the HAES files: Uncommon knowledge about changes in body weight–part 2

by Health At Every Size® Blog

by Lily O’Hara, BSc, Postgrad Dip Hlth Prom, MPH, PhD (c)

In Part 1 of this article I addressed some of the less well known contributors to increased body weight, including the strong role played by genetics, proteins and bacteria in the gut, and infections with bacteria and adenovirus. I also discussed factors such as inadequate sleep duration and quality, chronic work or life stress, and exposure to endocrine disrupting chemicals. Finally I discussed the studies that demonstrate the contribution of dieting and weight control behaviors to weight gain. In part 2 of this article, I examine a range of environmental factors and their contribution to increased body weight. The article draws on the PhD thesis I am currently completing, and is therefore written in an academic tone, and includes a number of references.

In recent years, antiobesity researchers, policy makers and health professionals have increasingly pointed to the contribution of environmental change to the obesity epidemic [1-8]. So called ‘obesogenic’ environmental factors are most commonly described as those environmental factors that contribute to changes in nutrition and physical activity – the ‘Big Two’ [9] – by making unhealthy behaviors the easy or default choice for people [6]. On the nutrition side, ‘obesogenic’ environmental factors are purported to include the heavy promotion of fast food, energy dense snacks and sweetened beverages, the ready availability of these foods in schools, the low cost and large serving sizes of these foods, the density of fast food outlets in poor neighborhoods, the high cost of fresh foods, the lack of time to prepare fresh meals and the reduction in family meal time. On the physical activity side, ‘obesogenic’ environmental factors are purported to include changes to the urban environment and perceptions of safety which have led to reduced use of active transport, increased car use, reduced outdoor play and increased indoor (sedentary) play and recreation, technological advancements which have resulted in reduced need for physical activity and increased opportunity for sedentary behaviors at home and at work, and reduced time dedicated to physical activity in schools.

The arguments for the ‘Big Two’ [9] ‘obesogenic’ environments have relied on a combination of ‘common sense’ about presumed mechanisms of action together with results from ecological studies that show associations between the specific ‘obesogenic’ environmental factors and aggregate population rates of ‘obesity’ prevalence or incidence. However critics point out that correlation is not the same as causation [10] and the ‘ecological fallacy’ refers to the inability of ecological studies to attribute any causal relationship between exposure to any putative ‘obesogenic’ factor and the development of disease in individuals [11]. As such these studies are considered to be useful for generating hypotheses about the causation of changes in body weight and health outcomes, but not for testing them [11].

Only a small number of scientific studies have investigated the relationship between ‘obesogenic’ factors and their purported ‘obesogenic’ behavioral correlates. A systematic review of 28 studies examined the relationship between physical, social, cultural and economic environmental factors, ‘obesogenic’ dietary behaviors and body weight in adults [3]. BMI was consistently associated with the food environment, whereas ‘obesogenic’ dietary behaviors were not. Living in a socio-economically deprived area was the only environmental factor consistently associated with ‘obesogenic’ dietary behaviors. There were no other consistent relationships between ‘obesogenic’ environments and ‘obesogenic’ dietary behaviors.

On the physical activity side, ‘obesity’ researchers and public health policy makers have focused a lot of attention on the physical environment and its relationship with active transport (walking or riding a bicycle as a means of transport rather than for recreation or leisure). The assumption, based on ‘common knowledge’ about the relationship between physical activity and body weight, is that people who use active transport are more physically active than those who don’t, and will therefore have lower body weight. This ‘common knowledge’ has been tested in numerous studies, and the findings are at best equivocal. A recently published systematic review of studies focused on adults concluded that there is “limited evidence” that active transport is associated with more physical activity or with body weight [12]. A systematic review of the evidence with respect to active school transport by children and adolescents showed that children who walked or rode their bikes to school tended to be more physically active overall than passive commuters, however only one study of the 10 that examined the effect showed any impact of active school transport on body weight. The authors concluded that “evidence for the impact of active school transport in promoting healthy body weight for children and youth is not compelling [13].

