The problem with "cause"
I received a flurry of feedback and comments on my post about Anorexia Mythbusting, and the discussion managed to be passionate and respectful. Which just goes to show that I have the best readers ever. The discussion was fantastic and engaging, and one comment in particular prompted me to do a follow-up post.
Earlier today, Jane (one of the co-chairs of the organization Maudsley Parents) wrote:
I wonder if a lot of the problem here is the word "cause." It seems to me like too simple a construct to be very useful. I find the genetic and neurobiological research on AN very compelling, but I'd be hesitant to say genes or neurobiology cause AN (maybe Radford or others would--I don't know). It seems to me more accurate to say they are responsible for risk. I really think the predisposing/precipitating/perpetuating model makes much more sense than saying, " X causes (or does not cause) AN."
Although I have a special interest in adolescent AN, I agree with Adria and Melissa other eating disorders (as well as disordered eating) merit consideration. Social influence might not be the same across eating disorders.
Humans like to look for "cause," myself included. We want to be able to answer why, to draw conclusions, to figure it out. But as Jane pointed out, the word "cause" as it points to a single factor--be it genetics, models, or mothers--is probably a little over simplistic. The predisposing/precipitating/perpetuating model that Jane mentioned is based on our relatively new understanding of the complex causes of many illnesses.
Take tuberculosis. It was originally thought that you got TB because you came from a bad family or you breathed in bad air. Even after the discovery of the TB bacterium, there was thought to be a simple cause and effect. You breathed in the bacterium, you developed TB. Except it's not that simple. Ninety percent of the people who harbor the TB bacterium in their lungs (after the initial infection, the body walls off the bacteria in the lungs) will never progress to clinical illness or transmit the disease to anyone else. So what's the difference between them and the 10% who do go on to develop clinical disease? Often, TB re-emerges at a point in a person's life when their immune system is weakened, and the bacteria can break free from their "jail" in the lungs. Many things can contribute to a weakened immune system, not the least of which is HIV or other severe infection, but factors also include severe stress and malnutrition. Assuming two people had latent TB infections in their lungs, and one was of a higher socioeconomic class than the other, the person who was wealthier would probably be less likely to develop TB simply because their immune system might have been in better shape. Furthermore, poor people are more likely to live in the types of close quarters that promote TB transmission, and so are probably more likely to inhale the bacterium in the first place.
Does poverty "cause" TB? No. But you can't study TB without realizing the effects of poverty. Just understanding the microbiology isn't enough. It isn't a simple matter of infection causes disease. The infection is a necessary but not sufficient aspect of TB. Vulnerability to TB infection doesn't just start with the infection (or the re-emergence of the infection). It starts with your access to food, with air quality, with a whole host of things that don't have anything to do with the actual bacteria.
It's similar with eating disorders. I would argue that the genetic predisposition is a necessary but not sufficient cause of eating disorders. You don't really see eating disorders in people without the genetic background, but the genetic background alone isn't enough.
So what the heck are these predisposing, precipitating, and perpetuating factors anyway? A good explanation of these factors comes from a continuing education course from the American Dental Hygenists' Association:
[Eating disorders are] considered to be developmental more so than mental. Therefore, predisposing, precipitating, and perpetuating factors are more useful to consider than actual causes.
Factors considered to predispose an individual to anorexia include female gender, family history of eating disorders, perfectionist personality, difficulty communicating negative emotions, difficulty resolving conflict, and low self-esteem. Precipitating factors associated with anorexia focus on developmental changes, such as sexual development and menarche in persons aged 10 to 14 years, which leads to a spurt in weight gain; independence and autonomy struggles in individuals aged 15 to 16 years; and identity conflicts in individuals aged 17 to 18 as they transition from home to college or married life. Perpetuating factors are those that maintain the eating disorder. Examples of these include signs and symptoms of starvation and coping strategies engendered by the eating disorder.
I personally would add illness, efforts towards "healthy eating," dieting, teasing, and other forms of trauma as precipitating factors. But I think this is a good breakdown of what these different factors are and what forms they make take.
A longer explanation (it's slightly dated as it was published in 1988) can be found here: Predisposing, Precipitating, Perpetuating, Professional Help and Prevention for Eating Disorders. This paper also wins the award for today's Best Use of Alliteration.
I promise you that I tried to find other analogies for this, but the best explanation I could think of was a cooking analogy. It's kind of like baking a cake: there are certain basic items that you need to make a cake (flour, sugar, baking soda, etc). You don't typically see anchovies called for in baking. Different cakes have different ingredients (chocolate birthday cake vs. flourless chocolate cake vs. chocolate cheesecake*), and even the same type of cake can have the same ingredients that vary in amounts (more sugar, less leavening). You can add frosting--or not. You can add filling. In the end, though, most cakes have a few staple ingredients that you combine and then bake in the oven. I don't make up a box of Betty Crocker yellow cake mix and expect to pull a Caesar salad out of the oven. It might be over- or under-baked, but it's still cake.
