Search

Background: A high plasma total homocysteine concentration is associated with increased risk of cardiovascular disease. Consumption of unfiltered or filtered coffee raises total homocysteine concentrations in healthy volunteers. The responsible compound, however, is unknown. Objective: The objective was to determine whether caffeine explains the homocysteine-raising effect of coffee. Design: Forty-eight subjects aged 19–65 y completed this randomized crossover study with 3 treatments, each lasting 2 wk. Subjects consumed 6 capsules providing 870 mg caffeine/d (test treatment), 0.9 L paper-filtered coffee providing 870 mg caffeine/d, or 6 placebo capsules. Blood samples were drawn fasting and 4 h after consumption of 0.45 L coffee or 3 capsules. Results: The mean fasting plasma homocysteine concentration after the placebo treatment was 9.6 ± 3.1 ?mol/L. The caffeine and coffee treatments increased fasting homocysteine by 0.4 ?mol/L (95% CI: 0.1, 0.7; P = 0.04), or 5%, and by 0.9 ?mol/L (95% CI: 0.6, 1.2; P = 0.0001), or 11%, respectively, compared with placebo. The increase in homocysteine concentrations 4 h after consumption of 0.45 L coffee relative to consumption of 3 placebo capsules was 19% (P = 0.0001). Caffeine treatment had a much weaker acute effect on homocysteine (4%; P = 0.09). Effects of caffeine were stronger in women than in men, but the effects of coffee did not differ significantly between men and women. Conclusions: Caffeine is partly responsible for the homocysteine-raising effect of coffee. Coffee, but not caffeine, affects homocysteine metabolism within hours after intake, although the effect is still substantial after an overnight fast. Key Words: Caffeine … paper-filtered coffee … homocysteine … B vitamins … crossover experiment

Item does not contain fulltext

Item does not contain fulltext

Boiled coffee raises blood levels of cholesterol and triglycerides in man. Cafestol and kahweol are responsible. These diterpenes also raise blood levels of alanine aminotransferase (ALT). The objective of the present studies was to further specify the health effects of cafestol and kahweol.Unfiltered coffee contains up to 5 g of grounds per liter. Intake of 8 g/day of such grounds for 3 weeks raised cholesterol by 0.65 mmol/L and ALT by 18 U/L in healthy volunteers. Diterpenes in floating grounds thus contribute to the hyperlipidaemic and ALT- elevating effects of unfiltered coffee. Chemical analyses showed that boiled, cafeti6re (also called French press), and Turkish coffee are rich in diterpenes. Levels are moderate in espresso and mocha coffee, and negligible in percolated, instant, and filtered coffee.We studied the separate activities of cafestol and kahweol in a randomised, double-blind cross-over study with 10 male volunteers. Intake of 63 mg/day of cafestol for 4 weeks raised cholesterol by 17%, triglycerides by 86%, and ALT by 78%. Additional intake of 51 mg/d of kahweol only marginally raised the lipid responses, but more than doubled the ALT responses. Cafestol therefore is more hyperlipidaemic than kahweol, but both affect liver cells.To study long term effects, we gave 46 volunteers 0.9 liter/day of either filtered or cafetiere coffee for 6 months in a randomised experiment. ALT levels were still raised by 45%, and LDL by 9%, after 6 months of intake of cafetiere coffee, but most of the initial rise in triglycerides had disappeared.Lipoprotein(a) is an atherogenic particle made by the liver. We found that lipoprotein(a) levels were 65% higher in chronic drinkers of boiled coffee than in peers drinking filtered coffee. However, supplements rich in diterpenes lowered lipoprotein(a) in four experiments.In conclusion, the strong and persistent effects on total and LDL cholesterol levels are a good reason to advise patients with a high coronary risk to lim

