Childhood Obesity and Cardiovascular Disease
Childhood Obesity and Cardiovascular Disease
During the final decades of the twentieth century there was an alarming increase in the occurrence of obesity, accompanied by upward shifts in population body-fat distributions. The increase in obesity has been particularly marked in children and has not been confined to the Western world. There is strong evidence that adult obesity is a risk factor for atherosclerotic disease, cardiovascular events, and cardiac dysfunction—partly a consequence of its strong association with the risk of developing type 2 diabetes.
The unprecedented nature of the current childhood obesity phenomenon, in which a widespread increase in body fat from early life will lead to an increasing burden of obesity of longer duration, makes it difficult to predict the consequences with certainty. Childhood obesity carries a greatly increased risk of adult obesity, which is likely to be accentuated as adult obesity prevalence increases. 'Tracking' of body mass with increasing strength through childhood and adolescence, to obesity in adult life is probably reinforced by the tracking of related health behaviors, particularly in diet and exercise, from childhood onwards. The long-term consequences of childhood obesity are, therefore, at least partly those of adult obesity; the direct consequences of childhood obesity on long-term cardiovascular risk are, however, less certain.
Some studies have related BMI in childhood, adolescence or early adult life to mortality. Most have suggested that higher indices of body mass at these early stages are associated with increased mortality during adult life. Studies relating early BMI to cardiovascular risk, however, have not shown consistent associations. Despite this, childhood obesity has appreciable short-term effects on the cardiovascular system, including impaired endothelial function, diminished arterial distensibility, adverse changes in intimamedia thickness and increased risk of atherosclerosis in early adult life. These could be mediated by the strong associations between obesity and insulin resistance, the metabolic syndrome, higher mean total cholesterol, LDL cholesterol and blood pressure, and raised inflammatory and hemostatic vascular markers. It is possible that the cardiovascular consequences of obesity are cumulative, so obesity duration becomes an important risk factor in its own right.
The cardiovascular consequences of obesity in a population will also depend strongly on the associated pattern of other major cardiovascular disease risk factors. In many Western countries, the last two decades have seen a drop in mortality from coronary heart disease and stroke, attributed to reductions in the prevalence of cigarette smoking, favorable changes in blood cholesterol and blood pressure, and improvements in treatment. Diminishing exposure to other major risk factors, through lifestyle changes and treatment patterns, might limit the adverse cardiovascular effects of obesity, as appears to be happening in the US. It is possible, however, that rising levels of obesity, type 2 diabetes, insulin resistance and metabolic syndrome components will reverse the current favorable mortality trends. Moreover, the current social distribution of obesity, which is more prevalent in lower social groups, suggests that the increasing importance of obesity as a determinant of cardiovascular risk could exacerbate social inequalities in cardiovascular disease in the West. In developing countries, however, which account for most of the global cardiovascular disease burden, the rising obesity prevalence is occurring alongside rising levels of cardiovascular disease and unfavorable changes in blood lipids and blood pressure. In these circumstances, which are strongly associated with urbanization, the consequences of obesity for cardiovascular disease could be amplified.
The increase in childhood obesity presents substantial challenges for clinicians and those concerned with public health. The substantial increase in childhood obesity reflects a widespread decline in physical activity and energy expenditure, without a compensatory decline in dietary energy intake. The first reflects shifts in modes of transport used (from walking and cycling to motorized transport, particularly car use) and changes in leisure activities. The second might well reflect the increasing calorie density of many foods and drinks directed at children, which make control of calorie intake increasingly difficult. A reversal of these trends to increase physical activity levels and rebalance calorie intakes in childhood will require action by individuals, families and schools, and by both local and national governments, to influence the context in which individual decisions on exercise and diet are made. Controls on the marketing of calorie-dense food and drinks to children and making walking, cycling and recreational options available, safer and more attractive are likely to be particularly important. Learning from the natural experiments presented by variations in the urban environment across different countries and cities will also be important.
