scholarly journals Cigarette smoking increases coffee consumption: findings from a Mendelian randomisation analysis

2017 ◽  
Author(s):  
Johan H Bjørngaard ◽  
Ask Tybjærg Nordestgaard ◽  
Amy E Taylor ◽  
Jorien L Treur ◽  
Maiken E. Gabrielsen ◽  
...  
Keyword(s):  
Causal Effect ◽  
Coffee Consumption ◽  
Cigarette Consumption ◽  
Mendelian Randomisation ◽  
Caffeine Intake ◽  
Tea Consumption ◽  
Coffee Intake ◽  
General Population Study ◽  
Weak Evidence ◽  
The Uk

AbstractBackgroundSmokers tend to consume more coffee than non-smokers and there is evidence for a positive relationship between cigarette and coffee consumption in smokers. Cigarette smoke increases the metabolism of caffeine, so this association may represent a causal effect of smoking on caffeine intake.MethodsWe performed a Mendelian randomisation analysis in 114,029 individuals from the UK Biobank, 56,664 from the Norwegian HUNT study and 78,650 from the Copenhagen General Population Study. We used a genetic variant in the CHRNA5 nicotinic receptor (rs16969968) as a proxy for smoking heaviness. Coffee and tea consumption were self-reported. Analyses were conducted using linear regression and meta-analysed across studies.ResultsEach additional cigarette per day consumed by current smokers was associated with higher coffee consumption (0.10 cups per day, 95% CI:0.03,0.17). There was weak evidence for an increase in tea consumption per additional cigarette smoked per day (0.04 cups per day, 95% CI:-0.002,0.07). There was strong evidence that each additional copy of the minor allele of rs16969968 (which increases daily cigarette consumption) in current smokers was associated with higher coffee consumption (0.15 cups per day, 95% CI:0.11,0.20), but only weak evidence for an association with tea consumption (0.04 cups per day, 95% CI:- 0.01,0.09). There was no clear evidence that rs16969968 was associated with coffee or tea consumption in never or former smokers.ConclusionThese findings suggest that higher cigarette consumption causally increases coffee intake. This is consistent with faster metabolism of caffeine by smokers, but may also reflect behavioural links between smoking and coffee.

scholarly journals Evidence for causal effects of lifetime smoking on risk for depression and schizophrenia: a Mendelian randomisation study

2019 ◽  
Vol 50 (14) ◽  
pp. 2435-2443 ◽  
Author(s):  
Robyn E. Wootton ◽  
Rebecca C. Richmond ◽  
Bobby G. Stuijfzand ◽  
Rebecca B. Lawn ◽  
Hannah M. Sallis ◽  
...  
Keyword(s):  
Causal Effect ◽  
Association Studies ◽  
Smoking Initiation ◽  
Smoking Behaviour ◽  
Positive Control ◽  
Mendelian Randomisation ◽  
Genome Wide Association Studies ◽  
Weak Evidence ◽  
Smoking Duration ◽  
The Uk

AbstractBackgroundSmoking prevalence is higher amongst individuals with schizophrenia and depression compared with the general population. Mendelian randomisation (MR) can examine whether this association is causal using genetic variants identified in genome-wide association studies (GWAS).MethodsWe conducted two-sample MR to explore the bi-directional effects of smoking on schizophrenia and depression. For smoking behaviour, we used (1) smoking initiation GWAS from the GSCAN consortium and (2) we conducted our own GWAS of lifetime smoking behaviour (which captures smoking duration, heaviness and cessation) in a sample of 462690 individuals from the UK Biobank. We validated this instrument using positive control outcomes (e.g. lung cancer). For schizophrenia and depression we used GWAS from the PGC consortium.ResultsThere was strong evidence to suggest smoking is a risk factor for both schizophrenia (odds ratio (OR) 2.27, 95% confidence interval (CI) 1.67–3.08, p < 0.001) and depression (OR 1.99, 95% CI 1.71–2.32, p < 0.001). Results were consistent across both lifetime smoking and smoking initiation. We found some evidence that genetic liability to depression increases smoking (β = 0.091, 95% CI 0.027–0.155, p = 0.005) but evidence was mixed for schizophrenia (β = 0.022, 95% CI 0.005–0.038, p = 0.009) with very weak evidence for an effect on smoking initiation.ConclusionsThese findings suggest that the association between smoking, schizophrenia and depression is due, at least in part, to a causal effect of smoking, providing further evidence for the detrimental consequences of smoking on mental health.

