Obesity is a global epidemic, yet successful interventions are rare. Up to 60% of people fail to achieve clinically meaningful, short-term weight loss (5-10% of start weight), whereas up to 72% are unsuccessful at achieving long-term weight loss (5-10% loss for ≥5years). Understanding how biological, cognitive, and self-regulatory factors work together to promote or to impede weight loss is clearly needed to optimize obesity treatment. This paper describes the methodology of the Cognitive and Self-regulatory Mechanisms of Obesity Study (the COSMOS trial). COSMOS is the first randomized controlled trial to investigate how changes in multiple biopsychosocial and cognitive factors relate to weight loss and one another across two weight loss treatments. The specific aims are to: 1) Confirm that baseline obesity-related physiological dysregulation is linked to cognitive deficits and poorer self-regulation, 2) Evaluate pre- to post-treatment change across time to assess individual differences in biomarkers, cognition, and self-regulation, and 3) Evaluate whether the acceptance-based treatment (ABT) group has greater improvements in outcomes (e.g., greater weight loss and less weight regain, improvements in biomarkers, cognition, and self-regulation), than the standard behavioral treatment group (SBT) from pre- to post-treatment and 1-year follow-up. The results of COSMOS will provide critical information about how dysregulation in biomarkers, cognition, and/or self-regulation is related to weight loss and whether weight loss treatments are differentially associated with these factors. This information will be used to identify promising treatment targets that are informed by biological, cognitive, and self-regulatory factors in order to advance obesity treatment.
Neurocognitive deficits induced by a diet high in refined carbohydrates may manifest before overt obesity or metabolic disease onset, suggesting that researchers and providers may need to target subclinical metabolic, inflammatory, and vascular dysregulation factors in efforts to preserve cognitive function across the lifespan.
Objective Examine the indirect association between parents’ experience of stigma (i.e., associative stigma) and youth depressive symptoms through the serial effects of associative stigma on parent and youth illness intrusiveness in pediatric inflammatory bowel disease (IBD). Methods During routine clinic visits, 150 youth with well-controlled IBD (ages 10–18 years) completed measures of perceived illness intrusiveness and depressive symptoms. Parents completed measures of associative stigma and illness intrusiveness. Pediatric gastroenterologists provided ratings of IBD disease severity. Results Structural equation modeling revealed significant direct associations for associative stigma → parent illness intrusiveness, parent illness intrusiveness → youth illness intrusiveness, and youth illness intrusiveness → youth depressive symptoms. Results also revealed a significant associative stigma → parent illness intrusiveness → youth illness intrusiveness→ youth depressive symptoms serial mediation path, indicating that parents’ experience of associative stigma indirectly influenced youth depressive symptoms through its sequential effects on parent and youth perceived illness intrusiveness. Conclusions Parents who face stigma related to their child’s IBD (i.e., associative stigma) are more likely to experience IBD-induced lifestyle intrusions (i.e., illness intrusiveness), which in turn is associated with youths’ illness intrusiveness and ultimately youth depressive symptoms. These findings provide further evidence for the important role of illness-related stigma in pediatric IBD, particularly the transactional relation between parents’ associative stigma and youths’ illness appraisals and emotional functioning. The clinical implications of our results for addressing adjustment difficulties in youth with IBD are also discussed.
Adverse childhood experiences (ACEs) may be an early life factor associated with adult weight stigma via biological (e.g., stress response), cognitive (e.g., self-criticism/deprecation), and/or emotional (e.g., shame) mechanisms. This pilot study investigated relationships between ACEs and internalized and experienced weight stigma in adult women with overweight/obesity and explored differential relationships between weight stigma and ACE subtypes (i.e., abuse, neglect, household dysfunction). Adult women (68% white, Mage = 33 ± 10 years, MBMI = 33.7 ± 7.2 kg/m2) completed measures of ACEs (ACE Questionnaire), internalized weight stigma (IWS; Weight Bias Internalization Scale—Modified; WBIS—M), and lifetime experiences of weight stigma (yes/no). Data were analyzed with linear and logistic regression (n = 46), adjusting for age, race, and body mass index (BMI). Linear regressions revealed a positive association between ACE and WBIS—M scores (β = 0.40, p = 0.006), which was driven by Abuse-type ACEs (β = 0.48, p = 0.009). Relationships between WBIS—M scores and Neglect- and Household-Dysfunction-type ACEs did not reach significance (β = 0.20, p = 0.173; β = −0.16, p = 0.273). Though descriptive statistics revealed greater rates of experienced weight stigma endorsement by those with high-3+ ACEs (81%) vs. medium-1–2 ACEs (67%) or low/no-0 ACEs (60%), ACE scores were not significantly associated with experienced weight stigma in logistic regression (Wald = 1.36, p = 0.244, OR = 1.324, 95%, CI = 0.825–2.125). ACEs may be an early life factor that increase the risk for internalizing weight stigma in adulthood. Larger studies should confirm this relationship and follow-up on descriptive findings suggesting a potential association between ACEs and experienced weight stigma.
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