Roberto Ferdman recently wrote an article for the Washington Post titled “Why you shouldn’t blame yourself for binge eating.” Long story short, Mr. Ferdman concluded:
“… the next time you find yourself in a rut, and eating too much, know that the unbecoming scene isn’t merely a question of will power – it’s rather, in all likelihood, a matter of your genetic makeup.”
In other words, it’s not you being “lazy” or “weak-willed” or a “bad decision maker” that is causing you to binge-eat. Your binge eating is a consequence of your genes – “a matter of your genetic makeup.”
This claim is one of a growing, widespread belief that the definitive way of understanding psychological disorders is by identifying biological correlates and pathologies. However, the evidence strongly suggests that this belief is wrong and dangerous.
Below, I discuss three general topics. First, I discuss the significance of the issue. To do this, I briefly discuss the power of beliefs as well as some theory surrounding biological explanations of psychological disorders. I’ll also touch on the importance these theories have to individuals struggling with psychological disorders. Second, I discuss the stigma surrounding psychological disorders. Here, I try to relate how the strong emotions related to this topic contribute to the motivation to explain maladaptive behavior as biologically determined. Third, I examine the evidence Ferdman used to justify his claim that binge eating is caused by genetics. I will discuss the study he referred to, some important methodological features involved in determining the genetic contribution to psychological disorders, and some sociological features of behavioral genetics. What I want to show is that this article dramatically exaggerates the genetic contribution to binge eating and that this type of presentation is probably harmful to the individuals struggling to overcome their psychological challenges.
Ferdman’s article has the potential to change what individuals believe about binge eating. That’s why he urges his readers, “…next time you find yourself in a rut, and eating too much, know that the unbecoming scene isn’t merely a question of will power…” Ferdman is suggesting to his readers that struggle with binge eating not to beat themselves up – at least not nearly to the extent they have in the past. And they shouldn’t beat themselves up for binge eating because it’s not really in their control. Their genetics are causing the behavior. So, Ferdman appears to reason, even if those who binge eat cannot change their genetics, they can change how they evaluate their behavior.
There’s a lot I admire about this approach (and plenty I don’t, as I’ll discuss below). Centrally, Ferdman is pointing out that what individuals believe can have significant impacts on what they think, feel, and do. So, if Ferdman is successful in changing what his readers believe about binge eating, this could powerfully change how they think of themselves. Maybe they won’t beat themselves up or at least beat themselves up less.
Before I discuss the evidence involved in Ferdman’s article, I want to establish the powerful impacts an individual’s beliefs can have.
Consider the placebo effect. The “placebo effect” is a well-studied, and powerful, phenomena. In short, people who are given placebo treatments – whether a pill, a cream, or even types of surgery – often get as better as those given the supposedly efficacious treatment (Kirsch, 2010).
Precisely how placebo’s work is still an open question. Nevertheless, researchers have some good hypotheses. Montgomery and Kirsch (1997) argued that placebos involve the beliefs – the expectancies – of those who take them. The power of expectancies is extraordinary. Consider a powerful passage from a placebo expert at Harvard: “Although placebo responses generally mimic the effects of the active drug, when people have response expectancies that are contrary to the pharmacological effects of the active drug, their response to placebo is consistent with their expectations rather than with the drug’s pharmacological effects” (Kirsch, 1985, p. 1192). In other words, the placebo effect is so strong that even when individuals are administered a drug that is, for example, a stimulant, if they are told the drug is a depressant, their expectancy to feel depressant effects can trump the pharmacological effects of the stimulant. Further, many studies have shown that individuals administered placebo’s exhibit measurable biological effects comparable to actually taking a drug. So, for example, when individuals are given caffeine they exhibit particular measurable biological changes. They also exhibit these changes when they are told they are being given caffeine which, in fact, is just placebo. This suggests a “mind/body interaction that is guided by subjective factors, such as expectations, beliefs, meaning, [and] hope for improvement” (Beauregard , 2007, p. 227).
In psychological disorders, the power of the placebo effect has been extensively examined in, among other studies, randomized controlled trials (RCTs) of antidepressants. Oddly, there is no clinically meaningful difference in the improvement between individuals taking antidepressants and individuals taking placebo pills (Moncrieff & Kirsch, 2015). That is, in RCTs, individuals taking placebo pills improve nearly just as much as individuals taking powerful psychotropic medications. This may come as a shock to those of who’ve been repeatedly exposed to commercials portraying depression as a chemical imbalance – a theory that, despite its prevalence, has next to no evidence supporting it (Schultz, 2015). It may also come as a shock to see once again how powerful the placebo effect can be.
