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1.  Beyond Obesity and Lifestyle: A Review of 21st Century Chronic Disease Determinants 
BioMed Research International  2014;2014:731685.
The obesity epidemic and associated chronic diseases are often attributed to modern lifestyles. The term “lifestyle” however, ignores broader social, economic, and environmental determinants while inadvertently “blaming the victim.” Seen more eclectically, lifestyle encompasses distal, medial, and proximal determinants. Hence any analysis of causality should include all these levels. The term “anthropogens,” or “…man-made environments, their by-products and/or lifestyles encouraged by these, some of which may be detrimental to human health” provides a monocausal focus for chronic diseases similar to that which the germ theory afforded infectious diseases. Anthropogens have in common an ability to induce a form of chronic, low-level systemic inflammation (“metaflammation”). A review of anthropogens, based on inducers with a metaflammatory association, is conducted here, together with the evidence for each in connection with a number of chronic diseases. This suggests a broader view of lifestyle and a focus on determinants, rather than obesity and lifestyle per se as the specific causes of modern chronic disease. Under such an analysis, obesity is seen more as “a canary in a mineshaft” signaling problems in the broader environment, suggesting that population obesity management should be focused more upstream if chronic diseases are to be better managed.
doi:10.1155/2014/731685
PMCID: PMC3997940  PMID: 24804239
2.  Earlier Mother's Age at Menarche Predicts Rapid Infancy Growth and Childhood Obesity 
PLoS Medicine  2007;4(4):e132.
Background
Early menarche tends to be preceded by rapid infancy weight gain and is associated with increased childhood and adult obesity risk. As age at menarche is a heritable trait, we hypothesised that age at menarche in the mother may in turn predict her children's early growth and obesity risk.
Methods and Findings
We tested associations between mother's age at menarche, mother's adult body size and obesity risk, and her children's growth and obesity risk in 6,009 children from the UK population-based Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort who had growth and fat mass at age 9 y measured by dual-energy X-ray absorptiometry. A subgroup of 914 children also had detailed infancy and childhood growth data. In the mothers, earlier menarche was associated with shorter adult height (by 0.64 cm/y), increased weight (0.92 kg/y), and body mass index (BMI, 0.51 kg/m2/y; all p < 0.001). In contrast, in her children, earlier mother's menarche predicted taller height at 9 y (by 0.41 cm/y) and greater weight (0.80 kg/y), BMI (0.29 kg/m2/y), and fat mass index (0.22 kg/m2/year; all p < 0.001). Children in the earliest mother's menarche quintile (≤11 y) were more obese than the oldest quintile (≥15 y) (OR, 2.15, 95% CI 1.46 to 3.17; p < 0.001, adjusted for mother's education and BMI). In the subgroup, children in the earliest quintile showed faster gains in weight (p < 0.001) and height (p < 0.001) only from birth to 2 y, but not from 2 to 9 y (p = 0.3–0.8).
Conclusions
Earlier age at menarche may be a transgenerational marker of a faster growth tempo, characterised by rapid weight gain and growth, particularly during infancy, and leading to taller childhood stature, but likely earlier maturation and therefore shorter adult stature. This growth pattern confers increased childhood and adult obesity risks.
Earlier age at menarche may be a transgenerational marker of faster growth, particularly during infancy, leading to taller childhood stature but earlier maturation and hence shorter adult stature.
Editors' Summary
Background.
Childhood obesity is a rapidly growing problem. Twenty-five years ago, overweight children were rare. Now, 155 million of the world's children are overweight and 30–45 million are obese. Overweight and obese children—those having a higher than average body mass index (BMI; weight divided by height squared) for their age and sex—are at increased risk of becoming obese adults. Such people are more likely to develop heart disease, diabetes, and other health problems than lean people. Many factors are involved in the burgeoning size of children. Parental obesity, for example, predisposes children to being overweight. In part, this is because parents influence the eating habits of their offspring and the amount of exercise they do. In addition, though, children inherit genetic factors from their parents that make them more likely to put on weight.
Why Was This Study Done?
To prevent childhood obesity, health care professionals need ways to predict which infants are likely to become obese so that they can give parents advice on controlling their children's weight. In girls, early menarche (the start of menstruation) is associated with an increased risk of childhood and adult obesity and tends to be preceded by rapid weight gain in the first two years of life. Because age at menarche is inherited, the researchers in this study have investigated whether mothers' age at menarche predicts rapid growth in infancy and childhood obesity in their offspring using data from the Avon Longitudinal Study of Parents and Children (ALSPAC). In 1991–1992, this study recruited nearly 14,000 children born in Bristol, UK. Since then, the children have been regularly examined to investigate how their environment and genetic inheritance interact to affect their health.
What Did the Researchers Do and Find?
The researchers measured the growth and fat mass of 6,009 children from ALSPAC at 9 years of age. For 914 of these children, the researchers had detailed data on their growth during infancy and early childhood. They then looked for any associations between the mother's age at menarche (as recalled during pregnancy), mother's adult body size, and the children's growth and obesity risk. In the mothers, earlier menarche was associated with shorter adult height and increased weight and BMI. In the children, those whose mothers had earlier menarche were taller and heavier than those whose mothers had a later menarche. They also had a higher BMI and more body fat. The children whose mothers had their first period before they were 11 were twice as likely to be obese as those whose mothers did not menstruate until they were 15 or older. Finally, for the children with detailed early growth data, those whose mothers had the earliest menarche had faster weight and height gains in the first two years of life (but not in the next seven years) than those whose mothers had the latest menarche.
What Do These Findings Mean?
These findings indicate that earlier mother's menarche predicts a faster growth tempo (the speed at which an individual reaches their adult height) in their offspring, which is characterized by rapid weight and height gain during infancy. This faster growth tempo leads to taller childhood stature, earlier sexual maturity, and—because age at puberty determines adult height—shorter adult stature. An inherited growth pattern like this, the researchers write, confers an increased risk of childhood and adult obesity. As with all studies that look for associations between different measurements, these findings will be affected by the accuracy of the measurements—for example, how well the mothers recalled their age at menarche. Furthermore, because puberty, particularly in girls, is associated with an increase in body fat, a high BMI at age nine might indicate imminent puberty rather than a risk of long-standing obesity—further follow-up studies will clarify this point. Nevertheless, the current findings provide a new factor—earlier mother's menarche—that could help health care professionals identify which infants require early growth monitoring to avoid later obesity.
Additional Information.
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.0040132.
The Avon Longitudinal Study of Parents and Children has a description of the study and results to date
The US Centers for Disease Control and Prevention provides information on overweight and obesity (in English and Spanish)
US Department of Health and Human Services's program, Smallstep Kids, is an interactive site for children about healthy eating (in English and Spanish)
The International Obesity Taskforce has information on obesity and its prevention
The World Heart Federation's Global Prevention Alliance provides details of international efforts to halt the obesity epidemic and its associated chronic diseases
The Child Growth Foundation has information on childhood growth and its measurement
doi:10.1371/journal.pmed.0040132
PMCID: PMC1876410  PMID: 17455989
3.  Association between Class III Obesity (BMI of 40–59 kg/m2) and Mortality: A Pooled Analysis of 20 Prospective Studies 
PLoS Medicine  2014;11(7):e1001673.
In a pooled analysis of 20 prospective studies, Cari Kitahara and colleagues find that class III obesity (BMI of 40–59) is associated with excess rates of total mortality, particularly due to heart disease, cancer, and diabetes.
Please see later in the article for the Editors' Summary
Background
The prevalence of class III obesity (body mass index [BMI]≥40 kg/m2) has increased dramatically in several countries and currently affects 6% of adults in the US, with uncertain impact on the risks of illness and death. Using data from a large pooled study, we evaluated the risk of death, overall and due to a wide range of causes, and years of life expectancy lost associated with class III obesity.
Methods and Findings
In a pooled analysis of 20 prospective studies from the United States, Sweden, and Australia, we estimated sex- and age-adjusted total and cause-specific mortality rates (deaths per 100,000 persons per year) and multivariable-adjusted hazard ratios for adults, aged 19–83 y at baseline, classified as obese class III (BMI 40.0–59.9 kg/m2) compared with those classified as normal weight (BMI 18.5–24.9 kg/m2). Participants reporting ever smoking cigarettes or a history of chronic disease (heart disease, cancer, stroke, or emphysema) on baseline questionnaires were excluded. Among 9,564 class III obesity participants, mortality rates were 856.0 in men and 663.0 in women during the study period (1976–2009). Among 304,011 normal-weight participants, rates were 346.7 and 280.5 in men and women, respectively. Deaths from heart disease contributed largely to the excess rates in the class III obesity group (rate differences = 238.9 and 132.8 in men and women, respectively), followed by deaths from cancer (rate differences = 36.7 and 62.3 in men and women, respectively) and diabetes (rate differences = 51.2 and 29.2 in men and women, respectively). Within the class III obesity range, multivariable-adjusted hazard ratios for total deaths and deaths due to heart disease, cancer, diabetes, nephritis/nephrotic syndrome/nephrosis, chronic lower respiratory disease, and influenza/pneumonia increased with increasing BMI. Compared with normal-weight BMI, a BMI of 40–44.9, 45–49.9, 50–54.9, and 55–59.9 kg/m2 was associated with an estimated 6.5 (95% CI: 5.7–7.3), 8.9 (95% CI: 7.4–10.4), 9.8 (95% CI: 7.4–12.2), and 13.7 (95% CI: 10.5–16.9) y of life lost. A limitation was that BMI was mainly ascertained by self-report.
Conclusions
Class III obesity is associated with substantially elevated rates of total mortality, with most of the excess deaths due to heart disease, cancer, and diabetes, and major reductions in life expectancy compared with normal weight.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
The number of obese people (individuals with an excessive amount of body fat) is increasing rapidly in many countries. Worldwide, according to the Global Burden of Disease Study 2013, more than a third of all adults are now overweight or obese. Obesity is defined as having a body mass index (BMI, an indicator of body fat calculated by dividing a person's weight in kilograms by their height in meters squared) of more than 30 kg/m2 (a 183-cm [6-ft] tall man who weighs more than 100 kg [221 lbs] is obese). Compared to people with a healthy weight (a BMI between 18.5 and 24.9 kg/m2), overweight and obese individuals (who have a BMI between 25.0 and 29.9 kg/m2 and a BMI of 30 kg/m2 or more, respectively) have an increased risk of developing diabetes, heart disease, stroke, and some cancers, and tend to die younger. Because people become unhealthily fat by consuming food and drink that contains more energy (kilocalories) than they need for their daily activities, obesity can be prevented or treated by eating less food and by increasing physical activity.
Why Was This Study Done?
Class III obesity (extreme, or morbid, obesity), which is defined as a BMI of more than 40 kg/m2, is emerging as a major public health problem in several high-income countries. In the US, for example, 6% of adults are now morbidly obese. Because extreme obesity used to be relatively uncommon, little is known about the burden of disease, including total and cause-specific mortality (death) rates, among individuals with class III obesity. Before we can prevent and treat class III obesity effectively, we need a better understanding of the health risks associated with this condition. In this pooled analysis of prospective cohort studies, the researchers evaluate the risk of total and cause-specific death and the years of life lost associated with class III obesity. A pooled analysis analyzes the data from several studies as if the data came from one large study; prospective cohort studies record the characteristics of a group of participants at baseline and follow them to see which individuals develop a specific condition.
What Did the Researchers Do and Find?
The researchers included 20 prospective (mainly US) cohort studies from the National Cancer Institute Cohort Consortium (a partnership that studies cancer by undertaking large-scale collaborations) in their pooled analysis. After excluding individuals who had ever smoked and people with a history of chronic disease, the analysis included 9,564 adults who were classified as class III obese based on self-reported height and weight at baseline and 304,011 normal-weight adults. Among the participants with class III obesity, mortality rates (deaths per 100,000 persons per year) during the 30-year study period were 856.0 and 663.0 in men and women, respectively, whereas the mortality rates among normal-weight men and women were 346.7 and 280.5, respectively. Heart disease was the major contributor to the excess death rate among individuals with class III obesity, followed by cancer and diabetes. Statistical analyses of the pooled data indicate that the risk of all-cause death and death due to heart disease, cancer, diabetes, and several other diseases increased with increasing BMI. Finally, compared with having a normal weight, having a BMI between 40 and 59 kg/m2 resulted in an estimated loss of 6.5 to 13.7 years of life.
What Do These Findings Mean?
These findings indicate that class III obesity is associated with a substantially increased rate of death. Notably, this death rate increase is similar to the increase associated with smoking among normal-weight people. The findings also suggest that heart disease, cancer, and diabetes are responsible for most of the excess deaths among people with class III obesity and that having class III obesity results in major reductions in life expectancy. Importantly, the number of years of life lost continues to increase for BMI values above 50 kg/m2, and beyond this point, the loss of life expectancy exceeds that associated with smoking among normal-weight people. The accuracy of these findings is limited by the use of self-reported height and weight measurements to calculate BMI and by the use of BMI as the sole measure of obesity. Moreover, these findings may not be generalizable to all populations. Nevertheless, these findings highlight the need to develop more effective interventions to combat the growing public health problem of class III obesity.
Additional Information
Please access these websites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001673.
The US Centers for Disease Control and Prevention provides information on all aspects of overweight and obesity (in English and Spanish)
The World Health Organization provides information on obesity (in several languages); Malri's story describes the health risks faced by an obese child
The UK National Health Service Choices website provides information about obesity, including a personal story about losing weight
The Global Burden of Disease Study website provides the latest details about global obesity trends
The US Department of Agriculture's ChooseMyPlate.gov website provides a personal healthy eating plan; the Weight-Control Information Network is an information service provided for the general public and health professionals by the US National Institute of Diabetes and Digestive and Kidney Diseases (in English and Spanish)
MedlinePlus provides links to other sources of information on obesity (in English and Spanish)
doi:10.1371/journal.pmed.1001673
PMCID: PMC4087039  PMID: 25003901
4.  BMI and Risk of Serious Upper Body Injury Following Motor Vehicle Crashes: Concordance of Real-World and Computer-Simulated Observations 
PLoS Medicine  2010;7(3):e1000250.
Shankuan Zhu and colleagues use computer crash simulations, as well as real-world data, to evaluate whether driver obesity is associated with greater risk of body injury in motor vehicle crashes.
Background
Men tend to have more upper body mass and fat than women, a physical characteristic that may predispose them to severe motor vehicle crash (MVC) injuries, particularly in certain body regions. This study examined MVC-related regional body injury and its association with the presence of driver obesity using both real-world data and computer crash simulation.
Methods and Findings
Real-world data were from the 2001 to 2005 National Automotive Sampling System Crashworthiness Data System. A total of 10,941 drivers who were aged 18 years or older involved in frontal collision crashes were eligible for the study. Sex-specific logistic regression models were developed to analyze the associations between MVC injury and the presence of driver obesity. In order to confirm the findings from real-world data, computer models of obese subjects were constructed and crash simulations were performed. According to real-world data, obese men had a substantially higher risk of injury, especially serious injury, to the upper body regions including head, face, thorax, and spine than normal weight men (all p<0.05). A U-shaped relation was found between body mass index (BMI) and serious injury in the abdominal region for both men and women (p<0.05 for both BMI and BMI2). In the high-BMI range, men were more likely to be seriously injured than were women for all body regions except the extremities and abdominal region (all p<0.05 for interaction between BMI and sex). The findings from the computer simulation were generally consistent with the real-world results in the present study.
Conclusions
Obese men endured a much higher risk of injury to upper body regions during MVCs. This higher risk may be attributed to differences in body shape, fat distribution, and center of gravity between obese and normal-weight subjects, and between men and women.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
Worldwide, accidents involving motor vehicles kill 1.2 million people and injure as many as 50 million people every year. Collisions between motor vehicles, between vehicles and stationary objects, or between vehicles and pedestrians are responsible for one in 50 deaths and are the 11th leading cause of death globally. Many factors contribute to the risk of motor traffic accidents and the likelihood of subsequent injury or death. These risk factors include vehicle design, vehicle speeds, road design, driver impairment through, for example, alcohol use, and other driver characteristics such as age. Faced with an ever-increasing death toll on their roads, many countries have introduced lower speed limits, mandatory seat belt use, and greater penalties for drunk driving to reduce the carnage. Road design and traffic management initiatives have also been introduced to try to reduce the incidence of road traffic accidents and cars now include many features that provide protection in crashes for their occupants such as airbags and crumple zones.
Why Was This Study Done?
Although these measures have reduced the number of crashes and casualties, a better understanding of the risk factors associated with motor vehicle crashes is needed to deal with this important public-health problem. Another major public-health problem is obesity—having excess body fat. Obesity increases the risk of heart disease and diabetes but also contributes to the severity of motor vehicle crash injuries. Men with a high body mass index (an individual's weight in kilograms divided by height in meters squared; a BMI of 30 or more indicates obesity) have a higher risk of death after a motor vehicle accident than men with a normal BMI (18.5–24.9). This association between death and obesity is not seen in women, however, possibly because men and women accumulate fat on different parts of their body and the resultant difference in body shape could affect how male and female bodies move during traffic collisions and how much protection existing car safety features afford them. In this study, therefore, the researchers investigated how driver obesity affects the risk of serious injuries in different parts of the body following real and simulated motor vehicle crashes in men and women.
