What causes anorexia nervorsa?

What causes anorexia nervorsa?

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I've heard of anorexia nervosa being a severe loss of appetite. I'm wondering what causes such disease in humans?

What is anorexia nervosa?

Generally, it is an eating disorder which is characterised by a tremendous fear of food as well as an extreme weight loss. Patients with anorexia nervosa do not necessarily lose their appetite but rather obsessively control and restrict their food intake.

Anorexia Nervosa as an inherited disease/genetic factors

There has been a lot of research proposing that eating disorders are often biologically inherited and tend to run in families.

Recent research suggests that inherited biological and genetic factors contribute approximately 56% of the risk for developing an eating disorder. Individuals who have a mother or a sister with anorexia nervosa are approximately twelve times more likely to develop anorexia and four times more likely to develop bulimia than other individuals without a family history of these disorders. Studies of twins have shown a higher rate of eating disorders when they are identical (compared to fraternal twins or other siblings).

The hormone serotonin

There has been found that anorexics have an overproduction of serotonin, which can cause a continual state of acute stress and anxiety.

Researchers are still puzzled as to why, if anorexics already have high levels of serotonin, then SSRIs (medications like Prozac which raise serotonin levels) are successful treatments for some individuals. These scientists speculate that that there may be different subtypes of this disease, and that different groups of anorexics may have different neurochemical characteristics.

Researchers have also noted that abnormal eating behaviours and the resulting changes in the body can actually cause a disruption in serotonin levels, thus contributing to an already existing problem. Abnormalities in serotonin levels can lead to depression and anxiety. Studies also suggest that there are genetic predispositions to serotonin disruptions that appear to run in some families.

The hormone dopamine

Research suggests that women who develop anorexia nervosa may have altered levels of dopamine in their brains. Dopamine disturbances can cause hyperactivity, repetition of behaviour (such as food restriction), and anhedonia (a decreased sense of pleasure). This neurotransmitter also affects reward-motivated behaviour.

The hormone cortisol/hydrocortisone

Numerous other hormones in the brain have also been linked to eating disorders. Stress triggers the production and release of a hormone called cortisol; chronically elevated cortisol levels have been observed in patients with anorexia. Cortisol can inhibit appetite.

The hormone leptin

Leptin is a protein hormone produced by the body's adipose tissue. Leptin is regarded as a hormone which can regulate fact storage and appetite. If individuals with anorexia nervosa lose extreme amounts of body fat, their levels of leptin drop which is known as hypoleptinaemia. The side effects of hypoleptinaemia can include amenorrhea, impaired metabolism, and bone loss.

Also, if people receive treatment, their leptin levels do not immediately return to normal. Initially during the treatment, leptin levels rise through the sky, which is also the reason why most patients are most susceptible of relapsing back into an eating order, since very high levels of leptin may cause a weight gain.


  • ENGEL, BRIDGET, NATALIE STAATS REISS, and MARK DOMBECK. "Causes Of Eating Disorders - Biological Factors Continued." Mental Help Causes of Eating Disorders Biological Factors Continued Comments. 2 Feb. 2007

Neurobiology of anorexia and bulimia nervosa

Anorexia nervosa (AN) and bulimia nervosa (BN) are related disorders of unknown etiology that most commonly begin during adolescence in women. AN and BN have unique and puzzling symptoms, such as restricted eating or binge-purge behaviors, body image distortions, denial of emaciation, and resistance to treatment. These are often chronic and relapsing disorders, and AN has the highest death rate of any psychiatric disorder. The lack of understanding of the pathogenesis of this illness has hindered the development of effective interventions, particularly for AN. Individuals with AN and BN are consistently characterized by perfectionism, obsessive-compulsiveness, and dysphoric mood. Individuals with AN tend to have high constraint, constriction of affect and emotional expressiveness, ahendonia and asceticism, whereas individuals with BN tend to be more impulsive and sensation seeking. Such symptoms often begin in childhood, before the onset of an eating disorder, and persist after recovery, suggesting they are traits that create a vulnerability for developing an ED. There is growing acknowledgement that neurobiological vulnerabilities make a substantial contribution to the pathogenesis of AN and BN. Considerable evidence suggests that altered brain serotonin (5-HT) function contributes to dysregulation of appetite, mood, and impulse control in AN and BN. Brain imaging studies, using 5-HT specific ligands, show that disturbances of 5-HT function occur when people are ill, and persist after recovery from AN and BN. It is possible that a trait-related disturbance of 5-HT neuronal modulation predates the onset of AN and contributes to premorbid symptoms of anxiety, obsessionality, and inhibition. This dysphoric temperament may involve an inherent dysregulation of emotional and reward pathways which also mediate the hedonic aspects of feeding, thus making these individuals vulnerable to disturbed appetitive behaviors. Restricting food intake may become powerfully reinforcing because it provides a temporary respite from dysphoric mood. Several factors may act on these vulnerabilities to cause AN to start in adolescence. First, puberty-related female gonadal steroids or age-related changes may exacerbate 5-HT dysregulation. Second, stress and/or cultural and societal pressures may contribute by increasing anxious and obsessional temperament. Individuals with AN may discover that reduced dietary intake, by reducing plasma tryptophan availability, is a means by which they can modulate brain 5-HT functional activity and anxious mood. People with AN enter a vicious cycle which accounts for the chronicity of this disorder because caloric restriction results in a brief respite from dysphoric mood. However, malnutrition and weight loss, in turn, produce alterations in many neuropeptides and monoamine function, perhaps in the service of conserving energy, but which also exaggerates dysphoric mood. In summary, this article reviews findings in brain chemistry and neuroimaging that shed new light on understanding the psychopathology of these difficult and frustrating disorders.


Comparison of CSF concentrations of…

Comparison of CSF concentrations of neuropeptide and monoamine metabolites in individuals who were…

Compared to CW, values for…

Compared to CW, values for recovered anorexia and bulimia subjects expressed as a…

Trauma: A Cause of Anorexia

Trauma comes in all forms, from sexual abuse physical assault, or severe discipline in childhood, to witnessing a violent attack, natural disasters, or war. Trauma can result from emotional, physical, and verbal battle wounds. Maybe you were continuously disciplined in a harsh manner as a child or you were in an abusive romantic relationship. Or maybe you were bullied in school and always compared to your siblings while growing up. Individuals who have experienced any form of trauma are more at risk for developing an eating disorder if these unresolved feelings from the traumatic experience are not appropriately dealt with.

Diagnosis and Tests

How is anorexia nervosa diagnosed?

If symptoms are present, the doctor will begin an evaluation by performing a complete medical history and physical examination. Diet history will be taken – the individual will be asked about the quantity and variety of foods/food groups and thoughts about food. The doctor will ask about body image and weight loss history and measure weight and height and compare with age-based weight and growth charts. Binge and purging frequency and elimination habits (diet pills, laxatives, supplements) will be discussed. Current medications will also be reviewed. The doctor will also ask about menstrual history, exercise history and family history of eating disorders, substance abuse and psychological disorders (mood, depression, suicidal thoughts).

Although there are no laboratory tests to specifically diagnose anorexia nervosa, the doctor might use various diagnostic tests, including laboratory values (a blood test), to rule out physical illness as the cause of the weight loss, as well as to evaluate the severity of illness or the effects of the weight loss on the body’s organs. The doctor may order an electrocardiogram (ECG) to check for slow heart rate, chest pain, abnormal heart rhythm, or heart flutter.

To be diagnosed with anorexia nervosa, the doctor will determine if three criteria have been met:

  • Does the person weigh less than the minimum that is considered normal for their age, sex, stage of growth and development, and physical health?
  • Does the person have an intense fear of gaining weight or becoming fat or display ongoing behavior that interferes with weight gain even though the individual is at a significantly low weight?
  • Does the person show a disturbance in the way they view their body weight or shape does their body weight or shape have a strong influence on their self-image does the person lack recognition of the seriousness of their current low body weight?

What Are the Causes of Anorexia Nervosa?

With a blend of contributing factors such as past experiences and personality, anorexia is more complicated than you might think.

Anorexia nervosa is an eating disorder involving weight loss, food restriction, and sometimes compulsive exercise.

Body image distress and fear of weight gain often drive these behaviors, but the condition goes deeper than that.

Biological and environmental factors can:

  • make you more likely to develop anorexia
  • trigger behaviors related to anorexia
  • get in the way of healing and recovery

In addition, the following factors can contribute to anorexia:

  • genetics
  • brain chemistry
  • family behaviors
  • other mental health conditions
  • past trauma
  • social attitudes about weight

Learning about the risk factors and causes of anorexia can help people at many stages of recovery gain a better understanding of their condition. It can often be a validating process.

Whether you’re still figuring out if you have an eating disorder or you’re far along on your path to recovery, learning about the roots of anorexia could be a step toward healing.

Environmental and social factors play a large role in who develops anorexia.

Eating disorders are often connected to having a history of trauma, especially childhood sexual trauma.

Research suggests that people with eating disorders are also more likely to have experienced:

  • physical abuse
  • emotional abuse
  • teasing and bullying
  • parental divorce
  • loss of a family member

Some other environmental risk factors of anorexia are:

  • bullying, especially about weight
  • childhood adversity or trauma
  • isolation and loneliness
  • being in environments with high pressure to have a smaller body (like modeling and ballet)
  • history of family or generational trauma
  • living in a culture that promotes small bodies as ideal

One study in women with anorexia found that 13.7% met criteria for post-traumatic stress disorder (PTSD). Most of the women with PTSD reported that their first traumatic event happened before they’d developed anorexia.

The most common traumatic events were connected to sexual trauma.

Other research suggests that childhood bullying can predict eating disorder symptoms in both kids who bully and kids who experience bullying.

