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Coffee, CYP1A2 Genotype, and Risk of Myocardial Infarction
Open accessAbstract
CONTEXT: The association between coffee intake and risk of myocardial infarction (MI) remains controversial. Coffee is a major source of caffeine, which is metabolized by the polymorphic cytochrome P450 1A2 (CYP1A2) enzyme. Individuals who are homozygous for the CYP1A2*1A allele are "rapid" caffeine metabolizers, whereas carriers of the variant CYP1A2*1F are "slow" caffeine metabolizers. OBJECTIVE: To determine whether CYP1A2 genotype modifies the association between coffee consumption and risk of acute nonfatal MI. DESIGN, SETTING, AND PARTICIPANTS: Cases (n = 2014) with a first acute nonfatal MI and population-based controls (n = 2014) living in Costa Rica between 1994 and 2004, matched for age, sex, and area of residence, were genotyped by restriction fragment-length polymorphism polymerase chain reaction. A food frequency questionnaire was used to assess the intake of caffeinated coffee. MAIN OUTCOME MEASURE: Relative risk of nonfatal MI associated with coffee intake, calculated using unconditional logistic regression. RESULTS: Fifty-five percent of cases (n = 1114) and 54% of controls (n = 1082) were carriers of the slow *1F allele. For carriers of the slow *1F allele, the multivariate-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) of nonfatal MI associated with consuming less than 1, 1, 2 to 3, and 4 or more cups of coffee per day were 1.00 (reference), 0.99 (0.69-1.44), 1.36 (1.01-1.83), and 1.64 (1.14-2.34), respectively. Corresponding ORs (95% CIs) for individuals with the rapid *1A/*1A genotype were 1.00, 0.75 (0.51-1.12), 0.78 (0.56-1.09), and 0.99 (0.66-1.48) (P = .04 for gene x coffee interaction). For individuals younger than the median age of 59 years, the ORs (95% CIs) associated with consuming less than 1, 1, 2 to 3, or 4 or more cups of coffee per day were 1.00, 1.24 (0.71-2.18), 1.67 (1.08-2.60), and 2.33 (1.39-3.89), respectively, among carriers of the *1F allele. The corresponding ORs (95% CIs) for those with the *1A/*1A genotype were 1.00, 0.48 (0.26-0.87), 0.57 (0.35-0.95), and 0.83 (0.46-1.51). CONCLUSION: Intake of coffee was associated with an increased risk of nonfatal MI only among individuals with slow caffeine metabolism, suggesting that caffeine plays a role in this association.
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“The Panel notes that, although this case-control study suggests that polymorphisms of the CYP1A2 gene may affect the risk of MI in relation to caffeine consumption, which may be further affected by polymorphisms of the serotonin receptor gene HTR2A, the results have not yet been replicated and the hypothesis has not been tested in prospective cohort studies.”
From Scientific Opinion on the safety of caffeine (2015) · cites this paper as Cornelis et al., 2006
In the citing paper
“In total, 55 % of cases (n = 1 114) and 54 % of controls (n = 1 082) were carriers of the slow *1F allele, for which the multivariate-adjusted odds ratios (ORs) and 95 % CIs for non-fatal MI associated with the consumption of less than one, one, two to three and four or more cups of coffee per day were 1.00 (reference), 0.99 (0.69-1.44), 1.36 (1.01-1.83)and 1.64 (1.14-2.34),respectively.Cor”
From Scientific Opinion on the safety of caffeine (2015) · cites this paper as Cornelis et al., 2006
In the citing paper
“A study by Cornelis MC et al.47 showed that CYP1A2 genotype was an effect modifier between coffee consumption and risk of myocardial infarction: coffee consumption was related to higher risk of myocardial infarction for the slow caffeine metabolizer, and was not related to myocardial infarction for the fast caffeine metabolizer.”
From Long-Term Coffee Consumption and Risk of Cardiovascular Disease: A Systematic Review and a Dose–Response Meta-Analysis of Prospective Cohort Studies (2014) · cites this paper as [47]
In the citing paper
“However, this analysis was based on a case-control study conducted in Costa Rico and the results have not been replicated in prospective cohort studies yet.”
From Long-Term Coffee Consumption and Risk of Cardiovascular Disease: A Systematic Review and a Dose–Response Meta-Analysis of Prospective Cohort Studies (2014) · cites this paper as [47]
Citations
Cites
Willett, W. C. (1998) · doi:10.1093/acprof:oso/9780195122978.001.0001 · Cited by 4,541
Tunstall-Pedoe, H., Kuulasmaa, K., Amouyel, P., Arveiler, D., Rajakangas, A.-M., & Pająk, A. (1994) · Circulation · doi:10.1161/01.cir.90.1.583 · Cited by 2,260
Effects of caffeine on human health
Nawrot, P., Jordan, S., Eastwood, J., Rotstein, J., Hugenholtz, A., & Feeley, M. (2003) · Food Additives and Contaminants · doi:10.1080/0265203021000007840 · Cited by 1,199
Sachse, C., Brockmöller, J., Bauer, S., & Roots, I. (1999) · British Journal of Clinical Pharmacology · doi:10.1046/j.1365-2125.1999.00898.x · Cited by 751
How introns influence and enhance eukaryotic gene expression
Hir, H. L., Nott, A., & Moore, M. J. (2003) · Trends in Biochemical Sciences · doi:10.1016/s0968-0004(03)00052-5 · Cited by 734
Butler, M. A., Iwasaki, M., Guengerich, F. P., & Kadlubar, F. F. (1989) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.86.20.7696 · Cited by 638
Shryock, J. C., & Belardinelli, L. (1997) · The American Journal of Cardiology · doi:10.1016/s0002-9149(97)00256-7 · Cited by 578
Caffeine as a psychomotor stimulant: mechanism of action
Fisone, G., Borgkvist, A., & Usiello, A. (2004) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-003-3269-3 · Cited by 558
Nakajima, M., Yokoi, T., Mizutani, M., Kinoshitah, M., Funayama, M., & Kamataki, T. (1999) · The Journal of Biochemistry · doi:10.1093/oxfordjournals.jbchem.a022352 · Cited by 345
Gu, L., Gonzalez, F. J., KALOW, W., & Tang, B. K. (1992) · Pharmacogenetics · doi:10.1097/00008571-199204000-00004 · Cited by 326
Cited by
Sorted by citations
Zanger, U. M., & Schwab, M. (2013) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2012.12.007 · Cited by 4,169
“controversial association between coffee intake and risk of MI was investigated with respect to the CYP1A2 –163C/A polymorphism by the same researchers (Cornelis et al., 2006).”
