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 . Nonetheless, average body weight is still increasing to some degree in specific population groups as well as in countries that are rapidly industrialising , 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 . 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 , and with the number of eating episodes per day, after controlling for body weight . 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 .
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 . 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 . 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 . 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 . 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 . 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 , metabolic endotoxemia caused by bacterial lipopolysaccharide from Gram-negative intestinal microbiota, which leads to low grade chronic inflammation , 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  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 . 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 .
Different types of stress have been shown to impact on body weight, including life stress [42, 43] and cumulative work stress or job strain . 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 . 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 , perfluorooctanoate , dichlorodiphenyldichloroethylene (DDE), polychlorinated biphenyl, polychlorinated dibenzodioxins and polychlorinated dibenzofurans . 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 , or over nutrition in-utero . Parental factors that may contribute to increased body weight include maternal smoking  and child feeding practices, particularly pressure to eat and concern for child’s weight .
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 . 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 . 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 . 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.
Lily 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.