Sometimes anorexia can be triggered when a person who has other anorexia risk factors spends a lot of time in situations where the pressure to have a small body is very strong.

Certain personality traits are more common in people with anorexia.

Anorexia has been linked to:

  • body dissatisfaction and frequent thoughts about an “ideal” appearance such as social anxiety disorder, generalized anxiety disorder, and obsessive-compulsive disorder (OCD)
  • history of dieting or other weight-control methods
  • autistic features
  • rigid ideas, beliefs, or plans

Some research estimates that anywhere from 8 to 37% of people with an eating disorder could be autistic.

One study found the chances of autism were more than 15 times greater in people with anorexia than in those without.

Researchers also looked at the link between eating disorder symptoms and cognitive inflexibility. Cognitive flexibility is the ability to think about something in a new way, such as finding a new way to solve a problem.

People with cognitive inflexibility may have a harder time adapting to unexpected conditions. They might stay more focused or get stuck on one issue longer.

The study found that eating disorder symptoms and social anxiety were both tied to cognitive inflexibility. And when researchers took social anxiety out of the picture, the link between eating disorder symptoms and cognitive inflexibility stayed strong.

Perfectionism could also play a major role in anorexia, both before and after recovery. Researchers suggest that perfectionism in people with anorexia could be related to self-doubt.

Treatment and Recovery

Treatment of eating disorders varies according to the type and severity of the eating disorder. Usually, more than one treatment option is used. Treatment typically includes mental health counseling, which can take place in a variety of settings, such as a community program, private practice, or hospital. Treatment may also include the use of antidepressants or other medications because many people with eating disorders also suffer from depression or other mental health disorders. Nutritional counseling is often recommended as well. Hospitalization is occasionally required, in many cases to treat the adverse physical health consequences of the disordered eating.

The goal of treatment is recovery, including gaining control of eating, adopting normal eating habits, and attaining a normal weight. About 50 to 85 percent of people with eating disorders recover with treatment. However, some may have to struggle to maintain normal eating behaviors throughout the rest of their life.

People with anorexia nervosa, as with many other health problems, may seek information and advice online before or instead of contacting a healthcare professional. The web offers a plethora of useful information on eating disorders, including anorexia nervosa, but some websites, blogs, and social media pages actually have the agenda of promoting disordered eating. The term pro-ana (from &ldquopro-anorexia&rdquo) refers to organizations, websites, and other sources that promote anorexia nervosa. Their mission is to normalize or even glamorize anorexia nervosa. They defend it as a lifestyle choice and an accomplishment of self-control rather than as a mental disorder. Research has shown that visiting pro-ana sites can have a negative impact on eating behavior in people both with and without eating disorders. After visiting such sites, people tend to decrease their Caloric intake, although most of them do not actually perceive that they have reduced their intake of Calories.

Following a 2001 episode of the Oprah Winfrey Show that focused on pro-ana, the mainstream press started covering the issue. Pressure from the public and pro-recovery organizations led to some social media and other websites adopting policies of blocking pro-ana pages or labeling them with warning messages. As a result, many pro-ana groups have taken steps to conceal themselves. For example, they may claim that they are simply providing a nonjudgmental forum for people with anorexia nervosa to discuss their disorder. They may also claim that they exist in part to provide support for those who choose to enter recovery.

Some clues that a website or page may be pro-ana include providing information on topics such as:

  • crash dieting techniques and recipes.
  • socially acceptable pretexts for refusing food, such as veganism.
  • ways to hide weight loss from parents and doctors.
  • reducing the adverse health effects of anorexia.
  • ways to ignore or suppress hunger pangs.

Do you think you can tell the difference between pro-ana websites and legitimate pro-recovery websites, which are designed to encourage the development and maintenance of healthy behaviors and cognition? Go online and try to find at least one pro-ana website and at least one pro-recovery website. Then write a brief explanation of how you made your choices.

Integrating Risk Factor Research with a Genetic Epidemiological Perspective on Eating Disorders G-E

Relationships Potentially Influencing Eating Disorder Etiology

For decades, parenting styles have been unrightfully blamed for causing eating disorders. Considerable care must be taken when discussing gene x environment interplay not to convey the message that somehow parenting is to blame for these pernicious illnesses. Conversely, a purely genetic explanation should not be taken to mean that parents need not examine their parenting style and the influence that might have on their children. The context for the following discussion is that parenting does matter. Moreover, parenting style is in part influenced by the parents’ genes, and the effect of parenting style is similarly influenced by the offsprings’ genotype. For an example outside of the eating disorders world, alcoholism has a known genetic component. An alcoholic father’s erratic and authoritarian parenting is in part influenced by his genetic predisposition to alcoholism. His two children may be differentially influenced by that parenting style due to their own genetically influenced constitution—one may be vulnerable and sensitive to rejection and verbal abuse whereas the other may remain effectively impervious to rejecting parenting. We will now explore some of the identified risk factors for eating disorders through this complex lens.

Parental Role Modeling of Eating Disordered Behavior

In the clinic, it is not uncommon to see either frank eating disorders or shadows of disordered eating, appearance focus, exercise obsession, body preoccupation, or personality traits associated with eating disorders such as perfectionism or obsessionality in parents of individuals with eating disorders. Of course, this is not always the case, and there are many examples of families in which these traits are not evident. Through their relationships with food and their own bodies, parental role modeling of unhealthy eating behaviors and attitudes likely represents an example of passive G-E correlation. The literature suggests that such modeling has an effect on offspring, as case studies indicate that children do indeed imitate their mothers’ purging and restricting behaviors [30�]. Studies conducted in non-treatment-seeking samples have found similarities between mothers’ and daughters’ restraint and dieting behaviors among children as young as 10 years old [33]. Mothers’ comments about their own weight and appearance are associated with the body esteem of their fourth and fifth grade daughters and sons [34], and mothers who complain about their own weight are more likely to have daughters who are weight concerned. Moreover, maternal drive for thinness and restraint are associated with the development of overeating behaviors among children in their first five years of life [35]. Thus, although not solely causal, the principle of children being more likely to 𠇍o as you do” rather than 𠇍o as you say” renders parental role modeling of healthy eating and weight behaviors important to the task of creating a protective environment𠅎specially in genetically vulnerable offspring.

Problematic Feeding Behaviors

A second area where parental genotype and environment intersect dramatically is in the feeding behaviors of children. Mothers tend to retain primary responsibility for nurturing their offspring. For most mothers this is a joyous part of motherhood however, for women with eating disorders this can represent an emotionally charged and highly challenging part of the job. Clinicians working with mothers with eating disorders should be keenly aware of the potential difficulties they may encounter in what should be this very natural mother-child interaction. Studies have shown that mothers with eating disorders are more likely to use food for nonnutritive purposes, such as rewarding, comforting, or punishing their children [36,37]. One retrospective study found that adults whose parents used food in this manner were more likely to exhibit disordered eating behaviors than those who did not recall such parenting behaviors, even when factors such as current Body Mass Index (BMI), childhood weight status, ethnicity and age were controlled [38].

Mothers’ own eating restraint and disinhibition also appear to influence their approach to feeding their children. In two studies of five year old girls, mothers’ restraint and weight concerns were positively associated with the degree of restriction they imposed on their daughters’ eating [39,40]. Maternal disinhibition of eating was also related to children’s eating behavior. For example, Johnson and Birch [41] found that parental disinhibition was inversely associated with children’s ability to self-regulate energy intake. For both sexes, a tendency to overeat in the presence of food-related cues may be transmitted across generations.

Parental Over-Emphasis on Child Weight and Shape

In addition to having concerns about their own shape and weight, women with eating disorders may similarly be over-concerned about their children’s weight, even when it is well within normal limits [30,36,37]. One study [36] found that 15% of mothers with a history of bulimia nervosa had attempted to “slim down” their normal weight infants. Similarly, Waugh and Bulik [42] found that 20% of the mothers with eating disorder histories in their sample tried to change their children’s appearance. Maternal restriction of children’s eating is a concern, as previous research [41] suggests that maternal control of children’s eating interferes with the development of dietary self-regulation. These effects have been found among children as young as two years of age [41].

In another example of how genes and environment may interact, mothers’ disordered eating attitudes appear to influence their perceptions of their children’s appearance. For example, Stein and colleagues [43] found that mothers’ satisfaction with their children’s size was inversely related to the severity of their own eating disorder symptomatology. Further, other research has found that mothers’ comments about their children’s weight were associated with children’s body esteem and the frequency of children’s weight loss attempts [44].

The influence of maternal perceptions on daughters’ eating disordered behavior appears to continue into adolescence and young adulthood. For example, mothers whose daughters engaged in eating disordered behavior were more likely to view their daughters as overweight [45,46] than were mothers of non-eating disordered daughters (controlling for weight differences between groups). Further, this appearance pressure is not necessarily limited to weight, as mothers of daughters with eating disorder symptomatology also rated their daughters as less attractive than the daughters rated themselves [46]. These results are concerning, as they suggest that daughters who engage in eating disordered behaviors may not only lack a maternal role model of healthy eating, but also feel maternal pressure to lose weight and enhance their appearance. This of course could reflect several complex intergenerational processes. On one hand, mothers may harbor threshold or subthreshold eating disturbances themselves, and their comments or behaviors could reflect their underlying pathology. Alternatively or complementarily, the daughters’ pathology could render them more sensitive to maternal comments that in other situations may be perceived as culturally normative. These environmental experiences could facilitate the expression of an existing genetic predisposition for eating disorder symptomatology.

