A. Janet Tomiyama

Medicare's search for effective obesity treatments: Diets are not the answer.

The prevalence of obesity and its associated health problems have increased sharply in the past 2 decades. New revisions to Medicare policy will allow funding for obesity treatments of proven efficacy. The authors review studies of the long-term outcomes of calorie-restricting diets to assess whether dieting is an effective treatment for obesity. These studies show that one third to two thirds of dieters regain more weight than they lost on their diets, and these studies likely underestimate the extent to which dieting is counterproductive because of several methodological problems, all of which bias the studies toward showing successful weight loss maintenance. In addition, the studies do not provide consistent evidence that dieting results in significant health improvements, regardless of weight change. In sum, there is little support for the notion that diets lead to lasting weight loss or health benefits.

Cultural Models, Socialization Goals, and Parenting Ethnotheories A Multicultural Analysis

This study conceptualizes a cultural model of parenting. It is argued that cultural models are expressed in the degree of familism, which informs socialization goals that are embodied in parenting ethnotheories. Three cultural models were differentiated a priori: independent, interdependent, and autonomous-related. Samples were recruited that were expected to represent these cultural models: German, Euro-American, and Greek middle-class women representing the independent cultural model; Cameroonian Nso and Gujarati farming women representing the interdependent cultural model; and urban Indian, urban Chinese, urban Mexican, and urban Costa Rican women representing the autonomous-related model. These a priori classifications were confirmed with data that addressed different levels of the cultural models of parenting. The authors further confirmed that socialization goals mediate between broader sociocultural orientations (familism) and parenting ethnotheories concerning beliefs about good parenting. The data reveal that the model of autonomous relatedness needs further theoretical and empirical refinement. Problems with empirical studies comparing participants with very different lifestyles are discussed.

Low Calorie Dieting Increases Cortisol

Objective: To test the hypothesis that dieting, or the restriction of caloric intake, is ineffective because it increases chronic psychological stress and cortisol production—two factors that are known to cause weight gain; and to examine the respective roles of the two main behaviors that comprise dieting—monitoring ones caloric intake and restricting ones caloric intake—on psychological and biological stress indicators. Methods: In a 2 (monitoring vs. not) × 2 (restricting vs. not) fully crossed, controlled experiment, 121 female participants were assigned randomly to one of four dietary interventions for 3 weeks. The monitoring + restricting condition tracked their caloric intake and restricted their caloric intake (1200 kcal/day); the monitoring only condition tracked their caloric intake but ate normally; the restricting only condition was provided 1200 kcal/day of food but did not track their calories, and the control group ate normally and did not track their intake. Before and after the interventions, participants completed measures of perceived stress and 2 days of diurnal saliva sampling to test for cortisol. Results: Restricting calories increased the total output of cortisol, and monitoring calories increased perceived stress. Conclusions: Dieting may be deleterious to psychological well-being and biological functioning, and changes in clinical recommendations may be in order. HPA = hypothalamic-pituitary-adrenocortical; PSS = Perceived Stress Scale; CAR = cortisol awakening response.

Hypothalamic-pituitary-adrenal axis dysregulation and cortisol activity in obesity: A systematic review

BACKGROUND Although there is substantial evidence of differential hypothalamic-pituitary-adrenal (HPA) axis activity in both generalized and abdominal obesity, consistent trends in obesity-related HPA axis perturbations have yet to be identified. OBJECTIVES To systematically review the existing literature on HPA activity in obesity, identify possible explanations for inconsistencies in the literature, and suggest methodological improvements for future study. DATA SOURCES Included papers used Pubmed, Google Scholar, and the University of California Library search engines with search terms body mass index (BMI), waist-to-hip ratio (WHR), waist circumference, sagittal diameter, abdominal versus peripheral body fat distribution, body fat percentage, DEXA, abdominal obesity, and cortisol with terms awakening response, slope, total daily output, reactivity, feedback sensitivity, long-term output, and 11β-HSD expression. STUDY ELIGIBILITY CRITERIA Empirical research papers were eligible provided that they included at least one type of obesity (general or abdominal), measured at least one relevant cortisol parameter, and a priori tested for a relationship between obesity and cortisol. RESULTS A general pattern of findings emerged where greater abdominal fat is associated with greater responsivity of the HPA axis, reflected in morning awakening and acute stress reactivity, but some studies did show underresponsiveness. When examined in adipocytes, there is a clear upregulation of cortisol output (due to greater expression of 11β-HSD1), but in hepatic tissue this cortisol is downregulated. Overall obesity (BMI) appears to also be related to a hyperresponsive HPA axis in many but not all studies, such as when acute reactivity is examined. LIMITATIONS The reviewed literature contains numerous inconsistencies and contradictions in research methodologies, sample characteristics, and results, which partially precluded the development of clear and reliable patterns of dysregulation in each investigated cortisol parameter. CONCLUSIONS AND IMPLICATIONS The literature to date is inconclusive, which may well arise from differential effects of generalized obesity vs. abdominal obesity or from modulators such as sex, sex hormones, and chronic stress. While the relationship between obesity and adipocyte cortisol seems to be clear, further research is warranted to understand how adipocyte cortisol metabolism influences circulating cortisol levels and to establish consistent patterns of perturbations in adrenal cortisol activity in both generalized and abdominal obesity.

