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New Dean-Fowkes Deprenyl Article Critiqued

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Steve Farmer

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Jun 14, 1996, 3:00:00 AM6/14/96
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The new issue of CERI's newsletter ("Smart Drug News") arrived in this
afternoon's mail. It contains a report entitled "Recent Developments
with Deprenyl," authored by Ward Dean, MD, and Steve Fowkes. We're told
that the article, which is dubbed an "interim report," was written in
response to the "furor being generated on the Internet" over deprenyl.
Unfortunately, the article doesn't say *where* on the Internet that
furor is taking place, so few CERI readers will ever read the severe
criticisms of the Dean-Fowkes article that follow.

The new Dean-Fowkes article discusses only *one* of the three negative
long-term studies that have been published in the last six months on
deprenyl. The study it discusses was published in December by the
Parkinson's Disease Research Group of the United Kingdom. The study
showed a 60% increase in death rates in patients treated with deprenyl
(also known as selegiline) and levodopa.(1) The Dean-Fowkes article does
not mention the important editorial that accompanied the British study
(2) nor the two negative studies of deprenyl published in January by the
Parkinson Study Group of the United States. (3, 4)

Ignoring this evidence, Dean and Fowkes suggest that the combination of
levodopa + deprenyl, rather than deprenyl alone, was the probable cause
for the high death rates seen in the British study. The article's main
conclusions appear in the following paragraph:

Although we agree that there are life-and-death issues that need
addressing, we believe that the reassessment should focus primarily
on the combined use of L-dopa with deprenyl in Parkinson's
disease. Much evidence has accumulated in recent years that dopa
adversely effects [sic] several key receptor and enzyme systems and
may actually *accelerate* the progression of Parkinson's disease.
In our judgment, recent suggestions on the Internet that
deprenyl therapy for Parkinson's disease be abandoned is premature
and hardly justified by the results of this study. However, we do
believe that the simultaneous use of dopa and deprenyl should be
discouraged.

The latter claim is a huge concession, since groups like the Life
Extension Foundation (LEF) continue to claim that deprenyl and dopa
(levodopa) should be used conjunctively. Nevertheless, by ignoring a
wide spectrum of data, the new "Smart Drug News" report obscures the
most critical issues in the deprenyl debate. I list the article's most
obvious omissions of evidence below:

1. The Dean-Fowkes article doesn't tell readers that the *only*
tentative hypothesis that the Parkinson's Disease Research Group put
forward concerning the high death rates in their study concerned
deprenyl alone - and not deprenyl only when it is used conjunctively
with levodopa. The Parkinson's Group acknowledged that the precise cause
of the high death rates wasn't known. But the Group also pointed out
that deprenyl "increased the number of early adverse events" in
Parkinson's patients, and suggested that deprenyl "may have deleterious
effects on the cardiovascular and cerebrovascular system." As evidence
for this suggestion, the researchers pointed out that in an earlier
American study "a higher incidence of cardiac rhythm disturbance was
reported in patients treated with selegiline [deprenyl]." The
Dean-Fowkes article quotes the statement that deprenyl "increased the
number of early adverse events," but omits all that follows on
deprenyl's apparent toxicities.

2. The CERI article doesn't mention the very negative editorial on
deprenyl/selegiline that accompanied the Parkinson's Disease Research
Group study (2). The editorial again points to deprenyl alone - and not
combination therapy - as the probable culprit. Indeed, the editorial
concludes that in light of recent studies "the controversy over the role
of selegiline [deprenyl] in the management of Parkinson's disease can
perhaps now be put behind us." The editorial's stark title is:
"Selegiline [deprenyl] in Parkinson's disease. No neuroprotective
effect: increased mortality." It is therefore not surprising that the
Dean-Fowkes article doesn't mention the editorial, which was written by
D.B. Calne, one of the world's leading authorities on neurodegenerative
diseases.

3. The CERI article conspicuously fails to discuss (or even mention) the
two recent negative studies of deprenyl by the Parkinson Study Group of
the United States, published in the _Annals of Neurology_ in January (3,
4). The U.S. studies, which involved 189 researchers and 800 patients,
found that adverse effects showed up in deprenyl-treated patients long
*before* levodopa was administered. Hence once again the problem appears
to lie in deprenyl and *not* deprenyl only when combined with levodopa.
I pointed out these studies to CERI long ago, and indeed posted
abstracts of the studies in sci.life-extension right in the middle of a
debate with Fowkes. The evidence in these crucial articles has been
discussed repeatedly, so their exclusion from the new Dean-Fowkes
article was clearly intentional.

