FOOD TO EAT. DISHES AND MENUS
postmenopausal estrogen, and risk of Parkinson's disease.
||Effects of caffeine
on human health.
||Effects of coffee and
caffeine on fertility, reproduction, lactation, and development.
Review of human and animal data.
||Caffeine: an update.
||Coffee, tea, and caffeine
consumption and breast cancer incidence in a cohort of
||Effects of caffeine
on bone and the calcium economy.
||Caffeine and coffee:
effects on health and cardiovascular disease.
||Caffeine intake and
low birth weight: a population-based case-control study.
||Selected health and
behavioral effects related to the use of caffeine.
||Regular caffeine consumption:
a balance of adverse and beneficial effects for mood and
||Caffeine affects cardiovascular
and neuroendocrine activation at work and home.
||Effect of coffee consumption
on intraocular pressure.
||Coffee intake and
risk of hypertension: the Johns Hopkins precursors study.
||Coffee, caffeine and
blood pressure: a critical review.
||The effect of caffeine
on ambulatory blood pressure in hypertensive patients.
||A prospective study
of coffee drinking and suicide in women.
and risk of ischaemic heart disease - a settled issue?
||Coffee intake and
coronary heart disease.
and cause-specific mortality. Association with age at
death and compression of mortality.
of coffee consumption in the aged: the CASTEL epidemiologic
among hypertensives by reported level of caffeine consumption.
and blood pressure: an Italian study.
and the incidence of coronary heart disease.
||Coffee and health.
and the risk of coronary heart disease and death.
||Coffee and tea consumption
in the Scottish Heart Health Study follow up: conflicting
relations with coronary risk factors, coronary disease,
and all cause mortality.
and coronary heart disease in women. A ten-year follow-up.
a complex mixture of chemical compounds. Some components,
particularly those related to the aroma, are produced during
roasting of the green beans. The substances which during "brewing"
dissolve in water to form the beverage are classified as nonvolatile
taste components (including caffeine, trigonelline, chlorogenic
acid, phenolic acids, amino acids, carbohydrates, and minerals)
and volatile aroma components including organic acids, aldehydes,
ketones, esters, amines, and mercaptans.
The major physiologically active substance
in coffee is the alkaloid caffeine (C_8 H_10 O_2 N_4·H_2
O), also called guaranine or methyltheobromine, which acts
as a mild stimulant. Caffeine is a naturally occurring substance
found in the leaves, seeds or fruits of more than 60 plants,
including coffee and cocoa beans, cola nuts and tea leaves.
These are used to make beverages such as coffee, tea and
cola drinks, and foods such as chocolate. Caffeine is also
contained in many over-the-counter (OTC) and prescription
medications. In the United States, most of the population
uses caffeine in some form.
A cup of coffee, depending on the strength,
may contain some 20-100mg of caffeine. Some types of coffee
may also contain significant amounts of the B-vitamin niacin,
although this nutrient is of course readily available from
other foods as well. Caffeine-containing tablets or medications
should not be taken as well as cups of coffee or tea, since
this would increase the true dosage. The effects of caffeine
vary from person to person; some individuals can drink several
cups of coffee in an hour and notice no effects, while others
may feel a strong effect after just one serving. Caffeine
is prohibited for competition athletes.
People who wish to avoid or minimise caffeine intake (see
below) often use decaffeinated coffee, or coffee substitutes.
One method of decaffeination is by treating the green beans
(before roasting) with chlorinated hydrocarbon solvents;
other methods are also used. Important coffee substitutes
are chicory, and roasted cereals such as barley; although
these are commonly used not as total substitutes but as
"extenders". Under U.S. law, the addition of chicory
or any other substance must be clearly stated on the label.
Caffeine is a drug that has been widely
used for centuries. Its main
effect is that it is a mild stimulant of the central nervous
system (CNS), helping to reduce feelings of drowsiness and
fatigue. However, regular use may lead to "habituation";
that is, no net benefit from use but, rather, a negative
effect if the drug is not taken.
Besides the above-mentioned CNS stimulant
effect, caffeine also temporarily increases heartbeat, increases
the blood pressure, and stimulates the action of the lungs;
increases basal metabolic rate (BMR), and promotes urine
production; and it relaxes smooth muscles, notably the bronchial
muscle. Caffeine is used in treating migraine, either alone
or in combination. It enhances the action of the ergot alkaloids
used for the treatment of this problem, and also increases
the potency of analgesics such as aspirin. It can somewhat
relieve asthma attacks by dilating the bronchial airways.
Too much caffeine can produce restlessness,
nausea, headache, tense muscles, sleep disturbances, and
cardiac arrhythmias (irregular heartbeats). Because caffeine
increases the production of stomach acid it may worsen ulcer
symptoms or cause acid reflux ("heartburn"). Evening
use of caffeine may disrupt sleep and cause insomnia.
Caffeine should be used with caution by
people with heart disease and high blood pressure (hypertension),
and by those suffering from the eye disease glaucoma. Caffeine
medications should generally not be used in children. Many
children are already consuming significant amounts of caffeine
in drinks and food. In this connection, a nutritional concern
is that children may choose fizzy drinks in preference to
milk, thus getting "empty" calories at the expense
of valuable nutrients.
