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Low-dose caffeine physical dependence in humans
Abstract
This study investigated the effects of terminating low dose levels of caffeine (100 mg/day) in 7 normal humans. Substitution of placebo capsules for caffeine capsules occurred under double-blind conditions while subjects rated various dimensions of their mood and behavior. In the first phase of the study, substitution of placebo for 12 consecutive days resulted in an orderly withdrawal syndrome in 4 subjects which peaked on days 1 or 2 and progressively decreased toward prewithdrawal levels over about 1 week. Data from the remaining three subjects provided no evidence of withdrawal. In the second phase of the study, the generality of the withdrawal effect was examined by repeatedly substituting placebo for 100 mg/day of caffeine for 1-day periods separated by an average of 9 days. Despite differences within and across subjects with respect to the presence, nature and magnitude of symptoms, each of the seven subjects demonstrated a statistically significant withdrawal effect. Although the phenomenon of caffeine withdrawal has been described previously, the present report documents that the incidence of caffeine withdrawal is higher (100% of subjects), the daily dose level at which withdrawal occurs is lower (roughly equivalent to the amount of caffeine in a single cup of strong brewed coffee or 3 cans of caffeinated soft drink) and the range of symptoms experienced is broader (including headache, fatigue and other dysphoric mood changes, muscle pain/stiffness, flu-like feelings, nausea/vomiting and craving for caffeine) than heretofore recognized.
... The primary outcomes were symptoms of withdrawal, measured by (1) a modified scale of mood, behavior, and physical symptoms (Griffiths et al., 1990) for identifying symptoms of caffeine withdrawal, and (2) dimensions of mood, including SSB craving, assessed five times per day via check-in questions. We focused on withdrawal and craving, common manifestations of addiction/substance use disorders, because (1) withdrawal perpetuates continued use of a substance to alleviate symptoms, and (2) craving predicts frequency of substance use and relapse (American Psychiatric Association, 2013;Epstein, Marrone, Heishman, Schmittner, & Preston, 2010;Oslin, Cary, Slaymaker, Colleran, & Blow, 2009). ...
... We used 11 items sensitive to caffeine cessation from a scale by Griffiths et al. (1990). This scale asked, "How do you feel right now?" for each dimension: having a headache, feeling energetic, awake/alert, tired, good overall, drowsy/sleepy, content/satisfied, motivated to do work, outgoing, self-confident, and able to concentrate. ...
... These questions assessed SSB cravings as well as perceptions of overall well-being, tiredness, and irritability. Griffiths et al. (1990) identified craving and irritability as also sensitive to caffeine withdrawal (Griffiths et al., 1990). Check-in questions were completed at 10am, 12pm, 4pm, 6pm, and 9pm on days 2-3 of the usual SSB phase and on each day of SSB cessation. ...
... Second, Dews et al. (2002) argue that the considerable variability in onset and incidence of caffeine withdrawal symptoms cannot be explained by the pure pharmacological effects of caffeine, implicating psychological factors like expectancy. For example, estimates of the prevalence of headache in abstinent caffeine users range from 9% (Hughes et al., 1995) to 100% (Naismith et al., 1970); and in the individuals who experience headaches, there is considerable variance in peak onset, ranging from 27 to 51 hours of abstinence (Griffiths et al., 1990). ...
... It was interesting that headache, which is generally the most robust and commonly reported of the caffeine withdrawal symptoms (Juliano and Griffiths, 2004), was not significantly affected by expectancy, with a small numerical change from 1.97 pre-beverage to 1.57 post-beverage, out of 8 points. There is evidence that headaches due to caffeine withdrawal do not peak until 27-51 h after abstinence (Griffiths et al., 1990); therefore, it is possible that the 24-hr abstinence period used in the current study created a floor effect, in the sense that headaches prior to the intervention were already too low to be significantly reduced by the expectancy manipulation. ...
... Fourth, the average daily coffee consumption of participants in this study (554 mg) was relatively high, compared with the average (280 mg) for the US population (Barone and Roberts, 1996). Thus, it is possible that both the withdrawal and the expectancy effects that were observed in this study were more pronounced than they would be in a sample population whose consumption was lower; however, participants in Griffiths et al. (1990) displayed marked withdrawal symptoms, despite their daily caffeine consumption being considerably lower that the US average. Thus, the effects of expectancy may occur irrespective of average consumption, as long as the level of use leads to at least some withdrawal symptoms, although this needs to be tested. ...
Background:
Expectancies have been shown to play a role in the withdrawal syndrome of many drugs of addiction; however, no studies have examined the effects of expectancies across a broad range of caffeine withdrawal symptoms, including craving.
Aims:
The purpose of the current study was to use caffeine as a model to test the effect of expectancy on withdrawal symptoms, specifically whether the belief that one has ingested caffeine is sufficient to reduce caffeine withdrawal symptoms and cravings in abstinent coffee drinkers.
Methods:
We had 24-h abstinent regular coffee drinkers complete the Caffeine Withdrawal Symptom Questionnaire (CWSQ) before and after receiving decaffeinated coffee. One-half of the participants were led to believe the coffee was regular caffeinated coffee (the 'Told Caffeine' condition) and one-half were told that it was decaffeinated (the 'Told Decaf' condition).
Results:
Participants in the Told Caffeine condition reported a significantly greater reduction in the factors of cravings, fatigue, lack of alertness and flu-like feelings of the CWSQ, than those in the Told Decaf condition.
Conclusions:
Our results indicated that the belief that one has consumed caffeine can affect caffeine withdrawal symptoms, especially cravings, even when no caffeine was consumed.
... Low doses of caffeine act positively on mood; subjects ingesting 20 to 200 mg of caffeine report that they feel energetic, imaginative, efficient, self-confident, alert, able to concentrate, and motivated to work (Casas, Ramos-Quiroga, Prat, & Qureshi, 2004;Griffiths et al., 1990;Griffiths & Mumford, 1995;. Positive effects of low doses of caffeine (40 to 60 mg) on performance and well-being may be more beneficial in situations of low arousal, such as the postlunch decrease in vigilance, the common cold (Smith, 1994;Smith, Rusted, Eaton-Williams, Savory, & Leathwood, 1990;Smith, Sturgess, & Gallagher, 1999;Smith, Thomas, Perry, & Whitney, 1997), and fatigue in drivers (Reyner & Horne, 2000) or during attention-requiring tasks (Lorist, Snel, Kok, & Mulder, 1994). ...
... At abrupt cessation, caffeine induces a withdrawal syndrome in a subset of sensitive individuals, about 11 to 22% of the population (Dews, O'Brien, & Bergman, 2002). This syndrome is mostly characterized by headaches, feelings of weakness, impaired concentration, fatigue, irritability, and withdrawal feelings (Griffiths et al., 1990; for review, see Nehlig, 1999Nehlig, , 2004. These symptoms usually start 12 to 24 h after caffeine cessation and reach a peak after 20 to 48 h. ...
... They never occur when caffeine consumption is progressively decreased. Therefore, the possible physical dependence on the methyxanthine has been considered for about two decades (Griffiths et al., 1990;Griffiths & Mumford, 1995Griffiths & Woodson, 1988b;Holtzman, 1990;Strain, Mumford, Silverman, & Griffiths, 1994), but appears quite low compared to common drugs of abuse such as cocaine, amphetamine, morphine, and nicotine. Drugs of abuse selectively activate the shell of the nucleus accumbens, which plays a critical role in drug dependence (Di Chiara, 1995;Self & Nestler, 1995). ...
... Tolerance is not observed for all effects of the drug, such as fat cell lipolysis (Holtzman et al., 1991), but is seen for certain behavioral actions, such as some of its stimulant properties (increase in locomotor activity in rats) (Finn and Holtzman, 1986). Following the cessation of caffeine use, withdrawal-like symptoms are sometimes seen in humans, such as headache, irritability, nervousness, and a reduction in energy (Griffiths et al., 1986(Griffiths et al., , 1990. The physiological bases for these symptoms are not known. ...
... James (1994James ( , 1995James ( , 1998 argued that the majority of studies reporting the effects of caffeine in rested subjects studied moderate caffeine consumers (200-300 mg/d) who were required to abstain from caffeine for some period of time prior to cognitive testing (2-24 hr). Abstinence for regular caffeine users could have resulted in symptoms of withdrawal which include headaches, fatigue, and irritability (Griffiths and Mumford, 1995;Griffiths et al., 1990). James (1994James ( , 1995James ( , 1998, hypothesized that comparisons between caffeine and placebo conditions in experiments assessing the effects of caffeine on cognitive behavior could represent a reversal of deteriorated performance. ...
