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COFFEE AND
HEALTH
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| There
are many different coffee drinks available, we will list
the three most popular ones. |
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COFFEE
AND ALZHEIMER’S DISEASE |
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Interest in the possibility that the consumption of coffee
or caffeine might protect against the development of Alzheimer’s
disease is growing. A retrospective Portuguese study of
54 cases of Alzheimer’s disease and 54 controls recently
demonstrated that caffeine intake over the preceding 20
years was inversely and significantly associated with risk
of Alzheimer’s disease (1). A prospective Canadian
cohort study of 4,615 elderly subjects diagnosed 194 cases
of Alzheimer’s disease and showed that coffee consumption
was inversely associated with disease risk (2). More prospective
cohort studies of the relationship between coffee and caffeine
intake and Alzheimer’s disease risk are needed.
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| COFFEE,
CAFFEINE AND ASTHMA |
|
Two large cross-sectional studies have examined the relationship
between the intake of coffee and tea and the prevalence
of asthma. A study of 72,284 Italians showed that there
was an inverse association between intake of coffee and
prevalence of asthma (1). Risk of asthma fell by 28% when
three or more cups of coffee were drunk every day. The Second
National Health and Nutrition Examination Survey (NHANES
II) studied 20,322 Americans and found that risk of current
asthma fell significantly by 29% and risk of wheeze fell
insignificantly by 13% when regular coffee drinkers were
compared with non-coffee drinkers (2). There was also a
significant dose response relationship with current asthma.
Intervention trials of effects of caffeine intake on asthma
have recently been critically reviewed (3). Nine intervention
trials of effects of caffeine on pulmonary function were
identified although three of them were excluded from the
analysis due to a variety of design faults (4, 5, 6). A
randomised controlled trial on 7 adult asthmatics was unable
to show any difference between 6 mg caffeine/kg body weight
and placebo on airway responsiveness to methacholine (7).
By contrast, a double-blind randomised crossover study of
9 adult asthmatics using four doses of caffeine up to 7.2
mg/kg body weight showed a dose response effect of caffeine
on forced expiratory volume (FEV), forced expiratory flow
(FEF) and specific airway conductance (Gaw/VL) (8). This
suggests that caffeine is an effective bronchodilator. The
effect of caffeine on FEV was confirmed in a second trial
on 8 adult asthmatics using a dose of 5 mg/kg body weight
(9). However, in 10 mild asthmatics 5 mg caffeine/kg body
weight had little if any effect on histamine provoked bronchoconstriction
(10). By contrast, the higher of two doses of caffeine (3.5
and 7 mg/kg body weight) prevented exercise- induced bronchoconstriction
in 10 asthmatics (11). In a subsequent double-blind, placebo
controlled randomised crossover trial, it was shown that
10 but not 5 mg caffeine/kg body weight reduced bronchoconstriction
induced by eucapnic voluntary hyperventilation in 11 asthmatics
(12).
The beneficial effects of caffeine on asthma have been appreciated
for over 100 years. In Scotland, caffeine has been used
to treat asthma since at least 1859 (13). Marcel Proust,
an asthmatic, wrote in A l’Ombre de Jeunes Filles
en Fleur that he used caffeine as a child which “was
prescribed to help me breathe”. He was born in 1871.
As reviewed above, modern research has confirmed that caffeine
and hence caffeine-containing beverages have a role to play
in the management of asthma.
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| COFFEE,
CAFFEINE, CALCIUM BALANCE ANDBONE HEALTH GENERAL
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A 2002 review of the scientific literature by Professor
Heaney concluded that “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" (1).
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| CALCIUM
BALANCE |
It is generally assumed that a decrease in the supply of
calcium, an essential mineral for bone formation, would
be likely to decrease bone mass and hence increase the risk
of fracture. A number of intervention trials have focused
on the effects of coffee, tea or caffeine on calcium balance.
Although such studies can show cause effect relationships
they cannot establish whether the magnitude of the effects
on calcium balance observed are large enough to influence
bone health.
