Genes load the gun, but the environment pulls the trigger

Eating disorders are a psychological phenomenon that both clinicians and the media have focused intensively on for decades. There has been a recent “boom” in research to investigate the background causes and development behind them. Recent research has begun to inform our understanding of eating disorders so that traditional stereotypes are increasingly redundant. Young, white, affluent teenage girls used to be considered the primary group at risk of eating disorders, but now the problem has crossed socioeconomic, ethnic and gender boundaries. For example N.H.S direct 2010 quote that “in the last decade the number of men with anorexia has doubled, of anorexia sufferers 2.5 out of 10 are now men, whereas it used to be 1.2 out of 10.” As awareness of the diversity of eating disorders has increased, researchers have come to questions both the origin and growth of these intriguing conditions. Underlying causes of eating disorders include a number of complex interwoven, social, psychological and biological factors. Both biological and psychosocial factors are implicated in the pathophysiology, but the causes and mechanisms underlying eating disorders remain uncertain. Early theories of eating disorders focused on aversive family and sociocultural factors as central to the development of these problems, for example Minuchin’s concept of psychosomatic families. However a progression of family, twin and molecular genetic studies has demonstrated a substantial role for genetic factors in the development of anorexia nervosa, bulimia nervosa and related traits. With research continuing to increase, one of the most controversial and heavily researched areas of eating disorders is whether genetic or the environment play the biggest role. A common query is whether and how they intervene together. Thus how far does each one “loads the gun” for the other, which is what this essay will continue to explore.

          One of the most controversial topics in the development of eating disorders is whether or not there is a stress vulnerability model much like the stress diathesis model of depression. According to the stress diathesis model of depression some people inherit a diathesis (genetic susceptibility) which is in itself not a cause for the disorder, but if a trigger from the environment is endured these people are more likely to suffer from depression. The central idea is that if susceptible individuals are exposed to stress early in life, their systems become permanently sensitised and they overact to mild stressors for the rest of their life (John Pinel, 2005). If indeed there is a stress vulnerability model for eating disorders the implication for treatment could be huge, and the question of genes loading the gun for the development of these disorders will be answered further. Evidence for a stress diathesis model is linked to all developmental areas of eating disorders, be it genetic or environmental. It implies that there must first be some kind of genetic vulnerability but an environmental trigger is needed to activate the susceptibility.  Several cognitive models of eating disorders now exist, these tend to drawn on Beck et al’s 1979 theory of depression and the stress diathesis model. In this essay I will go on to discuss how specific genetic factors, biological changes at puberty, the media, sociocultural influences, familial influences and personality traits can all be linked to a stress vulnerability model and hence support the very idea that genes do indeed load the gun whilst environment pulls the trigger.

        For decades, environmental factors have been singled out and held responsible for eating disorders. However this simplistic approach has greatly damaged and hampered efforts to understand the neurobiology of eating disorders which is now seen as essential for developing effective interventions and treatments. Recently there has been an increasing availability of genetic analytic techniques and neuroimaging technology that has enabled more biological research. More recently family, twin, hormone and neurobiological studies into the development of eating disorders has exploded at an alarming rate. Firstly twin and family studies have rapidly become part of the forefront of new research into eating disorders and their development; they provide strong evidence for the genetic transmission of eating disorders. For example concordance rates for narrowly defined bulimia nervosa have been found to be 22.9% in monozygotic and 8.7% in dizygotic twins (Kendlar et al 1991.) Furthermore the majority of twin studies on anorexia nervosa have shown that the concordance rate for monozygotic twins is higher on average (44%) than for dizygotic twins on average (12.5%.) (Kipman et al 1999.) As can be seen by these results and many more alike there is a very high heritability coefficient, reflecting the relative importance of genetic factors, that has been claimed for both anorexia nervosa and bulimia nervosa. Indeed Klump et al’s (2000) reading of the literature surrounding eating disorders leads them to conclude that between 24-42% of the variance in eating disorders is strictly down to just genetics.  These differences in concordance rates shows that genetic factors, may explain why there could be a phenotype for eating disorders that runs in families.

