WIKIPEDIA:
OBESITY:
Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have an adverse effect on health, leading to reduced life expectancy and/or increased health problems. Body mass index (BMI), a measurement which compares weightand height, defines people as overweight (pre-obese) if their BMI is between 25 and 30 kg/m2, and obese when it is greater than 30 kg/m2.
Obesity increases the likelihood of various diseases, particularly heart disease, type 2 diabetes, obstructive sleep apnea, certain types ofcancer, and osteoarthritis.Obesity is most commonly caused by a combination of excessive food energy intake, lack of physical activity, and genetic susceptibility, although a few cases are caused primarily by genes, endocrine disorders, medications or psychiatric illness. Evidence to support the view that some obese people eat little yet gain weight due to a slow metabolism is limited; on average obese people have a greater energy expenditure than their thin counterparts due to the energy required to maintain an increased body mass.
Dieting and physical exercise are the mainstays of treatment for obesity. Moreover, it is important to improve diet quality by reducing the consumption of energy-dense foods such as those high in fat and sugars, and by increasing the intake of dietary fiber. To supplement this, or in case of failure, anti-obesity drugs may be taken to reduce appetite or inhibit fat absorption. In severe cases, surgery is performed or an intragastric balloon is placed to reduce stomach volume and/or bowel length, leading to earlier satiation and reduced ability to absorb nutrients from food.
Obesity is a leading preventable cause of death worldwide, with increasing prevalence in adults and children, and authorities view it as one of the most serious public health problems of the 21st century.Obesity is stigmatized in much of the modern world (particularly in theWestern world), though it was widely perceived as a symbol of wealth and fertility at other times in history, and still is in some parts of the world.
Excess body fat underlies 64% of cases of diabetes in men and 77% of cases in women.[29]
Main article: Classification of obesity
Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have an adverse effect on health.[1] It is defined by body mass index (BMI) and further evaluated in terms of fat distribution via the waist–hip ratio and total cardiovascular risk factors.[10][11] BMI is closely related to both percentage body fat and total body fat.[12]
In children, a healthy weight varies with age and sex. Obesity in children and adolescents is defined not as an absolute number, but in relation to a historical normal group, such that obesity is a BMI greater than the 95th percentile.[13] The reference data on which these percentiles were based date from 1963 to 1994, and thus have not been affected by the recent increases in weight.[14]
| BMI | Classification |
|---|---|
| < 18.5 | underweight |
| 18.5–24.9 | normal weight |
| 25.0–29.9 | overweight |
| 30.0–34.9 | class I obesity |
| 35.0–39.9 | class II obesity |
| ≥ 40.0 | class III obesity |
BMI is calculated by dividing the subject's mass by the square of his or her height, typically expressed either in metric or US "customary" units:
- Metric: BMI = kilograms / meters2
- US customary and imperial: BMI = lb * 703 / in2
The most commonly used definitions, established by the World Health Organization (WHO) in 1997 and published in 2000, provide the values listed in the table at right.[3]
Some modifications to the WHO definitions have been made by particular bodies. The surgical literature breaks down "class III" obesity into further categories whose exact values are still disputed.[15]
- Any BMI ≥ 35 or 40 is severe obesity
- A BMI of ≥ 35 or 40–44.9 or 49.9 is morbid obesity
- A BMI of ≥ 45 or 50 is super obesity
Diet
Main article: Diet and obesity
The per capita dietary energy supply varies markedly between different regions and countries. It has also changed significantly over time.[68] From the early 1970s to the late 1990s the average calories available per person per day (the amount of food bought) increased in all parts of the world except Eastern Europe. The United States had the highest availability with 3,654 calories per person in 1996.[68] This increased further in 2003 to 3,754.[68] During the late 1990s Europeans had 3,394 calories per person, in the developing areas of Asia there were 2,648 calories per person, and in sub-Saharan Africa people had 2,176 calories per person.[68][69] Total calorie consumption has been found to be related to obesity.[70]
