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Table 10.4 Relative strength of physiological effects exerted by caffeine, theobromine and theophylline.

System

Caffeine

Theobromine

Theophylline

Brain

Strong

Weak

Moderate

Heart

Weak

Moderate

Strong

Bronchia

Weak

Moderate

Strong

Skeletal muscle

Strong

Weak

Moderate

Kidneys

Weak

Moderate

Strong

of caffeine can stimulate the cortex, resulting in reduced fatigue, shortened reaction time, sensory stimulation and increased motor activity. High blood concentrations produced by the same amount of caffeine administered parenterally can also stimulate the medullary respiratory, vasomotor and vagal centers. Amounts of 200500 mg can cause headaches, tremulousness, nervousness and irritability (28).

Delay in sleep has been noted after caffeine doses of 100 mg, although there appears to be considerable variation between and even within individuals (29). Estimated time to go to sleep after 300 mg of caffeine varied from 15240 min for one individual, but never exceeded 45 min after consuming a placebo (30). In other studies, regular coffee consumers were relatively insensitive to caffeine's effect on their sleep habits while non-coffee drinkers experienced a delayed onset of sleep (31, 32). Sleep patterns can be influenced by temperature, noise and fatigue as well as habitual caffeine consumption, complicating the evaluation of study results.

In contrast to caffeine, theobromine is virtually inactive as a CNS stimulant, although headaches have been reported after ingestion of 50 g of cocoa per day, and sweating, trembling and severe headaches after long-term ingestion of 100 g of cocoa per day (25). Even in large doses, theobromine appears to be ineffective in relieving drowsiness and fatigue, and does not prolong the time required to fall asleep (29).

Interest in the behavioral and autonomic effects of caffeine led to investigations of the hormonal effects of caffeine. Increases in brain levels of serotonin and 5-hydroxyindoleacetic acid were observed after both acute and chronic administration of caffeine (33). Plasma epinephrine and norepinephrine were increased after 220250 mg caffeine consumption (34, 35). Higher doses on the order of 500 mg can cause endocrine stress symptoms characterized by increased serum adrenocorticotropic hormone (ACTH) and cortisol (36). After 7 days of caffeine consumption, no increases in hormone levels were observed, suggesting that habitual consumers are the least sensitive to caffeine's effects on the endocrine system. Based on the high doses of caffeine required to produce these effects, it is unlikely that normal consumption of cocoa and chocolate-containing foods would produce any observable endocrine effects.

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Cardiovascular/Circulatory

The methylxanthines can affect cardiovascular function directly or indirectly influence it through their effects on the neurocrine and endocrine systems. Although caffeine is the weaker of the two, both theobromine and caffeine stimulate cardiac muscle, increasing the force of contraction, heart rate and cardiac output (28, 34). At the same time, these compounds can also stimulate the medullary vagal nuclei, producing a decrease in heart rate. The result of these opposing actions may be no change in heart rate, bradycardia or tachycardia. Occasionally, arrhythmias have been observed in persons who use excessive amounts of caffeine.

Caffeine and theobromine briefly dilate coronary, pulmonary and general systemic blood vessels, and thereby increase blood flow. The methylxanthines have been therapeutically used to dilate coronary arteries and increase coronary blood flow, although there is controversy over the effectiveness of this practice. They also stimulate the medullary vasomotor center to constrict blood vessels and decrease cerebral blood flow and oxygen tension. The vasoconstrictive action is believed to be responsible for the efficiency of xanthines in relieving hypertensive headaches. Conversely, sudden withdrawal of caffeine results in a dilatation of cerebral blood vessels and reports of headaches (37).

Due to the multiple physiological effects of the methylxanthines, their overall impact on systemic blood pressure is usually minimal or, at worst, unpredictable (28, 38). Stimulation of the central vasomotor and myocardium tend to increase blood pressure; central vagal stimulation and peripheral vasodilation tend to decrease blood pressure. Pulse pressure is increased by the vasodilation and enhanced cardiac output while pulmonary arterial pressure is usually reduced.

As with the neurocrine and endocrine effects, cardiovascular effects appear to be minimized by habitual methylxanthine intake. Blood pressure, heart rate, plasma renin activity and plasma and urinary catecholamines increase after a single dose of caffeine is ingested by caffeine-naive individuals (35). However, levels return to baseline within 47 days of repeated caffeine administration (38).

Caffeine consumption has been considered as a possible risk factor for coronary heart disease, although results from both animal and human studies have not been consistent. Interpretation of study results is confounded by a host of factors, including age, sex, adiposity, alcohol consumption, exercise, smoking habits, occupational stress and ethnicity. Two studies by the Boston Collaborative Drug Surveillance Program suggested that coffee consumption is associated with an increased risk of myocardial infarction (39, 40). In another study, coffee raised cholesterol, phospholipids and triglycerides, but tea caused a fall in all three fractions (41). Retrospective and prospective studies since that time have failed to consistently find a correlation between coffee consumption and ischemic heart disease (42-44). A number of the reported correlations actually may have been due to other confounding factors such as brewing techniques, non-caffeine

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