Nocturnal levels of ghrelin and leptin and sleep in chronic insomnia.

Experimental sleep deprivation in healthy humans affects levels of ghrelin and leptin, two primary hormones involved in energy balance that regulate appetite and body weight. No study to date has examined levels of these hormones in patients with chronic insomnia. In this study, men diagnosed with primary insomnia using DSM-IV criteria (n=14) and age and body weight comparable healthy control men (n=24) underwent polysomnography. Circulating levels of ghrelin and leptin were measured at 2300h, 0200h and 0600h. As compared to controls, insomnia patients showed less total sleep time, stage 2 and REM sleep and decreased sleep efficiency and more stage 1 sleep than controls (ps<.05). Ghrelin levels across the night were significantly lower in insomnia patients (p<.0001). Leptin was not significantly different between the groups. In conclusion, decreased nocturnal ghrelin in insomnia is consistent with findings for nighttime levels in sleep deprivation studies in healthy sleepers. These findings suggest that insomnia patients have a dysregulation in energy balance that may play a role in explaining prospective weight gain in this population.

Weight labeling and obesity: a longitudinal study of girls aged 10 to 19 years.

Letters RESEARCH LETTER Weight Labeling and Obesity: A Longitudinal Study of Girls Aged 10 to 19 Years Anti-obesity efforts that rely on stigmatizing weight (eg, using harsh language or stereotypical portrayals of over- weight individuals) may impede health promotion efforts, as weight stigma is often negatively related to behavior change and thus seems unlikely to result in weight loss. 1 Indeed, considerable research underscores the detrimental effects of weight stigma on the physical health and well-being of chil- dren and adolescents, 2 and nationally representative, longi- tudinal data show weight-based discrimination is associated with weight gain among older individuals. 3 Although the childhood weight stigma literature frequently examines overt and often malicious behaviors (eg, bullying), stigma pro- cesses can begin when an individual experiences weight labeling. 4 By labeling someone as overweight, the negative stereotypes, status loss, and mistreatment associated with this label may now be applicable to the individual. Recent research suggests that the negative psychological effects of weight stigma can begin when one is simply labeled as “too fat” by others. 5 However, the relationship between weight labeling and weight gain remains unknown. Thus, we exam- ined if weight labeling during childhood was related to the likelihood of having an obese body mass index (BMI) nearly a decade later. Methods | Sample . The National Heart, Lung, and Blood Insti- tute Growth and Health Study followed up girls who self- identified as black (n = 1213) or white (n = 1166) from age 10 years until age 19 years. Extensive study information is avail- able at https://biolincc.nhlbi.nih.gov/static/studies/nghs /Protocol.pdf. The National Heart, Lung, and Blood Institute Growth and Health Study protocol was approved by institu- tional review boards at all 3 sites (University of California, Berkeley; University of Cincinnati; and Westat/Group Health Association, Rockville, Maryland). The University of Califor- nia, Los Angeles Institutional Review Board provided human subjects approval for the current study. The child provided writ- ten assent and a parent/guardian provided written informed consent until the child became 18 years old, at which point she provided written informed consent. Measures. A parent or guardian provided income and educa- tion information at baseline. Certified staff conducted anthro- pometry and collected information on pubertal timing and weight labeling. Weight labeling was assessed by asking par- ticipants, “Have any of these people told you that you were too fat?” followed by a list that included father, mother, brother, sister, best girlfriend, boy you like best, any other girl, any other boy, and teacher. Participants reporting “yes” to any item were considered “labeled.” Results | Participants without BMI data at age 19 years (n = 317) were excluded from analyses. These participants did not dif- fer in baseline BMI, weight labeling, or race but had slightly lower levels of household income and parental education. At baseline, 57.9% (n = 1188) of participants reported being la- beled. Black girls reported more weight labeling than white girls (χ 21 = 16.13, P < .001), although this difference was small (φ = 0.089). Baseline BMI and weight labeling status were mod- erately correlated (r = 0.41, P < .001). Logistic regression analy- ses (Table) evaluated the association between baseline label- ing and obesity 10 years later. Adjusting for baseline BMI, household income, parental education, race, and age at men- arche, being labeled “too fat” at age 10 years remained a sig- nificant predictor of obesity at age 19 years (odds ra- tio = 1.66). The odds ratio was 1.62 when family members were the source of labeling and 1.40 when nonfamily members were the source. These effects were not modulated by race. Discussion | Being labeled “too fat” in childhood was associ- ated with higher odds of having an obese BMI nearly a decade later. Importantly, this relationship was independent of ini- tial BMI and thus not attributable simply to participants’ ob- jective weight at baseline. These data provide novel evidence that the relationship between weight stigma and weight gain may begin early in life; these findings also demonstrate that this relationship can emerge even for a seemingly innocuous Table. Results of Logistic Regression Analyses Predicting Obesity Status at Age 19 Years From Baseline Weight Labeling a Source of Labeling, OR (95% CI) Predictor Model 1: Anyone Model 2: Family Baseline BMI Model 3: Nonfamily Race Parental education Household income Age at menarche Baseline labeling jamapediatrics.com Abbreviations: BMI, body mass index; OR, odds ratio. a The pattern of results was the same when modeling both weight labeling and BMI as continuous variables; these full results are available from the authors. JAMA Pediatrics Published online April 28, 2014 Copyright 2014 American Medical Association. All rights reserved. Downloaded From: http://archpedi.jamanetwork.com/ by a University of California - Los Angeles User on 04/28/2014 E1