MethodGene–environment interactions in psychiatry: joining forces with neuroscience
Caspi, A., & Moffitt, T. E. (2006) · Nature Reviews Neuroscience · doi:10.1038/nrn1925 · Cited by 1,300
“Caffeine is metabolized by an enzyme (CYP1A2) in the liver, knowledge that allowed researchers to test (and confirm) the hypothesis that carriers of the slow metabolizer variant of the CYP1A2 gene are at a heightened risk of myocardial infarctio”
BackgroundGenome-wide association study identifies eight loci associated with blood pressure
Wellcome Trust Case Control Consortium, Newton-Cheh, C., Johnson, T., Gateva, V., Tobin, M. D., Bochud, M., Coin, L., Najjar, S. S., Zhao, J. H., Heath, S. C., et al. (2009) · Nature Genetics · doi:10.1038/ng.361 · Cited by 1,215
Heckman, M. A., Weil, J., & de Mejía, E. G. (2010) · Journal of Food Science · doi:10.1111/j.1750-3841.2010.01561.x · Cited by 1,116
Polymorphism of human cytochrome P450 enzymes and its clinical impact
Zhou, S., Liu, J., & Chowbay, B. (2009) · Drug Metabolism Reviews · doi:10.1080/03602530902843483 · Cited by 857
International society of sports nutrition position stand: caffeine and performance
Goldstein, E. R., Ziegenfuss, T., Kalman, D., Kreider, R., Campbell, B., Wilborn, C., Taylor, L., Willoughby, D., Stout, J., Graves, B. S., et al. (2010) · Journal of the International Society of Sports Nutrition · doi:10.1186/1550-2783-7-5 · Cited by 686
International Society of Sports Nutrition Position Stand: Caffeine and Exercise Performance
Guest, N. S., VanDusseldorp, T. A., Nelson, M. T., Grgic, J., Schoenfeld, B. J., Jenkins, N. D. M., Arent, S. M., Antonio, J., Stout, J. R., Trexler, E. T., et al. (2021) · Journal of the International Society of Sports Nutrition · doi:10.1186/s12970-020-00383-4 · Cited by 665
Interindividual Differences in Caffeine Metabolism and Factors Driving Caffeine Consumption
Nehlig, A. (2018) · Pharmacological Reviews · doi:10.1124/pr.117.014407 · Cited by 632
“Carriers of the C allele, 54% of the population (163A/C and 163C/C genotypes; CYP1A2*1F), metabolize caffeine more slowly than individuals homozygous for the 163A/A allele (CYP1A2*1A) who are considered rapid caffeine metabolizers and represent 46% of the population (Sachse et al., 1999; Cornelis et al., 2006).”
BackgroundCoffee and its Consumption: Benefits and Risks
Butt, M. S., & Sultan, M. T. (2011) · Critical Reviews in Food Science and Nutrition · doi:10.1080/10408390903586412 · Cited by 631
“Some genetic factors also influence the speed and fate of caffeine as effects are more pronounced in subjects showing slow caffeine metabolism (Cornelis et al., 2006).”
BackgroundScientific Opinion on the safety of caffeine
EFSA Panel on Dietetic Products, N. A. A. (. (2015) · EFSA Journal · doi:10.2903/j.efsa.2015.4102 · Cited by 613
“This polymorphism is also referred to as CYP1A2*1F or -163C>A (AA, AC, CC) genotypes (Cornelis et al., 2006; Djordjevic et al., 2010) or as single nucleotide polymorphism (SNP) “rs762551” registered in the SNP Database of the US National Center for Biotechnology Information (http://www.”
BackgroundDing, M., Bhupathiraju, S. N., Satija, A., van Dam, R. M., & Hu, F. B. (2014) · Circulation · doi:10.1161/circulationaha.113.005925 · Cited by 565
Coffee, Caffeine, and Health Outcomes: An Umbrella Review
Grosso, G., Godos, J., Galvano, F., & Giovannucci, E. L. (2017) · Annual Review of Nutrition · doi:10.1146/annurev-nutr-071816-064941 · Cited by 531
Food as exposure: Nutritional epigenetics and the new metabolism
Landecker, H. L. (2011) · BioSocieties · doi:10.1057/biosoc.2011.1 · Cited by 502
“For example, people process caffeine at different rates if they possess different alleles of a gene coding for an enzyme expressed in the liver involved in caffeine metabolism (Cornelis et al, 2006).”
Backgroundde Toro‐Martín, J., Arsenault, B. J., Després, J., & Vohl, M. (2017) · Nutrients · doi:10.3390/nu9080913 · Cited by 534
“For instance, that is the case of genetic tests based on the specific metabolism of caffeine (slow or fast metabolizers) [13,14], the predisposition to weight gain by saturated fat intake [15,16], or the increased risk of developing hypertension by high salt intake [17,18], among others.”
