Abstract
Currently, we are experiencing an epidemic of cardiorenal disease characterized by increasing rates of obesity, hypertension, the metabolic syndrome, type 2 diabetes, and kidney disease. Whereas excessive caloric intake and physical inactivity are likely important factors driving the obesity epidemic, it is important to consider additional mechanisms. We revisit an old hypothesis that sugar, particularly excessive fructose intake, has a critical role in the epidemic of cardiorenal disease. We also present evidence that the unique ability of fructose to induce an increase in uric acid may be a major mechanism by which fructose can cause cardiorenal disease. Finally, we suggest that high intakes of fructose in African Americans may explain their greater predisposition to develop cardiorenal disease, and we provide a list of testable predictions to evaluate this hypothesis.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Cardiovascular Diseases / chemically induced
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Cardiovascular Diseases / epidemiology
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Comorbidity
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Diabetes Mellitus, Type 2 / chemically induced
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Diabetes Mellitus, Type 2 / epidemiology
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Fructose / administration & dosage
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Fructose / adverse effects*
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Fructose / metabolism
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Genetic Predisposition to Disease
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Humans
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Hypertension / chemically induced
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Hypertension / epidemiology
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Hyperuricemia / chemically induced
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Hyperuricemia / epidemiology*
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Kidney Diseases / chemically induced
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Kidney Diseases / epidemiology
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Metabolic Syndrome / chemically induced
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Metabolic Syndrome / epidemiology
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Obesity / chemically induced
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Obesity / epidemiology
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Risk Factors
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Sweetening Agents / administration & dosage
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Sweetening Agents / adverse effects*
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Sweetening Agents / metabolism
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Uric Acid / blood
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Uric Acid / metabolism
Substances
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Sweetening Agents
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Uric Acid
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Fructose