I find myself on the cusp of another coming out – this will make the third in my lifetime. First as gay, then as eating disordered and now, in many ways, as a ‘non-believer’. I suspect my directness when filming a recent documentary for BBC Inside Out may, for some, feel too controversial. Personally, do I believe there is a genetic connection as far as my own eating disorder is concerned? Disappointing as it is for some to hear, no I do not. Do I believe that there is a genetic cause for eating disorders? Similarly no, I do not. However, the use of the word ‘cause’ is key here as this is what is most commonly asked by presenters and interviewers: “what causes eating disorders?” or “what do you think caused your eating disorder?”
Do I believe the swiftly growing body of research evidence about the possible genetic vulnerability or genetic susceptibility as one of several risk indicators of the potential development of an eating disorder? Yes, I certainly do. There are a number of rigorous studies conducted by scholars whose bodies of work I greatly admire and value. As you can tell at this point I’m moving away from personal opinion and experience toward the literature analysis I’ve conducted on a substantial number of books and research articles as part of my doctoral work (over 300 sources and counting). I continue to dig deeper, as I embrace keeping an open mind about what the literature from a wide range of disciplines has to offer my understanding of eating disorders in males.
Does my research evidence any genetic connection whatsoever for men’s eating disorder – that’s a resounding no – none whatsoever – because to claim so would be grossly untrue. My research is hermeneutic. I am examining and interpreting texts men have written about their experience of eating disorder. If I were to extrapolate genetic findings from what is an interpretive social research study this would be at best, no way to pass a PhD and, at worst, utterly unethical. The men’s texts are directing the focus, scope and angle of what I’m writing about. This means I find myself examining the multiple risk factors that may combine in a complex way to result in disordered eating as just one facet of the larger life stories about men’s experiences of living with their disorders.
There’s another issue skulking behind the question of there being a genetic link to the development of an eating disorder: conflating ‘genetic vulnerability’ with deeply ingrained familial acculturation to certain coping mechanisms and tendencies may somewhat confuse the public’s understanding of the debate. Family history does not always translate directly as ‘genetic connection’. This is a confusion that the peer-reviewed scientific literature is duly cautious about when publishing its findings. Indeed, as Morgan (2008) asserts, the more genetic vulnerability is studied the more complex the issue becomes.
Even back in 1991, Kendler et al. were studying the potential impact of genetic liability on female susceptibility to the development of bulimia nervosa. They found some substantial influence but the study is also indicative of a pattern that was to dominate until recent times: they necessarily pointed out the “incompleteness” (p.1636) of their data. This by no means renders their findings redundant. It does, however, suggest that a complete picture, offering certainty, was not arrived at.
Instead, what we are faced with is a lack of consistent findings, sustained over time, between clinical and scientific data. Flash forward to 2012, for example, and a study which included 111 males who had presented for eating disorders treatment (Weltzin et al., p.448) found only 18 of those patients had a family history of eating disorder. In very recent studies the importance of taking into account biological data when examining the propensity for eating disorders is clearly argued but there is an interesting change of perspective over time – what is suggested is an issue of epigenetics, that gene expression is itself altered by the environment:
“Indeed, individual differences in thin-ideal internalization demonstrate significant heritability, supporting the need for expanded biopsychosocial risk models, that account for a multitude of factors including how adverse family environments may alter gene expression through epigenetic processes.” (Keel & Forney, 2013, p.433)
So, here there is a useful take on the conflation I was critical of above. In fact, the researchers posit a real need for factors not to be seen in isolation – as any genetic vulnerabilities may be specifically ‘influenced’ by the family and societal context. This is not a ‘genetic connection’, instead it begins to appear that genetic findings may be evidencing the results of what a person’s nutritional and psychological development has undergone, suggesting the sheer power of the environment an organism finds itself in. Whilst, Bulik suggests that the genetic study of eating disorders is the ‘next generation’ of research, it is quite clear that this will only lead to adequate risk identification with the presence of other risk factors. This is compelling for what the future will yield but certainly not conclusive. Rather than there being the data we need to be irrevocably convinced of a 100% genetic connection, we appear to be at an early point in the research where it is important to be more circumspect, following Wildes and Marcus’s lead that genetic liability or vulnerability is currently hypothesized, not proven (2013).
Citing one of Bulik’s studies, Wade et al (2006) while investigating transdiagnostic approaches to the understanding of eating disorders found “genetic influence to be an important factor” (p.515), once again, the researchers were clear to point out some of the limitations of their study; namely, that they were drawing of small sample to twins and the reliability of using qualitative self-report methods for some of their data. Just this year another study by Wade et al, Genetic Variants Associated with Disordered Eating, which examined specific susceptibility genes managed to work with a vastly greater sample size – some 2564 female twins. As there were no data about men, this still requires investigation to be able to offer something definitive about the people I’m studying. Additionally, and carefully stated, out of this significant number only 45 people from their genotyped sample would have been accorded a diagnosis of anorexia or bulimia – leaving the number much lower than appears at first glance. Whilst they already have stated confidence in their being an genetic liability in AN at the beginning of their paper, by the end they state: “our analyses should make a useful contribution toward improving the power to identify genetic variants influencing symptoms and behaviours related to eating disorders…”, this suggests that whilst progress is being made, the genetic understanding is clearly not quite ‘there’ yet.