... A number of studies have demonstrated that cessation of caffeine consumption may result in a distinct withdrawal syndrome, typified by the occurrence of headaches (Dreisbach and Pfeiffer, 1943;Griffiths et al., 1990;Strain et al., 1994;van Dusseldorp and Katan, 1990). In the light of this evidence, caffeine withdrawal syndrome has been included in DSM-IV. ...
... The most frequently-reported effect of caffeine withdrawal is headaches (Juliano & Griffiths, 2004;Rogers et al., 2005;Silverman, Evans, Strain, & Griffiths, 1992), which can manifest following overnight cessation of caffeine consumption (Lane & Phillips-Bute, 1998;Rogers et al., 2005) and may last up to a week (Griffiths et al., 1990;Hofer & Battig, 1994;van Dusseldorp & Katan, 1990). As noted in the section on Pain/Injury (see page 28), headaches from caffeine withdrawal, as with other forms of pain, are likely to draw cognitive resources away from a task, resulting in decreased performance. ...
... Caffeine withdrawal also has a number of negative effects on subjective ratings of mood. Following caffeine cessation, individuals report higher levels of fatigue, drowsiness, and irritability, as well as decreased friendliness and amicability compared to baseline (Griffiths et al., 1990;Juliano & Griffiths, 2004;Keane, James, & Hogan, 2007;Lane & Phillips-Bute, 1998;Mills, Boakes, & Colagiuri, 2016;Rogers, Heatherley, Mullings, & Smith, 2013;Sigmon, Herning, Better, Cadet, & Griffiths, 2009;Silverman et al., 1992). The degree of these mood changes is typically associated with the magnitude of caffeine dependence prior to cessation (Juliano & Griffiths, 2004). ...
... Due to the psychoactive nature of caffeine, it produces physical dependence following chronic use, and habituated individuals experience physiological withdrawal when caffeine is no longer consumed (Strain et al., 1994). The incidence and severity of the effects of caffeine withdrawal vary based on how much caffeine one typically consumes; however, research suggests that individuals who typically consume as little as 100 mg/day may experience withdrawal symptoms following cessation (Evans & Griffiths, 1999;Griffiths et al., 1990). Given the prevalence of caffeine use among submariners, caffeine withdrawal could be rampant in a DISSUB scenario. ...
... Caffeine withdrawal has a number of negative effects on subjective ratings of mood in individuals. Following caffeine cessation, individuals report higher levels of fatigue, drowsiness, and irritability, as well as decreased friendliness and amicability compared to baseline (Griffiths et al., 1990;Juliano & Griffiths, 2004;Keane et al., 2007;Lane & Phillips-Bute, 1998;Mills et al., 2016;Rogers et al., 2013;Sigmon et al., 2009;Silverman et al., 1992). The degree of these mood changes is typically associated with the magnitude of caffeine dependence prior to cessation (Juliano & Griffiths, 2004). ...
... Caffeine causes increased well-being in small to moderate doses and its overuse has the potential to cause physical dependence (60). The caffeine dependence syndrome has been recognized by the World Health Organization as a behavioral disorders due to frequent use of caffeine (61). ...
... Further, two of the migraineurs had migraine attacks on the height of the caffeine stimulation, and in one of these subjects this reoccurred in a second trial. In these trials, and in later studies the headache is described to typically evolve gradually (60,77,78), being diffuse (79), throbbing (9), severe (60, 80), intensified with exercise (77), and Valsalva manoeuver (9) and having a mean duration for 2-3 days (81). Despite being claimed that caffeine-related headache has a non-migrainous clinical presentation (82), the description of caffeine withdrawal headache given in the literature is not very different from migraine. ...
Background: The actions of caffeine as an antagonist of adenosine receptors have been extensively studied, and there is no doubt that both daily and sporadic dietary consumption of caffeine has substantial biological effects on the nervous system. Caffeine influences headaches, the migraine syndrome in particular, but how is unclear. Materials and Methods: This is a narrative review based on selected articles from an extensive literature search. The aim of this study is to elucidate and discuss how caffeine may affect the migraine syndrome and discuss the potential pathophysiological pathways involved. Results: Whether caffeine has any significant analgesic and/or prophylactic effect in migraine remains elusive. Neither is it clear whether caffeine withdrawal is an important trigger for migraine. However, withdrawal after chronic exposure of caffeine may cause migraine-like headache and a syndrome similar to that experienced in the prodromal phase of migraine. Sensory hypersensitivity however, does not seem to be a part of the caffeine withdrawal syndrome. Whether it is among migraineurs is unknown. From a modern viewpoint, the traditional vascular explanation of the withdrawal headache is too simplistic and partly not conceivable. Peripheral mechanisms can hardly explain prodromal symptoms and non-headache withdrawal symptoms. Several lines of evidence point at the hypothalamus as a locus where pivotal actions take place. Conclusion: In general, chronic consumption of caffeine seems to increase the burden of migraine, but a protective effect as an acute treatment or in severely affected patients cannot be excluded. Future clinical trials should explore the relationship between caffeine withdrawal and migraine, and investigate the effects of long-term elimination.
... Considering the analysis of relevant experimental research in caffeine abuse, and its comparison with DSM-V, we concluded that caffeine can be considered a drug of abuse, with the special characteristic of possible auto-regulatory effects occurring when higher doses are ingested. In particular, the view of caffeine as an abuse drug is better supported when we consider the symptoms observed by chronic users who report an ingestion of caffeinated beverages per day, starting from 100 to 200 mg of caffeine when compared to placebo ingestion, 100 mg produced significant increases in subjective positive effects (i.e., content/at ease/relaxed/satisfied and active/stimulated/energetic) and decrease in negative effects (i.e., tired/ drowsy/half-awake) (Griffiths and Woodson 1988a;Griffiths et al. 1990;Juliano and Griffiths 2004). ...
... These studies also confirm the specific criterion for Blow control,^that is continued use despite harm, and points, to another guiding criterion, that is Brisky use of substance,^in which the individual fails to refrain from using the substance. Experimental works also base pharmacological (American Psychiatric Association 2013) and withdrawal criteria (Evans and Griffiths 1992;Schuh and Griffiths 1997;Daly and Fredholm 1998;Nehlig 1999;Dews et al. 2002;Juliano et al. 2012) although excessive and problematic caffeine use has not been associated with serious medical consequences such those observed with alcohol or tobacco use (Budney et al. 2015); on its singularity, excessive caffeine use and abrupt withdrawal are in general associated with increased anxiety, insomnia, headache, drowsiness, and fatigue (Stringer and Watson 1987;Griffiths and Woodson 1988b, c;Griffiths et al. 1990;Evans and Griffiths 1992;Strain and Griffiths 1995;Dews et al. 2002;Juliano and Griffiths 2004;Juliano et al. 2012). Therefore, we point to a need for more clinical studies in the field, to possibly identify specific susceptibility factors for caffeine abuse within the population. ...
Caffeine is the most consumed psychoactive substance in the world; in general, it is not associated to potentially harmful effects. Nevertheless, few studies were performed attempting to investigate the caffeine addiction. The present review was mainly aimed to answer the following question: is caffeine an abuse drug? To adress this point, the effects of caffeine in preclinical and clinical studies were summarized and critically analyzed taking account the abuse disorders described in the Diagnostic and Statistical Manual of Mental Disorders (DSM-V). We concluded that the diagnostic criteria evidenced on DSM-V to intoxication-continued use and abstinence are not well supported by clinical studies. The fact that diagnostic criteria is not widely supported by preclinical or clinical studies may be due specially to a controversy in its exactly mechanism of action: recent literature point to an indirect, rather than direct modulation of dopamine receptors, and auto-limitant consumption due to adverse sensations in high doses. On the other hand, it reports clear withdrawal-related symptoms. Thus, based on a classical action on reward system, caffeine only partially fits its mechanism of action as an abuse drug, especially because previous research does not report a clear effect of dopaminergic activity enhance on nucleus accumbens; despite this, there are reports concerning dopaminergic modulation by caffeine on the striatum. However, based on human and animal research, caffeine withdrawal evokes signals and symptoms, which are relevant enough to include this substance among the drugs of abuse.