What Did the Researchers Do and Find?
The researchers extracted data about injuries and BMIs for nearly 11,000 adult men and women who were involved in a frontal motor vehicle collision between 2001 and 2005 from the Crashworthiness Data System of the US National Automotive Sampling System. They then used detailed statistical methods to look for associations between specific injuries and driver obesity. The researchers also constructed computer models of obese drivers and subjected these models to simulated crashes. Their analysis of the real-world data showed that obese men had a substantially higher risk of injury to the upper body (the head, face, chest, and spine) than men with a normal weight. Serious injury in the abdominal region was most likely at low and high BMIs for both men and women. Finally, obese men were more likely to be seriously injured than obese women for all body regions except the extremities and the abdominal region. The researchers' computer simulations confirmed many of these real-world findings.
What Do These Findings Mean?
These findings suggest that obese men have a higher risk of injury, particularly to their upper body, from motor vehicle crashes than men with a normal body weight or than obese women. The researchers suggest that this higher risk may be attributed to differences in body shape, fat distribution, and center of gravity between obese and normal weight individuals and between men and women. These findings, although limited by missing data, suggest that motor vehicle safety features should be adjusted to take into account the ongoing obesity epidemic. Currently, two-thirds of people in the US are overweight or obese, yet a crash test dummy with a normal BMI is still used during the design of car cabins. Finally, although more studies are needed to understand the biomechanical responses of the human body during vehicle collisions, the findings in this study could aid the identification of groups of people at particularly high risk of injury or death on the roads who could then be helped to reduce their risk.
Additional Information
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1000250.
Wikipedia has a page on traffic collision (note that Wikipedia is a free online encyclopedia that anyone can edit; available in several languages)
The World Health Organization has information about road traffic injuries as a public-health problem; its World report on road traffic injury prevention is available in several languages
The US Centers for Disease Control and Prevention provides detailed information about overweight and obesity (in several languages)
MedlinePlus provides links to further resources about obesity (in English and Spanish)
The US National Automotive Sampling System Crashworthiness Data System contains detailed data on thousands of US motor vehicle crashes
doi:10.1371/journal.pmed.1000250
PMCID: PMC2846859  PMID: 20361024
5.  Acute-Phase Serum Amyloid A: An Inflammatory Adipokine and Potential Link between Obesity and Its Metabolic Complications 
PLoS Medicine  2006;3(6):e287.
Background
Obesity is associated with low-grade chronic inflammation, and serum markers of inflammation are independent risk factors for cardiovascular disease (CVD). However, the molecular and cellular mechanisms that link obesity to chronic inflammation and CVD are poorly understood.
Methods and Findings
Acute-phase serum amyloid A (A-SAA) mRNA levels, and A-SAA adipose secretion and serum levels were measured in obese and nonobese individuals, obese participants who underwent weight-loss, and persons treated with the insulin sensitizer rosiglitazone. Inflammation-eliciting activity of A-SAA was investigated in human adipose stromal vascular cells, coronary vascular endothelial cells and a murine monocyte cell line. We demonstrate that A-SAA was highly and selectively expressed in human adipocytes. Moreover, A-SAA mRNA levels and A-SAA secretion from adipose tissue were significantly correlated with body mass index ( r = 0.47; p = 0.028 and r = 0.80; p = 0.0002, respectively). Serum A-SAA levels decreased significantly after weight loss in obese participants ( p = 0.006), as well as in those treated with rosiglitazone ( p = 0.033). The magnitude of the improvement in insulin sensitivity after weight loss was significantly correlated with decreases in serum A-SAA ( r = −0.74; p = 0.034). SAA treatment of vascular endothelial cells and monocytes markedly increased the production of inflammatory cytokines, e.g., interleukin (IL)-6, IL-8, tumor necrosis factor alpha, and monocyte chemoattractant protein-1. In addition, SAA increased basal lipolysis in adipose tissue culture by 47%.
Conclusions
A-SAA is a proinflammatory and lipolytic adipokine in humans. The increased expression of A-SAA by adipocytes in obesity suggests that it may play a critical role in local and systemic inflammation and free fatty acid production and could be a direct link between obesity and its comorbidities, such as insulin resistance and atherosclerosis. Accordingly, improvements in systemic inflammation and insulin resistance with weight loss and rosiglitazone therapy may in part be mediated by decreases in adipocyte A-SAA production.
Editors' Summary
Background.
Obesity often alters an individual's overall metabolism, which in turn leads to complications like diabetes, high blood pressure, and an increased risk of cardiovascular disease (disease of the heart and blood vessels, such as stroke or heart attacks). Having established a strong link between inflammation and cardiovascular disease, scientists now think that obesity might cause persistent low-level inflammation, and that this is the reason for the cardiovascular problems seen in many obese people. By better understanding the links between obesity, inflammation, and cardiovascular disease, the hope is that scientists may be able to find medications that can be given to obese people to reduce their risk of heart attacks and strokes.
Why Was This Study Done?
Previous research had suggested that a substance in the blood called A-SAA, which is raised by inflammation, might be a “missing link” between inflammation and cardiovascular disease, since an individual's baseline level of A-SAA is associated with the risk for cardiovascular disease (in other words, the higher the A-SAA, the higher the risk of cardiovascular disease). In the new study, researchers wanted to know whether the reason that obese people have a higher risk of cardiovascular disease is because they have higher blood levels of A-SAA.
What Did the Researchers Do and Find?
They found that obese people had higher levels of A-SAA in their blood. A-SAA appears to be produced in fat cells (or adipocytes) and then released into the blood. Obese people have higher numbers of fat cells, which could by itself account for the higher blood levels of A-SAA, but the researchers also found that the average fat cell from an obese individual produces and secretes higher levels of A-SAA than fat cells from lean individuals. When the researchers studied people who underwent weight loss, they found that A-SAA levels fell in response to weight loss, and this was associated with improvements in their metabolism. They then studied obese individuals who received the diabetes drug rosiglitazone (which is known to reduce inflammation). They found that even though these individuals did not lose weight, their A-SAA levels dropped as their metabolism improved. Trying to get at the mechanisms by which A-SAA might cause inflammation and diabetes, the researchers found that exposure to A-SAA can stimulate the activation of proinflammation molecules in a number of different cells, including blood vessel cells. It can also stimulate cells to break down fat stores and release fats, which could lead to metabolic complications and ultimately contribute to diabetes.
What Do These Findings Mean?
Together with similar results from other studies, the findings here suggest that A-SAA could promote inflammation, and that elevated levels of A-SAA in obese individuals could contribute to the chronic low-level inflammatory state that puts them at higher risk for cardiovascular complications. The authors speculate that drugs that reduce the blood levels of A-SAA might be useful as treatments for obese patients (to lower their risk of heart attacks and strokes). However, as they acknowledge, additional studies are needed to establish that A-SAA is indeed a causal link between obesity and inflammation and whether it plays a major role before it could be considered a promising drug target.
Additional Information.
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.0030287.
• MedlinePlus pages on obesity and cardiovascular disease
• US Centers for Disease Control and Prevention pages on obesity and cardiovascular disease
• Wikipedia pages on obesity and cardiovascular disease (note: Wikipedia is a free Internet encyclopedia that anyone can edit)
Higher levels of Acute-phase serum amyloid A (A-SAA), a proinflammatory adipokine, in obese individuals may contribute to the chronic low-level inflammatory state that puts them at higher risk for cardiovascular complications.
doi:10.1371/journal.pmed.0030287
PMCID: PMC1472697  PMID: 16737350
6.  Scientific Decision Making, Policy Decisions, and the Obesity Pandemic 
Rising and epidemic rates of obesity in many parts of the world are leading to increased suffering and economic stress from diverting health care resources to treating a variety of serious, but preventable, chronic diseases etiologically linked to obesity, particularly type 2 diabetes mellitus and cardiovascular diseases. Despite decades of research into the causes of the obesity pandemic, we seem to be no nearer to a solution now than when the rise in body weights was first chronicled decades ago. The case is made that impediments to a clear understanding of the nature of the problem occur at many levels. These obstacles begin with defining obesity and include lax application of scientific standards of review, tenuous assumption making, flawed measurement and other methods, constrained discourse limiting examination of alternative explanations of cause, and policies that determine funding priorities. These issues constrain creativity and stifle expansive thinking that could otherwise advance the field in preventing and treating obesity and its complications. Suggestions are made to create a climate of open exchange of ideas and redirection of policies that can remove the barriers that prevent us from making material progress in solving a pressing major public health problem of the early 21st century.
doi:10.1016/j.mayocp.2013.04.005
PMCID: PMC3759398  PMID: 23726399
7.  TV Viewing and Physical Activity Are Independently Associated with Metabolic Risk in Children: The European Youth Heart Study 
PLoS Medicine  2006;3(12):e488.
Background
TV viewing has been linked to metabolic-risk factors in youth. However, it is unclear whether this association is independent of physical activity (PA) and obesity.
Methods and Findings
We did a population-based, cross-sectional study in 9- to 10-y-old and 15- to 16-y-old boys and girls from three regions in Europe (n = 1,921). We examined the independent associations between TV viewing, PA measured by accelerometry, and metabolic-risk factors (body fatness, blood pressure, fasting triglycerides, inverted high-density lipoprotein (HDL) cholesterol, glucose, and insulin levels). Clustered metabolic risk was expressed as a continuously distributed score calculated as the average of the standardized values of the six subcomponents. There was a positive association between TV viewing and adiposity (p = 0.021). However, after adjustment for PA, gender, age group, study location, sexual maturity, smoking status, birth weight, and parental socio-economic status, the association of TV viewing with clustered metabolic risk was no longer significant (p = 0.053). PA was independently and inversely associated with systolic and diastolic blood pressure, fasting glucose, insulin (all p < 0.01), and triglycerides (p = 0.02). PA was also significantly and inversely associated with the clustered risk score (p < 0.0001), independently of obesity and other confounding factors.
Conclusions
TV viewing and PA may be separate entities and differently associated with adiposity and metabolic risk. The association between TV viewing and clustered metabolic risk is mediated by adiposity, whereas PA is associated with individual and clustered metabolic-risk indicators independently of obesity. Thus, preventive action against metabolic risk in children may need to target TV viewing and PA separately.
A study of over 1,900 European children showed that TV viewing and physical activity in children are separately associated with obesity and metabolic risk.
Editors' Summary
Background.
Childhood obesity is a rapidly growing problem. Twenty-five years ago, overweight children were rare. Now, 155 million of the world's children are overweight, and 30–45 million are obese. Both conditions are diagnosed by comparing a child's body mass index (BMI; weight divided by height squared) with the average BMI for their age and sex. Being overweight during childhood is worrying because it is one of the so-called metabolic-risk factors that increase the chances of developing diabetes, heart problems, or strokes later in life. Other metabolic-risk factors are fatness around the belly, blood-fat disorders, high blood pressure, and problems with how the body uses insulin and blood sugar. Until recently, like obesity, these other metabolic-risk factors were seen only in adults, but now they are becoming increasingly common in children. In the US, 1 in 20 adolescents has metabolic syndrome—three or more of these risk factors. Environmental and behavioural changes have probably contributed to the increase in metabolic syndrome in children. As a group, they tend to be less physically active nowadays and they eat bigger portions of energy-dense foods more often. Increased TV viewing during childhood (and the use of other media such as computer games) has also been linked to increased obesity and to poorer health as an adult.
Why Was This Study Done?
One popular theory is that TV viewing may affect obesity and other metabolic-risk factors by displacing PA. Instead of playing in the yard after school, the theory suggests, children laze about in front of the TV. However, there is limited evidence to support this idea, and health professionals need to know whether TV viewing and PA are related, and how they affect metabolic-risk factors, in order to improve children's health. In this study, the researchers examined the associations between TV viewing, PA, and metabolic-risk factors in European children.
What Did the Researchers Do and Find?
The researchers enrolled nearly 2,000 children in two age groups from three areas in Europe. They measured the children's height and weight, estimated how fat they were by measuring skin fold thickness, measured their blood pressure, and examined the levels of glucose, insulin, and different fats in their blood. The children completed a computer questionnaire about the lengths of time for which they watched TV and how often they ate while doing so, and their PA was measured using a device called an accelerometer that each child wore for four days. When these data were analyzed statistically, the researchers found that TV viewing was slightly associated with clustered metabolic risk (the average of the individual metabolic-risk factors). This association was due to an association between TV viewing and obesity—the children who watched most TV tended to be the fattest children. However, TV viewing was not related to PA. The most active children were not necessarily those who watched least TV. Most importantly, PA was related to all individual risk factors except for obesity and with clustered metabolic risk. These associations were independent of obesity.
What Do These Findings Mean?
These results suggest that TV viewing does not damage children's health by displacing PA as popularly believed. The finding that the association between TV viewing and clustered metabolic-risk factors is mediated by obesity suggests that targeting behaviours like eating while watching TV might be a good way to improve children's health. Indeed, the researchers provide some evidence that eating while watching TV is associated with being overweight, but the results of this post hoc analysis—one that was not planned in advance—need to be confirmed. Another limitation of the study is the possibility that the children inaccurately reported their TV watching habits. Also, because measurements of metabolic-risk factors were made only once, it is impossible to say whether TV viewing or lack of PA actually causes an increase in metabolic-risk factors.
Nevertheless, these results strongly suggest that promoting PA is beneficial in relation to metabolic-risk factors, but less so in relation to obesity in childhood. TV viewing and PA should be treated as separate targets in programs designed to reverse the obesity and metabolic-syndrome epidemic in children.
Additional Information.
Please access these Web sites via the online version of this summary at http://dx.doi.org/doi:10.1371/journal.pmed.0030488.
US Centers for Disease Control and Prevention, information on overweight and obesity
International Obesity Taskforce, information on obesity and its prevention, particularly in childhood
Global Prevention Alliance, details of international efforts to halt the obesity epidemic and its associated chronic diseases
American Heart Association, information for patients and professionals on metabolic syndrome and children's health
doi:10.1371/journal.pmed.0030488
PMCID: PMC1705825  PMID: 17194189
8.  Genetic Markers of Adult Obesity Risk Are Associated with Greater Early Infancy Weight Gain and Growth 
PLoS Medicine  2010;7(5):e1000284.
Ken Ong and colleagues genotyped children from the ALSPAC birth cohort and showed an association between greater early infancy gains in weight and length and genetic markers for adult obesity risk.
Background
Genome-wide studies have identified several common genetic variants that are robustly associated with adult obesity risk. Exploration of these genotype associations in children may provide insights into the timing of weight changes leading to adult obesity.
Methods and Findings
Children from the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort were genotyped for ten genetic variants previously associated with adult BMI. Eight variants that showed individual associations with childhood BMI (in/near: FTO, MC4R, TMEM18, GNPDA2, KCTD15, NEGR1, BDNF, and ETV5) were used to derive an “obesity-risk-allele score” comprising the total number of risk alleles (range: 2–15 alleles) in each child with complete genotype data (n = 7,146). Repeated measurements of weight, length/height, and body mass index from birth to age 11 years were expressed as standard deviation scores (SDS). Early infancy was defined as birth to age 6 weeks, and early infancy failure to thrive was defined as weight gain between below the 5th centile, adjusted for birth weight. The obesity-risk-allele score showed little association with birth weight (regression coefficient: 0.01 SDS per allele; 95% CI 0.00–0.02), but had an apparently much larger positive effect on early infancy weight gain (0.119 SDS/allele/year; 0.023–0.216) than on subsequent childhood weight gain (0.004 SDS/allele/year; 0.004–0.005). The obesity-risk-allele score was also positively associated with early infancy length gain (0.158 SDS/allele/year; 0.032–0.284) and with reduced risk of early infancy failure to thrive (odds ratio  = 0.92 per allele; 0.86–0.98; p = 0.009).
Conclusions
The use of robust genetic markers identified greater early infancy gains in weight and length as being on the pathway to adult obesity risk in a contemporary birth cohort.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
The proportion of overweight and obese children is increasing across the globe. In the US, the Surgeon General estimates that, compared with 1980, twice as many children and three times the number of adolescents are now overweight. Worldwide, 22 million children under five years old are considered by the World Health Organization to be overweight.
Being overweight or obese in childhood is associated with poor physical and mental health. In addition, childhood obesity is considered a major risk factor for adult obesity, which is itself a major risk factor for cancer, heart disease, diabetes, osteoarthritis, and other chronic conditions.
