Archive for ‘Lily O’Hara’

May 15, 2012

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

by healthateverysizeblog

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.

May 1, 2012

the HAES files: Uncommon knowledge about changes in body weight–part 1

by healthateverysizeblog

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

The ‘common knowledge’ about body weight is that an increase or decrease in body weight is caused by a simple imbalance between the choices an individual makes regarding energy intake and energy expenditure, and that body weight is therefore ultimately within the conscious control of the individual. Although this mechanistic ‘common knowledge’ about body weight is extremely widespread, it is completely inadequate to explain changes in body weight over recent decades.

There is a growing body of evidence that demonstrates that physiological characteristics such as body weight are not simple at all, but result from complex interactions between genes, other biological factors, behaviours, life course experiences and exposures to biophysical and socioeconomic environments [1-4]. In this two part article, I discuss the contribution of a range of factors to increased body weight, beyond the ‘common knowledge’ of conscious choices about eating and physical activity. I do not explore the contribution to increased body weight of medical conditions such as hypothyroidism, Cushing’s syndrome, etc.

This article draws on the PhD thesis I am currently completing, and is therefore written in an academic tone, and includes a large number of references. (In fact I’ve been writing in this tone for so long now, I don’t really know how to write any other way.)

Before exploring the factors that may contribute to increased body weight at the individual and population levels, it is worth revisiting the evidence about trends in body weight over the past 40 years. Average body weight in many industrialized countries increased from about the 1970s onwards, though not equally across the weight spectrum. In contrast to the commonly held belief that ‘obesity’ rates are continuing to increase, high quality studies have shown that ‘obesity’ rates for children, adolescents and adults in fact stabilized in many countries around the turn of the 21st Century, and in some countries, such as England, ‘obesity’ rates for adolescents have actually decreased over the past decade [5]. Nonetheless, average body weight is still increasing to some degree in specific population groups as well as in countries that are rapidly industrialising [5], and so it is worth exploring the factors that may be contributing to this trend.

Whilst it may seem self-evident that what people eat and how much they move are voluntary, conscious (and therefore manipulable) decisions, it is becoming clear that the balance between energy intake and energy output is largely controlled by a powerful unconscious biological system [6, 7]. This biological system regulates body mass by regulating the unconscious desire to eat and to move. It is possible for an individual to wilfully manipulate this biological system to a certain degree, just as you can hold your breath for a short time, but ultimately the biological system wins out and ensures that the body returns to homeostasis through unconsciously increasing food intake and reducing movement. There are numerous mechanisms used by the body to makes these subtle changes. For example, increases in food intake result in part from increases in the production of the hormone that signals hunger (ghrelin) and decreases in the production of the hormone that signals fullness (leptin) [6, 7].

The precise ways that the components in the biological system work together in any individual are strongly genetic, and therefore associations between dietary behaviours and adiposity are strongly attenuated by genetic factors [8]. Exploration of the pathways between genetic factors, behaviors and adiposity has revealed multiple mechanisms at play. For example, the fat mass and obesity (FTO) gene, located on chromosome 16, has been consistently associated with adiposity. Recent studies have confirmed that the presence of the FTO gene is strongly associated with appetite and satiety [9], and with the number of eating episodes per day, after controlling for body weight [10]. The presence of other genes has been shown to be associated with more servings of dairy products, and different genes seem to either increase or decrease intake of proteins [10].

Genetics, environment and chance all contribute to the variation in body weight between individuals in any given population. The relative contribution of genetics to the variability in body weight in a population is referred to as heritability. Research on monozygotic (identical) twins, non-identical twins and siblings provides strong evidence for the heritability of body weight [6, 11, 12]. These studies show that between 70 and 80% of the variability in body weight can be attributed to genetic variation within the population that the twins are from. Body weight is therefore classified as 70 – 80% heritable. Heritability does not refer to the contribution of genetics to the weight of an individual person, or the relative chance of being fat if one’s parents are fat. Heritability is high when genes contribute proportionately more to the variation of body weight within the population than the environment. The heritability of body weight is second only to height, and higher than heart disease, diabetes and cancer, all of which are considered to have high levels of heritability.