A careful study of calcium balance in 170 healthy middle-aged
women examined the effects of tea and coffee consumption
(2). Multiple regression analysis showed that caffeine consumption
in the form of tea or coffee was significantly associated
with a small negative calcium balance. It was calculated
that for every cup of coffee consumed less than 5 mg calcium
was lost, probably due to increased urinary or faecal excretion.
This trial was followed by a series of studies (3, 4, 5)
from a second laboratory showing that caffeine induced a
loss of calcium in the urine. For example, it was shown
that when 37 healthy women consumed 6 mg caffeine/kg body
weight the urinary calcium loss increased in the two hour
period following caffeine consumption (5). However, it should
be noted that these caffeine intakes were unrealistically
high and that the two-hour study period was too short. A
further study from the same laboratory (6) looked at the
effects of 6 mg caffeine/kg body weight in 17 healthy males
and females on calcium excretion over a longer time period.
They found that caffeine significantly increased urinary
calcium excretion for six hours after intake, had no effect
in the subsequent nine hours and significantly decreased
urinary calcium excretion in the following three hours.
Although there was an overall net increase in urinary calcium
excretion in response to high intakes of caffeine it is
clear that two-hour study periods seriously overestimate
calcium loss in response to caffeine.
Two studies were unable to reveal any effects of more moderate
doses of caffeine on 24-hour calcium loss (7, 8, 9). A double-blind
placebo controlled crossover study with a 37-day washout
compared the effects of 400 mg caffeine/day for 19 days
with placebo in 16 healthy pre-menopausal women (7). There
were no significant effects of caffeine on calcium absorption,
urinary calcium excretion or faecal calcium excretion. This
is an important study as it looks at the effects of caffeine
consumption over the longer-term i.e. 19 days. Most other
studies have only looked at the effects of caffeine over
periods ranging from two hours to twenty-four hours.
The original calcium balance study (2) has since been expanded
by examining 191 healthy perimenopausal women on two or
three occasions over a 15-year period, generating a total
of 518 balance studies (8, 9). There were no significant
effects of caffeine-containing beverages on either urinary
calcium loss (8) or faecal calcium loss (9). However, the
negative calcium balance observed in the original study
(2) persisted in the expanded study (8,9). It was estimated
that 4 mg calcium were lost for every cup of coffee consumed
and multivariate analysis suggested that this was due to
a small but significant decrease in calcium absorption efficiency.
However, calcium intakes in the study population were only
660 mg/day or about half the recommended intake in the USA
so the effects of caffeine observed on calcium balance may
only be relevant to women with inadequate calcium intakes.
Three other studies of effects of caffeine on 24-hour urinary
calcium excretion have given mixed results (10,11,12). In
eight pre-menopausal women given 1.4 l diet cola per day
(equivalent to approximately four and a half cans) as the
sole source of caffeine for two weeks, there were no effects
on 24-hour calcium excretion (10). In twenty-five pre- and
postmenopausal women normally consuming at least 5.8 mg
caffeine/kg body weight, abstinence for 2 weeks had no effect
on urinary calcium excretion (11). By contrast, in eighty-five
postmenopausal women suffering from osteoporosis, multiple
regression analysis showed that coffee intake was inversely
associated with calcium balance (12). It was calculated
that for every 100 ml coffee consumed 6 mg calcium/day was
lost.
It can be concluded that the consumption of caffeine is
associated with a small negative calcium balance probably
arising from reduced calcium absorption efficiency. The
negative balance has been variously estimated as between
4 and 6 mg calcium/day. However, this effect is seen only
in women with inadequate calcium intakes. In addition, it
has been estimated that this small calcium deficit can be
compensated for by the addition of only 1-2 tablespoons
of milk to a caffeine-containing beverage such as coffee
(8).
|
| BONE
HEALTH |
Osteoporosis has been defined as “a disease characterised
by low bone mass and micro-architectural deterioration of
bone tissue, leading to enhanced bone fragility and a consequent
increase in fracture risk”. Like many chronic diseases
it is multifactorial. Risk factors for osteoporosis include
age, cigarette smoking, alcohol consumption, level of physical
activity and calcium intake.
