Caffeine & Anxiety: A Stress Interaction

The study began with the hypothesis that caffeine, as a central nervous system stimulant, could be beneficial in modulating arousal levels for improved performance under stress. It was suggested that low-anxiety individuals might use caffeine to reach an optimal arousal state for tasks like exams or public speaking, while high-anxiety individuals might perform better by avoiding caffeine. This initial premise was based on the understanding that caffeine affects alertness, tension, and performance, but lacked prior experimental comparison of high and low trait anxiety subjects.

The core of the experiment involved a mental arithmetic task as a measure of performance under stress. Participants, categorized as having either high or low anxiety traits, were administered either caffeine (400mg) or a placebo. This allowed for a direct comparison of caffeine's effects on performance within both anxiety groups. The study measured multiple variables alongside performance, such as blood pressure, heart rate, subjective alertness, and subjective tension, providing a comprehensive picture of the overall stress response and how it is affected by caffeine.

The study's primary finding was the absence of a significant effect of caffeine on performance on the mental arithmetic task in both high and low anxiety groups. This directly contradicted the initial hypothesis. Contrary to expectations, caffeine administration did not provide a noticeable benefit for either high or low anxiety individuals in terms of task completion or accuracy. This unexpected result suggests that using caffeine to manipulate arousal and improve performance under stress is not a reliable strategy.

While caffeine failed to improve performance, the study did reveal effects on other physiological and psychological variables. Blood pressure responses, specifically diastolic blood pressure, were significantly higher during the stressful mental arithmetic task in both groups following caffeine administration compared to the placebo. Additionally, subjective alertness was increased by caffeine in both groups. Interestingly, the order in which caffeine was administered (first or second testing session) had a greater influence on reported tension levels than the caffeine itself. The interaction between sex, anxiety level, and caffeine also impacted blood pressure responses, with low-anxiety males exhibiting the most significant diastolic blood pressure elevation during stress.

The research concludes that a 400mg dose of caffeine is not effective in optimizing arousal or stress levels to enhance performance in stressful situations, regardless of anxiety level. While caffeine did increase subjective alertness and diastolic blood pressure under stress, its impact on performance was negligible. High anxiety females showed the most notable increase in resting systolic blood pressure after caffeine consumption, suggesting potential cardiovascular risks. The overall findings suggest a complex interplay between caffeine, anxiety, sex, and stress, highlighting the need for further research considering individual variability and using multiple physiological measures.

Caffeine, pharmacologically, is a powerful central nervous system (CNS) stimulant. This stimulatory action is largely responsible for the widespread popularity of caffeinated beverages. The text cites Ritchie (1975) and Graham (1978) who claimed that coffee and tea improve mental activity, enhance intellectual effort, reduce drowsiness and fatigue, and decrease reaction time—all highly valued in achievement-oriented societies. These effects are attributed to caffeine's impact on the cortex, and at high doses, on the medulla's respiratory, vasomotor, and vagal centers, as well as the spinal cord. Importantly, the dosages frequently exceeded in daily life are of clinical significance, with potential cumulative effects.

A key physiological effect of caffeine is its influence on blood pressure. Lane (1983) demonstrated that moderate caffeine doses (two or three cups of coffee) raised blood pressure in healthy young males during both rest and stress. Crucially, Lane concluded that the blood pressure elevation caused by caffeine is additive to that caused by stress. The text further notes that caffeine's impact on the circulatory system is complex, with the ability to both dilate and constrict blood vessels, highlighting the need for multiple measurements of multiple variables in any comprehensive study of its effects on the circulatory system and medullary centers. The lack of research on caffeine's effect on populations with pre-existing cardiovascular conditions is also mentioned as an important area of future research.

Beyond its effects on the cardiovascular system, caffeine also affects respiratory function. Robertson et al. (1978) found that 250mg of caffeine significantly increased respiratory rate in non-coffee drinkers, with the degree of acceleration correlating with plasma caffeine levels. The document also mentions that caffeine affects other systems. For instance, it impacts gastric acid secretion, possibly independently of its stimulant effects. Caffeine has also been shown to increase cyclic 3',5' adenosine monophosphate, a compound likely involved in stimulating hydrogen ion secretion by the gastric mucosa (Harris et al., 1965, 1969). This indicates that the effects of caffeine are not limited to just the CNS but have broader physiological implications.

