The American Heart Association conference entitled
"Obesity: Impact on Cardiovascular Disease" was
held May 22–24, 1998, in Amelia Island, Fla. It was cosponsored by
Futura Media Services and the American Heart Association Councils on
Cardiovascular Nursing;
Arteriosclerosis, Thrombosis, and Vascular Biology;
Cardiovascular Disease in the Young; Clinical
Cardiology; Epidemiology and
Prevention; and High Blood Pressure Research; the AHA Nutrition
Committee; and the AHA Prevention Coordinating Committee. The
proceedings are summarized briefly in this report. A monograph of the
conference will be published by Futura Publishing Company, Inc.
Obesity is an important determinant of cardiovascular
disease (CVD). Previous epidemiological studies of obesity have
documented a modest association of obesity and risk of CVD, especially
in younger age groups. The study of obesity and CVD should now focus on
weight change over time, especially differences between childhood
versus younger and older adult weight gains, and the distribution of
body fat, especially visceral or intra-abdominal fat. Weight gain
during young adult life may be one of the most important determinants
of cardiovascular risk factors. Increased
intra-abdominal fat, or waist circumference, is probably related to a
constellation of risk factors, the so-called insulin resistance
syndrome. It is also associated with higher levels of inflammatory
markers such as C-reactive protein and fibrinogen.
Age and Sex as Determinants of Obesity
The increasing prevalence of obesity in children is cause for
great concern. There is no definition of obesity in children that
relates body mass index (BMI) to health outcomes. However, >20% of
children aged 6 to 17 years are >20% overweight at the 85th
percentile of BMI, and 10% of children aged 6 to 17 are overweight at
the 95th percentile. It appears that 50% of children who are
overweight are also overweight as adults, but it is not possible to
identify any individual child who will become an overweight adult. CVD
risk factors, such as elevated blood pressure, elevated total
cholesterol and LDL cholesterol (LDL-C), and
low levels of HDL cholesterol (HDL-C) track from childhood,
although less strongly than BMI. Overweight children also tend to have
a cluster of risk factors. Risk factors tend to occur in families and
are especially evident in children when an adult relative is obese.
Children with a family history of CVD are heavier than those without
family history of disease. All of this suggests that the obese child
has an elevated risk of developing CVD in adulthood. A few studies have
linked childhood obesity with adult morbidity and mortality. One study
showed a trend toward an increase in all-cause mortality; in another,
very obese children (before and after puberty) were at greater risk for
adult mortality from CVD. A BMI greater than the 70th percentile versus
the 25th to 50th percentiles in childhood resulted in a greater
relative risk of coronary heart disease (CHD) mortality in men
but not in women. Increased relative risk for all-cause mortality was
present in both men and women in this study population.
Weight gain occurs differently in men and women. The greatest weight
gain in men occurs in those with the highest BMI and those in the older
age groups. Compared with women, men live longer and are obese later in
life. In women, the greatest weight gain is in the younger age groups.
Recent epidemiological studies have shown that in women, weight loss is
also accompanied by bone loss. Another difference in weight gain
between men and women is that as women's educational level rises,
obesity decreases, for both white and black women, whereas in men,
educational level appears not to be related to obesity.
Genetics
The causes of obesity are many, but there is little doubt that
genetic factors play an important role in its etiology. Humans carry
probably dozens of genes that are directly related to body size. One of
the specific roles for genes is the determination of set points.
Identification of such genes is important, and several types of studies
must be performed to address this. Linkage analysis can be used
to find physical locations of genes that are relevant to a
phenotype. If a specific gene plays a role in the determination
of a given phenotype, the gene and the phenotype will
be transmitted together (cosegregate) across generations. The fact that
the etiology of obesity is so complex underscores the need for better
understanding of genetic determinants as a basis for more rational
interventions to treat obesity.
