A brief induction of loving kindness meditation to reduce anti-fat bias.

Weight stigma is highly prevalent. However, existing weight stigma interventions are only modestly effective at reducing anti-fat attitudes. The current research proposes a novel approach using a loving kindness meditation (LKM). Experiment 1 tests whether random assignment to the LKM intervention reduces explicit and implicit anti-fat bias and increases empathy based on the LKM recipient with higher weight (close other vs. stranger). Experiment 2 tests whether LKM outperforms an empathy intervention or control to increase empathy or reduce stigmatizing behavior. Results revealed that the LKM increased empathic care but did not reduce anti-fat bias compared to control; the LKM intervention, but not the empathy intervention, reported greater empathy compared to control in unadjusted analyses; and participants in the LKM and empathy interventions (vs. control) were more likely to engage in stigmatizing behavior. These findings suggest that the LKM may not be effective at reducing weight stigma despite increasing empathy.

Weight stigma as a stressor: A preliminary multi-wave, longitudinal study testing the biobehavioral pathways of the cyclic obesity/weight-based stigma (COBWEBS) model.

Higher weight individuals often face significant weight stigma. According to the Cyclic Obesity/Weight-Based Stigma (COBWEBS) model, weight stigma operates as a stressor that increases the stress hormone cortisol and promotes comfort eating, thus resulting in weight gain. Such weight gain is harmful as it exposes individuals to further stigmatization. Thus far, no study has yet tested the mechanistic pathways of the COBWEBS model and prospective longitudinal studies are severely lacking. To fill this gap, the current study tested the biobehavioral pathways of the COBWEBS model using a 4-wave yearlong longitudinal study comprising 348 higher weight individuals. Using a structural equation modeling framework, we tested three cross lagged panel models for the putative mediator, comfort eating. The models examined either synchronous and/or lagged effects across weight stigma, perceived stress, comfort eating, weight, and future weight stigma. The best fitting model revealed significant associations between baseline weight stigma, perceived stress, and comfort eating within the same month. However, comfort eating did not significantly predict weight four months later. Weight status and baseline weight stigma both predicted future weight stigma as expected. Additionally, a separate path model with hair cortisol found that weight stigma predicted perceived stress four months later, but stress did not predict aggregate cortisol levels from months 10 and 11. Hair cortisol also did not predict later weight. This preliminary work lays the foundation for identifying modifiable targets of weight stigma, thereby offering potential avenues to reduce weight stigma's harm on higher weight individuals.

Measuring context-response associations that drive habits.

People achieve important life outcomes of health, financial security, and productivity by repeating operant behavior. To identify whether such operants reflect goal pursuit or habit, the present research introduces a new paradigm that yields objective measures of learning and controls for the motivations of goal pursuit. In two experiments, participants practiced a sequential task of making sushi and then completed a test of the strength of cue-response (habit) associations in memory. Finally, they repeated the sushi task without instructions while under cognitive load (designed to impede deliberation about goals). As predicted, greater task practice yielded stronger cue-response associations, which in turn promoted task success. Practice did not improve performance by enhancing goal intentions or other task motivations. We conclude that repetition facilitates performance by creating mental associations that automatically activate practiced, habitual responses upon perception of recurring context cues.

Healthy versus unhealthy comfort eating for psychophysiological stress recovery in low-income Black and Latinx adults.

Low-income Black and Latinx individuals are disproportionately vulnerable to chronic stress and metabolic disease. Evidence suggests that these populations engage in elevated levels of comfort eating (i.e., eating comforting food to alleviate stress), which can harm diet quality. For this reason, many interventions discourage comfort eating. However, if comfort eating does indeed buffer stress, it may be a protective health behavior, particularly if healthy foods (e.g., strawberries) buffer stress as effectively as traditional unhealthy comfort foods (e.g., brownies). By choosing healthy foods, people may be able to simultaneously improve their nutrition and reduce their stress levels, both of which have the potential to reduce health disparities among chronically stressed populations. The present study tested the efficacy of healthy and unhealthy comfort eating for improving psychophysiological stress recovery. A sample of low-income Black and Latinx individuals (N = 129) were randomly assigned to consume a healthy food (e.g., grapes), unhealthy comfort food (e.g., chips), or no food after exposure to a laboratory stressor. Throughout, we measured participants' psychophysiological stress responses, including self-reported stress, rumination, autonomic nervous system activation (i.e., electrodermal activity (EDA), heart rate variability (HRV)) and neuroendocrine responses (i.e., salivary cortisol). We compared participants' stress recovery trajectories by condition and found no significant group differences (p = 0.12 for self-reported stress; p = 0.92 for EDA; p = 0.22 for HRV, p = 1.00 for cortisol). Participants in all conditions showed decreases in self-reported stress and in cortisol post-stressor (ps < 0.01), but rates of decline did not differ by condition (i.e., healthy or unhealthy comfort food, brief no-food waiting period). Although null, these results are important because they challenge the widely-held assumption that comfort foods help people decrease stress.

Hunchback activates Bicoid in Pair1 neurons to regulate synapse number and locomotor circuit function.