scholarly journals Caffeinated Coffee and Tea Consumption, Genetic Variation and Cognitive Function in the UK Biobank

2020 ◽  
Vol 150 (8) ◽  
pp. 2164-2174
Author(s):  
Marilyn C Cornelis ◽  
Sandra Weintraub ◽  
Martha Clare Morris
Keyword(s):  
Genetic Variation ◽  
Cognitive Function ◽  
Poor Performance ◽  
Sociodemographic Factors ◽  
Caffeine Intake ◽  
Tea Consumption ◽  
Uk Biobank ◽  
Trail Making ◽  
Caffeine Metabolism ◽  
The Uk

ABSTRACT Background Coffee and tea are the major contributors of caffeine in the diet. Evidence points to the premise that caffeine may benefit cognition. Objective We examined the associations of habitual regular coffee or tea and caffeine intake with cognitive function whilst additionally accounting for genetic variation in caffeine metabolism. Methods We included white participants aged 37–73 y from the UK Biobank who provided biological samples and completed touchscreen questionnaires regarding sociodemographic factors, medical history, lifestyle, and diet. Habitual caffeine-containing coffee and tea intake was self-reported in cups/day and used to estimate caffeine intake. Between 97,369 and 445,786 participants with data also completed ≥1 of 7 self-administered cognitive functioning tests using a touchscreen system (2006–2010) or on home computers (2014). Multivariable regressions were used to examine the association between coffee, tea, or caffeine intake and cognition test scores. We also tested interactions between coffee, tea, or caffeine intake and a genetic-based caffeine-metabolism score (CMS) on cognitive function. Results After multivariable adjustment, reaction time, Pairs Matching, Trail Making test B, and symbol digit substitution, performance significantly decreased with consumption of 1 or more cups of coffee (all tests P-trend &lt; 0.0001). Tea consumption was associated with poor performance on all tests (P-trend &lt; 0.0001). No statistically significant CMS × tea, CMS × coffee, or CMS × caffeine interactions were observed. Conclusions Our findings, based on the participants of the UK Biobank, provide little support for habitual consumption of regular coffee or tea and caffeine in improving cognitive function. On the contrary, we observed decrements in performance with intakes of these beverages which may be a result of confounding. Whether habitual caffeine intake affects cognitive function therefore remains to be tested.

Abstract 021: C-reactive Protein Partially Mediates The Inverse Association Between Coffee Consumption And Risk Of Type 2 Diabetes: Findings From The UK Biobank And The Rotterdam Studies

Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Carolina Ochoa-Rosales ◽  
Niels van der Schaft ◽  
Kim V Braun ◽  
Frederick Ho ◽  
Fanny Petermann ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Coffee Consumption ◽  
Inverse Association ◽  
Statistical Regression ◽  
Uk Biobank ◽  
C Reactive Protein ◽  
Coffee Intake ◽  
Reactive Protein ◽  
The Uk

Background: Coffee intake has been linked to lower type 2 diabetes (T2D) risk. We hypothesized this may be mediated by coffee’s effects on inflammation. Methods: Using participants from the UK Biobank (UKB n=145370) and Rotterdam Study (RS n=7172) cohorts, we studied associations of coffee intake with incident T2D; longitudinally measured insulin resistance (HOMA IR); serum levels of inflammation markers; and the mediating role of inflammation. Statistical regression models were adjusted for sociodemographic, lifestyle and health factors. Results: The median follow up was 7 (UKB) and 9 (RS) years. An increase of one coffee cup/day was associated with 4-6% lower T2D risk (RS HR=0.94 [95% CI 0.90; 0.98]; UKB HR=0.96 [0.94; 0.98]); lower HOMA IR (RS β=-0.017 [-0.024; -0.010]); with lower C reactive protein (CRP) and higher adiponectin (Figure1). Consumers of filtered coffee had the lowest T2D risk (UKB HR=0.88 [0.83; 0.93]). CRP levels mediated 9.6% (UKB) and 3.4% (RS) of the total effect of coffee on T2D (Figure 1). Conclusions: We suggest that coffee’s beneficial effects on lower T2D risk are partially mediated by improvements in systemic inflammation.Figure 1. a CRP and a adiponectin refer to the effect of coffee intake on CRP and adiponectin levels. a CRP RS : β=-0.014 (-0.022; -0.005); UKBB a CRP UKB : β=-0.011 (-0.012; -0.009) and RS a adiponectin : β=0.025 (0.007; 0.042). b CRP and b adiponectin refer to the effect of coffee related levels in CRP and adiponectin on incident T2D, independent of coffee. RS b CRP : HR=1.17 (1.04; 1.31); UKB b CRP : HR=1.45 (1.37; 1.54); and b adiponectin : HR=0.58 (0.32; 0.83). c′ refers to coffee’ effect on T2D going directly or via others mediators. UKB c′ independent of CRP : HR=0.96 (0.94; 0.99); RS c′ independent of CRP : HR=0.94 (0.90; 0.99); and RS c′ independent of CRP+adiponectin : HR=0.90 (0.80; 1.01). Coffee related changes in CRP may partially explain the beneficial link between coffee and T2D, mediating a 3.4% (0.6; 4.8, RS) and 9.6% (5.7; 24.4, UKB). Evidence of mediation was also found for adiponectin.

