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Abstract

Caffeine is the most widely consumed drug in the world with coffee representing a major source of intake. Despite widespread availability, various medical conditions necessitate caffeine-restricted diets. Patients on certain prescription medications are advised to discontinue caffeine intake. Such admonition has implications for certain psychiatric patients because of pharmacokinetic interactions between caffeine and certain anti-anxiety drugs. In an effort to abstain from caffeine, patients may substitute decaffeinated for caffeinated coffee. However, decaffeinated beverages are known to contain caffeine in varying amounts. The present study determined the caffeine content in a variety of decaffeinated coffee drinks. In phase 1 of the study, 10 decaffeinated samples were collected from different coffee establishments. In phase 2 of the study, Starbucks espresso decaffeinated (N=6) and Starbucks brewed decaffeinated coffee (N=6) samples were collected from the same outlet to evaluate variability of caffeine content of the same drink. The 10 decaffeinated coffee samples from different outlets contained caffeine in the range of 0-13.9 mg/16-oz serving. The caffeine content for the Starbucks espresso and the Starbucks brewed samples collected from the same outlet were 3.0-15.8 mg/shot and 12.0-13.4 mg/16-oz serving, respectively. Patients vulnerable to caffeine effects should be advised that caffeine may be present in coffees purported to be decaffeinated. Further research is warranted on the potential deleterious effects of consumption of "decaffeinated" coffee that contains caffeine on caffeine-restricted patients. Additionally, further exploration is merited for the possible physical dependence potential of low doses of caffeine such as those concentrations found in decaffeinated coffee.
Journal of Analytical Toxicology, Vol. 30, October 2006
Technical Note I
Caffeine Content of Decaffeinated Coffee
Rachel R. McCusker 1, Brian Fuehrlein 2, Bruce
A. Goldberger 1,3,*, Mark S. Gold 3, and Edward J.
Cone 4
I Department of Pathology, Immunology and Laboratory Medicine, 2Department of Biomedical Engineering,
3Department of Psychiatry, University of Florida College of Medicine, Gainesville, Florida and 4ConeChem Research, LL C
441 Fairtree Drive, Severna Park, Maryland 21146
Abstract
Caffeine is the most widely consumed drug in the world with
coffee representing a major source of intake. Despite widespread
availability, various medical conditions necessitate caffeine-
restricted diets. Patients on certain prescription medications are
advised to discontinue caffeine intake. Such admonition has
implications for certain psychiatric patients because of
pharmacokinetic interactions between caffeine and certain anti-
anxiety drugs. In an effort to abstain from caffeine, patients may
substitute decaffeinated for caffeinated coffee. However,
decaffeinated beverages are known to contain caffeine in varying
amounts. The present study determined the caffeine content in a
variety of decaffeinated coffee drinks. In phase I of the study, 10
decaffeinated samples were collected from different coffee
establishments. In phase 2 of the study, Starbucks | espresso
decaffeinated (N -- 6) and Starbucks brewed decaffeinated coffee
(N = 6) samples were collected from the same outlet to evaluate
variability of caffeine content of the same drink. The 10
decaffeinated coffee samples from different outlets contained
caffeine in the range of 0-13.9 mg/16-oz serving. The caffeine
content for the Starbucks espresso and the Starbucks brewed
samples collected from the same outlet were 3.0-15.8 mg/shot and
12.0-13.4 mg/16-oz serving, respectively. Patients vulnerable to
caffeine effects should be advised that caffeine may be present in
coffees purported to be decaffeinated. Further research is
warranted on the potential deleterious effects of consumption of
"decaffeinated" coffee that contains caffeine on caffeine-restricted
patients. Additionally, further exploration is merited for the
possible physical dependence potential of low doses of caffeine
such as those concentrations found in decaffeinated coffee.
