This essay is dedicated to my mother and grandmother, two inspiring women of great strength and love.
How many do you do?
When I was ten, I could barely eat three WeetBix. But I was proud of it: at least I could top my seven-year-old sister, who just managed to swallow two of Australia’s favorite breakfast bricks. On the other hand, my dad, a beach-brown West Aussie bloke, could ‘do’ up to five or six of the fibrous slabs when he put his mind to it.
Looking back now, WeetBix offers a neat metric to track the development of my eating disorder (ED). At the voracious onset of puberty, I was putting away up to eight each morning. First, I was triumphant of my newfound appetite. Then, slowly, I became frightened by my loss of control. My compulsion to eat surpassed hunger and enjoyment. It filled haunted spaces inside me I hadn’t noticed before. Anxious gaps, questions unanswered, feelings misunderstood. I would excuse myself from class to ‘get water’, sobbing into my locker as I stuffed down my entire lunch before we even reached recess.
I went to a private school where image was everything. We wore blazers and format hats, hitched our skirts up and donned mascara and fake tans. My classmates brought celery to school, shared diet tips, binged in groups, then signed up for gym memberships out of guilt. People’s bodies changed drastically in a short period of time. With no guarantee that we might not end up looking like the Michelin Man at the end of our transformation, we did all we could to slow the tide. The kind of feminism our principal sermonised was the neoliberal sort: you have to be the woman with everything, career, family and looks included. We learnt that being a woman meant being in control. And yet, being a woman wasn’t something I wanted to sign on to, not yet.
From the same stone
The woman I knew best, of course, was my own mother. I could see my hips, legs and breasts becoming hers, and I heard her every self-abasement as my own. She’d take up walking regimes, or cut out bread for a month, and then on weeknights I’d come into the kitchen to find she’d caved and drunk an entire bottle of white wine. It was a cliche, a stock-standard Electra complex, but there was no way in hell I was going to become her.
She describes her twenties as a kind of manic montage: aerobics in the morning before a full day of teaching, then sometimes a late night at the club. She took over-the-counter slimming pills to give her energy and help with her ‘weight issues’. She didn’t want to tell me which pill, or talk about it much, though she did admit pharmacies had stopped selling them due to the amphetamine levels. My initial reaction was disapproval. But then I realised that what I really felt was jealousy. If I’d had access to chemist-sanctioned speed, I’d have done it too. What an easy shortcut that would’ve been.
Eating disorders suffer from a serious research lag, which is not surprising. These diseases represent the intersection of a number of factors historically thrown in the ‘too hard’ basket: they’re a mental health problem, they’ve long been thought of as ‘female’ diseases, and many of their outward symptoms (weight loss, ‘healthy’ eating and exercise), at least in the early stages, are seen as cause for celebration, not concern.
A review of ED research by Whitehouse and Harris was published in the late 90s, and they found most papers agreed there was some intergenerational influence on whether a child develops an ED or not:
If food has become more, or less, to the primary caregiver than a fuel to enable the body to function, it is possible that the child will not develop a normal relationship with food.
This vague blanket statement cites four different sources, and its ambiguity is apt. Researchers can all seem to agree that how a child is raised, their family life, and even certain genes can increase the risk of developing an ED. There have even been studies that find correlations between, for instance, a parent’s ED and the child’s weight and growth, or a child’s ED and a parent’s attitude towards their own parents, or the presence of certain genes and a child’s likelihood of developing an ED. But the specific risk factors are still only that: correlations, possibilities.
Honey? / You look so underfed
I certainly feel my own ED had at least something do with the other women in my family. Tasked as my mother was with bringing us together around a dinner table in some kind of nuclear family tableaux, I made her the enemy of my weight-loss goals, as I dropped down to a single dry WeetBix at breakfast every morning (59 calories), and very little else for the rest of the day. It became even easier to antagonise her when she started forcing me into treatment, and then again when she refused my psychologist’s suggestion that she also see a therapist during the process. She said it was me who was sick, not her. She thought they meant she’d been a terrible mother. That it was her fault I was dying.
Sometimes I thought it was: I still believed I had a lot of autonomy over my disease, that I was making a statement. I wrote angry poems about her fake nails, her attempts to make our family appear wealthier or more cohesive than we really were. Back then I had no sympathy: I was spiteful and hypercritical of her attitudes towards food, how she’d dealt with body image. And yet, how could I blame her for being a product of her environment, just as I was of my own?