Other areas of research also demonstrate the power an individual’s beliefs can have. For example, one important feature of cognitive-behavioral therapy is that individuals struggling with psychological disorders often have a variety of troublesome beliefs which significantly contribute to their problems (Beck & Dozois, 2011) Nearly fifty-years ago, psychological theories identified that individuals who experience clinical depression frequently hold a cluster of beliefs such as “I can’t stand myself because” or “I’m no good” or “I’ll never amount to anything” (Beck, 1963; Ellis, 1962). It’s not that these individuals consciously choose to believe phrases like these. These beliefs are generally automatic – they’re deeply rooted habits. Nevertheless, these beliefs can be changed – and new, more positive and adaptive, emotions tend to follow.
Finally, beliefs can impact our behavior even when those beliefs are about very abstract subjects. For example, Baumeister (2008) reviewed numerous studies which demonstrated that participants who are induced to disbelieve in free will (usually by reading passages which argue there is no free will) are not only significantly impacted by these abstract beliefs but often in negative ways, such as increased cheating and aggression and less willingness to help others.
So I hope the above has shown that beliefs can have powerful consequences. Now I’d like to tie this discussion in more directly with the Ferdman article.
Individuals have beliefs about lots of different things. Critically, individuals have beliefs about psychological disorders, such as beliefs about what causes psychological disorders. Research on the effects these types of beliefs have is only about five years old, but the studies conducted thus far have consistently found that individuals who believe their psychological disorder(s) is caused by purely or primarily biological causes have increased prognostic pessimism (they believe they are less likely to get better) and are less likely to seek psychotherapy (Lebowitz, 2014).
Increased prognostic pessimism is an important consideration in clinical practice. Recall the discussion above: we just finished reviewing a variety of different ways in which beliefs have significant consequences. In this case, the research is fairly conclusive that the same holds with individual’s beliefs about whether or not they will improve in treatment. That is, an individual’s expectancy of getting better influences whether or not they in fact do get better (Constantino, 2012).
Now we’re finally in a position to see the significance and the danger of Ferdman’s article. Explaining to someone struggling with binge eating that their binge eating is “part of their genetic makeup” probably contributes to a belief something along the lines of “this is just how I am” and implies that their binge eating will be unlikely to change. This, in turn, can increase their prognostic pessimism and discourages psychotherapy [probably because someone struggling with binge eating who also believes a genetic explanation might wonder: “How is talking to a clinician going to change my genes?” (Kemp, Lickel, & Deacon, 2014)]. And since an increase in prognostic pessimism is related to worse treatment outcomes, a genetic explanation of binge eating can have a significant negative impact on treatment outcomes. That’s not good.
An important, but mostly implicit, theme of Ferdman’s article seems to be that understanding, not blaming, is important when considering individuals struggling with binge eating. And so he argued, “people…turning to binge eating when they’re depressed, are not merely demonstrating a lack of willpower…They’re engaging in a biologically driven behavior” and “depression and binge eating share a deep, biological relationship that might explain why some of us will finish a box of Oreos after a tough day at work” and those who binge eat “are likely wired to.” In each of this quotations, an underlying idea is that we should move beyond thinking of binge eating as being weak willed or undisciplined. We should move beyond thinking in this way because a deeper understanding of what is actually causing binge eating, the article claims, is our “genetic makeup.” Since individuals are not responsible for their genetic makeup, they aren’t responsible for their binge eating. Thus, just as we would for anyone else who is subject to the misfortune of fate, it makes sense to adopt an empathetic, not accusatory and judgmental, approach to individuals struggling with binge eating,
There are at least two important considerations on the above. First of all, a biological understanding of psychological disorders is not the only way to combat stigma. We can adopt a compassionate attitude toward those struggling with binge eating even if we don’t also accept the view that their binge eating is biologically determined. For example, individuals who binge eat may simply not know other ways to manage their emotions or they may be dealing with a variety of stressors which overwhelm their ability to cope in a more adaptive way. Neither of these views suggests that the proper attitude is to judge and chastise individuals who binge eat as being weak willed.
On the other hand, they suggest a variety of approaches, such as psychotherapy, behavioral changes, or social interventions. Evidence strongly suggests these can be helpful. For example, a recent study by Kristeller, Wolever, & Sheets (2014) achieved a 95% remission rate in binge eating disorder via mindfulness psychotherapy. Meta-analytic findings suggest that psychotherapeutic interventions for binge eating consistently produce large treatment effects (Godfrey, Gallo, & Afari, 2015; Hilbert, Bishop, Stein, Tanofsky-Kraff, Swenson, Welch, & Wilfley, 2012).). The powerful effectiveness of psychotherapeutic interventions for binge eating is a curious finding for behavior that Ferdman argued is determined by our genetic makeup.