Introduction
Caffeine (1,3,7-trimethylxanthine) is the most widely con-
sumed psychostimulant in the world. Its physiological effects in-
clude diuresis, central nervous system stimulation, coronary
vessel dilation, gastric acid secretion stimulation, and free fatty
* Author to whom correspondence should be addressed: Bruce A. Goldberger, Ph.D.,
Department of Pathology, Immunology and Laboratory Medicine, University of Florida
College of Medicine, P.O. Box 100275, Gainesville, FL 32610-0275.
E-mail: bruce-goldberger@u fl.edu.
acids and glucose elevation (1). Caffeine containing beverages
are popular, in part, due to decreased fatigue, increased mental
acuity and improved cognitive functioning following the in-
take of moderate doses (2). Despite these desirable effects, var-
ious medical conditions including hypertension and arrhyth-
mias call for health care professionals to recommend
caffeine-free diets. Additionally, patients on certain prescription
medications are also advised to discontinue their caffeine intake.
The U.S. Food and Drug Administration has suggested the
avoidance of the concomitant administration of caffeine with
bronchodilators, anti-anxiety drugs, and quinolones (3). In
those patients with autosomal dominant polycystic kidney dis-
ease, caffeine is a risk factor for the promotion of cyst enlarge-
ment. For this reason, the Polycystic Kidney Foundation rec-
ommends that these patients eliminate the use of caffeinated
substances (4). In an effort to abstain from caffeine for the pre-
viously mentioned health concerns, many people substitute
decaffeinated for caffeinated coffee, sometimes unaware that
these beverages contain caffeine. In the present study, the caf-
feine content of decaffeinated coffee beverages was determined
for beverages collected from a variety of coffee establishments.
Methods
Twenty-two decaffeinated coffee beverages were purchased
and evaluated for caffeine content. In phase I of the study, six
brewed decaffeinated coffee beverages (D1-D6) were purchased
from various coffee shops in Severna Park and Bethesda, MD.
In addition, four brewed decaffeinated beverages (D13-D16)
were purchased from various restaurants in Gainesville, FL. In
phase 2 of the study, six decaffeinated espresso coffee beverages
(El-E6) brewed from the same batch and six brewed decaf-
feinated coffee beverages (D7-D12) from the same batch were
purchased from the same Starbucks coffee shop in Gainesville,
FL on Day 1 and Day 2, respectively. Caffeine was quantitated
in the coffee beverages utilizing a gas chromatographic tech-
nique previously reported (5). Quantitation of caffeine was
based on a calibration curve prepared in a concentration range
of 10-100 mg/L, with the limit of quantitation arbitrarily set at
the concentration of the lowest standard.
Reproduction (photocopying) of editorial content of this journal is prohibited without publisher's permission.
611
Results
The results of the caffeine analyses of the various decaf-
feinated coffee samples purchased from various coffee shops
and eating establishments (phase 1) are shown in Table I. The
store, brand, and the country of origin, if known, along with
the measured caffeine dose (rag) based on a 16-oz serving size
are also listed. In phase 1 of the study, the 10 decaffeinated
coffee samples had a caffeine concentration in the range of
0-13.9 mg per 16-oz serving.