BackgroundWikoff, D. S., Welsh, B. T., Henderson, R. G., Brorby, G. P., Britt, J. K., Myers, E. F., Goldberger, J. J., Lieberman, H. R., O’Brien, C. P., Peck, J. D., et al. (2017) · Food and Chemical Toxicology · doi:10.1016/j.fct.2017.04.002 · Cited by 470
Fenech, M. F., El‐Sohemy, A., Cahill, L. E., Ferguson, L. R., French, T.-A. C., Tai, E. S., Milner, J. A., Koh, W., Xie, L. Y., Zucker, M., et al. (2011) · Lifestyle Genomics · doi:10.1159/000327772 · Cited by 374
“The incorporation of genetic polymorphisms into nutritional epidemiologic studies has helped to address several limitations inherent in such studies. These include recall bias among case-control studies and residual confoundingamong observational studies in general. One example of how nutrigenomics has been used to cl…”
BackgroundGenetics of caffeine consumption and responses to caffeine
Yang, A., Palmer, A. A., & de Wit, H. (2010) · Psychopharmacology · doi:10.1007/s00213-010-1900-1 · Cited by 330
“…does not appear to differ between the genotypes (Cornelis et al. 2007) Risk of nonfatal myocardial infarction higher for subjects with C/C genotype (Cornelis et al. 2006) No association found for risk of Parkinson's disease (Facheris et al. 2008) rs35694136 No association found for risk of…”
InfluentialThe neuroprotective effects of caffeine in neurodegenerative diseases
Kolahdouzan, M., & Hamadeh, M. J. (2017) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.12684 · Cited by 323
The clinical toxicology of caffeine: A review and case study
Willson, C. (2018) · Toxicology Reports · doi:10.1016/j.toxrep.2018.11.002 · Cited by 289
Cytochrome P450 variations in different ethnic populations
McGraw, J. E., & Waller, D. P. (2012) · Expert Opinion on Drug Metabolism & Toxicology · doi:10.1517/17425255.2012.657626 · Cited by 284
“have designated the CYP1A2*1F variant as the -163A allele (-163C > A) making the -163C allele CYP1A2*1A while others have adopted an opposite nomenclature [16,17].”
BackgroundThom, E. (2007) · Journal of International Medical Research · doi:10.1177/147323000703500620 · Cited by 280
Ghotbi, R., Christensen, M., Roh, H., Ingelman‐Sundberg, M., Aklillu, E., & Bertilsson, L. (2007) · European Journal of Clinical Pharmacology · doi:10.1007/s00228-007-0288-2 · Cited by 265
“Despite the fact that CYP1A2*1F is argued to have an effect on enzyme inducibility, a recent study reported an association between coffee intake and an increased risk of nonfatal myocardial infarction among individuals carrying the CYP1A2*1F allele, who are defined as slow metabolisers, in both smokers and non-smokers…”
BackgroundZhou, S.-F., Wang, B., Yang, L.-P., & Liu, J. (2009) · Drug Metabolism Reviews · doi:10.3109/03602530903286476 · Cited by 270
“…infarction among individuals carrying the CYP1A2*1F allele, who are defined as PMs, in both smokers (n = 368 for the *1A/*1A genotype; n = 437 for the *1A/*1F or *1F/*1F genotype) and nonsmokers (n = 531 for the *1A/*1A genotype; n = 677 for the *1A/*1F or *1F/*1F genotype) (Cornelis et al., 2006).”
BackgroundManach, C., Milenković, D., de Wiele, T. V., Rodriguez‐Mateos, A., de Roos, B., García‐Conesa, M., Landberg, R., Gibney, E. R., Heinonen, M., Tomás-Barberán, F. A., et al. (2016) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.201600557 · Cited by 247
“Subjects with the CYP1A2*1F variant (carriers of the -163 C allele) associated with a low enzyme inducibility are considered to be slow caffeine metabolizers in comparison with the rapid caffeine metabolizers carrying the wild-type allele [47].”
BackgroundCaffeine, CYP1A2 Genotype, and Endurance Performance in Athletes
GUEST, N., COREY, P., VESCOVI, J., & EL-SOHEMY, A. (2018) · Medicine & Science in Sports & Exercise · doi:10.1249/mss.0000000000001596 · Cited by 231
“Individuals with the AC or CC genotype (slow metabolizers) have an elevated risk of myocardial infarction (24), hypertension (25), and prediabetes (26) with increasing caffeinated coffee consumption, whereas those with the AA genotype show no such risk.”
BackgroundResultGenetic polymorphism of the adenosine A2A receptor is associated with habitual caffeine consumption
Cornelis, M. C., El‐Sohemy, A., & Campos, H. (2007) · American Journal of Clinical Nutrition · doi:10.1093/ajcn/86.1.240 · Cited by 231
“Details of the study design (case-control study) and participants were reported previously (25).”