Several approaches have been used to search for specific genes involved
in obesity: identification of mutations responsible for obesity in
rodent models, association or linkage of obesity measures with
candidate genes in humans, and chromosomal localization of genes by
linkage of polymorphic markers to obesity and related
phenotypes in humans and mice. To date, causative genes have
been found for 5 obese mouse models. Two, leptin and leptin receptor,
have been linked with variation in body fat in some human studies, but,
for leptin, causation has been shown only in 2 obese children with
homozygous missense mutations in the leptin gene. Linkages or
associations with body fat measures have been reported for >20 other
candidate genes in humans, but relationships involving these genes were
generally not strong and in some cases were inconsistent among
studies. Chromosomal sites of genes responsible for several rare
familial human obesity syndromes have been identified, but none to date
have been linked to obesity in the general population. On the other
hand, with genome-wide searches, quantitative trait linkages of body
fat indexes have been reported for several genetic markers in both
humans and mouse models. Although multiple genetic influences on
obesity phenotypes are suggested by these studies, in most
cases the responsible gene variants, their
pathophysiological effects, and their interactions
with other genes and environmental factors remain to be determined.
Environmental Factors
Environmental as well as genetic factors greatly affect the
expression of obesity across the lifespan. The relative contribution of
each of these factors to the phenotypic variance of obesity is not
fully understood. Knowledge of the nongenetic determinants of
obesity-CVD risk factor clustering is essential for planning effective
multidisciplinary interventions focused on primary prevention of CVD.
Data from a longitudinal twin-family study and co-twin control studies
combined with population-based data on patterns of dietary intake and
physical activity provide persuasive evidence for an environmental
hypothesis. Collectively, these data point to the importance of primary
prevention beginning early in life, emphasize the role of health
behaviors including physical activity and dietary intake, and suggest
the need for modification of health-related practices and policies
focused on consumers, providers, schools, and communities.
Obesity and Cardiovascular Health
The effects of obesity on cardiovascular health
and disease are many, one of the most profound of which is
hypertension. Risk estimates from population studies suggest that
Obesity has a strong effect on lipoprotein metabolism,
regardless of ethnic group. Increased weight is a determinant of higher
levels of triglycerides, elevated LDL-C, and low HDL-C.
Conversely, weight loss is associated with a healthier lipoprotein
profile in both men and women: triglycerides decrease,
HDL-C increases, and LDL-C decreases. Changes in HDL-C levels are more
pronounced in women than in men. The association between obesity and
LDL-C is more complex. LDL-C concentrations increase with BMI in men,
but such increases are not as pronounced in women, the elderly, and
some ethnic groups. Increasing BMI is associated with small,
atherogenic LDL. Furthermore, central obesity in women is associated
with elevated LDL-C concentrations. Research should be directed toward
understanding the relative importance of obesity-related changes in
lipoproteins in predicting actual and potential CVD.
There is a strong link between obesity and a generalized
metabolic disorder of which insulin resistance is an
indicator. It is difficult to define the precise contribution of
obesity to insulin resistance, but most analyses suggest that
it can account for
The response of various ethnic groups to insulin resistance is
variable; eg, Asian Indians are more susceptible to insulin
resistance than are other ethnic groups and are at very high risk of
coronary disease. The role of body fat distribution in insulin
resistance is important; the key may be abdominal fat, which is highly
correlated with insulin resistance. It is also necessary to consider
the role of aging, exercise, diet, and genetics in insulin
resistance.
Biological Factors in Obesity
Currently, little is known about the basic causes of obesity, but
a great deal is happening in the area of translational research that
will lead to the therapeutics of tomorrow. An important focus of
research is the biology of weight reduction. The role of proteins and
receptors in the regulation of obesity is not yet fully understood. A
good example is orphan receptors, the recent screening of which
revealed orexin A and B. These receptors are found in the lateral
hypothalamus of the brain, the area known to be associated with
regulation of body weight. Orexin peptides A and B are
neurotransmitters responsible for regulation of fasting and feeding. It
is possible that other peptides and amines that regulate energy are
present, but this remains to be demonstrated. The function of such
peptides and amines and their relationship to obesity remains to be
shown and is an area for future research.
The uncoupling proteins UCP-2 and -3 may be important in regulating
metabolic rate and therefore in obesity. The relationships
between these proteins, which act in the mitochondria, and obesity are
not completely understood. Because UCP-3 is thought to regulate energy
balance, research in this area would be valuable.
