Keywords: obesity, weight gain, health promotion, nutrition, lifestyle, food, genetics, physical activity, public health. Obesity is a medical condition defined as disproportionate fat storage in the body that might adversely affect health. More than million of them are considered obese. The global prevalence of obesity has increased by threefold between and If the trend continues to rise, it is estimated that close to one third of the world adult population will be overweight and more than1 billion will be obese by The WHO recognises this limitation and recommends its use as a screening tool only.
Obesity infers a huge economic burden on the already outstretched health systems in many countries. With its sharply rising prevalence, complex aetiology and incapacitating adverse health and economic outcome, Obesity is now considered a global epidemic. Several published epidemiological studies examined different aspects of the complex aetiology of Obesity. Utilising evidence from these studies, this review aims at carrying an in-depth analysis of the different factors contributing to the development of the obesity epidemic.
This takes place when energy intake exceeds energy expenditure over time. To start with, the importance of genetical predisposition to obesity has been demonstrated in several studies. In a study that examined the effect of increased caloric intake on monozygotic twins in Canada, 12 pairs of identical male twins were provided with extra intake of kcal per day for six days a week over a period of days.
Within pairs of twins, the weight gain patterns were almost similar in terms of overall weight, fat distribution and percentage. These similar patterns of response of identical twins clearly highlights the effect of genetical susceptibility on weight. There was greater variation in weight gain in between different twin pairs than within the same pair. Another study published in the New England Journal of Medicine reviewing adopted adults provides additional evidence of the influence of genetics on body weight.
There was no significant relationship between the adoptees BMI class and their adopting parents. An additional example of the significance of polygenic susceptibility to weight gain is the Pima Indians of Arizona who are well known as a group to have a high prevalence rate of obesity. This could be related to polygenic aetiology.
However, there is considerable variability in the overall response to high calorie intake among them. Weyer et al. The genetic predisposition to obesity can be polygenic, monogenic or syndromic. These are similar to known genetic defects causing obesity in rats and are secondary to either relative or absolute leptin deficiency and leptin receptor defects.
Leptin is an adipocyte driven hormone that acts on the hypothalamus to induce satiety and reduce food intake. Patients with leptin deficiency develop sever obesity secondary to boosted food intake mainly due to lack of satiety and reduced energy expenditure. Some other rare genetic conditions can lead to syndromic obesity due to single gene defect or large chromosomal region of multiple genes. However, the exact molecular mechanism that causes weight gain in most of them remains unclear.
The association between several endocrinological conditions and obesity is well recognised. Polycystic ovary syndrome leading to insulin resistance may contribute to obesity as well. Lithium is associated with lesser but significant weight gain of up to 10 kg.
In addition, many antidepressants including Tricyclic antidepressants like Amitriptyline Average weight gain of 0. Glucose lowering medications including Insulin, Sulfonylureas and Thiazolidinediones and some antihypertensives like Clonidine and Atenolol can result in significant weight gain as well. Three main factors contribute to energy expenditure.
In addition, energy is required for the breaking down of food, and lastly there is the energy required for any physical activity. Both calorie intake and energy expenditure are controlled by the central nervous system. This involves different neurotransmitters and complex mechanisms within the hypothalamus to induce either satiety or hunger.
This is guided by genetic predisposition, but it is also subject to voluntary control to some extent. In evolution most of these systems are set to save energy in times of scarcity rather than reducing or wasting it at times of redundancy. The significance of the contribution of environmental factors is shown on a study carried on 2 groups of Pima Indians.
Those living in Arizona in the United states have a recognised high rate of obesity. In spite of the similar genetic susceptibility as they share the same ancestors , Pima Indians living in an isolation in Mexico had considerably lower BMI. The Mexican Pima Indians consume a simpler diet lower in fat and caloric density than their peers in Arizona and their heavy physical work lead to greater levels of energy expenditure.
When considering environmental factors, the fundamental factors that have likely contributed to the obesity epidemics are the changes to the amount and quality of food in the diet energy density and the changes in the level of energy expenditure in terms of physical activity carried out by the population.
The redundancy and easy accessibility to a variety of high caloric diets, rich in fat and processed carbohydrate is a crucial factor in the obesity epidemic. Car driving and time spent on TV viewing significantly correlate with the rise in obesity in England. TV viewing time in specific is a growing concern amongst children as a contributor to the rise in childhood obesity prevalence.
The point of purchase effect has a major role in the obesity epidemic. People are often unable to recognize and avoid purchasing a product due to the complex marketing strategies that sometimes work through non-cognitive processes. The food industry recognises the role of product presentation in influencing purchasing. Obesity, although mainly seen in the economically privileged western countries, is more prevalent in subjects from lower socio-economic classes.