As already mentioned, some potentially
harmful effects of coffee are recognized, particularly for
people who should take few or no stimulants. Beyond this
however, scientific studies of the effects of caffeine have
in general failed to prove negative effects, although some
have produced contradictory conclusions. An individual study
may produce interesting results which may suggest fruitful
directions for further research, but usually it is only
when several independent studies confirm one another, and
any contradictory results can be accounted for, that one
can have reasonable confidence in the safety of a drug --
particularly an " optional" one like coffee.
Although caffeine does not fall into the
class of "addictive" drugs, it may be habit-forming.
Some people may experience headache, fatigue, irritability
and nervousness when their daily intake of caffeine is quickly
and substantially altered.
Such "withdrawal effects" may
be responsible for confusing results in some studies. There
are many complicating factors in long-term studies. One
is the familiar "convergence of risk-factors"
(e.g. that coffee-drinkers may be more likely to be smokers).
Another is that many of the study subjects may deliberately
change (or have previously changed) their consumption habits
or behaviour, e.g. in response to discovering that they
suffer from hypertension. There may also be significant
differences in methods of coffee preparation between study
populations, or over long periods of time.
Moderate caffeine consumption during pregnancy
is generally considered safe. A study has not found any
effect on low birth-weight or incidence of premature births.
However, although it has been suggested that caffeine may
stimulate milk production, cautious mothers may prefer to
avoid such beverages during pregnancy or while breastfeeding.
Furthermore, a large study has not shown
any connection of coffee or tea consumption with breast-cancer
incidence. Osteoporosis is another condition which particularly
affects women. Previous studies have suggested caffeine
consumption as a risk-factor, but a recent analysis concludes
that such an effect is probably not significant except in
conditions of calcium-deficiency, which can be easily corrected.
There is even some actual positive news.
The effect of caffeine on the risk of developing Parkinson's
disease, which usually affects older people, has been found
to be favourable for men. For women, previous results have
been confusing; but a recent study suggests that a crucial
factor may be the effect of hormone levels. Often caffeine
may have a favourable effect against developing this disease;
but when combined with hormone replacement therapy (HRT),
it may have a negative one.
One study has found (for women) a
strong inverse association between coffee intake and risk
of suicide. However, even if confirmed, to determine whether
this might be actual cause and effect is, as usual, a much
more challenging problem.
BACKGROUND: Men who regularly
consume caffeinated drinks have a lower risk of PD than
do nondrinkers, but this relation has not been found
in women. Because this sex difference could be due to
hormonal effects, the authors examined prospectively
the risk of PD according to use of postmenopausal hormones
and caffeine intake among participants in the Nurses'
Health Study. METHODS: The study population comprised
77,713 women free of PD, stroke, or cancer at baseline,
who were postmenopausal at baseline or reached menopause
before the end of the study. During 18 years of follow-up
the authors documented 154 cases of PD. RESULTS: Overall,
the risk of PD was similar in women using hormones and
women who never used hormones (relative risk 1.02, 95%
CI 0.69 to 1.52). Use of hormones, however, was associated
with a reduced risk of PD among women with low caffeine
consumption (RR 0.39, 95% CI 0.13 to 1.17), and with
increased risk among women with high caffeine consumption
(RR 2.44, 95% CI 0.75 to 7.86; p for interaction = 0.01).
Among hormone users, women consuming six or more cups
of coffee per day had a fourfold higher risk of PD (RR
3.92, 95% CI 1.49 to 10.34; p = 0.006) than did women
who never drink coffee. CONCLUSION: These results suggest
that caffeine reduces the risk of PD among women who
do not use postmenopausal hormones, but increases risk
among hormone users. Clinical trials of caffeine or
estrogens in women should avoid the combined use of
Caffeine is probably the most
frequently ingested pharmacologically active substance
in the world. It is found in common beverages (coffee,
tea, soft drinks), in products containing cocoa or chocolate,
and in medications. Because of its wide consumption
at different levels by most segments of the population,
the public and the scientific community have expressed
interest in the potential for caffeine to produce adverse
effects on human health. The possibility that caffeine
ingestion adversely affects human health was investigated
based on reviews of (primarily) published human studies
obtained through a comprehensive literature search.
Based on the data reviewed, it is concluded that for
the healthy adult population, moderate daily caffeine
intake at a dose level up to 400 mg day(-1) (equivalent
to 6 mg kg(-1) body weight day(-1) in a 65-kg person)
is not associated with adverse effects such as general
toxicity, cardiovascular effects, effects on bone status
and calcium balance (with consumption of adequate calcium),
changes in adult behaviour, increased incidence of cancer
and effects on male fertility. The data also show that
reproductive-aged women and children are 'at risk' subgroups
who may require specific advice on moderating their
caffeine intake. Based on available evidence, it is
suggested that reproductive-aged women should consume
=300 mg caffeine per day (equivalent to 4.6 mg kg(-1)
bw day(-1) for a 65-kg person) while children should
consume =2.5 mg kg(-1) bw day(-1).