Given the high heritability of body weight, there has been extensive research looking for the genes that contribute to body weight. Genetic contribution can arise from either specific locations of genetic sequences within a gene that make an individual more susceptible to higher body weight (referred to in the literature as ‘obesity susceptible loci’) or variant forms of whole genes associated with increased susceptibility (referred to as ‘obesity risk alleles’). In 2010, researchers examined the genetic makeup of almost 250,000 individuals and confirmed previous findings of 14 obesity susceptible loci associated with higher body weight. They also identified 18 new loci associated with higher body weight [13]. A 2012 meta-analysis of 14 studies of genes related to ‘common childhood obesity’ found strong evidence for 2 previously unknown obesity susceptible loci associated with children’s body weight, and some evidence for a further 2 loci [14]. Not all adiposity genes are the same; there appears to be different genetic influences on BMI and waist circumference, with only a 60% overlap in genes associated with both [12]. Not surprisingly, the influence of genetics extends beyond susceptibility to higher body weight and fat accumulation to responses to attempted weight loss. The presence of some obesity risk alleles associated with ‘early onset obesity’ in children is strongly associated with reduced weight loss in children and adolescents from behavioral weight loss interventions [15]. The role of genes and genetic loci in influencing energy regulating behaviors, heritability and weight regulation is now well established. Research in genetic mutations has also demonstrated the role of genetic changes in increased adiposity [11, 13, 16-20].

Genes however, only tell part of the story. The Foresight Report in 2007 produced an extremely complex model with 108 factors contributing to increased body weight [21]. Despite the large number of identified factors, the map only included factors related to energy intake and expenditure. There are many other factors that have been found to contribute to increased body weight for individuals, including physiological factors related to the gut, such as deficiency in Toll-like receptor 5, an immune system protein present in the gut [22], metabolic endotoxemia caused by bacterial lipopolysaccharide from Gram-negative intestinal microbiota, which leads to low grade chronic inflammation [23], the composition of microbiota in the gut [22, 24-32], and infection with helicobacter pylori [31-33]. Other types of infection have also been identified as contributing to increased body weight, including chlamydia pneumonia [33] and human adenovirus 36 [34-37].

Sleep duration and quality has been demonstrated in numerous studies to impact on body weight [38-40]. A recent review of the literature examined experimental, cross-sectional (single point in time) and prospective studies [41]. Experimental studies included in the review showed that short-term sleep restriction leads to impaired glucose metabolism, dysregulation of appetite and increased blood pressure. The cross-sectional studies reviewed demonstrated associations between sleeping less than 6 hours per night and increased body mass index, diabetes, and hypertension, but of course these types of studies cannot prove causality. Prospective studies have demonstrated a significant increase in risk of weight gain, and development of diabetes and hypertension in association with chronic inadequate sleep. Interestingly, too much sleep may also be problematic as some studies have shown an association between sleeping longer than 8 hours a night and incidence of cardiometabolic disease [41].

Different types of stress have been shown to impact on body weight, including life stress [42, 43] and cumulative work stress or job strain [44]. Brunner et al. investigated the effect that stress at work had on the development of central adiposity over a 19 year period in over 10,000 participants in the Whitehall study [44]. In addition to having a large number of participants, the Whitehall study is extremely useful because the researchers controlled for socio-economic status, eating behaviors and physical inactivity. They were therefore able to look at the effect of job stress on body weight, independent of these factors. They found that employees experiencing chronic work stress (which they defined as 3 or more episodes of stress) had a 50% increased risk of developing central adiposity compared with those without chronic work stress.