The most commonly used measure of whether an adult is a healthy weight is body mass index (BMI), defined as weight in kilograms/(height in metres)2. However, adult categories of obese (>30) and overweight (>25) BMI are not directly applicable to children, whose BMI naturally varies as they grow. BMI can be used to screen children for being overweight and or obese but a diagnosis requires further information.
Why Was This Study Done?
As the numbers of obese and overweight children increase, a corresponding rise in future numbers of overweight and obese adults is also expected. This in turn is expected to lead to an increasing incidence of poor health. As a result, there is great interest among health professionals in possible pathways between childhood and adult obesity. It has been proposed that certain periods in childhood may be critical for the development of obesity.
In the last few years, ten genetic variants have been found to be more common in overweight or obese adults. Eight of these have also been linked to childhood BMI and/or obesity. The authors wanted to identify the timing of childhood weight changes that may be associated with adult obesity. Knowledge of obesity risk genetic variants gave them an opportunity to do so now, without following a set of children to adulthood.
What Did the Researchers Do and Find?
The authors analysed data gathered from a subset of 7,146 singleton white European children enrolled in the Avon Longitudinal Study of Parents and Children (ALSPAC) study, which is investigating associations between genetics, lifestyle, and health outcomes for a group of children in Bristol whose due date of birth fell between April 1991 and December 1992. They used knowledge of the children's genetic makeup to find associations between an obesity risk allele score—a measure of how many of the obesity risk genetic variants a child possessed—and the children's weight, height, BMI, levels of body fat (at nine years old), and rate of weight gain, up to age 11 years.
They found that, at birth, children with a higher obesity risk allele score were not any heavier, but in the immediate postnatal period they were less likely to be in the bottom 5% of the population for weight gain (adjusted for birthweight), often termed “failure to thrive.” At six weeks of age, children with a higher obesity risk allele score tended to be longer and heavier, even allowing for weight at birth.
After six weeks of age, the obesity risk allele score was not associated with any further increase in length/height, but it was associated with a more rapid weight gain between birth and age 11 years. BMI is derived from height and weight measurements, and the association between the obesity risk allele score and BMI was weak between birth and age three-and-a-half years, but after that age the association with BMI increased rapidly. By age nine, children with a higher obesity risk allele score tended to be heavier and taller, with more fat on their bodies.
What Do These Findings Mean?
The combined obesity allele risk score is associated with higher rates of weight gain and adult obesity, and so the authors conclude that weight gain and growth even in the first few weeks after birth may be the beginning of a pathway of greater adult obesity risk.
A study that tracks a population over time can find associations but it cannot show cause and effect. In addition, only a relatively small proportion (1.7%) of the variation in BMI at nine years of age is explained by the obesity risk allele score.
The authors' method of finding associations between childhood events and adult outcomes via genetic markers of risk of disease as an adult has a significant advantage: the authors did not have to follow the children themselves to adulthood, so their findings are more likely to be relevant to current populations. Despite this, this research does not yield advice for parents how to reduce their children's obesity risk. It does suggest that “failure to thrive” in the first six weeks of life is not simply due to a lack of provision of food by the baby's caregiver but that genetic factors also contribute to early weight gain and growth.
The study looked at the combined obesity risk allele score and the authors did not attempt to identify which individual alleles have greater or weaker associations with weight gain and overweight or obesity. This would require further research based on far larger numbers of babies and children. The findings may also not be relevant to children in other types of setting because of the effects of different nutrition and lifestyles.
Additional Information
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1000284.
Further information is available on the ALSPAC study
The UK National Health Service and other partners provide guidance on establishing a healthy lifestyle for children and families in their Change4Life programme
The International Obesity Taskforce is a global network of expertise and the advocacy arm of the International Association for the Study of Obesity. It works with the World Health Organization, other NGOs, and stakeholders and provides information on overweight and obesity
The Centers for Disease Control and Prevention (CDC) in the US provide guidance and tips on maintaining a healthy weight, including BMI calculators in both metric and Imperial measurements for both adults and children. They also provide BMI growth charts for boys and girls showing how healthy ranges vary for each sex at with age
The Royal College of Paediatrics and Child Health provides growth charts for weight and length/height from birth to age 4 years that are based on WHO 2006 growth standards and have been adapted for use in the UK
The CDC Web site provides information on overweight and obesity in adults and children, including definitions, causes, and data
The CDC also provide information on the role of genes in causing obesity.
The World Health Organization publishes a fact sheet on obesity, overweight and weight management, including links to childhood overweight and obesity
Wikipedia includes an article on childhood obesity (note that Wikipedia is a free online encyclopedia that anyone can edit; available in several languages)
doi:10.1371/journal.pmed.1000284
PMCID: PMC2876048  PMID: 20520848
9.  Physical Activity Attenuates the Genetic Predisposition to Obesity in 20,000 Men and Women from EPIC-Norfolk Prospective Population Study 
PLoS Medicine  2010;7(8):e1000332.
Shengxu Li and colleagues use data from a large prospective observational cohort to examine the extent to which a genetic predisposition toward obesity may be modified by living a physically active lifestyle.
Background
We have previously shown that multiple genetic loci identified by genome-wide association studies (GWAS) increase the susceptibility to obesity in a cumulative manner. It is, however, not known whether and to what extent this genetic susceptibility may be attenuated by a physically active lifestyle. We aimed to assess the influence of a physically active lifestyle on the genetic predisposition to obesity in a large population-based study.
Methods and Findings
We genotyped 12 SNPs in obesity-susceptibility loci in a population-based sample of 20,430 individuals (aged 39–79 y) from the European Prospective Investigation of Cancer (EPIC)-Norfolk cohort with an average follow-up period of 3.6 y. A genetic predisposition score was calculated for each individual by adding the body mass index (BMI)-increasing alleles across the 12 SNPs. Physical activity was assessed using a self-administered questionnaire. Linear and logistic regression models were used to examine main effects of the genetic predisposition score and its interaction with physical activity on BMI/obesity risk and BMI change over time, assuming an additive effect for each additional BMI-increasing allele carried. Each additional BMI-increasing allele was associated with 0.154 (standard error [SE] 0.012) kg/m2 (p = 6.73×10−37) increase in BMI (equivalent to 445 g in body weight for a person 1.70 m tall). This association was significantly (pinteraction = 0.005) more pronounced in inactive people (0.205 [SE 0.024] kg/m2 [p = 3.62×10−18; 592 g in weight]) than in active people (0.131 [SE 0.014] kg/m2 [p = 7.97×10−21; 379 g in weight]). Similarly, each additional BMI-increasing allele increased the risk of obesity 1.116-fold (95% confidence interval [CI] 1.093–1.139, p = 3.37×10−26) in the whole population, but significantly (pinteraction = 0.015) more in inactive individuals (odds ratio [OR] = 1.158 [95% CI 1.118–1.199; p = 1.93×10−16]) than in active individuals (OR = 1.095 (95% CI 1.068–1.123; p = 1.15×10−12]). Consistent with the cross-sectional observations, physical activity modified the association between the genetic predisposition score and change in BMI during follow-up (pinteraction = 0.028).
Conclusions
Our study shows that living a physically active lifestyle is associated with a 40% reduction in the genetic predisposition to common obesity, as estimated by the number of risk alleles carried for any of the 12 recently GWAS-identified loci.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
In the past few decades, the global incidence of obesity—defined as a body mass index (BMI, a simple index of weight-for-height that uses the weight in kilograms divided by the square of the height in meters) of 30 and over, has increased so much that this growing public health concern is now commonly referred to as the “obesity epidemic.” Once considered prevalent only in high-income countries, obesity is an increasing health problem in low- and middle-income countries, particularly in urban settings. In 2005, at least 400 million adults world-wide were obese, and the projected figure for 2015 is a substantial increase of 300 million to around 700 million. Childhood obesity is also a growing concern. Contributing factors to the obesity epidemic are a shift in diet to an increased intake of energy-dense foods that are high in fat and sugars and a trend towards decreased physical activity due to increasingly sedentary lifestyles.
However, genetics are also thought to play a critical role as genetically predisposed individuals may be more prone to obesity if they live in an environment that has abundant access to energy-dense food and labor-saving devices.
Why Was This Study Done?
Although recent genetic studies (genome-wide association studies) have identified 12 alleles (a DNA variant that is located at a specific position on a specific chromosome) associated with increased BMI, there has been no convincing evidence of the interaction between genetics and lifestyle. In this study the researchers examined the possibility of such an interaction by assessing whether individuals with a genetic predisposition to increased obesity risk could modify this risk by increasing their daily physical activity.
What Did the Researchers Do and Find?
The researchers used a population-based cohort study of 25,631 people living in Norwich, UK (The EPIC-Norfolk study) and identified individuals who were 39 to 79 years old during a health check between 1993 and 1997. The researchers invited these people to a second health examination. In total, 20,430 individuals had baseline data available, of which 11,936 had BMI data at the second health check. The researchers used genotyping methods and then calculated a genetic predisposition score for each individual and their occupational and leisure-time physical activities were assessed by using a validated self-administered questionnaire. Then, the researchers used modeling techniques to examine the main effects of the genetic predisposition score and its interaction with physical activity on BMI/obesity risk and BMI change over time. The researchers found that each additional BMI-increasing allele was associated with an increase in BMI equivalent to 445 g in body weight for a person 1.70 m tall and that the size of this effect was greater in inactive people than in active people. In individuals who have a physically active lifestyle, this increase was only 379 g/allele, or 36% lower than in physically inactive individuals in whom the increase was 592 g/allele. Furthermore, in the total sample each additional obesity-susceptibility allele increased the odds of obesity by 1.116-fold. However, the increased odds per allele for obesity risk were 40% lower in physically active individuals (1.095 odds/allele) compared to physically inactive individuals (1.158 odds/allele).
What Do These Findings Mean?
The findings of this study indicate that the genetic predisposition to obesity can be reduced by approximately 40% by having a physically active lifestyle. The findings of this study suggest that, while the whole population benefits from increased physical activity levels, individuals who are genetically predisposed to obesity would benefit more than genetically protected individuals. Furthermore, these findings challenge the deterministic view of the genetic predisposition to obesity that is often held by the public, as they show that even the most genetically predisposed individuals will benefit from adopting a healthy lifestyle. The results are limited by participants self-reporting their physical activity levels, which is less accurate than objective measures of physical activity.
Additional Information
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1000332.
This study relies on the results of previous genome-wide association studies The National Human Genome Research Institute provides an easy-to-follow guide to understanding such studies
The International Association for the Study of Obesity aims to improve global health by promoting the understanding of obesity and weight-related diseases through scientific research and dialogue
The International Obesity Taskforce is the research-led think tank and advocacy arm of the International Association for the Study of Obesity
The Global Alliance for the Prevention of Obesity and Related Chronic Disease is a global action program that addresses the issues surrounding the prevention of obesity
The National Institutes of Health has its own obesity task force, which includes 26 institutes
doi:10.1371/journal.pmed.1000332
PMCID: PMC2930873  PMID: 20824172
10.  Cars, corporations, and commodities: Consequences for the social determinants of health 
Social epidemiologists have drawn attention to health inequalities as avoidable and inequitable, encouraging thinking beyond proximal risk factors to the causes of the causes. However, key debates remain unresolved including the contribution of material and psychosocial pathways to health inequalities. Tools to operationalise social factors have not developed in tandem with conceptual frameworks, and research has often remained focused on the disadvantaged rather than on forces shaping population health across the distribution. Using the example of transport, we argue that closer attention to social processes (capital accumulation and motorisation) and social forms (commodity, corporation, and car) offers a way forward. Corporations tied to the car, primarily oil and vehicle manufacturers, are central to the world economy. Key drivers in establishing this hegemony are the threat of violence from motor vehicles and the creation of distance through the restructuring of place. Transport matters for epidemiology because the growth of mass car ownership is environmentally unsustainable and affects population health through a myriad of pathways. Starting from social forms and processes, rather than their embodiment as individual health outcomes and inequalities, makes visible connections between road traffic injuries, obesity, climate change, underdevelopment of oil producing countries, and the huge opportunity cost of the car economy. Methodological implications include a movement-based understanding of how place affects health and a process-orientated integration of material and psychosocial explanations that, while materially based, contests assumptions of automatic benefits from economic growth. Finally, we identify car and oil corporations as anti-health forces and suggest collaboration with them creates conflicts of interest.
doi:10.1186/1742-7622-5-4
PMCID: PMC2289830  PMID: 18291031
11.  The Double Burden of Obesity and Malnutrition in a Protracted Emergency Setting: A Cross-Sectional Study of Western Sahara Refugees 
PLoS Medicine  2012;9(10):e1001320.
Surveying women and children from refugee camps in Algeria, Carlos Grijalva-Eternod and colleagues find high rates of obesity among women as well as many undernourished children, and that almost a quarter of households are affected by both undernutrition and obesity.
Background
Households from vulnerable groups experiencing epidemiological transitions are known to be affected concomitantly by under-nutrition and obesity. Yet, it is unknown to what extent this double burden affects refugee populations dependent on food assistance. We assessed the double burden of malnutrition among Western Sahara refugees living in a protracted emergency.
Methods and Findings
We implemented a stratified nutrition survey in October–November 2010 in the four Western Sahara refugee camps in Algeria. We sampled 2,005 households, collecting anthropometric measurements (weight, height, and waist circumference) in 1,608 children (6–59 mo) and 1,781 women (15–49 y). We estimated the prevalence of global acute malnutrition (GAM), stunting, underweight, and overweight in children; and stunting, underweight, overweight, and central obesity in women. To assess the burden of malnutrition within households, households were first classified according to the presence of each type of malnutrition. Households were then classified as undernourished, overweight, or affected by the double burden if they presented members with under-nutrition, overweight, or both, respectively.
The prevalence of GAM in children was 9.1%, 29.1% were stunted, 18.6% were underweight, and 2.4% were overweight; among the women, 14.8% were stunted, 53.7% were overweight or obese, and 71.4% had central obesity. Central obesity (47.2%) and overweight (38.8%) in women affected a higher proportion of households than did GAM (7.0%), stunting (19.5%), or underweight (13.3%) in children. Overall, households classified as overweight (31.5%) were most common, followed by undernourished (25.8%), and then double burden–affected (24.7%).
Conclusions
The double burden of obesity and under-nutrition is highly prevalent in households among Western Sahara refugees. The results highlight the need to focus more attention on non-communicable diseases in this population and balance obesity prevention and management with interventions to tackle under-nutrition.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
Good nutrition is essential for human health and survival. Insufficient food intake causes under-nutrition, which increases susceptibility to infections; intake of too much or inappropriate food, in particular in interaction with sedentary behaviour, can lead to obesity, which increases the risk of non-communicable diseases such as diabetes. During the past 30 years, the prevalence (the proportion of a population affected by a condition) of obesity has greatly increased, initially among adults in industrialized countries, but more recently among children and in less-affluent populations. Now, worldwide, overweight people outnumber under-nourished people. Furthermore, some populations are affected by both under-nutrition and obesity, forms of malnutrition that occur when the diet is suboptimal for health. So, for example, a child can be both stunted (short for his or her age, an indicator of long-term under-nutrition) and overweight (too heavy for his or her age). The emergence of this double burden of malnutrition has been attributed to the nutrition transition—the rapid move because of migration or urbanization to a lifestyle characterized by low levels of physical activity and high consumption of refined, energy-dense foods—without complete elimination of under-nutrition.
Why Was This Study Done?
Refugees are one group of people in whom under-nutrition and obesity sometimes coexist. Worldwide, in 2010, 15.4 million refugees were dependent on host governments and international humanitarian agencies for their food security and well-being. It is essential that these governments and organizations provide appropriate food assistance programs to refugees—policies that are appropriate during acute emergencies may not be appropriate in protracted emergencies and may contribute to the emergence of the double burden of malnutrition among refugees. Unfortunately, the extent to which the double burden of malnutrition affects refugees in protracted emergencies is unknown. In this cross-sectional study (an investigation that looks at the characteristics of a population at a single time), the researchers assessed the double burden of malnutrition among people from Western Sahara who have been living in four refugee camps near Tindouf city, Algeria, since 1975.
What Did the Researchers Do and Find?
The researchers used data from a 2010 survey that measured the height and weight of children and the height, weight, and waist circumference of women living in 2,005 households in the Algerian refugee camps. For the children, they estimated the prevalence of global acute malnutrition (which includes thin, “wasted” children, as indicated by a low weight for height based on the World Health Organization growth standards, and those with nutritional oedema), stunting, and underweight and overweight (low and high weight for age and gender, respectively). For the women, they estimated the prevalence of stunting, underweight (body mass index less than 18.5 kg/m2), overweight (body mass index greater than 25 kg/m2), and central obesity (a waist circumference of more than 80 cm). Among the children, 9.1% had global acute malnutrition, 29.1% were stunted, 8.6% were underweight, and 2.4% were overweight. Among the women, 14.8% were stunted, 53.7% were overweight, and 71.4% had central obesity. Notably, central obesity and overweight in women affected more households than global acute malnutrition, stunting, and underweight in children. Finally, based on whether a household included members with under-nutrition or overweight, alone or in combination, the researchers classified a third of households as overweight, a quarter as undernourished, and a quarter as affected by the double burden of malnutrition.
