Sunday, 1 December 2013

Eating Disorders: Bulimia nervosa - The Do's and Do not's list

Bulimia nervosa is defined as a medical condition of  consuming a large amount of food in a short amount of time or one setting (binge eating), followed by self induced vomiting, taking a laxative or diuretic and/or excessive exercise, etc. to compensate for the binge. Bulimia nervosa also effects almost 90% of female. Unlike anorexia nervosa, people suffering from bulimia nervosa are usually normal or slightly over weight.
VI. Preventions
A. The Do's and Do not's list
A.1. Primary prevention 
Dt. Michael Sidiropoulos in the article of Anorexia Nervosa: The physiological consequences of starvation and the need for primary prevention efforts indicated that there are numerous actions that the physician, along with the family, allied health care workers and/or through a broader public health initiative can accomplish in this particular case that will have longstanding implications on the patient's future development and growth and will increase the likelihood of healthy outcomes through primary
prevention(37).
1. Minimizing social pressures
In the study to evaluation the Sociological factors in the development of eating disorders, Dr Nagel KL, andand Dr. Jones KH. at the University of Georgia indicated that professionals in the educational and physical and mental health care fields need to be aware of the influence of social pressures on teenagers' perceptions of body image and appearance. This article reviews the sociocultural, socioeconomic, and sex-related factors which contribute to the development of eating disorders. It is recommended that professionals help adolescents resist societal pressure to conform to unrealistic standards of appearance, and provide guidance on nutrition, realistic body ideals, and achievement of self-esteem, self-efficacy, interpersonal relations and coping skills(38).

2. Minimizing family issues
Dr. Yager J. in the study of the family issues in the pathogenesis of anorexia nervosa, suggested that factors residing in family systems have been implicated in the pathogenesis of anorexia nervosa. In this paper I critically review literature that bears on this issue: the transmission of anorexia nervosa in families; family stress patterns, personality and psychopathological characteristics of parents, parent-child interactions, and whole family systems. Much additional research is needed to accurately determine the precise nature of such factors and the extent to which they actually contribute to the appearance of this syndrome(39).

3. Reducing individual factors
In the study to examine which unique factors (genetic and environmental) increase the risk for developing anorexia nervosa by using a case-control design of discordant sister pairs, Dr. Karwautz A, and the research team at University of London, suggested that he sisters with anorexia nervosa differed from their healthy sisters in terms of personal vulnerability traits and exposure to high parental expectations and sexual abuse. Factors within the dieting risk domain did not differ. However, there was evidence of poor feeding in childhood. No difference in the distribution of genotypes or alleles of the DRD4, COMT, the 5HT2A and 5HT2C receptor genes was detected. These results are preliminary because our calculations indicate that there is insufficient power to detect the expected effect on risk with this sample size(40).

A.2. Secondary prevention
Secondary prevention focuses early detection and intervention as  early detection is often difficult as individuals with eating problems often attempt to conceal their behavior. People such as Parents, peers and siblings, teacher and family doctor are in good position to detect changing attitudes around food,weight, and shape for detecting eating disorder early for effective treatment(41)
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Sources
(37) http://www.ncbi.nlm.nih.gov/pubmed/19633611
(38) http://www.ncbi.nlm.nih.gov/pubmed/9582008
(39) http://www.ncbi.nlm.nih.gov/pubmed/20709593
(40) http://www.ncbi.nlm.nih.gov/pubmed/421844 
(41) http://www.ncbi.nlm.nih.gov/pubmed/22162675

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