Demystifying the Genetic and Environmental Influences on Disordered Eating

Genetics play an important role in the development of eating disorders and disordered eating behaviours. To date, many (over 30!) twin studies have been done and all but two found significant genetic effects on the development of eating disorders and disordered eating. However, no methodology is without limitations and tentative conclusions become more convincing when the findings are confirmed using different experimental approaches.

Twin studies, while they offer many advantages, are not that good when it comes to detecting shared environmental effects on a particular trait (literally, evens that happen to both twins and affect them in the same way). Fortunately, twin studies are just one of several different ways that researchers can use to study heritability(A quick reminderHeritability measures the amount of the variability in an observable trait/behaviour that can be attributed to genetic variation. This is NOT the same as stating that a particular fraction of an individual’s trait is caused by genetics.) 

Adoption studies (scroll to bottom of link) provide a powerful alternative method to assess heritability and they are particularly useful in overcoming some of the inherent limitations of twin studies.

Adoption studies compare similarity for a trait or disorder in biological versus adoptive relatives to determine the degree to which genetic and shared environmental factors contribute to a phenotype (Plomin et al., 2001). Genetic factors are implicated if biological relatives are more highly correlated for a trait or disorder than are adoptive relatives. By contrast, shared environmental effects are implicated if adoptive and biological relatives are similarly correlated for a trait or disorder. Perhaps more importantly, because they do not share segregating genetic material, significant associations between adoptive siblings function as a “direct” estimate of shared environmental influences.

One major drawback of conducting an adoption study is that it is really hard to find eligible participants. But in 2009, Kelly Klump and colleagues overcame this hurdle and published the first adoption study to examine the genetic and environmental effects on disordered eating.

As the PDF of the paper is freely available here, I’m not going to go into details about the participants and the statistical analyses, but if you have any questions, do raise them in the comments. Instead, I want to skip to the juicy part: Results.


  • No significant differences in levels of disordered eating between biological and adoptive siblings (and a lot of variability in levels of disordered eating in both groups)
  • Levels of disordered eating among biological siblings were moderately correlated
  • Levels of disordered eating were not correlated among adoptive siblings
  • Differences between adoptive sibling and biological sibling correlations were statistically significant suggesting significant genetic effects but little shared environmental influence on disordered eating 


  1. The findings in this study converge with the findings from twin studies and establishes that genetics are an important factor in the development of eating disorders. 
  1. These results support previous findings that shared environmental effects are not an important contributor to the development of disordered eating during adolescence and young adulthood.
  1. Finally, heritability estimates for eating disorders are on par with other psychiatric disorders (which, by the way, are commonly acknowledged to be “biologically-based”) such as schizophrenia and bipolar disorder (~50-80%).


Often more important than what the findings of a particular study suggest is what they don’t suggest, particularly for studies on heritability, which are (like neuroimaging, I’d argue) quite prone to misinterpretation.

ONE. Although the findings suggest that shared environmental factors do not have strong main effects,  they CAN impact the development of disordered eating through interactions with other factors:

For example, family conflict may interact with genetic risk to increase susceptibility to disordered eating in both siblings […] Likewise, family conflict could interact with a nonshared environmental factor (i.e., peer group) to increase susceptibility to disordered eating in one sibling relative to another […] Thus, while our findings rule out the main effects of shared environment, they do not rule out interactive effects that may be equally important and potent.

TWO, and this is important: The lack of shared environmental effects DOES NOT say much about the role of culture in causing eating disorders. I’ll quote at length here because it is too good to paraphrase:

A common misconception is to think that broad sociocultural factors (e.g., the thin beauty ideal for women) are implicated if shared environment is significant, and are excluded if shared environment is negligible. To the contrary, cultural factors may influence disordered eating in the face of non-significant shared environmental effects. For example, cultural factors (i.e., pressures for thinness) may increase risk for disordered eating in genetically susceptible siblings via gene × environment interactions. Indeed, in the absence of a culture that emphasizes thinness […] disordered eating may be diminished [note, diminished doesn’t mean it will disappear] (Keel & Klump, 2003)

Remember: Genetics load the gun and environment pulls the trigger. If the genetic risk is relatively high (for example, family history of eating disorders and conditions highly comorbid with eating disorders, such as OCD, anxiety, and depression), it might take relatively few environmental factors to “pull the trigger”; if the genetic risk is not as high, it might take relatively more environmental factors to “pull the trigger” (maybe, for example, childhood trauma/stressors or being involved in a sport like ballet or gymnastics).

The following, which is that shared environmental factors may act through unique (nonshared) environmental factors, is equally important to remember:

In addition, cultural factors may also influence disordered eating through nonshared environmental mechanisms. The prototypical example in this regard is participation in weight-focused sports. A sibling who participates in ballet will presumably experience more pressures to be thin than her sister who is a softball player. In this example, the cultural factor is a non-shared rather than shared environmental effect and is therefore included in the nonshared environmental variance that is significant […] for the development of disordered eating.

THREE. This study, because it evaluated individuals during late adolescence and young adulthood, says nothing about the role of shared environmental factors during other developmental stages (i.e., pre-puberty). Indeed, previous findings by this group suggest that shared environmental factors ARE important on the variance of disordered eating during pre-adolescent and pre-pubertal periods. (I believe I mentioned some of those findings here; heritability values DO NOT seem to stay stable throughout development. On a side note, I really enjoyed that study, so I urge you to check out that post if you haven’t already.)