scholarly journals Polynomial Mendelian Randomization reveals widespread non-linear causal effects in the UK Biobank

2021 ◽  
Author(s):  
Jonathan Sulc ◽  
Jenny Sjaarda ◽  
Zoltan Kutalik
Keyword(s):  
Causal Inference ◽  
Large Scale ◽  
Causal Effect ◽  
Causal Effects ◽  
Mendelian Randomisation ◽  
Uk Biobank ◽  
Individual Level ◽  
Glucose Levels ◽  
Causal Function ◽  
The Uk

Causal inference is a critical step in improving our understanding of biological processes and Mendelian randomisation (MR) has emerged as one of the foremost methods to efficiently interrogate diverse hypotheses using large-scale, observational data from biobanks. Although many extensions have been developed to address the three core assumptions of MR-based causal inference (relevance, exclusion restriction, and exchangeability), most approaches implicitly assume that any putative causal effect is linear. Here we propose PolyMR, an MR-based method which provides a polynomial approximation of an (arbitrary) causal function between an exposure and an outcome. We show that this method provides accurate inference of the shape and magnitude of causal functions with greater accuracy than existing methods. We applied this method to data from the UK Biobank, testing for effects between anthropometric traits and continuous health-related phenotypes and found most of these (84%) to have causal effects which deviate significantly from linear. These deviations ranged from slight attenuation at the extremes of the exposure distribution, to large changes in the magnitude of the effect across the range of the exposure (e.g. a 1 kg/m2 change in BMI having stronger effects on glucose levels if the initial BMI was higher), to non-monotonic causal relationships (e.g. the effects of BMI on cholesterol forming an inverted U shape). Finally, we show that the linearity assumption of the causal effect may lead to the misinterpretation of health risks at the individual level or heterogeneous effect estimates when using cohorts with differing average exposure levels.

scholarly journals 861Mendelian randomization on habitual coffee intake and plasma lipid profile: evidence from UK Biobank

2021 ◽  
Vol 50 (Supplement_1) ◽  
Author(s):  
Ang Zhou ◽  
Elina Hyppönen
Keyword(s):  
Lipid Profile ◽  
Plasma Lipid ◽  
Coffee Consumption ◽  
Plasma Lipid Profile ◽  
Robust Methods ◽  
Uk Biobank ◽  
Cvd Risk ◽  
Coffee Intake ◽  
The Uk

Abstract Background Long-term heavy coffee consumption may adversely affect individuals’ cardiovascular disease (CVD) risk. As hyperlipidemia is a well-established contributor to CVD, we investigated the association between habitual coffee intake and plasma lipid profile. Methods We used data from up to 362,571 UK Biobank participants to examine associations between coffee intake and plasma lipid profiles, including LDL-C, HDL-C, total-C, triglycerides, ApoA1 and ApoB. Inverse variance weighted mendelian randomization (MR) was used to interrogate the causal nature of coffee-lipid associations, complemented by pleiotropy-robust methods, including MR-median, MR-Mode, MR-PRESSO and MR-Egger. Results We observed positive dose-dependent associations between self-reported coffee intake and plasma concentration of LDL-C, ApoB and total-C, with the highest lipid levels seen among participants drinking &gt;6 cups/day (Plinear trend≤1.97E-57 for all). Genetic instrument for coffee intake was robustly associated with self-reported intake in the UK Biobank (F-statistic = 416). One cup increase in genetically instrumented intake was associated with 0.07 mmol/L (95%CI 0.03 to 0.12), 0.02 g/L (95%CI 0.01 to 0.03), and 0.09 mmol/L (95%CI 0.04 to 0.14) increase in LDL-C, ApoB, and total-C, respectively. Pleiotropy-robust methods provided largely consistent results albeit with greater imprecision when using MR-Egger. Conclusions Our phenotypic and genetic analysis consistently suggests that long-term heavy coffee consumption can lead to unfavourable lipid profile, which could potentially increase individuals’ risk for CVD. Individuals with elevated cholesterol may need to reduce their daily coffee intake. Key messages Our study provides evidence that long-term heavy coffee consumption can lead to unfavourable lipid profile.