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      Furthermore adding argument to the genetic debate is the emergence of recent research proposing that there could be a specific gene implicated in the development of eating disorders. Work in this area has focused mainly on neuropeptide and monoamine (especially 5-HT systems) because they are thought to be important in the regulation of eating and weight with respect to anorexia nervosa. The most promising research has been on serotonin genes, the serotonin 2a receptor (5-HT2a) and serotonin transporter (5-HTT) genes. “The A allele of the 5-HT2a-1438 gene has been associated with anorexia nervosa in several studies” (Gobrogge 2005). This gene has indeed been found to be more prevalent in both people with anorexia nervosa and bulimia nervosa (Ricca et al 2002). It has been argued that the specific gene 5-HT2A may be an important vulnerability factor for both anorexia nervosa and bulimia nervosa. In addition to the research of specific gene function in the development of eating disorders is research into the endocrine system especially in women. For the first time scientists have discovered a possible biological element in the development of eating disorders during puberty. Adolescence is a time of huge biological change for both the body and mind, this demands flexibility to successfully manage the transition into adulthood. Change may challenge the rigidity of those already vulnerable to anorexia nervosa and open a new window of vulnerability to dysregualtion in relevant biopsychosocial systems. This could well be implicated to the timing and onset of eating disorders, especially as the onset of eating disorders does stereotypically happen within teenage girls whilst hitting puberty. Several lines of evidence highlight the potential importance of estrogen and in particular a type of estrogen called estradiol, in the genetic underpinnings of eating pathology. Estrogen directly influences food intake and has been linked to eating pathology in women (Edler, Lipson, & Keel, 2007).  A groundbreaking pilot study led by Michigan State University found that influence of one’s genes on eating disorder symptoms was much greater in pubertal girls with higher levels of estradiol than pubertal girls with lower levels of estradiol (Journal of Psychological Medicine, 2009.) It is clear that this kind of genetic research cannot be ignored, and ultimately could open up a new window to all kinds of treatment and interventions.

        Finally on the side of biology, researchers have recently identified associations between eating disorders and self report measures of specific personality traits; the highest associated trait is that of perfectionism. Perfectionism is characterised by the tendency to set and pursue high standards despite the often occurrence of adverse consequences. (Shafran, Cooper & Farbum 2002). Hewitt et al 1995 argue that perfectionism can contribute to eating disorders by making normal shortcomings more traumatic or by making a normal body a sign of imperfection. Both adding more stress to the individual and making this individual more vulnerable to any form of criticism. Indeed it has been shown in many experiments that both patients with anorexia nervosa and bulimia nervosa have elevated traits of perfectionism. For example in a study by Halmi et al 2000 the multidimensional perfectionism scale and the perfectionism subscale of the eating disorder inventory were administered to 322 women with a history of anorexia nervosa. The results showed that persons who had previously suffered from anorexia nervosa had a significantly higher total score (an average of a 45% increase) on both scales than the healthy comparison group. What was also as interesting as these elevated percentages, was the fact that out of 322 women 302 said that their perfectionism was self imposed, and not as a result to other’s expectations. Hence seemingly more to do with their own biological make up than others opinions, pressures or comments. This finding of seemingly biological origin to eating disorders leads to an associated and equally worrying finding about a lot of the associated attitudes and traits with eating disorders (especially perfectionism). Common findings show that it is not only the disorder itself but also the associated attitudes (concerns, fears and preoccupations) that are highly heritable (Klump et al 2000.) Hence there is strong evidence of familial transmission of perfectionism and it has been hypothesized that perfectionism is one of several phenotypic temperamental or personality trait markers expressing a genotypic vulnerability to eating disorders.

     It can be seen that there seem to be vast theories and a sterling amount of research and evidence into how genes play a role in the development of eating disorders. These factors are perceived to be the sole causal mechanism operating in the development of eating disorders, by many people. Nevertheless while looking at this highly persuasive evidence it is important to remember that unpacking the interplay between gene and environment is very challenging. For example when studying the differences in monozygotic and dyzygotic twins it seems that due to a higher association and cocordence rate in monozygotic twins that it has to be down to genetics. However perhaps it can be said to be more likely that monozygotic twins environment is more commonly identical than that on dyzygotic twins as monozygotic twins can often (wrongly) be assumed to be the same person, thus treated in the same way. Like Hewiit 1997 said it seems to be true that “although there is consistent evidence of genetic factors influencing vulnerability to eating disorders, the details are far from clear”. With all these genetic factors the stress vulnerability model can be implicated, it is indeed true that perhaps there is a genetic vulnerability to eating disorders, but a certain environmental situation needed for them to emerge. The second part of this essay will go on to examine the environment and this suggested interplay further.

            As has been previously said there are several ways in which genes and the environment can intervene together in the development of eating disorders. The most familiar is the gene-environment interaction, whereby a person’s genes may influence how sensitive he or she is to the effects of the environment a “genetic loading”. We have earlier discussed how indeed genetic research into this area has implied a loaded gun waiting for a trigger, so what about the environment. What does this specific environment look like, and what drives someone to rely on these destructive attitudes and behaviours towards food in an effort to deal with emotional distress? The interaction between the gene-environment nexus is particularly relevant in the study of eating disorders, given the nearly ubiquitous exposure of young girls in western societies to ideals of slenderness. The rest of this essay will try to answer questions on what an environmental trigger constitutes, and the suggested integrated idea of a stress vulnerability model.

