Regional fat distribution in adolescent and adult females with anorexia nervosa: A longitudinal study

2015 ◽  
Vol 34 (6) ◽  
pp. 1224-1232 ◽  
Author(s):  
Marwan El Ghoch ◽  
Chiara Milanese ◽  
Simona Calugi ◽  
Manfred J. Müller ◽  
Maryam Pourhassan ◽  
...  
2007 ◽  
Vol 157 (4) ◽  
pp. 473-479 ◽  
Author(s):  
María Teresa García De Álvaro ◽  
María Teresa Muñoz-Calvo ◽  
Vicente Barrios ◽  
Guillermo Martínez ◽  
Gabriel Ángel Martos-Moreno ◽  
...  

Objective: This study addresses the influence of the duration of malnutrition and the effect of weight recovery on regional fat mass distribution in moderately malnourished adolescents with anorexia nervosa (AN). Study design: We measured total and regional fat mass and leptin levels in 42 restrictive AN female adolescents and 23 controls. AN patients, followed over 2 years, were divided into three groups: prolonged moderate malnutrition (PM; secondary amenorrhea for over 1 year, n = 14); SM, short period of moderate malnutrition (secondary amenorrhea for less than 1 year, n = 13); and R, recovered from AN (BMI, body mass index and menses recovered for over 6 months, n = 15). Results: Total, trunk, and extremity fat mass were reduced in the PM and SM groups (P < 0.05), whereas only PM patients showed altered regional fat distribution with a low trunk to extremity fat ratio (P < 0.05). BMI increased after 12 months only in the SM group (P < 0.05), with menses resumption in 69% of these patients and BMI normalization at 24 months. Their regional fat distribution was similar to controls throughout the study. No difference in any parameter was found between the R group and the controls. Conclusion: Prolonged malnutrition, but not weight recovery, is associated with an abnormal regional fat distribution pattern in moderately malnourished AN adolescents.


2016 ◽  
Vol 29 (5) ◽  
pp. 662-666 ◽  
Author(s):  
M. El Ghoch ◽  
S. Calugi ◽  
E. Chignola ◽  
P. V. Bazzani ◽  
R. Dalle Grave

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
E. Caitlin Lloyd ◽  
Hannah M. Sallis ◽  
Bas Verplanken ◽  
Anne M. Haase ◽  
Marcus R. Munafò

Abstract Background Evidence from observational studies suggests an association between anxiety disorders and anorexia nervosa (AN), but causal inference is complicated by the potential for confounding in these studies. We triangulate evidence across a longitudinal study and a Mendelian randomization (MR) study, to evaluate whether there is support for anxiety disorder phenotypes exerting a causal effect on AN risk. Methods Study One assessed longitudinal associations of childhood worry and anxiety disorders with lifetime AN in the Avon Longitudinal Study of Parents and Children cohort. Study Two used two-sample MR to evaluate: causal effects of worry, and genetic liability to anxiety disorders, on AN risk; causal effects of genetic liability to AN on anxiety outcomes; and the causal influence of worry on anxiety disorder development. The independence of effects of worry, relative to depressed affect, on AN and anxiety disorder outcomes, was explored using multivariable MR. Analyses were completed using summary statistics from recent genome-wide association studies. Results Study One did not support an association between worry and subsequent AN, but there was strong evidence for anxiety disorders predicting increased risk of AN. Study Two outcomes supported worry causally increasing AN risk, but did not support a causal effect of anxiety disorders on AN development, or of AN on anxiety disorders/worry. Findings also indicated that worry causally influences anxiety disorder development. Multivariable analysis estimates suggested the influence of worry on both AN and anxiety disorders was independent of depressed affect. Conclusions Overall our results provide mixed evidence regarding the causal role of anxiety exposures in AN aetiology. The inconsistency between outcomes of Studies One and Two may be explained by limitations surrounding worry assessment in Study One, confounding of the anxiety disorder and AN association in observational research, and low power in MR analyses probing causal effects of genetic liability to anxiety disorders. The evidence for worry acting as a causal risk factor for anxiety disorders and AN supports targeting worry for prevention of both outcomes. Further research should clarify how a tendency to worry translates into AN risk, and whether anxiety disorder pathology exerts any causal effect on AN.


2012 ◽  
Vol 25 (1) ◽  
pp. 63-70 ◽  
Author(s):  
Aldo Scafoglieri ◽  
Jonathan Tresignie ◽  
Steven Provyn ◽  
Mike Marfell-Jones ◽  
Keith George ◽  
...  

1999 ◽  
Vol 42 (2) ◽  
pp. 191-200
Author(s):  
C. Xie ◽  
E. Albrecht ◽  
J. Wegner ◽  
G. A. Brockmann ◽  
C. Kazala ◽  
...  

Abstract. Leptin is a hormone involved in the regulation of feed intake and energy balance in animals. The expression and secretion of leptin is highly correlated with body fat mass and adipocyte size. The regulation of leptin is integrated into a broad regulatory network including other hormones and cytokines. Leptin's effects on food intake and energy expenditure is thought to be mediated centrally via various neurotransmitters. Peripheral hormones, including insulin and glucocorticoids, stimulate the expression of leptin. While leptin action has been well studied in rodents and humans, its role in farm animals remains to be determined in relation to feed intake and energy metabolism. Leptin may play a role in the regulation of regional fat distribution. The deposition of intramuscular fat (marbling) is positively correlated with the palatability of beef and, therefore, investigations into the mechanisms underlying fat aecretion in this depot are underway. Studying the relationship between leptin and lipid metabolizing enzymes may provide us with clues on the mechanisms governing site-specific fat aecretion in farm animals.


1995 ◽  
Vol 27 (Supplement) ◽  
pp. S117
Author(s):  
K. T. Farrell-Lee ◽  
D. L. Alekel ◽  
C. B. Christ ◽  
J. L. Clasey ◽  
P. C. Fehling ◽  
...  

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