Finally, as I mentioned in the very beginning, all studies have limitations. Some limitations in this study are that (1) the sample sizes are not exactly large, (2) the sample is more diverse in age and ethnicity than twin studies tended to be, (3) the authors did not assess biological relatives of the adoptees (but of course, logistically, this is pretty challenging), (4) the authors examined disordered eating symptoms rather than anorexia nervosa or bulimia nervosa specifically, and (5) the authors only examined women.

Before I wrap up, I want to, again, stress a couple of things about heritability:

Heritability is a population statistic. It CAN vary depending on the population studied (ethnicity, age, gender, for example) and the surrounding environment. Which means, all in all, we don’t know much about the heritability of eating disorders/disordered eating in non-Western cultures as most studies examining heritability were almost exclusively focused on middle classes from Western nations. We need more research to sort this stuff out. Way more.

I know I have quoted a lot from this paper, but let me still finish with yet another quote. It is just too good:

Before ending, it is important to highlight implications of our findings. Perhaps most importantly, we hope that our work will help change perceptions of eating disorders as purely psychosocial phenomena. Currently, some US legislation and insurance statutes limit mental health parity for eating disorders because they are not considered to be “biologically based” (Klump, Bulik, Kaye, Treasure, & Tyson, 2009). While no psychiatric disorder is entirely “biologically based”, we hope that our findings will contribute to increased recognition of the genetic basis for eating disorders and the ways in which genes may interact with environmental factors to create differential risk.

The key take home message: Psychiatric disorders are not 100% genetic or 100% environmental, they result from complex interactions between genes and the environment, but, the extent of genetic and environmental influences will vary from person to person, which is part of why the notion that everyone can (or worse, should!) fully recover is, well, in my opinion, kind of silly. Despite similar behavioural or cognitive traits (fear of weight gain, similar symptom frequency, etc.), the causative factors are very heterogeneous and can vary a lot from person to person, and it is reasonable to expect that some of those factors are more readily manipulated/altered by behavioural and pharmacological interventions than others.

If you have any questions about the study, the methodology, or what the results mean, please ask! I know when I’m tired I tend to fall back on jargon, and I feel I might have done that more in this post than usual, so, call me out on it!


Klump, K.L., Suisman, J.L., Burt, S.A., McGue, M., & Iacono, W.G. (2009). Genetic and environmental influences on disordered eating: An adoption study. Journal of Abnormal Psychology, 118 (4), 797-805 PMID: 19899849

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Tetyana is the creator and manager of the blog. She has an Honours BSc in Neuroscience and an MSc in Medical Science. She can be reached at tetyana[at]scienceofeds[dot]org.


  1. This is really helpful Tetyana… Thanks!

    So often have I heard people claim that ‘genetic studies show that EDs are X% genetic and Y% environmental’… It’s really helpful that you have spelt out what heritability actually means.

    What I am interested to learn is how knowledge of the candidate genes involved in the development of (some) people’s EDs can actually help with treatment.. I would guess that it such knowledge could help professionals to better tailor treatment in accordance with individual aetiology – and possibly also help identify those at risk of developing an ED in the future?

    • Regarding you question, I don’t think anyone knows the answer to that. I highly doubt that it will help a lot in diagnostics or developing predictors because it is very heterogenous and there are likely lots of alterations in the system that can result in similar phenotypes. That’s my opinion, though. What it might help with is understanding what the particular alleles associated with eating disorders (or related disorders) *do* and what’s the effect on overall brain function. THAT, I think, can help in treatment. But how, who knows. I think it is hard to predict. It depends on what we find.

      • What also interests me in all this is the issue of ‘attribution’. (I prefer the term ‘attribution’ to ‘blame’). Knowledge of heritability in the development of EDs has led some to conclude that a person will only develop an ED if they are genetically pre-disposed. I am a little sceptical of this assumption. Some people’s EDs may be highly influenced inherent factors, while others’ EDs may be almost solely environmental – as you imply above.

        I would hope that in the future it is possible to better tease out the influence of inherent risks and environmental risks to better tailor treatment. But this may be a LONG way in the future. Even though some of the behaviours of people with EDs are comparable, the cognitive processes and precise thoughts can vary considerably from person to person.

  2. Just. Amazing.

    That’s all I have to say. You do the best job of explaining genetics and its accompanying misconceptions than anyone I’ve ever met. . . but perhaps that’s not surprising given your intellect 😉

  3. THIS…extremely thorough, well-written offering that certainly strikes more than a few “chords” with me personally.

    I am an identical twin…and while we both shared boughts of bulimia during our university years (attending different schools in different states..and not KNOWING of each other’s “problem” until after graduation!)…she has gone on to full recovery…whilst I myself am currently battling a “re-surfacing”…ten years long …with anorexia nervosa.

    I believe this is partly because of the difference in our personalities/lifestyles AND environment. She lives alone in the States…has always enjoyed sports such as softball, tackle football etc…has always preferred to wear pants …doesn’t give a hoot about “fashion”…and is gay. I, on the other hand, have always cared too much about such frivolities…always loved dresses, preferred classical dance…am married with three children and live in France…a culture where thinness is legion…and this study really reflects the importance of biological AND environmental factors…Thank you for this.

    • Hi Donna,

      Thanks so much for your comment! Your personal experiences are very interesting and speak volumes about gene and environment interactions. It is fascinating.

      I’m glad you enjoyed the post.


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