Nicotine and soluble semi-stable
aldehydes and
ketones in cigarette
smoke are key mediators of the elevated risks for
vascular disease,
cancer, and
chronic obstructive pulmonary disease observed in smokers.
Nicotine, via sympathetic stimulation, increases risk for both
vascular disease and
cancer. Comprehensive suppression of sympathetic activity with the well-tolerated drug
carvedilol, which inhibits betal 1, beta2 and alphal
adrenergic receptors, may be protective to smokers and other
nicotine addicts. The soluble
aldehydes and
ketones in tobacco
smoke appear to exert their adverse effects through activation of
NADPH oxidase complexes in vascular tissues and in the lungs. The
phytochemical phycocyanobilin (PhyCB), richly supplied by the edible cyanobacterium spirulina, in studies on rodents and in human cell cultures has shown the ability to safely mimic intracellular
bilirubin's physiological role as an inhibitor ofNADPH
oxidase activity. It therefore may have potential for mitigating the pro-oxidative effects of tobacco
smoke aldehydes and
ketones. Joint administration of
carvedilol and spirulina merits exploration as a strategy for moderating the pathogenic impact of smoking in chronic tobacco users who either fail to quit or refuse to try cessation of tobacco.
Carvedilol may be appropriate for those who manage a
nicotine addiction in other ways (smokeless tobacco, e-cigarettes,
nicotine gum). Further clinical studies to evaluate the impact of
carvedilol on cardiovascular risk factors in
nicotine addicts, and rodent studies to assess markers of
lung inflammation in
smoke- exposed rodents fed PhyCB, are recommended.