The widespread availability of nutritional guidelines[71] has done little to address the problems of overeating and poor dietary choice.[72] From 1971 to 2000, obesity rates in the United States increased from 14.5% to 30.9%.[73] During the same period, an increase occurred in the average amount of food energy consumed. For women, the average increase was 335 calories per day (1,542 calories in 1971 and 1,877 calories in 2004), while for men the average increase was 168 calories per day (2,450 calories in 1971 and 2,618 calories in 2004). Most of this extra food energy came from an increase in carbohydrate consumption rather than fat consumption.[74] The primary sources of these extra carbohydrates are sweetened beverages, which now account for almost 25 percent of daily food energy in young adults in America,[75] and potato chips.[76] Consumption of sweetened drinks is believed to be contributing to the rising rates of obesity.[77][78]
As societies become increasingly reliant on energy-dense, big-portions, and fast-food meals, the association between fast-food consumption and obesity becomes more concerning.[79] In the United States consumption of fast-food meals tripled and food energy intake from these meals quadrupled between 1977 and 1995.[80]
Agricultural policy and techniques in the United States and Europe have led to lower food prices. In the United States, subsidization of corn, soy, wheat, and rice through the U.S. farm bill has made the main sources of processed food cheap compared to fruits and vegetables.[81]
Obese people consistently under-report their food consumption as compared to people of normal weight.[82] This is supported both by tests of people carried out in a calorimeter room[83] and by direct observation.
Sedentary lifestyle
See also: Sedentary lifestyle and Exercise trends
A sedentary lifestyle plays a significant role in obesity.[84] Worldwide there has been a large shift towards less physically demanding work,[85][86][87] and currently at least 60% of the world's population gets insufficient exercise.[86] This is primarily due to increasing use of mechanized transportation and a greater prevalence of labor-saving technology in the home.[85][86][87] In children, there appear to be declines in levels of physical activity due to less walking and physical education.[88] World trends in active leisure time physical activityare less clear. The World Health Organization indicates people worldwide are taking up less active recreational pursuits, while a study from Finland[89] found an increase and a study from the United States found leisure-time physical activity has not changed significantly.[90]
In both children and adults, there is an association between television viewing time and the risk of obesity.[91][92][93] A 2008 meta-analysis found 63 of 73 studies (86%) showed an increased rate of childhood obesity with increased media exposure, with rates increasing proportionally to time spent watching television.[94]
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ANOREXIA
Anorexia nervosa is an eating disorder characterized by an obsessive fear of gaining weight. The terms anorexia nervosa and anorexia are often used interchangeably, however anorexia is simply a medical term for lack of appetite. Anorexia nervosa has many complicated implications and may be thought of as a lifelong illness that may never be truly cured, but only managed over time.
Anorexia nervosa is often coupled with a distorted self image[1][2] which may be maintained by various cognitive biases[3] that alter how the affected individual evaluates and thinks about her or his body, food and eating. Persons with anorexia nervosa continue to feel hunger, but deny themselves all but very small quantities of food. The average caloric intake of a person with anorexia nervosa is 600–800 calories per day, but extreme cases of complete self-starvation are known.[4] It is a serious mental illness with a high incidence of comorbidity and the highest mortality rate of any psychiatric disorder.[5]
Anorexia most often has its onset in adolescence and is most prevalent among adolescent girls. [6] However, more recent studies show that the onset age of anorexia decreased from an average of 13 to 17 years of age to 9 to 12. [7] While it can affect men and women of any age, race, and socioeconomic and cultural background,[8] Anorexia nervosa occurs in females 10 times more than in males.[9]
The term anorexia nervosa was established in 1873 by Sir William Gull, one of Queen Victoria's personal physicians.[10] The term is of Greek origin: an- (ἀν-, prefix denoting negation) and orexis (ὄρεξις, "appetite"), thus meaning a lack of desire to eat.
