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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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