Genome-Wide Meta-Analysis Identifies Regions on 7p21 (AHR) and 15q24 (CYP1A2) As Determinants of Habitual Caffeine Consumption

Cornelis, Marilyn C.; Monda, Keri L.; Yu, Kai; Paynter, Nina P.; Azzato, Elizabeth M.; Bennett, Siiri N.; Berndt, Sonja I.; Boerwinkle, Eric; Chanock, Stephen J.; Chatterjee, Nilanjan; Couper, David J.; Curhan, Gary C.; Heiss, Gerardo; Hu, Frank B.; Hunter, David J.; Jacobs, Kevin B.; Jensen, Majken K.; Kraft, Peter; Landi, Maria Teresa; Nettleton, Jennifer A.; Purdue, Mark P.; Rajaraman, Preetha; Rimm, Eric B.; Rose, Lynda M.; Rothman, Nathaniel; Silverman, Debra T.; Stolzenberg-Solomon, Rachael; Subar, Amy F.; Yeager, Meredith; Chasman, Daniel I.; Dam, Rob M. van; Caporaso, Neil E.

doi:10.1371/journal.pgen.1002033

Cited by 198 publications

(221 citation statements)

References 35 publications

(45 reference statements)

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“…It is not clear if either alcohol or caffeine is indeed responsible for the protective feature or if there is a genetic setup that makes individuals be alcohol or coffee lowers and at the same time protects them form diabetes. Very recently, Cornelis et al (60) reported the a genome-wide association study of habitual caffeine intake on large number (>47,000) individuals within the United States. They found two loci: 7p21 (P=2.4x10 -19 ), near AHR, and 15q24 (P=5.2x10 -14 ), between CYP1A1 and CYP1A2 associated with high daily caffeine intake.…”

Section: Risk Of Diabetes and Life Stylementioning

confidence: 99%

Can inactivators of plasminogen activator inhibitor alleviate the burden of obesity and diabetes? (Review)

Jankun

Al-Senaidy²,

Skrzypczak‐Jankun³

2011

Int J Mol Med

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Section: Risk Of Diabetes and Life Stylementioning

confidence: 99%

Can inactivators of plasminogen activator inhibitor alleviate the burden of obesity and diabetes? (Review)

Jankun

Al-Senaidy²,

Skrzypczak‐Jankun³

2011

Int J Mol Med

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“…Genome-wide association studies have identified several genetic loci associated with caffeine/coffee consumption (26)(27)(28)(29). We extracted results for these SNPs from our genomewide G-E interaction analysis to better illustrate their potential functions.…”

Section: Resultsmentioning

confidence: 99%

A genome-wide analysis of gene–caffeine consumption interaction on basal cell carcinoma

Cornelis

Liang

et al. 2016

CARCIN

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Animal models have suggested that oral or topical administration of caffeine could inhibit ultraviolet-induced carcinogenesis via the ataxia telangiectasia and rad3 (ATR)-related apoptosis. Previous epidemiological studies have demonstrated that increased caffeine consumption is associated with reduced risk of basal cell carcinoma (BCC). To identify common genetic markers that may modify this association, we tested gene-caffeine intake interaction on BCC risk in a genome-wide analysis. We included 3383 BCC cases and 8528 controls of European ancestry from the Nurses' Health Study and Health Professionals Follow-up Study. Single nucleotide polymorphism (SNP) rs142310826 near the NEIL3 gene showed a genome-wide significant interaction with caffeine consumption (P = 1.78 × 10 -8 for interaction) on BCC risk. There was no gender difference for this interaction (P = 0.64 for heterogeneity). NEIL3, a gene belonging to the base excision DNA repair pathway, encodes a DNA glycosylase that recognizes and removes lesions produced by oxidative stress. In addition, we identified several loci with P value for interaction <5 × 10 -7 in gender-specific analyses (P for heterogeneity between genders < 0.001) including those mapping to the genes LRRTM4, ATF3 and DCLRE1C in women and POTEA in men. Finally, we tested the associations between caffeine consumption-related SNPs reported by previous genome-wide association studies and risk of BCC, both individually and jointly, but found no significant association. In sum, we identified a DNA repair gene that could be involved in caffeine-mediated skin tumor inhibition. Further studies are warranted to confirm these findings.

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“…Some previous studies have examined the relationship between caffeine metabolism and genetics [83][84][85][86][87][88][89][90]. Most of them examined the relationship between coffee consumption and gene polymorphism of the caffeine receptor (A2A) or liver enzymes (cytochrome P450).…”

Section: Discussionmentioning

confidence: 99%

The effect of caffeine on energy balance

Harpaz

Tamir

Weinstein

et al. 2016

Journal of Basic and Clinical Physiology and Pharmacology

120

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Abstract:The global prevalence of obesity has increased considerably in the last two decades. Obesity is caused by an imbalance between energy intake (EI) and energy expenditure (EE), and thus negative energy balance is required to bring about weight loss, which can be achieved by either decreasing EI or increasing EE. Caffeine has been found to influence the energy balance by increasing EE and decreasing EI, therefore, it can potentially be useful as a body weight regulator. Caffeine improves weight maintenance through thermogenesis, fat oxidation, and EI. The sympathetic nervous system is involved in the regulation of energy balance and lipolysis (breakdown of lipids to glycerol and free fatty acids) and the sympathetic innervation of white adipose tissue may play an important role in the regulation of total body fat. This article reviews the current knowledge on the thermogenic properties of caffeine, and its effects on appetite and EI in relation to energy balance and body weight regulation.

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Genome-Wide Meta-Analysis Identifies Regions on 7p21 (AHR) and 15q24 (CYP1A2) As Determinants of Habitual Caffeine Consumption

Cited by 198 publications

References 35 publications

Can inactivators of plasminogen activator inhibitor alleviate the burden of obesity and diabetes? (Review)

Can inactivators of plasminogen activator inhibitor alleviate the burden of obesity and diabetes? (Review)

A genome-wide analysis of gene–caffeine consumption interaction on basal cell carcinoma

The effect of caffeine on energy balance

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