Signs and symptoms
A person with anorexia nervosa may exhibit a number of signs and symptoms, some of which are listed below. The type and severity vary in each case and may be present but not readily apparent. Anorexia nervosa and the associated malnutrition that results from self-imposed starvation, can cause severe complications in every major organ system in the body.[12][13][14]
- Refusal to maintain a normal BMI for their age [15]
- amenorrhea: The absence of 3 consecutive menstural cycles [16]
- Fearful of even the slightest weight gain and takes all precautionary measures to avoid weight gain and becoming overweight [16]
- obvious, rapid, dramatic weight loss
- lanugo: soft, fine hair grows on face and body[17]
- obsession with calories and fat content
- preoccupation with food, recipes, or cooking; may cook elaborate dinners for others but not eat themselves[18]
- dieting despite being thin or dangerously underweight
- rituals: cuts food into tiny pieces; refuses to eat around others; hides or discards food
- purging: uses laxatives, diet pills, ipecac syrup, or water pills; may engage in self-induced vomiting; may run to the bathroom after eating in order to vomit and quickly get rid of thecalories[19][20] (see also bulimia nervosa).
- may engage in frequent, strenuous exercise[21]
- perception: perceives self to be overweight despite being told by others they are too thin
- becomes intolerant to cold: frequently complains of being cold from loss of insulating body fat or poor circulation resulting from extremely low blood pressure; body temperature lowers (hypothermia) in effort to conserve energy[22]
- depression: may frequently be in a sad, lethargic state[23]
- solitude: may avoid friends and family; becomes withdrawn and secretive
- cheeks may become swollen because of enlargement of the salivary glands caused by excessive vomiting[24]
- swollen joints[citation needed]
- abdominal distension[citation needed]
- bad breath[citation needed]
- hair loss or thinning[citation needed]
Biological
- Obstetric complications: various prenatal and perinatal complications may factor into the development of AN such as maternal anemia, diabetes mellitus, preeclampsia, placentalinfarction, and neonatal cardiac abnormalities. Neonatal complications may also have an influence on harm avoidance, one of the personality traits associated with the development of AN.[49][50]
- Genetics: anorexia nervosa is believed to be highly heritable, with estimated inheritance rates ranging from 56% to 84%.[51][52][53] Association studies have been performed, studying 128 different polymorphisms related to 43 genes including genes involved in regulation of eating behavior, motivation and reward mechanics, personality traits and emotion. Consistent associations have been identified for polymorphisms associated with agouti-related peptide, brain derived neurotrophic factor, catechol-o-methyl transferase, SK3 andopioid receptor delta-1.[54] In one study, variations in the norepinephrine transporter gene promoter were associated with restrictive anorexia nervosa, but not binge-purge anorexia.[55] Recent studies have advanced the theory that the sex difference in incidence and the common onset at the age of puberty may reflect an abnormal response of the brain to anorexic (feeding suppressing) effects of the female sex hormone, estrogen.[56] This viewpoint has been recently supported by a report that abnormal forms of the estrogen receptor are more common in women with anorexia nervosa of the restricting type.[57]
- epigenetics: Epigenetic mechanisms: are means by which genetic mutations are caused by environmental effects that alter gene expression via methods such as DNA methylation, these are independent of and do not alter the underlying DNA sequence. They are heritable, as was shown in the Överkalix study, but also may occur throughout the lifespan, and are potentially reversible. Dysregulation of dopaminergic neurotransmission and Atrial natriuretic peptide homeostasis resulting from epigenetic mechanisms has been implicated in various eating disorders.[58]"We conclude that epigenetic mechanisms may contribute to the known alterations of ANP homeostasis in women with eating disorders."[58][59]
- serotonin dysregulation;[64] particularly high levels in those areas in the brain with the 5HT1A receptor - a system particularly linked toanxiety, mood and impulse control. Starvation has been hypothesized to be a response to these effects, as it is known to lowertryptophan and steroid hormone metabolism, which might reduce serotonin levels at these critical sites and ward off anxiety. Other studies of the 5HT2A serotonin receptor (linked to regulation of feeding, mood, and anxiety), suggest that serotonin activity is decreased at these sites. There is evidence that both personality characteristics associated with AN, and disturbances to the serotonin system are still apparent after patients have recovered from anorexia.[65]
