Body size overestimation and its association with body mass index, body dissatisfaction, and drive for thinness in anorexia nervosa.

BACKGROUND: Body size overestimation is a fundamental feature in anorexia nervosa (AN). There have been inconclusive findings about the extent to which this feature distinguishes psychopathology and some authors have argued that overestimation may be a function of lower body mass index (BMI). METHODS: We examine body size estimation accuracy and body dissatisfaction in 74 females with AN and 11 age-matched female controls using two well-established psychophysical procedures. RESULTS: Participants with AN overestimated their body size more and had greater body dissatisfaction than controls. Size accuracy was found to be independent of BMI and correlated with body dissatisfaction and drive for thinness in participants with AN. CONCLUSIONS: We conclude that overestimation of body size in AN is related to the psychopathology associated with the disorder and is not due to any perceptual tendency for people with lower BMI to overestimate their body size. We discuss the implications of these findings for treatment of AN.

Body size estimation in anorexia nervosa: a brief review of findings from 2003 through 2013.

Body size overestimation is a fundamental feature in anorexia nervosa (AN). The extent or even existence of body size overestimation in AN is controversial. The most recent review (Farrell et al., 2005) found that only half the studies reported overestimation of body size in individuals diagnosed with AN. The remaining studies found no overestimation or in some instances underestimation. The discrepancy in these findings has been attributed to the wide variety of assessment techniques that are used, including many with questionable psychometric properties. We review all 9 contemporary studies conducted in this area since the last review in 2005. For each study we describe the number of participants, methodology, reliability/validity data, amount of whole body distortion, effect sizes, and a summary of findings. In all studies that included a healthy control group, individuals with AN overestimated their whole body size more than healthy controls did. The difference was significant in all except two studies. Based on these contemporary findings, we conclude that individuals with AN overestimate their body size and that the greater consistency of findings in the studies conducted over the last decade is attributable to the use of improved methodologies and assessment tools with documented psychometric properties.

Using Amazon's Mechanical Turk website to measure accuracy of body size estimation and body dissatisfaction.

This study investigated Amazon.com's website Mechanical Turk (MTurk) as a research tool for measuring body size estimation and dissatisfaction. 160 U.S. participants completed the BIAS-BD figural drawing scale and demographic questions posted on the MTurk website. The BIAS-BD consists of 17 drawings of various male and female body sizes based on anthropometric data corresponding to a range of 60% below to 140% above the average U.S. adult. Respondents selected a drawing that best reflected their current size and ideal size. Results revealed that respondents overestimated their body size by 6% and desired an ideal size 9.2% smaller than their perceived size. Findings are compared with three previous studies using the BIAS-BD scale. A general correspondence in findings between the four studies was found. We conclude that the MTurk can serve as a viable method for collecting data on the perceptual and attitudinal aspects of body image quickly and inexpensively.

Method of presentation and sex differences when using a revised figural drawing scale to measure body size estimation and dissatisfaction.

The present study examined whether a revision of the Gardner, Jappe, and Gardner (2009) BIAS-BD figural drawing scale gave more accurate estimations of body size estimation and body dissatisfaction than a prior version. It also examined whether the order of figure presentation led to differing values for body size estimation and body dissatisfaction. The revised BIAS-BD scale included a continuous line beneath 17 figural drawings ordered in either ascending or descending size. Results were compared with previous studies using the original scale in which the 17 figural drawings were presented in a random order and, additionally, with a method using an adjustable video image by which the participants estimated their perceived body size by adjusting the width of their static image. The scale was presented to 330 undergraduate university students, including 199 women and 131 men. Overall, compared to BMIs calculated from the participants' reports of their height and weight, men and women participants gave less accurate estimations of body size using the revised scale when compared to the original BIAS-BD scale and video methodology. Participants reported significantly less body dissatisfaction than with the original scale. There was no significant difference in body size estimation when the figures were presented in ascending or descending size. Body dissatisfaction was greater for women than men, and when the figures were presented in descending order. Methodological considerations for using figural drawing scales in body image research are discussed.