BackgroundResultCYP1A2 genotype modifies the association between coffee intake and the risk of hypertension
Palatini, P., Ceolotto, G., Ragazzo, F., Dorigatti, F., Saladini, F., Papparella, I., Mos, L., Zanata, G., & Santonastaso, M. (2009) · Journal of Hypertension · doi:10.1097/hjh.0b013e32832ba850 · Cited by 230
Mineharu, Y., Koizumi, A., Wada, Y., Iso, H., Watanabe, Y., Date, C., Yamamoto, A., Kikuchi, S., Inaba, Y., Toyoshima, H., et al. (2009) · Journal of Epidemiology & Community Health · doi:10.1136/jech.2009.097311 · Cited by 230
“Although the relationship between coffee consumption and CVD has been extensively studied,”
BackgroundCaffeine Consumption through Coffee: Content in the Beverage, Metabolism, Health Benefits and Risks
DePaula, J., & Farah, A. (2019) · Beverages · doi:10.3390/beverages5020037 · Cited by 258
Caffeine and cardiovascular health
Turnbull, D., Rodricks, J. V., Mariano, G. F., & Chowdhury, F. (2017) · Regulatory Toxicology and Pharmacology · doi:10.1016/j.yrtph.2017.07.025 · Cited by 216
“…or AMI only among individuals with a genotype associated with slow caffeine metabolism (CYP1A2*1F instead of CYP1A2*1A) when analyzed separately (Cornelis et al., 2006), or low COMT activity genotype (low catecholamine metabolism) (Happonen et al., 2006) compared to non- or lowconsumption of…”
BackgroundCaffeine Use Disorder: A Comprehensive Review and Research Agenda
Meredith, S. E., Juliano, L. M., Hughes, J. R., & Griffiths, R. R. (2013) · Journal of Caffeine Research · doi:10.1089/jcr.2013.0016 · Cited by 230
“Moreover, individuals who carry the variant of the CYP1A2 gene that slows caffeine metabolism have been shown to be at increased risk for hypertension and myocardial infarction associated with coffee use.(66,77) Recent genome-wide meta-analyses have found associations between caffeine use and variants of the CYP1A2 ge…”
BackgroundPickering, C., & Kiely, J. (2017) · Sports Medicine · doi:10.1007/s40279-017-0776-1 · Cited by 228
“The variable effects of this SNP are most well-established in regard to health, with myocardial infarction and hypertension risk increased in slow metabolisers consuming moderate (3–4 cups) amounts of coffee, whilst fast metabolisers exhibit a protective effect of moderate coffee consumption [40, 41].”
BackgroundBožina, N., Bradamante, V., & Lovrić, M. (2009) · Archives of Industrial Hygiene and Toxicology · doi:10.2478/10004-1254-60-2009-1885 · Cited by 201
Crippa, A., Discacciati, A., Larsson, S. C., Wolk, A., & Orsini, N. (2014) · American Journal of Epidemiology · doi:10.1093/aje/kwu194 · Cited by 191
Wu, J.-N., Ho, S. C., Zhou, C., Ling, W.-H., Chen, W.-Q., Wang, C.-L., & Chen, Y.-M. (2009) · International Journal of Cardiology · doi:10.1016/j.ijcard.2008.06.051 · Cited by 185
“In addition, different genotypes and gene–environment interactions may also partially account for the variations in coffee effects on CHD among individuals, populations and studies [46,57].”
BackgroundHabitual Coffee Consumption and Risk of Heart Failure: A Dose-Response Meta-Analysis
Mostofsky, E., Rice, M. S., Levitan, E. B., & Mittleman, M. A. (2012) · Circulation: Heart Failure · doi:10.1161/circheartfailure.112.967299 · Cited by 185
Nebert, D. W., Zhang, G., & Vesell, E. S. (2008) · Drug Metabolism Reviews · doi:10.1080/03602530801952864 · Cited by 181
“…showed a statistically significant (P 0.05) association between CYP1A2 metabolic activity (Nakajima et al., 1999), rate of caffeine metabolism (Chen et al., 2005), or risk of myocardial infarction from drinking coffee (Cornelis et al., 2006) with a particular SNP in or near the CYP1A2 gene.”
BackgroundInfluentialZordoky, B. N. M., & El‐Kadi, A. O. S. (2010) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2009.12.002 · Cited by 179
Association of Coffee Drinking With Mortality by Genetic Variation in Caffeine Metabolism
Loftfield, E., Cornelis, M. C., Caporaso, N. E., Yu, K. F., Sinha, R. R., & Freedman, N. D. (2018) · JAMA Internal Medicine · doi:10.1001/jamainternmed.2018.2425 · Cited by 178
The influence of a CYP1A2 polymorphism on the ergogenic effects of caffeine
Womack, C. J., Saunders, M. J., Bechtel, M. K., Bolton, D. J., Martin, M., Luden, N. D., Dunham, W., & Hancock, M. (2012) · Journal of the International Society of Sports Nutrition · doi:10.1186/1550-2783-9-7 · Cited by 178
“This polymorphism has clinical importance, as caffeine increases risk for cardiovascular disease in individuals who possess the C variant, but not in individuals homozygous for the A variant [11,12], presumably due to a slower caffeine clearance in the former group.”
BackgroundResultInfluentialSport Nutrigenomics: Personalized Nutrition for Athletic Performance
Guest, N. S., Horne, J. R., Vanderhout, S. M., & El‐Sohemy, A. (2019) · Frontiers in Nutrition · doi:10.3389/fnut.2019.00008 · Cited by 199
“Individuals who are considered slow metabolizers, that is with the AC or CC genotype, have an elevated risk of myocardial infarction (56), hypertension and elevated blood pressure (57, 58), and pre-diabetes (59), with increasing caffeinated coffee consumption, whereas those with the AA genotype (fast metabolizers) do…”
BackgroundRamos-López, O., Milagro, F. I., Allayee, H., Chmurzyńska, A., Choi, M. S., Curi, R., Caterina, R. D., Ferguson, L. R., Goñi, L., Kang, J. X., et al. (2017) · Lifestyle Genomics · doi:10.1159/000477729 · Cited by 172
Acute and long-term cardiovascular effects of coffee: Implications for coronary heart disease
Riksen, N. P., Rongen, G. A. P. J. M., & Smits, P. (2008) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2008.10.006 · Cited by 166
“, who showed in a case-control study that coffee consumption was only associated with an increased risk of acute myocardial infarction in patients with the cytochrome P450 (CYP) 1A2 genotype which predicts slow hepatic metabolism of caffeine, suggesting that caffeine plays a role in this association (Cornelis et al.,…”
BackgroundZhang, Z., Hu, G., Caballero, B., Appel, L., & Chen, L. (2011) · The American Journal of Clinical Nutrition · doi:10.3945/ajcn.110.004044 · Cited by 166
“Because the Australia study used residuals of BP in their regression models (16) and the Amsterdam Growth and Health Longitudinal Study in the Netherlands used mean arterial BP [arterial BP = (2 · DBP + SBP)/3] in the analyses (14), we conducted a meta-analysis for a pooled estimation.”