The coffee diterpene cafestol occurs in both robusta and arabica beans. It is present in unfiltered coffee brews and raises serum concentrations of cholesterol, triacylglycerols, and alanine aminotransferase in humans. The effects are linear with the cafestol dose. Unfiltered coffee also contains the related compound kahweol, which occurs only in the major coffee strain arabica. The activity of kahweol is unknown. In a randomized, double-blind crossover study, we gave 10 healthy male volunteers either pure cafestol (61-64 mg/d) or a mixture of cafestol (60 mg/d) and kahweol (48-54 mg/d) for 28 d. Relative to baseline values, cafestol raised mean ( /-SEM) total serum cholesterol concentrations by 0.79 /- 0.14 mmol/L (31 /- 5 mg/dL), low-density-lipoprotein (LDL) cholesterol by 0.57 /- 0.13 mmol/L (22 /- 5 mg/dL), fasting triacy-glycerols by 0.65 /- 0.12 mmol/L (58 /- 11 mg/dL), and alanine aminotransferase by 18 /- 2 U/L (all P < 0.01). Relative to cafestol alone, the mixture of cafestol plus kahweol increased total cholesterol by another 0.23 /- 0.16 mmol/L (9 /- 6 mg/dL) (P = 0.08), LDL cholesterol by 0.23 /- 0.16 mmol/L (9 /- 6 mg/dL) (P = 0.09), triacylglycerols by 0.09 /- 0.10 mmol/L (8 /- 9 mg/dL) (P = 0.20), and alanine aminotransferase by 35 /- 11 U/L (P = 0.004). Thus, the effect of cafestol on serum lipid concentrations was much larger than the additional effect of kahweol, and the hyperlipidemic potential of unfiltered coffee mainly depends on its cafestol content. Both cafestol and kahweol raised alanine aminotransferase concentrations, and their hyperlipidemic effect thus seems not to be coupled with their effect on liver cells.

Objective: Unfiltered coffee raises serum LDL cholesterol in humans, owing to the presence of the diterpenes cafestol and kahweol. Norwegians with a chronic high intake of unfiltered coffee also had elevated serum levels of lipoprotein(a), an LDL-like particle which is insensitive toward dietary interventions. We now experimentally studied the influence of coffee diterpenes on lipoprotein(a) levels. Design: Four randomised controlled trials. Subjects: Healthy, normolipidemic volunteers. Interventions: Coffee, coffee oil, and pure diterpenes for 4-24 weeks. Main outcome measures: The circulating level of lipoprotein(a). Results: In 22 subjects drinking five to six strong cups of cafetiere coffee per day, the median fall in lipoprotein(a) was 1.5 mg/dL after two months (P=0.03), and 0.5 mg/dL after half a year (P>0.05), relative to 24 filter coffee drinkers. Coffee oil doses equivalent to 10-20 cups of unfiltered coffee reduced lipoprotein(a) levels by up to 5.5 mg/dL (P<0.05) in two separate trials (n=12-16 per group). A purified mixture of cafestol and kahweol, as well as cafestol alone, were also effective in reducing Lp(a) levels (n=10). Averaged over the four trials, each 10 mg/d of cafestol (plus kahweol)?the amount present in two to three cups of cafetiere coffee?decreased Lp(a) levels by 0.5 mg/dL or 4% from baseline values after four weeks (n=63). Conclusions: Coffee diterpenes are among the few dietary exceptions shown to influence serum lipoprotein(a) levels. However, the Lp(a)-reducing potency of coffee diterpenes may subside in the long run, and their adverse side effects preclude their use as lipoprotein(a)-reducing agents. Sponsorship: Supported by the Netherlands Heart Foundation through grant No. 900-562-091 of the Netherlands Organization of Scientific Research (NWO), plus supplemental funding by the Institute for Scientific Information on Coffee.

Specific fatty acids and sterols in food composites from seven countries were analyzed. In the 1960s, groups of 8 to 49 men from 16 cohorts, ages 40–59 years and living in the United States, Finland, the Netherlands, Italy, Greece, the former Yugoslavia, or Japan recorded their food intake. In 1987, we collected food composites representing the average food intake per cohort sample in the 1960s. The foods were transported to the Netherlands, pooled, and centrally analyzed for energy, total fat, 42 fatty acids, cholesterol, and four plant sterols. The fat content ranged from 12% of total daily energy in the Tanushimaru, Japan, cohort to 50% in the U.S. cohort sample, and the polyunsaturated to saturated fat ratio ranged from 0.17 in the east Finland cohort to 1.2 in Tanushimaru. The amount oftransfatty acids with 16 or 18 carbon atoms varied between 0.2 g/day in Corfu, Greece, and 8.6 g/day in Zutphen, Netherlands, and that of -linolenic acid between 0.8 g/day in Rome and 2.5 g/day in east Finland. The sum of eicosapentaenoic and docosahexanoic acid ranged from 0.1 (U.S. railroad) to 2.0 g/day (Ushibuka, Japan), and phytosterols from 170 (U.S. railroad) to 358 mg/day (Corfu, Greece). Thus the intake of various fatty acids and sterols with potential relevance for coronary heart disease occurrence varied 10-fold or more between cohorts. Our data can be used to generate new hypotheses about the causes of differences in incidence of diseases between countries.

