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Epidemiology of type 2 diabetes and cardiovascular disease: translation from population to prevention: the Kelly West award lecture 2009.

Meigs JB - Diabetes Care (2010)

Bottom Line: West recognized that pre-diabetes is recognizable as what we now call metabolic syndrome.He predicted that type 2 diabetes could be prevented by healthy lifestyle change.The challenge now is for us to translate these insights into effective strategies for the prevention of the modern epidemic of diabetes and vascular disease.

View Article: PubMed Central - PubMed

Affiliation: General Internal Medicine Unit, Massachusetts General Hospital, Boston, Massachusetts, USA. jmeigs@partners.org

ABSTRACT
In the book Epidemiology of Diabetes and Its Vascular Lesions (1978), Kelly West summarized extant knowledge of the distribution and causes of diabetes. The 30 years of epidemiological research that followed have seen remarkable advances in the understanding of obesity as a risk factor for type 2 diabetes, and diabetes and pre-diabetes as risk factors for cardiovascular disease. Increasingly detailed understanding of these relationships has, unfortunately, been accompanied by an alarming increase in the prevalence of obesity, diabetes, and cardiovascular disease. West recognized that pre-diabetes is recognizable as what we now call metabolic syndrome. He predicted that novel insight into diabetes pathogenesis would come from biochemical and genetic epidemiology studies. He predicted that type 2 diabetes could be prevented by healthy lifestyle change. The challenge now is for us to translate these insights into effective strategies for the prevention of the modern epidemic of diabetes and vascular disease.

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Related in: MedlinePlus

A genetic risk score of 18 SNPs predicts type 2 diabetes. A: Shows the distribution of an 18-SNP genetic risk score, where FHS individuals were scored with a 0 if they had no risk alleles at a given SNP, one if they were heterozygous, and two if they were homozygous for the risk allele. Individuals who developed type 2 diabetes over 28 years of follow-up have about 0.6 more risk alleles than those who remain free of diabetes (P < 0.0001). B: Shows that risk for type 2 diabetes increases with increasing genetic risk burden. Those with 16–20 risk alleles have a risk of diabetes of 1.6, and those with ≥21 risk alleles have a risk of 2.5 relative to those with ≤15 risk alleles (P < 0.001). However, the genetic risk score does not discriminate those who will develop type 2 diabetes from those who will not after accounting for common clinical risk factors (age, sex, family history of diabetes, and metabolic syndrome traits). C: Shows that the area under the receiver operating characteristic curve (the C statistic) was 0.900 for a simple clinical model including clinical risk factors (gray line), and 0.901 for a model including clinical risk factors and the genetic risk score (black line) (adapted from Meigs et al. [[29]).
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Figure 5: A genetic risk score of 18 SNPs predicts type 2 diabetes. A: Shows the distribution of an 18-SNP genetic risk score, where FHS individuals were scored with a 0 if they had no risk alleles at a given SNP, one if they were heterozygous, and two if they were homozygous for the risk allele. Individuals who developed type 2 diabetes over 28 years of follow-up have about 0.6 more risk alleles than those who remain free of diabetes (P < 0.0001). B: Shows that risk for type 2 diabetes increases with increasing genetic risk burden. Those with 16–20 risk alleles have a risk of diabetes of 1.6, and those with ≥21 risk alleles have a risk of 2.5 relative to those with ≤15 risk alleles (P < 0.001). However, the genetic risk score does not discriminate those who will develop type 2 diabetes from those who will not after accounting for common clinical risk factors (age, sex, family history of diabetes, and metabolic syndrome traits). C: Shows that the area under the receiver operating characteristic curve (the C statistic) was 0.900 for a simple clinical model including clinical risk factors (gray line), and 0.901 for a model including clinical risk factors and the genetic risk score (black line) (adapted from Meigs et al. [[29]).

Mentions: The possibility to use new biochemical and genetic discoveries for type 2 diabetes prediction and prevention would perhaps have most intrigued West. It is now possible for an individual to purchase a diabetes genetic risk profile from several different companies for just a few hundred dollars. However, the ability of these profiles to discriminate future disease risk remains, at present, somewhat uncertain. In FHS, a genetic risk score comprised of 18 confirmed type 2 diabetes risk SNPs was higher among individuals who developed type 2 diabetes over 28 years compared with those who remained free of diabetes, although the absolute magnitude of the difference was minute (about 0.6 risk alleles, although the probability that there was no difference was <0.0001) (Fig. 5A and B) (29).