BackgroundCoffee consumption and risk of type 2 diabetes, cardiovascular diseases, and cancer
van Dam, R. M. (2008) · Applied Physiology, Nutrition, and Metabolism · doi:10.1139/h08-120 · Cited by 161
“caffeine-metabolizing cytochrome P450 1A2 (CYP1A2) enzyme (Cornelis et al. 2006).”
Disclosure of genetic information and change in dietary intake: a randomized controlled trial
Nielsen, D. E., & El-Sohemy, A. (2014) · PLoS ONE · doi:10.1371/journal.pone.0112665 · Cited by 157
“Dietary Reports and Recommendations Subjects in the intervention group were genotyped for variants that affect caffeine metabolism (CYP1A2) [18,19], vitamin C utilization (GSTT1 and GSTM1) [17], sweet taste perception (TAS1R2) [20], and sodium-sensitivity (ACE) [21,22] (Table 1).”
MethodPharmacogenetics of Drug Metabolism
Flockhart, D. A., & Desta, Z. (2009) · Elsevier eBooks · doi:10.1016/b978-0-12-373639-0.00021-2 · Cited by 151
Coffee consumption and risk of coronary heart disease: a meta‐analysis
Sofi, F., Conti, A. A., Gori, A. M., Eliana Luisi, M. L., Casini, A., Abbate, R., & Gensini, G. F. (2007) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2006.07.013 · Cited by 148
“Interestingly, it has been reported recently that a genetic variant in the cytochrome P450 1A2 gene, which accounts for approximately 95% of caffeine metabolism, plays an important role in the association between coffee consumption and the occurrence of myocardial infarction [74].”
BackgroundThorn, C. F., Aklillu, E., Klein, T. E., & Altman, R. B. (2011) · Pharmacogenetics and Genomics · doi:10.1097/fpc.0b013e32834c6efd · Cited by 141
“There was some confusion because of incorrect use of nomenclature in this paper, which was later clarified in a letter stating that the AA genotype was considered ‘fast’ caffeine metabolizer and the C allele ‘slow’ [24,32]; however, this is still an oversimplification because, as mentioned above, the fast metabolizer…”
BackgroundkConFab Investigators, Amin, N., Byrne, E. M., Johnson, J., Chenevix‐Trench, G., Walter, S., Nolte, I. M., Vink, J. M., Rawal, R., Mangino, M., et al. (2011) · Molecular Psychiatry · doi:10.1038/mp.2011.101 · Cited by 139
Nutrigenomics in Cardiovascular Medicine
Corella, D., & Ordovas, J. M. (2009) · Circulation: Cardiovascular Genetics · doi:10.1161/circgenetics.109.891366 · Cited by 138
Predicting adverse side effects of drugs
Huang, L., Wu, X., & Chen, J. Y. (2011) · BMC Genomics · doi:10.1186/1471-2164-12-s5-s11 · Cited by 136
“Additional experimentally-based genotype-phenotype information, e.g., those derived from genome-wide association studies, may also be useful, as several recent studies of genetic polymorphisms of cardiotoxicity-inducing enzymes have already showed [37,38].”
BackgroundThorn, C. F., Aklillu, E., McDonagh, E. M., Klein, T. E., & Altman, R. B. (2012) · Pharmacogenetics and Genomics · doi:10.1097/fpc.0b013e3283505d5e · Cited by 124
Ferguson, J. F., Allayee, H., Gerszten, R. E., Ideraabdullah, F., Kris‐Etherton, P. M., Ordovás, J. M., Rimm, E. B., Wang, T. J., & Bennett, B. J. (2016) · Circulation Cardiovascular Genetics · doi:10.1161/hcg.0000000000000030 · Cited by 128
Zhou, A., & Hyppönen, E. (2018) · American Journal of Clinical Nutrition · doi:10.1093/ajcn/nqy297 · Cited by 125
“Although it could be argued that the consistency between earlier studies is a testament to the robustness of the CYP1A2-by-coffee interaction (12, 14), it is perhaps more likely that the perceived consistency may merely reflect publication bias toward positive results, which is a well-established phenomenon in studies…”
BackgroundResultInfluentialMalerba, S., Turati, F., Galeone, C., Pelucchi, C., Verga, F., La Vecchia, C., & Tavani, A. (2013) · European Journal of Epidemiology · doi:10.1007/s10654-013-9834-7 · Cited by 119
“and the fact that studies included in these meta-analyses did not consider genetic variants associated with coffee drinking, such as CYP1A2, which is responsible for more than 95 % of caffeine metabolism, and consequently of the effects of caffeine and coffee consumption [80].”
BackgroundCoffee, ADORA2A, and CYP1A2: the caffeine connection in Parkinson’s disease
Popat, R. A., Eeden, S. K. V. D., Tanner, C. M., Kamel, F., Umbach, D. M., Marder, K. S., Mayeux, R. P., Ritz, B. R., Ross, G. W., Petrovitch, H., et al. (2011) · European Journal of Neurology · doi:10.1111/j.1468-1331.2011.03353.x · Cited by 119
“For the most frequently studied intronic variant, rs762551, we expected the risk of PD to be lower among slow metabolizers (AC or CC) compared to fast metabolizers (AA) as the former would have higher caffeine levels [24,25,27] resulting in greater neuroprotection.”