Now to the second consideration regarding stigma. Although it makes sense to think that understanding binge eating (or other psychological disorders) as biologically driven pathologies would lessen the stigma associated with those who do so, there is reason to believe that attributing psychological disorders to biological causes does not simply and easily reduce stigma. Many studies have found that biological etiologies of psychological disorders are unlikely to be a cure all for stigma (Kvaale, Haslam, & Gottdiener, 2013). In fact, other studies suggest that explaining psychological disorders via biological explanations can increase stigma (Speerforck, Schomerus, Pruess, & Angermeyer, 2014). Thus, although it makes sense that attributing psychological disorders to uncontrollable features of an individual’s biology would lessen stigma, the research suggests that this is not the case.
Regardless of the power of beliefs, the clinical effects of biological explanations, or the complexities surrounding stigma, what about the evidence that binge eating is caused by our genes? That is, if it is the case that binge eating really is caused by genetic makeup, then the considerations above, though interesting, probably aren’t crucial.
In his article, Ferdman placed the entire weight of his assertion about genetics on one study (Racine, Keel, Burt, Sisk, Neale, Boker, & Klump, 2013). In order to critically assess the article, it’s important to understand how studies like Racine et al., (2013) attempt to show that genetic makeup is a contributing factor to a psychological disorder. (I’m going to leave aside, for now, the fact that no study I’ve ever reviewed makes claims that genetics determine psychological disorders in the way Ferdman suggests. Psychiatric genetic research is modest and only suggests a genetic contribution, not a genetic determinate.)
For quite some time, psychiatric researchers have been trying to identify genes responsible for psychological disorders. This process has, more or less, been a failure. No psychiatric disorder has been reliably associated with genetic findings (Deacon, 2013). Psychiatric researchers now conduct genome-wide association studies (GWAS) to see if large sample sizes lead to the identification of clusters of genes that are significantly more common in individuals diagnosed with a psychological disorder than in those not diagnosed. With such large sample sizes, it is not uncommon for researchers to identify statistically significant findings. However, these findings almost always fail to replicate and, even if they did, the increased risk of psychological disorders related to the cluster of genes, although statistically significant (unlikely to be due to chance), does not make a significant real world impact.
For example, large GWAS studies on schizophrenia – the psychological disorder with the largest research base and the strongest evidence for being a genuine biological disease (though even this evidence is surprisingly weak) – are only able to identify genes which account for “1.1% of the absolute risk” of an individual being diagnosed with schizophrenia (Gratten, Wray, Keller, & Visscher, 2014).
The evidence for a genetic contribution to other psychological disorders is even worse. For example, Ripke et al., (2013) described how, though the authors conducted the largest ever GWAS of major depression, they were “unable to identify robust and replicable” genetic markers.
Although the genetic search has failed, researchers continue to persist, arguing that more research will eventually make real gains. An important component of the belief that GWAS will finally yield results is rooted in the twin study methods. It is commonly thought that twin studies suggest a genetic component of psychological disorders. For example, the classical twin method compares concordance rates – if one, both, or neither twin is diagnosed with a psychological disorder — between identical twins (monozygotic twins [MZ]) and fraternal twins (dizygotic twins [DZ]). MZ twins share 100% the same genes. DZ twins share about 50% of the same genes. Crucially, in twin studies, the twins are raised in the same environment. Thus, if it turns out to be the case that MZ twins reliably have higher concordance rates of, for example, binge eating, than DZ twins, then this would seem to count as evidence that there is a genetic component to binge eating. In other words, if twins who share 100% of the same genes as well as the same environment are more concordant than twins who share 50% of the same genes as well as the same environment, then a plausible explanation of the elevated rates of concordance is the higher level of genetic similarity.
Even if we grant all of this (which we won’t, see below) the language of the article is still misleading. It’s misleading because even the Racine et al., (2013) study results show that there is not anywhere near a perfect concordance rate between MZ twins. Less than half of MZ twins both participate in binge eating. In other words, it’s common for one on the MZ twin pair to binge eat while the other twin does not. If genetic makeup is causing binge eating, why are twins with 100% of the same genes not having 100% of the same binge eating rates? There’s no question that any sort of genetic deterministic claim from Ferdman overstates even his own evidence.
Nevertheless, the Racine et al., (2013) study does seem to show that MZ twins have higher concordance rates for a variety of psychological features, including binge eating, than DZ twins. So, although it’s clear we should reject Federman’s stronger claim — that genes determine binge eating — we could adopt a weaker claim that genes somehow contribute to binge eating.