In the present review, we have
examined the effects of coffee ingestion on fertility,
reproduction, lactation and development. The potential
effects of coffee consumption on fertility, spontaneous
abortion and prematurity are not clearly established
but appear to be quite limited. In rodents, caffeine
can induce malformations but this effect appears in
general at doses never encountered in humans. Indeed,
as soon as the quantity of caffeine is divided over
the day, as is the case for human consumption, the teratogenic
effect of caffeine disappears in rodents. Coffee ingested
during gestation induces a dose-dependent decrease in
birth weight, but usually only when ingested amounts
are high (i.e. more than 7 cups/day), whereas coffee
has no effect at moderate doses. Caffeine consumption
during gestation affects hematologic parameters of the
new-born infant or rat. In animals, caffeine induces
long-term consequences on sleep, locomotion, learning
abilities, emotivity and anxiety, whereas, in children,
the effects of early exposure to coffee and caffeine
on behavior are not clearly established. The quantities
of caffeine found in maternal milk vary with authors,
but it appears clearly that caffeine does not change
maternal milk composition and has a tendency to stimule
milk production. In conclusion to this review, it appears
that maternal coffee or caffeine consumption during
gestation and/or lactation does not seem to have measurable
consequences on the fetus of the newborn, as long as
ingested quantities remain moderate. Therefore, pregnant
mothers should be advised to limit their coffee and
caffeine intake to 300 mg caffeine/day (i.e. 2-3 cups
of coffee or 2.5-3 l of coke) especially because of
the increase of caffeine half-life during the third
trimester of pregnancy and in the neonate.
While the total annual volume
of caffeine has increased over the years, the actual
per capita daily intake has not. This is based on the
fact that the quantity of caffeine in a soft drink is
about the same or, in the case of diet drinks, less
than in 1961 when the original GRAS (Generally Recognized
as Safe) determinations were made. Since that time,
there have been numerous studies on the effect of caffeine
on animals and humans. The Select Committee on GRAS
Substances (SCOGS) of the Federation of American Societies
for Experimental Biology (FASEB) in 1978 reviewed all
the data available at that time and concluded that there
is "no evidence in the available information on caffeine
[that] demonstrates a hazard to the public when it is
used in cola-type beverages at levels that are now current
and in the manner now practiced...", although they did
suggest further study was necessary. The Flavor and
Extract Manufacturers' Association (FEMA) Expert Panel
has now reviewed not only the same data s the FASEB
(SCOGS) Committee, but several more recent studies.
On the basis of this review, the Panel reaffirms the
GRAS status of caffeine under conditions of its current
use as an international ingredient in nonalcoholic beverages.
PURPOSE: Coffee, caffeinated tea,
and caffeine have been suggested to play a role in breast
carcinogenesis or in the promotion or inhibition of
tumor growth. Prior epidemiologic evidence has not supported
an overall association between consumption of caffeinated
beverages and risk of breast cancer, but consumption
in some studies was low. METHODS: We studied this relation
in the Swedish Mammography Screening Cohort, a large
population-based prospective cohort study in Sweden
comprising 59,036 women aged 40-76 years. Sweden has
the highest coffee consumption per capita in the world.
RESULTS: During 508,267 person-years of follow-up, 1271
cases of invasive breast cancer were diagnosed. Women
who reported drinking 4 or more cups of coffee per day
had a covariate-adjusted hazard ratio of breast cancer
of 0.94 [95% confidence interval (CI) 0.75-1.28] compared
to women who reported drinking 1 cup a week or less.
The corresponding hazard ratio for tea consumption was
1.13 (95% CI 0.91-1.40). Similarly, women in the highest
quintile of self-reported caffeine intake had a hazard
ratio of beast cancer of 1.04 (95% CI 0.87-1.24) compared
to women in the lowest quintile. CONCLUSIONS: In this
large cohort of Swedish women, consumption of coffee,
tea, and caffeine was not associated with breast cancer
Caffeine-containing beverage consumption
has been reported to be associated with reduced bone
mass and increased fracture risk in some, but not most,
observational studies. Human physiological studies and
controlled balance studies show a clear but only a very
small depressant effect of caffeine itself on intestinal
calcium absorption, and no effect on total 24-h urinary
calcium excretion. The epidemiologic studies showing
a negative effect may be explained in part by an inverse
relationship between consumption of milk and caffeine-containing
beverages. Low calcium intake is clearly linked to skeletal
fragility, and it is likely that a high caffeine intake
is often a marker for a low calcium intake. The negative
effect of caffeine on calcium absorption is small enough
to be fully offset by as little as 1-2 tablespoons of
milk. All of the observations implicating caffeine-containing
beverages as a risk factor for osteoporosis have been
made in populations consuming substantially less than
optimal calcium intakes. There is no evidence that caffeine
has any harmful effect on bone status or on the calcium
economy in individuals who ingest the currently recommended
daily allowances of calcium.
Caffeine is a methylxanthine whose
primary biological effect is the competitive antagonism
of the adenosine receptor. Its presence in coffee, tea,
soda beverages, chocolate and many prescription and
over-the-counter drugs makes it a commonly consumed
stimulant. Coffee and/or caffeine consumption has been
linked to many human diseases in epidemiologic studies.
Causal relationships have been difficult to substantiate.
Initial investigations, showing an association between
coffee and coronary heart disease, suffer from confounding
variables and have been difficult to replicate. Recent
studies, showing a significant effect over long follow-up
periods and with high coffee intake, have again raised
the question of a role for coffee and/or caffeine consumption
in the pathogenesis of atherosclerotic heart disease.
Contrary to common belief, the published literature
provides little evidence that coffee and/or caffeine
in typical dosages increases the risk of infarction,
sudden death or arrhythmia.