As reviewed recently (13), there are at least 31 cross-sectional,
case control and cohort studies of associations between
caffeine intake and bone health involving many thousands
of subjects. The aspects of bone health measured include
bone mineral density, change in bone mineral density, fracture
rate and osteoporosis. Although these studies have the advantage
of measuring aspects of bone health directly, such observational
epidemiological studies can only demonstrate associations
and not cause effect relationships. All such studies are
subject to confounding.
Twenty-two studies have looked at associations between bone
mineral density or change in bone mineral density and caffeine
intake. Four cross-sectional studies have shown inverse
associations between bone mineral density and caffeine intake
which were weak (14), present at one skeletal site but not
at others (15) or present in the hip but not in the spine
(16, 17). By contrast, a further ten cross-sectional studies
were unable to find any associations between caffeine intake
and bone mineral density at any skeletal site (18-27). A
fifteenth cross-sectional study was able to show a negative
association between caffeine intake and bone mineral density
but only in subjects consuming inadequate amounts of calcium
(28). This finding is supported by the results of a cohort
study which found a negative association between change
in bone mineral density and caffeine intake (29). By contrast,
four other cohort studies failed to find any associations
between caffeine intake and change in bone mineral density
(30, 31, 32,33) and two other cohort studies failed to find
any associations between caffeine intake and bone mineral
density (34,35).
Eight studies have looked at associations between risk of
fracture and intake of caffeine. Four case control studies
were unable to find any associations between risk of fracture
and caffeine intake (36, 37, 38,39). A fifth case control
study used osteoporosis as an endpoint but was unable to
find any association with caffeine intake (40). By contrast,
four cohort studies reported a significant association between
caffeine intake and risk of fracture. In a subset of the
Framingham cohort, there was an incremental increase in
fracture risk for coffee consumption above two cups per
day (41). In the Nurses Health Study, the risk of hip fracture
increased three-fold with caffeine intake but only in women
younger than 65 years old (42). In the Study of Fractures
cohort, the investigators identified 17 independent risk
factors and found that caffeine intake was one of the weakest
(43). In a Norwegian study, fracture risk increased with
caffeine intake but only when coffee consumption was greater
than nine cups per day.
Out of the 31 studies cited above, 10 showed an inverse
association between consumption of caffeine- containing
beverages and some aspect of bone health and 21 found no
association. Although the available evidence is contradictory,
the weight of evidence does not support the idea that caffeine-containing
beverages adversely affect bone health. One reason for the
contradictory results is confounding. Taking one study as
an example, the inverse association observed before adjustment
for confounders between intake of caffeine containing beverages
and bone mass disappeared after adjustment for other risk
factors (20). It is also possible that intake of caffeine-
containing beverages is acting as a marker for a true causal
factor. It is known that there is an inverse relationship
between the intake of milk and consumption of caffeine-containing
beverages (8). It is possible, therefore, that a low intake
of milk rather than a high intake of caffeine-containing
beverages is a true cause of impaired bone health. This
positon was supported by Hallstrom et al (44) who examined
the relationship between consumption of coffee and tea and
total caffeine intake associated with osteoporotic fracture
risk. They found that a daily intake of 330 mg caffeine,
or more, may be associated with a modestly increased risk
of osteoporotic fractures, especially in those women with
a low calcium intake.
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|
GENERAL |
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There are no intervention trials of effects of coffee consumption
on risk of cancer at any site and consequently there is
no cause effect evidence. By contrast, there are numerous
case control and cohort studies of associations between
coffee consumption and risk of cancer at various sites particularly
the bladder, breast, colon, ovary, pancreas and kidney.
Such studies of associations cannot prove cause effect relationships
and are subject to confounding by other risk factors and
to bias. In addition, coffee consumption might be a marker
for some other aspect of lifestyle such as smoking which
is a true cause of cancer.
