 1-month follow-up.

Conclusions

Training in mindful eating weakened the mood-craving association from pre- to post-intervention. The weakened association remained at follow-up. Our findings highlight the mood-craving link as a target-worthy mechanism of mindful eating that should be assessed in clinical trials.

Trial registration

NCT02694731.

Supplementary information

The online version contains supplementary material available at 10.1007/s12671-021-01760-z.