A significant body of work in recent years has demonstrated the effect on body weight of exposure to endocrine disrupting chemicals. Specific chemicals found to be associated with increases in body weight include bisphenol A (BPA) [45-48], diethylstilbestrol, tributyltin [45], perfluorooctanoate [49], dichlorodiphenyldichloroethylene (DDE), polychlorinated biphenyl, polychlorinated dibenzodioxins and polychlorinated dibenzofurans [50]. Exposure to these chemicals is widespread as they are found in products such as paints, pesticides and plastics, including food and beverage containers. Some of these studies suggest that exposure to endocrine-disrupting chemicals in-utero may cause permanent physiological damage to the fetus, reducing the capacity to regulate body weight throughout life and therefore predisposing to later weight gain [47, 50].

Other in-utero exposures have been associated with weight gain, including exposure to famine in-utero through true famine or maternal dieting [51], or over nutrition in-utero [52]. Parental factors that may contribute to increased body weight include maternal smoking [53] and child feeding practices, particularly pressure to eat and concern for child’s weight [54].

Paradoxically, one of the strongest predictors of weight gain is weight loss dieting. This is the case irrespective of actual body weight – in other words it is the case for both ‘normal weight’ people and people whose body weights are above ‘normal’. The evidence shows very clearly that the body weight that dieters are trying to reduce or avoid gaining is increased by the very behaviors used to do so. In other words, dieting is actually counterproductive to weight loss [55-59]. A study on the determinants of weight gain amongst first year university students examined a range of dieting behaviors and practices [58]. After controlling for BMI, dieting for weight loss strongly predicted weight gain over the course of the first year at university. Participants who reported currently dieting to lose weight gained twice as much weight (5.0 kg) as former dieters (2.5 kg) and three times as much weight as never dieters (1.6 kg).

One of the biggest studies to demonstrate this effect in adolescents was a prospective study of over 16,000 adolescents aged between 9 and 14 years [60]. The Growing Up Today Study (GUTS) assessed dieting behavior to control weight, binge eating, dietary intake and Body Mass Index (BMI) over a 3 year period. Over 9000 participants remained in the study for the entire period. Participants were classified as ‘frequent dieters’ (dieting 2 to 7 days a week), ‘infrequent dieters’ (dieting less than once a month to once a week) or ‘nondieters’. At the 3 year follow up period, both male and female adolescents that were frequent or infrequent dieters had gained significantly more weight than nondieters. The study controlled for potential confounding factors of BMI, age, physical development, physical activity, inactivity, caloric intake and height change over the period. Therefore the weight gain experienced by the adolescents in this study could reasonably be ascribed to the practice of dieting behaviors.

The longest running study that demonstrates this phenomenon is Project EAT (Eating and Activity in Teens and Young Adults), which involves a diverse population-based sample of middle and high school students [61]. Over 3 waves of data collection spanning 10 years, this study has demonstrated that the strongest predictors of weight gain in participants were dieting and unhealthy weight control behaviors. The analysis controlled for socioeconomic status and initial BMI, and the associations were found in participants from right across the weight spectrum. The behaviors associated with the largest increases in BMI over the 10 year period were skipping meals, eating very little, using food substitutes and taking diet pills.

In Part 1 of this article I have 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 have 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 over the short, medium and long term. In part 2 of this article, I will examine a range of environmental factors and their contribution to increased body weight.

Please click here to access the numbered references.

July 25, 2011

the Haes files: public health authorities need to be held accountable

by healthateverysizeblog

 by Lily O’Hara, Section Head for Health Promotion, Health Authority – Abu Dhabi

The dominant health paradigm  governing public health action from government departments and health care organisations is the weight centered health paradigm, where body weight is positioned as the single biggest problem in health today. But is this paradigm consistent with the values and principles of modern health promotion?(good rhetorical questions) Shouldn’t government departments and health care organisations be engaging in the most up to date practices? Would we accept other forms of health care that were based on outdated knowledge and beliefs? As our scientific and other forms of knowledge grow, sometimes exponentially, health care practices change and develop to take account of the new knowledge. This is what happens in most of the health care world EXCEPT in the area of weight.  