4. The Dean-Fowkes article mentions old claims about deprenyl
"alleviating symptoms" of Parkinson's disease. This is in direct
contradiction to the new long-term studies by the Parkinson Study Group
of the United States, (3,4) which found that after a transient period of
improvement, patients treated with deprenyl alone (i.e., not in
combination with levodopa) experienced *accelerated" development of
Parkinson's symptoms. This again contradicts CERI's claims that
levodopa, or combination therapy using deprenyl + levodopa, is the
culprit rather than deprenyl alone.

5. The new Dean-Fowkes article recommends antioxidant therapy (in
conjunction with deprenyl) as a useful treatment for Parkinson's
disease. It also complains that "scientists and doctors have been slow
to apply this technology." This is a strange claim, since the two giant
studies conducted by the Parkinson Study Group of the United States,
whose results were published in January, were designed *specifically* to
test antioxidants in combination with deprenyl. The clear finding of
these studies was that antioxidant therapy (in this case, large doses of
vitamin E) - used *with* or *without* deprenyl - is of no value in
treating Parkinson's disease.(3,4) Indeed, the free-radical theory of
the origin of the disease - a theory tied closely to antioxidant therapy
(5) - is a major victim of the recent negative studies of deprenyl.(2)
None of this is so much as mentioned in the Dean-Fowkes article.

6. Surprisingly, the Dean-Fowkes article makes no mention of CERI's
oft-repeated suggestions that "unidentified contaminant(s)" may be
responsible for the disastrous results found in the recent studies. In a
small sidebar story, CERI *does* call for readers to send in old samples
of deprenyl for analysis. It also suggests that at some unspecified time
CERI will "be addressing the purity of commercial deprenyl products in
more depth." But the article doesn't directly connect these points to
the disastrous results arising out of the two Parkinson's study groups.
I suspect that CERI realizes by now that the "unidentified
contaminant(s)" theory won't fly with Parkinson's researchers, and they
are hence afraid to discuss that theory in an article that they know
will be scrutinized closely. The omission of this claim says a great
deal about the credibility of the "unidentified contaminant(s)" theory,
however.

7. The new Fowkes-Dean article tells us that "Our present opinion favors
Discovery-brand liquid deprenyl as the deprenyl product of choice." But
the article does *not* repeat much stronger earlier claims by Fowkes and
Discovery (DEDI) that other brands are filled with "unidentified
contaminant(s)" whose neurotoxicities might explain the new studies'
negative results. The article's conservatism on this issue also speaks
legions about the credibility of the "unidentified contaminant(s)"
theory.

8. Finally, the article quietly drops CERI's old argument - which it
amazingly doesn't even *mention* - that deprenyl has "neuroprotective
effects" in regions of the brain linked to Parkinson's disease. This
argument, which has been thoroughly debunked by the new negative studies
(1,2,3,4), has been the linchpin of CERI's repeated claims concerning
deprenyl's "life-extension effects." Despite the quiet disappearance of
this argument, however, the new Dean-Fowkes article *continues* to claim
that deprenyl has "anti-aging applications"! This claim also continues
to be made on CERI's Web pages, in an article whose sensationalist views
have sold a lot of subscriptions to "Smart Drug News." For this article,
see http://www.ceri.com/deprenyl.htm. Needless to say, the new Dean-Ward
article offers no evidence for these views, which are soundly debunked
by the recent studies published by the Parkinson's Disease Research
Group of the United Kingdom (93 participating hospitals, 520 patients)
and the Parkinson Study Group of the United States (189 investigators,
800 patients). To continue at this point to claim that deprenyl is a
"life-extending" drug is highly irresponsible - to say the very least.

S.A.Farmer

References:

1. AJ Lees on behalf of the Parkinson's Disease Research Group of the
United Kingdom. "Comparison of therapeutic effects and mortality data of
levodopa and levodopa combined with selegiline [deprenyl] in patients
with early, mild Parkinson's disease." British Medical Journal (BMJ)
1995; 11: 1602-1607.