The results of the caffeine analyses of the Starbucks espresso
decaffeinated coffee samples purchased on Day 1 from the same
outlet (phase 2) appear in Table II. The caffeine concentration
Table I. Phase l mDecaffeinated Coffee Samples
Caffeine Dose
Sample # Store Type/Brand (mg/16 oz)
D1 The Big Bean
TM
Brewed, blended 10.1
D2 The Big Bean Brewed, Italian
Roast, country origin,
Columbia 10.6
D3 Starbucks Brewed 8.6
D4 Royal Farms | Brewed 8.6
D5 Dunkin' Donuts | Brewed 10.1
D6 Hampden Caf~ Brewed, Antigua, 10.6
Guatemala
D13 Krispy Kreme Brewed 13.9
Doughnuts |
D14 Krystal | Folgers | Instant none
detected
D15 Gainesville Doughnuts Brewed t0.1
DI6 McDonald's | Brewed 11.5
Table II. Phase 2--Starbucks
Espresso Decaffeinated
Caffeine Concentration
Sample
# (mg/shot)
E1 75.8
E2 3.3
E3 4.1
E4 3.0
E5 12.7
E6 3.2
Table Ill. Phase 2--Starbucks Brewed Decaffeinated
Caffeine Concentration
Sample
# (mg/16 oz)
D7 12.0
D8 12.5
D9 13.0
D10 13.4
Dll 13.4
D12 13.0
Journal of Analytical Toxicology, Vol. 30, October 2006
of these specialty drinks are in the range of 3.0-15.8 mg per
shot (1-oz). The intra-assay mean (N = 6), standard deviation,
and % C.V. were 7.0 mg/serving, 5.7 and 81.5, respectively. The
results of the caffeine analyses of the Starbucks brewed decaf-
feinated coffee purchased on Day 2 from the same outlet (also
phase 2) appear in Table III. The caffeine concentrations of
these drinks were in the range of 12.0-13.4 mg per 16-oz
serving. The intra-assay mean (N = 6), standard deviation, and
% C.V. were 12.9 rag/serving, 0.6, and 4.4, respectively.
Discussion
The caffeine content of decaffeinated coffee obtained from
different establishments was variable ranging from none de-
tected to 13.9 mg per 16-oz serving. The six espresso decaf-
feinated samples demonstrated considerable variability ranging
from 3.0 to 15.8 mg of caffeine per shot. The variability in the
espresso beverage may more accurately be attributed to human
manipulation involved in the production of the espresso ex-
traction. In comparison, an earlier study found a caffeine con-
centration range of 18-48 mg/]2-oz serving in a variety of
popular caffeinated carbonated sodas (6). Further, in another
study the average caffeine content of brewed caffeinated spe-
cialty coffees was found to be 188 mg/16-oz serving (5).
The finding that decaffeinated coffee contains caffeine has
far-reaching clinical consequences. Clinicians and patients
should be aware that decaffeinated coffee frequently contains
caffeine. Ingestion of multiple servings of decaffeinated bev-
erages could result in caffeine doses equivalent to a caffeinated
beverage. In addition, one must be mindful of the potential for
pharmacological interactions that exist between caffeine and
prescription medications (7).
Caffeine fits the criteria for physical dependence potential.
The literature lends support to the notion that caffeine exhibits
reinforcing effects. Even low doses of caffeine have been found
to exhibit these effects which are demonstrated by self-ad-
ministration greater than that of a placebo. One double-blind
study enlisting heavy coffee drinkers found evidence for the re-
inforcement of caffeine with doses as low as 25 rag/cup being
consumed at a slightly higher rate than decaffeinated coffee
containing 2 rag/cup (8).
One study reported the reinforcing effects of decaffeinated
coffee, finding higher levels of self-administration of decaf-
feinated prepared capsules than placebo capsules (9). One pos-
sible explanation for a steady consumption of decaffeinated
coffee might be due to the reinforcing effects of the low doses
of caffeine present in decaffeinated coffee, concentrations com-
parable to those found in the current study.
Further evidence for the reinforcing effects of low doses of
caffeine was found in another study among moderate caffeine
consumers. More than half of the subjects discriminated 18 mg
of caffeine, and one discriminated 10 mg of caffeine. All sub-
jects based their discrimination on changes in mood, such as
alertness, well-being, motivation, concentration, and energy
(10). Another double-blind study found that coffee containing
25 mg of caffeine was repeatedly self-administered in two of the
612
Journal of Analytical Toxicology, Vol. 30, October 2006
six moderate coffee drinkers. The authors suggested that these
reinforcing effects were not the result of a single dose, but a se-
ries of several caffeine doses (11).