However, there is an important argument that challenges even this weaker claim. The crucial assumption of the classical twin method is that MZ and DZ twins share an equal environment (Joseph, 2014). At first glance, this seems fairly straightforward. In the studies, both the MZ and the DZ twins are raised in the same household – so it’s close to a brute fact that they share equal environments.
However, many decades ago it was strongly argued that MZ twins share a much more similar environment than DZ twins. MZ twins have an “ego fusion” that is greater than DZ twins. That is, they are treated more alike, found together more often, and share more similar experiences. In short, MZ twins have a more similar environment than DZ twins and, thus, it could be the more similar environment causing the more similar concordance rates.
Jackson (1960) provided support for this argument in a number of ways. For example, he pointed out that female MZ twins were consistently more concordant than male MZ twins. This high concordance level couldn’t be because of genetic factors – whether male or female, MZ twins have the same genetic makeup. So what might cause the greater concordance rate? A variety of environmental factors, such as the fact that females (at that time) may have shared more similar environments because of being kept indoors more often than males and increased female closeness being more accepted than male closeness (which could be seen, in Jackson’s words, as “sissy” and “homosexual”).
A similar line of reasoning applies to the numerous other observations Jackson (1960) pointed out: that DZ twins were more concordant than siblings (despite the fact that DZ twins and siblings share approximately the same level of genetic similarity); that female DZ twins were more concordant than male DZ twins; and that same-sex DZ twins had higher concordance than opposite-sex DZ twins (Joseph, 2001). In each of these observations, the genetic hypothesis cannot explain the higher concordance rate while the environmental hypothesis has, at least, a plausible chance to (for those interested, Joseph (2014) discussed psychiatric research and twin studies in exhaustive detail).
But if the argument against the equal environment assumption is so strong, why do genetic accounts of psychological disorders continue to be so popular? Panofsky (2014) provides, I think, a good working hypothesis. He provided a detailed account of the history of behavioral genetics and its prominent advocates. In that history he explained that the behavioral geneticists “main techniques for demonstrating genetic influences on behavior – twin and adoption studies and the estimation of heritability – had been criticized and undermined from seemingly every possible angle” and they had not been able to produce adequate answers to these criticisms (loc. 2839). This prompted him to ask, “Facing these conditions, how could behavior geneticists promote genetics in psychology-the field from which most hailed-and other behavioral sciences?…[They] turned their weaknesses into strengths…they directed their attentions outward, seeking attention and recognition …[They] made it possible to use their tools without having to join their field or assume their identity. They accumulated findings that gave behavior genetics an imprimatur of scientific successes without addressing the fundamental critiques. Indeed, to this day the basic premises of behavior genetics’ claims and techniques are still controversial across the sciences” (loc. 2839). In other words, behavioral geneticists general response to the methodological criticism of their work was to complete more and more research which could be integrated with more and more disciplines. The breadth of their work covers the lack of depth associated with the methodological problems of the discipline.
Concretely, you wouldn’t know these types of problems existed by reading Ferdman. What you’d learn from him is that binge eating is a result of your genetic makeup: studies (study, really) show!
I think at least one of the factors involved here is that medical science has been very successful in treating medical conditions and we’d like that success to translate into increased understanding and treatment of psychological disorders. After all, many believe that human beings are, fundamentally, biological entities (that’s what I believe, at least) and so it makes sense to try and find biological causes for our psychological disorders. I’m sure that biological research can inform our understanding of psychological disorders. But I think it’s unlikely biological findings will ever explain psychological disorders. This is a topic far outside of the range of this piece, so I’ll conclude with a passage that captures at least one of the reasons for my thinking:
We should remind ourselves that, despite the unpopularity of dualism in mental health science, a distinction between mental and non-mental somatic or physical disorders is widely accepted within medicine… Does it imply that the mental is something non-physical? No, it does not…The world in which we live in is a hierarchically layered or multi-leveled world…Physics describes the most basic or general level, chemistry a level about that, and biology, psychology, and sociology each describe successively higher and more abstract and specialized levels…We persons are special or distinct in our detailed multi-level complexity…So to be us ultimately is to be physically based or realized. This does not mean, however, that each and every activity, state, aspect or component of us can be exhaustively or completely described in lower level physical scientific terms. (Graham, 2010, p. 87)
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Mad in America hosts blogs by a diverse group of writers. These posts are designed to serve as a public forum for a discussion—broadly speaking—of psychiatry and its treatments. The opinions expressed are the writers’ own.