... Next we tested whether the analgesic effects of acupuncture could be restored following caffeine removal. Caffeine is known to induce mild physical dependency associated with sustained physiological and molecular changes after daily consumption [11][12][13] . Thus, certain long-term changes caused by caffeine habituation may influence acupuncture treatment. ...
... Caffeine is known to induce mild physical dependency after regular consumption [11][12][13] , and alter gene expression 30,31 . Therefore, it is possible that caffeine influences gene expression of A1 receptors, such that there may be changes in the sensitivity to A1 receptor-mediated analgesia. ...
Acupuncture is an alternative treatment for wide spectrum chronic pain. However, its validity remains controversial due to the disputed efficacy assessed in various clinical studies. Moreover, variability amongst individuals complicates the predictability of outcome, which impedes the integration of acupuncture into mainstream pain management programs. In light of our previous finding that the analgesic effect of acupuncture is mediated by adenosine A1 receptor activation at the acupuncture point, we here report that in acute and chronic animal pain models, oral intake of caffeine, a potent adenosine receptor antagonist, interferes with acupuncture analgesia, even at a low dose. Local administration of caffeine at the acupuncture point was sufficient to eliminate the analgesic effect, dismissing the systemic action of caffeine. Such interference was reversible, as caffeine withdrawal fully restored the efficacy of acupuncture by the next day, and long-term exposure to caffeine did not alter A1 receptor expression at the acupuncture point. Combined, these data indicate that a trace amount of caffeine can reversibly block the analgesic effects of acupuncture, and controlling caffeine consumption during acupuncture may improve pain management outcomes.
... 17 Caffeinewithdrawal headache has been reported in individuals who consume the equivalent of about 1 cup of coffee/day. 18 Caffeine consumption and withdrawal headache might contribute to the development of CDH, although analytic epidemiologic studies are lacking and clinical trials would be difficult to perform. ...
... Caffeine-withdrawal headache is a self-limiting process that generally resolves in days or weeks after consumption ceases. 18 In addition, the headache disappears when consumption resumes, according to the International Headache Society criteria for withdrawal headache. 21 For these reasons, caffeinewithdrawal headache appears to be a less plausible model for CDH in those individuals with continuous headache or those with long-term duration of CDH. ...
Objective: To investigate the possible association of dietary caffeine consumption and medicinal caffeine use with chronic daily headache (CDH). Methods: Population-based cases and controls were recruited from the Baltimore, MD, Philadelphia, PA, and Atlanta, GA, metropolitan areas. Controls ( n = 507) reported 2 to 104 headache days/year, and cases ( n = 206) reported greater than or equal to 180 headache days/year. Current and past dietary caffeine consumption and medication use for headache were based on detailed self-report. High caffeine exposure was defined as being in the upper quartile of dietary consumption or using a caffeine-containing over-the-counter analgesic as the preferred headache treatment. Results: In comparison with episodic headache controls, CDH cases were more likely overall to have been high caffeine consumers before onset of CDH ( odds ratio [ OR] = 1.50, p = 0.05). No association was found for current caffeine consumption (i.e., post CDH) ( OR = 1.36, p = 0.12). In secondary analyses, associations were confined to younger ( age < 40) women ( OR = 2.0, p = 0.02) and those with chronic episodic ( as opposed to chronic continuous) headaches ( OR = 1.69, p = 0.01), without physician consultation ( OR = 1.67, p = 0.04) and of recent ( < 2 years) onset ( OR = 1.67, p = 0.03). Conclusion: Dietary and medicinal caffeine consumption appears to be a modest risk factor for chronic daily headache onset, regardless of headache type.
... Caffeine withdrawal syndrome is characterized by symptoms that arise up to 48 hours after reducing usual caffeine intake [206] or abstaining from caffeine following regular use [5,269]. ...
... Symptoms peak between 20 to 51 hours following abstinence [5] and can last for 2 to 9 days [269]. There are fourteen well-described caffeine withdrawal symptoms including headache, tiredness/ fatigue, decreased energy/activeness, drowsiness/sleepiness, decreased contentedness/well-being, anxiety, depressed mood, difficulty concentrating, irritability, muzzy/foggy/not clearheaded, flu-like symptoms, nausea/vomiting and muscle pain/stiffness [267]. ...
... This hypothesis is consistent with symptoms of caffeine withdrawal, which include headache, tiredness/fatigue, decreased energy, decreased well-being, difficulty concentrating, irritability (Juliano and Griffiths, 2004), and importantly for present purposes, decreased cognitive performance (e.g., James, 1998;Rogers et al., 2003Rogers et al., , 2013Yeomans et al., 2002). Symptoms may be felt within about 12-16 h, generally peak at around 24-48 h, and usually abate within 3-5 days, although occasionally may continue for up to a week (Griffiths et al., 1990;Hughes et al., 1993). Cessation of as little as 100 mg (approximately one cup of instant coffee) per day, and possibly considerably less, can produce symptoms of withdrawal (Griffiths et al., 1990;Lieberman et al., 1987;Smit and Rogers, 2000). ...
... Symptoms may be felt within about 12-16 h, generally peak at around 24-48 h, and usually abate within 3-5 days, although occasionally may continue for up to a week (Griffiths et al., 1990;Hughes et al., 1993). Cessation of as little as 100 mg (approximately one cup of instant coffee) per day, and possibly considerably less, can produce symptoms of withdrawal (Griffiths et al., 1990;Lieberman et al., 1987;Smit and Rogers, 2000). ...
Human cognitive performance is widely perceived to be enhanced by caffeine at usual dietary doses. However, the evidence for and against this belief continues to be vigorously contested. Controversy has centred on caffeine withdrawal and withdrawal reversal as potential sources of experimental confounding. In response, some researchers have enlisted "caffeine-naïve" experimental participants (persons alleged to consume little or no caffeine) assuming that they are not subject to withdrawal. This mini-review examines relevant research to illustrate general methodological challenges that have been the cause of enduring confusion in caffeine research. At issue are the processes of caffeine withdrawal and withdrawal reversal, the definition of caffeine-naïve, the population representativeness of participants deemed to be caffeine-naïve, and confounding due to caffeine tolerance. Attention to these processes is necessary if premature conclusions are to be avoided, and if caffeine's complex effects and the mechanisms responsible for those effects are to be illuminated. Strategies are described for future caffeine research aimed at minimising confounding from withdrawal and withdrawal reversal.
... Studies reported that caffeine at low (up to 100 mg) to moderate (up to 250 mg) doses increases alertness (24)(25)(26)(27)(28), energetic feeling (29), attention, and vigilance (30)(31)(32). However, the effects of caffeine on the spectrum of neuropsychological domains are inconsistent (26,29,(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43). ...
... Caffeine dependence and withdrawal have been described (105,106,109). ...
p>Caffeine is present in a variety of beverages and food and is widely consumed. Caffeine causes a reduction in cerebral blood flow (CBF) in healthy individuals. A similar reduction in ischaemic stroke patients could theoretically exacerbate pre- existing ischaemia. In a previous study of patients recovering from an acute ischaemic stroke using transcranial Doppler ultrasound a fall in middle cerebral artery (MCA) blood velocity (Vmca) of 12% was demonstrated after ingestion of caffeine. The aim of this study was to investigate if these velocity changes reflected changes in cerebral blood flow. The study used a randomised, double blind, cross over design. Twenty patients recovering from an acute ischaemic stroke in the MCA territory and ten controls attended two sessions having abstained from caffeine for 48hours prior to each. At each session CBF was measured 4 times using xenon clearance, twice before the oral administration of 250mg caffeine or matched placebo, and twice after. Similarly, three Vmca readings using transcranial Doppler were made prior to administration and four after. 250mg caffeine (equivalent to 2-3 cups of coffee) resulted in a significant fall in CBF and Vmca compared to placebo. This reduction occurred in stroke patients and controls and was similar on the affected stroke hemisphere and the unaffected side. Since caffeine is present in the diet of most patients recovering from an acute ischaemic stroke this effect may have adverse clinical consequences.</p
... All participants met the predetermined criteria: 18-35 yr of age (inclusive), consumed either 35 mg·d À1 of caffeine (NHAB), or ! 100 mg·d À1 of caffeine (HAB) (assessed over a 1-wk period), had a minimum oxygen consumption (V _ O 2max ) ! 28 mL·kg À1 · min À1 , and had not recently undertaken a heat acclimation protocol. The threshold for inclusion in the HAB group was set at 100 mg·d À1 based on caffeine dependence being present after 9 days of repeated caffeine (>100 mg) ingestion (13). Testing of HAB and NHAB participants was distributed evenly throughout the course of data collection. ...