Sleep apnea is a major factor to consider in obesity. This dysfunction
may be associated with the release of the cytokines tumor
necrosis factor and interleukin-6. Sequelae associated with sleep apnea
appear to play a role in mortality of severely obese patients.
Circulating estrogens increase with body weight. However, an
association of weight gain with hormone replacement therapy (HRT) has
not been supported by findings from scientific studies. The relation
between HRT and incidence of CVD is similar at all levels of BMI.
Breast cancer increases only in the group with the lowest BMI. HRT
appears to protect against initial myocardial infarction and hip
fracture in both obese and lean women.
Assessing the Obese Patient
In assessing the obese patient, it is critical to determine the
relative contributions made by fat and fat-free mass to total body
mass. Body composition assessment has improved over the century.
Various measures are used to grossly estimate the degree of obesity in
large-scale epidemiological settings, including body weight, BMI, waist
circumference, and the waist-to-hip ratio. In smaller-scale studies and
clinical settings, measurements of triceps and subscapular skinfolds
are more practical and accurate methods. Bioelectrical impedance, total
body electrical conductivity methods, and dual-energy x-ray
absorptiometry are also used in clinical settings. Indirect methods
such as hydrostatic weighing and measurement of total body potassium
and deuterated and
18O2-labeled water are used
in research settings.
It is essential that valid and reliable measures of dietary intake be
used in studies aimed at determining the links between dietary intake
and obesity. Various instruments are available, but a valid assessment
requires clear identification of the primary objective of the
assessment and the intended uses of the derived information. Other
considerations include defining what components of the diet will be
assessed, participant burden, and reporting bias. Understanding the
strengths and weakness of food records, dietary recalls, and food
frequency questionnaires is important for the selection of methods, the
development of strategies to minimize problems, and the appropriate
interpretation of the data.
A better understanding of why modest weight reduction benefits many of
the comorbidities and why the elderly may be relatively protected from
obesity-related consequences may better delineate who should be treated
and how aggressively. For example, in hypertensives, nonpharmacological
treatment combined with pharmacological treatment is the most
effective, and the development of diabetes can be prevented by weight
loss and exercise.
Another factor to consider is diet composition. The recommendations for
dietary intake for the prevention of CVD may require modification. The
following areas are being considered: increasing
monounsaturated fatty acids to replace saturated
fatty acids; the role of water in obesity; the role of high energy
density in obesity; and the role of meal replacements, diet
supplements, vitamin and mineral supplements, and macronutrients.
Altering the diet composition for short-term weight loss (12 to 20
weeks) adds little to the amount of weight loss achieved. However, diet
composition is important for weight maintenance. Small changes,
such as eating 50 fewer calories a day, exercising for 15 to 20 minutes
a day, or expending 100 additional calories per day, can result in a
10-lb weight loss per year or can help maintain weight. Small changes
are additive.
Obesity is the normal physiological response to an
environment in which energy intake exceeds energy output. It is an
adaptive mechanism. Major environmental changes that support this
adaptive mechanism are the greater availability of foods and the
increase in sedentary lifestyle. The social environment has moved from
being obesity retardant to being obesity conducive. This has important
implications for patients with certain genotypes.
Metabolic rates differ between patients and may be
important in determining who becomes obese.
Obesity can develop when an imbalance exists between energy intake and
energy expenditure. Despite this seemingly simple statement, the
relative contributions of energy intake and energy expenditure in
obesity development are poorly understood. Total energy expenditure can
be divided into the following components:
In the context of a 3000-calorie diet, typical energy expenditure
can be anywhere from 450 to 1500 calories. There is little
evidence that "defective" energy expenditure exists. Efforts to
increase energy expenditure by increasing physical activity are
considered an important treatment for obesity. Physical activity
is beneficial to cardiovascular health in many ways.
For example, HDL-C levels increase and triglyceride,
glucose, and blood pressure levels decrease. These changes occur in
connection with small changes in weight. Diet and exercise strategies
provide relatively equal amounts of weight loss in premenopausal and
postmenopausal women. In men, this combination is also a very effective
means of achieving weight loss. Further research is needed to
determine a "prescription" of exercise; that is, its intensity,
frequency, duration, and total amount as well as the length of the
training period. The most important factor in successful weight loss is
likely to be adherence to whatever exercise regimen a person
adopts.