      A question that has been continually linked to eating disorders especially within the last decade is whether the media can be partly if not fully held responsible for the recent “boom” in their development. The media’s association of feminity, success and desirability with being slender and having the “ideal thin figure” is a powerful message for young girls. The media are often blamed for the increasing incidence of eating disorders on the grounds that the media images of idealized (slim) physiques motivate or it can be suggested even force people to attempt to achieve this slimness themselves. It has been noted that as our culture becomes increasingly homogenized, with media images of the “perfect slim” women now permeating every corner of society, eating disorders have become correspondingly more democratic (Gord and Freeman 1996). The British Medical Association has called for the media to show “more realistic body shapes” to reduce the number of deaths caused by eating disorders. Research has continually shown that in recent years the gap between the perceived ideal body shape and reality is widening, with perceived slimness become thinner and more dangerous to obtain. Research from the British Medical Association showed that the majority of female characters on television are thinner than average. It was estimated that models and actresses in the 1990’s had 10-15% body fat, whereas a healthy women has 22-26%, the media can clearly be seen to be distorting true reality (British Medical association 1999). Interestingly and further evidence to support the hypothesis that media portrayals of women’s body shape have a strong causal influence over eating disorders, is the fact that eating disorders do not occur uniformly in all cultures at all times. In societies where there is no culture of equating thinness with beauty eating disorders are very rare, i.e. there is no environmental trigger. The trigger is that increasing westernisation has led to lowering of ideal body weight and hence an increase in eating disorders in several cultures. The key to this increasingly westernisation can be placed at the door of the mass media, with thinner women being heralded as the epitome of attractiveness.  For example a study by Groesz et al (2004) found that body image was significantly more negative after viewing thin media images than after viewing images of average, plus sized models or inanimate objects. These results along with many others alike support the sociocultural perspective that the mass media promulgates a slender ideal that elicits body dissatisfaction. There is also perturbing evidence that it is not just the obtainment of an eating disorder that the media effects but also the continuation of one. Research from the British journal of psychiatry in 1993 showed that eating disordered women over estimated their size when shown media portrayals of idealized female bodies in fashion magazine than when looking at neutral objects. None of these findings are overly surprising but the implications are huge when these thin media images are everywhere to be seen and continually hard-pressed as the idea of “perfection”.

          Much like the media peer influence is often cited as a significant contributor to the development and continuation of eating disorders. Peer influence has been found to be highly correlated to a host of harmful heath behaviours but is especially relevant to eating disorders. Adolescent girls learn certain attitudes and behaviours from their peers, both by example, encouragement and by way of teasing for failure to adhere to peer norms. These attitudes and behaviours are often the ones that shape children for later life. It has indeed been found that adolescent female friendship cliques tend to be homogeneous with respect to body image concerns (Parson et al 1999). The increasing incidence of body image dissatisfaction and eating concerns in childhood has led rearchers to question where, how and from whom are children developing these eating-related problems. Evidence has indicated that children especially girls learn a large amount of concerns from their peers. Teasing during childhood has been indicated as a very significant risk factor. Warren (1968) reported that 5 out of the 20 girls he studies with anorexia nervosa had been teased as children, which led to dieting and eventual eating disorders. Peers also directly seem to have an influence on body image and eating concerns simply through just modelling behaviour and interacting about these issues. There doesn’t have to be bullying or teasing about weight just the simple idea that children want to be like their friends believing this will make them more popular. Linked to this idea of modelling behaviour is the degree to which children believe being thin will increase how much peers like them, this may influence their own perceptions of their body as well as their eating practices. It has been shown that the likability construct of peer influence was the most significant predictor of disordered eating. For example in a study of boys and girls in grades 3 through to 6, 15% claimed that they believed their friends would like them more if they were thinner, and this belief significantly contributed to the prediction of eating disturbances (Maloney et al 1989).