Associations between coffee consumption and cancer risk
have been reviewed at regular intervals. In 1997 the World
Cancer Research Fund in association with the American Institute
for Cancer Research concluded that “Most evidence
on coffee suggests that coffee drinking has no relationship
with cancer risk” (1). The authors of a 2000 scientific
review wrote that “This updated and comprehensive
overview of coffee and cancer epidemiology provides further
reassuring information on the absence of any appreciable
association between coffee intake and most common cancers,
including cancer of the genital tract, digestive tract and
of the breast” (4).
Accordingly there is no scientific reason for believing
that moderate consumption of coffee increases the risk of
developing cancer at any site. |
| BLADDER
AND LOWER URINARY TRACT CANCER |
|
A 1991 review of associations between bladder cancer and
coffee consumption identified 26 studies and analysed 22
of them (3). Sixteen studies demonstrated a higher risk
of bladder cancer in coffee consumers. In 7 of these 16
studies the association was significant and in 3 there was
evidence of a dose response relationship. There were no
associations in the other 6 studies. When non-smokers were
considered separately in 7 of these studies, the association
weakened but persisted, suggesting that confounding by smoking
is not the only explanation for the association. It was
concluded that there was a weak positive association between
risk of bladder cancer and coffee consumption but the possibility
that this was due to bias or confounding could not be excluded.
A 2000 review of all types of study published since 1991
identified an additional 3 cohort studies and 12 case control
studies (4). The authors stated in their abstract “Thus,
a strong association between coffee drinking and bladder
cancer can be excluded, although it is still unclear whether
the weak association is causal or non-specific and due to
some bias or confounding”. A 2001 review and meta-analysis
identified 34 case control studies and 3 cohort studies
(5). In agreement with previous studies, it was found that
coffee consumption increased the risk of urinary tract cancer
by approximately 20%.
Two meta-analyses of case control studies have been published.
In 1993 thirty-five case control studies published between
1971 and 1992 were identified and 7 core studies selected
for meta-analysis according to strict methodological criteria
(6). The authors concluded that “the best available
data do not suggest a clinically important association between
the regular use of coffee and development of cancer of the
lower urinary tract in men or women”. In 2000 a pooled
analysis of 10 European case control studies attempted to
eliminate confounding by cigarette smoking by considering
non-smokers only (7). It was found that the risk of bladder
cancer in coffee drinkers was no greater than in non-coffee
drinkers unless consumption was ten cups or more per day.
This is considerably greater than the average consumption
in the United Kingdom of between 3 and 4 cups per day.
Although cohort studies have more robust designs than case
control studies they have never been separately analysed.
In the Californian Seventh Day Adventist Study, 52 cases
of bladder cancer were identified in a study population
of 34,198 but there was no significant association between
coffee consumption and risk of disease (8). In a study of
7,995 Japanese American men living in Hawaii, 96 cases of
bladder cancer were diagnosed and although coffee consumption
was associated with an increase in bladder cancer risk this
was not significant (9). In a study of almost 43,000 Norwegian
men and women, 53 cases of bladder cancer were identified,
but no significant associations between a coffee consumption
greater than or equal to 7 cups per day and disease risk
emerged either in men or women (10). The most recently published
study of a subcohort of the Netherlands Cohort Study identified
569 bladder cancer cases in a study population of 3,123
men and women (11). After adjustment for all confounders,
a non-significant association between bladder cancer risk
and coffee consumption was observed in men but a significant
inverse association in women. Hence there is no evidence
from cohort studies that coffee consumption increases the
risk of bladder cancer.
It can be concluded that the increased risk of bladder cancer
associated with coffee consumption which is sometimes observed
is probably due to confounding by smoking. In addition,
such associations are only observed in retrospective case
control studies which have weaker designs and not in prospective
cohort studies which have stronger designs.
|
| BREAST
CANCER
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|
A 1991 review of the literature identified 7 case control
studies none of which showed any association between coffee
consumption and risk of breast cancer (3). By 2000, a further
three cohort studies and four case control studies had been
published (4). The three cohort studies and three of the
four case control studies were also unable to show any association
between the risk of breast cancer and coffee consumption.
By contrast, the fourth case control study from Finland
demonstrated an inverse association between coffee consumption
and risk of breast cancer in postmenopausal women (12).