I can trace disordered eating back in my family through at least three generations. My grandmother was born in the 1940s, a time when dieting was thought of as a kind of glamorous hobby. I always associate my grandmother with Judy Garland in Wizard of Oz – the sweet, pastoral, overgrown girl child who helps the men (Scarecrow, Tin Man, Lion) attain their goals. Onscreen, Kansas looked just like the wheatbelt upbringing my grandmother had.
Judy Garland died of barbiturate overdose after a long life of trying to return to her Oz days. My grandma wasn’t in showbiz and she didn’t die – she didn’t take pills or even drink much – but this was her world, her idols. She worked in an elite section of the local department store where rich women would watch a private fashion show and buy clothes off the backs of models. I grew up with her singing ‘Zippidy Doo Dah’ and ‘Singin’ in the Rain’ and ‘Somewhere over the Rainbow’. She is a Metro-Goldwyn-Mayer woman, and she wears the MGM waistline to this day.
By the 70s, my grandma was wife to an Olympic-level yachtsman and the proud parent of my two uncles, and my mother (the youngest). As boys my uncles rowed, stayed out late, smoked weed and won the hearts of the prettiest girls at their regattas. My grandfather took them on long runs and advocated carrot juice, measuring his own food intake and exercise routines and, by proxy, the rest of the family’s. My mother, then a curvy teen with a nuisance bust that would later cause her major back pain, tried her best to keep up. My grandmother’s role in all of this was to provide a constant stream of nutrition for these hyperactive, growing young men and her elite athlete husband. When I imagine their family home, I picture Jimmy Dean’s exorbitant breakfast in Rebel Without a Cause. And I picture my slim, amiable grandmother earnestly feeding everyone but herself.
In ED circles a person who enjoys making food for others and seeing them eat it is known as a ‘feeder’. This behavior offers a way to engage with food that maybe you yourself crave, without having to consume it: instead, you can take some kind of vicarious pleasure out of watching others eat. My grandmother’s idea of herself as an ideal wife includes providing for her family domestically, always appearing the effervescent entertainer. But it also includes a slim figure – a sense of thrift and self-sacrifice. Add a dose of Calvinist WA wheatbelt martyrdom and my grandma fits the bill. Her food is always for someone else. She has no need, except where it concerns good manners and social engagement.
Blood is thicker
While researchers will never find a singular gene that guarantees disordered eating, they’ve identified a whole alphabet soup of different genomes that might contribute (I won’t bore you with the various HTR2As and 5-HTTLPRs of geneticists-only heiroglyphics). Results from the Anorexia Nervosa Genetics Initiative, due out sometime in 2019, ought to give a much better idea of the role of genetics in EDs. Meanwhile, the emerging field of epigenetics has revolutionised the idea of heredity in medicine and psychology, and appears to play a part in ED susceptibility.
Epigenetics basically mean that environmental factors – trauma, nutrition, activity et cetera – can change the way a parent’s genes are switched on/off, and that this programming is actually heritable. In one of the more recent studies on the epigenetics of EDs, Schroeder et al artificially raised the cortisol levels of some unfortunate pregnant mice. The scientists noticed this hormone scaled back their foetus’s nutrient supply, which in turn ‘programmed’ the genetic combo for a slower metabolism in the babies. From birth, the young mice were metabolically prepared for a life of scarcity, and, as many larger families will know, when there’s less to go around you just have to eat faster. If ample food was available, the younger mice would eat normally. But if the scientists placed them on extremely restricted diets for weeks, these little mice would scoff huge excesses of food in the scarce time they had, compared to the control group, whose mothers’ had been afforded relatively breezy, cortisol-free pregnancies.
We are not mice, but Schroeder’s study, along with the others I’ve mentioned, show a strong link between the attitudes to food of mothers and children. If phenotypes relating to anxiety, depression and addiction can be programmed across generations, why not food-related anxieties or addictions? In the past, anything to do with genetics sounded like a death sentence, but with the revolutionary discovery of this on/off switch, we’re now far better able to identify and avoid risky epigenetic triggers. Secondly, genetic framing could help reduce ED stigma, and provide practical physical steps towards treatment and recovery, which, amid all the experimental maybes that exist in ED treatment, would be a welcome change (trust me).