What Do These Findings Mean?
These findings indicate that there is a high prevalence of the double burden of malnutrition among households in Western Saharan refugee camps in Algeria. Although this study provides no information on men and does not investigate whether the obesity seen in these camps leads to an increased risk of diabetes and other non-communicable diseases, these findings have several important implications for the provision of food assistance and care for protracted humanitarian emergencies. For example, they highlight the need to promote long-term food security and to improve nutrition adequacy and food diversity in protracted emergencies. In addition, they suggest that current food assistance programs that are suitable for acute emergencies may not be suitable for extended emergencies. They also highlight the need to focus more attention on non-communicable diseases in refugee camps and to develop innovative ways to provide obesity prevention and management in these settings. However, as the researchers stress, careful policy and advocacy work is essential to ensure that efforts to deal with the threat of obesity among refugees do not jeopardize support for life-saving food assistance programs for refugees.
Additional Information
Please access these websites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001320.
Wikipedia provides background information about the Western Sahara refugee camps near Tindouf, Algeria (note that Wikipedia is a free online encyclopedia that anyone can edit)
The World Health Organization provides information on all aspects of nutrition and obesity (in several languages)
The United Nations World Food Programme is the world's largest humanitarian agency fighting hunger worldwide; its website provides detailed information about hunger and information about its work in the Western Sahara refugee camps in Algeria, including personal stories and photographs of food distribution
The United Nations High Commissioner for Refugees is the United Nations body mandated to lead and coordinate international action to protect refugees and resolve refugee problems worldwide; its website provides detailed information about its work in the Western Sahara refugee camps in Algeria
Oxfam also provides detailed information about its work in the Algerian refugee camps, a description of the camps, and personal stories from people living in the camps
An article published by the Food and Agriculture Organization of the United Nations explains the double burden of malnutrition
doi:10.1371/journal.pmed.1001320
PMCID: PMC3462761  PMID: 23055833
12.  The Effect of Rural-to-Urban Migration on Obesity and Diabetes in India: A Cross-Sectional Study 
PLoS Medicine  2010;7(4):e1000268.
Shah Ebrahim and colleagues examine the distribution of obesity, diabetes, and other cardiovascular risk factors among urban migrant factory workers in India, together with their rural siblings. The investigators identify patterns of change of cardiovascular risk factors associated with urban migration.
Background
Migration from rural areas of India contributes to urbanisation and may increase the risk of obesity and diabetes. We tested the hypotheses that rural-to-urban migrants have a higher prevalence of obesity and diabetes than rural nonmigrants, that migrants would have an intermediate prevalence of obesity and diabetes compared with life-long urban and rural dwellers, and that longer time since migration would be associated with a higher prevalence of obesity and of diabetes.
Methods and Findings
The place of origin of people working in factories in north, central, and south India was identified. Migrants of rural origin, their rural dwelling sibs, and those of urban origin together with their urban dwelling sibs were assessed by interview, examination, and fasting blood samples. Obesity, diabetes, and other cardiovascular risk factors were compared. A total of 6,510 participants (42% women) were recruited. Among urban, migrant, and rural men the age- and factory-adjusted percentages classified as obese (body mass index [BMI] >25 kg/m2) were 41.9% (95% confidence interval [CI] 39.1–44.7), 37.8% (95% CI 35.0–40.6), and 19.0% (95% CI 17.0–21.0), respectively, and as diabetic were 13.5% (95% CI 11.6–15.4), 14.3% (95% CI 12.2–16.4), and 6.2% (95% CI 5.0–7.4), respectively. Findings for women showed similar patterns. Rural men had lower blood pressure, lipids, and fasting blood glucose than urban and migrant men, whereas no differences were seen in women. Among migrant men, but not women, there was weak evidence for a lower prevalence of both diabetes and obesity among more recent (≤10 y) migrants.
Conclusions
Migration into urban areas is associated with increases in obesity, which drive other risk factor changes. Migrants have adopted modes of life that put them at similar risk to the urban population. Gender differences in some risk factors by place of origin are unexpected and require further exploration.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
India, like the rest of the world, is experiencing an epidemic of diabetes, a chronic disease characterized by dangerous levels of sugar in the blood that cause cardiovascular and kidney disease, which lower life expectancy. The prevalence of diabetes (the proportion of the population with diabetes) has been increasing steadily in India over recent decades, particularly in urban areas. In 1984, only 5% of adults living in the towns and cities of India had diabetes, but by 2004, 15% of adults in urban areas were affected by diabetes. In rural areas of India, diabetes is less common than in urban areas but even here, the prevalence of diabetes is now 6%. Obesity—too much body fat—is a major risk factor for diabetes and, in parallel with the greater increase in diabetes in urban India compared to rural India, there has been a greater increase in obesity in urban areas than in rural areas.
Why Was This Study Done?
Experts think that the increasing prevalence of obesity and diabetes in India (and in other developing countries) is caused in part by increased consumption of saturated fats and sugars and by reduced physical activity, and that these changes are related to urbanization—urban expansion into the countryside and migration from rural to urban areas. If living in an urban setting is a major determinant of obesity and diabetes risk, then people migrating into urban areas should acquire the high risk of the urban population for these two conditions. In this cross-sectional study (a study in which participants are studied at a single time point), the researchers investigate whether rural to urban migrants in India have a higher prevalence of obesity and diabetes than rural nonmigrants. They also ask whether migrants have a prevalence of obesity and diabetes intermediate between that of life-long urban and rural dwellers and whether a longer time since migration is associated with a higher prevalence of obesity and diabetes.
What Did the Researchers Do and Find?
The researchers recruited rural-urban migrants working in four Indian factories in north, central, and south regions and their spouses (if they were living in the same town) into their study. Each migrant worker and spouse asked one nonmigrant brother or sister (sibling) still living in their place of origin to join the study. The researchers also enrolled nonmigrant factory workers and their urban siblings into the study. All the participants (more than 6,500 in total) answered questions about their diet and physical activity and had their fasting blood sugar and their body mass index (BMI; weight in kg divided by height in meters squared) measured; participants with a fasting blood sugar of more than 7.0 nmol/l or a BMI of more than 25 kg/m2 were classified as diabetic or obese, respectively. 41.9% and 37.8% of the urban and migrant men, respectively, but only 19.0% of the rural men were obese. Similarly, 13.5% and 14.3% of the urban and migrant men, respectively, but only 6.2% of the rural men had diabetes. Patterns of obesity and diabetes among the women participants were similar. Finally, although the prevalence of diabetes and obesity was lower in the most recent male migrants than in those who had moved more than 10 years previously, this difference was small and not seen in women migrants.
What Do These Findings Mean?
These findings show that rural-urban migration in India is associated with rapid increases in obesity and in diabetes. They also show that the migrants have adopted modes of life (for example, reduced physical activity) that put them at a similar risk for obesity and diabetes as the urban population. The findings do not show, however, that migrants have an intermediate prevalence of obesity and diabetes compared to urban and rural dwellers and provide only weak support for the idea that a longer time since migration is associated with a higher risk of obesity and diabetes. Although the study's cross-sectional design means that the researchers could not investigate how risk factors for diabetes evolve over time, these findings suggest that urbanization is helping to drive the diabetes epidemic in India. Thus, targeting migrants and their families for health promotion activities and for treatment of risk factors for obesity and diabetes might help to slow the progress of the epidemic.
Additional Information
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1000268.
The International Diabetes Federation provides information about all aspects of diabetes, including information on diabetes in Southeast Asia (in English, French, and Spanish)
DiabetesIndia.com provides information on the Indian Task Forces on diabetes care in India
Diabetes Foundation (India) has an international collaborative research focus and provides information about health promotion for diabetes; it has also produced consensus guidelines on dietary change for prevention of diabetes in India
The US National Diabetes Information Clearinghouse provides detailed information about diabetes for patients, health care professionals, and the general public (in English and Spanish)
MedlinePlus provides links to further resources and advice about diabetes (in English and Spanish)
doi:10.1371/journal.pmed.1000268
PMCID: PMC2860494  PMID: 20436961
13.  Averting Obesity and Type 2 Diabetes in India through Sugar-Sweetened Beverage Taxation: An Economic-Epidemiologic Modeling Study 
PLoS Medicine  2014;11(1):e1001582.
In this modeling study, Sanjay Basu and colleagues estimate the potential health effects of a sugar-sweetened beverage taxation among various sub-populations in India over the period 2014 to 2023.
Please see later in the article for the Editors' Summary
Background
Taxing sugar-sweetened beverages (SSBs) has been proposed in high-income countries to reduce obesity and type 2 diabetes. We sought to estimate the potential health effects of such a fiscal strategy in the middle-income country of India, where there is heterogeneity in SSB consumption, patterns of substitution between SSBs and other beverages after tax increases, and vast differences in chronic disease risk within the population.
Methods and Findings
Using consumption and price variations data from a nationally representative survey of 100,855 Indian households, we first calculated how changes in SSB price alter per capita consumption of SSBs and substitution with other beverages. We then incorporated SSB sales trends, body mass index (BMI), and diabetes incidence data stratified by age, sex, income, and urban/rural residence into a validated microsimulation of caloric consumption, glycemic load, overweight/obesity prevalence, and type 2 diabetes incidence among Indian subpopulations facing a 20% SSB excise tax. The 20% SSB tax was anticipated to reduce overweight and obesity prevalence by 3.0% (95% CI 1.6%–5.9%) and type 2 diabetes incidence by 1.6% (95% CI 1.2%–1.9%) among various Indian subpopulations over the period 2014–2023, if SSB consumption continued to increase linearly in accordance with secular trends. However, acceleration in SSB consumption trends consistent with industry marketing models would be expected to increase the impact efficacy of taxation, averting 4.2% of prevalent overweight/obesity (95% CI 2.5–10.0%) and 2.5% (95% CI 1.0–2.8%) of incident type 2 diabetes from 2014–2023. Given current consumption and BMI distributions, our results suggest the largest relative effect would be expected among young rural men, refuting our a priori hypothesis that urban populations would be isolated beneficiaries of SSB taxation. Key limitations of this estimation approach include the assumption that consumer expenditure behavior from prior years, captured in price elasticities, will reflect future behavior among consumers, and potential underreporting of consumption in dietary recall data used to inform our calculations.
Conclusion
Sustained SSB taxation at a high tax rate could mitigate rising obesity and type 2 diabetes in India among both urban and rural subpopulations.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
Non-communicable diseases (NCDs) and obesity (excessive body mass) are major threats to global health. Each year NCDs kill 36 million people (including 29 million people in low- and middle-income countries), thereby accounting for nearly two-thirds of the world's annual deaths. Cardiovascular diseases, cancers, respiratory diseases, and diabetes (a condition characterized by raised blood sugar levels) are responsible for most NCD-related deaths. Worldwide, diabetes alone affects about 360 million people and causes nearly 5 million deaths annually. And the number of people affected by NCDs is likely to rise over the next few decades. It is estimated, for example, that 101.2 million people in India will have diabetes by 2030, nearly double the current number. In Asia and other low- and middle-income countries overweight as well as obesity represent a risk factor for NCDs and the global prevalence of obesity (the proportion of the world's population that is obese) has nearly doubled since 1980. Worldwide, around 0.5 billion people are now classified as obese and about 1.5 billion more overweight. That is, they have a body mass index (BMI) of 30 kg/m2 or more (25–30 for overweight); BMI is calculated by dividing a person's weight in kilograms by the square of their height in meters. In India individuals with a BMI of 25 or more (overweight/obese) are at very high risk of diabetes.
Why Was This Study Done?
The consumption of sugar-sweetened beverages (SSBs, soft drinks sweetened with cane sugar or other caloric sweeteners) is a major risk factor for overweight/obesity and, independent of total energy consumption and BMI, for type 2 diabetes (the commonest form of diabetes). In high-income countries, SSB taxation has been proposed as a way to lower the risk of obesity and type 2 diabetes, however it is unknown if this approach will work in low- and middle-income countries. Here, in an economic-epidemiologic modeling study, researchers estimate the potential health effects of SSB taxation in India, a middle-income country in which total SSB consumption is rapidly increasing, but where SSB consumption and chronic disease risk vary greatly within the population and where people are likely to turn to other sugar-rich beverages (for example, fresh fruit juices) if SSBs are taxed.
What Did the Researchers Do and Find?
The researchers used survey data relating SSB consumption to price variations to calculate how changes in the price of SSBs affect the demand for SSBs (own-price elasticity) and for other beverages (cross-price elasticity) in India. They combined these elasticities and data on SSB sales trends, BMIs, and diabetes incidence (the frequency of new diabetes cases) into a mathematical microsimulation model to estimate the effect of a 20% tax on SSBs on caloric (energy) consumption, glycemic load (an estimate of how much a food or drink raises blood sugar levels after consumption; low glycemic load diets lower diabetes risk), the prevalence of overweight/obesity, and the incidence of diabetes among Indian subpopulations. According to the model, if SSB sales continue to increase at the current rate, compared to no tax, a 20% SSB tax would reduce overweight/obesity across India by 3.0% and the incidence of type 2 diabetes by 1.6% over the period 2014–2023. In absolute figures, a 20% SSB tax would avert 11.2 million cases of overweight/obesity and 400,000 cases of type 2 diabetes between 2014 and 2023. Notably, if SSB sales increase more steeply as predicted by drinks industry marketing models, the tax would avert 15.8 million cases of overweight/obesity and 600,000 cases of diabetes. Finally, the model predicted that the largest relative effect of an SSB tax would be among young men in rural areas.
What Do These Findings Mean?
The accuracy of these findings is likely to be affected by the assumptions incorporated in the model and by the data fed into it. In particular, the accuracy of the estimates of the health effects of a 20% tax on SSBs is limited by the assumption that future consumer behavior will reflect historic behavior and by potential underreporting of SSB consumption in surveys. Nevertheless, these findings suggest that a sustained high rate of tax on SSBs could mitigate the rising prevalence of obesity and the rising incidence of diabetes in India in both urban and rural populations by affecting both caloric intake and glycemic load. Thus, SSB taxation might be a way to control obesity and diabetes in India and other low- and middle-income countries where, to date, large-scale interventions designed to address these threats to global health have had no sustained effects.
Additional Information
Please access these websites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001582.
The World Health Organization provides information about non-communicable diseases, obesity, and diabetes around the world (in several languages)
The US Centers for Disease Control and Prevention provides information on non-communicable diseases around the world and on overweight and obesity and diabetes (including some information in Spanish)
The US National Diabetes Information Clearinghouse provides information about diabetes for patients, health-care professionals, and the general public, including detailed information on weight control (in English and Spanish)
The UK National Health Service Choices website provides information for patients and carers about type 2 diabetes and about obesity; it includes personal stories about diabetes and about obesity
MedlinePlus provides links to further resources and advice about diabetes and diabetes prevention and about obesity (in English and Spanish)
A 2012 Policy brief from the Yale Rudd Center for food policy and obesity provides information about SSB taxes
doi:10.1371/journal.pmed.1001582
PMCID: PMC3883641  PMID: 24409102
14.  Bariatric Surgery 
Executive Summary
Objective
To conduct an evidence-based analysis of the effectiveness and cost-effectiveness of bariatric surgery.
Background
Obesity is defined as a body mass index (BMI) of at last 30 kg/m2.1 Morbid obesity is defined as a BMI of at least 40 kg/m2 or at least 35 kg/m2 with comorbid conditions. Comorbid conditions associated with obesity include diabetes, hypertension, dyslipidemias, obstructive sleep apnea, weight-related arthropathies, and stress urinary incontinence. It is also associated with depression, and cancers of the breast, uterus, prostate, and colon, and is an independent risk factor for cardiovascular disease.
Obesity is also associated with higher all-cause mortality at any age, even after adjusting for potential confounding factors like smoking. A person with a BMI of 30 kg/m2 has about a 50% higher risk of dying than does someone with a healthy BMI. The risk more than doubles at a BMI of 35 kg/m2. An expert estimated that about 160,000 people are morbidly obese in Ontario. In the United States, the prevalence of morbid obesity is 4.7% (1999–2000).
In Ontario, the 2004 Chief Medical Officer of Health Report said that in 2003, almost one-half of Ontario adults were overweight (BMI 25–29.9 kg/m2) or obese (BMI ≥ 30 kg/m2). About 57% of Ontario men and 42% of Ontario women were overweight or obese. The proportion of the population that was overweight or obese increased gradually from 44% in 1990 to 49% in 2000, and it appears to have stabilized at 49% in 2003. The report also noted that the tendency to be overweight and obese increases with age up to 64 years. BMI should be used cautiously for people aged 65 years and older, because the “normal” range may begin at slightly above 18.5 kg/m2 and extend into the “overweight” range.