The authors concluded that “there is no appreciable
relation between coffee and cancer of the breast”.
At least seven cohort studies of associations between coffee
consumption and breast cancer risk have been published.
Studies of 23,912 male and female Californian Seventh-day
Adventists (13), 2,891 Norwegian women (14), 14,593 Norwegian
women (15), 89,494 female nurses from the USA (16), 18,586
postmenopausal women living in New York State (17), 34,388
postmenopausal women living in Iowa (18) and 59,036 Swedish
women (19) found no significant associations between risk
of breast cancer and coffee consumption.
Male breast cancer also exists although it is a much rarer
disease. A recent population-based case control study from
Canada which compared 81 cases with 1905 controls found
an inverse and statistically significant association between
coffee consumption and risk of male breast cancer both before
and after correction for confounders (20). The possibility
that coffee consumption protects against male breast cancer
awaits confirmation by other studies.
There is no evidence whatever for an association between
female breast cancer and coffee consumption.
|
| COLORECTAL
CANCER |
|
Case control studies and cohort studies give different messages
about associations between coffee consumption and risk of
colorectal cancer. Out of the 12 “informative”
case control studies identified in a 1991 review, 11 showed
an inverse association between coffee consumption and the
risk of colorectal cancer (3). In 5 of these case control
studies the association was statistically significant and
a significant dose response relationship was demonstrated
in one of them. By contrast, none of the four cohort studies
reviewed showed any evidence of an inverse association between
coffee consumption and risk of colorectal cancer.
A 2000 review identified 2 new cohort studies and 11 new
case control studies published since 1991 (4). In their
abstract the authors wrote that “Overall evidence
on the coffee-colorectal cancer relation suggests an inverse
association, since most case control studies found odds
ratios below unity, particularly for colon cancer. The pattern
of risk is less clear for cohort studies”. A population
based case control study published since the 2000 review
was published also reported an inverse association between
coffee consumption and risk of colon cancer with evidence
of a significant dose response relationship (21).
A similar conclusion was arrived at in a meta-analysis published
in 1998 of the 12 case control studies and 5 cohort studies
which met the selection criteria of the study (22). When
the case control studies were analysed separately, then
coffee consumption lowered the risk of colorectal cancer
by 28%. However, when the 5 cohort studies were analysed
separately, then coffee consumption lowered the risk of
colorectal cancer by only 3%. When both types of study were
combined the reduction in risk was 24% due to the larger
number of case control studies. The lower risk of colorectal
cancer in heavy coffee drinkers was observed in studies
from Asia, Northern and Southern Europe and North America.
The author suggested that ongoing cohort studies might help
resolve the discrepancy between the results of case control
studies and cohort studies.
Cohort studies have a stronger experimental design than
case control studies. In a study of nearly 43,000 Norwegian
men and women where 130 cases of colon cancer and 79 cases
of rectal cancer were diagnosed, there were no significant
associations between coffee consumption and disease risk
(10). When 27,111 male Finnish smokers were studied, 106
cases of colon cancer and 79 cases of rectal cancer were
identified but no associations between coffee consumption
and disease risk were reported (23). In the most recently
published study, 460 new cases of colorectal cancer were
diagnosed in a cohort of 61,463 Swedish women but no association
between risk of colorectal cancer and coffee consumption
was shown (24).
The disagreement between the results of case control studies
and cohort studies remains to be resolved. On the one hand,
the results of prospective cohort studies showing no protective
effect of coffee against colorectal cancer are more reliable
than the results of retrospective case control studies showing
a protective effect. On the other hand, there is a remarkable
degree of consistency in the results of case control studies.
It is hard to imagine how a methodological artefact could
account for this consistency.
|
| OVARIAN
CANCER |
|
Twelve case control studies of associations between consumption
of coffee and risk of ovarian cancer have been published
(25-36). Nine of these studies were unable to show any consistent
or significant associations (25-33). However, two of these
studies indicated a consistent and significant association
between coffee consumption and risk of ovarian cancer was
demonstrated (34, 35). A population-based case control study
from the USA of 549 cases of ovarian cancer and 516 controls
showed no significant association between coffee or caffeine
consumption and risk of ovarian cancer (36).