- Brain-derived neurotrophic factor (BDNF) is a protein that regulates neuronal development and neuroplasticity, it also plays a role inlearning, memory and in the hypothalamic pathway that controls eating behavior and energy homeostasis. BDNF amplifiesneurotransmitter responses and promotes synaptic communication in the enteric nervous system. Low levels of BDNF are found in patients with AN and some comorbid disorders such as major depression.[66][67] Exercise increases levels of BDNF[68]
- leptin and ghrelin; leptin is a hormone produced primarily by the fat cells in white adipose tissue of the body it has an inhibitory (anorexigenic) effect on appetite, by inducing a feeling of satiety. Ghrelin is an appetite inducing (orexigenic) hormone produced in thestomach and the upper portion of the small intestine. Circulating levels of both hormones are an important factor in weight control. While often associated with obesity both have been implicated in the pathophysiology of anorexia nervosa and bulimia nervosa.[69]
- cerebral blood flow (CBF); neuroimaging studies have shown reduced CBF in the temporal lobes of anorectic patients, which may be a predisposing factor in the onset of AN.[70]
- autoimmune system; Autoantibodies against neuropeptides such as melanocortin have been shown to affect personality traits associated with eating disorders such as those that influence appetite and stress responses.[71]
- Nutritional deficiencies
- Zinc deficiency may play a role in anorexia. It is not thought responsible for causation of the initial illness but there is evidence that it may be an accelerating factor that deepens the pathology of the anorexia. A 1994 randomized, double-blind, placebo-controlled trial showed that zinc (14 mg per day) doubled the rate of body mass increase compared to patients receiving the placebo.[72]
[edit]Environmental
Sociocultural studies have highlighted the role of cultural factors, such as the promotion of thinness as the ideal female form in Western industrialized nations, particularly through the media.[73] A recent epidemiological study of 989,871 Swedish residents indicated that gender, ethnicity and socio-economic status were large influences on the chance of developing anorexia, with those with non-European parents among the least likely to be diagnosed with the condition, and those in wealthy, white families being most at risk.[74] People in professions where there is a particular social pressure to be thin (such as models and dancers) were much more likely to develop anorexia during the course of their career,[75] and further research has suggested that those with anorexia have much higher contact with cultural sources that promote weight-loss.[76]
Anorexia nervosa is more likely to occur in a person’s pubertal years, especially for girls.[77] Female students are 10 times more likely to suffer from anorexia nervosa than male students. According to a survey of 1799 Japanese female high school students, “85% who were a normal weight wanted to be thinner and 45% who were 10–20% underweight wanted to be thinner.”[78] Teenage girls concerned about their weight and who believe that slimness is more attractive among peers trend to weight-control behaviors. Teen girls are learning from each other to consume low-caloric, low-fat foods and diet pills. This results in lack of nutrition and a greater chance of developing anorexia nervosa.[79]
It has also been noted that anorexia nervosa is more likely to occur in populations in which obesity is more prevalent. It has been suggested that anorexia nervosa results from a sexually selected evolutionary drive to appear youthful in populations in which size becomes the primary indicator of age.[80]
There is also evidence to suggest that patients who have anorexia nervosa can be characterised by alexithymia[81] and also a deficit in certain emotional functions. A research study showed that this was the case in both adult and adolescent anorexia nervosa patients.[82]