BackgroundDoes caffeine alter muscle carbohydrate and fat metabolism during exercise?
Graham, T. E., Battram, D. S., Dela, F., El‐Sohemy, A., & Thong, F. S. L. (2008) · Applied Physiology, Nutrition, and Metabolism · doi:10.1139/h08-129 · Cited by 112
Coffee, caffeine, and coronary heart disease
Cornelis, M. C., & El‐Sohemy, A. (2007) · Current Opinion in Clinical Nutrition & Metabolic Care · doi:10.1097/mco.0b013e3282f05d81 · Cited by 113
Biological roles of cytochrome P450 1A1, 1A2, and 1B1 enzymes
Kwon, Y., Shin, S., & Chun, Y. (2021) · Archives of Pharmacal Research · doi:10.1007/s12272-021-01306-w · Cited by 112
Acute Effects of Coffee on Endothelial Function in Healthy Subjects
Buscemi, S., Verga, S., Batsis, J. A., Donatelli, M., Tranchina, M. R., Belmonte, S., Mattina, A., Re, A., & Cerasola, G. (2010) · European Journal of Clinical Nutrition · doi:10.1038/ejcn.2010.9 · Cited by 110
“An interesting potential hypothesis is that the effects that we observed on FMD and blood pressure may be even more relevant in subjects who are genetically ‘slow caffeine metabolizers,’ as recently defined by Cornelis et al. (2006).”
BackgroundMilenković, D., Morand, C., Cassidy, A., Konić‐Ristić, A., Tomás-Barberán, F. A., Ordovás, J. M., Kroon, P. A., Caterina, R. D., & Rodriguez‐Mateos, A. (2017) · Advances in Nutrition · doi:10.3945/an.116.013623 · Cited by 113
“In relation to myocardial infarction, in a case-control study coffee intake was only associated with an increased risk of nonfatal myocardial infarction among participants with slow-caffeine metabolism (*1F variant) (19).”
BackgroundCoffee, caffeine, and coronary heart disease
Cornelis, M. C., & El‐Sohemy, A. (2007) · Current Opinion in Lipidology · doi:10.1097/mol.0b013e3280127b04 · Cited by 110
Bidel, S., Hu, G., Qiao, Q., Jousilahti, P., Antikainen, R., & Tuomilehto, J. (2006) · Diabetologia · doi:10.1007/s00125-006-0435-9 · Cited by 107
“Some other, mostly case–control, studies found a positive association [16, 17].”
BackgroundSplenic Switch-off: A Tool to Assess Stress Adequacy in Adenosine Perfusion Cardiac MR Imaging
Manisty, C., Ripley, D. P., Herrey, A. S., Captur, G., Wong, T. C., Petersen, S. E., Plein, S., Peebles, C., Schelbert, E. B., Greenwood, J. P., et al. (2015) · Radiology · doi:10.1148/radiol.2015142059 · Cited by 107
Coffee for Cardioprotection and Longevity
O’Keefe, J. H., DiNicolantonio, J. J., & Lavie, C. J. (2018) · Progress in Cardiovascular Diseases · doi:10.1016/j.pcad.2018.02.002 · Cited by 106
Low, but not high, dose caffeine is a readily available probe for adenosine actions
Fredholm, B. B., Yang, J., & Wang, Y.-Q. (2016) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2016.11.011 · Cited by 99
The Crystal Structure of Anhydrous β‐Caffeine as Determined from X‐ray Powder‐Diffraction Data
Lehmann, C. W., & Stowasser, F. (2007) · Chemistry - A European Journal · doi:10.1002/chem.200600973 · Cited by 100
A scheme for a flexible classification of dietary and health biomarkers
Gao, Q., Praticò, G., Scalbert, A., Vergères, G., Kolehmainen, M., Manach, C., Brennan, L., Afman, L. A., Wishart, D. S., Andrés‐Lacueva, C., et al. (2017) · Genes & Nutrition · doi:10.1186/s12263-017-0587-x · Cited by 103
“Both polymorphisms represent (static) host factors but the latter may also be a risk modulator related to myocardial infarction [80].”
BackgroundGrosso, G., Micek, A., Godos, J., Pająk, A., Sciacca, S., Bes‐Rastrollo, M., Galvano, F., & Martínez‐González, M. Á. (2017) · Nutrients · doi:10.3390/nu9080890 · Cited by 102
“Carriers of the CYP1A2*1F allele have been demonstrated to be at higher risk of nonfatal myocardial infarction following intake of caffeinated coffee [31].”
BackgroundRodríguez‐Artalejo, F., & López‐García, E. (2017) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.7b04506 · Cited by 99
Josse, A. R., Costa, L. A. D., Campos, H., & El‐Sohemy, A. (2012) · American Journal of Clinical Nutrition · doi:10.3945/ajcn.112.038794 · Cited by 101
“Although no association with caffeine consumption was observed for rs762551 of CYP1A2 (17), where carriers of the C allele were considered slow caffeine metabolizers (24), according to the findings in the current study, an increased intake of caffeine was associated with having a T allele for CYP1A1-CYP1A2-rs2472297,…”
BackgroundMethodResultA randomized trial of genetic information for personalized nutrition
Nielsen, D. E., & El‐Sohemy, A. (2012) · Genes & Nutrition · doi:10.1007/s12263-012-0290-x · Cited by 96
Consumption of cocoa, tea and coffee and risk of cardiovascular disease
Castelnuovo, A. F. D., di Giuseppe, R., Iacoviello, L., & de Gaetano, G. (2011) · European Journal of Internal Medicine · doi:10.1016/j.ejim.2011.07.014 · Cited by 95
“Coffee Albeit coffee represents, along with tea, the most worldwide consumed beverage, its potential effect on cardiovascular disease is still controversial (Table 2) [42–53].”
