The Contribution of cocoa additive to cigarette smoking addiction

RIVM report 650270002 Page 39 of 207
Caffeine
DEPENDENCY
After sudden caffeine cessation, withdrawal symptoms develop in a small portion of
the population but are moderate and transient. Tolerance to caffeine-induced
stimulation of locomotor activity has been shown in animals. In humans, tolerance to
some subjective effects of caffeine seems to occur, but most of the time complete
tolerance to many effects of caffeine on the central nervous system does not occur. In
animals, caffeine can act as a reinforcer, but only in a more limited range of
conditions than with classical drugs of dependence. In humans, the reinforcing stimuli
functions of caffeine are limited to low or rather moderate doses while high doses are
usually avoided. The classical drugs of abuse lead to quite specific increases in
cerebral functional activity and dopamine release in the shell of the nucleus
accumbens, the key structure for reward, motivation and addiction. However, caffeine
doses that reflect the daily human consumption, do not induce a release of dopamine
in the shell of the nucleus accumbens but lead to a release of dopamine in the
prefrontal cortex, which is consistent with caffeine reinforcing properties. Moreover,
caffeine increases glucose utilization in the shell of the nucleus accumbens only at
rather high doses that stimulate most brain structures, non-specifically, and likely
reflect the side effects linked to high caffeine ingestion. That dose is also 5-10-fold
higher than the one necessary to stimulate the caudate nucleus, which mediates motor
activity and the structures regulating the sleep-wake cycle, the two functions the most
sensitive to caffeine. In conclusion, it appears that although caffeine fulfils some of
the criteria for drug dependence and shares with amphetamines and cocaine a certain
specificity of action on the cerebral dopaminergic system, the methylxanthine does
not act on the dopaminergic structures related to reward, motivation and addiction
(51, 52).
The pharmacology of caffeine in cocoa products has been thoroughly reviewed and
the conclusion seems to be that this agent is not responsible for the craving qualities
of chocolate (15, 53).
Effects of smoking cessation
There is a strong, significant relationship between coffee consumption and smoking.
In six epidemiological studies reviewed and analyzed, 86.4 % of smokers consumed
coffee versus 77.2 % of non-smokers. Ex-smokers use more coffee than non-smokers
do, but somewhat less than smokers do. Seventeen experimental studies suggest that
the pharmacological effect of caffeine in coffee may be partially but not totally
responsible for the relationship. Conditioning, a reciprocal interaction (caffeine intake
increases anxiety/arousal--nicotine decreases it), or joint effect of a third variable
(e.g., stress, alcohol) may account for the relationship. In abstinent smokers, blood
caffeine levels increase and remain elevated for as long as 6 months. These higher
caffeine plasma levels may be sufficient to produce caffeine toxicity syndrome (54).
Critical assessment
Caffeine has low addictive properties and some causal relationship exists between
caffeine intake from coffee and smoking. However, the low doses in the cigarettes is
marginal compared with the high intake from other caffeine sources, such as coffee.
At the other hand, caffeine could increase the nicotine availability through
bronchodilatation, which subsequently could increase the addictive property of