Studies on the chronic effects of caffeine show no growth retardation, reproductive impairment, or other pathological problems in rats at levels of 35-60mg/kg of body weight daily for 26 weeks. Similarly, there were no adverse effects on the fertility or mortality of rats after daily injections of 100mg/kg of body weight for four generations. Despite this, the document emphasizes that individual responses to caffeine vary dramatically, with some individuals exhibiting high tolerance while others have extremely sensitive responses. This variation is attributed to differences in metabolic half-life and biotransformation rates. The text points out that even 4 hours after one cup of coffee, substantial amounts of caffeine remain in the system, illustrating the importance of considering these individual differences when studying caffeine's effects.

The document defines caffeinism, a diagnosis included in the DSM-III, as the result of ingesting high doses of caffeine from various sources (tea, coffee, cola, over-the-counter medications). Symptoms include a constellation of affective, sleep, and psychophysiological manifestations. Innes and Nickerson (1975) list anxiety as a side effect of epinephrine and norepinephrine injections, hormones whose levels are increased by caffeine. Sawyer et al. (1981) point out that the causal link between caffeine and anxiety is unclear. They note that caffeine's effects on these hormones might interact with situational variables, exacerbating subclinical anxiety to clinical levels. Other reported symptoms of caffeinism include nervousness, tremulousness, muscle twitching, insomnia, sensory disturbances, palpitations, flushing, arrhythmias, diuresis, and periods of agitation and depression (Greden, 1974; Furlong, 1975). Greden et al. (1978) also found a correlation between prehospitalization caffeine consumption and anxiety and depression in psychiatric inpatients.

While popularly believed to elevate mood, the document notes that other central nervous system stimulants, like amphetamines and cocaine, cause depression after an initial mood lift. Veleber and Templer (1984) suggest the perceived mood-boosting effect of caffeine might be time-dependent. Their study, using the Multiple Affect Adjective Checklist (MAAC), found that caffeine increased anxiety, depression, and hostility, but the timing of the assessment relative to caffeine consumption could influence these results. Regarding sleep, the document notes that caffeine's sleep-disturbing properties are more pronounced in non-users than habitual users (Goldstein, 1964a). Goldstein (1964b) showed that 150-200mg of caffeine before bedtime prolongs sleep onset, though the effect is less in heavy caffeine consumers.

The document discusses caffeine's role in headaches, noting that it provides only temporary relief, creating a cycle of recurring headaches (Selbach, 1973; Miller, 1960). However, intravenous caffeine has been used to relieve hypertensive headaches, possibly by constricting cerebral arteries and reducing brain swelling (Selbach, 1973). Caffeine administration during the early stages of migraine headaches has also prevented further development in some cases. This dual role of caffeine in both causing and alleviating headaches highlights the complexity of its effects and the need for further research, particularly concerning the mechanisms involved and the potential for chronic usage to impact headache frequency and intensity.

The document describes a case study by Roller (1981) detailing caffeine withdrawal symptoms in a heavy user (900-1100mg/day). After 72 hours of abstinence, headaches, fatigue, rhinorrhea, leg pain, diaphoresis, and general muscle aches developed, resolving quickly upon resuming caffeine consumption. This highlights the potential for significant withdrawal symptoms. The document also connects caffeine to Restless Legs Syndrome (RLS). Lutz (1978), based on 11 years of experience with 62 patients, concluded that caffeine is a major factor in causing RLS. Other factors, like hereditary predisposition and environmental influences, may modify individual sensitivity to caffeine's effects in the context of RLS. The document suggests that caffeine's role in increasing nervous system arousal and striated muscle contractility might interfere with microcirculation, leading to increased irritability and the dysphoric sensations characteristic of RLS.