Life Events and Distress Tolerance

Historically, research on parenting and its relation to eating disorders has focused on family/parent characteristics, an important component of which is termed “shared environment” in twin research. Shared environment refers to those familial experiences that act to increase similarity amongst family members. However, genetic epidemiological research has suggested that the majority of environmental variance in eating disordered symptomatology is influenced by “unique environment,” or environmental factors experienced by only one member of a twin pair or family [23,47]. Unique environmental influences act to increase dissimilarity amongst family members. However, even the definitions and existence of shared and unique environmental factors are disputed. For example, adverse life events, such as abuse experiences to which only one member of a twin pair was subjected, might exemplify unique environmental factors salient to the development of an eating disorder. Yet, it has been posited that the frequency and intensity of defining unique environmental events [48], as well as the impact of these unique life experiences are at least partially under genetic control [49]. For example, Klump and colleagues [23] stated, “Genetic differences …may provide the mechanisms by which nonshared environment exerts its influence” (p. 123). Thus, it seems appropriate to review research on adverse life events and their association with eating disorder etiology from a genetic epidemiological perspective.

As noted above, adverse life events may be one significant way in which the unique environment can act to increase eating disorder risk. The association between negative life events and the onset of eating disorders has received significant clinical and research attention [23,50�]. However, as Schmidt and colleagues [51] have noted, the majority of studies in this area have used case reports to identify life events, and did not include non-eating disordered comparison groups. However, one case-control study [52] found that some adverse experiences were more common among women with bulimia nervosa in the year prior to illness onset (e.g., a major move, illness, pregnancy, physical abuse, and sexual abuse). Further, the more life events an individual experienced in the last year, the more likely she was to have bulimia nervosa. However, the frequency of several other life events (e.g., bereavement, illness of a close relative, friend or partner, and beginning or end of a new romantic relationship) did not differentiate women with and without the disorder. In addition, nearly one-third of women with bulimia nervosa did not experience any of the life events assessed in the previous year. Thus, although there appears to be some association between experiences of adverse life events and bulimia onset, there is also significant variability among affected individuals with respect to recent experiences.

The impact of recent life events on the development of binge eating disorder (BED) was investigated by Pike et al. using a case-control sample [50]. Women with BED experienced more adverse life events in the year prior to the onset of their eating disorder (compared to nonclinical and psychiatric controls), and the likelihood of BED was positively associated with the frequency of negative events. Compared to both the non-clinical and psychiatric control groups, women with BED more frequently reported major changes in life circumstances and relationships. Physical abuse, perceived risk of physical abuse, safety concerns, stress, and experiences of weight and shape-related criticism were also more common in the BED group (vs. non-clinical controls).

The impact of stressful life events is obviously at least partially dependent upon how individuals perceive, or think about these experiences, and how they attempt to cope with them. Thus, studies on the impact of life events on eating disorder etiology should also be considered in light of the significant body of research supporting the influence of cognitive appraisal on psychological outcomes [53,54]. According to appraisal theory, the impact of life events depends on how they are appraised by the individual [53,54]. The appraisal process involves both determining if a given situation is threatening to the individual (primary appraisal) and if so, evaluating whether his/her resources are sufficient to manage this threat (secondary appraisal). It seems plausible that both genetically-influenced traits (e.g., trait anxiety, fearfulness), and environmental factors (social support, SES) would influence primary and secondary appraisal. This hypothesis is supported by the results of a twin study [55] which found that specific coping behaviors (turning to others and problem solving) were significantly influenced by genetic factors.

Distress tolerance is another construct related to appraisal and coping processes. The degree to which a given individual possesses the ability to tolerate distress also is likely influenced by a complex combination of genetic and environmental factors. According to Corstorphine et al., distress tolerance is, “the ability to endure and accept negative affect, so that problem-solving can take place…[and it] manifests as high emotional vulnerability and an inability to regulate emotion” [56], p. 91). Although no extant research has investigated the heritability of the specific construct of distress tolerance, related variables, such as neuroticism, have been found to be strongly familial [57,58] and to predict the later development of anorexia nervosa [59]. Further, emotion regulation difficulties have been found in women with eating disorders of all subtypes (e.g., [60,61]). A recent study [56] found that eating disordered attitudes were associated with scores on two components of a distress tolerance measure: high avoidance of affect and low acceptance and management of problems.

Research in other clinical areas has indicated that distress tolerance skills can be improved with the implementation of a specific cognitive-behavioral intervention (e.g., Dialectical Behavioral Therapy [DBT] for Borderline Personality Disorder, [62]). Thus, interventions aimed at individuals at high-risk for eating disorders (and thus potentially genetically prone to low distress tolerance) should perhaps include elements of DBT focusing on affect regulation and coping skills training. Thus, in this manner, an environmental intervention could directly address genetic vulnerabilities. Future studies of G-E correlations should include the construct of distress tolerance, in order to evaluate its interaction with life events and specific genetic vulnerabilities.

Evocative G-E Correlations Potentially Influencing Eating Disorder Etiology

Interaction of Temperamental Style and Environment

Genes may also influence risk for eating disorders through the way in which one’s genotype evokes certain responses from the environment. For example, considerable work has explored temperamental style in individuals with eating disorders. In the current context, we are interested not only in how temperament may be associated with eating disorders risk, but also in the various ways that temperament influences interactions with the environment. As suggested above, personality characteristics (such as neuroticism) can make us more or less vulnerable to environmental insults but these traits can also influence our tendency to evoke certain responses from the environment.

Recent work on temperamental factors influencing eating disorder etiology indicates that anorexia nervosa is associated with a temperamental style characterized by perfectionism, a need for order and exactness, harm avoidance, and sensitivity to praise and reward [63�]. Bulimia nervosa shares many of these same characteristics, but commonly coupled with features of novelty seeking and impulsivity [64,65,67]. These temperamental traits have been shown to be influenced by genetic factors [68,69]. However, these temperamental characteristics also influence how individuals interface with their environment. Thus, it is plausible that individuals genetically susceptible to eating disorders due (to some degree) to their temperament, may hold themselves to extremely high standards, and through their own actions, actively seek out praise or evaluation of their efforts from others. Comments evoked from others, even if positive, may in turn reinforce perfectionist tendencies, including those relevant to eating disordered behavior.

On the other hand, parents may treat even identical (or monozygotic, MZ) twins differently, which could also influence eating disorder susceptibility. For example, in a study of MZ twins discordant for bulimia nervosa, Wade et al. [70] found that affected twins reported higher parental expectations than their unaffected co-twins. It is not possible from this study to determine if parents actually did hold one twin to higher standards, or, if this finding reflects the retrospectively recalled experience of the affected twin. That is, the answers may reflect the affected twin’s attempt to make sense of her childhood experiences and current symptomatology. Longitudinal studies are needed to clarify the role of parental expectations (both actual and perceived) in eating disorders etiology.

Teasing and Weight Shape Related Criticism

Another environmental issue relevant to eating disorders risk is weight related teasing, and critical comments about weight (particularly those made by parents) which have been identified as risk factors for a range of eating disordered behaviors (e.g., [18,50,70,71]), although not all studies have identified this association (e.g., [19]). The association between teasing and risk for eating disorders is unlikely to be a simple one and a complete understanding of risk mechanisms needs to consider gene x environment relationships.

Klump et al. [23] suggested that weight-related teasing may reflect an evocative G-E correlation relevant to eating disorders. For example, teasing experienced by an overweight adolescent may be in part evoked by his or her simply being overweight. Thus, in this case, a trait significantly influenced by genetic factors (BMI), influences the comments an individual is exposed to in the environment.

Another possible way in which genetic and environmental factors may interact to influence teasing–related risk is that teasing experiences may be appraised more negatively among individuals with different genetically-influenced temperaments. Individuals genetically predisposed to eating disorders and neuroticism for example, may be particularly prone to ruminate about weight-related teasing or critical comments about weight, thereby exacerbating the negative effects of these occurrences. Supporting this observation, clinicians report that many individuals with eating disorders recall triggering events that prompted their eating disorder. Although highly salient and even defining to these individuals, many of these events fall within normative experience and could easily be brushed off by individuals less sensitive to their salience. As in the case with the overweight teen above eliciting comments about weight, it is also possible that individuals genetically vulnerable to eating disorders may elicit comments about their appearance through their frequent seeking of reassurance (and these comments may, in some cases, be critical). These evoked responses may reinforce their eating disordered tendencies or behaviors.

Further, it should also be considered that, as noted above, even MZ twins may be treated differently by their parents, particularly with respect to appearance. Research on MZ twins discordant for anorexia and bulimia nervosa found that affected twins report receiving more critical comments regarding their weight than their non-affected co-twins [70]. As these twins are virtually identical genetically, this finding may represent a true nonshared environmental difference. Nonetheless, specific genetic vulnerabilities (e.g., to a higher-than average BMI, or sensitivity to praise) may still influence the etiology of eating disorders in this case. It is also possible that these findings are influenced by recall bias, as participants were not surveyed about their childhood experiences until they were already adults. Thus, perhaps affected twins affected were more likely to view parent comments regarding weight as salient to their current functioning.

Active G-E Correlations Potentially Influencing Eating Disorder Etiology


One potential pitfall of genetic research on eating disorders is the misinterpretation that environmental factors such as the media do not matter. Western media’s idealization of an ultra-thin female body type has long been viewed as an important sociocultural risk factor for eating disorders [72,73]. However, given the ubiquity of this influence in Western cultures, other factors must influence vulnerability to the thin cultural ideal. As Bulik [1] suggests, genetically vulnerable individuals might seek out experiences, such as exposure to thin-ideal media images, which reinforce their negative body image. This hypothesis is supported by a longitudinal study which found that adolescent girls whose eating disorder symptomatology increased over a 16 month period also reported significantly greater fashion magazine reading at Time 2, compared with Time 1 [74].

