Throughout childhood there is a shift from predominantly milk-based beverage consumption to other types of beverages, including those containing caffeine. Although a variety of health effects in children and adults have been attributed to caffeine, few data exist on caffeine intake in children aged one to five years.
Because beverages provide about 80% of total caffeine consumed in children of this age group, beverage consumption patterns and caffeine intakes were evaluated from two beverage marketing surveys: the 2001 Canadian Facts study and the 1999 United States Share of Intake Panel study.
Considerably fewer Canadian children than American children consume caffeinated beverages (36% versus 56%); Canadian children consume approximately half the amount of caffeine (7 versus 14 mg/day in American children). Differences were largely because of higher intakes of carbonated soft drinks in the US.
Caffeine intakes from caffeinated beverages remain well within safe levels for consumption by young children.
BACKGROUND: It is not known whether the consumption of caffeine is associated with excess risk of atrial fibrillation. OBJECTIVE: We evaluated the risk of atrial fibrillation or flutter in association with daily consumption of caffeine from coffee, tea, cola, cocoa, and chocolate. DESIGN: We prospectively examined the association between the amount of caffeine consumed per day and the risk of atrial fibrillation or flutter among 47 949 participants (x age: 56 y) in the Danish Diet, Cancer, and Health Study. Subjects were followed in the Danish National Registry of Patients and in the Danish Civil Registration System. The consumption of caffeine was analyzed by quintiles with Cox proportional-hazard models. RESULTS: During follow-up (x: 5.7 y), atrial fibrillation or flutter developed in 555 subjects (373 men and 182 women). When the lowest quintile of caffeine consumption was used as a reference, the adjusted hazard ratios (95% CIs) in quintiles 2, 3, 4, and 5 were 1.12 (0.87, 1.44), 0.85 (0.65, 1.12), 0.92 (0.71, 1.20), and 0.91 (0.70, 1.19), respectively. CONCLUSION: Consumption of caffeine was not associated with risk of atrial fibrillation or flutter.
Comment In: Am J Clin Nutr. 2005 Mar;81(3):539-4015755819
The coffee bean contains over 2000 chemical compounds, the health effects of which are known only to a limited extent. Previous coffee researchers and laymen focused solely on caffeine and its positive effect on mental alertness. Other ingredients in coffee, especially its polyphenols, also have an influence on our health. In Finland, coffee is the source of more than half of the so-called antioxidants that are thought to be important for health. Coffee drinkers have lower mortality and morbidity rates than non-drinkers in respect of many common chronic diseases.
Only a few cross-sectional studies have assessed the association between coffee, tea and caffeine and the risk of depression. Our aim was to determine the association in a population-based cohort study.
The population-based Kuopio Ischaemic Heart Disease Risk Factor Study cohort was recruited between 1984 and 1989 and followed until the end of 2006. We investigated the association between the intake of coffee, tea and caffeine and depression.
Middle-aged men (n 2232).
Altogether, forty-nine men received a discharge diagnosis of depression. We classified subjects into quartiles according to their mean daily coffee intake: non-drinkers (n 82), light drinkers (813 ml/d, n 390). Heavy drinkers had a decreased risk (RR = 0.28, 95 % CI 0.08, 0.98) for depression when compared with non-drinkers, after adjustment for age and examination years. Further adjustment for socio-economic status, alcohol consumption, smoking, maximal oxygen uptake, BMI and the energy-adjusted daily intakes of folate and PUFA did not attenuate this association (relative risk (RR) = 0.23, 95 % CI 0.06, 0.83). No associations were observed between depression and intake of tea (drinkers v. non-drinkers; RR = 1.19, 95 % CI 0.54, 2.23) or caffeine (highest quartile v. lowest quartile; RR = 0.99, 95 % CI 0.40, 2.45).
Coffee consumption may decrease the risk of depression, whereas no association was found for tea and caffeine intake.
The purpose of this work was to study how the type of post-harvest process, i.e. natural preparation known as the dry method, and two wet processes, affected contamination and toxin production up to the green coffee stage. Batches were contaminated with ochratoxin A or with OTA-producing strains of Aspergillus ochraceus and Aspergillus niger. For OTA artificial contamination, hulling or husk removal caused a reduction of OTA. When A. ochraceus was inoculated at low level, its growth was hampered by indigenous mould flora contrary that observed with A. niger. The fungal counts and OTA assays showed that the best way of limiting the development and impact of contaminating toxigenic flora "from the field" was the physical wet method.