The Chief Medical Officer of Health cautioned that these data may underestimate the true extent of the problem, because they were based on self reports, and people tend to over-report their height and under-report their weight. The actual number of Ontario adults who are overweight or obese may be higher.
Diet, exercise, and behavioural therapy are used to help people lose weight. The goals of behavioural therapy are to identify, monitor, and alter behaviour that does not help weight loss. Techniques include self-monitoring of eating habits and physical activity, stress management, stimulus control, problem solving, cognitive restructuring, contingency management, and identifying and using social support. Relapse, when people resume old, unhealthy behaviour and then regain the weight, can be problematic.
Drugs (including gastrointestinal lipase inhibitors, serotonin norepinephrine reuptake inhibitors, and appetite suppressants) may be used if behavioural interventions fail. However, estimates of efficacy may be confounded by high rates of noncompliance, in part owing to the side effects of the drugs. In addition, the drugs have not been approved for indefinite use, despite the chronic nature of obesity.
The Technology
Morbidly obese people may be eligible for bariatric surgery. Bariatric surgery for morbid obesity is considered an intervention of last resort for patients who have attempted first-line forms of medical management, such as diet, increased physical activity, behavioural modification, and drugs.
There are various bariatric surgical procedures and several different variations for each of these procedures. The surgical interventions can be divided into 2 general types: malabsorptive (bypassing parts of the gastrointestinal tract to limit the absorption of food), and restrictive (decreasing the size of the stomach so that the patient is satiated with less food). All of these may be performed as either open surgery or laparoscopically. An example of a malabsorptive technique is Roux-en-Y gastric bypass (RYGB). Examples of restrictive techniques are vertical banded gastroplasty (VBG) and adjustable gastric banding (AGB).
The Ontario Health Insurance Plan (OHIP) Schedule of Benefits for Physician Services includes fee code “S120 gastric bypass or partition, for morbid obesity” as an insured service. The term gastric bypass is a general term that encompasses a variety of surgical methods, all of which involve reconfiguring the digestive system. The term gastric bypass does not include AGB. The number of gastric bypass procedures funded and done in Ontario, and funded as actual out-of-country approvals,2 is shown below.
Number of Gastric Bypass Procedures by Fiscal Year: Ontario and Actual Out-of-Country (OOC) Approvals
Data from Provider Services, MOHLTC
Courtesy of Provider Services, Ministry of Health and Long Term Care
Review Strategy
The Medical Advisory Secretariat reviewed the literature to assess the effectiveness, safety, and cost-effectiveness of bariatric surgery to treat morbid obesity. It used its standard search strategy to retrieve international health technology assessments and English-language journal articles from selected databases. The interventions of interest were bariatric surgery and, for the controls, either optimal conventional management or another type of bariatric procedure. The outcomes of interest were improvement in comorbid conditions (e.g., diabetes, hypertension); short- and long-term weight loss; quality of life; adverse effects; and economic analysis data. The databases yielded 15 international health technology assessments or systematic reviews on bariatric surgery.
Subsequently, the Medical Advisory Secretariat searched MEDLINE and EMBASE from April 2004 to December 2004, after the search cut-off date of April, 2004, for the most recent systematic reviews on bariatric surgery. Ten studies met the inclusion criteria. One of those 10 was the Swedish Obese Subjects study, which started as a registry and intervention study, and then published findings on people who had been enrolled for at least 2 years or at least 10 years. In addition to the literature review of economic analysis data, the Medical Advisory Secretariat also did an Ontario-based economic analysis.
Summary of Findings
Bariatric surgery generally is effective for sustained weight loss of about 16% for people with BMIs of at least 40 kg/m2 or at least 35 kg/m2 with comorbid conditions (including diabetes, high lipid levels, and hypertension). It also is effective at resolving the associated comorbid conditions. This conclusion is largely based on level 3a evidence from the prospectively designed Swedish Obese Subjects study, which recently published 10-year outcomes for patients who had bariatric surgery compared with patients who received nonsurgical treatment. (1)
Regarding specific procedures, there is evidence that malabsorptive techniques are better than other banding techniques for weight loss and resolution of comorbid illnesses. However, there are no published prospective, long-term, direct comparisons of these techniques available.
Surgery for morbid obesity is considered an intervention of last resort for patients who have attempted first-line forms of medical management, such as diet, increased physical activity, behavioural modification, and drugs. In the absence of direct comparisons of active nonsurgical intervention via caloric restriction with bariatric techniques, the following observations are made:
A recent systematic review examining the efficacy of major commercial and organized self-help weight loss programs in the United States concluded that the evidence to support the use of such programs was suboptimal, except for one trial on Weight Watchers. Furthermore, the programs were associated with high costs, attrition rates, and probability of regaining at least 50% of the lost weight in 1 to 2 years. (2)
A recent randomized controlled trial reported 1-year outcomes comparing weight loss and metabolic changes in severely obese patients assigned to either a low-carbohydrate diet or a conventional weight loss diet. At 1 year, weight loss was similar for patients in each group (mean, 2–5 kg). There was a favourable effect on triglyceride levels and glycemic control in the low-carbohydrate diet group. (3)
A decision-analysis model showed bariatric surgery results in increased life expectancy in morbidly obese patients when compared to diet and exercise. (4)
A cost-effectiveness model showed bariatric surgery is cost-effective relative to nonsurgical management. (5)
Extrapolating from 2003 data from the United States, Ontario would likely need to do 3,500 bariatric surgeries per year. It currently does 508 per year, including out-of-country surgeries.
PMCID: PMC3382415  PMID: 23074460
15.  Pregnancy Weight Gain and Childhood Body Weight: A Within-Family Comparison 
PLoS Medicine  2013;10(10):e1001521.
David Ludwig and colleagues examine the within-family relationship between pregnancy weight gain and the offspring's childhood weight gain, thereby reducing the influence of genes and environment.
Please see later in the article for the Editors' Summary
Background
Excessive pregnancy weight gain is associated with obesity in the offspring, but this relationship may be confounded by genetic and other shared influences. We aimed to examine the association of pregnancy weight gain with body mass index (BMI) in the offspring, using a within-family design to minimize confounding.
Methods and Findings
In this population-based cohort study, we matched records of all live births in Arkansas with state-mandated data on childhood BMI collected in public schools (from August 18, 2003 to June 2, 2011). The cohort included 42,133 women who had more than one singleton pregnancy and their 91,045 offspring. We examined how differences in weight gain that occurred during two or more pregnancies for each woman predicted her children's BMI and odds ratio (OR) of being overweight or obese (BMI≥85th percentile) at a mean age of 11.9 years, using a within-family design. For every additional kg of pregnancy weight gain, childhood BMI increased by 0.0220 (95% CI 0.0134–0.0306, p<0.0001) and the OR of overweight/obesity increased by 1.007 (CI 1.003–1.012, p = 0.0008). Variations in pregnancy weight gain accounted for a 0.43 kg/m2 difference in childhood BMI. After adjustment for birth weight, the association of pregnancy weight gain with childhood BMI was attenuated but remained statistically significant (0.0143 kg/m2 per kg of pregnancy weight gain, CI 0.0057–0.0229, p = 0.0007).
Conclusions
High pregnancy weight gain is associated with increased body weight of the offspring in childhood, and this effect is only partially mediated through higher birth weight. Translation of these findings to public health obesity prevention requires additional study.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
Childhood obesity has become a worldwide epidemic. For example, in the United States, the number of obese children has more than doubled in the past 30 years. 7% of American children aged 6–11 years were obese in 1980, compared to nearly 18% in 2010. Because of the rising levels of obesity, the current generation of children may have a shorter life span than their parents for the first time in 200 years.
Childhood obesity has both immediate and long-term effects on health. The initial problems are usually psychological. Obese children often experience discrimination, leading to low self-esteem and depression. Their physical health also suffers. They are more likely to be at risk of cardiovascular disease from high cholesterol and high blood pressure. They may also develop pre-diabetes or diabetes type II. In the long-term, obese children tend to become obese adults, putting them at risk of premature death from stroke, heart disease, or cancer.
There are many factors that lead to childhood obesity and they often act in combination. A major risk factor, especially for younger children, is having at least one obese parent. The challenge lies in unravelling the complex links between the genetic and environmental factors that are likely to be involved.
Why Was This Study Done?
Several studies have shown that a child's weight is influenced by his/her mother's weight before pregnancy and her weight gain during pregnancy. An obese mother, or a mother who puts on more pregnancy weight than average, is more likely to have an obese child.
One explanation for the effects of pregnancy weight gain is that the mother's overeating directly affects the baby's development. It may change the baby's brain and metabolism in such a way as to increase the child's long-term risk of obesity. Animal studies have confirmed that the offspring of overfed rats show these kinds of physiological changes. However, another possible explanation is that mother and baby share a similar genetic make-up and environment so that a child becomes obese from inheriting genetic risk factors, and growing up in a household where being overweight is the norm.
The studies in humans that have been carried out to date have not been able to distinguish between these explanations. Some have given conflicting results. The aim of this study was therefore to look for evidence of links between pregnancy weight gain and children's weight, using an approach that would separate the impact of genetic and environmental factors from a direct effect on the developing baby.
What Did the Researchers Do and Find?
The researchers examined data from the population of the US state of Arkansas recorded between 2003 and 2011. They looked at the health records of over 42,000 women who had given birth to more than one child during this period. This gave them information about how much weight the women had gained during each of their pregnancies. The researchers also looked at the school records of the children, over 91,000 in total, which included the children's body mass index (BMI, which factors in both height and weight). They analyzed the data to see if there was a link between the mothers' pregnancy weight gain and the child's BMI at around 12 years of age. Most importantly, they looked at these links within families, comparing children born to the same mother. The rationale for this approach was that these children would share a similar genetic make-up and would have grown up in similar environments. By taking genetics and environment into account in this manner, any remaining evidence of an impact of pregnancy weight gain on the children's BMI would have to be explained by other factors.
The results showed that the amount of weight each mother gained in pregnancy predicted her children's BMI and the likelihood of her children being overweight or obese. For every additional kg the mother gained during pregnancy, the children's BMI increased by 0.022. The children of mothers who put on the most weight had a BMI that was on average 0.43 higher than the children whose mothers had put on the least weight.
The study leaves some questions unanswered, including whether the mother's weight before pregnancy makes a difference to their children's BMI. The researchers were not able to obtain these measurements, nor the weight of the fathers. There may have also been other factors that weren't measured that might explain the links that were found.
What Do These Findings Mean?
This study shows that mothers who gain excessive weight during pregnancy increase the risk of their child becoming obese. This appears to be partly due to a direct effect on the developing baby.
These results represent a significant public health concern, even though the impact on an individual basis is relatively small. They could contribute to several hundred thousand cases of childhood obesity worldwide. Importantly, they also suggest that some cases could be prevented by measures to limit excessive weight gain during pregnancy. Such an approach could prove effective, as most mothers will not want to damage their child's health, and might therefore be highly motivated to change their behavior. However, because inadequate weight gain during pregnancy can also adversely affect the developing fetus, it will be essential for women to receive clear information about what constitutes optimal weight gain during pregnancy.
Additional Information
Please access these websites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001521.
The US Centers for Disease Control and Prevention provide Childhood Obesity Facts
The UK National Health Service article “How much weight will I put on during my pregnancy?” provides information on pregnancy and weight gain and links to related resources
doi:10.1371/journal.pmed.1001521
PMCID: PMC3794857  PMID: 24130460
16.  Exploring the Developmental Overnutrition Hypothesis Using Parental–Offspring Associations and FTO as an Instrumental Variable 
PLoS Medicine  2008;5(3):e33.
Background
The developmental overnutrition hypothesis suggests that greater maternal obesity during pregnancy results in increased offspring adiposity in later life. If true, this would result in the obesity epidemic progressing across generations irrespective of environmental or genetic changes. It is therefore important to robustly test this hypothesis.
Methods and Findings
We explored this hypothesis by comparing the associations of maternal and paternal pre-pregnancy body mass index (BMI) with offspring dual energy X-ray absorptiometry (DXA)–determined fat mass measured at 9 to 11 y (4,091 parent–offspring trios) and by using maternal FTO genotype, controlling for offspring FTO genotype, as an instrument for maternal adiposity. Both maternal and paternal BMI were positively associated with offspring fat mass, but the maternal association effect size was larger than that in the paternal association in all models: mean difference in offspring sex- and age-standardised fat mass z-score per 1 standard deviation BMI 0.24 (95% confidence interval [CI]: 0.22 to 0.26) for maternal BMI versus 0.13 (95% CI: 0.11, 0.15) for paternal BMI; p-value for difference in effect < 0.001. The stronger maternal association was robust to sensitivity analyses assuming levels of non-paternity up to 20%. When maternal FTO, controlling for offspring FTO, was used as an instrument for the effect of maternal adiposity, the mean difference in offspring fat mass z-score per 1 standard deviation maternal BMI was −0.08 (95% CI: −0.56 to 0.41), with no strong statistical evidence that this differed from the observational ordinary least squares analyses (p = 0.17).
Conclusions
Neither our parental comparisons nor the use of FTO genotype as an instrumental variable, suggest that greater maternal BMI during offspring development has a marked effect on offspring fat mass at age 9–11 y. Developmental overnutrition related to greater maternal BMI is unlikely to have driven the recent obesity epidemic.
Using parental-offspring associations and theFTO gene as an instrumental variable for maternal adiposity, Debbie Lawlor and colleagues found that greater maternal BMI during offspring development does not appear to have a marked effect on offspring fat mass at age 9-11.
Editors' Summary
Background.
Since the 1970s, the proportion of children and adults who are overweight or obese (people who have an unhealthy amount of body fat) has increased sharply in many countries. In the US, 1 in 3 adults is now obese; in the mid-1970s it was only 1 in 7. Similarly, the proportion of overweight children has risen from 1 in 20 to 1 in 5. An adult is considered to be overweight if their body mass index (BMI)—their weight in kilograms divided by their height in meters squared—is between 25 and 30, and obese if it is more than 30. For children, the healthy BMI depends on their age and gender. Compared to people with a healthy weight (a BMI between 18.5 and 25), overweight or obese individuals have an increased lifetime risk of developing diabetes and other adverse health conditions, sometimes becoming ill while they are still young. People become unhealthily fat when they consume food and drink that contains more energy than they need for their daily activities. It should, therefore, be possible to avoid becoming obese by having a healthy diet and exercising regularly.
Why Was This Study Done?
Some researchers think that “developmental overnutrition” may have caused the recent increase in waistline measurements. In other words, if a mother is overweight during pregnancy, high sugar and fat levels in her body might permanently affect her growing baby's appetite control and metabolism, and so her offspring might be at risk of becoming obese in later life. If this hypothesis is true, each generation will tend to be fatter than the previous one and it will be very hard to halt the obesity epidemic simply by encouraging people to eat less and exercise more. In this study, the researchers have used two approaches to test the developmental overnutrition hypothesis. First, they have asked whether offspring fat mass is more strongly related to maternal BMI than to paternal BMI; it should be if the hypothesis is true. Second, they have asked whether a genetic indicator of maternal fatness—the “A” variant of the FTO gene—is related to offspring fat mass. A statistical association between maternal FTO genotype (genetic make-up) and offspring fat mass would support the developmental nutrition hypothesis.
What Did the Researchers Do and Find?
In 1991–1992, the Avon Longitudinal Study of Parents and Children (ALSPAC) enrolled about 14,000 pregnant women and now examines their offspring at regular intervals. The researchers first used statistical methods to look for associations between the self-reported prepregnancy BMI of the parents of about 4,000 children and the children's fat mass at ages 9–11 years measured using a technique called dual energy X-ray absorptiometry. Both maternal and paternal BMI were positively associated with offspring fat mass (that is, fatter parents had fatter children) but the effect of maternal BMI was greater than the effect of paternal BMI. When the researchers examined maternal FTO genotypes and offspring fat mass (after allowing for the offspring's FTO genotype, which would directly affect their fat mass), there was no statistical evidence to suggest that differences in offspring fat mass were related to the maternal FTO genotype.
What Do These Findings Mean?
Although the findings from first approach provide some support for the development overnutrition hypothesis, the effect of maternal BMI on offspring fat mass is too weak to explain the recent obesity epidemic. Developmental overnutrition could, however, be responsible for the much slower increase in obesity that began a century ago. The findings from the second approach provide no support for the developmental overnutrition hypothesis, although these results have wide error margins and need confirming in a larger study. The researchers also note that the effects of developmental overnutrition on offspring fat mass, although weak at age 9–11, might become more important at later ages. Nevertheless, for now, it seems unlikely that developmental overnutrition has been a major driver of the recent obesity epidemic. Interventions that aim to improve people's diet and to increase their physical activity levels could therefore slow or even halt the epidemic.
Additional Information.
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.0050033.
