Table 3.
Selected studies showing statistically significant gene-diet interactions in determining final CVD phenotyes
| Authors | Phenotype | Description of the gene-diet interaction | Year, Ref. |
|---|---|---|---|
| Fumeron et al |
Myocardial infarction |
Alcohol consumption interacted with the CETP-TaqIB SNP in determining myocardial infarction. The increasing effect of the B2 allele on plasma HDL-C was absent in subjects drinking < 25 grams/d of alcohol but increased commensurably, with higher values of alcohol consumption. Accordingly, the OR for myocardial infarction of B2B2 subjects decreased from 1 in nondrinkers to 0.34 in those drinking 75 grams/d or more. |
1995, (82) |
| Markus et al |
Ischemic cerebrovascular disease |
The C677T SNP in the MTHFR gene interacted with serum folate concentrations in determining the risk of ischaemic stroke. The TT genotype was a risk when serum folate was low. |
1997, (83) |
| Yoo et al | Coronary artery disease |
The C677T SNP in the MTHFR gene interacted with a low folate status in determining coronary artery disease risk. |
2000, (84) |
| Hines et al |
Myocardial infarction |
Alcohol consumption interacted with the alcohol dehydrogenase type 3 (ADH3) SNP in determining myocardial infarction. Moderate drinkers who are homozygous for the slow-oxidizing ADH3 allele (gamma2) have higher HDL levels and a substantially decreased risk of myocardial infarction. |
2001, (85) |
| Yates et al. |
Thrombotic event | The C677T SNP in the MTHFR gene interacted with B- vitamin nutritional in determining homocysteine levels and risk for a thrombotic event. |
2003 (86) |
| Younis et al |
Coronary heart disease |
Significant alcohol-ADH3 genotype interaction on coronary heart disease risk was observed, with gamma2 homozygotes, who were modest drinkers, displaying 78% risk reduction compared to gamma1 homozygotes. |
2005 (87) |
| Cornelis et al |
Myocardial infarction |
A cytochrome P450 1A2 (CYP1A2) polymorphism interacted with coffee intake in determining myocardial infarction risk. Individuals who are homozygous for the CYP1A2*1A allele are "rapid" caffeine metabolizers, whereas carriers of the variant CYP1A2*1F are "slow" caffeine metabolizers. Intake of coffee was associated with an increased risk of nonfatal myocardial infarction only among individuals with slow caffeine metabolism |
2006, (88) |
| Volcik et al |
Coronary heart disease |
The PON1 polymorphism interacted with heavy alcohol intake in determining coronary heart disease in black men. |
2007, (89) |
| Yang et al |
Myocardial infarction |
The APOE SNP interacted with saturated fat intake in determining myocardial infarction. E2 and E4 gene variants increase susceptibility to myocardial infarction in the presence of high saturated fat diet. |
2007, (90) |
| Ruiz- Narvaez et al |
Myocardial infarction |
The Pro12Ala PPARG polymorphism interacted with PUFA intake to affect the risk of myocardial infarction. The protective effect of PUFA intake on myocardial infarction is attenuated in carriers of the Ala12 allele of PPARG. |
2007, (91) |
| Cornelis et al |
Myocardial infarction |
Cruciferous vegetables are a major dietary source of isothiocyanates. Isothiocyanates induce glutathione S- transferases (GSTs), polymorphic genes. The GST genotypes modified the association between cruciferous vegetable intake and the risk of myocardial infarction. Compared with the lowest tertile of cruciferous vegetable intake, the highest tertile was associated with a lower risk of MI among persons with the functional GSTT1*1 allele but not among those with the GSTT1*0*0 genotype. |
2007, (92) |
| Allayee et al |
Myocardial infarction |
A 5-Lipoxygenase (5-LO) SNP interacted with dietary arachidonic acid (AA) in determining myocardial infarction. The variant alleles were associated with greater risk of myocardial infarction in the context of a high-AA diet. |
2008, (93) |
| Jensen et al |
Myocardial infarction |
The CETP-TaqIB SNP interacted with alcohol consumption in determining myocardial infarction risk. Alcohol consumption was associated with lower risk in carriers of the B2 alleles |
2008, (94) |
All of these were observational studies and habitual dietary intake was analyzed