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3
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Division of Basic Medical Sciences and
The Department of Pediatrics, Mercer University School of Medicine, Macon, GA 31207 and
**
Dairy Management Incorporated, Rosemont, IL
3To whom correspondence should be addressed. E-mail: tobin.b{at}gain.mercer.edu.
| INTRODUCTION |
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A number of earlier symposia have dealt effectively with the individual
topics of population variability, nutrient-gene interactions,
obesity, cardiovascular disease
(CVD),4
diabetes and epidemiology. None, however, have approached the problem
of obesity, diabetes and cardiovascular disease within an
interdisciplinary effort. There is good reason to consider obesity,
diabetes and CVD as a topic best enumerated in an interdisciplinary
format. The comorbid associated conditions of obesity and diabetes
include many aspects of CVD (Montague and ORahilly 2000
). In addition, CVD is strongly associated with obesity and
diabetes (Timar et al. 2000
). It is becoming increasing
apparent that no one discipline can solve the complex genetic,
molecular, cellular, whole-body and population-based issues and
design research initiatives necessary to sustain continued progress in
this area.
The manuscripts included in this symposium profile genetic, molecular, subcellular, whole-body and statistical approaches to identify and understand specific examples of nutritional and metabolic variance in the human population. The authors represent a breadth of disciplines, including the clinical and basic sciences. Together and individually, these manuscripts provide a broad view and a focused perspective of research performed and future initiatives aimed at furthering our understanding of nutrition and metabolic diversity. We propose that a major advancement in the nutritional sciences will occur when we understand the biologic basis of nutritional individuality, identify the genotype and phenotype, and prescribe nutritional management appropriate to individual variation in obesity, diabetes and cardiovascular disease.
| Links among obesity, diabetes and CVD |
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In 1961, the Framingham Study illustrated that cholesterol, blood
pressure and electrocardiogram abnormalities are associated with an
increase in the risk for heart disease (Kannel et al. 1961
). By 1967, it was apparent that physical activity could
reduce CVD, and obesity could increase the risk of CVD (Kannel 1967
). The role of high blood pressure as a contributor to
increased risk of stroke was later established (Kannel 1970
). The association of increased HDL cholesterol with a
reduced incidence of CVD was published in 1988 (Campos et al. 1988
, Castelli 1988
). Obesity has been
demonstrated to enhance the development of diabetes, increasing insulin
resistance, insulin secretion and CVD risk (Haffner 2000
). Thus, from an historical perspective, a robust body of
epidemiologic data links the coexistent conditions of obesity, diabetes
and cardiovascular disease (Hiller et al. 1988
).
The relationship between the secondary complications of diabetes and
the role of pharmacologic and dietary intervention in reducing these
complications was firmly established in the Diabetes Control and
Complications Trials (DCCT 1993
). Overall, >60% of the
morbidity and mortality of diabetes is attributable to CVD. However,
before the DCCT, it could not be stated that enhanced metabolic control
reduced the complications of diabetes. However, although improved
metabolic control reduced the incidence of microvascular renal, retinal
and neural complications by 4060%, there were individuals in the
DCCT who did not improve, suggesting variability within the population,
i.e., glucose concentration alone did not completely explain the
variation in diabetes complications (Santiago 1993
).
Stern (1995)
later proposed that diabetes and
cardiovascular disease may coexist as a "common soil" condition,
yet may have mutually exclusive attributes.
| The lack of published literature on diversity and individuality |
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| Recent interdisciplinary nutrition initiatives |
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| SUMMARY |
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The manuscripts that follow illustrate a broad spectrum of approaches to understanding nutritional diversity. Our geneticist, Dr. Robert Eckhardt, argues convincingly that our fundamental knowledge of genetics dictates that a combination of biochemical individuality and allelic variants could be a basis for identifying an individual nutritional optimum. Dr. Ronald Krauss, physician and molecular biologist, provides substantive data that diet-gene interactions alter LDL subclass patterns, which contributes to substantial interindividual variability and thus dictates consideration of the fat content of a diet for CVD prevention and treatment. An international expert in diet-gene interactions, Dr. Carolyn Berdanier, nutrition scientist and genetics researcher, presents novel and innovative data on a variation in diabetes linked not to immunologically altered insulin secretion or genetic insulin receptor defects, but to a genetic defect in mitochondrial function, and subsequent energy metabolism pathways. From a diagnostic and clinical perspective, Dr. Steven Kahn, physician and diabetes researcher, provides one of the most unique and useful models to date, the disposition index, as a mathematical and physiologic tool to quantify individual variability in insulin secretion and insulin sensitivity and thus predict potential risk for developing diabetes and ultimately, CVD. Dr. Suzanne Murphey, nutrition researcher and statistician, provides the epidemiologic and statistical framework for understanding how current dietary recommendations are derived, and how those recommendations can overlook segments of our population who, on the basis of their nutritional individuality, do not fit population-based approaches to dietary prescription. The manuscripts that follow, thus, depict a portion of the data necessary to further an interdisciplinary approach to the nutritional sciences and present genetic, molecular, cellular, whole-body and population-based data that elucidate the biologic basis of nutritional individuality in the obesity, diabetes and CVD connection.
| FOOTNOTES |
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2 Dr. Tobin is funded by the National Institutes of Aging (AG13776), and the National Heart, Lung and Blood Institute (HL04305). ![]()
4 Abbreviations used: ASCN, American Society for Clinical Nutrition; CDC, Centers for Disease Control and Prevention; CVD, cardiovascular disease; DCCT, Diabetes Control and Complications Trials. ![]()
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