Purpose:
To assess the impact of acute caffeine ingestion on thermoregulatory responses during steady-state exercise under moderate heat stress conditions in caffeine-habituated and non-habituated individuals.
Methods:
28 participants (14 habituated (HAB) (4 females); and 14 non-habituated (NHAB) (6 females)) cycled at a fixed metabolic heat production (7 W·kg-1) for 60 minutes on two separate occasions 1 hour after ingesting i) 5 mg·kg-1 caffeine (CAF) or ii) 5 mg·kg-1 placebo (PLA), in a double-blinded, randomized and counter-balanced order. Environmental conditions were 30.6±0.9°C, 31±1% RH.
Results:
The end-exercise rise in esophageal temperature (ΔTes) from baseline was greater with CAF in the HAB group (CAF=0.88±0.29°C, PLA=0.62±0.34°C, P<0.001), but not the NHAB group (CAF=1.00±0.42°C, PLA=1.00±0.39°C, P=0.94). For a given change in mean body temperature, rises in % of maximum skin blood flow were attenuated with CAF on the forearm (P=0.015) and back (P=0.021) in the HAB group, but not in the NHAB group (P≥0.65). Dry heat loss similar in the HAB (CAF=31±5 W·m-2, PLA=33±7 W·m-2) and NHAB groups (CAF=31±3 W·m-2, PLA 30±4 W·m-2) (P≥0.37). There were no differences in whole-body sweat losses in both groups (HAB: CAF=0.59±0.15 kg, PLA=0.56±0.17 kg, NHAB:CAF=0.53±0.19 kg, PLA 0.52±0.19 kg) (P≥0.32).
Conclusion:
As the potential for both dry and evaporative heat loss was uninhibited by caffeine, we suggest the observed ΔTes differences with CAF in the HAB group were due to alterations in internal heat distribution. Our findings support the common practice of participants abstaining from caffeine prior to participation in thermoregulatory research studies in compensable conditions.
... [54] Caffeine causing withdrawal migraine has been accounted in individuals who intake about 1 cup of coffee/day. [55] Few patients are very conscious to caffeine when they consume 1-2 cups per day and can lead to withdrawal symptoms of Migraine reported by Scher et al., [56] narrowing down caffeine slowly is significant. ...
Migraine is a disease known as polyneuropathy, which is intolerable to the sufferer, family and community. Persistent headaches mark this condition in patients with migraine. The primary focus of this review article is to summarise the current findings of the migraine epidemiology, prevalence, neuroimaging tools, risk factors and prospects. Currently, a rise in migraine cases has been reported for persons of age between 25 and 55 years. A rapid increase in migraine cases was reported for people having lower socioeconomic status. Patients with migraine have shown an increase in the incidence of mental illness and co-morbidity. These patients are diagnosed using various neuroimaging tools such as (a) computerized tomography (CT), (b) magnetic resonance imaging (MRI), (c) functional (fMRI), (d) PET (Positron Emission Tomography), (e) SPECT (Single-Photon Emission Computed Tomography), (f) CEPs (Cortical Evoked Potentials), (g) MEG (Magnetoencephalography), and (h) Diffusion Tensor Imaging (DTI). In clinical practice, Headache Impact Test (HIT-6 ™) is used to measure the pain impact in patients with migraine. Precipitating factors such as (a) caffeine, (b) sleep apnea, (c) sleep deprivation, (d) stress, and (e) depression that cause migraine have been discussed in detail. The prospects for the future research have been discussed based on (a) Pain and psychological factors, (b) cognitive techniques, (c) new developments in treatment, and (d) neuromodulation. In this review, it is concluded with the possibility of reducing the progression of migraine disease through pathopsychological knowledge. Also, the progression can be reduced by implementing high research standards in clinical studies. © 2020 International Journal of Nutrition, Pharmacology, Neurological Diseases | Published by Wolters Kluwer - Medknow.
... The symptoms of caffeine withdrawal, the most common of which is headache, begin 12-24 h after the last dose of caffeine. Griffiths et al. (1990) also found that in addition to headache, other caffeine withdrawal symptoms include tiredness/fatigue, sleepiness/ drowsiness, dysphoric mood (e.g., miserable, decreased well-being/ contentedness), difficulty concentrating/decreased cognitive performance, depression, irritability, nausea/vomiting, and muscle aches/stiffness. Therefore, public should know how many present caffeine concentration per serving and what level is negative impact level of caffeine especially in infant, children and pregnancy. ...
... Reversal of withdrawal has been put forward as a possible explanation of effects of caffeine on cognition and alertness. [15][16][17][18][19][20][21][22][23][24][25][26] Many studies of caffeine withdrawal focus on symptoms such as headache [27][28][29][30][31] and it has been suggested that they may reflect expectancies based on perceptions of withdrawal. [32,33] Other researchers have argued that effects of caffeine on behaviour do not reflect reversal of caffeine withdrawal. ...
... 22 Caffeine can delay or prevent sleep and improves task performance during sleep deprivation. 23 Shift workers who use caffeine make fewer mistakes due to drowsiness. [39] Caffeine overdose can result in a state of central nervous system over-stimulation known as caffeine intoxication, a clinically significant temporary condition that develops during, or shortly after, the consumption of caffeine. ...
Diazepam is commonly used in clinical setting in treatment and management of several conditions such as convulsion, insomnia, anxiety disorder and sleep disorder. Caffeine is widely and regularly consumed for different purposes. A total of thirty (30) wister rats of 120–210 g of either sex were divided into five groups of
six mice per group. Rats in all group received diazepam (4 mg/Kg), while group 2, 3, 4 and 5 received
concurrent dose of caffeine (2.5, 5, 10 and 20 mg/Kg) intraperitoneally respectively. After 2 minutes
of administration of the drugs, sedative and hypnotic study were carried out. There was significant (P<0.05) dose dependent decreased in the time taken for rat in all groups
to return the widely parted hind limb to their normal position when compare to the control. There was
also significant (P<0.05) dose dependent increased in sleep latency and decreased in duration of sleep
in all group administered caffeine. Group 5 rats did not have sleep latency and duration of sleep
throughout the 90 minutes period of observation. result from the study showed that caffeine significantly reduced CNS effect of diazepam
induced rats which suggests that dose
... 22 Caffeine can delay or prevent sleep and improves task performance during sleep deprivation. 23 Shift workers who use caffeine make fewer mistakes due to drowsiness. [39] Caffeine overdose can result in a state of central nervous system over-stimulation known as caffeine intoxication, a clinically significant temporary condition that develops during, or shortly after, the consumption of caffeine. ...
Introduction/aim: Diazepam is commonly used in clinical setting in treatment and management of
several conditions such as convulsion, insomnia, anxiety disorder and sleep disorder. Caffeine is
widely and regularly consumed for different purposes. It is a central nervous system stimulant that
affects the body in numerous ways. The aim of this study is to investigate the effect of caffeine on
diazepam– induced in rat.
Method: A total of thirty (30) wister rats of 120–210 g of either sex were divided into five groups of
six mice per group. Rats in all group received diazepam (4 mg/Kg), while group 2, 3, 4 and 5 received
concurrent dose of caffeine (2.5, 5, 10 and 20 mg/Kg) intraperitoneally respectively. After 2 minutes
of administration of the drugs, sedative and hypnotic study were carried out.
Result: There was significant (P<0.05) dose dependent decreased in the time taken for rat in all groups
to return the widely parted hind limb to their normal position when compare to the control. There was
also significant (P<0.05) dose dependent increased in sleep latency and decreased in duration of sleep
in all group administered caffeine. Group 5 rats did not have sleep latency and duration of sleep
throughout the 90 minutes period of observation.
Conclusion: result from the study showed that caffeine significantly reduced CNS effect of diazepam
induced rats which suggests that dose adjustment should be considered to patients on diazepam who
may have been exposed to caffeine.
... Due to the psychoactive nature of caffeine, it produces physical dependence following chronic use and subsequent withdrawal when no longer consumed (Strain, Mumford, & Silverman, 1994). The incidence and severity of the effects of caffeine withdrawal vary based on how much caffeine one typically consumes; however, research suggests that individuals who typically consume as little as 100 mg/day may experience withdrawal symptoms following cessation (Evans & Griffiths, 1999;Griffiths et al., 1990). The effects of caffeine withdrawal (most commonly headaches, fatigue, and reduced alertness; Juliano & Griffiths, 2004) vary in magnitude among individuals and depend on one's maintenance dose. ...