The authors conducted a matched
case-control study to investigate the effects of caffeine
intake during pregnancy on birth weight. From January
to November 1992, in the first 24 hours after delivery,
1,205 mothers (401 cases and 804 controls) were interviewed
and their newborns were examined to assess birth weight
and gestational age by means of the method of Capurro
et al. (J Pediatr 1978;93:120-2). The cases were children
with birth weight < 2,500 g and gestational age > or
= 28 weeks. Cases and controls were matched for time
of birth and hospital of delivery and were recruited
from the four maternity hospitals in Pelotas, southern
Brazil. Daily maternal caffeine intake during pregnancy
for each trimester was estimated. To assess caffeine
intake, 10% of the mothers were reinterviewed at their
households and samples of reported information on drip
coffee and mate (a caffeine-containing drink widely
used in South America) were collected and sent to the
laboratory for caffeine determination through liquid
chromatography. When instant coffee was reported, the
weight of powder was measured using a portable scale,
and caffeine intake was estimated from a reference table.
Caffeine intake from tea, chocolate, soft drinks, and
medicines was estimated from a reference table. Analyses
were performed by conditional logistic regression. Crude
analyses showed no effect of caffeine on low birth weight,
preterm births or intrauterine growth retardation. The
results did not change after allowing for confounders.
This paper reviews the research
literature concerning health and selected behavioral
effects of caffeine. Epidemiological and laboratory
findings are reviewed to determine the health risks
associated with both acute and chronic caffeine exposure.
Common sources of caffeine, its properties, and physiological
effects are considered. The relationships between caffeine
and various health conditions are examined including
caffeine's association with heart disease, cancer, and
benign breast disease. Caffeine's possible contribution
to enhanced exercise performance is discussed along
with a brief overview of caffeine's effects on mental
and emotional health. Over 100 references cited in this
review were part of a more extensive literature base
obtained from several on-line services including MEDLINE
and LEXIS/NEXIS medical data bases. Other sources of
relevant literature included manual searches of research
journals and the use of selected references from appropriate
articles. The relationship between caffeine consumption
and various illnesses such as cardiovascular disease
and cancer remains equivocal. Prudence might dictate
that pregnant women and chronically ill individuals
exercise restraint in their use of caffeine, although
research suggests relatively low or nonexistent levels
of risk associated with moderate caffeine consumption.
It has often been pointed out
that caffeine is the most widely "used" psychoactive
substance in the world, and accordingly, there is a
very large amount of research available on the effects
of caffeine on body and mind. In particular, a psychostimulant
action of caffeine is generally accepted as well established;
for example, caffeine has been found to quicken reaction
time and enhance vigilance performance, and to increase
self-rated alertness and improve mood. There is, however,
a real difficulty in determining the net effects of
caffeine. In a typical experiment the subjects have
a history of regular caffeine consumption, and they
are tested on caffeine and a placebo after a period
of caffeine deprivation (often overnight). The problem
with relying solely on this approach is that it leaves
open the question as to whether the results obtained
are due to beneficial effects of caffeine or to deleterious
effects of caffeine deprivation. The present article
briefly reviews this evidence on the psychostimulant
effects of caffeine, and presents some new data testing
the hypothesis that caffeine may enhance cognitive performance
to a greater extent in older adults than in young adults.
No age-related differences in the effects of caffeine
on psychomotor performance were found. We conclude that
overall there is little unequivocal evidence to show
that regular caffeine use is likely to substantially
benefit mood or performance. Indeed, one of the significant
factors motivating caffeine consumption appears to be
OBJECTIVE: This study investigated
the effects of moderate doses of caffeine on ambulatory
blood pressure and heart rate, urinary excretion of
epinephrine, norepinephrine, and cortisol, and subjective
measures of stress during normal activities at work
and at home in the evening. METHODS: Healthy, nonsmoking,
habitual coffee drinkers (N = 47) participated in 3
days of ambulatory study. After a day of ad lib caffeine
consumption, caffeine (500 mg) and placebo were administered
double-blind in counter-balanced order on separate workdays.