Shorter Leukocyte Telomere Length in Midlife Women with Poor Sleep Quality

Background. Accumulating evidence supports leukocyte telomere length (LTL) as a biological marker of cellular aging. Poor sleep is a risk factor for age-related disease; however, the extent to which sleep accounts for variation in LTL is unknown. Methods. The present study examined associations of self-reported sleep duration, onset latency, and subjective quality with LTL in a community-dwelling sample of 245 healthy women in midlife (aged 49–66 years). Results. While sleep duration and onset latency were unrelated to LTL, women reporting poorer sleep quality displayed shorter LTL (r = 0.14, P = 0.03), independent of age, BMI, race, and income (b = 55.48, SE = 27.43, P = 0.04). When analyses were restricted to participants for whom sleep patterns were chronic, poorer sleep quality predicted shorter LTL independent of covariates and perceived psychological stress. Conclusions. This study provides the first evidence that poor sleep quality explains significant variation in LTL, a marker of cellular aging.

Weight bias in 2001 versus 2013: Contradictory attitudes among obesity researchers and health professionals

To assess levels of two types of anti‐fat bias in obesity specialists, explicit bias, or consciously accessible anti‐fat attitudes, and implicit bias, or attitudes that are activated outside of conscious awareness, were examined. This study also assessed changes over time by comparing levels of bias in 2013 to published data from 2001.

Neural systems underlying the reappraisal of personally craved foods

Craving of unhealthy food is a common target of self-regulation, but the neural systems underlying this process are understudied. In this study, participants used cognitive reappraisal to regulate their desire to consume idiosyncratically craved or not craved energy-dense foods, and neural activity during regulation was compared with each other and with the activity during passive viewing of energy-dense foods. Regulation of both food types elicited activation in classic top–down self-regulation regions including the dorsolateral prefrontal, inferior frontal, and dorsal anterior cingulate cortices. This main effect of regulation was qualified by an interaction, such that activation in these regions was significantly greater during reappraisal of craved (versus not craved) foods and several regions, including the dorsolateral prefrontal, inferior frontal, medial frontal, and dorsal anterior cingulate cortices, were uniquely active during regulation of personally craved foods. Body mass index significantly negatively correlated with regulation-related activation in the right dorsolateral PFC, thalamus, and bilateral dorsal ACC and with activity in nucleus accumbens during passive viewing of craved (vs. neutral, low-energy density) foods. These results suggest that several of the brain regions involved in the self-regulation of food craving are similar to other kinds of affective self-regulation and that others are sensitive to the self-relevance of the regulation target.

Physical activity moderates effects of stressor-induced rumination on cortisol reactivity

Objective: Physically active individuals have lower rates of morbidity and mortality, and recent evidence indicates that physical activity may be particularly beneficial to those experiencing chronic stress. The tendency to ruminate increases and prolongs physiological stress responses, including hypothalamic-pituitary-adrenal (HPA) axis responses as indexed by cortisol reactivity to stressful experiences. We examined the association between ruminating in response to a laboratory stressor task and HPA axis reactivity and recovery and examined whether a physically active life-style moderates the associations between rumination and cortisol output trajectories. Methods: Forty-six postmenopausal women underwent the Trier Social Stress Test, whereas salivary cortisol was repeatedly measured. Twenty-five minutes after the end of the stressor, participants reported level of rumination in response to the stress. Results: Findings indicate that physical activity moderated the initial rate (B = −0.10, standard error = 0.04, p < .05) and curvature (B = −0.03, standard error = 0.01, p = .06) of the relationship between rumination and log-transformed cortisol trajectory. Among sedentary participants, those who responded to the stressor with higher levels of rumination had a more rapid initial increase in cortisol level (0.26 versus 0.21, p < .001), a later peak in cortisol reactivity (56 versus 39 minutes), and a delayed recovery from stress (curvature: −0.07 versus −0.08, p < .001) compared with those with lower levels of rumination. In active participants, cortisol trajectories were equivalent, regardless of the level of rumination. Conclusions: In sum, individuals who maintain a physically active life-style may be protected against the effects of rumination on HPA axis reactivity to and recovery from acute stress.HPA = hypothalamic-pituitary-adrenal; TSST = Trier Social Stress Task; RRS = Ruminative Responses Scale; BMI = body mass index; REML = restricted maximum likelihood; HRT = hormone replacement therapy.