... The symptoms (Griffiths et al., 1990;Juliano & Griffiths, 2004;Mills et al., 2016). Day 2 headache was the only dose effect still present 24 hr postadministration. ...
Objective
This study investigated psychological influences on drug withdrawal symptomatology using a caffeine‐based model.
Methods
Using the 2 × 2 balanced placebo design caffeine dose (given caffeinated vs decaffeinated coffee) was crossed with dose expectancy (told caffeine vs. decaf) among 87 (16‐hr abstinent) regular coffee consumers in a 2‐day study.
Results
There were effects of expectancy and pharmacology that differed depending on the measure. Those told decaf reported greater caffeine cravings than those told caffeine 45 min and 8 hr postmanipulation. There were no expectancy effects on withdrawal symptoms or cognitive performance. There were pharmacological effects on all measures. Those given decaf reported greater withdrawal symptoms and showed poorer cognitive performance 45 min and 8 hr postmanipulation, with effects for headache and flu‐like symptoms first emerging 8 hr postmanipulation (i.e., 24 hr abstinence in given decaf conditions). Caffeine readministration alleviated all withdrawal symptoms and cognitive decrements within 45 min. No drug by expectancy interactions were observed.
Conclusions
These findings confirm a strong pharmacological basis for caffeine withdrawal and an important role of cognition in drug craving. Future research should investigate the role of expectancy in drug withdrawal and craving and the potential use of expectancy manipulations in symptom prevention and management.
... A indução floral é definida como um evento que ativa processos que permitem que a planta esteja apta para o florescimento, por meio da transcrição e da expressão de genes, que ocorrem antes da iniciação. Bernier et al. (1981) (TATEFUJI et al., 1996); características antimutagênicas (STICH et al., 1982;WATTENBERG, 1983); a indução da diminuição dos níveis sanguíneos de glicose por meio da inibição da enzima glicose-6-fosfatase (ARION et al., 1998;HERLING et al., 1998) Os sintomas associados à abstinência de cafeína têm sido observados em estudos envolvendo a cessação desde o consumo regular, de alta (≤ 1250 mg/dia) (GRIFFITHS et al., 1986); ≤ 2548 mg/dia (STRAIN et al., 1994) e doses muito mais baixas (100 mg dia) (GRIFFITHS et al., 1990); 235 mg/dia (SILVERMAN et al., 1992); 290 mg/dia (WEBER et al., 1993); 428 mg/dia (BRUCE et al., 1991); quatro a seis xícaras de café por dia (VAN DUSSELDORP; KATAN, 1990); cinco xícaras de café por dia (HUGHES et al., 1991). ...
Este trabalho tem como objetivo responder aos questionamentos: quais as indicações do uso da espécie Coffea arabica, quais as principais formas desse uso e quais são as partes da planta aplicadas com finalidade medicinal? Para esta revisão foram utilizados apenas recursos primários como os bancos de dados SciELO, ScienceDirect e Web CAPES. Foram selecionados documentos e artigos compreendendo os aspectos envolvidos direto ou indiretamente nas propriedades de C. arabica, a exposição humana e animal e consequências da intoxicação, incluindo artigos originais e de revisão. Como resultados, nos artigos explorados os principais assuntos abordados referentes ao café foram: atividade antioxidante: alta atividade de inibição da peroxidação lipídica; efeitos fisiológicos: respostas psicoativas (estado de alerta e mudanças de humor) e neurológicas (hiperatividade infantil e doença de Parkinson); efeito anti-inflamatório; bioatividade dos ácidos clorogênicos, que possuem propriedades antioxidantes e bacterianas. Assim, C. arabica apresenta em sua composição química: alcaloides, ácidos orgânicos, flavonoides, diterpenos, salicilatos, EDTA, ácido benzoico, derivados nicotínicos, óleos essenciais, vitaminas, minerais e ações medicinais relacionadas ao Alzheimer, hiperatividade, doenças crônicas, efeito anti-inflamatório, doenças cardiovasculares e outros benefícios à saúde humana.
... Abstinence from intermediate doses in daily coffee and cola consumers (579 mg/day), increased ratings of drowsy/sleepy, fatigue/tired, lazy/sluggy/slow-moving, decreased ratings of active/energetic/excited and motivation to work, and impaired performance on psychomotor tasks (Liguori and Hughes, 1997). Even at low quantities (100 mg/day, in a controlled study), caffeine withdrawal increased ratings of lethargy, fatigue, tiredness, and sluggishness, and decreased ratings of energy, motivation and urge to work (Griffiths et al., 1990). ...
Major depressive disorder is one of the most common and debilitating psychiatric disorders. Some of the motivational symptoms of depression, such anergia (lack of self-reported energy) and fatigue are relatively resistant to traditional treatments such as serotonin uptake inhibitors. Thus, new pharmacological targets are being investigated. Epidemiological data suggest that caffeine consumption can have an impact on aspects of depressive symptomatology. Caffeine is a non-selective adenosine antagonist for A1/A2A receptors, and has been demonstrated to modulate behavior in classical animal models of depression. Moreover, selective adenosine receptor antagonists are being assessed for their antidepressant effects in animal studies. This review focuses on how caffeine and selective adenosine antagonists can improve different aspects of depression in humans, as well as in animal models. The effects on motivational symptoms of depression such as anergia, fatigue, and psychomotor slowing receive particular attention. Thus, the ability of adenosine receptor antagonists to reverse the anergia induced by dopamine antagonism or depletion is of special interest. In conclusion, although further studies are needed, it appears that caffeine and selective adenosine receptor antagonists could be therapeutic agents for the treatment of motivational dysfunction in depression.
... The majority of studies on the effects of caffeine on cognitive function utilize people who regularly consume caffeine and who are instructed to abstain from caffeine prior to the study. If these habitual users demonstrate physical dependence, abstinence leads to withdrawal symptoms such as headache, fatigue, and difficulty concentrating (Griffiths et al., 1990;Juliano & Griffiths, 2004). Thus, withdrawn consumers may have diminished performance on cognitive tasks than would be expected in nonhabitual users of caffeine. ...
Previous studies have shown that caffeine can improve performance on cognitive tasks in adults, but little work has been done in children and adolescents, who use caffeine less habitually. The primary aim of this study was to test the hypothesis that acute caffeine enhances performance on cognitive tasks in children and adolescents. Two secondary aims were to determine if these effects differ as a function of sex, puberty, and menstrual cycle phase and if these effects can be attributed to withdrawal reversal. Children were given a cognitive test battery using the Automated Neurological Assessment Metrics (ANAM) before and 60 min after administration of placebo or caffeine (1 or 2 mg/kg). The number of correct responses and throughput on the Stroop task were increased after caffeine administration. Caffeine also decreased reaction time on the Stroop and decreased the standard deviation of the reaction time on the Go/No-Go task. We further analyzed these data based on presence or absence of withdrawal symptoms and by usual caffeine use and found that the effects of caffeine remained. We found interactions between sex and caffeine for Go/No-Go task time and the standard deviation of the reaction time on the Stroop task and an interaction between caffeine dose and menstrual cycle phase on the standard deviation of the reaction time on the Go/No-Go task. These results are consistent with previous studies showing caffeine facilitates performance on some cognitive tasks and that these improvements are not related to reversal of withdrawal effects. This study is among the first to report sex differences in responses to caffeine on cognitive tasks in children and adolescents.
... 17 Caffeine withdrawal headache has been reported in persons consuming the equivalent of as little as one cup of coffee per day. 39 As R192Q mice exhibit a genetically enhanced CSD susceptibility and are particularly sensitive to migraine modulators 6 while being less susceptible to stimulation of adenosine receptors, 40 we tested whether withdrawal from caffeine has an effect on CSD in this group of mice, but no such effects were observed in this group either. ...