Medical Treatment of Obesity
One group of medications currently available for treatment of
obesity works primarily by reducing food intake. The central regulation
of food intake involves both monoamine and peptide neurotransmitters.
Sibutramine, a newly approved sympathomimetic drug, reduces food intake
and increases thermogenesis in experimental animals. There is a
dose-related reduction in body weight. Sibutramine is associated with a
1 to 3 mm Hg increase in blood pressure and a 4 to 5 bpm increase
in heart rate. Another group of drugs works by altering
metabolism; orlistat, a lipase inhibitor, is in
this group. Five long-term trials lasting 1 to 2 years have been
reported in which drug-treated patients lost significantly more weight
than control subjects. Gastrointestinal symptoms were rather severe the
first year but subsided the second year. Yet another way to increase
energy expenditure is through thermogenic mechanisms; however, no drugs
are currently available that work in this manner. The impact of
drug treatment on cardiac mechanics was discussed at the conference.
The most striking example, of course, was the recent withdrawal of the
combination of fenfluramine and phentermine (fen/phen) from the market
by the Food and Drug Administration (FDA). This was prompted by a
report from the Mayo Clinic of 24 cases of valvular heart
disease in women who were treated with fen/phen. In addition,
unpublished data on the World Wide Web provided the basis for the
withdrawal of the combination drug. The percentage of patients meeting
the FDA criteria for valvulopathy was 31.7%; 68.3% of patients taking
these drugs did not exhibit valvular changes. It will be
necessary to determine whether obesity without pharmacological
intervention is associated with valvular changes before cause
can be attributed to any drug used to treat human obesity. There is
clearly a need to first identify which heart valve changes occur as a
direct result of obesity before deciding that pharmacological therapy
is the cause of valvular disease. At present, little is
known about the incidence of new, significant valvular
disorders associated with fen/phen. Information will come from
case-control studies and smaller retrospective studies with patients
serving as their own control subjects. The risk factors for
valvulopathy must be identified, as well as whether the valve
abnormalities are reversible if the obesity drugs are discontinued.
Nondrug Treatment of Obesity
Lifestyle and psychosocial treatments have their roots in behavior
modification and include techniques and approaches that focus on
changing behaviors that are thought to contribute to or maintain
obesity. Most of the various lifestyle approaches have several factors
in common, including the following: the use of self-monitoring and goal
setting; stimulus control; modification of eating style and habits; the
use of reinforcement for healthy behaviors; nutrition education;
moderate physical activity; and cognitive restructuring, including
stress management, relaxation skills, meditation, and
relapse-prevention training. These approaches produce moderate weight
loss and have minimal side effects. They are most useful for
individuals with mild obesity (BMI of 27 to 30). Individuals who follow
such an approach to weight loss maintain on average about two thirds of
their initial weight loss 12 months after treatment termination. In
studies with extended follow-up, patients return gradually to baseline
within a few years after treatment termination. Thus far, only a
continuous-care model of lifestyle intervention that views obesity as a
chronic disease requiring support or contact after the conclusion of
formal treatment produces significant results in terms of long-term
maintenance. Future research needs to address the
barriers to this approach, such as insurance reimbursement for
obesity-related treatments and the lack of data to support the
cost-effectiveness and feasibility of continuous care. Research should
also focus on methods of implementing lifestyle interventions at the
lowest cost possible and evaluating which elements of multicomponent
treatments are most effective for which individuals. Despite the
lack of substantive evidence to support specific strategies to achieve
weight maintenance, empirical evidence has provided some
insight into this problem. Factors related to weight
maintenance are different from those involved in initial weight
loss. Regular exercise is crucial, as is social support. Effective
strategies for maintaining weight loss include ongoing contact with a
physician or counselor, provision of problem solving, and
enhancement of interactions. These can be accomplished by telephone
and/or mail contacts. Multicomponent and home-based strategies appear
to be the most effective. Social support can be enhanced by looking
beyond the usual sources. For example, program participants can be
asked to bring in 3 friends. Intragroup activities and intergroup
competition have been shown to be effective. In summary, weight
maintenance requires ongoing contact with a physician or other
weight-loss counselor, exercise, social support, and extended
treatment. In the long term, the most effective approach to controlling
obesity may be to view it as a chronic disease.