See a related PLoS Medicine Perspective article
The MedlinePlus encyclopedia has a page on obesity (in English and Spanish)
The US Centers for Disease Control and Prevention provides information on all aspects of obesity (in English and Spanish)
The UK National Health Service's health Web site (NHS Direct) provides information about obesity
The International Obesity Taskforce provides information about preventing obesity and on childhood obesity
The UK Foods Standards Agency, the United States Department of Agriculture, and Shaping America's Health all provide useful advice about healthy eating for adults and children
The ALSPAC Web site provides information about the Avon Longitudinal Study of Parents and Children and its results so far
doi:10.1371/journal.pmed.0050033
PMCID: PMC2265763  PMID: 18336062
17.  The Arctic Human Health Initiative: a legacy of the International Polar Year 2007–2009 
International Journal of Circumpolar Health  2013;72:10.3402/ijch.v72i0.21655.
Background
The International Polar Year (IPY) 2007–2008 represented a unique opportunity to further stimulate cooperation and coordination on Arctic health research and increase the awareness and visibility of Arctic regions. The Arctic Human Health Initiative (AHHI) was a US-led Arctic Council IPY coordinating project that aimed to build and expand on existing International Union for Circumpolar Health (IUCH) and Arctic Council human health interests. The project aimed to link researchers with potential international collaborators and to serve as a focal point for human health research, education, outreach and communication activities during the IPY. The progress of projects conducted as part of this initiative up until the end of the Arctic Council Swedish chairmanship in May 2013 is summarized in this report.
Design
The overall goals of the AHHI was to increase awareness and visibility of human health concerns of Arctic peoples, foster human health research, and promote health strategies that will improve health and well-being of all Arctic residents. Proposed activities to be recognized through the initiative included: expanding research networks that will enhance surveillance and monitoring of health issues of concern to Arctic peoples, and increase collaboration and coordination of human health research; fostering research that will examine the health impact of anthropogenic pollution, rapid modernization and economic development, climate variability, infectious and chronic diseases, intentional and unintentional injuries, promoting education, outreach and communication that will focus public and political attention on Arctic health issues, using a variety of publications, printed and electronic reports from scientific conferences, symposia and workshops targeting researchers, students, communities and policy makers; promoting the translation of research into health policy and community action including implementation of prevention strategies and health promotion; and promoting synergy and strategic direction of Arctic human health research and health promotion.
Results
As of 31 March, 2009, the official end of the IPY, AHHI represented a total of 38 proposals, including 21 individual Expressions of Intent (EoI), and 9 full proposals (FP), submitted to the IPY Joint Committee for review and approval from lead investigators from the US, Canada, Greenland, Norway, Finland, Sweden and the Russian Federation. In addition, there were 10 National Initiatives (NI-projects undertaken during IPY beyond the IPY Joint Committee review process). Individual project details can be viewed at www.arctichealth.org. The AHHI currently monitors the progress of 28 individual active human health projects in the following thematic areas: health network expansion (5 projects), infectious disease research (7 projects), environmental health research (7 projects), behavioral and mental health research (4 projects), and outreach education and communication (5 projects).
Conclusions
While some projects have been completed, others will continue well beyond the IPY. The IPY 2007–2008 represented a unique opportunity to further stimulate cooperation and coordination on Arctic health research and increase the awareness and visibility of Arctic regions.
doi:10.3402/ijch.v72i0.21655
PMCID: PMC3749855  PMID: 23971017
International Polar Year; Arctic Health; research; education outreach communication; Arctic Council
18.  Lifetime Medical Costs of Obesity: Prevention No Cure for Increasing Health Expenditure 
PLoS Medicine  2008;5(2):e29.
Background
Obesity is a major cause of morbidity and mortality and is associated with high medical expenditures. It has been suggested that obesity prevention could result in cost savings. The objective of this study was to estimate the annual and lifetime medical costs attributable to obesity, to compare those to similar costs attributable to smoking, and to discuss the implications for prevention.
Methods and Findings
With a simulation model, lifetime health-care costs were estimated for a cohort of obese people aged 20 y at baseline. To assess the impact of obesity, comparisons were made with similar cohorts of smokers and “healthy-living” persons (defined as nonsmokers with a body mass index between 18.5 and 25). Except for relative risk values, all input parameters of the simulation model were based on data from The Netherlands. In sensitivity analyses the effects of epidemiologic parameters and cost definitions were assessed. Until age 56 y, annual health expenditure was highest for obese people. At older ages, smokers incurred higher costs. Because of differences in life expectancy, however, lifetime health expenditure was highest among healthy-living people and lowest for smokers. Obese individuals held an intermediate position. Alternative values of epidemiologic parameters and cost definitions did not alter these conclusions.
Conclusions
Although effective obesity prevention leads to a decrease in costs of obesity-related diseases, this decrease is offset by cost increases due to diseases unrelated to obesity in life-years gained. Obesity prevention may be an important and cost-effective way of improving public health, but it is not a cure for increasing health expenditures.
Using a simulation model, Pieter van Baal and colleagues conclude that obesity prevention leads to a decrease in costs of obesity-related diseases, but this is offset by cost increases due to diseases unrelated to obesity in life-years gained.
Editors' Summary
Background.
Since the mid 1970s, the proportion of people who are obese (people who have an unhealthy amount of body fat) has increased sharply in many countries. One-third of all US adults, for example, are now classified as obese, and recent forecasts suggest that by 2025 half of US adults will be obese. A person is overweight if their body mass index (BMI, calculated by dividing their weight in kilograms by their height in meters squared) is between 25 and 30, and obese if BMI is greater than 30. Compared to people with a healthy weight (a BMI between 18.5 and 25), overweight and obese individuals have an increased risk of developing many diseases, such as diabetes, coronary heart disease and stroke, and tend to die younger. People become unhealthily fat by consuming food and drink that contains more energy than they need for their daily activities. In these circumstances, the body converts the excess energy into fat for use at a later date. Obesity can be prevented, therefore, by having a healthy diet and exercising regularly.
Why Was This Study Done?
Because obesity causes so much illness and premature death, many governments have public-health policies that aim to prevent obesity. Clearly, the improvement in health associated with the prevention of obesity is a worthwhile goal in itself but the prevention of obesity might also reduce national spending on medical care. It would do this, the argument goes, by reducing the amount of money spent on treating the diseases for which obesity is a risk factor. However, some experts have suggested that these short-term savings might be offset by spending on treating the diseases that would occur during the extra lifespan experienced by non-obese individuals. In this study, therefore, the researchers have used a computer model to calculate yearly and lifetime medical costs associated with obesity in The Netherlands.
What Did the Researchers Do and Find?
The researchers used their model to estimate the number of surviving individuals and the occurrence of various diseases for three hypothetical groups of men and women, examining data from the age of 20 until the time when the model predicted that everyone had died. The “obese” group consisted of never-smoking people with a BMI of more than 30; the “healthy-living” group consisted of never-smoking people with a healthy weight; the “smoking” group consisted of lifetime smokers with a healthy weight. Data from the Netherlands on the costs of illness were fed into the model to calculate the yearly and lifetime health-care costs of all three groups. The model predicted that until the age of 56, yearly health costs were highest for obese people and lowest for healthy-living people. At older ages, the highest yearly costs were incurred by the smoking group. However, because of differences in life expectancy (life expectancy at age 20 was 5 years less for the obese group, and 8 years less for the smoking group, compared to the healthy-living group), total lifetime health spending was greatest for the healthy-living people, lowest for the smokers, and intermediate for the obese people.
What Do These Findings Mean?
As with all mathematical models such as this, the accuracy of these findings depend on how well the model reflects real life and the data fed into it. In this case, the model does not take into account varying degrees of obesity, which are likely to affect lifetime health-care costs, nor indirect costs of obesity such as reduced productivity. Nevertheless, these findings suggest that although effective obesity prevention reduces the costs of obesity-related diseases, this reduction is offset by the increased costs of diseases unrelated to obesity that occur during the extra years of life gained by slimming down.
Additional Information.
Please access these Web sites via the online version of this summary at http://dx.doi.org/doi:10.1371/journal.pmed.0050029.
The MedlinePlus encyclopedia has a page on obesity (in English and Spanish)
The US Centers for Disease Control and Prevention provides information on all aspects of obesity (in English and Spanish)
The UK National Health Service's health Web site (NHS Direct) provides information about obesity
The International Obesity Taskforce provides information about preventing obesity
The UK Foods Standards Agency, the United States Department of Agriculture, and Shaping America's Health all provide useful advice about healthy eating
The Netherlands National Institute for Public Health and the Environment (RIVM) Web site provides more information on the cost of illness and illness prevention in the Netherlands (in English and Dutch)
doi:10.1371/journal.pmed.0050029
PMCID: PMC2225430  PMID: 18254654
19.  Causal Relationship between Obesity and Vitamin D Status: Bi-Directional Mendelian Randomization Analysis of Multiple Cohorts 
PLoS Medicine  2013;10(2):e1001383.
A mendelian randomization study based on data from multiple cohorts conducted by Karani Santhanakrishnan Vimaleswaran and colleagues re-examines the causal nature of the relationship between vitamin D levels and obesity.
Background
Obesity is associated with vitamin D deficiency, and both are areas of active public health concern. We explored the causality and direction of the relationship between body mass index (BMI) and 25-hydroxyvitamin D [25(OH)D] using genetic markers as instrumental variables (IVs) in bi-directional Mendelian randomization (MR) analysis.
Methods and Findings
We used information from 21 adult cohorts (up to 42,024 participants) with 12 BMI-related SNPs (combined in an allelic score) to produce an instrument for BMI and four SNPs associated with 25(OH)D (combined in two allelic scores, separately for genes encoding its synthesis or metabolism) as an instrument for vitamin D. Regression estimates for the IVs (allele scores) were generated within-study and pooled by meta-analysis to generate summary effects.
Associations between vitamin D scores and BMI were confirmed in the Genetic Investigation of Anthropometric Traits (GIANT) consortium (n = 123,864). Each 1 kg/m2 higher BMI was associated with 1.15% lower 25(OH)D (p = 6.52×10−27). The BMI allele score was associated both with BMI (p = 6.30×10−62) and 25(OH)D (−0.06% [95% CI −0.10 to −0.02], p = 0.004) in the cohorts that underwent meta-analysis. The two vitamin D allele scores were strongly associated with 25(OH)D (p≤8.07×10−57 for both scores) but not with BMI (synthesis score, p = 0.88; metabolism score, p = 0.08) in the meta-analysis. A 10% higher genetically instrumented BMI was associated with 4.2% lower 25(OH)D concentrations (IV ratio: −4.2 [95% CI −7.1 to −1.3], p = 0.005). No association was seen for genetically instrumented 25(OH)D with BMI, a finding that was confirmed using data from the GIANT consortium (p≥0.57 for both vitamin D scores).
Conclusions
On the basis of a bi-directional genetic approach that limits confounding, our study suggests that a higher BMI leads to lower 25(OH)D, while any effects of lower 25(OH)D increasing BMI are likely to be small. Population level interventions to reduce BMI are expected to decrease the prevalence of vitamin D deficiency.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
Obesity—having an unhealthy amount of body fat—is increasing worldwide. In the US, for example, a third of the adult population is now obese. Obesity is defined as having a body mass index (BMI, an indicator of body fat calculated by dividing a person's weight in kilograms by their height in meters squared) of more than 30.0 kg/m2. Although there is a genetic contribution to obesity, people generally become obese by consuming food and drink that contains more energy than they need for their daily activities. Thus, obesity can be prevented by having a healthy diet and exercising regularly. Compared to people with a healthy weight, obese individuals have an increased risk of developing diabetes, heart disease and stroke, and tend to die younger. They also have a higher risk of vitamin D deficiency, another increasingly common public health concern. Vitamin D, which is essential for healthy bones as well as other functions, is made in the skin after exposure to sunlight but can also be obtained through the diet and through supplements.
Why Was This Study Done?
Observational studies cannot prove that obesity causes vitamin D deficiency because obese individuals may share other characteristics that reduce their circulating 25-hydroxy vitamin D [25(OH)D] levels (referred to as confounding). Moreover, observational studies cannot indicate whether the larger vitamin D storage capacity of obese individuals (vitamin D is stored in fatty tissues) lowers their 25(OH)D levels or whether 25(OH)D levels influence fat accumulation (reverse causation). If obesity causes vitamin D deficiency, monitoring and treating vitamin D deficiency might alleviate some of the adverse health effects of obesity. Conversely, if low vitamin D levels cause obesity, encouraging people to take vitamin D supplements might help to control the obesity epidemic. Here, the researchers use bi-directional “Mendelian randomization” to examine the direction and causality of the relationship between BMI and 25(OH)D. In Mendelian randomization, causality is inferred from associations between genetic variants that mimic the influence of a modifiable environmental exposure and the outcome of interest. Because gene variants do not change over time and are inherited randomly, they are not prone to confounding and are free from reverse causation. Thus, if a lower vitamin D status leads to obesity, genetic variants associated with lower 25(OH)D concentrations should be associated with higher BMI, and if obesity leads to a lower vitamin D status, then genetic variants associated with higher BMI should be associated with lower 25(OH)D concentrations.
What Did the Researchers Do and Find?
The researchers created a “BMI allele score” based on 12 BMI-related gene variants and two “25(OH)D allele scores,” which are based on gene variants that affect either 25(OH)D synthesis or breakdown. Using information on up to 42,024 participants from 21 studies, the researchers showed that the BMI allele score was associated with both BMI and with 25(OH)D levels among the study participants. Based on this information, they calculated that each 10% increase in BMI will lead to a 4.2% decrease in 25(OH)D concentrations. By contrast, although both 25(OH)D allele scores were strongly associated with 25(OH)D levels, neither score was associated with BMI. This lack of an association between 25(OH)D allele scores and obesity was confirmed using data from more than 100,000 individuals involved in 46 studies that has been collected by the GIANT (Genetic Investigation of Anthropometric Traits) consortium.
What Do These Findings Mean?
These findings suggest that a higher BMI leads to a lower vitamin D status whereas any effects of low vitamin D status on BMI are likely to be small. That is, these findings provide evidence for obesity as a causal factor in the development of vitamin D deficiency but not for vitamin D deficiency as a causal factor in the development of obesity. These findings suggest that population-level interventions to reduce obesity should lead to a reduction in the prevalence of vitamin D deficiency and highlight the importance of monitoring and treating vitamin D deficiency as a means of alleviating the adverse influences of obesity on health.
Additional Information
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001383.
The US Centers for Disease Control and Prevention provides information on all aspects of overweight and obesity (in English and Spanish); a data brief provides information about the vitamin D status of the US population
The World Health Organization provides information on obesity (in several languages)
The UK National Health Service Choices website provides detailed information about obesity and a link to a personal story about losing weight; it also provides information about vitamin D
The International Obesity Taskforce provides information about the global obesity epidemic
The US Department of Agriculture's ChooseMyPlate.gov website provides a personal healthy eating plan; the Weight-control Information Network is an information service provided for the general public and health professionals by the US National Institute of Diabetes and Digestive and Kidney Diseases (in English and Spanish)
The US Office of Dietary Supplements provides information about vitamin D (in English and Spanish)
MedlinePlus has links to further information about obesity and about vitamin D (in English and Spanish)
Wikipedia has a page on Mendelian randomization (note: Wikipedia is a free online encyclopedia that anyone can edit; available in several languages)
Overview and details of the collaborative large-scale genetic association study (D-CarDia) provide information about vitamin D and the risk of cardiovascular disease, diabetes and related traits
doi:10.1371/journal.pmed.1001383
PMCID: PMC3564800  PMID: 23393431
20.  Characterizing the Epidemiological Transition in Mexico: National and Subnational Burden of Diseases, Injuries, and Risk Factors 
PLoS Medicine  2008;5(6):e125.
Background
Rates of diseases and injuries and the effects of their risk factors can have substantial subnational heterogeneity, especially in middle-income countries like Mexico. Subnational analysis of the burden of diseases, injuries, and risk factors can improve characterization of the epidemiological transition and identify policy priorities.
Methods and Findings
We estimated deaths and loss of healthy life years (measured in disability-adjusted life years [DALYs]) in 2004 from a comprehensive list of diseases and injuries, and 16 major risk factors, by sex and age for Mexico and its states. Data sources included the vital statistics, national censuses, health examination surveys, and published epidemiological studies. Mortality statistics were adjusted for underreporting, misreporting of age at death, and for misclassification and incomparability of cause-of-death assignment. Nationally, noncommunicable diseases caused 75% of total deaths and 68% of total DALYs, with another 14% of deaths and 18% of DALYs caused by undernutrition and communicable, maternal, and perinatal diseases. The leading causes of death were ischemic heart disease, diabetes mellitus, cerebrovascular disease, liver cirrhosis, and road traffic injuries. High body mass index, high blood glucose, and alcohol use were the leading risk factors for disease burden, causing 5.1%, 5.0%, and 7.3% of total burden of disease, respectively. Mexico City had the lowest mortality rates (4.2 per 1,000) and the Southern region the highest (5.0 per 1,000); under-five mortality in the Southern region was nearly twice that of Mexico City. In the Southern region undernutrition and communicable, maternal, and perinatal diseases caused 23% of DALYs; in Chiapas, they caused 29% of DALYs. At the same time, the absolute rates of noncommunicable disease and injury burdens were highest in the Southern region (105 DALYs per 1,000 population versus 97 nationally for noncommunicable diseases; 22 versus 19 for injuries).