Several factors that modulate migraine, a common primary headache disorder, also affect susceptibility to cortical spreading depolarization (CSD). CSD is a wave of neuronal and glial depolarization and thought to underlie the migraine aura and possibly headache. Here, we tested whether caffeine, known to alleviate or trigger headache after acute exposure or chronic use/withdrawal, respectively, modulates CSD. We injected C57BL/6J mice with caffeine once (30, 60, or 120 mg/kg; i.p.) (acute) or twice per day for one or two weeks (chronic). Susceptibility to CSD was evaluated by measuring the electrical CSD threshold and by assessing KCl-induced CSD. Simultaneous laser Doppler flowmetry was used to assess CSD-induced cortical blood flow changes. Recordings were performed 15 min after caffeine/vehicle administration, or 24 h after the last dose of chronic caffeine in the withdrawal group. The latter paradigm was also tested in mice carrying the familial hemiplegic migraine type 1 R192Q missense mutation, considered a valid migraine model. Neither acute/chronic administration nor withdrawal of caffeine affected CSD susceptibility or related cortical blood flow changes, either in WT or R192Q mice. Hence, adverse or beneficial effects of caffeine on headache seem unrelated to CSD pathophysiology, consistent with the non-migrainous clinical presentation of caffeine-related headache.
... served as the upper limit for participation~cf. Griffiths et al., 1990aGriffiths et al., , 1990b RAs escorted all toilet visits although subjects' privacy was obviously maintained. On such occasions participants were required to sing or whistle throughout. ...
We investigated the potential influence of sustained wakefulness on pre-attentive capacities by recording the mismatch negativity (MMN), an electrophysiological manifestation associated with nonintentional detection of auditory oddball stimuli. The MMN was elicited by pitch deviants presented to both ears via earphones, at the beginning of a total sleep deprivation session (baseline), after 24 hr, and after 36 hr of continuous controlled wakefulness. A conspicuous MMN response was elicited at all three sessions. With time, however, a small yet significant gradual reduction in the MMN amplitude was evident. Whereas previous research suggested that controlled attention-demanding tasks are hampered by sleep deprivation, the balance of the present results suggests that passive (total) sleep deprivation may also bring about some degradation in the pre-attentive detection of environmental irregularities and as a consequence may disrupt the reflexive shift of attention induced by such events.
... Because caffeine is a strong central nervous system stimulant, stopping use of caffeine after regular use can result in withdrawal effects, such as headache, irritability, inability to concentrate, and insomnia (Griffiths et al., 1990;Jones & Lejuez, 2005;Juliano & Griffiths, 2004;Silverman et al., 1992;Svikis et al., 2005). Energy drink researchers have previously highlighted concerns over the high levels of caffeine as well as other herbal ingredients in energy drinks (Sepkowitz, 2013;Wolk et al., 2012;Woolsey et al., 2014). ...
Introduction: The combined-use of alcohol and energy drinks can increase risky behaviors increase motivations to drink, reduce perceptions of impairment, and reduce users’ perceived levels of intoxication. This study examined differences in drinking and driving behaviors among combined-users and those who consumed alcohol-only.
Methods: College students (n=549) from a large mid-western university completed a web-based survey assessing drinking and driving, riding with an intoxicated driver, and energy drink use behaviors. Chi-square analyses and Mann-Whitney U tests were used to examine differences between the alcohol-only (AO; n=281) and combined-use (CU; n=268) groups.
Results: Compared to AO drinkers, in the past 30 days, combined-users were significantly more likely to drive both over the .08 blood alcohol content limit (CU 35.0% vs. AO 18.1%; p<.001) and after knowing they were too drunk to drive (CU 36.3% vs. AO 17.0%; p<.001). CU were also more likely to ride as a passenger when they knew the driver had too much alcohol to drive safely (44.1% vs. 23.6%; p<.001). Combined users also reported more indicators of high-risk alcohol use, such as larger number of drinks consumed, number of days drinking, number of days drunk, number of heavy episodic drinking episodes, greatest number of drinks on one occasion, and average hours of consumption (p<.001).
Discussion: In addition to increased high-risk alcohol consumption, combined-users exhibit an increased likelihood to drive after drinking and drive while knowingly drunk, as well as an increased likelihood to ride in a car with a driver who had too much alcohol to drive safely. Students who combine alcohol and ED are more likely to participate in multiple high-risk behaviors including frequency of drinking and driving over the .08 legal-limit. Public health professionals should target the combined use of alcohol and energy drinks in campus-based prevention efforts.
... Symptoms, appear within about 12-16 hours of abstinence, with a peak at around 24-48 hours, are likely to abate within 3-5 days though infrequently may extend for up to a week or more. 4 Notably, caffeine withdrawal symptoms are rapidly alleviated by ingestion of caffeine (i.e., reversal of withdrawal effects). Studies show that decreases in cognitive performance (not necessarily discernible to the individual) are detectable after as little as 6-8 hours since caffeine was last ingested. ...
... The extent of the development of tolerance towards caffeine's effects is unclear [153,154]. The uncertainty regarding this issue may be partly due to methodological limitations. ...
Caffeine use is increasing worldwide. The underlying motivations are mainly concentration and memory enhancement and physical performance improvement. Coffee and caffeine-containing products affect the cardiovascular system, with their positive inotropic and chronotropic effects, and the central nervous system, with their locomotor activity stimulation and anxiogenic-like effects. Thus, it is of interest to examine whether these effects could be detrimental for health. Furthermore, caffeine abuse and dependence are becoming more and more common and can lead to caffeine intoxication, which puts individuals at risk for premature and unnatural death. The present review summarizes the main findings concerning caffeine’s mechanisms of action (focusing on adenosine antagonism, intracellular calcium mobilization, and phosphodiesterases inhibition), use, abuse, dependence, intoxication, and lethal effects. It also suggests that the concepts of toxic and lethal doses are relative, since doses below the toxic and/or lethal range may play a causal role in intoxication or death. This could be due to caffeine’s interaction with other substances or to the individuals&apos preexisting metabolism alterations or diseases.be due to caffeine’s interaction with other substances or to individuals’ pre-existing diseases or metabolism alterations.
... Caffeine, an alkaloid belonging to the methylxanthine family, is a strong central nervous system stimulant that exhibits physically addictive properties (Jones & Lejuez, 2005;Juliano & Griffiths, 2004;Svikis, Berger, Haug, & Griffiths, 2005). Similar to alcohol, withdrawal symptoms of caffeine appear 12-24 hours after discontinuation of use and include: headache, irritability, inability to concentrate, drowsiness, insomnia, and pain in the stomach, upper body, and joints (Griffiths et al., 1990;Juliano & Griffiths, 2004;Silverman, Evans, Strain, & Griffiths, 1992). Caffeine warnings have been mentioned extensively by ED safety researchers; however, the accompanying herbal ingredients found EDs are equally concerning because of the potentially interactive, additive, or synergistic effects. ...
Background:
The combined-use of alcohol and energy drinks is an emerging public health issue. This investigation examined differences in drinking and driving behaviors among combined-users (CU) and participants who consumed alcohol-only (AO).
Objectives:
This study was specifically designed to investigate potential differences in drinker's perceptions of (a) what it means to them to drive over the .08 Blood Alcohol Content (BAC) driving limit and (b) what it means to drive after knowing they have had too much to drink to drive safely.
Methods:
College students (N = 355) were surveyed to assess differences in drinking and driving-related behaviors between the AO (n = 174) and CU (n = 107) groups.
Results:
CU were more likely than AO to drive over the .08 BAC driving limit (53% vs. 38%; p = .009) and after knowing they were too drunk to drive (57% vs. 44%; p = .025). CU were also more likely (56% vs. 35%; p = .000) to ride with an intoxicated driver while knowing it was unsafe. Conclusions/Importance: Combined-users are more likely to drive after drinking, drive while knowingly drunk, and participate in other high-risk behaviors such as heavy drinking that increase the potential for injury. Public policy makers and health professionals should focus prevention efforts to reduce high-risk combined-use behavior.
... Over the past 30 years, there have been a large number of studies characterizing caffeine withdrawal symptoms (for reviews, see Griffiths and Woodson [6] and Juliano and Griffiths [7]). As a result, the DSM-5 includes diagnostic criteria for caffeine withdrawal, which consists of prolonged daily use of caffeine and three or more withdrawal symptoms occurring within 24 h of abrupt cessation or reduction of caffeine use. ...