These studies on just a few select components of the Big Two ‘obesogenic’ environments show that the ‘common knowledge’ about the environmental influences on eating and physical activity, and therefore on body weight, may not be quite as straightforward or simple as portrayed. Although the research literature and public health policy continues to be dominated by the Big Two, some studies have examined other factors for their potential effect on body weight. The remainder of this article focuses on these factors.

A narrative review of ‘obesogenic’ environmental factors beyond the Big Two proposed 10 factors for which there is strong evidence of a causative role in increased average weight in the population [9]. In addition to sleep debt, exposure to endocrine disruptors, and in-utero effects of under and over-nutrition discussed in part 1 of this article, the review found strong evidence of a range of other environmental and social factors that contribute to increased body weight.

Reduction in variability in ambient temperature has resulted from increases in the temperature control of living, working and leisure environments. The ‘thermoneutral zone’ is the range of ambient air temperatures in which the body does not need to expend any energy to remain at a comfortable temperature. Ambient temperatures outside of this zone – too hot or too cold – require energy expenditure, and spending time in temperatures above the thermoneutral zone also reduces food intake. As countries become more industrialised, the proportion of homes with central air conditioning increases, and people spend more time in the thermoneutral zone. The energy expenditure required to maintain physical comfort has therefore been significantly reduced and the review authors propose that this reduction has contributed to increased body weight [9].

Another widespread social change, in western countries in particular, is decreased smoking rates. Nicotine has a thermogenic (heat generating) effect and is also well known as an appetite suppressant, both of which contribute to body weight regulation. Smoking rates have decreased steadily since their peak rates in the 1940s and the Centers for Disease Control and Prevention in the US estimate that the reduction in the prevalence of smoking has made a significant contribution to increases in average body weight [9].

Increases in the prescription rates of medications that lead to weight gain is proposed as a likely cause of population weight gain [9]. Medications known to contribute to weight gain include antipsychotics, antidepressants, mood stabilizers, anticonvulsants, antidiabetics, antihypertensives, steroid hormones, contraceptives, antihistamines, protease inhibitors and HIV antiretroviral drugs. Most of these drugs have either been introduced to the market in the same period that average body weight increased, or their use increased dramatically. The authors therefore regard the case for this putative cause as very strong.

Demographic changes have also been proposed as likely candidates for increased average body weight at the population level [9]. These include changes in the distribution of ethnicity and age, and increased average age of childbirth, all of which are associated with increased average body weight.

Finally the authors of the review point to biological factors related to mating that may have contributed to increased average population weight [9]. Firstly they present evidence that there is a reproductive selection bias for higher BMI, which means that fatter people are more likely to have more babies, and that this genotype is therefore more likely to be passed on to their offspring. Secondly, they propose that assortative mating means that there is a higher probability that phenotypically similar individuals will mate – in other words that fat people are more likely to mate with other fat people [9].

A recent study proposed that increases in acidic load from rising atmospheric carbon dioxide have contributed to increases in average weight for humans [14]. A large study published in 2011 examined changes in average mid-life body weight over the past few decades of over 20,000 animals from 24 populations living in close proximity to humans including primates and rodents in research colonies, domestic dogs and cats, and feral rodents [15]. Across all of the animal populations studied there were significant increases in average mid-life body weight, providing further evidence that the aetiology of increasing body weight is not yet well understood.

Despite the significant body of evidence on the contribution of genetics and a multitude of other factors to weight gain, antiobesity researchers and policy makers continue to posit the ‘common knowledge’ that eating too much and moving too little results in fatness, and that people have the capacity to consciously change these behaviours and thereby change their body weight. This two part article sheds light on some ‘uncommon knowledge’ about factors that contribute to body weight at the individual and population levels. Already it is clear that ‘common knowledge’ about body weight is about as accurate as the 16th Century ‘common knowledge’ that the sun revolves around earth. No doubt, with the enormous sums of money currently being invested in ‘obesity’ research, we will witness even more discoveries that shed new light on the incredible complexity of body weight regulation.