Till’s doctoral study charted the journey of male anorexia and the various dominant discourses that have encapsulated understanding of this phenomenon over time and finds:
“The completion of the project to map the human genome finally disposed of the myth that there might be an individual gene for every disease; that there would be discovered a normal and a pathological genetic framework. With a much smaller amount of genes than predicted being discovered, the rationality for genetic aetiologies shifts from one of causation to susceptibilities (McGuffin, Riley and Plomin 2001: 1232). In terms of AN: ‘It is likely that what is inherited is not a disorder, but risk factors for the development of a disorder, such as, perhaps, a tendency toward obsessionality. Thus, even if a gene or genes is identified, it will probably not be a gene for an eating disorder but a gene for a related factor…’ (Walsh, 2004: 7)” (2010, p.193)
Where does this leave us? Dr John Morgan in The Invisible Man is clear that genes are significant in “your vulnerability to an eating problem” (2008, p.59) but at the time felt the jury was still out – something that has continued to be echoed in more recent papers. Another scholar with a personal connection to eating disorders and someone whose analysis of the current landscape I trust, Dr Derek Botha, is keen to warn against dangers of the evidence from the proliferation twin-limited studies, female-driven studies and small sample studies being absorbed and regurgitated as “grand over-arching, scientific truths… [materializing] in social discourses as dominant ‘knowledge’ of universal theories…” (2012, p.88).
Finally, Strober and Johnson’s study (2012) of the complexities of biological, environmental psychological ideas inherent in anorexia nervosa would satisfy most scrutinizers in terms of the case they present about the incontrovertibility of genetic factors. However, these are still termed as vulnerabilities and their further examination and assertion added to my overall, more personalised, thinking (apologies for the excessive extract):
“Exactly what are parents and patients being told about the ‘‘new’’ paradigms for understanding AN? Well, they certainly hear more about genes and the brain; but unfortunately, without much clarification or context, the result of which has been no small measure of confusion and misunderstanding as they are to wonder in private if they were just told they/their child has ‘‘brain damage’’ or a ‘‘genetic defect.’’ It goes without saying that explanations serve a clinical purpose only if they are authoritative and complete; if not, they do harm since fragments of truth are never a good substitute for no explanation at all.
This is why it is not a good thing for patients and the public to be told that AN is a genetic disorder” (p.16)
Eating disorders AS genetic is, it would seem, a most unhelpful message to be misconstruing publicly, and so this makes me resist supporting a claim to a genetic ‘connection’ for the time being. For now, we know there continues to be growing evidence for a susceptibility to obsessional behaviours.
And therein lies an issue of things being taken out of context. Even ethical documentary makers want to spark interest by finding the angle where the most ‘controversial’ views can be presented; after all, it creates a personal, emotional response (as evidenced by some of the conversations in the blogosphere). And that’s good, it should be personal – so many people are personally affected by the issue of eating disorders, including me. Film-makers want people to watch, they want their work to be remembered, and so they’ll make it memorable in whatever way they can.
Public conversation and debate is crucial to the continued awareness of the risks eating disorders pose to men’s health – it ignites and motivates researchers, campaigners and clinicians in their continued work. Most of all, good debate allows sufferers and their families to engage with one another and professionals in the field to improve the lot of those who live with Ana, Mia, Rex or Bully (or their various combined ‘relatives’) on a daily basis as I do. I enjoy and welcome the debate because of both my academic interest and my personal benefit but I would hate for anyone out there to get the impression, whatever the content of the Inside Out broadcast ends up being, that I do not take my reading seriously or that I disregard the nuances of what scientific findings about genetics has to offer the wider body of sociological literature about eating disordered male identities and experiences that I study. Just because something doesn’t chime about my own personal experience does not mean I should or would leave it out of my thesis. However, like Sam at MGEDT, I think that the research is not yet at a ‘proof beyond reasonable doubt’ stage to warrant public health funds, diagnosticians, clinicians and health services (for that is surely what this might boil down to when a man is in crisis) focusing too narrowly upon genetic vulnerability as risk factor at the expense of the myriad life experiences that lead men to such a destructive and obsessive coping mechanism.
I would be very personally dismayed if anyone were to suggest that the last six years of my life committed to conducting research into men’s experiences of eating disorder were not a serious attempt to understand the phenomenon in as fulsome a way as I possibly could. Hence, I certainly have already read, amongst the other sources briefly presented above, Alexander and Treasure (Eds) but I certainly welcome the other recommendations for texts that I’ve recently been made aware of and these are gratefully received. Researchers (and even clinicians with incomplete specialist subject knowledge) are human too. We try our best, we make mistakes and we continue to strive to know more, to help better and to process our own trying histories. I would offer the same advice back to my fellow blogger – we do need to dig a little deeper, read a range of literature (not just that which supports our own personal views) and challenge the myths rather than perpetuate them.
This blog entry is dedicated to Jay Taylor, 24, who is reported as having died from heart failure following her eating disorder.
I have never met you but this evening I read the brief details of what you had been through, the love of your family and supporters, and your hope for others’ recovery – it made me cry and it made me sit and write all this straightaway. I hope you are at peace.