The latest edition of the Diagnostic and Statistical Manual of Mental Disorders (5th edition; DSM-5) has introduced new provisions for caffeine-related disorders. Caffeine withdrawal is now an officially recognized diagnosis, and criteria for caffeine use disorder have been proposed for additional study. Caffeine use disorder is intended to be characterized by cognitive, behavioral, and physiological symptoms indicative of caffeine use despite significant caffeine-related problems, similar to other substance use disorders. However, since non-problematic caffeine use is so common and widespread, it may be difficult for some health professionals to accept that caffeine use can result in the same types of pathological behaviors caused by alcohol, cocaine, opiates, or other drugs of abuse. Yet there is evidence that some individuals are psychologically and physiologically dependent on caffeine, although the prevalence and severity of these problems is unknown. This article reviews the recent changes to the DSM, the concerns regarding these changes, and some potential impacts these changes could have on caffeine consumers.
... A amostra foi composta por 15 voluntários do sexo masculino, com idade entre 18 e 30 anos, não engajados em programas de treinamento com finalidades competitivas e não consumidores habituais de bebidas que contenham cafeína (consumo inferior a 100mg/dia) (12) . Todos os indivíduos assinaram termo de consentimen-to livre e esclarecido em duas vias, e o presente estudo foi aprovado pelo Comitê de Ética em Pesquisa da Rede Metodista de Educação do Sul (protocolo nº 002/2008). ...
The purpose of this study was to evaluate the effect of acute caffeine consumption on lipid oxidation and performance during aerobic exercise. Fifteen healthy male individuals, 22.3 ± 2.7 years old, performed a progressive test on treadmill for determination of maximal oxygen uptake (VO2max) and ventilatory thresholds. Each volunteer performed three submaximal tests at the intensity of 10% below the second ventilatory threshold, being guided to remain on exercise until exhaustion. Thirty minutes before each submaximal test, the subjects ingested 250ml of one of following drinks: coffee with sweetener (CSW), coffee with sugar (CS) or decaffeinated coffee with sweetener (CD). During the exercise, the individuals's heart rate was monitored and respiratory gases analyses were done. The lipid oxidation was predicted by the respiratory quotient (RQ) during the test and performance was verified by exercise duration. In order to compare the RQ results and time of exercise among the three groups, factorial Anova was used, and a value of p < 0.05 was considered as statistically significant. The individuals had VO2max of 50.18 ± 9.9 ml/kg/min. CAD ingestion caused RQ average of 0.98 ± 0.18, and the average exercise duration was of 24.1 ± 17.04 min; CA ingestion caused RQ average of 0.96 ± 0.2 and the average exercise duration was 24.4 ± 17.8 min. Finally, CD ingestion caused the RQ average of 1.01 ± 0.24, and the average exercise duration was of 20.6 ± 9.7 min. There were no significant differences in the RQ values or exercise duration among the three interventions (p = 0.697 and p = 0.598, respectively). Caffeine did not increase lipid oxidation or performance of young male individuals.
The initial hours after surgery are a critical time in the care of the surgical patient. Familiarity with the clinical presentation of perioperative complications is important to achieving optimal outcomes. By taking an approach to complications based upon signs and symptoms seen in the early post-operative period among adult patients undergoing non-cardiac surgery, this book aids the practitioner in the clinical management of surgical patients during the often turbulent hours after surgery. After a brief introduction to PACU organization, this manual discusses the common and most serious symptoms encountered in the post-operative patient, giving guidance on diagnosis of the underlying disorder and the treatment options available. The book also includes chapters dedicated to subspecialty patients, including patients requiring post-operative mechanical ventilation, pediatric patients, patients with implantable cardiac devices, morbidly obese patients and the complex pain patient. This practical manual is essential reading for all practitioners working in the PACU environment.
Purpose:
The purpose of this paper is to review some of the causes of secondary headache particularly focusing on the subcategories of secondary headache in the International Classification of Headache Disorders, 3rd edition, the clinical features of these headaches, and their associated features and management.
Overview:
Headache attributed to trauma or injury to the head and/or neck, headache attributed to cranial or cervical vascular disorder, headache attributed to non-vascular intracranial disorder, headache attributed to a substance or its withdrawal, headache attributed to infection, headache attributed to disorder of homeostasis, and headache or facial pain attributed to disorder of the cranium, neck, eye, ears, nose, sinuses, teeth, mouth, or other facial or cervical structure are discussed in this paper.
Discussion:
Headache is a common symptom of multiple medical conditions. Although a minority of headache patients have a secondary basis for their headaches, it is important to identify clinical features of secondary headache disorders including both the headache and non-headache features of the condition, diagnose the secondary etiology correctly, and treat them appropriately.
Background:
The role of diet in the management of the headache patient is a controversial topic in the headache field.
Objectives:
To review the evidence supporting the hypothesis that specific foods or ingredients within foods and beverages trigger attacks of headache and/or migraine and to discuss the use of elimination diets in the prevention of headache disorders METHODS: This represents part 1 of a narrative review of the role of diet in the prevention of migraine and other headache disorders. A PubMed search was performed with the following search terms: "monosodium glutamate," "caffeine," "aspartame," "sucralose," "histamine intolerance syndrome," "tyramine," "alcohol," "chocolate," "nitrites," "IgG elimination diets," and "gluten." Each of these search terms was then cross-referenced with "headache" and "migraine" to identify relevant studies. Only studies that were written in English were included in this review.
Results:
Caffeine withdrawal and administration of MSG (dissolved in liquid) has the strongest evidence for triggering attacks of headache as evidenced by multiple positive provocation studies. Aspartame has conflicting evidence with two positive and two negative provocation studies. Observational studies provide modest evidence that gluten- and histamine-containing foods as well as alcohol may precipitate headaches in subgroups of patients. Two of three randomized controlled trials reported that an elimination diet of IgG positive foods significantly decreased frequency of headache/migraine during the treatment as compared to baseline time period.
Conclusions:
Certain foods, beverages, and ingredients within foods may trigger attacks of headache and/or migraine in susceptible individuals. Elimination diets can prevent headaches in subgroups of persons with headache disorders.
Caffeine, a central nervous system (CNS) stimulant, is the most widely used psychotropic drug in the world (Gilbert, 1984). In the United States, more than 85% of adults consume caffeine daily (Gilbert, 1976; Graham, 1978) and the average daily consumption is estimated to be 200 mg (Barone & Roberts, 1984). Caffeine is found in a wide variety of beverages (e.g., coffee, tea, colas), prescription drugs and over-the-counter stimulants, analgesics and cold preparations, and food items such as chocolate. Caffeine has been considered to be a model drug for studying and understanding drugs of abuse (Holtzman, 1990; Rush, Sullivan, & Griffiths, 1995), in part due to caffeine’s widespread use, and because caffeine produces a range of behavioral effects that are common to classic drugs of abuse.
In this chapter, five disorders associated with caffeine use are reviewed: the Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5) diagnoses of Caffeine Intoxication, Caffeine Withdrawal, Caffeine Use Disorder, Caffeine-Induced Anxiety Disorder, and Caffeine-Induced Sleep Disorder. The DSM-5 diagnosis of Caffeine Use Disorder includes symptoms that can also contribute to a diagnosis of caffeine intoxication and caffeine withdrawal, and both of these conditions should be included in the differential diagnosis of a patient with possible caffeine use disorder. When considering a patient for a possible diagnosis of caffeine use disorder, the clinician should also consider other substance use disorders, especially those related to stimulants. The possible presence of other psychiatric conditions, such as depressive and anxiety disorders, should be assessed. The chapter documents that the prevalence of caffeine-induced psychiatric syndromes is higher than may be commonly appreciated.
Caffeine is the most widely consumed psychoactive substance in history. This chapter provides an overview of the effects of caffeine on human health and well-being, with particular reference to the chronic effects of dietary use. Consideration is given to the main sources of caffeine and prevailing patterns of usage; the pharmacology of the drug, including the main mechanism of action and the key processes of physical dependence and tolerance; and the psychopharmacology of caffeine, with particular attention to psychomotor performance and mood, and the processes of withdrawal and withdrawal reversal. Regarding health consequences, attention is first given to mental health and well-being. This is followed by considerations of physical health, including cardiovascular disease, cancer, maternal use, and potential adverse interactions between caffeine and other drugs. Attention is given to whether caffeine may be regarded as a drug of addiction, whether there is a safe level of consumption, and processes for reducing and quitting caffeine consumption. Claims concerning possible health benefits of habitual caffeine use are examined, with particular reference to Type 2 diabetes mellitus and Parkinson’s disease, and mention is made of the growing interest in compounds other than caffeine in caffeine beverages. In the final section, consideration is given to major threats to the integrity of caffeine science, a topic that has thus far received too little attention in the literature. The main conclusions are that dietary caffeine is harmful to health. In particular, periods of caffeine abstinence in habitual users have negative effects on psychomotor performance and mood; habitual use produces modest increases in blood pressure that probably have negative effects on population cardiovascular health; caffeine interacts adversely with some medicines, and use during pregnancy may increase the risk of spontaneous abortion and lower birth weight. In contrast, there is little or no satisfactory evidence of net benefits of dietary caffeine. The extensive involvement of industry in caffeine research raises serious questions concerning the current and continued integrity of caffeine science.