Ambulatory blood pressure and heart rate were monitored
from the start of the workday until bedtime. Urinary
excretion of catecholamines and cortisol was assessed
during the workday and evening. RESULTS: Caffeine administration
significantly raised average ambulatory blood pressure
during the workday and evening by 4/3 mm Hg and reduced
average heart rate by 2 bpm. Caffeine also increased
by 32% the levels of free epinephrine excreted during
the workday and the evening. In addition, caffeine amplified
the increases in blood pressure and heart rate associated
with higher levels of self-reported stress during the
activities of the day. Effects were undiminished through
the evening until bedtime. CONCLUSIONS: Caffeine has
significant hemodynamic and humoral effects in habitual
coffee drinkers that persist for many hours during the
activities of everyday life. Furthermore, caffeine may
exaggerate sympathetic adrenal-medullary responses to
the stressful events of normal daily life. Repeated
daily blood pressure elevations and increases in stress
reactivity caused by caffeine consumption could contribute
to an increased risk of coronary heart disease in the
BACKGROUND: Many ophthalmologists
instruct patients with glaucoma to avoid coffee, although
data supporting this practice are insufficient. OBJECTIVE:
To estimate the effect of drinking coffee on intraocular
pressure (IOP). METHODS: In this crossover study, the
effect of the consumption of regular (180 mg caffeine
in 200 mL beverage) and decaffeinated coffee (3.6 mg
caffeine in 200 mL beverage) was compared in patients
with normotensive glaucoma (n = 6) or ocular hypertension
(n = 22). IOP was monitored in both groups at 30, 60,
and 90 minutes after coffee ingestion. RESULTS: In patients
with normotensive glaucoma who drank regular coffee,
the mean +/- SD changes in IOP at 30, 60, and 90 minutes
were 0.9 +/- 0.5, 3.6 +/- 1.1, and 2.3 +/- 0.66 mm Hg,
respectively; in those who drank decaffeinated coffee,
they were 0.75 +/- 0.36, 0.70 +/- 0.4, and 0.4 +/- 0.6
mm Hg, respectively. The corresponding values in patients
with ocular hypertension were as follows: after regular
coffee, 1.1 +/- 0.7, 3.4 +/- 1.0, and 3.0 +/- 2.7 mm
Hg; and after decaffeinated coffee, 0.6 +/- 0.4, 0.9
+/- 0.2, and 0.5 +/- 0.5 mm Hg. The difference in the
change in IOP from baseline after ingestion of regular
versus decaffeinated coffee was statistically significant
in each group at 60 and 90 minutes. Subjects who drank
regular coffee demonstrated a greater elevation in IOP;
this elevation may be clinically significant. CONCLUSIONS:
Intake of caffeinated beverage (>/=180 mg caffeine)
may not be recommended for patients with normotensive
glaucoma or ocular hypertension.
BACKGROUND: Whether the increase
in blood pressure with coffee drinking seen in clinical
trials persists over time and translates into an increased
incidence of hypertension is not known. METHODS: We
assessed coffee intake in a cohort of 1017 white male
former medical students (mean age, 26 years) in graduating
classes from 1948 to 1964 up to 11 times over a median
follow-up of 33 years. Blood pressure and incidence
of hypertension were determined annually by self-report,
demonstrated to be accurate in this cohort. RESULTS:
Consumption of 1 cup of coffee a day raised systolic
blood pressure by 0.19 mm Hg (95% confidence interval,
0.02-0.35) and diastolic pressure by 0.27 mm Hg (95%
confidence interval, 0.15-0.39) after adjustment for
parental incidence of hypertension and time-dependent
body mass index, cigarette smoking, alcohol drinking,
and physical activity in analyses using generalized
estimating equations. Compared with nondrinkers at baseline,
coffee drinkers had a greater incidence of hypertension
during follow-up (18.8% vs. 28.3%; P =.03). Relative
risk (95% confidence interval) of hypertension associated
with drinking 5 or more cups a day was 1.35 (0.87-2.08)
for baseline intake and 1.60 (1.06-2.40) for intake
over follow-up. After adjustment for the variables listed
above, however, these associations were not statistically
significant. CONCLUSION: Over many years of follow-up,
coffee drinking is associated with small increases in
blood pressure, but appears to play a small role in
the development of hypertension.
OBJECTIVE: We review the published
data relating to intake of coffee and caffeine on blood
pressure in man. We also refer to studies on the possible
mechanisms of actions of these effects of caffeine.
DESIGN: The MEDLINE and Current Contents databases were
searched from 1966 to April 1999 using the text words
'coffee or caffeine' and 'blood pressure or hypertension'.
Controlled clinical and epidemiologic studies on the
blood pressure effects of coffee or caffeine are reviewed.
We also refer to studies on the possible mechanisms
of action of these effects of caffeine. RESULTS: Acute
intake of coffee and caffeine increases blood pressure.
Caffeine is probably the main active component in coffee.
The pressor response is strongest in hypertensive subjects.
Some studies with repeated administration of caffeine
showed a persistent pressor effect, whereas in others
chronic caffeine ingestion did not increase blood pressure.
Epidemiologic studies have produced contradictory findings
regarding the association between blood pressure and
coffee consumption. During regular use tolerance to
the cardiovascular responses develops in some people,
and therefore no systematic elevation of blood pressure
in long-term and in population studies can be shown.
CONCLUSIONS: We conclude that regular coffee may be
harmful to some hypertension-prone subjects. The hemodynamic
effects of chronic coffee and caffeine consumption have
not been sufficiently studied. The possible mechanisms
of the cardiovascular effects of caffeine include the
blocking of adenosine receptors and the inhibition of
Because the potential impact of
habitual caffeine intake on blood pressure is a controversial
issue, a study was carried out to explore the relationship
between caffeine and various humoral factors that could
account for a coffee-induced rise in blood pressure.
Twenty-three hypertensive patients who refrained from
caffeine for 2 to 3 weeks were given 250 mg oral caffeine
powder dissolved in water. Blood pressure was recorded
every 15 min by blood pressure monitor. Caffeine blood
level, renin and endothelin were measured before and
1, 2, 3, and 6 h after caffeine intake. Urinary electrolytes
and catecholamines were measured under caffeine influence
(period I), and for the next 6 h (period II). A significant
increase in systolic (P = .017) and diastolic blood
pressure (P = .023) occurred in 13 subjects who were
58 +/- 10.4 years old. Nonresponders were younger (44.5
+/- 15.8 years). A statistically significant decrease
in heart rate was seen during the first hour after caffeine
intake in both responders (P = .008) and nonresponders
(P = .004). Marked diuresis and natriuresis were observed
during period I in both groups. Renin and endothelin
levels were unchanged. Although chronic studies point
to development of tolerance to long-term caffeine ingestion,
acute studies like the one described are essential to
obtain data on the immediate effects that can be of
practical importance, especially in the elderly.