The different ingredients are the predisposing and precipitating factors- not everyone has exactly the same genetic or environmental experiences, but there are often variations on a theme. The "baking" part is where I see the precipitating factors becoming the perpetuating factors. Different ingredients, different baking times, different cakes...but they're still cakes. No one ingredient causes these cakes to spring forth into being (unless you count the baker). Flour doesn't "cause" a cake, nor does sugar, nor does flipping the oven on and popping in a pan.
When trying to figure out what went wrong with a recipe, I often zero in on something. Maybe the oven is on the fritz. Or the baking soda was ancient. Or I was a little short on sugar but hoped for the best. That doesn't mean that that is the only thing wrong with the recipe, just that I focused on one thing. So with eating disorders, focusing on our culture's expectations of beauty as a cause of eating disorders is a little myopic. So is focusing on just genetics and neuroscience.
And a total gold star to whoever made it this far and muddled through my hopeless analogies!
*Yes, I know cheesecake is essentially a custard, but it has "cake" in the name so I'm running with it for the purposes of this analogy.
10 comments:
I am glad we're discussing this topic more Carrie, because it is clearly a topic that stimulates quite heated debate.
Like you (and many others) I have endeavoured to understand 'why', 'how' (etc.) with regard to my very long history of anorexia nervosa (AN). I felt that if I could answer these questions I could cure myself.
I knew the point at which my AN started (age 12 yrs). This point was when I felt totally COMPELLED to restrict and to over-exercise in a very specific manner. I had no choice in the matter; I simply HAD to do it. If I deviated from my diet and exercise rules I experienced intolerable panic, confusion and self-hatred. Initially I had derived satisfaction from these self-set rules, had lost weight having never intended to lose weight (I just wanted to to 'feel better'). But there came a point of no return. I knew I was too thin. I was feeling unwell. I wanted to be able to break my rules but I couldn't.
I had always had anxiety, but I had felt utterly overwhelmed with anxiety in the months preceding the onset of my AN. The era was 1977 and media images of thin women didn't really exist. However, had such images existed I might have been drawn to them in the context of my illness and concluded at the time that they were the cause of my AN. Who knows?
Nowadays, with the media emphasis on 'perfect bodies', people would consider me to have been the least likely person to develop AN. I have little interest in fashion and beauty, and was a geeky kid with 'tomboy' interests. But, I had always had terrible anxiety, phobias, self doubt and compulsive behaviours. My anxiety escalated following bullying and abuse. The rules of my AN helped me to feel more in control of my anxiety.
So, if we are looking for common themes that apply to people who are at risk of developing AN, then we are probably looking at temperament and character traits, which are in part inherent. Almost any environmental or interpersonal stimulus could serve as 'the final trigger'.
I did note that some comments on your previous post about 'cause' related to bulimia nervosa (BN). There is much more research evidence to suggest a cause-effect relationship between body dissatisfaction and BN than body dissatisfaction and AN. On the basis of this research it is not inaccurate to describe some cases of BN as 'disorders of body image'. But in terms of cases of (restricting?) AN in which the individual becomes totally emaciated, as I did, then I do question the role of 'body image' as a driving factor.
Cause is such a tricky word. I actually tend to compartmentalise it in the opposite direction to Jane - the biology/genetics as the cause, the environment/culture the trigger. I know that non fat-phobia anorexics are supposed to be less common in western cultures, but I've actually met very, very few people who exactly fit the stereotypical view of an anorexic, most others have some awareness that their behaviours feel like a coping mechanism or addiction. I agree with Cathy in that I am probably the last person a member of the general public would expect to develop anorexia, because I'm just not interested in fashion, celebrities, etc. And of course the disorder is not a modern or western phenomenon, where it appears in cultures without an emphasis on thinness, the sufferers just give different reasons for their behaviours. Culture provides the context for our explanations.
I'm also aware that I am someone who really loves clear, factual answers. This has helped me a lot in recovery in learning to think about and find solutions to problems rather than panic, but it's not so great when I end up overanalysing or jumping on something as the answer to all my problems :P so knowing this I am always willing to accept that other people have different view points, and that it is unlikely that there will ever be an absolute consensus as to what causes eating disorders.
Wow, I'm flattered to have made your blog!
Katie, I'm not sure see this from opposite directions. I'm inclined to think of genetics/neurobiology/temperament as predisposing.
Carrie, you said "You don't really see eating disorders in people without the genetic background, but the genetic background alone isn't enough." What did you mean by this? Do people with EDs always have a relative who also had one? If so, how close must that familial relationship be? My daughter has an ED, and I recently discovered that 2 of my husband's first cousins have EDs, but there is no other history of them in either of our families that I know of. Or are you referring to anxiety issues as being part of the genetic background? My mom had anxiety, but no ED.