One study also explored the relationship of caffeine tolerance
to the reinforcing effects of caffeine. Subjects who had previ-
ously consumed caffeinated coffee for an average of 10 days
were given the choice between caffeinated and decaffeinated
coffee, all preferred the caffeinated, stating that it was more
stimulating. These subjects also complained that the decaf-
feinated provided low stimulation. In contrast, another group
was subjected to a decaffeinated background condition (i.e.,
subjects consumed decaffeinated coffee for one week or more
before being given a choice) and upon given a choice, all found
the decaffeinated to be satisfactory. However, when the decaf-
feinated group was given caffeinated beverages, all complained
about the high stimulatory effects (12). It may be plausible
based on this study that caffeine served as a reinforcer only for
caffeine-tolerant subjects.
Another study evaluated the effects of substituting various
doses of caffeine or placebo for a 300 rag/day maintenance
dose. It was found that substituting lower doses of caffeine or
placebo resulted in an increase in withdrawal symptoms, such
as drowsiness, headache, impaired concentration and decreased
sociability. When caffeine doses in the range of 25-100 rag/day
were substituted for the 300 mg/day maintenance dose, such
withdrawal symptoms were reported as mild. Ratings of severe
withdrawal with the main symptom being headache were sig-
nificantly increased only when placebo was substituted. Thus,
it may be concluded that caffeine physical dependence can
occur with lower caffeine doses than previously thought (13).
Although it may be concluded that caffeine is responsible for
the reinforcing effects as seen in the previously mentioned
studies, one study found the total amount of decaffeinated
coffee and caffeinated coffee consumed did not differ greatly
(8). Such evidence has led to the proposal that other sub-
stances in decaffeinated coffee might be responsible for its re-
inforcing effects. One explanation for such effects suggests
that the decaffeinated coffee self-administration is due to the
presence of one or more chemical components found in both
decaffeinated and caffeinated coffee that exhibit opiate receptor
binding activity (14).
As reflected by the data collected in the present study, low
doses of caffeine are present in coffees purported to be decaf-
feinated. Therefore, substitution of decaffeinated coffee for caf-
feinated in an effort to eliminate caffeine consumption may
not be effective for patients on a caffeine-restricted or abstinent
diet. Further, it is possible that consumption of low doses of caf-
feine such as those found in decaffeinated coffee may demon-
strate physical dependence through its reinforcing effects and
avoidance of withdrawal symptoms. Consumption of multiple
servings throughout the day of decaffeinated coffee with an av-
erage caffeine concentration as found in the current study may
achieve concentrations supporting the physical dependence
potential of caffeine. On the other hand, the steady consumption
of decaffeinated coffee may be attributed merely to its pleasing
taste or the desire for the ingestion of a warm beverage.
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Using comet assay DNA damage in the cells of Hypothenemus hampei adults was assessed following irradiation from a 60Co source at gamma radiation doses 10, 20, 40, 80, 160, 320, 640, 1600 and 3200 Gy. The survival of exposed adults at different interval of time was assessed for the same doses of radiation. Radiation-induced DNA damage measured by increased strand breaks at higher doses was significantly different from intact cells found in control, where the increase in damage was dose-dependent. The survival of the exposed adults was dose-dependent. Doses of 1600 and 3200 Gy resulted in 100% mortality within 15 days of irradiation. The absence of significant radiation induced changes in DNA damage and survival of adults at lower doses indicates greater tolerance to radiation. The study provides useful information about the radiation sensitivity of H. hampei to develop an effective method for the control of the borer in harvested coffee.
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In a residential research ward the reinforcing and subjective effects of caffeine were studied under double-blind conditions in volunteer subjects with histories of heavy coffee drinking. In Experiment 1, 6 subjects had 13 opportunities each day to self-administer either a caffeine (100 mg) or a placebo capsule for periods of 14 to 61 days. All subjects developed a clear preference for caffeine, with intake of caffeine becoming relatively stable after preference had been attained. Preference for caffeine was demonstrated whether or not preference testing was preceded by a period of 10 to 37 days of caffeine abstinence, suggesting that a recent history of heavy caffeine intake (tolerance/dependence) was not a necessary condition for caffeine to function as a reinforcer. In Experiment 2, 6 subjects had 10 opportunities each day to self-administer a cup of coffee or (on different days) a capsule, dependent upon completing a work requirement that progressively increased and then decreased over days. Each day, one of four conditions was studied: caffeinated coffee (100 mg/cup), decaffeinated coffee, caffeine capsules (100 mg/capsule), or placebo capsules. Caffeinated coffee maintained the most self-administration, significantly higher than decaffeinated coffee and placebo capsules but not different from caffeine capsules. Both decaffeinated coffee and caffeine capsules were significantly higher than placebo capsules but not different from each other. In both experiments, subject ratings of "linking" of coffee or capsules covaried with the self-administration measures. These experiments provide the clearest demonstrations to date of the reinforcing effects of caffeine in capsules and in coffee.