Please click here to access the numbered references.

Lily O'Hara_3Lily O’Hara, BSc, Postgrad Dip Hlth Prom, MPH, PhD (c)  is the Section Head for Health Promotion, Health Authority – Abu Dhabi.  Lily  is passionate about social justice and the need for health promotion to be truly health promoting. Lily has worked in health promotion positions with government, non-government, university, private and community organisations for over 25 years. Lily has been in her current role with the Health Authority – Abu Dhabi since January 2011. Prior to that she spent 13 years as an academic at the University of the Sunshine Coast, Australia, where she established, taught in and led the health promotion and public health undergraduate and graduate programs. She and a colleague have developed and tested a new model of health promotion called the Red Lotus Health Promotion Model, which is the first health promotion model to explicitly incorporate a system of values and principles. Lily has held leadership roles in a number of scientific associations including the Australian Health Promotion Association (National President) and the Association for Size Diversity and Health (International Vice President). And a recipient of  the National Association to Advance Fat Acceptance International Size Acceptance Trailblazer Award for diligent work in bringing  the HAES® message to colleagues in the health education field.

16 Responses to “the HAES files: Uncommon knowledge about changes in body weight–part 2”

  1. There is some serious cherry picking of evidence going on here. While dismissing the idea of an obesogenic environment without much discussion, you have also failed to mention data from agriculture that shows the amount of calories that are being put into the market and consumed have risen dramatically since the 1980s. See Stephen Guyenet and his work on sugar, for example.There is also no discussion here of the role that poverty plays in obesity, or of the growth in food and snack advertising budgets over the past 30 years, or the changes in dietary habits that they have driven, some of which have been egregious, such as the rise in snacking, eating on the run and outsourcing food from the home kitchen.

    Far from relying on ‘common sense’ there is a huge body of reliable information about this. Much of it is to be found in government statistics, particularly of agriculture.

    While anti-psychotics, anti-depressants and the like are well known causes of rapid weight gain, you would need to show that a very significant portion of the population was taking them to suggest that it’s these drugs that have led to a massive rise in body weights. Simply pointing out that they have entered the market and suggesting a correlation doesn’t prove anything about their impact on the population at large. (The original paper is not linked – if they have made the above case, then surely you need to also make it.)

    This appears to be written with a very clear agenda: to decouple the idea of food intake from obesity. It may be that there are endocrine disruptors that are largely responsible for the rise in weights. This paper does not prove that, however.

    • Anna, there are some good points here for speculating, but the fact is, no one has been able to show that fat people eat more/differently/in a different pattern than thin people – dieters certainly do, and that is often conflated with higher weight; and people seeking help sometimes do, which is often overgeneralized to the non-clinical population. Also, your statement “a massive rise in body weights” makes me think you are unfamiliar with the actual data that the average weight rose 10-15 pounds from 1980 -2000 and that is it.

      Perhaps we are all eating more than before but only some people’s bodies are reacting by gaining some weight. There has also been a big rise in the amount of food waste, apparently, as the food supply increased. Hard to parse.

      It may seem like common sense to think that higher weight means someone ate more – certainly we all know if we individually eat less we temporarily lose weight. But it falls apart when you look across individuals – much the same as trying to look at someone’s bank account and make an assumption about how hard they work.

  2. Great work, Lily! So much to digest here. Can you just clarify for me what you refer to with “obesogenic dietary factors”? I just want to make sure I am understanding correctly. Thanks!

  3. I was very interested in your comments about “active transport.” About five years ago, I got rid of my car. Most reasons were economic, but while saving money is really nice, it’s also caused me to learn a lot about self-reliance. I’ve become very resourceful when it comes to getting around. I remember when I first started getting around on foot and on my bike; I thought “I’m gonna lose so much weight!” Well, it’s been five years, and you know how much weight I’ve lost? Not one pound. I thought maybe it was me! It was good to read this and find out that my experience is not unique. It’s got me doing more research on active transport and its effects. Thanks!