 Modern health promotion is the process of enabling people to increase control over the determinants of health. Research over the last 100 years has taught us that the determinants of health are extensive, multilayered and interconnected. Determinants are biological (such as genes and age), cognitive or psychological (such as knowledge, attitudes and beliefs), behavioral (including physical, mental, social and spiritual practices), and environmental (social, cultural, economic, political, natural and built environments). These determinants operate at the individual, family, group, community, population and global levels. In ecological science, these levels are referred to as nested hierarchies and the interconnections are referred to as feedback loops. So we know that health is complex.

 But that’s not the message we hear from our public health authorities. In fact, it’s just the opposite. Health is simple – it’s about how fat you are. And the answer is simple – eat less bad/wrong/unhealthy food, eat more good/right/healthy food, and move more and you will lose weight and therefore be healthier. Unfortunately for the authorities that is Just. Not. True. And saying it is will not make it so.

 Clearly body weight casts such a long dark shadow over the practice of modern health care that it has effectively created an enormous blind spot. Otherwise thoughtful and evidence based health practitioners still uncritically buy into the fat=bad story and act accordingly.  

 In my own field of health promotion, the big picture story since 1978 at least, when the World Health Organisation adopted the goal of Health for All by the Year 2000, has been the need to address systemic health inequities within and between countries by focusing on the environmental determinants of health – commonly referred to as the social determinants of health – which are basically all of those factors beyond the control of the individual. Major conferences have been devoted to the social determinants of health, and there was even a World Health Organisation Commission addressing them. When it became clear we would not achieve health for all by 2000, the goal became Health for All by the 21st Century.

 Although criticized for being unrealistic, this aspirational goal has sought to focus our attention on reducing health inequities through addressing the structural determinants of health. As a result you’d think that modern health promotion practice would be focused on addressing poverty, reducing income inequity, creating peace, improving social relations, social security and social justice, empowering women, respecting human rights, and creating healthier, sustainable environments in which we live, work, play, learn and love. These are the health determinants that all countries participating in the World Health Assembly made a legal commitment to address through health promotion programs.

 But they are not living up to this commitment. A significant chunk of the global, national, state and local health promotion effort is still directed towards trying to change behaviors, and a narrow range of behaviors at that – what people eat and drink, how much they move and what drugs they use. These are the holy trinity of health promotion that you will find on the agenda of pretty much every health promotion government department, conference or journal.

 Many practitioners that are vociferous and outspoken advocates for programs that address the social determinants of health can somehow also engage in ‘obesity prevention’ practice. In the past few years ‘obesity prevention’ at a public health level has broadened to address the ‘obesogenic environment’. The rationale is that by altering the environment then the behaviors that ‘create obesity’ will be altered. So what sounds on the surface like a more sophisticated argument about the role of the environment in creating health, basically boils down to the same simplistic beliefs about body weight.

 It doesn’t seem possible that the same articulate and passionate health promotion practitioners that advocate for a socio-ecological approach to reducing structural inequities in health are the same people arming up in the ‘war on obesity’. The dissonance between the two approaches seems so obvious to me and everyone else using the HAESSM approach, but it’s a great big blind spot for them. I guess you just can’t see what you can’t see.

 The Health at Every Size® principles advocate practices that are known to enhance the health of people of ALL sizes (In addition the HAESSM approach opposes practices that perpetuate body size oppression. This means any form of oppression including bias, exploitation, marginalisation, discrimination, powerlessness, cultural imperialism, harassment or violence against people based on their body image, body size or weight. Furthermore, the HAESSM approach opposes any approach to health, eating or exercise, the provision of products, services or amenities which focuses on body weight or perpetuates body size oppression.

 Body size oppression is a social determinant of poor health. Public health authorities are supposed to improve the social determinants of health, not make them worse. They are meant to be working towards health for ALL people.  Governments have signed up to this through a succession of charters at the World Health Assembly. It’s time we held them accountable and demand the adoption of modern health promotion practice that is enhances health for all.

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