BackgroundCoffee consumption attenuates short-term fructose-induced liver insulin resistance in healthy men
Lecoultre, V., Carrel, G., Egli, L., Binnert, C., Boss, A., MacMillan, E. L., Kreis, R., Boesch, C., Darimont, C., & Tappy, L. (2013) · American Journal of Clinical Nutrition · doi:10.3945/ajcn.113.069526 · Cited by 95
“This issue may be even more complex because there may be genetically determined interindividual variations regarding the health effects of coffee (51).”
BackgroundRole of coffee in modulation of diabetes risk
Natella, F., & Scaccini, C. (2012) · Nutrition Reviews · doi:10.1111/j.1753-4887.2012.00470.x · Cited by 94
Multi-ingredient, Caffeine-containing Dietary Supplements: History, Safety, and Efficacy
Gurley, B. J., Steelman, S. C., & Thomas, S. L. (2014) · Clinical Therapeutics · doi:10.1016/j.clinthera.2014.08.012 · Cited by 96
Horne, J. R., Madill, J., O’Connor, C. P., Shelley, J., & Gilliland, J. (2018) · Lifestyle Genomics · doi:10.1159/000488086 · Cited by 94
Xie, C., Cui, L., Zhu, J., Wang, K., Sun, N., & Sun, C. (2018) · Journal of Human Hypertension · doi:10.1038/s41371-017-0007-0 · Cited by 95
Cardiovascular effects of caffeinated beverages
Voskoboinik, A., Koh, Y., & Kistler, P. M. (2018) · Trends in Cardiovascular Medicine · doi:10.1016/j.tcm.2018.09.019 · Cited by 92
The pharmacogenetics of natural products: A pharmacokinetic and pharmacodynamic perspective
Rao, T., Tan, Z., Peng, J., Guo, Y., Chen, Y., Zhou, H., & Ouyang, D. (2019) · Pharmacological Research · doi:10.1016/j.phrs.2019.104283 · Cited by 94
Coffee and Arterial Hypertension
Surma, S., & Oparil, S. (2021) · Current Hypertension Reports · doi:10.1007/s11906-021-01156-3 · Cited by 92
Coffee intake and incidence of hypertension
Uiterwaal, C. S., Verschuren, W. M., Bueno-de-Mesquita, H. B., Ocké, M., Geleijnse, J. M., Boshuizen, H. C., Peeters, P. H., Feskens, E. J., & Grobbee, D. E. (2007) · The American Journal of Clinical Nutrition · doi:10.1093/ajcn/85.3.718 · Cited by 91
“Finally, there is recent evidence to suggest that genetically determined slow caffeine metabolism in relation to cardiovascular disease risk is present only in relatively younger persons (29).”
BackgroundTea Consumption and All-Cause and Cause-Specific Mortality in the UK Biobank
Inoue‐Choi, M., Ramirez, Y., Cornelis, M. C., de González, A. B., Freedman, N. D., & Loftfield, E. (2022) · Annals of Internal Medicine · doi:10.7326/m22-0041 · Cited by 90
“Tea also contains caffeine, and concerns have been raised about high caffeine intake, particularly among persons genetically predisposed to impaired caffeine metabolism (13 – 15).”
BackgroundThe Cardiovascular Effects of Methylxanthines
Riksen, N. P., Smits, P., & Rongen, G. A. P. J. M. (2010) · Handbook of experimental pharmacology · doi:10.1007/978-3-642-13443-2_16 · Cited by 89
Doepker, C., Lieberman, H. R., Smith, A. P., Peck, J. D., El-Sohemy, A., & Welsh, B. T. (2016) · Annual Review of Food Science and Technology · doi:10.1146/annurev-food-041715-033243 · Cited by 87
“The protective effect of moderate intakes of coffee on CVD is evidenced by an inverse or U- or J-shaped association (Andersen et al. 2006, Azevedo & Barros 2006, de Koning Gans et al. 2010, Happonen et al. 2004, Kleemola et al. 2000, Panagiotakos et al. 2003, Woodward & Tunstall-Pedoe 1999).”
BackgroundInfluentialKotsopoulos, J., Ghadirian, P., El‐Sohemy, A., Lynch, H. T., Snyder, C., Daly, M. B., Domchek, S. M., Randall, S., Karlan, B. Y., Zhang, P., et al. (2007) · Cancer Epidemiology Biomarkers & Prevention · doi:10.1158/1055-9965.epi-06-1074 · Cited by 87
“reported an increased risk of myocardial infarction with increasing coffee consumption among carriers of the variant C allele of the CYP1A2 gene (8).”
BackgroundThe Influence of Caffeine Expectancies on Sport, Exercise, and Cognitive Performance
Shabir, A., Hooton, A., Tallis, J. A., & Higgins, M. F. (2018) · Nutrients · doi:10.3390/nu10101528 · Cited by 92
Coffee Consumption and Incident Tachyarrhythmias
Kim, E., Hoffmann, T. J., Nah, G., Vittinghoff, E., Delling, F. N., & Marcus, G. M. (2021) · JAMA Internal Medicine · doi:10.1001/jamainternmed.2021.3616 · Cited by 81
Fabozzi, G., Verdone, G., Allori, M., Cimadomo, D., Tatone, C., Stuppia, L., Franzago, M., Ubaldi, N., Vaiarelli, A., Ubaldi, F. M., et al. (2022) · Nutrients · doi:10.3390/nu14091918 · Cited by 101
“Numerous studies showed that different individuals have different degradation capacities and that the risk associated with caffeine consumption, for example, myocardial infarction, varies according to the enzymatic capacity dictated by the genetic profile [265].”