Maintenance of quality of life (QOL) has recently emerged as
a standard for the successful treatment of obesity. Investigators agree
that QOL consists of the following domains: physical functioning,
psychological functioning, social functioning, overall life
satisfaction, and perceptions of health status. In one focus group of
moderately obese individuals, an attempt to gain insight into
patients' perceptions of why obesity is problematic
revealed that in the area of physical functioning, such things as lack
of energy, esophageal reflux, and pain emerged. In the psychological
arena, patients felt out of control and were entangled in a cycle of
depression and weight gain. Socially, they were withdrawn, they avoided
certain situations such as air travel because of the seating
difficulties, and they felt embarrassed to take part in their
children's activities. Finally, the economic costs were significant
with regard to food and clothing. The economic cost of obesity is
enormous. The monetary burden on society of illness and premature death
is measured in terms of direct and indirect costs. Direct costs
represent the value of resources (personal health care, other
professional services, and drugs) that could be allocated to other uses
in the absence of disease. Indirect costs are the value of lost output
because of the cessation or reduction of productive activity due to
morbidity and mortality. The direct costs of CHD,
non–insulin-dependent diabetes mellitus, and hypertension attributed
to obesity have been shown in 1 study to amount to $42.62 billion. The
indirect costs of non–insulin-dependent diabetes attributed to obesity
were $30.74 billion. A 1998 article showed that 17% of the costs of
CHD were related to obesity. The economic costs of weight-related
disease become significant at a BMI >25. In 1995, 5.7% ($99.2
billion) of the US health expenditure was related to individuals with a
BMI of 29. Using a BMI of 25, this cost would be even greater. It is
important to recognize that obesity is not confined to the United
States; it is an international problem. With regard to personal
costs, >$16 million is spent on diet sodas, $9 million in health
clubs, $600 million in medically supervised programs, $5 million on
diet meals, $4 million on exercise equipment, and $2 million on
commercial weight reduction programs. The cost and benefits of obesity
to society represent a very important issue that needs to be
thoroughly examined. The challenge is how to reduce the
increasing prevalence of obesity and its sequelae in both children and
adults. It is difficult to lose weight and maintain the loss; there are
side effects; people tend to regain weight once pharmacological agents
are withdrawn; and surgery is not without problems. These concepts
clearly support a preventive approach to obesity beginning in early
childhood, with a focus on eating and activity patterns and on health
as opposed to cosmetics. A family approach should be adopted. Two
strategies should be used, ie, the population approach and the
individual approach. The population-based effort should focus on such
areas as the media, community, and schools. The individual strategy
will probably require a multidisciplinary approach consisting of
physicians, dietitians, nurses, and physical therapists. To date,
health professionals have focused most of their efforts on an
individual approach, but serious consideration should be given to a
population approach. The scientific community has not yet reached
consensus on viable ways to approach the problems associated with
obesity. However, several lines of attack are being investigated.
Because of the complexity of the obesity problem, a multifactorial
approach will undoubtedly be required. The pharmacological approach has
yielded disappointing results, but promise is on the horizon regarding
possible drugs to modify appetite and others that reduce absorption of
foods or enhance energy expenditure. The public health approach
requires a systematic education of the public about the dangers of
obesity. Various health agencies could work together to promulgate such
a message that would reach all population groups. There is a great need
to address the social factors that contribute to obesity and to
initiate efforts on a broad scale to modify these factors. Much
skepticism exists regarding the possibility of achieving success in the
treatment of obesity. It is important to note that many of the
cardiovascular complications of obesity arise as a
result of mild to moderate degrees of overweight. The availability of
ancillary personnel, eg, dietitians and exercise therapists, will be
required to assist physicians in the treatment of obesity in the
clinical setting. Finally, management of associated risk factors
(atherogenic dyslipidemia, hypertension, prothrombic state,
and insulin resistance) will help prevent the
cardiovascular complications of obesity.
Footnotes
A single reprint of this article is available by calling 800-242-8721 (US only) or writing the American Heart Association, Public Information, 7272 Greenville Avenue, Dallas, TX 75231-4596. Ask for reprint No. 71–0152.