Peer Group Selection

Similarly, individuals genetically predisposed to eating disorder symptomatology such as thin-ideal internalization might also actively choose to affiliate with peers who place a similar high value on weight and appearance [23]. One potential example of this form of active selection could be the decision to join a sorority (particularly for European-American women). European-American sorority members report high levels of eating disorder symptomatology, including weight preoccupation, drive for thinness, and body dissatisfaction [75]. A longitudinal study [76] found that sorority and non-sorority members did not differ on three measures of disordered eating (EDI Drive for Thinness, Body Dissatisfaction, and Bulimia) at Time 1 and Time 2 (first and second year of undergraduate, respectively). However, by Time 3 (third year of undergraduate), non-members’ drive for thinness scores had decreased, while members’ scores on this measure remained roughly the same, and this difference was statistically significant. Thus, the authors concluded that characteristics of the sorority environment could contribute to the persistence of a higher degree of drive for thinness. Although this study did not include a measure of actual or putative genetic vulnerability to eating disorders, it is plausible to speculate that an environment that promotes the maintenance of eating disordered characteristics would be particularly problematic for a genetically vulnerable individual.

Potential Environmental Buffering Effects for High-Risk Groups

We have focused primarily on environmental risk factors and how they could plausibly interact with various facets of genetic vulnerability to increase risk for eating disorders. Given our inability to modify genetic risk in this point in time, it is critical to present a balanced picture of the environment. Just as both risk and protective genetic factors can exist, so can both risk and protective environmental factors. Also, protective factors may function differentially depending on the genotype of the exposed individual. Given the field’s focus on pathology, much less is known about differential effects of buffering environmental factors based on genetic differences.

Family meals and breakfast eating

One fascinating and modifiable environmental factor that has emerged as a possible buffer against the development of eating disorders in adolescent girls is family meals [77]. Likewise, breakfast eating may also play a role in preventing the development of eating problems. For example, Fernández-Aranda and colleagues [78] found that women with eating disorders were less likely to have eaten breakfast regularly during childhood compared to non-eating disordered controls. Although retrospective, these findings are consistent with those of a large (n = 2216), longitudinal study which found that breakfast eating frequency was inversely associated with dieting and weight-control behaviors, and positively related to dietary quality and physical activity in adolescents [79]. Overall, these studies offer preliminary insight into potential buffers against eating disorders however, research in this area has not yet progressed to assess the differential effect of these protective factors in individuals at high-risk for eating disorders versus the general population.

Distress tolerance/anxiety management

Another factor that offers promise as a potential buffer against the development of eating disorders is the enhancement of emotion regulation skills. As noted above, individuals with eating disorders experience relatively high levels of perceived stress and difficulties regulating emotion [56,61]. Thus, interventions aimed at enhancing emotion regulation skills might be of particular benefit to high-risk groups. However, research incorporating mindfulness techniques has not specifically targeted high-risk groups. For example, a recent study investigated the effectiveness of a primary prevention program incorporating elements of mindfulness (e.g., yoga), targeting fifth-grade girls [80]. This program integrated mindfulness into an empirically-based curriculum, which also included other elements, such as media literacy, and the promotion of dissonance regarding idealization of an ultra-slim body type. Compared to a control group, girls in the intervention reported lower body dissatisfaction and uncontrolled eating, and higher social self-concept at post-testing. However, there were no significant changes on other variables assessed including drive for thinness, perceived stress, physical self-concept and perceived competence. Nonetheless, these outcomes do provide some support for the inclusion of mindfulness-based activities in prevention. In contrast, a study with undergraduate women [81] did not find any differences between participants in a yoga program and a control group on eating disorder symptoms at post-testing. Future studies should target high-risk groups, to evaluate the efficacy of mindfulness-based techniques within this specific sample.

Reducing Weight and Shape-Related Attentional Biases

Previous studies have found that individuals with eating disorders manifest attentional biases (or selective attention) toward weight and shape-related information [82,83]. These biases are likely influenced by both genetic and environmental factors. However, a recent study [83] found that these biases were reduced in women with eating disorders following completion of a specific form of cognitive-behavioral therapy. Future research should investigate the effectiveness of incorporating some of these specific cognitive-behavioral techniques into prevention programs targeting high-risk individuals.

In summary, simplistic nature versus nurture explanations could never suffice to capture the many ways in which genes and environment may interact to influence eating disorder risk. Moreover, many of these processes are likely to be operative over time in any given individual and risk may be cumulative. The critical message for the clinician working with eating disorders is not necessarily to educate patients and parents about all potential forms of gene x environment interplay, but definitely to guard against simplistic explanations that lead to inaccurate conclusions and inappropriate solutions.

Clinical Implications

After reviewing the various and complex ways that genes and environment can interact and correlate, the clinician, although enlightened, will want to know how best to incorporate this knowledge into clinical practice. Given the state of the science of treatment for eating disorders𠅎specially in the absence of any effective medications for anorexia nervosa—the question remains how best to work with the patient and family to bolster protective environmental influences, reduce evoked environmental exposures, and develop strategies in the patient to minimize the deleterious effects that sensitivity to the environment can create.

Focus on the parents

One prong in the approach to incorporating genetics into clinical work focuses on the parents of individuals with eating disorders. Whether the parents are involved in parent training, traditional family therapy, or other types of supportive interventions, they can be educated about genetic factors influencing eating disorders. A sensitive explanation that incorporates knowledge about complex genetic etiology (not the one gene-one disease model) and about how genes and environment interact can serve to relieve guilt in parents who have been blamed for creating the illness in their offspring (or alternatively erroneously assumed that their parenting was to blame). A genetic and biological explanation can help parents understand that their child’s resistance is not just stubbornness or deviousness, but that in his or her recovery, their child is fighting an uphill battle against his or her biology. This knowledge can empower parents to understand and can decrease frustration. Care should be taken that parents do not transform this knowledge into a new form of guilt (i.e., feeling guilty for passing on risk genes), as the roll of the genetic dice is one thing over which we have no control. Likewise, care should be taken not to allow the genetic information to impart complete absolution on parents, as parenting can always improve and positive parenting changes should also be prescribed as part of treatment. Finally, symptomatic parents should be referred for treatment. Although few data exist, clinically, it is an uphill battle for offspring to recover from an eating disorder if they are faced on a day to day basis with a parent who is actively suffering from the illness.

Focus on the next generation

Intervention with mothers with eating disorders can be viewed as a form of targeted prevention. Eating disorder prevention is a complicated endeavor. Although primary prevention deserves additional research attention, interventions targeting individuals at risk of developing eating disorders may be a particularly promising focus of prevention efforts [84,85]. Such intervention could serve to improve maternal efficacy and confidence in feeding their children, increase modeling of healthy eating behaviors and attitudes, decrease mothers’ anxiety regarding parenting behaviors, and increase self-efficacy and confidence in general parenting skills. In the long term, this type of intervention may assist mothers with developing a healthy buffering environment which minimizes modeling of behaviors and attitudes associated with disordered eating.

Results from focus groups [86] and clinical case studies [87] suggest that mothers with eating disorders are eager to learn about how best to care for their children, especially with respect to feeding. However, they report that the level of assistance they desire is not routinely offered by their health care providers. In one of the only published interventions conducted with this population, Stein et al. [59] studied 80 mothers with eating disorders and their four to six month old infants to test whether a 13 session intervention of video-feedback treatment in conjunction with cognitive behavioral self-help was more effective than cognitive behavioral self-help alone in reducing mealtime conflict and other aspects of maternal-child interaction. Those mothers in the video-feedback group exhibited significantly less conflict than control mothers as well as significant improvements in infant autonomy and several other interaction measures. In addition, maternal eating psychopathology was reduced across both groups. Such interventions could help break the 𠇌ycle of risk” associated with eating disorders [16], by providing parents with useful buffering strategies.

Focus on the patient

Patients read enormous amounts about their illness and are often aware of the genetic research on eating disorders yet they struggle to understand what the data mean for them and the challenges they face every day during recovery. Helping patients to understand the genetic literature is a first step. Although they might not initially see its relevance to their situation, helping them map how disordered eating and temperamental traits track in their families by using techniques such as labeling family trees can provide a useful context for understanding genetic and environmental contributions to their current situation. An understanding of genetic and environmental interplay can provide them with an explanatory model for not only their illness, but also for understanding their sensitivity to the environment. It can help provide them with the motivation to acquire skills that may help buffer them from the environment and combat their biology most effectively.

What Causes Anorexia Nervosa?

I’m often asked, “what causes anorexia nervosa?” The exact causes are unknown, but experts agree that it is probably a combination of 3 factors: Biological, Psychological, and Environmental.

1. Biological Factors

While it’s not yet known exactly which genes are involved or associated with developing anorexia nervosa, some inherited personality traits are thought to be associated with a higher risk of developing anorexia. These factors include a tendency towards trying to be perfect (perfectionism), being sensitive, and high goal directed behavior – All traits found to be associated with anorexia.

In addition, there seems to be a genetic link to anorexia and individuals who have a family history of substance abuse, depression, OCD and eating disorders. In fact, studies published in NCBI suggest that a person whose close relative suffers from anorexia is 7 to 12 times more likely to develop anorexia than someone whose close relatives don’t suffer from anorexia. Other studies show that there is a 50 to 80% heritability factor that contributes to anorexia nervosa.

2. Psychological Factors

Psychological factors may play a part in causing anorexia nervosa. There are specific personality and behavioral traits that are thought to be connected in the development of anorexia nervosa. These traits include:

  • Having excessive fear or doubt about one’s future
  • Difficulty coping with stress or being highly sensitive to the effects of stress
  • Having a history of depression or anxiety related disorders
  • Difficulty expressing emotions, especially Alexithymia (the inability to put feelings into words)
  • Having a tendency towards perfectionism
  • Experiences that causes one to overvalue looks or being thin
  • Obsessive compulsive tendencies
  • A tendency to put the needs of others before your own

When a person has one or more of these psychological traits, they may find that the eating disorder helps them cope with these issues, that the eating disorder soothes or distracts them from these feelings.

