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The Contribution of cocoa additive to cigarette smoking addiction

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RIVM report 650270002 Page 101 <strong>of</strong> 207<br />

Tryp<strong>to</strong>phan<br />

activity, leading <strong>to</strong> increased catabolism <strong>of</strong> tryp<strong>to</strong>phan and thus making less<br />

tryp<strong>to</strong>phan available <strong>to</strong> the brain. Allopurinol, an inhibi<strong>to</strong>r <strong>of</strong> hepatic tryp<strong>to</strong>phan<br />

pyrrolase activity, prevented the reduction in the indole levels induced by 5-ALA<br />

(40).<br />

<strong>The</strong> tryp<strong>to</strong>phan degradation in the brain is reduced by methamphetamine due <strong>to</strong><br />

inhibition <strong>of</strong> tryp<strong>to</strong>phan hydroxylase (41).<br />

Critical assessment<br />

Chemical<br />

Both the amino group and the carboxy group form potential sites for a wide variety <strong>of</strong><br />

reactions. It has been shown that numerous compounds react with tryp<strong>to</strong>phan in<br />

<strong>cigarette</strong>s during <strong>smoking</strong> and resulting in complex compounds with potential<br />

hazardous effect in the body.<br />

In vivo<br />

Several compounds affect the tryp<strong>to</strong>phan level in plasma or brain either by inducing<br />

or inhibiting the tryp<strong>to</strong>phan degradation or by interaction with the binding site <strong>of</strong><br />

tryp<strong>to</strong>phan in albumin or in the transport system through the blood-brain-barrier.<br />

Conclusion<br />

Chemical<br />

Tryp<strong>to</strong>phan can react with numerous compounds during <strong>smoking</strong> resulting in<br />

potentially hazardous compounds for the body.<br />

In vivo<br />

Several compounds affect the tryp<strong>to</strong>phan level in plasma and brain.<br />

DEPENDENCY<br />

Effects <strong>of</strong> <strong>smoking</strong> cessation<br />

It is known that nicotine enhances the sero<strong>to</strong>nin release in the brain and that nicotine<br />

withdrawal has the opposite effect. Sero<strong>to</strong>nin-releasing brain neurons are unique in<br />

that the amount <strong>of</strong> neurotransmitter they release is normally controlled by food<br />

intake: carbohydrate consumption--acting via insulin secretion and the ‘plasma<br />

tryp<strong>to</strong>phan ratio’--increases sero<strong>to</strong>nin release; protein intake lacks this effect. This<br />

ability <strong>of</strong> neurons <strong>to</strong> couple neuronal signalling properties <strong>to</strong> food consumption is a<br />

link in the feedback mechanism that normally keeps carbohydrate and protein intakes<br />

more or less constant. Hence many patients learn <strong>to</strong> overeat carbohydrates<br />

(particularly snack foods, like pota<strong>to</strong> chips or pastries, which are rich in<br />

carbohydrates and fats) <strong>to</strong> make themselves feel better. This tendency <strong>to</strong> use certain<br />

foods as though they were drugs is a frequent cause <strong>of</strong> weight gain, and can also be<br />

seen in people who are attempting <strong>to</strong> give up <strong>smoking</strong> (42). Sero<strong>to</strong>nin-enhancing<br />

substances, such as tryp<strong>to</strong>phan and high-carbohydrate diets, have been used in<br />

clinical disorders <strong>to</strong> relieve negative affect, a classic symp<strong>to</strong>m <strong>of</strong> <strong>cigarette</strong><br />

withdrawal. In a study it was investigated whether the use <strong>of</strong> tryp<strong>to</strong>phan (50<br />

mg/kg/day) and high-carbohydrate diets, <strong>to</strong>gether with more traditional <strong>smoking</strong><br />

cessation treatment techniques, was able <strong>to</strong> ameliorate the <strong>smoking</strong> withdrawal<br />

syndrome and <strong>to</strong> improve abstinence rates. Subjects were randomly assigned <strong>to</strong><br />

receive either tryp<strong>to</strong>phan (n = 16) or placebo (n = 15). Standard <strong>smoking</strong> cessation<br />

treatment was identical for the experimental and control groups and consisted <strong>of</strong> four<br />

2-hr weekly sessions <strong>of</strong> multicomponent group therapy. Smoking behaviour,<br />

symp<strong>to</strong>ms <strong>of</strong> nicotine withdrawal, and negative effect were assessed during a 2-week

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