Linked to peer influence is the idea that a group can encourage and help contribute to the continuation of an eating disorder, there is a new “online predator” in the form of pro anorexia and pro eating disorder websites. As recently as two years ago, putting pro anorexia into any search site brought up articles, blogs, petitions and general sites condemning the use of pro eating disorder websites. Today, an internet search using such terms turns up hundreds of forums, sites and blogs geared towards the promotion of the so-called “lifestyle.” Thousands of young women log on every day to glean tips and tricks from their fellow disordered, and to gain encouragement. There can even be competition and encouragement on who can lose the most weight. A recent study at Stanford University 2009 found that patients who used pro-eating-disorder sites were sicker longer. Even sites like House of Thin, which claim to be “pro-recovery”, are harmful. In the Stanford Study, patients who used both pro-eating-disorder and pro-recovery sites were admitted to hospital more times than nonusers. Eating-disorder patients can get new, often harmful ideas from pro-eating disorder sites. According to the research, 96 percent of respondents who visited pro-eating-disorder sites said they learned new weight-loss or purging techniques; so did 46 percent of respondents who visited pro-recovery sites. Seven out of 10 users of pro-eating-disorder sites said they used the new techniques they learned; a third used new diet pills, supplements or laxatives (Stanford University 2009.) What is increasingly worrying is the idea that these sites can also encourage people with no previous history of eating disorders. In a study by Jett et al in 2010, Female college students with a body mass index (BMI) higher than 18 and no history of an ED were exposed to either pro-ED websites, healthy/exercise websites or tourist websites for 1.5 hours. They were then asked to keep a food diary for the next week. The pro-ED website group experienced a significant one-week decrease in caloric intake from pre- to post-exposure, and participants reported using techniques on the websites to aid with food reduction and had strong emotional reactions to the websites. This study shows that even modest exposure to these pro eating disorder websites has a significant effect. Hence the implications for women already with eating disorders, and who are using these websites frequently is phenomenal. It is clear that both the media and peer influence quite often come together in helping with the development of eating disorders. Without this continual Westernisation and idealized images of “beautiful” slim women would friendship groups be homogenized towards eating patterns and dieting, and thus clearly influencing the development of eating disorders within young adolescents.

There is a strong tendency to hold the media and our Western culture of unachievable beauty ideals responsible for the development of eating disorders. Research as we can clearly see does suggest that both the media and peer influence can play a substantial role in the development of body dissatisfaction, particularly in young women. “Normative discontent” is the term used to describe the unsettling finding that most women in Western societies are dissatisfied with their bodies. However we have to remember that we are talking about both the media and peer influence as environmental triggers not a sole cause. It is true that in the media all these images, advertisement and messages are indeed counterproductive to both a good self image and societies overall acceptance of size and shape. However it is important to point out that most young women are exposed to the same media images and are not all developing anorexia equally. Similarly there is a billion dollar dieting industry, with advertisings on the TV., radio, newspapers and magazines, but not everyone who see’s or hears them is on a diet. Additionally most children are teased by someone about their size or shape be it too thin, too fat, too short, to tall etc at some point but again not everyone developing some form of disordered eating. It seems that a lot of the time both the media and peer influence are necessary but not sufficient for the development of eating disorders. There seems to need to be a vulnerability already there, i.e. genetics loading the gun.