There is a high rate of reported child sexual abuse experiences in clinical groups of who have been diagnosed with anorexia. The connection between eating disorders and abuse has been convincingly evidenced by a number of studies, including one published in Epidemiology (and strengthened by blind hypothesis survey), which showed in a comparison of women with no history of eating disorders, women with a history of eating disorders were twice as likely to have reported childhood sexual abuse.[83] While the joint effect of both physical and sexual abuse resulted in a nearly 4-fold risk of eating disorders that met DSM-IV criteria.[83] It is thought that links between childhood abuse and sexual abuse are complex, such as by influencing psychologic processes that increase a woman's susceptibility to the development of an eating disorder, or perhaps by producing changes in psychobiologic process and neurotransmitting function, associated with eating behaviour.[83]
Recent efforts have been made to dispel some of the myths around anorexia nervosa and eating disorders, such as the misconception that families, in particular mothers, are responsible for their daughter developing an eating disorder.[84]
[edit]Relationship to autism
Since Gillberg's (1983 & 1985)[86][87] and others' initial suggestion of relationship between anorexia nervosa and autism,[88][89] a large-scalelongitudinal study into teenage-onset anorexia nervosa conducted in Sweden confirmed that 23% of people with a long-standing eating disorder are on the autism spectrum.[90][91][92][93][94][95][96] Those on autism spectrum tend to have a worse outcome,[97] but may benefit from the combined use of behavioural and pharmacological therapies tailored to ameliorate autism rather than anorexia nervosa per se.[98][99]Other studies, most notably research conducted at the Maudsley Hospital, UK, furthermore suggest that autistic traits are common in people with anorexia nervosa; shared traits include, e.g., poor executive function, autism quotient score, central coherence, theory of mind, cognitive-behavioural flexibility, emotion regulation and understanding facial expressions.[100][101][102][103][104][105]
Zucker et al. (2007) proposed that conditions on the autism spectrum make up the cognitive endophenotype underlying anorexia nervosa and appealed for increased interdisciplinary collaboration (see figure to right).[85] A pilot study into the effectiveness Cognitive Behaviour Therapy, which based its treatment protocol on the hypothesised relationship between anorexia nervosa and an underlying autistic like condition, reduced perfectionism and rigidity in 17 out of 19 participants.
Psychological
Anorexia nervosa is classified as an Axis I[135] disorder in the Diagnostic and Statistical Manual of Mental Health Disorders (DSM-IV), published by the American Psychiatric Association. The DSM-IV should not be used by laypersons to diagnose themselves.
- DSM-IV-TR: diagnostic criteria for AN includes intense fear of gaining weight, a refusal to maintain body weight above 85% of the expected weight for a given age and height, and three consecutive missed periods and either refusal to admit the seriousness of the weight loss, or undue influence of shape or weight on one's self image, or a disturbed experience in one's shape or weight. There are two types: the binge-eating/purging type is characterized by overeating or purging, and the restricting type is not.[136]
- Criticism of DSM-IV There has been criticisms over various aspects of the diagnostic criteria utilized for anorexia nervosa in the DSM-IV. Including the requirement of maintaining a body weight below 85% of the expected weight and the requirement of amenorrhea for diagnosis; some women have all the symptoms of AN and continue to menstruate.[137] Those who do not meet these criteria are usually classified as eating disorder not otherwise specified this may affect treatment options and insurance reimbursments.[138] The validity of the AN subtype classification has also been questioned because of the considerable diagnostic overlap between the binge eating/ purging type and the restricting type and the propensity of the patient to switch between the two.[139][140]
- ICD-10: The criteria are similar, but in addition, specifically mention:
- The ways that individuals might induce weight-loss or maintain low body weight (avoiding fattening foods, self-induced vomiting, self-induced purging, excessive exercise, excessive use of appetite suppressants or diuretics).
- If onset is before puberty, that development is delayed or arrested.
- Certain physiological features, including "widespread endocrine disorder involving hypothalamic-pituitary-gonadal axis is manifest in women as amenorrhoea and in men as loss of sexual interest and potency. There may also be elevated levels of growth hormones, raised cortisol levels, changes in the peripheral metabolism of thyroid hormone and abnormalities of insulin secretion".