This is likely due to the high fat content in diet in these groups and reduced physical activity especially with the regression in customary manual occupations. A systemic review carried out in 22 showed that ethnic minority and low-socioeconomic-status groups in the United States are more affected by obesity at all ages. These differences where recognised more among males than females. In developing countries with higher income, the previously noted correlation becomes mixed for men and nearly non-existent for women.
Childhood obesity seems to mostly affect the higher socioeconomic class in developing countries. A clear likely explanation for that, would be food scarcity in low-income countries which leads to reduced food intake among the unfortunate families with low income. In addition, those individuals are likely to be very physically active engaging in labour manual work.
Conversely, the rich are more prone to obesity due to accessibility to excess food and less involvement in manual occupations. It is also common in many cultures to consider obesity and overweight as a sign of affluency. By contrast, in developing countries with higher income, food scarcity becomes less of an issue. In its place, access to healthy food becomes the driving factor differentiating the more from the less affluent. Healthy food with low energy density e.
The effect of workplace environment on the prevalence obesity is well recognised. Long working hours can result in increased BMI due to reduced time for exercise and physical activity. It can also result in shifting towards ready processed meals and fast food rather than home-made meals. Another observational study that reviewed more than participants 26 reported increased BMI with long working hours in women ORs for obesity attributable to long working hours were 2. Long working hours can lead to reduced sleeping hours and contribute to obesity.
However, the questionnaire utilised in the study was broadly general and there was lack of assessment of reliability creating measurement bias. Nevertheless, this study reaffirmed the speculated association between longer working hours, lack of sleep and obesity.
Lack of sleep can result in hormonal imbalance impaired glucose tolerance and increased nocturnal cortisol and adversely affect the cognitive function leading to obesity. Among the strengths of this. However, due to the observational nature of the study, confounding factors cannot be ruled out. The inverse association between sleeping hours and obesity was demonstrated in several studies globally.
More than children in Japan were reviewed in a study in Similarly, another study involving subjects demonstrated increased risk of obesity with less than 6 hours of sleep or sleeping beyond midnight. They noted that longer hours of work are associated with increased BMI.
Interestingly, there was no association between job strain and BMI, however high psychological demand and low reward contributed to raised BMI. In addition, the built environment can influence travel and commuting choices in a financial and behavioural perspectives.
Households would make less vehicle trips if located in areas with denser land use development and better transit service. In other words, in order to reduce vehicle use, planning neighbourhoods should focus on high land use developments to shorten the distance to transit and make destinations more accessible by providing easy access to trip attractions. A systemic review 33 on the relationship between the built environment and obesity showed that access to physical activity opportunities and access to food outlet can significantly affect body weight.
While increased mixed land use and daily distance walked were associated with reduced obesity, increased time spent in a car was associated with the reverse. Increased open spaces and local parks availability was associated with reduced obesity.
Finally, the role of social networks and peer effect in the rise of obesity prevalence cannot be ignored. The determinants of obesity are summarised in Table 1. Certain medications: Anti-psychotics, Anti-depressants, Anti-Diabetic, Antihypertensives, and steroids. Energy intake exceeding energy expenditure due to excessive intake of energy-dense food and reduced physical activity. The built environment: poor access to recreational facilities, lack of sidewalks, Food deserts due to lack of food outlets.
The sharp rise in Obesity prevalence has raised major global concern. Clearly, the obesity epidemic is the outcome of multifaceted interaction between the environmental factors, genetic susceptibility, and human behaviour. In the context of the Brazilian Unified Health System i. Obesity is a major contributor to preventable disease and death across the globe, and poses a nearly unprecedented challenge not just to those tasked with addressing it at the public health level, or at the healthcare provider level, but to each of us as individuals, for none of us are immune.
Increasing ease of life, owing to reduced physical labor and automated transportation, an increasingly sedentary lifestyle, and liberal access to calorie-dense food, driven by dramatic economic growth in many parts of the world in the last century, have turned a once rare disease of the affluent into one of the most common diseases—increasingly of the poor. That barely one in three people in the USA today are normal weight portends, quite simply, an astounding and frightening future.
Obesity is complex. Although its risk factors are myriad and compounding, there is an urgent need for deeper understanding of the way risk factors interact with each other, and the potential solutions to the epidemic are as multi-leveled and complex as its causes. There are calls for applying systems-level and systems epidemiology approaches to this and related nutrition and metabolic diseases, approaches which attempt to comprehensively address biological, behavioral, and environmental contributors to disease as well as their intricate feedback loops.
For example, we could attempt to limit national production and import of sugar-sweetened beverages, tax sugar-sweetened beverages, or restrict fast food restaurant zoning. These largely political acts seem relatively inexpensive, but may have economic impacts in communities and regions beyond what we currently understand.