BACKGROUND: Among the many reported
central nervous system effects of long-term caffeine
use is improvement in mood. OBJECTIVE: To examine prospectively
the relationship of coffee and caffeine intake to risk
of death from suicide. METHODS: We conducted a 10-year
follow-up study (1980 to 1990) in an ongoing cohort
of 86 626 US female registered nurses aged 34 to 59
years in 1980, who were free of diagnosed coronary heart
disease, stroke, or cancer. Information on coffee and
caffeine intake was collected by a semiquantitative
food frequency questionnaire in 1980. Deaths from suicide
were determined by physician review of death certificates.
RESULTS: Fifty-six cases of suicide occurred during
832 704 person-years of observation. Compared with non-drinkers
of coffee, the age-adjusted relative risk of suicide
in women who consumed two to three cups per day was
0.34 (95% confidence interval [CI, 0.17 to 0.68) and
0.42 (95% CI, 0.21 to 0.86) in women who consumed four
or more cups per day (P for linear trend=.002). These
findings remained essentially unchanged after adjusting
for a broad range of potential confounding factors,
including smoking habit, alcohol intake, medication
use (diazepam and phenothiazine), history of comorbid
disease (hypertension, hypercholesterolemia, or diabetes),
marital status, and self-reported stress. A strong inverse
relationship was similarly found for caffeine intake
from all sources and risk of suicide. CONCLUSIONS: The
data suggest a strong inverse association between coffee
intake and risk of suicide. Whether regular intake of
coffee or caffeine has clinically significant effects
on the maintenance of affect or the prevention of depression
merits further investigation in clinical trials and
population-based prospective studies.
OBJECTIVE. Based on a meta-analysis,
it was recently stated that there is no association
between coffee consumption and the risk of coronary
heart disease. Why then, have studies on the issue shown
quite variable results? DESIGN SETTING AND SUBJECTS.
A prospective study was performed in the Copenhagen
Male Study on 2975 men (53-74 years) without cardiovascular
disease at baseline in 1985/1986. They were classified
according to self-reported consumption of filter coffee.
Some 147 men (5%) were coffee abstainers. Potential
confounders were alcohol use, physical activity, smoking,
serum cotinine, serum lipids, serum selenium, body mass
index, blood pressure, Lewis blood group, hypertension,
non-insulin-dependent diabetes mellitus and social class.
MAIN OUTCOME MEASURES. The incidence of ischaemic heart
disease (IHD) 1985/86-1991. RESULTS. Some 184 men had
a first IHD event. There was no significant difference
between those consuming 1-4, 5-8 or > or = 9 cups per
day after controlling for confounders (P-value of trend
test: 0.14). The crude incidence rates were 6.8, 6.7
and 4.6%, respectively; the adjusted rates were 6.8,
6.7 and 4.0%, respectively. Coffee consumption was significantly
(P < 0.05) inversely correlated with serum selenium
concentration (never previously described) and, positively
or negatively, with a number of other potential risk
factors: smoking, alcohol use, serum triglycerides,
serum cholesterol, blood pressure, social class, body
mass index, and serum selenium. In nonsmokers and smokers
of only a small amount of tobacco, coffee consumption
was associated with a lower risk of IHD (P < 0.05).
CONCLUSION. We conclude that the association between
coffee consumption and risk of IHD is conditioned by
known risk factors correlated with use of coffee, which
may partly explain the inconsistencies in the results
of previous studies.
We examined the risk of coronary
heart disease (CHD) associated with coffee intake in
1040 male medical students followed for 28 to 44 years.
During the follow-up, CHD developed in 111 men. The
relative risks (95% confidence interval) associated
with drinking 5 cups of coffee/d were 2.94 (1.27, 6.81)
for baseline, 5.52 (1.31, 23.18) for average, and 1.95
(0.86, 4.40) for most recent intake after adjustment
for baseline age, serum cholesterol levels, calendar
time, and the time-dependent covariates number of cigarettes,
body mass index, and incident hypertension and diabetes.
Risks were elevated in both smokers and nonsmokers and
were stronger for myocardial infarction. Most of the
excess risk was associated with coffee drinking prior
to 1975. The diagnosis of hypertension was associated
with a subsequent reduction in coffee intake. Negative
results in some studies may be due to the assessment
of coffee intake later in life or to differences in
methods of coffee preparation between study populations
or over calendar time.
The relationship between reported
coffee consumption and specific causes of death was
examined in 9484 males enrolled in the Adventist Mortality
Study in 1960 and followed through 1985. Coffee consumption
was divided into three levels: less than 1 cup per day,
1-2 cups per day, and greater than or equal to 3 cups
per day. Approximately one third of the subjects did
not drink coffee. Cause-specific mortality rates were
compared using survival analysis including Cox's proportional
hazard model, and controlling for potential confounders
such as body mass index, heart disease and hypertension
at baseline, race, physical activity, marital status,
educational level, smoking history, and dietary pattern.
