Puberty at an early age increases the risk for disordered eating behaviours such as bingeing and purging (Jacobi et al., 2004; Kaltiala-Heino et al., 2001). What’s more, the hormone estradiol moderates the risk of disordered eating behaviours. More precisely, in a group of twins with low estradiol levels, differences in disordered eating are likely due to environmental factors (such as family, school, friends), but in a group of twins with high estradiol levels, the differences in disordered eating are more likely due to genetic factors. (I blogged about it here.)
Essentially, estradiol partially moderates the extent to which genes affect disordered eating.
This is interesting because the estrogen system has a role in regulating body weight and food intake, influences eating behaviours during the menstrual cycle, and obviously plays an important role during puberty. Moreover, one study showed that estrogen receptor genes (proteins that bind estrogen) are associated with eating disorder symptomatology (Eastwood et al., 2002), though I don’t know if that finding has been replicated.
All of this is even more interesting because genetic effects on disordered eating are basically non-existent in prepubertal girls but increase to 50-60% postpuberty. This means that any variation we see in disordered eating in a group of 8 year olds is due to environmental factors (“nurture”). But, after puberty, genes account for 50-60% of the variation we see in disordered eating behaviours.
The idea is that estradiol might “turn on” genes that influence eating disorder behaviours.
Previous studies showed that estradiol moderates the genetic risk for eating disorders. In this study, Baker et al wanted to see if ovarian hormones, like estradiol, also mediates the risk. Mediate? Moderate? Isn’t that the same thing? I must admit, I had to go and look this up.
The difference boils down to the fact that mediators explain the relationship between two variables and moderators influence the strength or direction of that relationship. Here’s an example from a website:
Let’s consider the relation between social class (SES) and frequency of breast self-exams (BSE). Age might be a moderator variable, in that the relation between SES and BSE could be stronger for older women and less strong or nonexistent for younger women. Education might be a mediator variable in that it explains why there is a relation between SES and BSE. When you remove the effect of education, the relation between SES and BSE disappears.
Getting back to our study, the authors hypothesized that younger age of menarche (menarche is the first menstrual cycle) will be associated with increased disordered eating. To test this hypothesis, they compared the age of menarche and disordered eating behaviours in female monozygotic twins (who share ~100% of their genetic make-up) and dizygotic twins (who share ~50% of theirs).
They found a significant, albeit small, overlap between the genetic factors that contribute to early menarche and those that contribute to disordered eating. What are the shared genetic factors? How does the estrogen system influence the vulnerability to disordered eating? At this time, no one knows. But, there are some ideas:
Ovarian hormones, specifically estradiol, may also directly moderate genetic vulnerability by activating the genetic risk for disordered eating and/or indirectly influence risk through the physical, psychological, and emotional changes that occur with puberty. We also speculate that ovarian hormones influence the genetic vulnerability of disordered eating, at least in part, through epigenetic moderating mechanisms. Reproductive hormone splay a role in epigenetic changes in the brain by altering DNA methylation, which alters gene expression (Kaminsky et al., 2006). Preliminary studies suggest profound DNA methylation changes at pubertal onset in humans (Lintas et al., 2010) and rats (Ojeda et al., 2010). Although purely speculative, epigenetic changes at puberty could, in part, be responsible for the association between reproductive hormones and disordered eating.
What was curiously omitted from the discussion was that this finding (that there is an overlap between genes that influence age of menarche and disordered eating) provides a clue as to why eating disorders might be more prevalent among females than males. It can’t be the whole picture, of course, but it is suggestive. (Another factor might be that dieting produces greater alterations in the serotonin system in females than males, leading to a greater decrease in mood. I touched on that here.)
The authors conclude,
Our results confirm the association between puberty and disordered eating and suggest this association is the result of to genetic factors. Adolescence and puberty are well-documented vulnerability markers for eating disorders in girls, and our results suggest this is in part due to shared genetic factors between pubertal timing and disordered eating. These shared genetic factors may be the result of reproductive hormones.
There are some limitations to keep in mind. This study was cross-sectional, meaning that researchers only looked at one time point, so causal relationships cannot be determined. Moreover, the age range of the subjects was between 16-17 and there was only one cohort. Finally, the study looked at disordered eating attitudes and behaviours NOT eating disorder diagnoses, so it is possible that these findings do not translate to a clinical population.
Future work should probably include a more varied sample population. Moreover, longitudinal studies that monitor hormone levels and disordered eating attitudes/behaviours in prepubetal-to-postpubertal adolescents would also be great.
Until then, I think this is pretty cool!
By the way, check out my guest post on Ashley Miller’s/Kate Donovan’s blog about bulimia nervosa. In the post I go over the “basics” about bulimia (what is it, what are the causes, prevalence, mortality, treatments, common myths, etc..). Check it out, leave a comment!