    • Stacey, ditto! I started riding my bike again modestly (up to ~20 miles/week at its height) in the late 1990s, then stopped driving for four years ~2004-2009. I used bus only for 1 year (walking a lot to bus stops) and bike/bus for 3 years. I lost no weight. I had to stop biking 3 years ago, and put on ~15 lbs. I’ve read that exercise is more effective as a weight suppressant than for weight loss.

      Thank you for affirming what I experienced when biking.

  4. bodypolitic – actually, there is data that shows that obese individuals under-report calorie intake, and that the idea of ‘slow metabolism’ in obese individuals is a myth. Look up the studies such as Lichtman et al, Lansky et al, Herbert et al, dating back to the 1970s. The reports (e.g. Hanes) that purport to show that obese individuals eat the same or less as normal weight individuals are based on self reporting and are thus suspect.

    You can dispute this body of evidence. In fact, a large scale study would be welcome in the field, because the studies on both sides are problematic.

    The issue with this post is that the evidence is cherry picked. Throwing around studies of genetic propensity towards fat sounds very scientific. It’s true. It’s very clear that genes control fat gain. But this information needs context – the genotype needs the right environment to express an obese phenotype. The evidence, so far, suggests that we are living in that right environment. There is nothing to suggest that we don’t live in an obesogenic environment, where the number of calories available has gone up, the amount of money and advertising available to convince people to eat more has gone up, and so on. Dismissing the ‘obesogenic environment’ hypothesis without considering things like the food environment is pretty lame, to be honest.

    The science has serious consequences for policy. If the sudden and rapid weight gain across the population – and it has been both sudden and rapid – is the result of prescription medication, endocrine disruptors and genotype, then the public health policy solutions should be aimed at the way medicine is practised.

    If, on the other hand, the rapid rise in weight is clearly tied to the economics of food and marketing, then a different policy is required, such as the cessation of farm subsidies.

    There is a strong link between obesity and poverty that has not been touched on in these posts. Obesity is here presented as something random, that may be the result of unnamed, unidentified endocrine disruptors in the environment, or an unspecified number of pharmaceuticals prescribed for an unspecified number of people.

    Fat people are not served by bogus, cherry picked science. Nor is the HAES paradigm.

    • Anna, If you read my post more carefully, I am quite familiar with the “dietary underreporting” research and outlined its methodological flaws. Agree with you that better studies need to be done but until there is evidence of a difference in eating, the burden of proof has not been met. I would also let Lily respond to some of your other concerns because she is quite capable of talking about the SES factors here and has done so elsewhere. Again, I agree that those factors are incredibly important and often overlooked. Did you read Part 1?

      Enjoying your transformation of my user name, too!

  5. Bodypositive – apologies for getting your handle wrong. I did read both posts.

    The dietary intake studies for both camps are either poorly done, or use very small sample sizes. No argument about that. The burden of proof, however, as always lies with whoever is making the biggest claim. To suggest that the accumulation of fat is not driven by energy balance (calories) is a pretty big claim that would overturn a lot of science if it were true.

    • Not really – there is plenty of research showing that calories in-calories out is not the best fit model of mammalian weight dynamics. I would submit that the “common sense” idea that fat people must eat more is a bias, and so it feels like asking people to prove that feels to you like a “big claim.” I think the neutral position is that we don’t know if they eat more until we fins out that they eat more. Thanks for the discussion, you are a thoughtful debater.

      • Hi Deb and Anna,

        What about this study, which shows “obese” women with binge eating disorder who eat less earlier in the day, both on binge and non-binge days, consume significantly more kcals (especially on the day they restrict and then binge the most) than obese women who do not have BED. “Energy Intake Patterns in Obese Women with Binge Eating Disorder,” Nancy C. Raymond, 2003,

        Any thoughts from either of you on the findings, and on the quality of the study, please? The table, and figures 1-5 give a quick overview.