scholarly journals The Association between Coffee and Caffeine Consumption and Renal Function: Insight from Individual-Level Data, Mendelian Randomization, and Meta-Analysis

2021 ◽  
Author(s):  
Mohsen Mazidi ◽  
Abbas Dehghan ◽  
Dimitri Mikhailidis ◽  
Jacek Jóźwiak ◽  
Adrian Covic ◽  
...  
Keyword(s):  
Renal Function ◽  
Mendelian Randomization ◽  
Meta Analysis ◽  
Coffee Consumption ◽  
Caffeine Intake ◽  
Diabetic Patients ◽  
Caffeine Consumption ◽  
Coffee Intake ◽  
Level Data ◽  
Significant Difference

IntroductionBy applying on two-sample Mendelian randomization and systematic review and meta-analysis we investigated the association between caffeine and coffee intake with prevalent CKD and markers of renal function.Material and methodsFor the individual data analysis we analysed the NHANES data on renal function markers and caffeine intake. MR was implemented by using summary-level data from the largest ever GWAS conducted on coffee intake (N=91,462) and kidney function.ResultsFinally, we included the data of 18,436 participants, 6.9% had prevalent CKD (based on eGFR). Caffeine intake for general population was 131.1±1.1 mg. The percentage of participants with CKD, by caffeine quartile was 16.6% in the first (lowest) quartile, 13.9% in the second, 12.2% in the third and 11.0% in the top quartile (p<0.001). After adjustment, for increasing quartiles for caffeine consumption, mean urine albumin, albumin-creatinine ratio and estimated glomerular filtration rate (GFR) did not change significantly (p>0.234). In fully adjusted logistic regression models, there was no significant difference in chances of CKD prevalence (p-trend=0.745). In the same line, results of MR showed no impact of coffee intake on CKD (IVW=β: -0.0191, SE: 0.069, p=0.781), on eGFR (overall= IVW= β: -0.0005, SE: 0.005, p=0.926) both in diabetic (IVW= β: -0.006, SE: 0.009, p=0.478), and non-diabetic patients (IVW= β: -6.772, SE: 0.006, p=0.991). Results from the meta-analysis indicted that coffee consumption was not significantly associated with CKD (OR: 0.85, 95%CI 0.71-1.02, p=0.090, n=6 studies, I2=0.32).ConclusionsBy implementing on different strategies, we have highlighted no significant association between coffee consumption with renal function and chance of CKD.

Coffee and caffeine intake and risk of ovarian cancer: a systematic review and meta-analysis

2019 ◽  
Vol 29 (3) ◽  
pp. 579-584 ◽  
Author(s):  
Fateme Shafiei ◽  
Asma Salari-Moghaddam ◽  
Alireza Milajerdi ◽  
Bagher Larijani ◽  
Ahmad Esmaillzadeh
Keyword(s):  
Systematic Review ◽  
Ovarian Cancer ◽  
Meta Analysis ◽  
Coffee Consumption ◽  
Effect Sizes ◽  
Caffeine Intake ◽  
Case Control Studies ◽  
Coffee Intake ◽  
Decaffeinated Coffee ◽  
Caffeinated Coffee