3. Environmental Factors

Individuals who are raised or live in Western Cultures are exposed to a high level of pressure related to weight and appearance. Societal norms place a high importance on beauty and thinness. This concept is reinforced by media messaging, magazines, social media, and other online sources. Pressure mounts and places a high degree of stress, especially on young women.

Other environmental factors can include:

  • Being overly stressed at work or school
  • Having difficult family relations
  • Being bullied about body weight, shape, or how you look
  • Adverse life events that cause stress or trauma
  • Being physically or sexually abused


Stress is something that affects people every day. Reasons for stress can range from normal daily things such as work, school, and even relationships. Among anorexic victims, stress can be caused by both environmental and social factors. Social factors include the pressure to have the “”perfect body. People suffering from anorexia have higher stress levels which can cause destructive behavior and mental patterns. To cope with the stress, the anorexic victims turn to bad eating habits due to them not knowing how to transform the stress into something productive. These impulses can cause the person to not eat enough food or even purge after a meal, which is by vomiting up your food intentionally.


Anorexia nervosa is an eating disorder characterized by attempts to lose weight to the point of starvation. A person with anorexia nervosa may exhibit a number of signs and symptoms, the type and severity of which may vary and be present but not readily apparent. [23]

Anorexia nervosa, and the associated malnutrition that results from self-imposed starvation, can cause complications in every major organ system in the body. [24] Hypokalaemia, a drop in the level of potassium in the blood, is a sign of anorexia nervosa. [25] [26] A significant drop in potassium can cause abnormal heart rhythms, constipation, fatigue, muscle damage, and paralysis. [27]

Signs and symptoms may include:

  • A low body mass index for one's age and height. , a symptom that occurs after prolonged weight loss, causing menstruation to stop, hair to become brittle, and skin to become yellow and unhealthy.
  • Fear of even the slightest weight gain taking all precautionary measures to avoid weight gain or becoming "overweight". [28]
  • Rapid, continuous weight loss. [29] : soft, fine hair growing over the face and body. [26]
  • An obsession with counting calories and monitoring fat contents of food.
  • Preoccupation with food, recipes, or cooking may cook elaborate dinners for others, but not eat the food themselves or consume a very small portion.
  • Food restrictions despite being underweight or at a healthy weight.
  • Food rituals, such as cutting food into tiny pieces, refusing to eat around others, and hiding or discarding of food.
  • Purging: may use laxatives, diet pills, ipecac syrup, or water pills to flush food out of their system after eating or engage in self-induced vomiting, though this is a more common symptom of bulimia.
  • Excessive exercise, [30] including micro-exercising, for example making small persistent movements of fingers or toes. [31] of self as overweight, in contradiction to an underweight reality.
  • Intolerance to cold and frequent complaints of being cold body temperature may lower (hypothermia) in an effort to conserve energy due to malnutrition. [32] or orthostatic hypotension. or tachycardia. , anxiety disorders and insomnia. : may avoid friends and family and become more withdrawn and secretive. . (from vomiting or starvation-induced ketosis).
  • Dry hair and skin, as well as hair thinning.
  • Chronic fatigue. [28]
  • Rapid mood swings.
  • Orange discoloration of the skin, particularly the feet (Carotenosis).
  • Having severe muscle tension, aches and pains.
  • Evidence/habits of self harming or self-loathing.
  • Admiration of thinner people.
  • Infertility.

Interoceptive Edit

Interoception involves the conscious and unconscious sense of the internal state of the body, and it has an important role in homeostasis and regulation of emotions. [33] Aside from noticeable physiological dysfunction, interoceptive deficits also prompt individuals with anorexia to concentrate on distorted perceptions of multiple elements of their body image. [34] This exists in both people with anorexia and in healthy individuals due to impairment in interoceptive sensitivity and interoceptive awareness. [34]

Aside from weight gain and outer appearance, people with anorexia also report abnormal bodily functions such as indistinct feelings of fullness. [35] This provides an example of miscommunication between internal signals of the body and the brain. Due to impaired interoceptive sensitivity, powerful cues of fullness may be detected prematurely in highly sensitive individuals, which can result in decreased calorie consumption and generate anxiety surrounding food intake in anorexia patients. [36] People with anorexia also report difficulty identifying and describing their emotional feelings and the inability to distinguish emotions from bodily sensations in general, called alexithymia. [35]

Interoceptive awareness and emotion are deeply intertwined, and could mutually impact each other in abnormalities. [36] Anorexia patients also exhibit emotional regulation difficulties that ignite emotionally-cued eating behaviors, such as restricting food or excessive exercising. [36] Impaired interoceptive sensitivity and interoceptive awareness can lead anorexia patients to adapt distorted interpretations of weight gain that are cued by physical sensations related to digestion (e.g., fullness). [36] Combined, these interoceptive and emotional elements could together trigger maladaptive and negatively reinforced behavioral responses that assist in the maintenance of anorexia. [36] In addition to metacognition, people with anorexia also have difficulty with social cognition including interpreting others’ emotions, and demonstrating empathy. [37] Abnormal interoceptive awareness and interoceptive sensitivity shown through all of these examples have been observed so frequently in anorexia that they have become key characteristics of the illness. [35]

Associated problems Edit

Other psychological issues may factor into anorexia nervosa some fulfill the criteria for a separate Axis I diagnosis or a personality disorder which is coded Axis II and thus are considered comorbid to the diagnosed eating disorder. Some people have a previous disorder which may increase their vulnerability to developing an eating disorder and some develop them afterwards. [38] The presence of Axis I or Axis II psychiatric comorbidity has been shown to affect the severity and type of anorexia nervosa symptoms in both adolescents and adults. [39]

Obsessive-compulsive disorder (OCD) and obsessive-compulsive personality disorder (OCPD) are highly comorbid with AN. [40] [41] OCPD is linked with more severe symptomatology and worse prognosis. [42] The causality between personality disorders and eating disorders has yet to be fully established. [43] Other comorbid conditions include depression, [44] alcoholism, [45] borderline and other personality disorders, [46] [47] anxiety disorders, [48] attention deficit hyperactivity disorder, [49] and body dysmorphic disorder (BDD). [50] Depression and anxiety are the most common comorbidities, [51] and depression is associated with a worse outcome. [51]

Autism spectrum disorders occur more commonly among people with eating disorders than in the general population. [52] 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. [53]

There is evidence for biological, psychological, developmental, and sociocultural risk factors, but the exact cause of eating disorders is unknown. [54]

Genetic Edit

Anorexia nervosa is highly heritable. [54] Twin studies have shown a heritability rate of between 28 and 58%. [55] First-degree relatives of those with anorexia have roughly 12 times the risk of developing anorexia. [56] 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 and opioid receptor delta-1. [57] Epigenetic modifications, such as DNA methylation, may contribute to the development or maintenance of anorexia nervosa, though clinical research in this area is in its infancy. [58] [59]

A 2019 study found a genetic relationship with mental disorders, such as schizophrenia, obsessive–compulsive disorder, anxiety disorder and depression and metabolic functioning with a negative correlation with fat mass, type 2 diabetes and leptin. [60]

Environmental Edit

Obstetric complications: prenatal and perinatal complications may factor into the development of anorexia nervosa, such as preterm birth, [61] maternal anemia, diabetes mellitus, preeclampsia, placental infarction, and neonatal heart abnormalities. [62] Neonatal complications may also have an influence on harm avoidance, one of the personality traits associated with the development of AN. [ medical citation needed ]

Neuroendocrine dysregulation: altered signalling of peptides that facilitate communication between the gut, brain and adipose tissue, such as ghrelin, leptin, neuropeptide Y and orexin, may contribute to the pathogenesis of anorexia nervosa by disrupting regulation of hunger and satiety. [63] [64]

Gastrointestinal diseases: people with gastrointestinal disorders may be more at risk of developing disorders of eating practices than the general population, principally restrictive eating disturbances. [65] An association of anorexia nervosa with celiac disease has been found. [66] The role that gastrointestinal symptoms play in the development of eating disorders seems rather complex. Some authors report that unresolved symptoms prior to gastrointestinal disease diagnosis may create a food aversion in these persons, causing alterations to their eating patterns. Other authors report that greater symptoms throughout their diagnosis led to greater risk. It has been documented that some people with celiac disease, irritable bowel syndrome or inflammatory bowel disease who are not conscious about the importance of strictly following their diet, choose to consume their trigger foods to promote weight loss. On the other hand, individuals with good dietary management may develop anxiety, food aversion and eating disorders because of concerns around cross contamination of their foods. [65] Some authors suggest that medical professionals should evaluate the presence of an unrecognized celiac disease in all people with eating disorder, especially if they present any gastrointestinal symptom (such as decreased appetite, abdominal pain, bloating, distension, vomiting, diarrhea or constipation), weight loss, or growth failure and also routinely ask celiac patients about weight or body shape concerns, dieting or vomiting for weight control, to evaluate the possible presence of eating disorders, [66] especially in women. [67]

Studies have hypothesized the continuance of disordered eating patterns may be epiphenomena of starvation. The results of the Minnesota Starvation Experiment showed normal controls exhibit many of the behavioral patterns of AN when subjected to starvation. This may be due to the numerous changes in the neuroendocrine system, which results in a self-perpetuating cycle. [68] [69] [70]

Anorexia nervosa is more likely to occur in a person's pubertal years. Some explanatory hypotheses for the rising prevalence of eating disorders in adolescence are "increase of adipose tissue in girls, hormonal changes of puberty, societal expectations of increased independence and autonomy that are particularly difficult for anorexic adolescents to meet [and] increased influence of the peer group and its values." [71]