Every time I catch up with my mother she shares my grandmother’s latest food-related peculiarities, or how loudly she criticised an obese stranger at the shopping mall. Before my diagnosis, my mother had no words for what she saw in her own mother; now she agrees that what we all went through in my recovery sent ripples back through our family. It must be strange to realise so late in life that your mother, that first and fundamental model of woman, is only human, capable of flaw and disorder. Now, just as I am able to differentiate my own body image and my mother’s, she too can deflect her own mother’s attitudes to food, body and womanhood.
At the recovery-end of my ED, the years of therapeutic solipsism have culminated in this conclusion: my experience was, in some ways, the inevitably malnourished fruit of years – if not generations – of cultural conditioning, women’s trauma, even genetic inheritance. But though two in every ten Anorexia patients will remain chronically ill for the long term, I find it hard to imagine a relapse at this stage. This realisation relieved me of the burden of blame, and it gave me hope that, like any other disease, there’s some chance of figuring out how to prevent it taking more lives.
I’m rather relieved to have been born in 1994, with my own adolescence set to a backdrop of ever-reducing mental health stigma, accelerating ED research, and more nuanced and pervasive feminism. And I’m glad that my mum gets to live through this time, too. No matter how inevitable EDs may be for some people, there’s always the opportunity to change, and get that quality of life back. Reclaiming my mind from the obsessive nonsense of a severe mental illness has been a rewarding experience, and I’m glad to see the positive impact it’s had on the rest of my family. I wish the same for anyone else going through this.
Finally: no more WeetBix for me. I would add, however, that it’s nice to know breakfast is no longer about how many I can ‘do’, but rather, what I will ‘do’ with it.
 When I say woman, I guess I refer more broadly to anyone with any form of feminine experience. This cultural coding can affect anyone born female, who identifies as woman, or who falls anywhere on the feminine spectrum. It’s also worth noting men can experience eating disorders too, but the manifestation is often quite different.
 Even the etymology of ‘Anorexia Nervosa’ is loaded. The first part translates from Greek to ‘a loss of appetite’, which I can humbly assure you does not describe the real experience of this disease. At best I’d describe my experience of anorexia as a deliberate, competitive attempt to look better and feel in control. At worst, I was caught between dizzy spells and fatigue and a totally crippling phobia of anything entering my mouth. This resulted in nights spent punching at the hunger cramps in my stomach as I lay awake conjuring pornographic visions of whipped cream sundaes, deep fried Mars Bars, and whatever other food fantasies I could dream up. Even thinking about these things made me feel fatter. But it definitely wasn’t appetite loss: more like appetite perversion.The ‘Nervosa’ half – nervousness – is therefore a little more apt, and thank God it replaced the late-19th century aberration which was ‘Anorexia Hysteria’ (mind you, they only went with ‘Nervosa’ because there were some reports of men experiencing the disease; not out of any charitable gesture towards the affected women).
 My family was, until my generation, staunchly anti-therapy. The classic stigma that therapy’s just for ‘crazy people’ definitely rang true in our household. The crazy person in this instance, of course, was me.
 I used to do this myself, baking all kinds of sweet fatty things in the middle of the night with no intention of ever eating them myself. I once drove my father so crazy with this weird behavior that he threw several muffin tins off the second-storey of our house.
 An international study on the genetic component of anorexia, with over 13,000 anorexia sufferers and 9,327 non-anorexia volunteers recruited world-wide for genetic analysis.
 Cortisol being the hormone released when we’re stressed or our blood sugars drop, which instructs our body how to manage under these circumstances.
Baker et al., ‘Genetics of Anorexia Nervosa’, Current Psychiatry Reports, vol. 19, no. 11, 2017, p. 84.
Schroeder et al., ‘A methyl-balanced diet prevents CRF-induced prenatal stress-triggered predisposition to binge eating-like phenotype’, Cell Metabolism, vol. 25, no. 6, 2017, pp. 1269–1281.
Balottin et al., ‘The parental bonding in families of adolescents with anorexia: attachment representations between parents and offspring’, Neuropsychiatric Disease and Treatment, vol. 1, no. 13, 2017, pp. 319–327.
Eating Disorders in Australia, by National Eating Disorders Collaboration, 2013.
Stein et al., ‘An observational study of mothers with eating disorders and their infants’, Journal of Child Psychology and Psychiatry, and Allied Disciplines, vol. 35, 1994, pp. 733–748.
Whitehouse and Harris, ‘The inter-generational transmission of eating disorders’, European Eating Disorders Review, vol. 6, no. 4, 1998, pp. 238–254.
Image: Bird circus / flickr
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