Boiled coffee contains an unidentified lipid that raises serum cholesterol. We studied the effects of the ingestion of coffee oil fractions of increasing purity in volunteers in order to identify the cholesterol-raising factor. In 15 volunteers who ingested 0.75 g/d of a non-triglyceride-fraction from coffee oil for 4 weeks, mean cholesterol increased by 48 mg/dl (1.2 mmol/l) relative to placebo. In contrast, a coffee oil stripped of the non-triglyceride lipids cafestol and kahweol had no effect. In three volunteers, purified cafestol (73 mg/d) plus kahweol (58 mg/d) increased cholesterol by 66 mg/dl (1.7 mmol/l) after 6 weeks. Oil from Robusta beans, which contains cafestol but negligible kahweol, also raised serum cholesterol. These findings show that cafestol is at least partly responsible for the cholesterol-raising effect of boiled coffee. Coffee oils and brews containing cafestol consistently increased serum triglycerides and alanine amino-transferase, and depressed serum creatinine and gamma-glutamyl-transferase (GGT). After withdrawal GGT activity rose above baseline. Norwegians who habitually consumed 5-9 cups of boiled coffee per day had higher serum cholesterol levels and lower GGT but no higher alanine aminotransferase activity than controls. Thus, serum cholesterol is raised by cafestol and possibly also kahweol, both natural components of coffee beans. The mechanism of action is unknown but is accompanied by alterations in liver function enzymes.
Coffee is a widely consumed beverage, and studies suggest that drinking coffee has beneficial health effects. The phytohormone trigonelline is present in large amounts in coffee beans, and circulating concentrations of trigonelline have been shown to be positively related to dietary intake of coffee and to increase significantly after the consumption of a bolus dose of coffee.
We cross-sectionally investigated the utility of plasma trigonelline as a marker of coffee consumption in an epidemiologic setting. We secondarily investigated if coffee intake is related to plasma concentrations of vitamin B-3 (niacin) forms.
In a Norwegian cohort of 3503 participants, we combined questionnaire data on the number of cups of coffee consumed per day with plasma trigonelline to evaluate trigonelline as a marker of coffee intake. The suitability of plasma trigonelline to discriminate those not consuming from those consuming coffee was investigated by receiver operating characteristic (ROC) analysis. Plasma collected at 2 time points 1 y apart was used to determine the within-person reproducibility of trigonelline.
We found that plasma trigonelline concentrations increased strongly with increasing amounts of coffee consumed. ROC analysis showed that trigonelline had an area under the curve of 0.92 (95% CI: 0.90, 0.94) for distinguishing coffee abstainers from coffee drinkers. Plasma trigonelline had a good within-person reproducibility (0.66; 95% CI: 0.64, 0.68) for samples collected 1 y apart. The amount of coffee consumed was not associated with plasma concentrations of the niacin vitamers nicotinamide and N1-methylnicotinamide.
Plasma trigonelline performs well as a marker of coffee intake. Data used in this study were derived from the clinical trial registered at www.clinicaltrials.gov as NCT00354081.
One-hundred and one specimens of coffee were gathered from retail outlets across Canada and analysed for ochratoxin A. Seventy-one specimens were roasted beans or roasted ground coffee, and 30 were instant (or 'soluble') coffees. All samples were extracted with methanol-sodium bicarbonate. The extracts were cleaned up either by immunoaffinity column chromatography or by a combination of solid-phase extraction and immunoaffinity column chromatography. Ochratoxin A was quantified by liquid chromatography (LC) with fluorescence detection. The minimum quantifiable level was 0.1 ng g(-1). Ochratoxin A was present, above the minimum quantifiable level, in 42 (59%) of 71 beans and ground coffee and in 20 (67%) of 30 instant coffees. The mean ochratoxin A level in the positive samples of beans and ground coffee was 0.6 ng g(-1), and the mean level in the positive samples of instant coffee was 1.1 ng g(-1).