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LE Magazine March 2001
In The News
SAMe works when other anti-depressants
fail
 In a study published in the journal Movement Disorders (Nov 15, 2000),
s-adenosyl-methionine (SAMe) was administered to 13 depressed
patients with Parkinson's disease. All patients had been
previously treated with other antidepressant agents and had no
significant benefit or had intolerable side effects. SAMe was
administered in doses of 800 to 3600 mg per day for a period
of 10 weeks. Eleven patients completed the study, and 10 had
at least a 50% improvement on the 17-point Hamilton Depression
Scale. One patient did not improve. Two patients prematurely
terminated participation in the study because of increased
anxiety. One patient experienced mild nausea, and another two
patients developed mild diarrhea, which resolved
spontaneously. The mean improvement in depression scores from
before to after treatment was approximately 64%.
Although this study was uncontrolled and preliminary, it
suggests that SAMe is well tolerated and may be a safe and
effective alternative to the antidepressant agents currently
used in patients with Parkinson's disease. Please note that
some of these Parkinson's patients received very high doses of
SAMe, which could account for the few side effects observed.
Previous clinical studies show that doses of 800 to 1600 mg a
day of SAMe produce remarkable anti-depressant benefits in
otherwise healthy people without significant side effects.
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Aspirin &
Alzheimer's
In the November 2000 issue of Life Extension we reported that
ibuprofen, aspirin and other anti-inflammatories slow the
progression of Alzheimer's disease (AD). People who
chronically take anti-inflammatory drugs lower their risk
of getting AD in the first place. Most studies have looked
at people who take non-steroidal anti-inflammatory drugs
(NSAIDs) for other conditions such as rheumatoid arthritis.
Most of these people are taking moderate to high doses. A
new study looks at whether or not lower doses of NSAIDs and
other anti-inflammatories also reduce risk. It was found
that they do, at least in people over 75. As in previous
studies, aspirin seems to work about half as well as NSAIDs
such as ibuprofen-but it still can reduce risk about
25%.
High doses are not needed for beneficial effects. Aspirin
in doses less than 175 mg/day and NSAIDs in doses less than
500 mg/day provide protection against AD. This is good news
for people worried about intestinal bleeding and potential
kidney damage (the latter due to high-dose NSAIDs). The
very group that is most at risk for AD (over age 75) is
also more likely to get serious side effects from
anti-inflammatories.
The fact that it only takes low doses of the drugs to
get the effects means, also, that anti-inflammatories work
by some mechanism other than reducing inflammation. The
authors suggest that low levels of anti-inflammatories may
work by inhibiting the release of b-amyloid from platelets
and/or by inhibiting excess levels of cyclooxygenase
(COX).
A surprising finding of the study was the strong showing
of ACE-inhibitors. Taking these drugs also appears to lower
the risk of Alzheimer's. ACE (which stands for
“angiotensin converting enzyme”) inhibitors are
used to treat heart disease and lower blood pressure.
The study, conducted in Sydney, examined 78 patients with
probable AD (as assessed by National Institute of
Neurological and Communicative Disorders and
Stroke-Alzheimer's Disease and Related Disorders
Association criteria). It also looked at 45 people with
possible AD and/or vascular dementia, and 40 people with
other dementias. The effects of anti-inflammatories held up
only for AD, not for dementias of other types. The study
did not, however, look at duration. In other words, we
don't know how long a person has to take
anti-inflammatories to get the beneficial effects. Other
studies suggest that a person has to take NSAIDs for years,
while aspirin may start working immediately. (Two plus
years of NSAID use in the Baltimore Longitudinal Study of
Aging reduced the risk 60%). While this question is still
up-in-the-air, it seems that the question of whether a
person can get anti-Alzheimer's effects by taking low doses
of anti-inflammatories has been answered in the affirmative
for now.
Anthony JC, et al. 2000. Reduced
prevalence of AD in users of NSAIDs and H2 receptor
antagonists: the Cache County study. Neurology 54:2066-71.
Broe GA, et al. 2000. Anti-inflammatory drugs protect
against Alzheimer [sic] disease at low doses. Arch Neurol 57:1586-91.
Stewart WF, et al. 1997. Risk of Alzheimer's disease and
duration of NSAID use. Neurology 48:626-32.
Sugaya K, et al. 2000. New anti-inflammatory treatment
strategy in Alzheimer's disease. Jpn J Pharmacol
82:85-94.
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All in the Genes
 Genetics' contribution to the risk of breast,
colorectal and prostate cancer is 27%, 35% and 42%
respectively, according to a study of 44,788 pairs of twins
from Scandinavian registries, published in the New England Journal of Medicine last
summer. But for most of more than 15 other anatomic sites, the
study found little or no genetic contribution to risk.
This study sheds additional light on a controversy that has
raged over the genetic vs. environmental contribution to
cancer, Robert M. Hoover, M.D., of the National Cancer
Institute wrote in an editorial accompanying the article. Most
researchers agree that 80% to 90% of human cancer is
environmentally caused. The findings, Hoover writes, are
consistent with the literature behind this consensus,
including studies of certain cancers among immigrant
populations that come to match rates in the new homeland after
several generations. Nonetheless, the discovery over the last
15 years of the genetic mechanisms underlying cancer has
overshadowed environmental explanations in the minds of
researchers, doctors, policymakers and the public, according
to Hoover.
For cancer researchers, the most intriguing implication is
that “there must be major gaps in our understanding of
the genetic basis of colorectal, breast and prostate
cancer.” According to the authors, who were led by Paul
Lichtenstein of the Karolinska Institute, Stockholm, the
frequency of known high-risk mutations is insufficient to
account for observed rates of these cancers in the study.
Hoover adds that the nature/nurture debate obscures the fact
that “. . .genes and environment interact to produce a
risk greater than the sum of their independent effects,”
which can be reduced by advances in either area. For
health-care professionals and individuals who wish to take
charge of their health, the message is an optimistic one:
genetics is not destiny.
-David Holtzman
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