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          Coffee and Parkinson Disease: Is Starbucks the treatment ?
     By Abraham Lieberman MD, Medical Director, National Parkinson
Foundation


     Coffee drinking has, in some studies, been inversely
     associated with Parkinson disease. But the evidence, to
     date, has been equivocal.

     Thus, in an earlier study from the Honolulu Heart
     Program, coffee drinking appeared to be protective against
     Parkinson disease. But there were confounding factors
     and the evidence was not compelling.

     A recent article, from the same group, with Dr. G. Webster Ross as
the lead researcher,
     revisited the study between coffee drinking and the risk of
developing Parkinson disease. The
     new study is based on a longer follow-up and nearly twice the
number of new Parkinson
     cases. The role of other risk factors was analyzed separately. The
study appeared in the 24/31
     May 2000 widely-read and respected Journal of the American Medical
Association (JAMA).

     ABSTRACT

     Design, Setting, and Participants:
     Data were analyzed from 30 years of follow-up of 8004
Japanese-American men (aged 45-68
     years) enrolled in the prospective longitudinal Honolulu Heart
Program between 1965 and
     1968.

     Main Outcome Measure:
     Incident Parkinson disease (number of participants who developed
Parkinson during the study)
     by amount of coffee intake (measured at study enrollment and 6-year
follow-up) and by total
     dietary caffeine intake (measured at enrollment).

     Results:
     During follow-up, 102 men were identified as having Parkinson
disease. Age-adjusted
     incidence of Parkinson disease declined consistently with increased
amounts of coffee intake,
     from 10.4/10,000 person-years in men who drank no coffee to
1.9/10,000 person-years in
     men who drank at least 28 oz/d ( these results were significant
with).

     Similar relationships were observed with total caffeine intake and
caffeine from non-coffee
     sources. Consumption of increasing amounts of coffee was also
associated with lower risk of
     Parkinson disease in men who were never, past, and current smokers
at baseline.

     Other nutrients in coffee, including niacin, were unrelated to
Parkinson disease incidence. The
     relationship between caffeine and PD was unaltered by intake of
milk and sugar.

     Conclusions:
     Our findings indicate that higher coffee and caffeine intake is
associated with a significantly
     lower incidence of Parkinson disease. This effect appears to be
independent of smoking. The
     data suggest that the mechanism is related to caffeine intake and
not to other nutrients
     contained in coffee.

     Comment:
     The median age of the 8004 men at study enrollment (1965-1968) was
53 years (range, 45-68
     years). The median length of follow-up was 27 years, minimum
follow-up was 0.8 years to the
     first death, and maximum follow-up was 30 years from the baseline
examination.

     Among the men, 102 developed Parkinson disease over the 30 years of
follow-up. The median
     age of PD diagnosis was 73.6 years (range, 54-89 years), and the
median interval between
     baseline examination and Parkinson onset was 16.6 years (range,
2-30 years).

     Coffee drinkers had significantly lower incidence of Parkinson
disease than nondrinkers. This
     effect was apparent when examining incidence of Parkinson disease
based on 30 years of
     follow-up according to amounts of coffee consumed at the time of
study enrollment and at the
     1971 examination.

     At each examination, increasing amounts of coffee consumed were
associated with a decline in
     Parkinson disease. Based on data collected at the time of study
enrollment, nondrinkers of
     coffee had a risk of developing Parkinson disease more than 5 times
that of men who
     consumed 28 oz of coffee or more per day ( 4 or 5 cups of coffee,
6-oz in each cup).

     The progressively lower risk of developing Parkinson disease with
increasing amounts of
     coffee consumed was also observed in men who were never, past, and
current smokers. This
     is important because there may be a decreased risk of developing
Parkinson disease among
     cigarette smokers. Thus the two factors, coffee drinking and
cigarette smoking, must be
     analyzed separately.

     Among the other nutrients contained in coffee that were analyzed,
including niacin, no
     associations were observed with risk of Parkinson disease.

     Adjustment for alcohol consumption, hypertension, cholesterol
level, total energy intake, and
     saturated fat level had no effect on the development of Parkinson
disease.

     Parkinson disease afflicts 3% of the population older than 65 years
and is a significant source
     of morbidity and health services use. Based on the projected growth
of the US population, this
     percentage could double in the next 30 - 40 years.

     While rare genetic forms exist, determinants of typical late-onset
disease appear to be largely
     environmental. No treatment has definitively been shown to prevent
disease or slow
     progression. Identification of risk factors may lead to an
understanding of pathogenic
     mechanisms and to effective strategies for prevention.

     This is the first prospective study demonstrating a significant
inverse association between
     coffee consumption and development of Parkinson disease. There are
several possible
     mechanisms.

        1.The lower frequency of coffee consumption during mid-life
among men who eventually
          developed Parkinson disease could reflect an intolerance to
caffeine among persons with
          a tendency to develop Parkinson disease.

        2.Regular exposure to caffeine over many years might counteract
the age-related
          degenerative processes that cause loss of dopamine cells.

        3.Caffeine could also modulate the receptors on pigmented cells
in the midbrain and/or
          striatum. Thus, caffeine is a known stimulant thought to act
by blocking adenosine
          receptors in the brain. Adenosine is an internally generated
brain chemical. Blocking
          adenosine receptors results in increased movement possibly
through increasing dopamine
          levels. Thus, rather than having a direct effect on the
development of Parkinson disease,
          coffee and other caffeine sources may be a form of
self-medication that decreases the
          expression of Parkinson symptoms.

     There are limits to the study as noted by the authors.

        1.The population is Japanese-American men with older age at
diagnosis. Generalizations to
          younger-onset cases, women, and other ethnic groups cannot be
made with certainty. A
          review of the worldwide frequency of Parkinson disease
suggests that incidence is lower
          in Japan, with rates ranging from 5.4 - 10.2 compared with
rates in North America and
          Europe (range, 6-23).

        2.The study design is such as to prevent the researchers from
concluding, definitively, that
          coffee or caffeine directly protect against development of
Parkinson disease.

     At this time there is not enough evidence to urge you to go to
Starbucks and drink 6
     café-latte's a day. However, the possibility that caffeine may have
a protective effect against
     developing Parkinson disease must be investigated further.

--
Cheers,
Joao Paulo - Salvador,BA,Brazil
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