Psychological Edit

Early theories of the cause of anorexia linked it to childhood sexual abuse or dysfunctional families [72] [73] evidence is conflicting, and well-designed research is needed. [54] The fear of food is known as sitiophobia [74] or cibophobia, [75] and is part of the differential diagnosis. [76] [77] Other psychological causes of anorexia include low self-esteem, feeling like there is lack of control, depression, anxiety, and loneliness. [78] Anorexic people are, in general, highly perfectionistic [79] and most have an obsessive compulsive personality traits [80] which may facilitate sticking to a restricted diet. [81] It has been suggested that anorexic patients are rigid in their thought patterns, and place a high level of importance upon being thin. [82] [83]

Sociological Edit

Anorexia nervosa has been increasingly diagnosed since 1950 [84] the increase has been linked to vulnerability and internalization of body ideals. [71] People in professions where there is a particular social pressure to be thin (such as models and dancers) were more likely to develop anorexia, [85] and those with anorexia have much higher contact with cultural sources that promote weight loss. [86] This trend can also be observed for people who partake in certain sports, such as jockeys and wrestlers. [87] There is a higher incidence and prevalence of anorexia nervosa in sports with an emphasis on aesthetics, where low body fat is advantageous, and sports in which one has to make weight for competition. [88] Family group dynamics can play a role in the cause of anorexia including negative expressed emotion in overprotective families where blame is frequently experienced among its members. [89] [90] [91] When there is a constant pressure from people to be thin, teasing and bullying can cause low self-esteem and other psychological symptoms. [78]

Media effects Edit

Persistent exposure to media that presents body ideals may constitute a risk factor for body dissatisfaction and anorexia nervosa. The cultural ideal for body shape for men versus women continues to favor slender women and athletic, V-shaped muscular men. A 2002 review found that, of the magazines most popular among people aged 18 to 24 years, those read by men, unlike those read by women, were more likely to feature ads and articles on shape than on diet. [92] Body dissatisfaction and internalization of body ideals are risk factors for anorexia nervosa that threaten the health of both male and female populations. [93]

Websites that stress the importance of attainment of body ideals extol and promote anorexia nervosa through the use of religious metaphors, lifestyle descriptions, "thinspiration" or "fitspiration" (inspirational photo galleries and quotes that aim to serve as motivators for attainment of body ideals). [94] Pro-anorexia websites reinforce internalization of body ideals and the importance of their attainment. [94]

The media portray a false view of what people truly look like. In magazines and movies and even on billboards most of the actors/models are digitally altered in multiple ways. People then strive to look like these "perfect" role models when in reality they are not near perfection themselves. [95]

Evidence from physiological, pharmacological and neuroimaging studies suggest serotonin (also called 5-HT) may play a role in anorexia. While acutely ill, metabolic changes may produce a number of biological findings in people with anorexia that are not necessarily causative of the anorexic behavior. For example, abnormal hormonal responses to challenges with serotonergic agents have been observed during acute illness, but not recovery. Nevertheless, increased cerebrospinal fluid concentrations of 5-hydroxyindoleacetic acid (a metabolite of serotonin), and changes in anorectic behavior in response to acute tryptophan depletion (tryptophan is a metabolic precursor to serotonin) support a role in anorexia. The activity of the 5-HT2A receptors has been reported to be lower in patients with anorexia in a number of cortical regions, evidenced by lower binding potential of this receptor as measured by PET or SPECT, independent of the state of illness. While these findings may be confounded by comorbid psychiatric disorders, taken as a whole they indicate serotonin in anorexia. [96] [97] These alterations in serotonin have been linked to traits characteristic of anorexia such as obsessiveness, anxiety, and appetite dysregulation. [70]

Neuroimaging studies investigating the functional connectivity between brain regions have observed a number of alterations in networks related to cognitive control, introspection, and sensory function. Alterations in networks related to the dorsal anterior cingulate cortex may be related to excessive cognitive control of eating related behaviors. Similarly, altered somatosensory integration and introspection may relate to abnormal body image. [98] A review of functional neuroimaging studies reported reduced activations in "bottom up" limbic region and increased activations in "top down" cortical regions which may play a role in restrictive eating. [99]

Compared to controls, recovered anorexics show reduced activation in the reward system in response to food, and reduced correlation between self reported liking of a sugary drink and activity in the striatum and anterior cingulate cortex. Increased binding potential of 11 C radiolabelled raclopride in the striatum, interpreted as reflecting decreased endogenous dopamine due to competitive displacement, has also been observed. [100]

Structural neuroimaging studies have found global reductions in both gray matter and white matter, as well as increased cerebrospinal fluid volumes. Regional decreases in the left hypothalamus, left inferior parietal lobe, right lentiform nucleus and right caudate have also been reported [101] in acutely ill patients. However, these alterations seem to be associated with acute malnutrition and largely reversible with weight restoration, at least in nonchronic cases in younger people. [102] In contrast, some studies have reported increased orbitofrontal cortex volume in currently ill and in recovered patients, although findings are inconsistent. Reduced white matter integrity in the fornix has also been reported. [103]

A diagnostic assessment includes the person's current circumstances, biographical history, current symptoms, and family history. The assessment also includes a mental state examination, which is an assessment of the person's current mood and thought content, focusing on views on weight and patterns of eating.

DSM-5 Edit

Anorexia nervosa is classified under the Feeding and Eating Disorders in the latest revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM 5). There is no specific BMI cutoff that defines low weight required for the diagnosis of anorexia nervosa. [104] [3]

The diagnostic criteria for anorexia nervosa (all of which needing to be met for diagnosis) include: [7]

  • Restriction of energy intake relative to requirements leading to a low body weight.
  • Intense fear of gaining weight or persistent behaviors that interfere with gaining weight.
  • Disturbance in the way a person's weight or body shape is experienced or a lack of recognition about the risks of the low body weight.

Relative to the previous version of the DSM (DSM-IV-TR), the 2013 revision (DSM5) reflects changes in the criteria for anorexia nervosa, most notably that of the amenorrhea criterion being removed. [7] [105] Amenorrhea was removed for several reasons: it does not apply to males, it is not applicable for females before or after the age of menstruation or taking birth control pills, and some women who meet the other criteria for AN still report some menstrual activity. [7]

Subtypes Edit

There are two subtypes of AN: [24] [106]

  • Binge-eating/purging type: the individual utilizes binge eating or displays purging behavior as a means for losing weight. [106] It is different from bulimia nervosa in terms of the individual's weight. An individual with binge-eating/purging type anorexia can maintain a healthy or normal weight, but is usually significantly underweight. People with bulimia nervosa on the other hand can sometimes be overweight. [28]
  • Restricting type: the individual uses restricting food intake, fasting, diet pills, or exercise as a means for losing weight [24] they may exercise excessively to keep off weight or prevent weight gain, and some individuals eat only enough to stay alive. [24][28] In the restrictive type, there are no recurrent episodes of binge-eating or purging present. [104]

Levels of severity Edit

Body mass index (BMI) is used by the DSM-5 as an indicator of the level of severity of anorexia nervosa. The DSM-5 states these as follows: [107]

  • Mild: BMI of greater than 17
  • Moderate: BMI of 16–16.99
  • Severe: BMI of 15–15.99
  • Extreme: BMI of less than 15

Investigations Edit

Medical tests to check for signs of physical deterioration in anorexia nervosa may be performed by a general physician or psychiatrist, including:

    (CBC): a test of the white blood cells, red blood cells and platelets used to assess the presence of various disorders such as leukocytosis, leukopenia, thrombocytosis and anemia which may result from malnutrition. [108] : a variety of tests performed on the urine used in the diagnosis of medical disorders, to test for substance abuse, and as an indicator of overall health [109] : Chem-20 also known as SMA-20 a group of twenty separate chemical tests performed on blood serum. Tests include cholesterol, protein and electrolytes such as potassium, chlorine and sodium and tests specific to liver and kidney function. [110] : Oral glucose tolerance test (OGTT) used to assess the body's ability to metabolize glucose. Can be useful in detecting various disorders such as diabetes, an insulinoma, Cushing's Syndrome, hypoglycemia and polycystic ovary syndrome. [111]cholinesterase test: a test of liver enzymes (acetylcholinesterase and pseudocholinesterase) useful as a test of liver function and to assess the effects of malnutrition. [112] : A series of tests used to assess liver function some of the tests are also used in the assessment of malnutrition, protein deficiency, kidney function, bleeding disorders, and Crohn's Disease. [113] (LH) response to gonadotropin-releasing hormone (GnRH): Tests the pituitary glands' response to GnRh, a hormone produced in the hypothalamus. Hypogonadism is often seen in anorexia nervosa cases. [25] (CK) test: measures the circulating blood levels of creatine kinase an enzyme found in the heart (CK-MB), brain (CK-BB) and skeletal muscle (CK-MM). [114] : urea nitrogen is the byproduct of protein metabolism first formed in the liver then removed from the body by the kidneys. The BUN test is primarily used to test kidney function. A low BUN level may indicate the effects of malnutrition. [115] : A BUN to creatinine ratio is used to predict various conditions. A high BUN/creatinine ratio can occur in severe hydration, acute kidney failure, congestive heart failure, and intestinal bleeding. A low BUN/creatinine ratio can indicate a low protein diet, celiac disease, rhabdomyolysis, or cirrhosis of the liver. [116][117] (EKG or ECG): measures electrical activity of the heart. It can be used to detect various disorders such as hyperkalemia. [118] (EEG): measures the electrical activity of the brain. It can be used to detect abnormalities such as those associated with pituitary tumors. [119]
  • Thyroid screen: test used to assess thyroid functioning by checking levels of thyroid-stimulating hormone (TSH), thyroxine (T4), and triiodothyronine (T3). [120]

Differential diagnoses Edit

A variety of medical and psychological conditions have been misdiagnosed as anorexia nervosa in some cases the correct diagnosis was not made for more than ten years.