However, when pre-menopausal and postmenopausal women were
analysed separately, the consumption of coffee or caffeine
was significantly associated with risk of ovarian cancer
in pre-menopausal but not in postmenopausal women.
Two cohort studies have also examined associations between
coffee consumption and ovarian cancer risk. A study of 23,912
Californian Seventh-day Adventists found no association
between coffee consumption and fatal ovarian cancer (13).
A study of 21,238 Norwegian women found 93 cases of ovarian
cancer but no significant associations with coffee consumption
(10).
It can be concluded that there is no consistent evidence
for a link between coffee or caffeine consumption and the
risk of developing ovarian cancer.
|
PANCREATIC
CANCER |
A case control study from the USA published in 1981 suggesting
a two to three fold increase in risk of pancreatic cancer
associated with drinking three or more cups of coffee per
day stimulated an enormous amount of research in this area
(37). In 1987 a pooled analysis of nine epidemiological
studies gave a relative risk of 1.3 for moderate coffee
drinkers and 1.6 for heavy coffee drinkers when the original
study was included in the analysis but only 1.2 and 1.4
when it was excluded (38). By 1990 when thirty epidemiological
studies were reviewed it was concluded that the evidence
did not support the hypothesis that coffee consumption increases
the risk of pancreatic cancer (39). In 1991 twenty-six case
control studies were reviewed and it was concluded that
“the data are suggestive of a weak relationship between
high levels of coffee consumption and the occurrence of
pancreatic cancer, but the possibility that this is due
to bias or confounding is tenable” (3). In addition
none of the six cohort studies reviewed reported a significant
association between pancreatic cancer risk and coffee consumption.
By 2000 an additional twelve case control studies and four
cohort studies had been published (4). Nine of these case
control studies reported no association, one reported an
inverse association and two reported a positive association.
None of the four cohort studies reported any significant
associations. It was concluded that “a strong association
between coffee and pancreatic cancer can now be excluded;
however, the presence of some moderate and inconsistent
association may deserve further investigations”.
As has recently been pointed out, there is a particular
reason for distrusting the results of case control studies
on pancreatic cancer as poor survival leads to reduced participation
rates by cases in interviews and consequently more interviews
with surrogates (40). A clearer picture of the relationship
between coffee consumption and pancreatic cancer is likely
to emerge from a consideration of cohort studies only.
At least thirteen cohort studies of associations between
coffee consumption and pancreatic cancer risk have been
published and the vast majority of these found no significant
associations. Thus studies of 23,912 Californian Seventh-day
Adventists (13), 50,000 USA college alumni (41), 7,355 Japanese
men living in Hawaii (42), nearly 43,000 Norwegian men and
women (10), 34,000 Californian Seventh-day Adventists (43),
122,894 men and women living in California (44), 17,633
American men (45), 13,979 elderly Americans (46), 175,000
Americans (47), 47,794 American men and 88,799 American
women (40) and 12,204 Swedish women and 9,608 Swedish men
(48) were all unable to show significant associations between
coffee consumption and risk of pancreatic cancer. By contrast,
a study of 265,118 Japanese men (49) and 33,976 postmenopausal
women from Iowa (50) reported a significant positive association
between pancreatic cancer risk and coffee consumption. Nevertheless
the weight of cohort evidence remains firmly against the
concept that coffee drinking increases the risk of developing
pancreatic cancer.
It can be concluded that while some case control studies,
particularly the earlier ones, suggest that coffee drinking
is associated with an increase in the risk of pancreatic
cancer, the vast majority of cohort studies do not support
the idea. Since there are no intervention trials published
on the effect of coffee drinking on the risk of pancreatic
cancer then there is no evidence for a cause effect relationship.
|
| RENAL
CANCER |
As noted on a 1991 review (3), out of four case control
studies, three showed that coffee consumption was associated
with a slight increase in risk of transitional cell cancers
of the renal pelvis and ureter but none of the associations
was significant. In addition, six case control studies and
one cohort study failed to provide consistent evidence of
an association between coffee drinking and adenocarcinoma
of the kidney.