Cafestol and kahweol–diterpenes present in unfiltered coffee— strongly raise serum VLDL and LDL cholesterol and slightly reduce HDL cholesterol in humans. The mechanism of action is unknown. We determined whether the coffee diterpenes may affect lipoprotein metabolism via effects on lipid transfer proteins and lecithin:cholesterol acyltransferase in a randomized, double-blind cross-over study with 10 healthy male volunteers. Either cafestol (61–64 mg/day) or a mixture of cafestol (60 mg/day) and kahweol (48–54 mg/day) was given for 28 days. Serum activity levels of cholesterylester transfer protein, phospholipid transfer protein and lecithin:cholesterol acyltransferase were measured using exogenous substrate assays. Relative to baseline values, cafestol raised the mean (±S.D.) activity of cholesterylester transfer protein by 18±12% and of phospholipid transfer protein by 21±14% (both P<0.001). Relative to cafestol alone, kahweol had no significant additional effects. Lecithin:cholesterol acyltransferase activity was reduced by 11±12% by cafestol plus kahweol (P=0.02). It is concluded that the effects of coffee diterpenes on plasma lipoproteins may be connected with changes in serum activity levels of lipid transfer proteins.

Coffee beans and some types of coffee brew - not the regular types of coffee prepared with a paper filter or with soluble coffee granules - contain the diterpenes cafestol and kahweol. Cafestol and kahweol raise the serum concentration of cholesterol and triglycerides in humans, and they also appear mildly to affect the integrity of liver cells. Both effects are transient after withdrawal of the diterpenes, and it is as yet unsure whether these effects are associated. Patients at increased risk of heart disease who drink large amounts of coffee should be advised to select brews low in diterpenes.

Objectives: To examine the association of plasma caffeine concentrations during pregnancy with fetal growth and to compare this with relations with reported caffeine intake. Design: Prospective population based study. Setting: District general hospital, inner London. Subjects: Women booking for delivery between 1982 and 1984. Stored plasma was available for 1500 women who had provided a blood sample on at least one occasion and for 640 women who had provided a sample on all three occasions (at booking, 28 weeks, and 36 weeks). Main outcome measure: Birth weight adjusted for gestational age, maternal height, parity, and sex of infant. The exposures of interest were reported caffeine consumption and blood caffeine concentration. Cigarette smoking was assessed by blood cotinine concentration. Results: Caffeine intake showed no changes during pregnancy, but blood caffeine concentrations rose by 75%. Although caffeine intake increased steadily with increasing cotinine concentration above 15 ng/ml, blood caffeine concentrations fell. Caffeine consumption was inversely related to adjusted birth weight, the estimated effect being a 1.3% fall in birth weight for a 1000 mg per week increase in intake (95% confidence interval 0.5% to 2.1%). The apparent caffeine effect was confined to cigarette smokers, among whom the estimated effect was -1.6%/1000 mg a week (-2.9% to -0.2%) after adjustment for cotinine and -1.3% (-2.7% to 0.1%) after further adjustment for social class and alcohol intake. Adjusted birth weight was unrelated to blood caffeine concentrations overall (P = 0.09, but a positive coefficient), after adjustment for cotinine (P = 0.73), or among current smokers (P = 0.45). Conclusions: Smokers consume more caffeine than non-smokers. Blood caffeine concentrations during pregnancy are not related to fetal growth, but caffeine intake is negatively associated with birth weight, with this effect being apparent only in smokers. The effect remains of borderline significanc