Conclusions
Mexico is at an advanced stage in the epidemiologic transition, with the majority of the disease and injury burden from noncommunicable diseases. A unique characteristic of the epidemiological transition in Mexico is that overweight and obesity, high blood glucose, and alcohol use are responsible for larger burden of disease than other noncommunicable disease risks such as tobacco smoking. The Southern region is least advanced in the epidemiological transition and suffers from the largest burden of ill health in all disease and injury groups.
Gretchen Stevens and colleagues estimate deaths and loss of healthy life years (measured in disability-adjusted life years, DALYs) for Mexico as a whole and its 32 states.
Editors' Summary
Background.
The impact that a particular disease has upon a population is known as the “burden of disease.” This burden is estimated by considering how many deaths the disease causes and how much it disables those still living. The relative contributions of different diseases and injuries to the loss of healthy life from death and disability vary greatly among countries. Broadly speaking, in low-income countries (such as many African countries), infectious diseases and undernutrition are the major causes of ill health and death whereas in high-income countries (for example, the United States), noncommunicable diseases such as heart disease, diabetes, and stroke are more important. As poor countries become richer, they experience a change in the pattern of disease away from infectious diseases and malnutrition and toward noncommunicable diseases. Health experts call this change the “epidemiological transition” (epidemiology is the study of the distribution and causes of diseases in populations). Governments need to know as much as possible about which diseases have the greatest burden—and about where the country is in the epidemiological transition—to help them implement effective health policies. For example, there is no point in setting up treatment centers for a specific infectious disease in a country where the disease no longer occurs. Equally importantly, governments need to know which lifestyle choices and other genetic and environmental factors affect the chances of people in their country developing specific diseases so that they can provide relevant educational and intervention programs.
Why Was This Study Done?
Most analyses of the burden of disease have been done at the national and global scale. However, in middle-income countries, different regions of the country may be at different stages of the epidemiological transition and may, therefore, have very different patterns of disease. In this study, the researchers investigate whether this is the case for Mexico, a middle-income country that has developed rapidly over the past few decades. Mexico recently reformed its health system to improve access to health care for the poor and underserved. Under this new system, individual states play an important role in allocating health-care resources (as they do in many other countries) so it is very important to know how the burden of disease varies in different states of the country.
What Did the Researchers Do and Find?
The researchers estimated deaths and loss of healthy life years caused by various diseases and injuries for Mexico and its states using data from death registers, censuses, health examination surveys, and epidemiological studies. Loss of healthy life years was measured using a metric called “disability-adjusted life years” (DALYs)—one DALY is equivalent to the loss of one year of healthy life because of premature death or disability. They also identified the major risk factors for these diseases and injuries across the country. Nationally, noncommunicable diseases (particularly heart disease, diabetes, stroke, and liver cirrhosis) caused 75% of deaths and 68% of DALYs. Undernutrition, infectious diseases, and problems occurring in mothers and infants around the time of birth (maternal and perinatal diseases) caused 14% of deaths and 18% of DALYs. The leading risk factors for disease in Mexico were being overweight, having high blood glucose, and alcohol use. When the researchers studied different regions of the country, they found that Mexico City had the lowest death rate whereas the relatively undeveloped Southern region of Mexico had the highest, particularly among young children. In Chiapas, the most southerly state of Mexico, undernutrition and infectious, maternal, and perinatal diseases caused nearly a third of DALYs. In addition to the highest infectious disease burden, the Southern region also had the highest noncommunicable disease and injury burden per head of population.
What Do These Findings Mean?
These findings indicate that Mexico as a nation is at an advanced stage of the epidemiological transition. In other words, because of the improvement in its economic status, the burden of disease caused by infectious diseases and undernutrition has decreased, and noncommunicable diseases now cause the largest share of the total burden of disease. However, the study also shows that the poorest regions of the country, which have the highest overall burden of disease, are lagging behind the richer regions in terms of their position in the epidemiological transition. Thus different health priorities need to be set in different regions of Mexico (and in other middle-income countries where the burden of disease is also likely to vary with region). Finally, the information provided by this study about the forces driving the epidemiological transition in Mexico, such as the importance of obesity and alcohol use, should help public-health officials decide how to improve the overall health of the Mexican population.
Additional Information.
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.0050125.
A related PLoS Medicine Perspective by Martin Tobias further discusses this research
The World Health Organization provides information on the Global Burden of Disease Project including links to other burden of disease resources. It also provides detailed information on various aspects of health in Mexico (in several languages), and an explanation of DALYs
Read a detailed article on the “epidemiological transition” by Abdel Omran, who proposed this idea in 1971
A large amount of Mexican data is available online for Spanish speakers. Complete raw mortality statistics can be found on the Mexican Ministry of Health's Web site http://sinais.salud.gob.mx/sinais.php. Also online is the complete report of the ENSANUT survey (Encuesta Nacional de Salud y Nutrición 2006) http://www.insp.mx/ensanut/, which was one of the major data sources used to determine risk factor exposure
doi:10.1371/journal.pmed.0050125
PMCID: PMC2429945  PMID: 18563960
21.  Projections of Global Mortality and Burden of Disease from 2002 to 2030 
PLoS Medicine  2006;3(11):e442.
Background
Global and regional projections of mortality and burden of disease by cause for the years 2000, 2010, and 2030 were published by Murray and Lopez in 1996 as part of the Global Burden of Disease project. These projections, which are based on 1990 data, continue to be widely quoted, although they are substantially outdated; in particular, they substantially underestimated the spread of HIV/AIDS. To address the widespread demand for information on likely future trends in global health, and thereby to support international health policy and priority setting, we have prepared new projections of mortality and burden of disease to 2030 starting from World Health Organization estimates of mortality and burden of disease for 2002. This paper describes the methods, assumptions, input data, and results.
Methods and Findings
Relatively simple models were used to project future health trends under three scenarios—baseline, optimistic, and pessimistic—based largely on projections of economic and social development, and using the historically observed relationships of these with cause-specific mortality rates. Data inputs have been updated to take account of the greater availability of death registration data and the latest available projections for HIV/AIDS, income, human capital, tobacco smoking, body mass index, and other inputs. In all three scenarios there is a dramatic shift in the distribution of deaths from younger to older ages and from communicable, maternal, perinatal, and nutritional causes to noncommunicable disease causes. The risk of death for children younger than 5 y is projected to fall by nearly 50% in the baseline scenario between 2002 and 2030. The proportion of deaths due to noncommunicable disease is projected to rise from 59% in 2002 to 69% in 2030. Global HIV/AIDS deaths are projected to rise from 2.8 million in 2002 to 6.5 million in 2030 under the baseline scenario, which assumes coverage with antiretroviral drugs reaches 80% by 2012. Under the optimistic scenario, which also assumes increased prevention activity, HIV/AIDS deaths are projected to drop to 3.7 million in 2030. Total tobacco-attributable deaths are projected to rise from 5.4 million in 2005 to 6.4 million in 2015 and 8.3 million in 2030 under our baseline scenario. Tobacco is projected to kill 50% more people in 2015 than HIV/AIDS, and to be responsible for 10% of all deaths globally. The three leading causes of burden of disease in 2030 are projected to include HIV/AIDS, unipolar depressive disorders, and ischaemic heart disease in the baseline and pessimistic scenarios. Road traffic accidents are the fourth leading cause in the baseline scenario, and the third leading cause ahead of ischaemic heart disease in the optimistic scenario. Under the baseline scenario, HIV/AIDS becomes the leading cause of burden of disease in middle- and low-income countries by 2015.
Conclusions
These projections represent a set of three visions of the future for population health, based on certain explicit assumptions. Despite the wide uncertainty ranges around future projections, they enable us to appreciate better the implications for health and health policy of currently observed trends, and the likely impact of fairly certain future trends, such as the ageing of the population, the continued spread of HIV/AIDS in many regions, and the continuation of the epidemiological transition in developing countries. The results depend strongly on the assumption that future mortality trends in poor countries will have a relationship to economic and social development similar to those that have occurred in the higher-income countries.
The presented projections suggest a dramatic shift in the distribution of deaths from younger to older ages and from communicable, maternal, perinatal, and nutritional causes to non-communicable disease causes. HIV/AIDS and tobacco remain major killers and possible targets for intervention.
Editors' Summary
Background.
For most of human history, little has been known about the main causes of illness in different countries and which diseases kill most people. But public-health officials need to know whether heart disease kills more people than cancer in their country, for example, or whether diabetes causes more disability than mental illness so that they can use their resources wisely. They also have to have some idea about how patterns of illness (morbidity) and death (mortality) are likely to change so that they can plan for the future. In the early 1990s, the World Bank sponsored the 1990 Global Burden of Disease study carried out by researchers at Harvard University and the World Health Organization (WHO). This study provided the first comprehensive, global estimates of death and illness by age, sex, and region. It also provided projections of the global burden of disease and mortality up to 2020 using models that assumed that health trends are related to a set of independent variables. These variables were income per person (as people become richer, they, live longer), average number of years of education (as this “human capital” increases, so does life expectancy), time (to allow for improved knowledge about various diseases), and tobacco use (a major global cause of illness and death).
Why Was This Study Done?
These health projections have been widely used by WHO and governments to help them plan their health policies. However, because they are based on the 1990 estimates of the global burden of disease, the projections now need updating, particularly since they underestimate the spread of HIV/AIDS and the associated increase in death from tuberculosis. In this study, the researchers used similar methods to those used in the 1990 Global Burden of Disease study to prepare new projections of mortality and burden of disease up to 2030 starting from the 2002 WHO global estimates of mortality and burden of disease.
What Did the Researchers Do and Find?
As before, the researchers used projections of socio-economic development to model future patterns of mortality and illness for a baseline scenario, a pessimistic scenario that assumed a slower rate of socio-economic development, and an optimistic scenario that assumed a faster rate of growth. Their analysis predicts that between 2002 and 2030 for all three scenarios life expectancy will increase around the world, fewer children younger than 5 years will die, and the proportion of people dying from non-communicable diseases such as heart disease and cancer will increase. Although deaths from infectious diseases will decrease overall, HIV/AIDS deaths will continue to increase; the exact magnitude of the increase will depend on how many people have access to antiretroviral drugs and the efficacy of prevention programs. But, even given the rise in HIV/AIDS deaths, the new projections predict that more people will die of tobacco-related disease than of HIV/AIDS in 2015. The researchers also predict that by 2030, the three leading causes of illness will be HIV/AIDS, depression, and ischaemic heart disease (problems caused by a poor blood supply to the heart) in the baseline and pessimistic scenarios; in the optimistic scenario, road-traffic accidents will replace heart disease as the third leading cause (there will be more traffic accidents with faster economic growth).
What Do These Findings Mean?
The models used by the researchers provide a wealth of information about possible patterns of global death and illness between 2002 and 2030, but because they include many assumptions, like all models, they can provide only indications of future trends, not absolute figures. For example, based on global mortality data from 2002, the researchers estimate that global deaths in 2030 will be 64.9 million under the optimistic scenario. However, the actual figure may be quite a bit bigger or smaller because accurate baseline counts of deaths were not available for every country in the world. Another limitation of the study is that the models used assume that future increases in prosperity in developing countries will affect their population's health in the same way as similar increases affected health in the past in countries with death registration data (these are mostly developed countries). However, even given these and other limitations, the projections reported in this study provide useful insights into the future health of the world. These can now be used by public-health officials to plan future policy and to monitor the effect of new public-health initiatives on the global burden of disease and death.
Additional Information.
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.0030442.
World Health Organization, provides information on the Global Burden of Disease Project and links to other related resources Global Burden of Disease Project
Harvard School of Public Health, Burden of Disease Unit, offers information on the 1990 Global Burden of Disease study and its projections Harvard School of Public Health
doi:10.1371/journal.pmed.0030442
PMCID: PMC1664601  PMID: 17132052
22.  Maternal Overweight and Obesity and Risks of Severe Birth-Asphyxia-Related Complications in Term Infants: A Population-Based Cohort Study in Sweden 
PLoS Medicine  2014;11(5):e1001648.
Martina Persson and colleagues use a Swedish national database to investigate the association between maternal body mass index in early pregnancy and severe asphyxia-related outcomes in infants delivered at term.
Please see later in the article for the Editors' Summary
Background
Maternal overweight and obesity increase risks of pregnancy and delivery complications and neonatal mortality, but the mechanisms are unclear. The objective of the study was to investigate associations between maternal body mass index (BMI) in early pregnancy and severe asphyxia-related outcomes in infants delivered at term (≥37 weeks).
Methods and Findings
A nation-wide Swedish cohort study based on data from the Medical Birth Register included all live singleton term births in Sweden between 1992 and 2010. Logistic regression analyses were used to obtain odds ratios (ORs) with 95% CIs for Apgar scores between 0 and 3 at 5 and 10 minutes, meconium aspiration syndrome, and neonatal seizures, adjusted for maternal height, maternal age, parity, mother's smoking habits, education, country of birth, and year of infant birth. Among 1,764,403 term births, 86% had data on early pregnancy BMI and Apgar scores. There were 1,380 infants who had Apgar score 0–3 at 5 minutes (absolute risk  = 0.8 per 1,000) and 894 had Apgar score 0–3 at 10 minutes (absolute risk  = 0.5 per 1,000). Compared with infants of mothers with normal BMI (18.5–24.9), the adjusted ORs (95% CI) for Apgar scores 0–3 at 10 minutes were as follows: BMI 25–29.9: 1.32 (1.10–1.58); BMI 30–34.9: 1.57 (1.20–2.07); BMI 35–39.9: 1.80 (1.15–2.82); and BMI ≥40: 3.41 (1.91–6.09). The ORs for Apgar scores 0–3 at 5 minutes, meconium aspiration, and neonatal seizures increased similarly with maternal BMI. A study limitation was lack of data on effects of obstetric interventions and neonatal resuscitation efforts.
Conclusion
Risks of severe asphyxia-related outcomes in term infants increase with maternal overweight and obesity. Given the high prevalence of the exposure and the severity of the outcomes studied, the results are of potential public health relevance and should be confirmed in other populations. Prevention of overweight and obesity in women of reproductive age is important to improve perinatal health.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
Economic, technologic, and lifestyle changes over the past 30 years have created an abundance of cheap, accessible, high-calorie food. Combined with fewer demands for physical activity, this situation has lead to increasing body mass throughout most of the world. Consequently, being overweight or obese is much more common in many high-income and low-and middle-income countries compared to 1980. Worldwide estimates put the percentage of overweight or obese adults as increasing by over 10%, between 1980 and 2008.
As being overweight becomes a global epidemic, its prevalence in women of reproductive age has also increased. Pregnant women who are overweight or obese are a cause for concern because of the possible associated health risks to both the infant and mother. Research is necessary to more clearly define these risks.
Why Was This Study Done?
In this study, the researchers investigated the complications associated with excess maternal weight that could hinder an infant from obtaining enough oxygen during delivery (neonatal asphyxia). All fetuses experience a loss of oxygen during contractions, however, a prolonged loss of oxygen can impact an infant's long-term development. To explore this risk, the researchers relied on a universal scoring system known as the Apgar score. An Apgar score is routinely recorded at one, five, and ten minutes after birth and is calculated from an assessment of heart rate, respiratory effort, and color, along with reflexes and muscle tone. An oxygen deficit during delivery will have an impact on the score. A normal score is in the range of 7–10. Body mass index (BMI) a calculation that uses height and weight, was used to assess the weight status (i.e., normal, overweight, obese) of the mother during pregnancy.
What Did the Researchers Do and Find?
Using the Swedish medical birth registry (a database including nearly all the births occurring in Sweden since 1973) the researchers selected records for single births that took place between 1992 to 2010. The registry also incorporates prenatal care data and researchers further selected for records that included weight and height measurement taken during the first prenatal visit. BMI was calculated using the weight and height measurement. Based on BMI ranges that define weight groups as normal, overweight, and obesity grades I, II, and III, the researchers analyzed and compared the number of low Apgar scoring infants (Apgar 0–3) in each group. Mothers with normal weight gave birth to the majority of infants with Apgar 0–3. In comparison the proportion of low Apgar scores were greater in babies of overweight and obese mothers. The researchers found that the rates of low Apgar scores increased with maternal BMI: the authors found that rates of low Apgar score at 5 minutes increased from 0.4 per 1,000 among infants of underweight women (BMI <18.5) to 2.4 per 1,000 among infants of women with obesity class III (BMI ≥40). Furthermore, overweight (BMI 25.0–29.9) was associated with a 55% increased risk of low Apgar scores at 5 minutes; obesity grade I (BMI 30–34.9) and grade II (BMI 35.0–39.9) with an almost 2-fold and a more than 2-fold increased risk, respectively; and obesity grade ΙΙΙ (BMI ≥40.0) with a more than 3-fold increase in risk. Finally, maternal overweight and obesity also increase the risks for seizures and meconium aspiration in the neonate.
