Dietary approaches that delay age-related diseases.
Reducing food intake in lower animals such as the rat decreases body weight, retards many aging processes, delays the onset of most diseases of old age, and prolongs life. A number of clinical trials of food restriction in healthy adult human subjects running over 2-15 years show significant reductions in body weight, blood cholesterol, blood glucose, and blood pressure, which are risk factors for the development of cardiovascular disease and diabetes. Lifestyle interventions that lower energy balance by reducing body weight such as physical exercise can also delay the development of diabetes and cardiovascular disease. In general, clinical trials are suggesting that diets high in calories or fat along with overweight are associated with increased risk for cardiovascular disease, type 2 diabetes, some cancers, and dementia. There is a growing literature indicating that specific dietary constituents are able to influence the development of age-related diseases, including certain fats (trans fatty acids, saturated, and polyunsaturated fats) and cholesterol for cardiovascular disease, glycemic index and fiber for diabetes, fruits and vegetables for cardiovascular disease, and calcium and vitamin D for osteoporosis and bone fracture. In addition, there are dietary compounds from different functional foods, herbs, and neutraceuticals such as ginseng, nuts, grains, and polyphenols that may affect the development of age-related diseases. Long-term prospective clinical trials will be needed to confirm these diet-disease relationships. On the basis of current research, the best diet to delay age-related disease onset is one low in calories and saturated fat and high in wholegrain cereals, legumes, fruits and vegetables, and which maintains a lean body weight. Such a diet should become a key component of healthy aging, delaying age-related diseases and perhaps intervening in the aging process itself. Furthermore, there are studies suggesting that nutrition in childhood and even in the fetus may influence the later development of aging diseases and lifespan.
Everitt
Arthur V
AV
Centre for Education and Research on Ageing and Anzac Research Institute, University of Sydney, Concord Repatriation General Hospital, Concord, NSW, Australia. arthureveritt@yahoo.com.au
Hilmer
Sarah N
SN
Brand-Miller
Jennie C
JC
Jamieson
Hamish A
HA
Truswell
A Stewart
AS
Sharma
Anita P
AP
Mason
Rebecca S
RS
Morris
Brian J
BJ
Le Couteur
David G
DG
D000368:Aged; D000375:Aging / Q000502:physiology*; D000428:Alcohol Drinking; D000975:Antioxidants / Q000008:administration & dosage; D002318:Cardiovascular Diseases / Q000517:prevention & control*; D002784:Cholesterol / Q000097:blood; D003704:Dementia / Q000517:prevention & control*; D003924:Diabetes Mellitus, Type 2 / Q000517:prevention & control*; D004032:Diet; D002149:Energy Intake; D005247:Feeding Behavior; D005396:Fish Products; D006304:Health Status; D006801:Humans; D008268:Macular Degeneration / Q000517:prevention & control*; D009765:Obesity / Q000517:prevention & control*; D010024:Osteoporosis / Q000517:prevention & control*
D000975:Antioxidants; D002784:Cholesterol