We may push for the increasing medicalization of obesity, including developing an obesity vaccine. However, preventing and remediating obesity in children and adults—e. Given these resource costs, perhaps greater attention should be given to pregnancy, a condition which is already highly medicalized and which may be an ideal preventive avenue for the provision of nutrition education and intensive monitoring of weight gain, to ensure that children have the most optimal start with respect to their future obesity risk.
Clearly, no single approach is optimal, but with limited resources, an evidence base supporting one or more approaches or their combination is needed, as is tenacity and perhaps some audacity by local government and public health authorities in testing some of these approaches within their populations. However, an epidemic of this magnitude needs, quite simply, more resources.
Despite the many unknowns, we can be cautiously optimistic about our ability to address the obesity epidemic. Indeed, we have relatively successfully faced similarly daunting public health challenges before: smoking, to name just one.
While tobacco can loosely be thought of as a single product, and our food culture is infinitely more complex, as a case study in how to approach obesity, it provides numerous lessons in multi-level solutions to a major health threat in terms of both mitigation and prevention.
It took over half a century to achieve the immense success we have with regard to smoking in the USA and still we are not yet tobacco-free ; other parts of the world continue to wrestle with it to a greater degree. It has only been a couple decades since we first deeply appreciated that obesity was epidemic. We clearly still have a long way to go. While the prevalence of adult obesity in the developed world seems to have stabilized, the prevalence of obesity in children and adolescents globally, as well as adults obesity in developing countries, is still increasing.
In addition, some developed countries continue to observe increasing prevalence of extreme classes of obesity. Overweight and obesity—defined as excess body weight for height—have genetic, behavioral, socioeconomic, and environmental origins. Obesity increases risk of major chronic diseases, including heart disease, diabetes, depression, and many cancers, as well as premature death. Given its complexity, the obesity epidemic requires multilevel and integrated solutions, from individual intervention, to broad food policy, industry, and agriculture initiatives.
The authors declare no conflict of interest. The authors broadly thank the researchers in this field for their consistent and tireless work in illuminating the etiology, sequelae, and solutions to this complex condition. We refer readers to recent reviews on the topic 35 , 36 , AH wrote the first draft of the paper. AH and FH contributed to writing, revised, and edited the paper. AH is the final guarantor of this work and takes full responsibility for its contents.
Both authors read and approved the final manuscript. National Center for Biotechnology Information , U. Author manuscript; available in PMC Jul 1. Author information Copyright and License information Disclaimer. Copyright notice. The publisher's final edited version of this article is available at Pharmacoeconomics.
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These categories, if not the exact terminology, of adult weight status have been adopted by other major health organizations, including the US National Heart, Lung, and Blood Institute and National Institute of Diabetes and Digestive and Kidney Diseases Classification of Body Weight in Children In children, body weight classifications Table 1 differ from those of adults because body composition varies greatly as a child develops, and further varies between boys and girls primarily owing to differences in sexual development and maturation.
Prevalence and Trends 4. Child Obesity—USA and Europe US children may be faring better than their adult counterparts in some ways 16 , potentially offsetting earlier dire predictions of rampant obesity by 5. Individual Behaviors 5. Diet In the decades preceding the 21st century, the vast majority of research on obesity risk factors focused on individual-level, largely modifiable behaviors.
Physical Activity, Sedentary Behaviors, and Sleep Personal behaviors beyond diet physical activity, sleep, sedentary and screen time, and stress have also been independently associated with weight change and maintenance in adulthood. Socioeconomic Risk Factors: Income and Education Income has had a shifting role in obesity risk over the last century.
Environmental 2 Risk Factors 5. The Built Environment Research on the built environment tends to focus on a few measurable characteristics of neighborhoods as they relate to weight status, while holding sociodemographic and other person-level characteristics constant. Costs of Obesity: Co-Morbidities, Mortality, and Economic Burden Obesity is associated with concomitant or increased risk of nearly every chronic condition, from diabetes, to dyslipidemia, to poor mental health.
Heart and Vascular Diseases Ischemic heart disease and stroke are the leading causes of death in the USA and globally Trauma and Infection A study in Pennsylvania USA trauma centers — showed that in-hospital mortality and risk of major complications of surgery were increased in obese patients as compared to non-obese patients. Mental Health The role of weight in mental health faces causal challenges, but what is clear is that obesity and adiposity are associated with anatomical as well as functional changes in the human brain.
Touching on Solutions, and Some Conclusions Obesity is a major contributor to preventable disease and death across the globe, and poses a nearly unprecedented challenge not just to those tasked with addressing it at the public health level, or at the healthcare provider level, but to each of us as individuals, for none of us are immune.
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