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In a residential research ward coffee drinking was studied in 9 volunteer human subjects with histories of heavy coffee drinking. A series of five experiments was undertaken to characterize adlibitum coffee consumption and to investigate the effects of manipulating coffee concentration, caffeine dose per cup, and caffeine preloads prior to coffee drinking. Manipulations were double-blind and scheduled in randomized sequences across days. When cups of coffee were freely available, coffee drinking tended to be rather regularly spaced during the day with intercup intervals becoming progressively longer throughout the day; experimental manipulations showed that this lengthening of intercup intervals was not due to accumulating caffeine levels. Number of cups of coffee consumed was an inverted U-shaped function of both coffee concentration and caffeine dose per cup; however, coffee-concentration and dose-per-cup manipulations did not produce similar effects on other measures of coffee drinking (intercup interval, time to drink a cup, within-day distribution of cups). Caffeine preload produced dose-related decreases in number of cups consumed. As a whole, these experiments provide some limited evidence for both the suppressive and the reinforcing effects of caffeine on coffee consumption. Examination of total daily coffee and caffeine intake across experiments, however, provides no evidence for precise regulation (i.e., titration) of coffee or caffeine intake.
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In a residential research ward coffee drinking was studied in nine volunteer human subjects with histories of heavy coffee drinking. The presence or absence of caffeine in the coffee was manipulated under double-blind conditions by using caffeinated (C) or decaffeinated (D) coffee. When subjects were switched alternately for 10 or more consecutive days between C and D, the daily number of cups consumed tended to be relatively stable. In a different experiment, preference for C vs. D was assessed. After experimenter-scheduled exposures, subjects were given choices between C and D. When subjects were presumably caffeine tolerant/dependent, C was rated as being better liked than D and was reliably preferred to D in choice tests. When subjects were not caffeine tolerant/dependent, C was not reliably preferred to D, nor were there pronounced differences in ratings of liking. Under these conditions, some subjects preferred D to C, citing adverse symptoms (suggesting caffeine toxicity) as reasons for avoiding C. The effects of caffeine withdrawal were studied by abruptly substituting D for C for 10 or more days. This resulted in an orderly withdrawal syndrome, having an onset latency of 19 hr, peaking on days 1 and 2, and decreasing progressively over the next 5 or 6 days. The withdrawal syndrome, which was detected on subject-rated, staff-rated and objective behavioral measures, was characterized by increased headache, sleepiness and laziness and decreased alertness and activeness. The present study demonstrates the reinforcing effects of caffeine in humans and also documents the severity of the caffeine withdrawal syndrome. It is concluded that caffeine has the cardinal features of a prototypic drug of abuse.
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Although caffeine is the most widely used behaviorally active drug in the world, caffeine physical dependence has been only moderately well characterized in humans. Four double-blind experiments were conducted in independent groups of healthy participants to assess the conditions under which withdrawal symptoms occur upon cessation of low to moderate doses of caffeine. In experiment 1, there was no evidence that the range or magnitude of caffeine withdrawal symptoms differed when 300 mg of caffeine was consumed as a single dose in the morning versus 100 mg at three time points across the day. In experiment 2, both the range and severity of withdrawal increased as a function of caffeine maintenance dose (100, 300, and 600 mg/day), with even the lowest dose (100 mg) producing significant caffeine withdrawal. Experiment 3 showed that when individuals were maintained on 300 mg caffeine/day and tested with a range of lower doses (200, 100, 50, 25, and 0 mg/day), a substantial reduction in caffeine consumption (</=100 mg/day) was necessary for the manifestation of caffeine withdrawal. Experiment 4 manipulated duration of exposure to caffeine (1, 3, 7, or 14 days of 300 mg/day) and showed that caffeine withdrawal occurred after as little as 3 days of caffeine exposure, with a somewhat increased severity of withdrawal observed after 7 or 14 days of exposure. As a whole, this set of experiments provides the most complete parametric characterization of caffeine withdrawal to date and suggests that caffeine physical dependence can occur under more modest conditions (i.e., fewer doses per day, lower daily dose, shorter duration of exposure) than previously recognized.
