Advances in genetics and molecular biology indicate that susceptibility to chronic diseases such as coronary artery disease (CAD), hypertension, diabetes, obesity, osteoporosis, alcoholism, cancer, etc., to a great ex...Advances in genetics and molecular biology indicate that susceptibility to chronic diseases such as coronary artery disease (CAD), hypertension, diabetes, obesity, osteoporosis, alcoholism, cancer, etc., to a great extent is genetically determined. Studies have shown that 50% of the variance in plasma cholesterol concentration is genetically determined, whereas 30% - 60% of the variance in blood pressure is genetically determined. For fibrinogen, an independent risk factor for CAD, 15%-50% of the variance is genetically determined. In the U. K. population the variance for the fibrinogen level is 15% whereas in the Hawaiian population, the variance is 50%, indicating significant differences between populations. Among Australians, 75% of the variance in bone density is found to be genetically determined. Genetic variation influences the response to diet. For example,individuals with ApoE4 have higher cholesterol levels and a higher risk of CAD than those with ApoE3. Additional studies show that women of the ApoE 3/2 phenotype stand to benefit the least from a high polyunsaturate: saturate (P:S) diet because of reduction in the more 'protective' high density lipoprotein cholesterol (HDL-C), whereas men of the ApoE 4/3 phenotype showed the greatest improvement in the LDL/HDL ratio. Therefore a general recommendation to increase the polyunsaturated content of the diet in order to decrease the risk for CAD is not appropriate for women with ApoE 3/2 phenotyPe. Thus, specific information is needed to define the optimal diet for an individual展开更多
文摘Advances in genetics and molecular biology indicate that susceptibility to chronic diseases such as coronary artery disease (CAD), hypertension, diabetes, obesity, osteoporosis, alcoholism, cancer, etc., to a great extent is genetically determined. Studies have shown that 50% of the variance in plasma cholesterol concentration is genetically determined, whereas 30% - 60% of the variance in blood pressure is genetically determined. For fibrinogen, an independent risk factor for CAD, 15%-50% of the variance is genetically determined. In the U. K. population the variance for the fibrinogen level is 15% whereas in the Hawaiian population, the variance is 50%, indicating significant differences between populations. Among Australians, 75% of the variance in bone density is found to be genetically determined. Genetic variation influences the response to diet. For example,individuals with ApoE4 have higher cholesterol levels and a higher risk of CAD than those with ApoE3. Additional studies show that women of the ApoE 3/2 phenotype stand to benefit the least from a high polyunsaturate: saturate (P:S) diet because of reduction in the more 'protective' high density lipoprotein cholesterol (HDL-C), whereas men of the ApoE 4/3 phenotype showed the greatest improvement in the LDL/HDL ratio. Therefore a general recommendation to increase the polyunsaturated content of the diet in order to decrease the risk for CAD is not appropriate for women with ApoE 3/2 phenotyPe. Thus, specific information is needed to define the optimal diet for an individual