What Do These Findings Mean?
These findings suggest that the risk of experiencing an oxygen deficit increases for the babies of women who are overweight or obese. Given the high prevalence of overweight and obesity in many countries worldwide, these findings are important and suggest that preventing women of reproductive age from becoming overweight or obese is therefore important to the health of their children.
A limitation of this study is the lack of data on the effects of clinical interventions and neonatal resuscitation efforts that may have been performed at the time of birth. Also Apgar scoring is based on five variables and a low score is not the most direct way to determine if the infant has experienced an oxygen deficit. However, these findings suggest that early detection of perinatal asphyxia is particularly relevant among infants of overweight and obese women although more studies are necessary to confirm the results in other populations.
Additional Information
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001648.
The US National Institutes of Health explains and calculates body mass index
The NIH also defines the Apgar scoring system
The United Kingdom's National Health Service has information for pregnant woman who are overweight
The UK-based Overseas Development Institute discusses how changes in diet have led to a worldwide health crisis in its “Future Diets” publication
Information about the Swedish health care system is available
Information in English is available from the National Board of Health and Welfare in Sweden
doi:10.1371/journal.pmed.1001648
PMCID: PMC4028185  PMID: 24845218
23.  Causes of metabolic syndrome and obesity-related co-morbidities Part 1: A composite unifying theory review of human-specific co-adaptations to brain energy consumption 
Archives of Public Health  2014;72(1):30.
One line summary
Metabolic syndrome and obesity-related co-morbidities are largely explained by co-adaptations to the energy use of the large human brain in the cortico-limbic-striatal and NRF2 systems.
The medical, research and general community is unable to effect significantly decreased rates of central obesity and related type II diabetes mellitus (TIIDM), cardiovascular disease (CVD) and cancer. All conditions seem to be linked by the concept of the metabolic syndrome (MetS), but the underlying causes are not known. MetS markers may have been mistaken for causes, thus many treatments are destined to be suboptimal.
The current paper aims to critique current paradigms, give explanations for their persistence, and to return to first principles in an attempt to determine and clarify likely causes of MetS and obesity related comorbidities. A wide literature has been mined, study concepts analysed and the basics of human evolution and new biochemistry reviewed. A plausible, multifaceted composite unifying theory is formulated.
The basis of the theory is that the proportionately large, energy-demanding human brain may have driven co-adaptive mechanisms to provide, or conserve, energy for the brain. A ‘dual system’ is proposed. 1) The enlarged, complex cortico-limbic-striatal system increases dietary energy by developing strong neural self-reward/motivation pathways for the acquisition of energy dense food, and (2) the nuclear factor-erythroid 2-related factor 2 (NRF2) cellular protection system amplifies antioxidant, antitoxicant and repair activity by employing plant chemicals, becoming highly energy efficient in humans.
The still-evolving, complex human cortico-limbic-striatal system generates strong behavioural drives for energy dense food procurement, including motivating agricultural technologies and social system development. Addiction to such foods, leading to neglect of nutritious but less appetizing ‘common or garden’ food, appears to have occurred. Insufficient consumption of food micronutrients prevents optimal human NRF2 function. Inefficient oxidation of excess energy forces central and non-adipose cells to store excess toxic lipid. Oxidative stress and metabolic inflammation, or metaflammation, allow susceptibility to infectious, degenerative atherosclerotic cardiovascular, autoimmune, neurodegenerative and dysplastic diseases.
Other relevant human-specific co-adaptations are examined, and encompass the unusual ability to store fat, certain vitamin pathways, the generalised but flexible intestine and microbiota, and slow development and longevity.
This theory has significant past and future corollaries, which are explored in a separate article by McGill, A-T, in Archives of Public Health, 72: 31.
doi:10.1186/2049-3258-72-30
PMCID: PMC4335398
Metabolic syndrome; Obesity-related co-morbidities; Theory review; Evolution and nutrition; Food micronutrient; Malnutritive obesity (Malnubesity); Cortico-limbic-striatal; Food addiction; Nuclear factor-erythroid 2-related factor 2 (NRF2); Human brain metabolism; Oxidative stress; Metabolic inflammation
24.  Socioeconomic Factors and All Cause and Cause-Specific Mortality among Older People in Latin America, India, and China: A Population-Based Cohort Study 
PLoS Medicine  2012;9(2):e1001179.
Cleusa Ferri and colleagues studied mortality rates in over 12,000 people aged 65 years and over in Latin America, India, and China and showed that chronic diseases are the main causes of death and that education has an important effect on mortality.
Background
Even in low and middle income countries most deaths occur in older adults. In Europe, the effects of better education and home ownership upon mortality seem to persist into old age, but these effects may not generalise to LMICs. Reliable data on causes and determinants of mortality are lacking.
Methods and Findings
The vital status of 12,373 people aged 65 y and over was determined 3–5 y after baseline survey in sites in Latin America, India, and China. We report crude and standardised mortality rates, standardized mortality ratios comparing mortality experience with that in the United States, and estimated associations with socioeconomic factors using Cox's proportional hazards regression. Cause-specific mortality fractions were estimated using the InterVA algorithm. Crude mortality rates varied from 27.3 to 70.0 per 1,000 person-years, a 3-fold variation persisting after standardisation for demographic and economic factors. Compared with the US, mortality was much higher in urban India and rural China, much lower in Peru, Venezuela, and urban Mexico, and similar in other sites. Mortality rates were higher among men, and increased with age. Adjusting for these effects, it was found that education, occupational attainment, assets, and pension receipt were all inversely associated with mortality, and food insecurity positively associated. Mutually adjusted, only education remained protective (pooled hazard ratio 0.93, 95% CI 0.89–0.98). Most deaths occurred at home, but, except in India, most individuals received medical attention during their final illness. Chronic diseases were the main causes of death, together with tuberculosis and liver disease, with stroke the leading cause in nearly all sites.
Conclusions
Education seems to have an important latent effect on mortality into late life. However, compositional differences in socioeconomic position do not explain differences in mortality between sites. Social protection for older people, and the effectiveness of health systems in preventing and treating chronic disease, may be as important as economic and human development.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
Worldwide, half of all deaths occur in people aged 60 or older. Yet mortality among older people is a neglected topic in global health. In high income countries, where 84% of people do not die until they are aged 65 years or older, the causes of death among older people and the factors (determinants) that affect their risk of dying are well documented. In Europe, for example, the leading causes of death among older people are heart disease, stroke, and other chronic (long-term) diseases. Moreover, as in younger age groups, having a better education and owning a house reduces the risk of death among older people. By contrast, in low and middle income countries (LMICs), where three-quarters of deaths of older people occur, reliable data on the causes and determinants of death among older people are lacking, in part because many LMICs have inadequate vital registration systems—official records of all births and deaths.
Why Was This Study Done?
In many LMICs, chronic diseases are replacing communicable (infectious) diseases as the leading causes of death and disability—health experts call this the epidemiological transition (epidemiology is the study of the distribution and causes of disease in populations)—and the average age of the population is increasing (the demographic transition). Faced with these changes, which occur when countries move from a pre-industrial to an industrial economy, policy makers in LMICs need to introduce measures to improve health and reduce deaths among older people. However, to do this, they need reliable data on the causes and determinants of death in this section of the population. In this longitudinal population-based cohort study (a type of study that follows a group of people from a defined population over time), researchers from the 10/66 Dementia Research Group, which is carrying out population-based research on dementia, aging, and non-communicable diseases in LMICs, investigate the patterns of mortality among older people living in Latin America, India, and China.
What Did the Researchers Do and Find?
Between 2003 and 2005, the researchers completed a baseline survey of people aged 65 years or older living in six Latin American LMICs, China, and India. Three to five years later, they determined the vital status of 12,373 of the study participants (that is, they determined whether the individual was alive or dead) and interviewed a key informant (usually a relative) about each death using a standardized “verbal autopsy” questionnaire that includes questions about date and place of death, and about medical help-seeking and signs and symptoms noted during the final illness. Finally, they used a tool called the InterVA algorithm to calculate the most likely causes of death from the verbal autopsies. Crude mortality rates varied from 27.3 per 1,000 person-years in urban Peru to 70.0 per 1,000 person-years in urban India, a three-fold difference in mortality rates that persisted even after allowing for differences in age, sex, education, occupational attainment, and number of assets among the study sites. Compared to the US, mortality rates were much higher in urban India and rural China; much lower in urban and rural Peru, Venezuela, and urban Mexico; but similar elsewhere. Although several socioeconomic factors were associated with mortality, only a higher education status provided consistent independent protection against death in statistical analyses. Finally, chronic diseases were the main causes of death; stroke was the leading cause of death at all the sites except those in rural Peru and Mexico.
What Do These Findings Mean?
These findings identify the main causes of death among older adults in a range of LMICs and suggest that there is an association of education with mortality that extends into later life. However, these findings may not be generalizable to other LMICs or even to other sites in the LMICs studied, and because some of the information provided by key informants may have been affected by recall error, the accuracy of the findings may be limited. Nevertheless, these findings suggest how health and mortality might be improved in elderly people in LMICs. Specifically, they suggest that efforts to ensure universal access to education should confer substantial health benefits and that interventions that target social and economic vulnerability in later life and promote access to effectively organized health care (particularly for stroke) should be considered.
Additional Information
Please access these websites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001179.
The World Health Organization provides information on mortality around the world and projections of global mortality up to 2030
The 10/66 Dementia Research Group is building an evidence base to inform the development and implementation of policies for improving the health and social welfare of older people in LMICs, particularly people with dementia; its website includes background information about demographic and epidemiological aging in LMICs
Wikipedia has a page on the demographic transition (note: Wikipedia is a free online encyclopedia that anyone can edit; available in several languages)
Information about the InterVA tool for interpreting verbal autopsy data is available
The US Centers for Disease Control and Prevention has information about healthy aging
doi:10.1371/journal.pmed.1001179
PMCID: PMC3289608  PMID: 22389633
25.  “Working the System”—British American Tobacco's Influence on the European Union Treaty and Its Implications for Policy: An Analysis of Internal Tobacco Industry Documents 
PLoS Medicine  2010;7(1):e1000202.
Katherine Smith and colleagues investigate the ways in which British American Tobacco influenced the European Union Treaty so that new EU policies advance the interests of major corporations, including those that produce products damaging to health.
Background
Impact assessment (IA) of all major European Union (EU) policies is now mandatory. The form of IA used has been criticised for favouring corporate interests by overemphasising economic impacts and failing to adequately assess health impacts. Our study sought to assess how, why, and in what ways corporations, and particularly the tobacco industry, influenced the EU's approach to IA.
Methods and Findings
In order to identify whether industry played a role in promoting this system of IA within the EU, we analysed internal documents from British American Tobacco (BAT) that were disclosed following a series of litigation cases in the United States. We combined this analysis with one of related literature and interviews with key informants. Our analysis demonstrates that from 1995 onwards BAT actively worked with other corporate actors to successfully promote a business-oriented form of IA that favoured large corporations. It appears that BAT favoured this form of IA because it could advance the company's European interests by establishing ground rules for policymaking that would: (i) provide an economic framework for evaluating all policy decisions, implicitly prioritising costs to businesses; (ii) secure early corporate involvement in policy discussions; (iii) bestow the corporate sector with a long-term advantage over other actors by increasing policymakers' dependence on information they supplied; and (iv) provide businesses with a persuasive means of challenging potential and existing legislation. The data reveal that an ensuing lobbying campaign, largely driven by BAT, helped secure binding changes to the EU Treaty via the Treaty of Amsterdam that required EU policymakers to minimise legislative burdens on businesses. Efforts subsequently focused on ensuring that these Treaty changes were translated into the application of a business orientated form of IA (cost–benefit analysis [CBA]) within EU policymaking procedures. Both the tobacco and chemical industries have since employed IA in apparent attempts to undermine key aspects of European policies designed to protect public health.
Conclusions
Our findings suggest that BAT and its corporate allies have fundamentally altered the way in which all EU policy is made by making a business-oriented form of IA mandatory. This increases the likelihood that the EU will produce policies that advance the interests of major corporations, including those that produce products damaging to health, rather than in the interests of its citizens. Given that the public health community, focusing on health IA, has largely welcomed the increasing policy interest in IA, this suggests that urgent consideration is required of the ways in which IA can be employed to undermine, as well as support, effective public health policies.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
The primary goal of public health, the branch of medicine concerned with the health of communities, is to improve lives by preventing disease. Public-health groups do this by assessing and monitoring the health of communities, by ensuring that populations have access to appropriate and cost-effective health care, and by helping to formulate public policies that safeguard human health. Until recently, most of the world's major public-health concerns related to infectious diseases. Nowadays, however, many major public-health concerns are linked to the goods made and marketed by large corporations such as fast food, alcohol, tobacco, and chemicals. In Europe, these corporations are regulated by policies drawn up both by member states and by the European Commission, the executive organ of the European Union (EU; an economic and political partnership among 27 democratic European countries). Thus, for example, the tobacco industry, which is widely recognized as a driver of the smoking epidemic, is regulated by Europe-wide tobacco control policies and member state level policies.
Why Was This Study Done?
Since 1997, the European Commission has been required by law to assess the economic, social (including health), and environmental consequences of new policy initiatives using a process called an “impact assessment” (IA). Because different types of IA examine the likely effects of policies on different aspects of daily life—a health impact assessment, for example, focuses on a policy's effect on health—the choice of IA can lead to different decisions being taken about new policies. Although the IA tool adopted by the European Commission aims to assess economic, environmental and social impacts, independent experts suggest this tool does not adequately assess health impacts. Instead, economic impacts receive the most attention, a situation that may favour the interests of large businesses. In this study, the researchers seek to identify how and why the EU's approach to IA developed. More specifically, the researchers analyze internal documents from British American Tobacco (BAT), which have been disclosed because of US litigation cases, to find out whether industry has played a role in promoting the EU's system of IA.
What Did the Researchers Do and Find?
The researchers analyzed 714 BAT internal documents (identified by searching the Legacy Tobacco Documents Library, which contains more than 10 million internal tobacco company documents) that concerned attempts made by BAT to influence regulatory reforms in Europe. They also analyzed related literature from other sources (for example, academic publications) and interviewed 16 relevant people (including people who had worked at the European Commission). This analysis shows that from 1995, BAT worked with other businesses to promote European regulatory reforms (in particular, the establishment of a business-orientated form of IA) that favor large corporations. A lobbying campaign, initiated by BAT but involving a “policy network” of other companies, first helped to secure binding changes to the EU Treaty that require policymakers to minimize legislative burdens on businesses. The analysis shows that after achieving this goal, which BAT described as an “important victory,” further lobbying ensured that these treaty changes were translated into the implementation of a business-orientated form of IA within the EU. Both the tobacco industry and the chemical industry, the researchers argue, have since used the IA to delay and/or weaken EU legislation intended to protect public health.
What Do These Findings Mean?
These findings suggest that BAT and its corporate allies have fundamentally altered the way in which EU policy is made by ensuring that all significant EU policy decisions have to be assessed using a business-orientated IA. As the authors note, this situation increases the likelihood that the EU will produce policies that favor big business rather than the health of its citizens. Furthermore, these findings suggest that by establishing a network of other industries to help in lobbying for EU Treaty changes, BAT was able to distance itself from the push to establish a business-orientated IA to the extent that Commission officials were unaware of the involvement of the tobacco industry in campaigns for IA. Thus, in future, to safeguard public health, policymakers and public-health groups must pay more attention to corporate efforts to shape decision-making processes. In addition, public-health groups must take account of the ways in which IA can be used to undermine as well as support effective public-health policies and they must collaborate more closely in their efforts to ensure effective national and international policy.
Additional Information
Please access these Web sites via the online version of this summary at http://dx.doi.org/0.1371/journal.pmed.1000202.
Wikipedia has a page on public health (note that Wikipedia is a free online encyclopedia that anyone can edit; available in several languages)
More information on the European Union (in several languages), on public health in the European Union, and on impact assessment by the European Commission is available
The Legacy Tobacco Documents Library is a public, searchable database of tobacco company internal documents detailing their advertising, manufacturing, marketing, sales, and scientific activities
The World Health Organization provides information about the dangers of tobacco (in several languages)
The Smoke Free Partnership contains more information about smoking prevalence in Europe and about European policies to tackle the public health issues associated with tobacco use
For more information about tobacco industry influence on policy see the 2009 World Health Organization report on tobacco industry interference with tobacco control
doi:10.1371/journal.pmed.1000202
PMCID: PMC2797088  PMID: 20084098

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