Neural circuit function underlies cognition, sensation, and behavior. Proper circuit assembly depends on the identity of the neurons in the circuit (gene expression, morphology, synapse targeting, and biophysical properties). Neuronal identity is established by spatial and temporal patterning mechanisms, but little is known about how these mechanisms drive circuit formation in postmitotic neurons. Temporal patterning involves the sequential expression of transcription factors (TFs) in neural progenitors to diversify neuronal identity, in part through the initial expression of homeodomain TF combinations. Here, we address the role of the Drosophila temporal TF Hunchback and the homeodomain TF Bicoid in the assembly of the Pair1 (SEZ_DN1) descending neuron locomotor circuit, which promotes larval pausing and head casting. We find that both Hunchback and Bicoid are expressed in larval Pair1 neurons, Hunchback activates Bicoid in Pair1 (opposite of their embryonic relationship), and the loss of Hunchback function or Bicoid function from Pair1 leads to ectopic presynapse numbers in Pair1 axons and an increase in Pair1-induced pausing behavior. These phenotypes are highly specific, as the loss of Bicoid or Hunchback has no effect on Pair1 neurotransmitter identity, dendrite morphology, or axonal morphology. Importantly, the loss of Hunchback or Bicoid in Pair1 leads to the addition of new circuit partners that may underlie the exaggerated locomotor pausing behavior. These data are the first to show a role for Bicoid outside of embryonic patterning and the first to demonstrate a cell-autonomous role for Hunchback and Bicoid in interneuron synapse targeting and locomotor behavior.

Weight Stigma by Association Among Parents of Children With Obesity: A Randomized Trial.

OBJECTIVE: To experimentally test weight stigma and weight stigma by association in a parent-child relationship using a large, community-based sample. METHODS: We conducted a randomized experiment on Amazon Mechanical Turk using an online survey. Participants were randomly assigned to view a picture of a parent-child dyad, for which the parent and child's gender (male vs. female) and weight status (with obesity vs. without obesity) were manipulated. Participants read identical parenting descriptions that adhered to the American Academy of Pediatrics' parenting recommendations, then rated the parent's perceived effectiveness, helpfulness, and level of caring using a parenting questionnaire based on Barnhart et al (2013). RESULTS: Participants (N = 1862; Mage = 36.8 [11.2] years) rated parents of children with obesity as less effective compared to parents of children without obesity (P = .010) and parents with obesity as less effective compared to parents without obesity (P = .033). Participants also rated parents with obesity as less helpful compared to parents without obesity (P = .021). No differences emerged in perceived caring. Parenting evaluations did not differ across daughters versus sons or mothers versus fathers. CONCLUSIONS: Parents of children with obesity may experience weight stigma by association, which could have direct consequences for the parents, the children, and the parent-child relationship.

Weight stigma and health behaviors: evidence from the Eating in America Study.

BACKGROUND: Weight stigma is pervasive across the U.S. and is associated with poor health outcomes including all-cause mortality. One potential reason that weight stigma may be detrimental to health is that it begets poorer health behaviors. Therefore, the present study tested for associations between weight stigma and four health behaviors (i.e., eating behavior, alcohol use, sleep disturbance, and physical activity), while controlling for BMI and other potential confounds. SUBJECTS/METHODS: Participants (N = 2022) in the U.S. were recruited for the Eating in America Study using a Qualtrics panel between December 2019 and January 2020 and were census-matched according to national quotas for age, gender, income, race/ethnicity, and census region. Participants completed questionnaires about weight stigma, health behaviors, demographics, and anthropometric measurements. The current study employed a two-stage investigation: exploratory analyses were first performed on a random sample of the dataset (n = 438), then the remaining unexamined data were used to conduct confirmatory analyses that were preregistered on the Open Science Framework. RESULTS: Controlling for BMI, weight stigma was significantly associated with greater disordered eating (b = 0.34, 95% CI [0.31, 0.38], p < 0.001), comfort eating (b = 0.32, 95% CI [0.25, 0.39], p < 0.001), sleep disturbance (b = 0.27, 95% CI [0.20, 0.33], p < 0.001), and alcohol use (b = 0.30, 95% CI [0.11, 0.49], p = 0.002), but not lower physical activity (b = -0.04, 95% CI [-0.13, 0.05], p = 0.402) for individuals across the weight spectrum. BMI and perceived weight status significantly moderated the effects of weight stigma on disordered eating and alcohol use. No gender differences were found. These confirmatory analyses partially replicated the exploratory stage 1 findings. CONCLUSIONS: This study provides preliminary evidence that weight stigma is linked to several poor health behaviors, which may impact physical health.

Tyramine synthesis, vesicular packaging, and the SNARE complex function coordinately in astrocytes to regulate Drosophila alcohol sedation.