Subsequent studies have also failed to provide any consistent
evidence for an association between coffee consumption and
renal cancer. No significant associations were shown between
coffee consumption and renal cancer in case control studies
of 203 cases from the USA (51), 240 cases from Italy (52),
196 cases from France (53) and 518 cases from Canada (54).
A cohort study from Norway was also unable to demonstrate
any significant associations between renal cancer and coffee
consumption (10). Finally, a case control study carried
out in Australia, Denmark, Sweden and the United States
which analysed 1,185 cases of renal cancer was also unable
to show any consistent or significant associations nor any
evidence for a dose response relationship (55). A 2000 review
of these data concluded that “epidemiological data
on the relation between coffee consumption and kidney cancer
risk are reassuring” (4).
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| OCHRATOXIN
A |
|
Ochratoxin A is one of a family of mycotoxins produced by
the mould Penicillium verrucosum and by several species
of Aspergillus including A. ochraceus, A. carbonarius and
A. niger. Chemically it consists of a chlorinated isocoumarin
moiety linked through a carboxyl group to L-phenylalanine
via an amide bond. The major food contaminated by ochratoxin
A is cereals but much lower levels of contamination may
be found in grape juice and red wine, coffee, cocoa, nuts,
spices and dried fruits, and other agricultural products
subjected to conditions that result in mould growth. Ochratoxin
A is an accepted nephrotoxin and in animals is a carcinogen
and is also teratogenic and immunotoxic. The Joint FAO/WHO
Expert Committee on Food Additives (JECFA) has set a provisional
tolerable weekly intake (PTWI) of 100 ng/kg body weight
although the Canadian authorities have set a lower tolerable
daily intake (TDI) of 1.5 to 5.7 ng/kg body weight and the
European Commission a TDI of not more than 5 ng/kg body
weight (56).
Ochratoxin A production by Penicillium verrucosum is characteristic
of cereals. By contrast, a recent study of 408 Brazilian
coffee samples identified Aspergillus ochraceus as the major
source of ochratoxin A followed by Aspergillus carbonarius
(57). Aspergillus niger was an unimportant source. It was
also found that there was little infection of coffee cherries
while on the tree but infection occurred postharvest, the
most likely sources being soil, equipment and drying yard
surfaces. Improvements in good agricultural practices have
reduced ochratoxin A contamination of coffee.
Processing also lowers the ochratoxin A content of coffee.
Roasting dramatically lowers the ochratoxin A content of
coffee by 50-90% (58), 30-90% (59) or 81% (60). It has also
been reported that decaffeination lowers the ochratoxin
A content of coffee by 92% (61).
It has recently been estimated that mean total intakes of
ochratoxin A are 45 ng/kg body weight per week assuming
a body weight of 60 kg (62). Cereals and wine contribute
about 25 and 10 ng/kg body weight per week respectively
whereas grape juice and coffee each contribute only 2-3
ng/kg body weight per week. Other foods such as dried fruits,
beer, tea, milk, cocoa, poultry and pulses contributed less
than 1 ng/kg body weight per week. These estimates underline
the conclusion of the Ministry of Agriculture, Fisheries
and Food that coffee is not a major source of ochratoxin
A in the normal diet (63).
|
| LIVER
CANCER |
In recent years studies have suggested that coffee drinking
may be protective against the development of hepatocellular
carcinoma independently of its aetiology. Coffee has been
studied extensively in relation to other conditions affecting
the liver and this is reported elsewhere on this site. In
2005 Japanese researchers (64) published their findings
after conducting a large-scale population-based cohort study
that confirmed a statistically significant inverse association
between habitual coffee drinking and hepatocellular carcinoma.
A further hospital based case-control study conducted in
Italy (65) with 250 cases and 500 controls reached similar
conclusions. Finally, the findings of these studies were
further endorsed by Shimazu et al (66) who, using pooled
analysis consisting of over 60,000 people, found a significant
inverse association between coffee consumption and the risk
of liver cancer.
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