BackgroundResults from earlier publications on the association of coffee and caffeine and risk of ovarian cancer are inconsistent.ObjectiveTo evaluate the link between coffee, caffeine, caffeinated coffee, and decaffeinated coffee consumption and risk of ovarian cancer.MethodsWe searched PubMed/Medline, ISI Web of Science, Scopus, and Google Scholar to identify relevant publications up to April 2018. All case–control studies that considered coffee, caffeine, caffeinated coffee, or decaffeinated coffee as the exposure variables and ovarian cancer as the main outcome variable or as one of the outcomes were included in the systematic review. Publications in which odds ratios (ORs) or rate or risk ratios (RRs) and 95% confidence intervals (CIs) were reported, were included in the meta-analysis.ResultsA total of 22 case–control studies were included in the systematic review, and 20 studies in the meta-analysis. Overall, 40 140 participants, including 8568 patients with ovarian cancer, aged ≥ 17 years were included. Combining 21 effect sizes from 18 studies, no significant association was observed between total coffee intake and risk of ovarian cancer (OR=1.09; 95% CI 0.94 to 1.26). There was no significant association between total caffeine intake and ovarian cancer risk (OR=0.89; 95% CI 0.55 to 1.45). In addition, caffeinated coffee intake was not significantly associated with ovarian cancer (OR=1.05; 95% CI 0.87 to 1.28). However, combining effect sizes from five studies, we found an inverse significant association between decaffeinated coffee intake and risk of ovarian cancer (OR=0.72; 95% CI 0.58 to 0.90).ConclusionsOur findings indicated an inverse association between decaffeinated coffee consumption and risk of ovarian cancer. No significant association was found between coffee, caffeine or caffeinated coffee intake and risk of ovarian cancer.

P5313The association between coffee and caffeine consumption and renal function: insight from individual-level data, Mendelian randomization, and meta-analysis

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Mazidi ◽  
D P Mikhailidis ◽  
A Dehghan ◽  
J Jozwiak ◽  
J Rysz ◽  
...  
Keyword(s):  
Renal Function ◽  
Mendelian Randomization ◽  
Meta Analysis ◽  
Coffee Consumption ◽  
Caffeine Intake ◽  
Caffeine Consumption ◽  
Coffee Intake ◽  
Urine Albumin ◽  
Level Data ◽  
Inverse Variance

Abstract Background The reported relationship between coffee intake and renal function is poorly understood. Purpose By applying on two-sample Mendelian randomization (MR) and systematic review and meta-analysis we investigated the association between caffeine and coffee intake with prevalent CKD and markers of renal function. Methods For the individual data analysis we analysed the NHANES data on renal function markers and caffeine intake. MR was implemented by using summary-level data from genome-wide association studies conducted on coffee intake (N=91,462) and kidney function (N=133,413). Inverse variance weighted method (IVW), weighted median-based method, MR-Egger, MR-RAPS, MR-PRESSO were applied. Random effects models and generic inverse variance methods were used for the meta-analysis. Results Finally, we included the data of 18,436 participants, 6.9% had prevalent CKD (based on eGFR). Caffeine intake for general population was 131.1±1.1 mg. The % of pts. with CKD, by caffeine quartile was 16.6% in Q1 (lowest), 13.9% in Q2, 12.2% in Q3 and 11.0% in Q4 (p<0.001). After adjustment, for increasing quartiles for caffeine consumption, mean urine albumin, albumin-creatinine ratio and eGFR did not change significantly (p>0.234). In fully adjusted logistic regression models, there was no significant difference in chances of CKD prevalence (p-trend=0.745) (Table). In the same line, results of MR showed no impact of coffee intake on CKD (IVW=β: −0.0191, SE: 0.069, p=0.781) (Figure), on eGFR (overall= IVW= β: −0.0005, SE: 0.005, p=0.926) both in diabetic (IVW= β: −0.006, SE: 0.009, p=0.478), and non-diabetic patients (IVW= β: −6.772, SE: 0.006, p=0.991). Results from the meta-analysis indicted that coffee consumption was not significantly associated with CKD (OR: 0.85, 95% CI 0.71–1.02, p=0.090, n=6 studies, I2=0.32). These findings were robust in sensitivity analyses. Levels of CKD markers across caffeine Qs Characteristics Quartiles of Caffeine p-value First Second Third Fourth Number of participants (n) 4609 4611 4608 4608 Log Urine Albumin (mg/L) 2.20±0.02 2.16±0.02 2.19±0.02 2.17±0.02 0.239 Serum Creatinine (mg/dL) 0.89±0.003 0.90±0.004 0.91±0.002 0.88±0.003 0.234 Log ACR (mg/g) 2.14±0.02 2.10±0.02 2.11±0.02 2.16±0.02 0.352 eGFR (ml/min/1.73m2) 91.2±0.7 92.8±0.4 90.2±0.5 89.6±0.3 0.415 MR on the impact of coffee intake on CKD Conclusions By implementing on different strategies we have highlighted no significant association between coffee consumption with renal function and chance of CKD. Acknowledgement/Funding None

scholarly journals Tendency towards being a “Morning person” increases risk of Parkinson’s disease: evidence from Mendelian randomisation