I thought your post was fascinating. My daughter "switched" from having had AN for years to binge eating. I know that a large percentage of other sufferers do the same thing, usually adding purging as well. So some factors have to account for those "changes" in ED symptoms as well.
Thanks for this post because you actually hit on what bothered me about a lot of the discussion brought on by the anorexia mythbusting post. Whereas I believe that there is a very strong biological component to EDs, I also feel that in the attempt to emphasize the biological aspects of EDs, people tend to grossly over simplify things and we end up with a narrative that looks something like: person with genetic predisposition gets hit with trigger, starts on cycle of disordered behaviors that they are unable to break. I know I'm oversimplifying too, but I think that trying to create a neat and simple narrative like this just doesn't work. It ignores the complexities of this disease and the many, many different ways that people experience it. Yes, there are many similarities but there are also quite a few differences. And I think it does an injustice to both science and people with ED to look at all these different manifestations of EDs and claim there is one root cause that will always present in the same way in every sufferer. Science and disease are just not that simple.
I think your cake analogy is so right--there are many, many ingredients that go into the mix and it's impossible to look at one thing and say it's the be-all and end-all cause.
I love a good debate and I'm rather interested by Jessa's response (above). Research and treatment of mental illness, and the DSM in particular, classifies such illness into discrete categories. The inference is that a person has a specific disease that is attributed to a specific 'fault' in the brain that can be corrected by taking drugs X + Y, and by following a specific programme of psychological therapy.
Such a model applies much better to physical illness than to mental illness. I am very much against a 'one-size-fits-all' approach to mental illness (as well as the over-use of medication) because we are each, after all, unique human beings with varying degrees of intellect, temperament and education. We each have a unique family and cultural background, interpersonal experiences etc.
I would never have recovered without a lot of one-to-one therapy to 'get to the roots' of my difficulties. Re-feeding alone never worked, but re-feeding AND tailored psychological therapy DID work.
I have many of the character traits that are purported to pre-dispose one to anorexia nervosa (AN) (i.e. anxiety, perfectionism, obsessions, compulsions, tendency towards depressive mood and many autistic traits), but there were specific mental barriers that I needed to work through in recovery, like coming to terms with having been bullied and abused (and associated PTSD), and dealing with my social anxiety and all the other issues that deeply and negatively affected my sense of self.
So I guess that what I am saying is that I agree that there is no single model/personal experience of AN or other EDs as categorised by DSM IV/V. The stereotypical behaviours of AN are very similar, but they can have hugely different personal 'meanings' to each and every individual.
Brilliant, as always. :)
Jessa,
You raise some good points--some people aren't going to find the biological model of EDs useful, just as I don't find the cultural model of EDs useful. You're right, there have been trends that have been trying to identify the biological basis for many mental illnesses, just as there are trends for many things in science. I am a scientist at heart and so this is probably a little biased, but I think science gives us the best shot at learning what is actually going on in the mind and body that results in an eating disorder. Science can't say anything about the meaning of ED symptoms and how a person integrates their experiences in their life.
Kristine,
What I meant by that was that many people engage in disordered eating behaviors, whether intentionally or not. But there must be some explanation why most people return to somewhat normalized patterns of eating (or at least less pathological) whereas those with EDs don't.
The switching between different diagnosis (known officially as "diagnostic migration") is one of the big scientific mysteries in eating disorders. Some have proposed that we don't subtype between eating disorders (ie, anorexia and bulimia) because crossover is so common. No one knows why it happens.
A family history of anxiety I would count as part of the genetic background. Besides other relatives with EDs, the strongest predictor of a future eating disorder is childhood anxiety.
I like your baking analogy! I think you're right that most of us like to hone in on "causes." We want to know WHY. We hope that if we find out why, we'll be able to solve the problem and move on. The thing is that eating disorders are so complex. I still don't know exactly why, except that I had the right (or wrong, depending on your perspective) ingredients, combined with the identity crisis at the age of 17-18. I was actually thinking today about how I wouldn't really know what to say to someone struggling and looking to get out of anorexia. It's still sort of a mystery to me. That unnerves me in a way, and humbles me to the complexities of eating disorders. It's funny that people try to simplify something that is really so complex that even those of us who suffer can't put our fingers on a "why" most of the time. I've stopped harping on cause and, instead, looked at my reality and how to be healthy. Seems to be going OK :)
I don't have anything constructive to add, I just wanted to say that I love your baking analogy. I appreciate that you focus on the scientific side of things, Carrie, especially when EDs are so often explained away with talk of only environmental factors. Thank you for dedicating your time and efforts to this lovely blog.
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