The study employed a double-blind design to assess the effects of acute caffeine administration (400mg, equivalent to approximately five cups of coffee) on stress response and performance. Participants were categorized into high and low anxiety groups based on trait anxiety scores. The stressor used was a mental arithmetic task. Physiological measures included blood pressure (systolic and diastolic) and heart rate, recorded at 3-minute intervals during a 15-minute pre-drug baseline and throughout the experiment. Subjective measures, alertness and tension, were assessed using Visual Analogue Scales (VAS) before and after caffeine or placebo administration, and during the stressor task. The order of drug administration (caffeine or placebo first) was also recorded, as it emerged as a crucial factor impacting results. This comprehensive design was intended to provide a detailed examination of the interplay between caffeine, anxiety, and stress on various physiological and psychological parameters.

The results indicated no significant effect of caffeine on performance on the mental arithmetic task, regardless of anxiety level. This contrasts with the initial hypothesis. However, caffeine administration did significantly elevate diastolic blood pressure during the stressor task in both high and low anxiety groups. While this elevation was significant, the order of drug presentation proved the most important factor influencing reported levels of tension. Notably, caffeine did not appear to significantly affect heart rate in either high or low anxiety subjects during rest or under stress. High-anxiety female participants showed the most substantial elevations in resting systolic blood pressure after caffeine consumption, a finding highlighted as potentially significant regarding cardiovascular health.

The study also collected subjective data on alertness and tension using VAS. Caffeine administration significantly increased subjective alertness in both high and low anxiety groups during the post-drug and stressor phases, indicating a clear subjective effect. However, subjective tension was more profoundly influenced by the order of drug presentation, indicating a potential learning effect or habituation to the drug which requires further study. High-anxiety participants showed a greater difference in reported alertness compared to low-anxiety participants following caffeine administration. These findings suggest that while caffeine increased alertness, its impact on tension was complex and possibly confounded by procedural factors.

A major limitation was the significant influence of the order of drug presentation, which confounded interpretations of the interactions between caffeine, anxiety, and sex. The study only measured blood pressure and heart rate as physiological variables; future research should include more physiological measurements to provide a more complete picture. The results did not fully support previous findings from other studies regarding the interaction between caffeine, stress, and physiological changes (Cobb, 1974; Henry and Stephens, 1980; Lane, 1983). The study’s findings, however, suggest that for individuals who regularly consume caffeine, the combined effect of caffeine and daily stress might not result in significantly higher blood pressure than either alone. The significant interaction between sex and anxiety levels on diastolic blood pressure also warrants further investigation.

One significant limitation was the unexpected and substantial influence of the order of drug presentation (caffeine or placebo first) on the results. This order effect overshadowed other factors like anxiety level, sex, and the drug condition itself in several key interactions. This made it difficult, if not impossible, to draw definitive conclusions about the specific interactions of interest, particularly those related to the effects of caffeine on blood pressure, heart rate, alertness, and tension in individuals with different anxiety levels. The study highlights the need for future research to account for and control this confounding variable, perhaps by employing a counterbalanced design to minimize this limitation.

The study’s reliance on primarily cardiovascular measurements (blood pressure and heart rate) is presented as a limitation. Ritchie (1975) is cited to emphasize that observing a single physiological function like blood pressure can be misleading because caffeine may influence a variety of circulatory factors, leading to seemingly unchanged overall blood pressure. Future studies should incorporate a broader range of physiological measures, including respiratory rate, hormonal levels, and other relevant indicators, to create a more complete understanding of caffeine's complex physiological effects. This would allow for a more thorough analysis of the interaction between caffeine and stress on the human body.

The study's failure to account for hormonal fluctuations in females, particularly those related to the menstrual cycle, is cited as a key limitation. The document argues that the menstrual cycle may significantly influence responses to caffeine, affecting behavior (e.g., tiredness, concentration, emotionality) and the interaction with caffeine. This suggests a need for future studies to consider the menstrual cycle and its impact on caffeine's effects, and to also consider the impact of hormone replacement therapies, such as contraceptive pills, on the influence of caffeine. More generally, the study indicates a future need to carefully record and account for additional individual differences, such as age, sex, mental state, personality type, and physical fitness, to fully explain the variability observed in responses to caffeine across different populations, including racial and ethnic groups.