This chapter explores the potential beneficial effects of caffeine in preventing cognition disorder in the elderly. The growing population of older people is likely to bring about an increase in the incidence of age-related cognitive decline and so strategies to prevent it have to be developed. The consumption of caffeine and other stimulants have potentially beneficial effects on cognition, including improved attention and enhanced information processing and improve mental function. An outline of caffeine chemistry is given and the mechanism of its stimulatory action. The effect of caffeine in aging, prevention of diseases such as Parkinson's and Alzheimer's is explored. The negative effects of caffeine include its hypertensive and anxiety-producing effects as well as withdrawal symptoms and possible drug interactions. The effect of caffeine on cognition is influenced by a number of dietary and lifestyle factors. It concludes that the small number of studies on older people makes firm conclusions difficult as well as interpretation of data related to the effect of caffeine on cognition due to the variation in assessment tools. It recommends further studies to identify the optimal caffeine dose, or more selective stimulants that can separate the apparent cognitive benefits from its side effects.
This study investigated the effects of both habitual caffeine use and dose administered in determining the ability of caffeine to reinforce conditioned changes in flavour preference. Thirty overnight-withdrawn moderate caffeine consumers and 30 non or low-dose caffeine (non/low) consumers evaluated five novel-flavoured fruit teas. Subsequently, their median-rated tea was used in four ensuing conditioning sessions. Either placebo, 1 or 2 mg/kg of caffeine (n=10 consumers, 10 non/low consumers in each condition), was added to the target tea, and all five teas were reevaluated at a final tasting. Pleasantness ratings over the four conditioning sessions indicated that non/low consumers' liking increased for the noncaffeinated fruit tea with no change for the tea containing either 1 or 2 mg/kg of caffeine. Among consumers, pleasantness ratings tended to decrease for the noncaffeinated fruit tea but increased significantly at the 1-mg dose and showed a tendency to increase at the 2-mg dose. Similar effects were shown in the evaluations made before and after conditioning, with no change in the nonexposed drinks. These results show that 1.0 mg/kg of caffeine reinforces changes in flavour pleasantness in acutely withdrawn habitual consumers but not in nonconsumers or nondependent low-caffeine consumers, further endorsing the negative-reinforcement theory of conditioning with caffeine.
History Identifying Characteristics Exposure Dose Effect Toxicokinetics Histopathology and Pathophysiology Clinical Response Diagnostic Testing Treatment References
Caffeine is an excellent model compound for understanding drugs of abuse/dependence (HOLTZMAN 1990). Historically, caffeine use dates back hundreds, possibly thousands, of years (GRAHAM 1984). Caffeine use spread worldwide from its initially constrained geographical origins, despite recurring efforts to restrict or eliminate its use motivated on moral, economic, political, religious or medical grounds (AUSTIN 1979). Currently, caffeine use is almost universal, with more than 80% of adults in North America regularly consuming behaviorally active doses of caffeine (GILBERT 1976; GRAHAM 1978; HUGHES et al. 1993b). The broad generality of caffeine self-administration is reflected in the facts that, worldwide, caffeine consumption occurs in markedly different vehicles (e.g., drinking of coffee, tea, maté, soft drinks; chewing of kola nuts; consumption of cocoa and guarana products) and in widely different, but culturally well-integrated, social contexts (e.g., the coffee break in the United States; tea time in the United Kingdom; kola nut chewing in Nigeria). The dependence-producing nature of caffeine is reflected in the experience of most people who know someone who has expressed a “need” for a cup of coffee or who claimed to be “addicted” to coffee or their morning caffeinated beverage of choice. Consistent with this anecdotal experience, a recent random–digit telephone survey found that about 17% of current caffeine users met the DSM-III-Rpsychiatric criteria for being moderately or severely drug dependent on caffeine (HUGHES et al. 1993b).
Objective:
The goal of the present investigation was to develop and test a brief therapist-guided manualized treatment for problematic caffeine use, including cognitive-behavioral strategies and 5 weeks of progressively decreased consumption.
Method:
Individuals seeking treatment for problematic caffeine use (mean daily caffeine consumption of 666 mg at baseline) were randomized using a waitlist-control design to receive immediate treatment (N = 33) or delayed treatment (∼6 weeks later; N = 34). A 1-hr treatment session designed to help individuals quit or reduce caffeine consumption was provided by a trained counselor along with a take-home booklet. After the treatment session, participants completed daily diaries of caffeine consumption for 5 weeks. They returned for follow-up assessments at 6, 12, and 26 weeks and had a telephone interview at 52-weeks posttreatment.
Results:
Treatment resulted in a significant reduction in self-reported caffeine use and salivary caffeine levels. No significant posttreatment increases in caffeine use were observed for up to 1 year follow-up. Comparisons to the waitlist-control condition revealed that reductions in caffeine consumption were due to treatment and not the passing of time, with a treatment effect size of R2 = .35 for the model.
Conclusion:
A brief 1-session manualized intervention with follow-up was efficacious at reducing caffeine consumption. Future researchers should replicate and extend these findings, as well as consider factors affecting dissemination of treatment for problematic caffeine use to those in need. (PsycINFO Database Record
Chronic migraine is a debilitating disorder that affects 2 % of the global population and imparts a significant societal and economic impact. The cornerstones of chronic migraine management include making an accurate diagnosis, patient education, treatment of comorbid conditions, and selection of an appropriate, evidence-based acute and preventive treatment regimen. Although it is common to treat chronic migraine with preventive medications effective for episodic migraine, a number of treatment options exist with specific evidence for effectiveness in chronic migraine. Currently, onabotulinumtoxinA injections are the only FDA-approved preventive treatment for chronic migraine. A number of non-medication treatment options including occipital nerve and supraorbital nerve stimulation have shown promise as effective prevention for patients either unable to tolerate or unable to obtain relief from oral medications, but more research is necessary.
INTRODUCTION: The combined-use of alcohol and energy drinks is an emerging public health issue. This investigation examined group differences in drinking and driving as well as other high-risk behaviors among combined-users (CU) and students who consumed alcohol-only (AO).
METHODS: College students (n=281) from a large mid-western university were surveyed to assess high-risk drinking and driving behaviors. Chi-square analyses and Mann-Whitney U tests were used to examine differences between the AO (n=174) and CU (n=107) groups.
RESULTS: Combined-users were significantly more likely to drive both over the .08 blood alcohol content (BAC) driving limit (CU 53% vs. AO 38%; p=.009) and after knowing they were too drunk to drive (CU 57% vs. AO 44%; p=.025). Past 30 day differences in the number of days driven while drunk were also examined. Results indicated combined-users drove more frequently with 11.6% of combined-users driving 3-7+days while drunk compared to 2.8% of AO consumers (1-2days, AO 6.9% vs. CU 15.5%; 3-4days, 2.3% vs. 5.8%; 5-6days, 0.0% vs. 3.9%; 7+days, 0.0% vs. 1.9%). Combined-users were also more likely to choose to ride with an intoxicated driver while knowing it was unsafe (CU 56% vs. AO 35%; X2 p=.000).
CONCLUSIONS: The current study suggests students who combine alcohol and energy drinks exhibit an increased likelihood to drive over the .08 BAC limit, to drive while knowingly drunk, to choose to ride with an intoxicated driver, and to drink considerably more alcohol per heavy drinking episode. Public health professionals should focus prevention and education efforts to reduce these high-risk combined-use behaviors.
Coffee is widely consumed and appreciated all over the world, both for their stimulating effect and organoleptic characteristics. Due to its complex chemical composition and the factors involving brews preparation, the consumer is exposed to a wide range of chemical compounds. Several investigations aimed to clarify and understand coffee health effects. There is no evidence that moderate consumption could be harmful. On the contrary, some benefits and possible protective effects against several pathologies have been suggested. This review compiles the main conclusions related with the "coffee and health" topic, reporting, when possible, the chemicals involved.
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