Nitric oxide and AMPK cooperatively regulate PGC-1 in skeletal muscle cells.

Nitric oxide (NO) induces mitochondrial biogenesis in skeletal muscle cells via upregulation of the peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α). Further, we have shown that nitric oxide interacts with the metabolic sensor enzyme, AMPK. Therefore, we tested the hypothesis that nitric oxide and AMPK act synergistically to upregulate PGC-1α mRNA expression and stimulate mitochondrial biogenesis in culture. L6 myotubes treated with nitric oxide donors, S-nitroso-N-penicillamine (SNAP, 25 µM) or diethylenetriamine-NONO (DETA-NO, 50 µM), exhibited elevated AMPK phosphorylation, PGC-1α mRNA and protein, and basal and uncoupled mitochondrial respiration (P < 0.05). Pre-treatment of cultures with the AMPK inhibitor, Compound C, prevented these effects. Knockdown of AMPKα1 in L6 myotubes using siRNA reduced AMPKα protein content and prevented upregulation of PGC-1α mRNA by DETA-NO. Meanwhile, siRNA knockdown of AMPKα2 had no effect on total AMPKα protein content or PGC-1α mRNA. These results suggest that NO effects on PGC-1α expression are mediated by AMPKα1. Paradoxically, we found that the AMPK-activating compound, AICAR, induced NO release from L6 myotubes, and that AICAR-induced upregulation of PGC-1α mRNA was prevented by inhibition of NOS with N(G)-nitro-L-arginine methyl ester (L-NAME, 1 mM). Additionally, incubation of isolated mouse extensor digitorum longus (EDL) muscles with 2 mM AICAR for 20 min or electrical stimulation (10 Hz, 13 V) for 10 min induced phosphorylation of AMPKα (P < 0.05), which was completely prevented by pre-treatment with the NOS inhibitor, L-N(G)-monomethyl arginine (L-NMMA, 1 mM). These data identify the AMPKα1 isoform as the mediator of NO-induced effects in skeletal muscle cells. Further, this study supports a proposed model of synergistic interaction between AMPK and NOS that is critical for maintenance of metabolic function in skeletal muscle cells.

Endothelial nitric oxide synthase is involved in calcium-induced Akt signaling in mouse skeletal muscle.

We hypothesized that targeted mutation of the endothelial nitric oxide synthase (eNOS) gene would reduce Akt-related signaling events in skeletal muscle cells, compared to wild type (WT) controls. Results show that slow myosin heavy chain (type I/beta) expression and the abundance of slow-twitch fibers are reduced in plantaris muscle of eNOS(-/-) mice, compared to WT. Further, basal phosphorylation of Akt (p-Akt (Ser-473)/total Akt) and GSK-3beta (GSK-3beta (Ser-9)/total GSK-3beta) are reduced 60-70% in primary myotubes from eNOS(-/-) mice. Treatment with the calcium ionophore, A23187 (0.4 microM, 1 h), increased phosphorylation of Akt and GSK-3beta by approximately 2-fold (P<0.05) in myotubes from WT mice, but had no effect on phosphorylation of these proteins in eNOS(-/-) myotubes. Additionally, A23187 treatment failed to induce nuclear translocation of the transcription factor, NFATc1, in eNOS(-/-) myotubes. Treatment with the nitric oxide donor, propylamine propylamine NONOate (PAPA-NO; 1 microM for 1 h) increased Akt and GSK-3beta phosphorylation, and induced NFATc1 nuclear translocation in WT and eNOS(-/-) myotubes, and eliminated differences from WT in the NOS knockout cultures. Parallel experiments in C2C12 myotubes found that Akt phosphorylation induced by NO or the guanylate cyclase activator, YC-1, is prevented by co-treatment with either a guanylate cyclase or PI3K inhibitor (10 microM ODQ or 25 microM LY2904002, respectively). These data suggest that eNOS activity is necessary for calcium-induced activation of the Akt pathway, and that nitric oxide is sufficient to elevate Akt activity in primary myotubes. NO appears to influence Akt signaling through a cGMP, PI3K-dependent pathway.