Inclusion of interaction terms between coffee consumption
and attained age as time-dependent covariates allowed
the hazard ratio to vary with age. Univariate analyses
showed a statistically significant association (p less
than 0.05) for coffee consumption and mortality for
most endpoints. Multivariate analyses showed a small
but statistically significant association between coffee
consumption and mortality from ischemic heart disease,
other cardiovascular diseases, all cardiovascular diseases,
and all causes of death. For the major causes of death,
the hazard ratios decreased from about 2.5 at 30 years
of age to 1.0 around 95 years of age. These results
indicate that abstinence from coffee leads to compression
of mortality rather than an increase in lifespan.
The data obtained from 2240 subjects
aged 65 years or more from the general population of
Castelfranco Veneto (Italy) included in the CASTEL (CArdiovascular
STudy in the ELderly) epidemiological Italian project
were analyzed in relation to coffee consumption. Subjects
were divided into 3 classes: class 1 (N = 109): non
coffee drinkers; class 2 (N = 1554): 1 to 2 cups of
coffee per day; class 3 (N = 577): 3 or more cups per
day. The results were described by ANOVA, Tukey post
hoc test and Pearson correlation coefficient with Bonferroni's
conservative correction. In classes 2 and 3 total cholesterol,
apolipoprotein B100 and calculated LDL-cholesterol were
higher than in class 1. The number of cups of coffee
per day directly correlated to both the number of cigarettes
per day and the number of drinks per week. Although
these data seem to indicate a convergence of risk factors
(cholesterol, smoking, alcohol) in coffee drinkers,
no increase in the prevalence of cardiovascular events
was found in coffee drinkers in comparison with non
drinkers. This could be attributed to the fact that
prevalence of hypertension and diabetes did not increase
with increasing coffee consumption; on the contrary,
they were lower in classes 2 and 3 than in class 1.
The effect of caffeine consumption
on mortality was evaluated in a historical cohort study
of 10,064 diagnosed hypertensive individuals participating
in the Hypertension Detection and Follow-up Program
from 1973 to 1979. Total caffeine intake level from
beverages (coffee and tea) and certain medications,
was estimated at the 1-year visit. No evidence was found
supporting an association between increased level of
caffeine consumption and increased all-cause mortality
or cardiovascular disease mortality during the following
4 years. Cigarette smoking was significantly associated
with mortality; the association being more pronounced
among non- and low-caffeine consumers for all-cause
mortality and among non-caffeine consumers for all cardiovascular
mortality except cerebrovascular mortality.
The relation between habitual
coffee consumption and blood pressure was studied in
500 Italian subjects, males and females, aged 18-62
years. After allowing for sex, age and weight, the pressure
levels showed a significant decrease with increasing
coffee consumption. Systolic blood pressure (SBP) and
diastolic blood pressure (DBP) were respectively 130.4
+/- 1.8 (SE) mmHg and 81.5 +/- 1.1 mmHg for non-coffee
drinkers, 129.4 +/- 1.4 and 82.2 +/- 0.9 mmHg for 1
cup per day, 128.4 +/- 0.8 and 81.4 +/- 0.5 mmHg for
2-3 cups per day, 124.9 +/- 1.1 and 78.8 +/- 0.7 mmHg
for 4-6 cups per day, and 124.1 +/- 2.5 and 78.7 +/-
1.6 mmHg for more than 6 cups of coffee daily (analysis
of covariance: SBP F = 3.46, 4 df, P less than 0.01;
DBP F = 3.46, 4 df, P less than 0.01). Even after correcting
pressure levels for habitual alcohol intake and cigarette
smoking, we observed a mean reduction in SBP and DBP
of 0.80 mmHg and 0.48 mmHg respectively per cup per
We conducted a prospective investigation
of the effect of coffee consumption on coronary heart
disease in 1130 male medical students who were followed
for 19 to 35 years. Changes in coffee consumption and
cigarette smoking during follow-up were examined in
relation to the incidence of clinically evident coronary
disease in comparisons of three measures of coffee intake--base-line
intake, average intake, and most recent intake reported
before the manifestation of coronary disease. Clinical
evidence of coronary disease included myocardial infarction,
angina, and sudden cardiac death. In separate analyses
for each measure of coffee intake, the relative risks
for men drinking five or more cups of coffee per day,
as compared with nondrinkers, were approximately 2.80
for all three measures in the univariate analyses (maximum
width of 95 percent confidence intervals, 1.27 to 6.51).
After adjustment for age, current smoking, hypertension
status, and base-line level of serum cholesterol, the
estimated relative risk for men drinking five or more
cups of coffee per day (using the most recent coffee
intake measure), as compared with those drinking none,
was 2.49 (maximum width of 95 percent confidence interval,
1.08 to 5.77). The association between coffee and coronary
disease was strongest when the time between the reports
of coffee intake and the coronary event was shortest.
These findings support an independent, dose-responsive
association of coffee consumption with clinically evident
coronary heart disease, which is consistent with a twofold
to threefold elevation in risk among heavy coffee drinkers.
Coffee as a rule develops stimulating
effects on the central nervous system, heart and circulation
which are mainly caused by caffeine. In certain cases
coffee may also have a sedative effect and sometimes
even it is useful to fall asleep quickly. Furthermore
coffee may be advantageous in the treatment of some
functional disorders caused by lacking of dopamine,
because coffee is able to increase the dopamine formation
in brain. Concerning the effects of coffee in the gastrointestinal-tract
and liver-bile system caffeine is only of secondary
importance. Hereby certain roasting substances, possibly
also chlorogenic acid or caffeic acid should be responsible
for the stimulating effects observed in these organs.