BackgroundFunctional foods for dyslipidaemia and cardiovascular risk prevention
Sirtori, C. R., Galli, C., Anderson, J. W., Sirtori, E., & Arnoldi, A. (2009) · Nutrition Research Reviews · doi:10.1017/s0954422409990187 · Cited by 79
“Cornelis and El-Sohemy tried to unravel the complex genetic factors favouring CHD or protecting from it((212,213)).”
BackgroundAcute consumption of a caffeinated energy drink enhances aspects of performance in sprint swimmers
Lara, B., Ruiz-Vicente, D., Areces, F., Abián‐Vicén, J., Salinero, J. J., Gonzalez-Millán, C., Gallo–Salazar, C., & Coso, J. D. (2015) · British Journal Of Nutrition · doi:10.1017/s0007114515002573 · Cited by 82
The Health Effect of Psychostimulants: A Literature Review
Favrod-Coune, T., & Broers, B. (2010) · Pharmaceuticals · doi:10.3390/ph3072333 · Cited by 84
“Defect of this enzyme is associated with prolonged caffeine half-life [15].”
BackgroundCoffee Consumption and Cardiovascular Health: Getting to the Heart of the Matter
Rebello, S. A., & van Dam, R. M. (2013) · Current Cardiology Reports · doi:10.1007/s11886-013-0403-1 · Cited by 78
“Results from a few studies have suggested that coffee consumption may be associated with risk of hypertension [71] and myocardial infarct (MI) [70] in slow-metabolizers but not in fast metabolizers, but confirmation of these findings in other studies is needed.”
Clinical cardioprotection and the value of conditioning responses
Peart, J. N., & Headrick, J. P. (2009) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00162.2009 · Cited by 77
Braam, W., Keijzer, H., Struijker-Boudier, H. A. J., Didden, R., Smits, M. G., & Curfs, L. (2012) · Journal of Intellectual Disability Research · doi:10.1111/j.1365-2788.2012.01595.x · Cited by 75
Yamagata, K. (2018) · Antioxidants · doi:10.3390/antiox7020026 · Cited by 78
“Third, none of the studies took into account genetic factors, which have been reported to affect the relationship between coffee and cardiovascular outcomes due to polymorphisms related to caffeine metabolization [49,50].”
BackgroundMinimal Effect of Acute Caffeine Ingestion on Intense Resistance Training Performance
Astorino, T. A., Martin, B. J., Schachtsiek, L., Wong, K., & Ng, K. (2011) · The Journal of Strength and Conditioning Research · doi:10.1519/jsc.0b013e3181ddf6db · Cited by 69
“(7) demonstrated that a small substitution in the gene regulating caffeine metabolism impairs this process, leading to slowed metabolism, whereas persons homozygous for this allele are rapid caffeine metabolizers.”
BackgroundCaffeine Prevents Protection in Two Human Models of Ischemic Preconditioning
Riksen, N. P., Zhou, Z., Oyen, W. J. G., Jaspers, R. M. A., Ramakers, B. P., Brouwer, R. M. H. J., Boerman, O. C., Steinmetz, N. D., Smits, P., & Rongen, G. A. P. J. M. (2006) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2006.04.083 · Cited by 71
Basrai, M., Schweinlin, A., Menzel, J., Mielke, H., Weikert, C., Dusemund, B., Putze, K., Watzl, B., Lampen, A., & Bischoff, S. C. (2019) · The Journal of Nutrition · doi:10.1093/jn/nxy303 · Cited by 71
“Previous studies noted that carriers of a slow CYP1A2∗1F allele have a higher risk for myocardial infarction and hypertension because of impaired caffeine metabolism (43, 44).”
Background
Metadata
- Authors
- Cornelis, M. C., El-Sohemy, A., Kabagambe, E. K., & Campos, H.
- Affiliations
- University of Toronto (CA)
- Harvard University (US)
- Venue
- JAMA
- Publisher
- American Medical Association (AMA)
- Published
- 2006-03-08
- Volume
- 295
- Issue
- 10
- Pages
- 1135
- ISSN
- 0002-9955 (ISSN-L)
- 0098-7484
- OpenAlex
- W1972508135
- Cited by
- 490
- References
- 52
- Citations by year
- 2026: 22 · 2025: 26 · 2024: 26 · 2023: 21 · 2022: 20 · 2021: 21 · 2020: 24 · 2019: 24 · 2018: 30 · 2017: 30 · 2016: 21 · 2015: 22 · 2014: 28 · 2013: 22 · 2012: 24
- FWCI
- 16.50
- Type
- journal article
- Language
- en
- Open access
- green
- jamanetwork.com
- Licence
- other-oa
- Locations
- JAMA (publishedVersion)
- PubMed (publishedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
- Investigative News in Education (Universidad de Costa Rica) (submittedVersion)
- Funders
- Harvard University
- Universidad de Costa Rica
- National Heart, Lung, and Blood Institute (HL 60692, HL 071888, R01HL071888, R01HL060692)
- Topics
- Health Sciences › Medicine › Pharmacology (medical) › Coffee research and impacts
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Pharmacogenetics and Drug Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- coffee consumption, myocardial infarction, caffeine metabolism, gene-environment interaction, cardiovascular risk, Costa Rica, young adults, hormone replacement therapy
- MeSH terms
- Aged, Catchment Area, Health, Coffee, Costa Rica, Female, Genotype, Humans, Male, Middle Aged, Myocardial Infarction, Polymorphism, Restriction Fragment Length, Risk Factors, Logistic Models, Polymerase Chain Reaction, Cytochrome P-450 CYP1A2, Amino Acid Substitution
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