The distinction between the diagnosis of anorexia nervosa, bulimia nervosa and eating disorder not otherwise specified (EDNOS) is often difficult to make as there is considerable overlap between people diagnosed with these conditions. Seemingly minor changes in people's overall behavior or attitude can change a diagnosis from anorexia: binge-eating type to bulimia nervosa. A main factor differentiating binge-purge anorexia from bulimia is the gap in physical weight. Someone with bulimia nervosa is ordinarily at a healthy weight, or slightly overweight. Someone with binge-purge anorexia is commonly underweight. [121] People with the binge-purging subtype of AN may be significantly underweight and typically do not binge-eat large amounts of food, yet they purge the small amount of food they eat. [121] In contrast, those with bulimia nervosa tend to be at normal weight or overweight and binge large amounts of food. [121] It is not unusual for a person with an eating disorder to "move through" various diagnoses as their behavior and beliefs change over time. [53]

There is no conclusive evidence that any particular treatment for anorexia nervosa works better than others however, there is enough evidence to suggest that early intervention and treatment are more effective. [122] Treatment for anorexia nervosa tries to address three main areas.

  • Restoring the person to a healthy weight
  • Treating the psychological disorders related to the illness
  • Reducing or eliminating behaviors or thoughts that originally led to the disordered eating. [123]

Although restoring the person's weight is the primary task at hand, optimal treatment also includes and monitors behavioral change in the individual as well. [16] There is some evidence that hospitalization might adversely affect long term outcome. [124]

Psychotherapy for individuals with AN is challenging as they may value being thin and may seek to maintain control and resist change. [125] Some studies demonstrate that family based therapy in adolescents with AN is superior to individual therapy. [126] Due to the nature of the condition, treatment of people with AN can be difficult because they are afraid of gaining weight. Initially developing a desire to change is important. [127]

Diet Edit

Diet is the most essential factor to work on in people with anorexia nervosa, and must be tailored to each person's needs. Food variety is important when establishing meal plans as well as foods that are higher in energy density. [128] People must consume adequate calories, starting slowly, and increasing at a measured pace. [30] Evidence of a role for zinc supplementation during refeeding is unclear. [16]

Therapy Edit

Family-based treatment (FBT) has been shown to be more successful than individual therapy for adolescents with AN. [8] [129] Various forms of family-based treatment 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, and separated family therapy (SFT) in which the parents and child attend therapy separately with different therapists. [8] Proponents of family therapy for adolescents with AN assert that it is important to include parents in the adolescent's treatment. [8]

A four- to five-year follow up study of the Maudsley family therapy, an evidence-based manualized model, showed full recovery at rates up to 90%. [130] Although this model is recommended by the NIMH, [131] critics claim that it has the potential to create power struggles in an intimate relationship and may disrupt equal partnerships. [130]

There is tentative evidence that family therapy is as effective as treatment as usual and it is unclear if family therapy is more effective than educational interventions. [132]

Cognitive behavioral therapy (CBT) is useful in adolescents and adults with anorexia nervosa [133] acceptance and commitment therapy is a type of CBT, which has shown promise in the treatment of AN. [134] Cognitive remediation therapy (CRT) is used in treating anorexia nervosa. [135]

Medication Edit

Pharmaceuticals have limited benefit for anorexia itself. [136] [104] There is a lack of good information from which to make recommendations concerning the effectiveness of antidepressants in treating anorexia. [137] Administration of olanzapine has been shown to result in a modest but statistically significant increase in body weight of anorexia nervosa patients. [138]

Admission to hospital Edit

AN has a high mortality [139] and patients admitted in a severely ill state to medical units are at particularly high risk. Diagnosis can be challenging, risk assessment may not be performed accurately, consent and the need for compulsion may not be assessed appropriately, refeeding syndrome may be missed or poorly treated and the behavioural and family problems in AN may be missed or poorly managed. [140] Guidelines published by the Royal College of Psychiatrists recommend that medical and psychiatric experts work together in managing severely ill people with AN. [141]

Nutrition Edit

The rate of refeeding can be difficult to establish, because the fear of refeeding syndrome (RFS) can lead to underfeeding. It is thought that RFS, with falling phosphate and potassium levels, is more likely to occur when BMI is very low, and when medical comorbidities such as infection or cardiac failure, are present. In those circumstances, it is recommended to start refeeding slowly but to build up rapidly as long as RFS does not occur. Recommendations on energy requirements vary, from 5–10 kcal/kg/day in the most medically compromised patients, who appear to have the highest risk of RFS, to 1900 kcal/day. [142] [143]

AN has the highest mortality rate of any psychological disorder. [8] The mortality rate is 11 to 12 times greater than in the general population, and the suicide risk is 56 times higher. [25] Half of women with AN achieve a full recovery, while an additional 20–30% may partially recover. [8] [25] Not all people with anorexia recover completely: about 20% develop anorexia nervosa as a chronic disorder. [122] If anorexia nervosa is not treated, serious complications such as heart conditions [23] and kidney failure can arise and eventually lead to death. [144] The average number of years from onset to remission of AN is seven for women and three for men. After ten to fifteen years, 70% of people no longer meet the diagnostic criteria, but many still continue to have eating-related problems. [145]

Alexithymia influences treatment outcome. [136] Recovery is also viewed on a spectrum rather than black and white. According to the Morgan-Russell criteria, individuals can have a good, intermediate, or poor outcome. Even when a person is classified as having a "good" outcome, weight only has to be within 15% of average, and normal menstruation must be present in females. The good outcome also excludes psychological health. Recovery for people with anorexia nervosa is undeniably positive, but recovery does not mean a return to normal. [ medical citation needed ]

Complications Edit

Anorexia nervosa can have serious implications if its duration and severity are significant and if onset occurs before the completion of growth, pubertal maturation, or the attainment of peak bone mass. [146] [ medical citation needed ] Complications specific to adolescents and children with anorexia nervosa can include the following: Growth retardation may occur, as height gain may slow and can stop completely with severe weight loss or chronic malnutrition. In such cases, provided that growth potential is preserved, height increase can resume and reach full potential after normal intake is resumed. [ medical citation needed ] Height potential is normally preserved if the duration and severity of illness are not significant or if the illness is accompanied by delayed bone age (especially prior to a bone age of approximately 15 years), as hypogonadism may partially counteract the effects of undernutrition on height by allowing for a longer duration of growth compared to controls. [ medical citation needed ] Appropriate early treatment can preserve height potential, and may even help to increase it in some post-anorexic subjects, due to factors such as long-term reduced estrogen-producing adipose tissue levels compared to premorbid levels. [ medical citation needed ] In some cases, especially where onset is before puberty, complications such as stunted growth and pubertal delay are usually reversible. [147]

Anorexia nervosa causes alterations in the female reproductive system significant weight loss, as well as psychological stress and intense exercise, typically results in a cessation of menstruation in women who are past puberty. In patients with anorexia nervosa, there is a reduction of the secretion of gonadotropin releasing hormone in the central nervous system, preventing ovulation. [148] Anorexia nervosa can also result in pubertal delay or arrest. Both height gain and pubertal development are dependent on the release of growth hormone and gonadotropins (LH and FSH) from the pituitary gland. Suppression of gonadotropins in people with anorexia nervosa has been documented. [149] Typically, growth hormone (GH) levels are high, but levels of IGF-1, the downstream hormone that should be released in response to GH are low this indicates a state of “resistance” to GH due to chronic starvation. [150] IGF-1 is necessary for bone formation, and decreased levels in anorexia nervosa contribute to a loss of bone density and potentially contribute to osteopenia or osteoporosis. [150] Anorexia nervosa can also result in reduction of peak bone mass. Buildup of bone is greatest during adolescence, and if onset of anorexia nervosa occurs during this time and stalls puberty, low bone mass may be permanent. [151]

Hepatic steatosis, or fatty infiltration of the liver, can also occur, and is an indicator of malnutrition in children. [152] Neurological disorders that may occur as complications include seizures and tremors. Wernicke encephalopathy, which results from vitamin B1 deficiency, has been reported in patients who are extremely malnourished symptoms include confusion, problems with the muscles responsible for eye movements and abnormalities in walking gait.

The most common gastrointestinal complications of anorexia nervosa are delayed stomach emptying and constipation, but also include elevated liver function tests, diarrhea, acute pancreatitis, heartburn, difficulty swallowing, and, rarely, superior mesenteric artery syndrome. [153] Delayed stomach emptying, or gastroparesis, often develops following food restriction and weight loss the most common symptom is bloating with gas and abdominal distension, and often occurs after eating. Other symptoms of gastroparesis include early satiety, fullness, nausea, and vomiting. The symptoms may inhibit efforts at eating and recovery, but can be managed by limiting high-fiber foods, using liquid nutritional supplements, or using metoclopramide to increase emptying of food from the stomach. [153] Gastroparesis generally resolves when weight is regained.