© 1998 American Heart Association, Inc.
AHA Conference Proceedings
Obesity
Impact on Cardiovascular Disease
Key Words: obesity • cardiovascular diseases • AHA Conference Proceedings • morbidity
75% of hypertension can be directly attributed to obesity. However,
the precise mechanisms of hypertension related to obesity are not fully
understood. Contemporary thinking concerning the link between obesity
and subsequent renal failure has evolved from repeated observations of
the relationship between body weight and blood pressure. It is well
documented that blood pressure increases with weight gain and decreases
with weight loss. In addition, there is increasing evidence that
obesity may provide the impetus for sympathetic nervous system
activation as well as for changes in renal structure and function.
There is considerable evidence that renal dysfunction, characterized by
increased tubular sodium reabsorption and resetting of pressure
natriuresis, plays a key role in increasing blood pressure in obese
subjects. The increased tubular pressure reabsorption is closely
related to the sympathetic nervous and renin-angiotensin
systems, as are structural changes that cause compression of the
renal medulla. Renal vasodilation, glomerular
hyperfiltration, and increased arterial pressure are
compensations that help overcome increased renal tubular reabsorption
and maintain sodium balance in obesity. This also leads to increased
glomerular capillary wall stress, which, along with
activation of the neurohumoral systems, increased lipids, and glucose
intolerance, eventually causes
glomerulosclerosis and loss of nephron function
in obese subjects. Further research is needed to identify the
mechanisms involved in sympathetic nervous system activation and
changes in renal structure and function that accompany obesity. 50% of the variance in insulin sensitivity in the
general population. Insulin resistance is associated with a
constellation of metabolic abnormalities, including
obesity, diabetes, dyslipoproteinemia, hypertension, and
atherosclerosis. It is also linked to a prothrombotic
state. Because of the complex nature of insulin resistance, it is not
known whether it is independently related to atherogenesis by an
unknown mechanism. Future research should explore whether insulin
resistance can promote atherosclerosis independently of
other risk factors.
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 J. H. Hays, A. DiSabatino, R. T. Gorman, S. Vincent, and M. E. Stillabower Effect of a High Saturated Fat and No-Starch Diet on Serum Lipid Subfractions in Patients With Documented Atherosclerotic Cardiovascular Disease Mayo Clin. Proc., November 1, 2003; 78(11): 1331 - 1336. [Abstract] [PDF]
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 K. C. Oeffinger, A. C. Mertens, C. A. Sklar, Y. Yasui, T. Fears, M. Stovall, T. A. Vik, P. D. Inskip, and L. L. Robison Obesity in Adult Survivors of Childhood Acute Lymphoblastic Leukemia: A Report from the Childhood Cancer Survivor Study J. Clin. Oncol., April 1, 2003; 21(7): 1359 - 1365. [Abstract] [Full Text] [PDF]
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V. Stangl, G. Baumann, and K. Stangl Coronary atherogenic risk factors in women Eur. Heart J., November 2, 2002; 23(22): 1738 - 1752. [Full Text] [PDF]
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 M. Rendell, U. L. Hulthén, C. Törnquist, L. Groop, and I. Mattiasson Relationship between Abdominal Fat Compartments and Glucose and Lipid Metabolism in Early Postmenopausal Women J. Clin. Endocrinol. Metab., February 1, 2001; 86(2): 744 - 749. [Abstract] [Full Text]
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 J. Lynch, X. L. Wang, and D. E L Wilcken Body mass index in Australian children: recent changes and relevance of ethnicity Arch. Dis. Child., January 1, 2000; 82(1): 16 - 20. [Abstract] [Full Text]
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 M. Barton, R. Carmona, H. Morawietz, L. V. d'Uscio, W. Goettsch, H. Hillen, C. C. Haudenschild, J. E. Krieger, K. Munter, T. Lattmann, et al. Obesity Is Associated With Tissue-Specific Activation of Renal Angiotensin-Converting Enzyme In Vivo : Evidence for a Regulatory Role of Endothelin Hypertension, January 1, 2000; 35(1): 329 - 336. [Abstract] [Full Text] [PDF]
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