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02/22/96 - 08:14 PM ET - Click reload often for latest version

Linking smoking, lower Parkinson's risk

http://web.usatoday.com/life/health/lhs411.htm

Something in cigarette smoke - but not nicotine - may not only boost
addiction but also may explain why smokers appear to have a lower risk
of Parkinson's disease.

Researchers have known for years that nicotine's pleasure comes in
part from its ability to increase production of a brain chemical
called dopamine. Now scientists understand that there is more than
nicotine at work: Something in smoke lowers the levels of an enzyme
known as MAO B. As those levels go down, dopamine goes up.

Smokers have about 40% less MAO B than nonsmokers or ex-smokers, says
Joanna Fowler of the Brookhaven National Laboratory, Upton, N.Y., who
studied MAO B levels in eight smokers, eight nonsmokers and four
ex-smokers.

Nicotine already has been ruled out as the cause of the MAO B
shortage, the researchers say.

"There is something in the smoke contributing to the addiction that
goes beyond just the nicotine itself. That's what it looks like" from
Fowler's research, says Dr. Alan Leshner, director of the National
Institute on Drug Abuse.

Among the implications from the study, published in Nature:

     Because reduced levels of MAO B result in greater amounts of
     dopamine, Fowler says, smokers may have a lower risk of
     Parkinson's, a nerve disease aggravated by dopamine shortages.
     Drugs that increase MAO B or reduce dopamine's effect may help
     smokers stop smoking, says Leshner. Higher smoking rates among
     drug abusers may be linked to reduced MAO B levels, says Dr. Neal
     Benowitz, the University of California, San Francisco. The
     lowered enzyme level from the smoke could make alcohol and
     cocaine more pleasurable.

By Doug Levy, USA TODAY

-------------------------------------------

     NICOTINE GENE & SMOKING BEHAVIOR

http://www.gene.com/ae/WN/SU/nicotine.html

     SAN DIEGO - Many of the forbidden pleasures of the modern
     day-nicotine, alcohol and over-eating- appear to be linked by
     common genetic factors, according to recent studies.

     Genetic variables appear to play a key role in every aspect of
     nicotine addiction, from the tendency to begin smoking, to the
     chances of quitting, reported researchers at the first conference
     of the Society for Research on Nicotine and Tobacco.

     Evidence is now converging from behavioral studies, twin studies
     and molecular genetic research that provides a clearer
     understanding of the biobehavioral basis for nicotine dependence.
     Ultimately this should lead to the development of improved
     methods for assessment and treatment of dependence, said Gary
     Swann, Ph.D., of the Stanford Research Institute.

     "Behavioral scientists have made great progress in defining the
     phenotype and carefully pointing out the variables that have to
     be taken into account in describing individual differences in
     smoking behaviors. Molecular biologists have made great progress
     in identifying an array of nicotinic receptors, the genes
     involved and their locations, and other neurochemicals
     (particularly dopamine) that may be involved in regulation and
     activation of nicotine related behavior," he noted.

     Dr. Swan and colleagues analyzed more than 20 studies of smoking
     behaviors in monozygotic and dizygotic twins. They found
     consistent evidence of genetic influences governing the
     developmental stages of smoking (initiation, maintenance,
     cessation), smoking intensity (light to heavy), as well as for
     level alcohol consumption.

     Five years ago, Dr. Ernest Noble and colleagues reported the
     discovery of a gene that appeared to be associated with
     alcoholism, the D2 dopamine receptor gene (DRD2). Since that time
     Dr. Noble has conducted further studies implicating this gene in
     behaviors associated with tobacco, cocaine and obesity.

     There are two main dopaminergic pathways in brain. The first
     begins in the area called the substantia nigra and is involved
     with movement. Defects in this part of the brain are associated
     with movement disorders such as Parkinson's disease. The second
     pathway, the mesolimbic dopamine system, is associated with
     emotion activation.

     "When alcohol, nicotine, cocaine, or food are ingested, dopamine
     levels increase in this area. Therefore, we think these areas are
     associated with reward and pleasure," noted Dr. Noble, a
     professor of psychiatry at UCLA.

     The DRD2 gene is found on chromosome 11, in the q22-23 region.
     There are two alleles of interest, A1 found in 25% of the
     population and A2 found in 75%. Studies comparing alcoholics to
     controls showed a significantly higher incidence of A1 allele.
     The A1 allele is associated with significantly reduced levels of
     D2 dopamine receptors in the brain.

     "This led us to hypothesize that individuals with the A1 allele
     may have an inherent deficit of the dopaminergic system. To
     compensate for that deficiency, they are high risk for using
     alcohol, and other substances which by releasing dopamine
     activate these areas," he explained.

     Dr. Noble recently completed a study of the association between
     this gene with smoking and obesity. This study showed that male,
     but not female, smokers with the A1 allele began to smoke at an
     earlier age than those with the A2 allele. Also, the female
     smokers with the A1 allele were less likely to be obese, while
     male smokers with the A1 allele were more likely to be obese. The
     study also showed that non-obese female smokers with the A1
     allele had higher levels of anxiety and depression, while obese
     female smokers had lower anxiety scores.

     "These studies add further support for the role of this gene in
     weight and mood in smokers and non-smokers. However, the
     differences seen in males and females suggest that besides DRD2
     gene, other epigenetic and environmental factors play a role in
     contributing to these gender differences," he said.

     These findings could point the way to useful therapies for those
     attempting to quit smoking or drinking. A recent study with
     bromocriptine, a drug that increases levels of DRD2, showed
     significant improvements in craving and anxiety among alcoholics
     trying to quit.

     For more information see: Nature Medicine, 4/4/95, Noble et al.;
     Science, 4/26/95, Wehner et al.; or contact the Society for
     Research on Nicotine and Tobacco at tel: (301) 251-2792.

     Transmitted: 95-05-10 15:15:27 EDT

------------------------------------------------------

SCIENTIFIC AMERICAN ARTICLE

This response submitted by MAY 1996 ISSUE on 7/30/96.

http://dem0nmac.mgh.harvard.edu/neurowebforum/ParkinsonsDiseaseArticle
s/SCIENTIFICAMERICANARTICLE.htmlA
Author's Email: [log in to unmask]

PAGE 20 OF THE MAY 1966 SCIENTIFIC AMERICAN ADVISES THAT JOANNA S.
FOWLER AND HER COLLEAGUES AT BROOKHAVEN NATIONAL LABORTORY FOUND THAT
MAO B WAS 40% LESS ACTIVE IN SMOKERS. THE ARTICLE CONCLUDED BY NOTING
THAT THIS MAY EXPLAIN WHY FEW SMOKERS ACQUIRE PD. WHILE NOT A LONG OR
LARGE ARTICLE IT GAVE ME THE INCENTIVE TO SMOKE A PIPE FOR TWO WEEKS.
THERE WAS A REDUCTIUON OF PAIN AFTER TEN DAYS. I GAVE UP SMOKING AFTER
15 DAYS. NOW AFTER 15 ADDITIONAL DAYS PAIN HAS RETURNED. I AM
PARTIALLY CONVINCED AND I AM GOING TO EXPERIMENT FURTHER. GORDON

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