    • Anna – considering the high failure rate of “eat less, move more,” who is actually making the bigger claim here? And certainly, “energy balance” plays a part, but assuming the body is a closed system that responds in a linear fashion to calorie reduction is incorrect. The body adjusts its metabolism to conserve calories. Considering that the much-ballyhooed 20 pound weight gain from a person’s 20s into their 40s works out to an energy imbalance of about a potato chip a day, it’s actually pretty amazing how closely our bodies maintain energy balance. Saying it is all about an “energy imbalance” doesn’t necessarily get at the root causes of how that that energy imbalance occurs.

      • That’s a big leap from talking about calories to the specific advice of eat less, move more. The two are not the same thing. It’s now well known that it’s not as simple as 3500 calories = the loss/addition of one pound.

        That doesn’t mean that the concept of an obesogenic environment can simply be dismissed out of hand, or that calories don’t matter. Calories, even with the above caveat in mind, are basic science. The fact that different bodies process food differently – some people extract more calories from the same food than others, for example – doesn’t change that. It’s still all about energy, it’s just that individual variation has to be recognised.

        You’re quite right when you say that only discussing energy doesn’t get at the root cause of how that energy imbalance occurs. Food is a basic source of energy. The most basic source of energy.

        For that reason, a paper that rejects the notion of the ‘obesogenic environment’ without discussing food can’t be taken seriously. The additional calories that have been pumped into the food system correlate very nicely with the gain in body mass. Indeed, they’re sufficient by themselves to account for much of the increased weight gain seen in the population.

        That doesn’t mean that the other things discussed here aren’t important – gut flora, endocrine disruptors etc etc. The science isn’t settled, by any stretch and the more contributions the better.

      • Ah. Thank you for the clarification, Anna, and forgive me if I misinterpreted your position. (Although I would note that at least in the popular culture it’s not well known that it’s not as simple as 3500 calories = +/- one pound.)

        As a society, we’ve tried laying ELMM on the backs of individuals, but haven’t really taken on food marketing. One has to wonder about the bizarre alliance of food companies + weight-loss companies that all seem to be sponsoring obesity initiatives. Fatten ’em up, slim ’em down, rinse, repeat and count your profits on both the ups and downs.

  6. Very interesting interchange of ideas. Few areas of life are as controversial as body weight, and how people get and stay fat.

    The majority of studies out there are seriously flawed because they start out by asking the wrong questions. That’s just my opinion.

    In grade school you learn to answer the questions the way the teacher wants, and will result in a higher grade, regardless of your own opinions–or else, get a lower grade. Likewise, research grant applicants learn to ask the questions in a way that are most likely to result in funding, regardless of what they would really like to ask.

    I found Lily’s approach to be refreshing. I am sure that given more space, she would have given far more detail about some of the unanswered questions. For contrast, read what a mathematician with the NIDDK has to say about the obesity “epidemic.” Go to:

    At least most experts are beginning to blame our food environment more, and blame fat people less for having a moral failing.

  7. I agree that discussion, debate and research need to occur for so many reasons. Whilst evidence can appear to support ideas that are currently pushed does not make them true, right or real and we all need to keep questioning and exploring. I am currently completing a masters in nutrition and dietetics and I am disgusted at the way nutrition is being taught with no debate or a patient-centred approach is ever considered. If I don’t include weightloss as a desired outcome if someone is at a higher BMI I am marked down to argue against an entrenched meme would be academic suicide at this point. It is immensley frustrating that we are placing people into categories with little to no regard for them as a person and we attempt to use fat=death as a justification for everything we wish them to do despite no evidence their weight is even the problem, much less that weightloss could even resolve their problem. The idea that higher weights have protective outcomes particularly in CVD is dismissed despite the evidence that supports this idea because it messes their mantra that if you’re fat you should just lose weight period.


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