2018 ◽  
Author(s):  
AJ Noyce ◽  
DA Kia ◽  
K Heilbron ◽  
JEC Jepson ◽  
G Hemani ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Circadian Rhythm ◽  
Causal Relationship ◽  
Odds Ratio ◽  
Causal Effect ◽  
Coffee Consumption ◽  
Sensitivity Analyses ◽  
Mendelian Randomisation ◽  
Effect Estimate

AbstractBackgroundCircadian rhythm may play a role in neurodegenerative diseases such as Parkinson’s disease (PD). Chronotype is the behavioural manifestation of circadian rhythm and Mendelian randomisation (MR) involves the use of genetic variants to explore causal effects of exposures on outcomes. This study aimed to explore a causal relationship between chronotype and coffee consumption on risk of PD.MethodsTwo-sample MR was undertaken using publicly available GWAS data. Associations between genetic instrumental variables (IV) and “morning person” (one extreme of chronotype) were obtained from the personal genetics company 23andMe, Inc., and UK Biobank, and consisted of the per-allele odds ratio of being a “morning person” for 15 independent variants. The per-allele difference in log-odds of PD for each variant was estimated from a recent meta-analysis. The inverse variance weight method was used to estimate an odds ratio (OR) for the effect of being a “morning person” on PD. Additional MR methods were used to check for bias in the IVW estimate, arising through violation of MR assumptions. The results were compared to analyses employing a genetic instrument of coffee consumption, because coffee consumption has been previously inversely linked to PD.FindingsBeing a “morning person” was causally linked with risk of PD (OR 1⋅27; 95% confidence interval 1⋅06-1⋅51; p=0⋅012). Sensitivity analyses did not suggest that invalid instruments were biasing the effect estimate and there was no evidence for a reverse causal relationship between liability for PD and chronotype. There was no robust evidence for a causal effect of high coffee consumption using IV analysis, but the effect was imprecisely estimated (OR 1⋅12; 95% CI 0⋅89-1⋅42; p=0⋅22).InterpretationWe observed causal evidence to support the notion that being a “morning person”, a phenotype driven by the circadian clock, is associated with a higher risk of PD. Further work on the mechanisms is warranted and may lead to novel therapeutic targets.FundingNo specific funding source.

scholarly journals A study on caffeine consumption and its association with stress and appetite among call centre employees in Mumbai city, India

2017 ◽  
Vol 4 (3) ◽  
pp. 835 ◽  
Author(s):  
Lakshmi B. Kale ◽  
Kejal Joshi Reddy
Keyword(s):  
Negative Impact ◽  
Coffee Consumption ◽  
Negative Association ◽  
Caffeine Intake ◽  
Call Centre ◽  
Caffeine Consumption ◽  
Coffee Intake ◽  
Cross Sectional ◽  
Significant Difference ◽  
Stress Levels

Background: Caffeine is a widely consumed chemical having controversial effects. Caffeine may interact with the satiety and may be associated with stress levels. The prevalence of caffeine consumption among call centre employees is known to be high. The aim of the study was to assess the caffeine intake, appetite levels, stress levels and correlate these parameters among call centre employees aged between 25-35 yearsMethods: A cross sectional study with purposive sampling was carried out among a call centre at Mumbai, India. Anthropometric measurements and structured questionnaires were used for data collection.  Results: The average caffeine intake was 200mg/day through coffee and 150mg/day through tea among the habitual consumers. As per the scoring categories of modified appetite questionnaire (CNAQ), 54.7% (n=64) of the participants were at risk to abnormally low appetite. The stress questionnaire results showed that 84.6% (n=99) of the participants were at high risk to stress. Significant negative association was found between coffee intake and appetite score (r- 0.55, p<0.001), indicating that with more coffee consumption the appetite score was lower, similarly significant negative association was seen between tea consumption and appetite score (r- 0.300, p<0.05). Habitual smoking along with daily coffee intake had a significant negative association with appetite score (r- 0.476, p<0.05). Significant difference (p<0.01) was observed between the mean appetite score of habitual smokers and non-smokers; mean appetite score of non-smokers was greater.Conclusions: Caffeine had a negative impact on the appetite levels. Smoking was observed to worsen the effect of caffeine on appetite. 

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