Identifying mechanisms underlying alcohol-related behaviors could provide important insights regarding the etiology of alcohol use disorder. To date, most genetic studies on alcohol-related behavior in model organisms have focused on neurons, leaving the causal roles of glial mechanisms less comprehensively investigated. Here, we report our studies on the role of Tyrosine decarboxylase 2 (Tdc2), which converts tyrosine to the catecholamine tyramine, in glial cells in Drosophila alcohol sedation. Using genetic approaches that drove transgene expression constitutively in all glia, constitutively in astrocytes and conditionally in glia during adulthood, we found that knockdown and overexpression of Tdc2, respectively, increased and decreased the sensitivity to alcohol sedation in flies. Manipulation of the genes tyramine ß-hydroxylase and tyrosine hydroxylase, which respectively synthesize octopamine and dopamine from tyramine and tyrosine, had no discernable effect on alcohol sedation, suggesting that Tdc2 affects alcohol sedation by regulating tyramine production. We also found that knockdown of the vesicular monoamine transporter (VMAT) and disruption of the SNARE complex in all glia or selectively in astrocytes increased sensitivity to alcohol sedation and that both VMAT and the SNARE complex functioned downstream of Tdc2. Our studies support a model in which the synthesis of tyramine and vesicle-mediated release of tyramine from adult astrocytes regulates alcohol sedation in Drosophila. Considering that tyramine is functionally orthologous to norepinephrine in mammals, our results raise the possibility that gliotransmitter synthesis release could be a conserved mechanism influencing behavioral responses to alcohol as well as alcohol use disorder.

Alcohol sedation in adult Drosophila is regulated by Cysteine proteinase-1 in cortex glia.

Although numerous studies have demonstrated that neuronal mechanisms regulate alcohol-related behaviors, very few have investigated the direct role of glia in behavioral responses to alcohol. The results described here begin to fill this gap in the alcohol behavior and gliobiology fields. Since Drosophila exhibit conserved behavioral responses to alcohol and their CNS glia are similar to mammalian CNS glia, we used Drosophila to begin exploring the role of glia in alcohol behavior. We found that knockdown of Cysteine proteinase-1 (Cp1) in glia increased Drosophila alcohol sedation and that this effect was specific to cortex glia and adulthood. These data implicate Cp1 and cortex glia in alcohol-related behaviors. Cortex glia are functionally homologous to mammalian astrocytes and Cp1 is orthologous to mammalian Cathepsin L. Our studies raise the possibility that cathepsins may influence behavioral responses to alcohol in mammals via roles in astrocytes.

Convergent Evidence From Humans and Drosophila melanogaster Implicates the Transcription Factor MEF2B/Mef2 in Alcohol Sensitivity.

BACKGROUND: Self-Rating of the Effects of Alcohol (SRE) measures level of response to ethanol (EtOH) in humans. Interestingly, there is a positive relationship between the SRE and risk for abusing alcohol, suggesting mechanistic connections between SRE and alcohol abuse. METHODS: To identify candidate genes with a role in SRE and alcohol-related behavior more generally, we coupled human genetic analyses with studies in Drosophila melanogaster. We first performed a gene-based analysis of Genomewide association studies (GWAS) summary statistics for SRE in the Avon Longitudinal Study of Parents and Children sample. Based on prior findings in humans, orthology to fly genes, and the availability of genetic reagents, we selected a subset of these genes for studies on EtOH behavior in Drosophila. RESULTS: We found 37 genes with nominal associations in our SRE GWAS. We explored the role of 6 orthologous genes in Drosophila EtOH sedation and rapid tolerance. We found that the transcription factor Mef2 is required for normal EtOH sedation in flies. Pan-neuronal expression of 2 independent Mef2 RNAi transgenes significantly reduced Mef2 expression and made flies resistant to EtOH sedation. Additionally, flies with multiple independent mutant alleles of Mef2 were also resistant to EtOH sedation, confirming a role for Mef2 in this behavior. Altered expression of Mef2 did not change EtOH rapid tolerance or cause a net change in internal EtOH concentrations. CONCLUSIONS: Our studies indicate that MEF2B influences SRE in humans and that Mef2 impacts EtOH sedation in Drosophila.

Measurement of solid food intake in Drosophila via consumption-excretion of a dye tracer.

Although the Drosophila melanogaster (fly) model is a popular platform for investigating diet-related phenomena, it can be challenging to measure the volume of agar-based food media flies consume. We addressed this challenge by developing a dye-based method called Consumption-Excretion (Con-Ex). In Con-Ex studies, flies consume solid food labeled with dye, and the volume of food consumed is reflected by the sum of the dye inside of and excreted by flies. Flies consumed-excreted measurable amounts of FD&C Blue No. 1 (Blue 1) and other dyes in Con-Ex studies, but only Blue 1 was readily detectable at concentrations that had no discernable effect on consumption-excretion. In studies with Blue 1, consumption-excretion (i) increased linearly with feeding duration out to 24 h at two different laboratory sites, (ii) was sensitive to starvation, mating status and strain, and (iii) changed in response to alteration of media composition as expected. Additionally, the volume of liquid Blue 1 consumed from capillary tubes was indistinguishable from the volume of Blue 1 excreted by flies, indicating that excreted Blue 1 reflects consumed Blue 1. Our results demonstrate that Con-Ex with Blue 1 as a food tracer is a useful method for assessing ingestion of agar-based food media in adult flies.