Dietary
- Zinc supplementation has been shown in various studies to be beneficial in the treatment of AN even in patients not suffering from zinc deficiency, by helping to increase weight gain.[169][170][171]
- Essential fatty acids:The omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) have been shown to benefit various neuropsychiatric disorders. There was reported rapid improvement in a case of severe AN treated with ethyl-eicosapentaenoic acid (E-EPA) and micronutrients.[172] DHA and EPA supplementation has been shown to be a benefit in many of the comorbid disorders of AN including: attention deficit/hyperactivity disorder (ADHD), autism, major depressive disorder (MDD),[173]bipolar disorder, and borderline personality disorder. Accelerated cognitive decline and mild cognitive impairment (MCI) correlate with lowered tissue levels of DHA/EPA, and supplementation has improved cognitive function.[174][175]
- Nutrition counseling[176][177]
- Medical Nutrition Therapy;(MNT) also referred to as Nutrition Therapy is the development and provision of a nutritional treatment or therapy based on a detailed assessment of a person's medical history, psychosocial history, physical examination, and dietary history.[178][179][180]
[edit]Medication
- Olanzapine: has been shown to be effective in treating certain aspects of AN including to help raise the body mass index and reduce obsessionality, including obsessional thoughts about food.[181][182]
[edit]Therapy
- Cognitive behavioral therapy (CBT) CBT is an evidence based approach which in studies to date has shown to be useful in adolescents and adults with anorexia nervosa.[183][184][185]
- Acceptance and commitment therapy: A type of CBT, has shown promise in the treatment of AN" participants experienced clinically significant improvement on at least some measures; no participants worsened or lost weight even at 1-year follow-up."[186]
- Cognitive Remediation Therapy (CRT): is a cognitive rehabilitation therapy developed at King's College in London designed to improve neurocognitive abilities such as attention,working memory, cognitive flexibility and planning, and executive functioning which leads to improved social functioning. Neuropsychological studies have shown that patients with AN have difficulties in cognitive flexibility. In studies conducted at Kings College[187] and in Poland with adolescents CRT was proven to be beneficial in treating anorexia nervosa,[187] in the United States clinical trials are still being conducted by the National Institute of Mental Health[188] on adolescents age 10-17 and Stanford University in subjects over 16 as a conjunctive therapy with Cognitive behavioral therapy.[189]
- Family therapy: The most effective form of therapy for adolescents with anorexia is family therapy.[190] There are various forms of family therapy that have been proven to work in the treatment of adolescent AN including "conjoint family therapy" (CFT), in which the parents and child are seen together by the same therapist, "separated family therapy" (SFT) in which parents and child attend therapy separately with different therapists. "Eisler's cohort show that, irrespective of the type of FBT, 75% of patients have a good outcome, 15% an intermediate outcome... ".[191][192]
- Maudsley Family Therapy: A 4 to 5 year follow up study of the Maudsley approach, a manualized model, that shows full recovery at rates up to 90%.[193
RESOURCES:
Further reading
Bulimia Nervosa:
Overcoming Binge Eating (1995). Christopher Fairburn. Guildford Press.
Bulimia Nervosa:
Getting Better Bit(e) by Bit(e) (1993). Ulrich Schmidt and Janet Treasure. Psychology Press.
The Essential Handbook of Eating Disorders (2005) Janet Treasure. John Wiley & Sons Ltd
When dieting becomes dangerous: a guide to understansing and treating anorexia and bulimia (2003) Arthur Crisp, Deborah M Michel and Susan G Willard Yale University Press.
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Self-help
beat (formerly the Eating Disorders Association, EDA)
A national charity offering help and information to people with anorexia and bulimia nervosa, their families and friends.
Bodywhys - The Eating Disorders Association of Ireland
Providing help and information to people affected by eating disorders.
Helpline: 1890 200 444
info@bodywhys.ie |
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