These stimulating effects could be caused whether directly
or indirect e.g. by liberating gastrin or other gastrointestinal
hormones. Vitamin niacin, which is formed in greater
amounts from trigonelline during the roasting process,
may also be important from the nutritional standpoint.
Therefore coffee may be prescribed as a true drug in
cases of deficiency in vitamin niacin or also in the
pellagra disease. By extensive epidemiological studies
performed lately it could be demonstrated that there
exists no correlation between coffee consumption and
certain risk factors as hypertension, heart infarction,
diabetes, gout or cancer diseases. Furthermore there
was no evidence that coffee or its caffeine content
are able to induce genetic alterations or even malformations.
OBJECTIVES: To study prospectively
the relation of coffee drinking with fatal and nonfatal
coronary heart disease (CHD) and all-cause mortality
and to perform a cross-sectional analysis at baseline
on the association between coffee drinking and CHD risk
factors, diagnosed diseases, self-reported symptoms,
and use of medicines. METHODS: The study cohort consisted
of 20 179 randomly selected eastern Finnish men and
women aged 30 to 59 years who participated in a cross-sectional
risk factor survey in 1972, 1977, or 1982. Habitual
coffee drinking, health behavior, major known CHD risk
factors, and medical history were assessed at the baseline
examination. Each subject was followed up for 10 years
after the survey using the national hospital discharge
and death registers. Multivariate analyses were performed
by using the Cox proportional hazards model. RESULTS:
In men, the risk of nonfatal myocardial infarction was
not associated with coffee drinking. The age-adjusted
association of coffee drinking was J shaped with CHD
mortality and U shaped with all-cause mortality. The
highest CHD mortality was found among those who did
not drink coffee at all (multivariate adjusted). Also,
in women, all-cause mortality decreased by increasing
coffee drinking. The prevalence of smoking and the mean
level of serum cholesterol increased with increasing
coffee drinking. Non-coffee drinkers more often reported
a history of various diseases and symptoms, and they
also more frequently used several drugs compared with
coffee drinkers. CONCLUSIONS: Coffee drinking does not
increase the risk of CHD or death. In men, slightly
increased mortality from CHD and all causes in heavy
coffee drinkers is largely explained by the effects
of smoking and a high serum cholesterol level.
STUDY OBJECTIVE: To relate habitual
(cups per day) tea and coffee consumption to conventional
coronary risk factors and subsequent risk of coronary
heart disease and death. DESIGN: Cohort study. SETTING:
Nationwide random population study. PARTICIPANTS: Over
11,000 men and women aged 40-59 who took part in the
Scottish Heart Health Study lifestyle and risk factor
survey in 1984-87. Participants were followed up to
the end of 1993, an average of 7.7 years, for all cause
mortality, coronary death, or any major coronary event
(death, non-fatal infarction or coronary artery surgery).
Cox's proportional hazards regression model was used
to estimate the hazard in consumers of tea and coffee
relative to the zero consumption group, both before
and after correction for other factors. MAIN RESULTS:
Coffee and tea consumption showed a strong inverse relation.
For many conventional risk factors, coffee showed a
weak, but beneficial, gradient with increasing consumption,
whereas increasing tea consumption showed the reverse.
Increasing coffee consumption was associated with beneficial
effects for mortality and coronary morbidity, whereas
tea showed the opposite. Adjusting for age and social
class had some effect in reducing associations. Multiple
adjustment for other risk factors removed the associations
for tea and most of those for coffee although there
was a residual benefit of coffee consumption in avoiding
heart disease among men. CONCLUSIONS: The epidemiological
differences shown in this study occurred despite the
pharmacological similarities between tea and coffee.
Either they differ more than is realised, or they identify
contrasting associated lifestyle and health risks, for
which this multiple adjustment was inadequate.
OBJECTIVE--To assess the relationship
between coffee consumption and risk of coronary heart
disease (CHD) among women. DESIGN--Prospective cohort
study with coffee consumption measured in 1980, 1984,
and 1986, and follow-up through 1990. SETTING--Female
registered nurses in the United States. PARTICIPANTS--A
total of 85,747 US women 34 to 59 years of age in 1980
and without history of CHD, stroke, or cancer. MAIN
OUTCOME MEASURE--Ten-year incidence of CHD (defined
as nonfatal myocardial infarction or fatal CHD). RESULTS--During
10 years of follow-up we documented 712 cases of CHD.
After adjustment for age, smoking, and other CHD risk
factors, we found no evidence for any positive association
between coffee consumption and risk of subsequent CHD.
For women drinking six or more cups of caffeine-containing
coffee per day in 1980, the relative risk was 0.95 (95%
confidence interval, 0.73 to 1.26) compared with women
who did not consume this beverage. Similarly, there
was no association when the first 4 years of follow-up
were excluded, when nonfatal and fatal CHD end points
were examined separately, or when we updated coffee
consumption in 1984 or 1986 and examined only CHD during
the next 2-year interval. Further, there was no association
with caffeine intake from all sources combined or with
decaffeinated coffee consumption. CONCLUSIONS--These
data indicate that coffee as consumed by US women is
not an important cause of CHD.