We have seen how peer influence can contribute to the development of eating disorders, but what about closer to home. Why are children so preoccupied with weight and body image at such an early age, where, how and whom is this idealized body image coming from. The very earliest reports of anorexia nervosa noted that families interacted with the patients in peculiar ways, which was usually believed to be detrimental to the patients (Lasegue 1873.) Factors residing in family systems have been implicated in the pathogenesis of eating disorders. For example along with peers family can often praise anorexia nervosa patient’s slenderness and envy the self control and discipline required to achieve it (Branch and Eurman 1980). Whereas this can be seen as a positive aspect to just simple dieting, it turns into worry that this reinforcement frequently persists even when the person in question becomes severely emaciated. Family dynamics have been implicated not only in the perpetuation of eating disorders, but also in their development. There is the common saying that everything starts at home. Indeed in most “stereotypical” families parents serve as our role models, providing most of what we know as young children. This extends into eating habits, the setting of standards for perfectionism, and what is acceptable and what is not (even in weight and shape.) Many researchers claim that family dynamics are at the root of eating disorders and a lot of associated problems that come with them. There is a current view of a “typical” anorexia nervosa family, this view is important to consider as it is enlightening and can be very informative into the family dynamics involved in eating disorders. This family is generally seen to be upper middle class, highly achievement orientated, where the mother and often others are constantly vigilant about their weights and value slimness and physical appearance (Yager 1982). These families may appear to have an ideal environment on the surface but upon close observation little expression of affection or warmth is seen. Underlying dissatisfaction and tension is often present within the parental dyad. It has been suggested that parents of anorexic offspring put high expectations on their children to over compensate for the lack of love in their own marriage (Blinder et al 1988). Indeed many case reports and studies of family interaction, show eating disordered families to be enmeshed, intrusive, hostile and negating of the patients emotional needs, or sometimes overly concerned with parenting (Minuchin 1974.) Although these two subtypes seem contradictory, several connections remain. They both suggest that mothers of children with eating disorders tend to focus all their attention on their children, set high expectations and foster ambitions for external achievement and there is clear overinvolvment. This parental overinvestiment and overdirectivness leads to a situation in which a vulnerable child becomes more concerned with external parental approval then with their own internal satisfaction. It is clearly stated by many researchers that eating disorders are not about food but about emotions and control. Family dynamics is one of the most prominent “control” areas in a lot of patients with eating disorders lives. Either a disordered family environment, or over protective mothers, or indeed hostile ambitious, high achieving parents seem to instigate a lack of control in the patient’s life’s eating disorders is a way in which they can take back this control. There also seems to be an extremely strong link between mothers and children/ adolescents with eating disorders. Direct maternal comments appear to be a more powerful influence than simple modelling of weight and shape concerns. Mothers of children with eating disorders may well also have an influence not just on their dieting behaviours, but also their child’s pathology. They think their daughters should lose more weight and describe them as less attractive than do comparison mothers or the girls themselves (Hill and Franklin 1998). Eating disorders seem to run in families especially in mother-daughter pairings, anorexia nervosa and bulimia nervosa until recently were relatively uncommon disorders, but its incidence among members of afflicted families is much higher than in the general population. This can be seen to be due to both the environment and genetics. On the side of the environment, mothers who themselves have an eating disorder tend to have a negative influence on their children’s attitudes and behaviours. Also feeding them irregularly, using food for non-nutritive purposes, and expressing concern about their daughters’ weight as early as the age of two. In a study by Hodes et al in 1997, thirteen mothers with eating disorders whom had twenty six children between them, participated in a study designed to investigate the extent of psychiatric disorders and abnormality of weight and growth on their children. It was found that amongst the children 50% had psychiatric disorders of some kind and 32% had abnormalities of weight or growth. In addition female offspring tended to have low body weight and mother’s underestimated their children’s dietary needs. The issue of familial transmission on eating disorders is extremely important and has huge implications for intervention theories. Indeed it has been argues that the entire family must be treated as a unit for therapy to be effective, and that children should also be considered when mothers request help for themselves. The Maudsley Method which incorporates the whole family unit for treatment is an extremely effective treatment for many young anorexia patients. Proving this line of argument, Daniel Le Grange 2010 assigned 121 patients aged 12 to 18, mostly girls, to a year of either family or individual therapy at the University of Chicago and at Stanford — 24 hours in all. Twelve months after the treatment had ended, 49 percent of those who had been in family therapy were in full remission, more than double the 23 percent of those who had been in individual therapy. Among patients, who were in remission at the end of the treatment itself, only 10 percent of the family-therapy group had relapsed a year later, compared with 40 percent of those who had individual therapy. With results such as these, familial influence on the development of eating disorders cannot be ignored.

As can be seen families can obviously transmit eating concerns and even behaviours on to their children. However it is doubtful that such transmission is solely sufficient for the emergence of an eating disorder. There must be some kind of addition “vulnerability factor”. As we have previously stated this vulnerability factor is genetics. For example if a mother or father has an eating disorder it can be likely that their child will also have a predisposition to this through their shared genetics. However there will need to be the environmental trigger to set it off. This environmental trigger can also be through the family, but not by transmission but by family dynamics. Family dynamics, peer influence and the media are likely to interact with the genetic predisposition in the emergence of an eating disorder.

In conclusion it is clear that the underlying causes of eating disorders are vast and span many different psychological areas. When we take into account that eating disorders didn’t emerge as a serious problem until the late 1970’s it is not surprising that a mere twenty five years later we still seem far from understanding their etiology. Throughout this essay it has become clear that there is a very strong possibility for a stress vulnerability model within the development of eating disorders. A genetic vulnerability interacts with the environment and life events to trigger the development of an eating disorder. With this idea at the forefront of research, the implication for treatment is huge, with possible medical treatments advancing in relation to the specific gene linked with anorexia nervosa. Additionally family therapy and a backlash against the media are also on the rise in the ongoing efforts against the development of both anorexia nervosa and bulimia nervosa. Specific genes, twin studies, biological changes at puberty, the media, sociocultural influences, familial influences and personality traits can all be linked to a stress vulnerability model and hence enforce the very idea that genes do indeed load the gun while environment pulls the trigger.