Cardiac complications Edit

Anorexia nervosa increases the risk of sudden cardiac death, though the precise cause is unknown. Cardiac complications include structural and functional changes to the heart. [154] Some of these cardiovascular changes are mild and are reversible with treatment, while others may be life-threatening. Cardiac complications can include arrhythmias, abnormally slow heart beat, low blood pressure, decreased size of the heart muscle, reduced heart volume, mitral valve prolapse, myocardial fibrosis, and pericardial effusion. [154]

Abnormalities in conduction and repolarization of the heart that can result from anorexia nervosa include QT prolongation, increased QT dispersion, conduction delays, and junctional escape rhythms. [154] Electrolyte abnormalities, particularly hypokalemia and hypomagnesemia, can cause anomalies in the electrical activity of the heart, and result in life-threatening arrhythmias. Hypokalemia most commonly results in anorexic patients when restricting is accompanied by purging (induced vomiting or laxative use). Hypotension (low blood pressure) is common, and symptoms include fatigue and weakness. Orthostatic hypotension, a marked decrease in blood pressure when standing from a supine position, may also occur. Symptoms include lightheadedness upon standing, weakness, and cognitive impairment, and may result in fainting or near-fainting. [154] Orthostasis in anorexia nervosa indicates worsening cardiac function and may indicate a need for hospitalization. [154] Hypotension and orthostasis generally resolve upon recovery to a normal weight. The weight loss in anorexia nervosa also causes atrophy of cardiac muscle. This leads to decreased ability to pump blood, a reduction in the ability to sustain exercise, a diminished ability to increase blood pressure in response to exercise, and a subjective feeling of fatigue. [155]

Some individuals may also have a decrease in cardiac contractility. Cardiac complications can be life-threatening, but the heart muscle generally improves with weight gain, and the heart normalizes in size over weeks to months, with recovery. [155] Atrophy of the heart muscle is a marker of the severity of the disease, and while it is reversible with treatment and refeeding, it is possible that it may cause permanent, microscopic changes to the heart muscle that increase the risk of sudden cardiac death. [154] Individuals with anorexia nervosa may experience chest pain or palpitations these can be a result of mitral valve prolapse. Mitral valve prolapse occurs because the size of the heart muscle decreases while the tissue of the mitral valve remains the same size. Studies have shown rates of mitral valve prolapse of around 20 percent in those with anorexia nervosa, while the rate in the general population is estimated at 2–4 percent. [156] It has been suggested that there is an association between mitral valve prolapse and sudden cardiac death, but it has not been proven to be causative, either in patients with anorexia nervosa or in the general population. [154]

Relapse Edit

Rates of relapse after treatment range from 9–52% with many studies reporting a relapse rate of at least 25%. [104] Relapse occurs in approximately a third of people in hospital, and is greatest in the first six to eighteen months after release from an institution. [157]

Anorexia is estimated to occur in 0.9% to 4.3% of women and 0.2% to 0.3% of men in Western countries at some point in their life. [17] About 0.4% of young females are affected in a given year and it is estimated to occur three to ten times less commonly in males. [3] [17] [157] Rates in most of the developing world are unclear. [3] Often it begins during the teen years or young adulthood. [1]

The lifetime rate of atypical anorexia nervosa, a form of ED-NOS in which the person loses a significant amount of weight and is at risk for serious medical complications despite having a higher body-mass index, is much higher, at 5–12%. [158]

While anorexia became more commonly diagnosed during the 20th century it is unclear if this was due to an increase in its frequency or simply better diagnosis. [2] Most studies show that since at least 1970 the incidence of AN in adult women is fairly constant, while there is some indication that the incidence may have been increasing for girls aged between 14 and 20. [17] According to researcher Ben Radford who wrote in Skeptical Inquirer "I found many examples of flawed, misleading, and sometimes completely wrong information and data being copied and widely disseminated among eating disorder organizations and educators without anyone bothering to consult the original research to verify its accuracy". Radford states that misleading statistics and data have been ignored by organizations like the National Eating Disorder Association who has not released data for "incidence of anorexia from 1984–2017" he states that each agency continues to report incorrect numbers assuming that someone else has checked the accuracy. [159]

Underrepresentation Edit

Eating disorders are less reported in preindustrial, non-westernized countries than in Western countries. In Africa, not including South Africa, the only data presenting information about eating disorders occurs in case reports and isolated studies, not studies investigating prevalence. Data shows in research that in westernized civilizations, ethnic minorities have very similar rates of eating disorders, contrary to the belief that eating disorders predominantly occur in white people. [160]

Men (and women) who might otherwise be diagnosed with anorexia may not meet the DSM IV criteria for BMI since they have muscle weight, but have very little fat. [161] Male and female athletes are often overlooked as anorexic. [161] Research emphasizes the importance to take athletes' diet, weight and symptoms into account when diagnosing anorexia, instead of just looking at weight and BMI. For athletes, ritualized activities such as weigh-ins place emphasis on gaining and losing large amounts of weight, which may promote the development of eating disorders among them. [162] While women use diet pills, which is an indicator of unhealthy behavior and an eating disorder, men use steroids, which contextualizes the beauty ideals for genders. [54] In a Canadian study, 4% of boys in grade nine used anabolic steroids. [54] Anorexic men are sometimes referred to as manorexic. [163]

Anorexia Nervosa and Men Edit

Despite the stereotype that eating disorders only occur in women, about one in three people struggling with an eating disorder is male. [164] However, this statistic may represent the minimum, due to the feminine stigma attached to Anorexia Nervosa many men go undiagnosed and they shy away from gaining help. Additionally, assessment tests are geared towards women leading to misconceptions and men not being rightfully diagnosed. There have been many media reports explaining that there has been a rise in men developing Anorexia Nervosa, however the National Health Service (NHS) explains that this could be an effect of men feeling able to seek help and ultimately society recognising that men can suffer from Anorexia Nervosa and eating disorders in general as well as women. [ citation needed ] This is a positive development in society, and the false stigma that men are not affected by Anorexia Nervosa is being combatted.

In a poll of adolescents, cited by the National Eating Disorders Association (NEDA), researchers found that 33 percent of males used unhealthy behaviours to control weight. [165] Many men like women feel pressures to look a certain way, causing them to use unhealthy mechanisms to reach a weight/body goal.

Who gets Anorexia Nervosa? Edit

Men Edit

Men who identify as gay have traditionally been associated with the development of Anorexia Nervosa. National Eating Disorders Association (NEDA) reports that among those with an eating disorder, 42 percent identify as gay. [166]

Those who have experienced trauma early in life. Victims of sexual abuse, harassment and those who have been taunted about weight at a young age could be affected by an eating disorder such as Anorexia Nervosa at a later stage in life. These abusive incidents can result in a feeling of lifelong victimisation and a loss of control. Anorexia can spring from those roots. Boys and men who change their diets might feel as though they are in control of how others perceive them, maybe for the first time, and that power of anorexia may become a little addictive. Changing body shape or size can also make a man feel as though he isn’t subject to the abuse he felt when he was a different body shape at a younger age, and that can be empowering. [167]

Participation in certain sports that include certain types of weight restriction can initiate an eating disorder to arise. Men may initially initiate the harmful behaviour (such as restriction) due to the demand of the sport, but they may keep up with the behaviour due to the changes Anorexia can bring in the brain.

The term "anorexia nervosa" was coined in 1873 by Sir William Gull, one of Queen Victoria's personal physicians. [19] The history of anorexia nervosa begins with descriptions of religious fasting dating from the Hellenistic era [168] and continuing into the medieval period. The medieval practice of self-starvation by women, including some young women, in the name of religious piety and purity also concerns anorexia nervosa it is sometimes referred to as anorexia mirabilis. [169] [170]

The earliest medical descriptions of anorexic illnesses are generally credited to English physician Richard Morton in 1689. [168] Case descriptions fitting anorexic illnesses continued throughout the 17th, 18th, and 19th centuries. [171]

In the late 19th century anorexia nervosa became widely accepted by the medical profession as a recognized condition. In 1873, Sir William Gull, one of Queen Victoria's personal physicians, published a seminal paper which coined the term "anorexia nervosa" and provided a number of detailed case descriptions and treatments. [171] In the same year, French physician Ernest-Charles Lasègue similarly published details of a number of cases in a paper entitled De l'Anorexie hystérique. [172]

Awareness of the condition was largely limited to the medical profession until the latter part of the 20th century, when German-American psychoanalyst Hilde Bruch published The Golden Cage: the Enigma of Anorexia Nervosa in 1978. Despite major advances in neuroscience, [173] Bruch's theories tend to dominate popular thinking. A further important event was the death of the popular singer and drummer Karen Carpenter in 1983, which prompted widespread ongoing media coverage of eating disorders. [174]

The term is of Greek origin: an- (ἀν-, prefix denoting negation) and orexis (ὄρεξις, "appetite"), translating literally to a nervous loss of appetite. [175]

Anorexia Nervosa | Symptoms & Causes

While each child may experience symptoms differently, some of the most common signs of anorexia include the following:

  • low body weight (under 85 percent of the normal weight for the child&rsquos height and age)
  • intense fear of weight gain, even as they are losing weight
  • distorted view of body weight, size, or shape see themselves as too fat or normal sized, even when very underweight.
  • refusal to maintain normal body weight
  • in females, absence of three consecutive menstrual cycles without another cause
  • excessive physical activity
  • denies feelings of hunger
  • preoccupation with food preparation
  • bizarre eating behaviors (e.g., using a fork to eat raisins or cutting food into very small pieces)

Other symptoms may include:

  • dry skin
  • dehydration
  • abdominal pain or bloating
  • constipation
  • fatigue
  • hypothermia (problems maintaining normal body temperature) and feeling cold when others are hot
  • emaciation
  • development of lanugo (fine, downy body hair)
  • yellowing of the skin
  • stress fractures

If your child is struggling with anorexia, they may also be socially withdrawn, irritable, moody or depressed.

Eating disorders are illnesses of denial and secrecy they're often very difficult to track down. So family members and friends shouldn't feel badly about not figuring out right away if their loved one has a problem.

That being said, there are some signs you can look for:

  • unexplained weight loss
  • dizziness
  • fainting
  • fatigue
  • irritability or moodiness
  • going to the bathroom often, especially after meals
  • cutting food into tiny pieces and pushing it around the plate

Also be on the lookout for major change in eating or exercise behavior.