Even if preventive measures to stem for early-onset obesity are implemented rapidly, in many countries at least one generation will enter adult life with a high prevalence of obesity from childhood, presenting a large-scale challenge to physicians. Medical attention will probably focus on individuals with severe degrees of obesity, and use medical and surgical treatment. As with other cardiovascular risk factors, however, it is likely that much of the burden of cardiovascular disease risk will be distributed among individuals with lesser degrees of obesity. Weight loss will be the most obvious strategy for protecting these individuals from cardiovascular disease and type 2 diabetes. Efforts to encourage weight loss should probably focus on early adult life, when behavioral change and vigorous forms of exercise are practicable. This might also be a stage of life when favorable correlates of weight loss—favorable changes in blood pressure, insulin resistance and other cardiovascular risk markers, and a reduced risk of type 2 diabetes—will be reflected in falls in cardiovascular morbidity and mortality. Confirmation is needed, however, because the gains from weight loss at later ages remain uncertain.
Many individuals with moderate obesity will find it difficult to lose weight. Other approaches will therefore need to be considered to protect such individuals from developing cardiovascular disease and diabetes. Recent experience in the prevention of cardiovascular disease and diabetes suggests that combined interventions producing modest changes in more than one component can reduce overall risk appreciably. Such combinations could be based primarily on moderate changes in diet and physical activity, or on combinations of cardioprotective medications, particularly antiplatelet drugs, statins and blood-pressure lowering drugs, as in the 'polypill'. The use of such combinations in young individuals without established cardiovascular disease, however, remains controversial.
Much of the existing evidence on the expected impact of obesity in the young is based on longitudinal studies and clinical trials carried out in an era in which the balance of chronic disease risk factors differed from those now prevalent in younger people. Decisions on the optimum strategies for cardiovascular disease prevention in obese young adults will depend on clinical trials using surrogate endpoints for vascular disease, which might be based on intermediate measures of the structure and function of the arterial wall, and on assessments of lifetime risk rather than absolute risks, which have limited value in early adulthood. A concerted effort is needed to ensure that the current obesity epidemic does not exacerbate the growing epidemic of cardiovascular disease in the developing world and reverse the favorable trends in cardiovascular risk being seen in many affluent countries.
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During the final decades of the twentieth century there was an alarming increase in the occurrence of obesity, accompanied by upward shifts in population body-fat distributions. The increase in obesity has been particularly marked in children and has not been confined to the Western world. There is strong evidence that adult obesity is a risk factor for atherosclerotic disease, cardiovascular events, and cardiac dysfunction—partly a consequence of its strong association with the risk of developing type 2 diabetes.
The unprecedented nature of the current childhood obesity phenomenon, in which a widespread increase in body fat from early life will lead to an increasing burden of obesity of longer duration, makes it difficult to predict the consequences with certainty. Childhood obesity carries a greatly increased risk of adult obesity, which is likely to be accentuated as adult obesity prevalence increases. 'Tracking' of body mass with increasing strength through childhood and adolescence, to obesity in adult life is probably reinforced by the tracking of related health behaviors, particularly in diet and exercise, from childhood onwards. The long-term consequences of childhood obesity are, therefore, at least partly those of adult obesity; the direct consequences of childhood obesity on long-term cardiovascular risk are, however, less certain.
Some studies have related BMI in childhood, adolescence or early adult life to mortality. Most have suggested that higher indices of body mass at these early stages are associated with increased mortality during adult life. Studies relating early BMI to cardiovascular risk, however, have not shown consistent associations. Despite this, childhood obesity has appreciable short-term effects on the cardiovascular system, including impaired endothelial function, diminished arterial distensibility, adverse changes in intimamedia thickness and increased risk of atherosclerosis in early adult life. These could be mediated by the strong associations between obesity and insulin resistance, the metabolic syndrome, higher mean total cholesterol, LDL cholesterol and blood pressure, and raised inflammatory and hemostatic vascular markers. It is possible that the cardiovascular consequences of obesity are cumulative, so obesity duration becomes an important risk factor in its own right.
