January 22, 2015

An Exploration of Weight Bias in the Primary Source Literature

by Health At Every Size® Blog

by Annie Goldsmith, RD, LDN

Recently, a research article with an interesting title landed in my inbox: “Metabolically Normal Obese People are Protected from Adverse Effects Following Weight Gain¹”. As a Dietitian who works from a Health At Every Size® perspective, it certainly caught my eye! At first scan, the article appeared to support what I already believe to be true: weight as an isolated variable is not a predictor of heath risk or outcomes. However, as I read closer, my heart began to sink. I found in this article what I so often find in the world around me: a blatant, unfounded weight bias.

The Study: The Bare Facts

Before I launch into commentary, I’ll present here the objective facts of the study design and the authors’ conclusions. The sample consisted of 20 participants identified to be obese and divided into two groups: Metabolically Normal Obese (MNO; n=12) and Metabolically Abnormal Obese (MAO; n=8). The marker used to classify the participants as MAO was increased intrahepatic triglyceride (IHTG), which is associated with adverse metabolic effects such as insulin resistance and cardiovascular disease risk factors. The question the authors investigated was whether the MNO group was somehow protected from adverse metabolic outcomes as compared with the MAO group when both groups gained a similar amount of weight. They also were interested in the possible mechanism driving any differences between the groups.

In order to test their hypothesis, the authors instructed each group to consume 1000 extra kcals per day from one of 5 restaurants: McDonald’s, Burger King, KFC, Pizza Hut and Taco Bell. The subjects continued on with this diet until they had gained ~5-7% of their original body weight and maintained it for 2 weeks. The authors then re-tested IHTG and associated metabolic risk factors. Results showed that the MNO participants displayed no adverse metabolic effects from the short-term calorie surplus and weight gain, while the MAO did suffer increased risk factors. The authors concluded, “MNO people with normal IHTG content represent a distinct phenotype and are not simply in a transition phase toward MAO¹” In other words, the results suggest that obesity alone is not an indicator that can be used to identify heath risk!

The Study: The Underlying Message

At first pass, this study might seem encouraging – one more result to add to the mounting body of work that demonstrates the obesity researchers need to ditch this weight bias thing once and for all. However, what the bare facts don’t reveal, the specific language the authors use surely does. They write in the introduction that a primary purpose of the article is,

“To evaluate some of the putative molecular mechanisms in adipose tissue responsible for the adverse metabolic effects of weight gain.¹” (italics mine).

This statement is made before collecting one ounce of data! The authors simply want to see if the results will help them explain the weight-related mechanism for poor health – whether or not it exists at all is never questioned.
The assumption that weight is the causative factor for poor health drives this article forward, and it is particularly evident in the discussion (where the authors have freedom to speculate!). They spend an entire paragraph hypothesizing about,

“…the cellular mechanisms responsible for the differences in metabolic function between MNO and MAO people.¹”

(spoiler alert: adipose tissue is implicated). However, they ultimately concede that the mechanisms are “not clear”. Then there’s the kicker: after being forced to conclude that MNO people are in fact phenotypically different from MAO people (in other words: healthy), the authors throw in for good measure,

“Nonetheless, we cannot exclude the possibility that our MNO subjects would develop metabolic abnormalities with greater weight gain.¹”

Wait – what?? The data reveal a perfectly clear outcome, and the authors undermine the entire result with one throw-away statement. Which, by the way, is quite useless and absurd. What do they think would happen to any of us at ANY BMI if we overate fast food into the unforeseeable future?  (Morgan Spurlock gave us a pretty good idea in his movie “Super Size Me” – and he started out in perfect health!)

A Missed Opportunity

Sadly, a study that started out with potential ended as a missed opportunity. What might the authors have found if they had controlled for the myriad of confounding variables left glaringly unaddressed in the research design? Not one mention is made of how lifestyle factors such as eating habits, physical activity, sleep hygiene, and stress management might have contributed to the differences between groups. Or how about genetics? Family history is not mentioned either. I will go out on a limb and make some speculations of my own: it’s very likely that had the authors been able to see past their blind certainty that weight alone is the mediator of disease risk, they might actually have tapped into some of the possible underlying factors differentiating the MNO and MAO groups. Additionally, conspicuously absent are control groups of metabolically normal and metabolically abnormal normal-weight participants. Thin people who are sick exist in this world too! What impact would a steady diet of Taco Bell have had on them? We can only speculate.

In their wonderful article “Weight Science: Evaluating the Evidence for a Paradigm Shift²” Linda Bacon and Lucy Aphramor state,

“Researchers have demonstrated ways in which bias and convention interfere with robust scientific reasoning such that obesity research seems to ‘enjoy special immunity from accepted standards in clinical practice and publishing ethics.’ “

Here we see an example of such research. Until there is a shift in how society as a whole – or at least the scientific community – views the relationship between weight and health, NIH funding will continue to be wasted on superfluous studies that tell us what we in the HAES® community already know: weight is not a proxy for health.

References

1. Fabbrini, E et. al. Metabolically Normal Obese People are Protected from Adverse
Effects Following Weight Gain. J Clin Invest. doi:10.1172/JCI78425: 2015.

2. Bacon, Linda and Aphramor, Lucy. Weight Science: Evaluating the Evidence for a
Paradigm Shift. Nutrition Journal 2011, 10:9

Annie Goldsmith

Annie Goldsmith is a Registered Dietitian practicing one-on-one nutrition counseling in Charlotte, NC. She has an undergraduate degree in Brain and Cognitive Sciences, a field she was drawn to because she possesses an infinite curiosity about that place where biology and psychology come together to guide behavior. Her transition to a career in nutrition was a natural one, as she believes that how we choose to feed ourselves is deeply rooted in human physiology and psychology. She sees health as multidimensional, and has embraced the HAES® philosophy in her own practice. When not working, Annie spends time hanging out with her wonderful husband Brian and their intrepid cat, Chicken.

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