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Caffeine from dietary sources (mainly coffee, tea and soft drinks) is the most frequently and widely consumed CNS stimulant in the world today. Because of its enormous popularity, the consumption of caffeine is generally thought to be safe and long term caffeine intake may be disregarded as a medical problem. However, it is clear that this compound has many of the features usually associated with a drug of abuse. Furthermore, physicians should be aware of the possible contribution of dietary caffeine to the presenting signs and symptoms of patients. The toxic effects of caffeine are extensions of their pharmacological effects. The most serious caffeine-related CNS effects include seizures and delirium. Other symptoms affecting the cardiovascular system range from moderate increases in heart rate to more severe cardiac arrhythmia. Although tolerance develops to many of the pharmacological effects of caffeine, tolerance may be overwhelmed by the nonlinear accumulation of caffeine when its metabolism becomes saturated. This might occur with high levels of consumption or as the result of a pharmacokinetic interaction between caffeine and over-the-counter or prescription medications. The polycyclic aromatic hydrocarbon-inducible cytochrome P450 (CYP) 1A2 participates in the metabolism of caffeine as well as of a number of clinically important drugs. A number of drugs, including certain selective serotonin reuptake inhibitors (particularly fluvoxamine), antiarrhythmics (mexiletine), antipsychotics (clozapine), psoralens, idrocilamide and phenylpropanolamine, bronchodilators (furafylline and theophylline) and quinolones (enoxacin), have been reported to be potent inhibitors of this isoenzyme. This has important clinical implications, since drugs that are metabolised by, or bind to, the same CYP enzyme have a high potential for pharmacokinetic interactions due to inhibition of drug metabolism. Thus, pharmacokinetic interactions at the CYP1A2 enzyme level may cause toxic effects during concomitant administration of caffeine and certain drugs used for cardiovascular, CNS (an excessive dietary intake of caffeine has also been observed in psychiatric patients), gastrointestinal, infectious, respiratory and skin disorders. Unless a lack of interaction has already been demonstrated for the potentially interacting drug, dietary caffeine intake should be considered when planning, or assessing response to, drug therapy. Some of the reported interactions of caffeine, irrespective of clinical relevance, might inadvertently cause athletes to exceed the urinary caffeine concentration limit set by sports authorities at 12 mg/L. Finally, caffeine is a useful and reliable probe drug for the assessment of CYP1A2 activity, which is of considerable interest for metabolic studies in human populations.
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This study tested the effects of dose on the reinforcing effects of caffeine in humans. Eight moderate coffee drinkers were given concurrent access to decaffeinated coffee vs. decaffeinated coffee to which different doses of caffeine (25, 50, 150 and 200 mg/cup) were added. Subjects were tested across several independent double-blind trials. The coffees with 25 mg of caffeine were repeatedly self- administered at a rate greater than that of decaffeinated coffee in two of six subjects, the 50 mg dose in four of eight subjects, the 150 mg dose in three of six subjects, and the 200 mg dose in none of the three subjects tested. Headaches, drowsiness and fatigue occurred with use of decaffeinated coffee in five subjects. When these symptoms occurred, there was a greater probability of self-administration of the caffeinated coffee. We conclude that doses of caffeine similar to those in tea or soda can serve as reinforcers. (C) Lippincott-Raven Publishers.