The cardiovascular consequences of obesity in a population will also depend strongly on the associated pattern of other major cardiovascular disease risk factors. In many Western countries, the last two decades have seen a drop in mortality from coronary heart disease and stroke, attributed to reductions in the prevalence of cigarette smoking, favorable changes in blood cholesterol and blood pressure, and improvements in treatment. Diminishing exposure to other major risk factors, through lifestyle changes and treatment patterns, might limit the adverse cardiovascular effects of obesity, as appears to be happening in the US. It is possible, however, that rising levels of obesity, type 2 diabetes, insulin resistance and metabolic syndrome components will reverse the current favorable mortality trends. Moreover, the current social distribution of obesity, which is more prevalent in lower social groups, suggests that the increasing importance of obesity as a determinant of cardiovascular risk could exacerbate social inequalities in cardiovascular disease in the West. In developing countries, however, which account for most of the global cardiovascular disease burden, the rising obesity prevalence is occurring alongside rising levels of cardiovascular disease and unfavorable changes in blood lipids and blood pressure. In these circumstances, which are strongly associated with urbanization, the consequences of obesity for cardiovascular disease could be amplified.
The increase in childhood obesity presents substantial challenges for clinicians and those concerned with public health. The substantial increase in childhood obesity reflects a widespread decline in physical activity and energy expenditure, without a compensatory decline in dietary energy intake. The first reflects shifts in modes of transport used (from walking and cycling to motorized transport, particularly car use) and changes in leisure activities. The second might well reflect the increasing calorie density of many foods and drinks directed at children, which make control of calorie intake increasingly difficult. A reversal of these trends to increase physical activity levels and rebalance calorie intakes in childhood will require action by individuals, families and schools, and by both local and national governments, to influence the context in which individual decisions on exercise and diet are made. Controls on the marketing of calorie-dense food and drinks to children and making walking, cycling and recreational options available, safer and more attractive are likely to be particularly important. Learning from the natural experiments presented by variations in the urban environment across different countries and cities will also be important.
Even if preventive measures to stem for early-onset obesity are implemented rapidly, in many countries at least one generation will enter adult life with a high prevalence of obesity from childhood, presenting a large-scale challenge to physicians. Medical attention will probably focus on individuals with severe degrees of obesity, and use medical and surgical treatment. As with other cardiovascular risk factors, however, it is likely that much of the burden of cardiovascular disease risk will be distributed among individuals with lesser degrees of obesity. Weight loss will be the most obvious strategy for protecting these individuals from cardiovascular disease and type 2 diabetes. Efforts to encourage weight loss should probably focus on early adult life, when behavioral change and vigorous forms of exercise are practicable. This might also be a stage of life when favorable correlates of weight loss—favorable changes in blood pressure, insulin resistance and other cardiovascular risk markers, and a reduced risk of type 2 diabetes—will be reflected in falls in cardiovascular morbidity and mortality. Confirmation is needed, however, because the gains from weight loss at later ages remain uncertain.
Many individuals with moderate obesity will find it difficult to lose weight. Other approaches will therefore need to be considered to protect such individuals from developing cardiovascular disease and diabetes. Recent experience in the prevention of cardiovascular disease and diabetes suggests that combined interventions producing modest changes in more than one component can reduce overall risk appreciably. Such combinations could be based primarily on moderate changes in diet and physical activity, or on combinations of cardioprotective medications, particularly antiplatelet drugs, statins and blood-pressure lowering drugs, as in the 'polypill'. The use of such combinations in young individuals without established cardiovascular disease, however, remains controversial.
Much of the existing evidence on the expected impact of obesity in the young is based on longitudinal studies and clinical trials carried out in an era in which the balance of chronic disease risk factors differed from those now prevalent in younger people. Decisions on the optimum strategies for cardiovascular disease prevention in obese young adults will depend on clinical trials using surrogate endpoints for vascular disease, which might be based on intermediate measures of the structure and function of the arterial wall, and on assessments of lifetime risk rather than absolute risks, which have limited value in early adulthood. A concerted effort is needed to ensure that the current obesity epidemic does not exacerbate the growing epidemic of cardiovascular disease in the developing world and reverse the favorable trends in cardiovascular risk being seen in many affluent countries.
CLICK HERE for subscription information about this journal.
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