Epidemiology of type 2 diabetes and cardiovascular disease: translation from population to prevention: the Kelly West award lecture 2009.

Meigs JB - Diabetes Care (2010)

A genetic risk score of 18 SNPs predicts type 2 diabetes. A: Shows the distribution of an 18-SNP genetic risk score, where FHS individuals were scored with a 0 if they had no risk alleles at a given SNP, one if they were heterozygous, and two if they were homozygous for the risk allele. Individuals who developed type 2 diabetes over 28 years of follow-up have about 0.6 more risk alleles than those who remain free of diabetes (P < 0.0001). B: Shows that risk for type 2 diabetes increases with increasing genetic risk burden. Those with 16–20 risk alleles have a risk of diabetes of 1.6, and those with ≥21 risk alleles have a risk of 2.5 relative to those with ≤15 risk alleles (P < 0.001). However, the genetic risk score does not discriminate those who will develop type 2 diabetes from those who will not after accounting for common clinical risk factors (age, sex, family history of diabetes, and metabolic syndrome traits). C: Shows that the area under the receiver operating characteristic curve (the C statistic) was 0.900 for a simple clinical model including clinical risk factors (gray line), and 0.901 for a model including clinical risk factors and the genetic risk score (black line) (adapted from Meigs et al. [[29]).
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2909080&req=5

Figure 5: A genetic risk score of 18 SNPs predicts type 2 diabetes. A: Shows the distribution of an 18-SNP genetic risk score, where FHS individuals were scored with a 0 if they had no risk alleles at a given SNP, one if they were heterozygous, and two if they were homozygous for the risk allele. Individuals who developed type 2 diabetes over 28 years of follow-up have about 0.6 more risk alleles than those who remain free of diabetes (P < 0.0001). B: Shows that risk for type 2 diabetes increases with increasing genetic risk burden. Those with 16–20 risk alleles have a risk of diabetes of 1.6, and those with ≥21 risk alleles have a risk of 2.5 relative to those with ≤15 risk alleles (P < 0.001). However, the genetic risk score does not discriminate those who will develop type 2 diabetes from those who will not after accounting for common clinical risk factors (age, sex, family history of diabetes, and metabolic syndrome traits). C: Shows that the area under the receiver operating characteristic curve (the C statistic) was 0.900 for a simple clinical model including clinical risk factors (gray line), and 0.901 for a model including clinical risk factors and the genetic risk score (black line) (adapted from Meigs et al. [[29]).
Mentions: The possibility to use new biochemical and genetic discoveries for type 2 diabetes prediction and prevention would perhaps have most intrigued West. It is now possible for an individual to purchase a diabetes genetic risk profile from several different companies for just a few hundred dollars. However, the ability of these profiles to discriminate future disease risk remains, at present, somewhat uncertain. In FHS, a genetic risk score comprised of 18 confirmed type 2 diabetes risk SNPs was higher among individuals who developed type 2 diabetes over 28 years compared with those who remained free of diabetes, although the absolute magnitude of the difference was minute (about 0.6 risk alleles, although the probability that there was no difference was <0.0001) (Fig. 5A and B) (29).

Bottom Line: West recognized that pre-diabetes is recognizable as what we now call metabolic syndrome.He predicted that type 2 diabetes could be prevented by healthy lifestyle change.The challenge now is for us to translate these insights into effective strategies for the prevention of the modern epidemic of diabetes and vascular disease.

View Article: PubMed Central - PubMed

Affiliation: General Internal Medicine Unit, Massachusetts General Hospital, Boston, Massachusetts, USA. jmeigs@partners.org

ABSTRACT
In the book Epidemiology of Diabetes and Its Vascular Lesions (1978), Kelly West summarized extant knowledge of the distribution and causes of diabetes. The 30 years of epidemiological research that followed have seen remarkable advances in the understanding of obesity as a risk factor for type 2 diabetes, and diabetes and pre-diabetes as risk factors for cardiovascular disease. Increasingly detailed understanding of these relationships has, unfortunately, been accompanied by an alarming increase in the prevalence of obesity, diabetes, and cardiovascular disease. West recognized that pre-diabetes is recognizable as what we now call metabolic syndrome. He predicted that novel insight into diabetes pathogenesis would come from biochemical and genetic epidemiology studies. He predicted that type 2 diabetes could be prevented by healthy lifestyle change. The challenge now is for us to translate these insights into effective strategies for the prevention of the modern epidemic of diabetes and vascular disease.

Show MeSH
Related in: MedlinePlus