2. DB Calne. "Selegiline in Parkinson's disease. No neuroprotective
effect: increased mortality." British Medical Journal (BMJ) 1995; 11:
1583-4.

3. Parkinson Study Group (189 authors). "Impact of deprenyl [selegiline]
and tocopherol [vitamin E] on Parkinson's disease in DATATOP subjects
not
requiring levodopa." Annals of Neurology 1996; 39(1): 29-36.

4. Parkinson Study Group (189 authors). "Impact of deprenyl and
tocopherol [vitamin E] on Parkinson's disease in DATATOP patients
requiring levodopa." Annals of Neurology 1996; 39(1): 37-45.

5. DB Calne. The free radical hypothesis in idiopathic parkinsonism:
Evidence against it. Annals of Neurology 1992; 32: 799-803.

Paul Anacker

unread,
Jun 15, 1996, 3:00:00 AM6/15/96
to xbyt...@ios.com

Steve Farmer wrote:
>
> The new issue of CERI's newsletter ("Smart Drug News") arrived in this
> afternoon's mail. It contains a report entitled "Recent Developments
> with Deprenyl," authored by Ward Dean, MD, and Steve Fowkes. We're told
> that the article, which is dubbed an "interim report," was written in
> response to the "furor being generated on the Internet" over deprenyl.
> Unfortunately, the article doesn't say *where* on the Internet that
> furor is taking place, so few CERI readers will ever read the egotistical
> rantings of the self-appointed savior of the world, Steve Farmer.

>
> The new Dean-Fowkes article discusses only *one* of the three negative
> long-term studies that have been published in the last six months on
> deprenyl. The study it discusses was published in December by the
> Parkinson's Disease Research Group of the United Kingdom. The study
> showed a 60% increase in death rates in patients treated with deprenyl
> (also known as selegiline) and levodopa.(1) The Dean-Fowkes article does
> not mention the important editorial that accompanied the British study
> (2) nor the two negative studies of deprenyl published in January by the
> Parkinson Study Group of the United States. (3, 4)

Farmer Steve means they stuck to the scientific evidence, instead of arguing
with the editor's opinion? Tsk, tsk, for shame! Steve Farmer, without stop-
ping to think, correctly noted that discussing only one of three reports would
automatically mean the other two reports weren't discussed in an interim report.
I can only guess that he thinks someone has to address all of his issues imme-
diately. How dare they only respond to one report at a time!

> Ignoring this evidence, Dean and Fowkes suggest that the combination of
> levodopa + deprenyl, rather than deprenyl alone, was the probable cause
> for the high death rates seen in the British study. The article's main
> conclusions appear in the following paragraph:

They also ignored the weather in Kansas, Dorothy! But so what! In science, if
not in the History of Science, professor, one tries to differentiate things one
element at a time. It's very difficult to reach a valid conclusion when you
just lump everything into a Farmer's stew and then try to decide which ingredient
caused the food poisoning!



> Although we agree that there are life-and-death issues that need
> addressing, we believe that the reassessment should focus primarily
> on the combined use of L-dopa with deprenyl in Parkinson's
> disease. Much evidence has accumulated in recent years that dopa
> adversely effects [sic] several key receptor and enzyme systems and
> may actually *accelerate* the progression of Parkinson's disease.
> In our judgment, recent suggestions on the Internet that
> deprenyl therapy for Parkinson's disease be abandoned is premature
> and hardly justified by the results of this study. However, we do
> believe that the simultaneous use of dopa and deprenyl should be
> discouraged.
>
> The latter claim is a huge concession, since groups like the Life
> Extension Foundation (LEF) continue to claim that deprenyl and dopa
> (levodopa) should be used conjunctively. Nevertheless, by ignoring a
> wide spectrum of data, the new "Smart Drug News" report obscures the
> most critical issues in the deprenyl debate. I list the article's most
> obvious omissions of evidence below:

Sorry, Stevie, but Ward Dean, MD, CERI, Steve Fowkes, nor "Smart Drug News"
can't make any concessions for LEF. They ain't it! Get it? If you want
to say that any of them made the claim (with proof, of course) and then
made the previous statement, you could say that THEY were making a conces-
sion. But you can't take one person's (group's) statement and make it some-
one else's concession. Well, not unless you live in Farmer World...Isn't
that a cartoon show that comes on Saturday mornings?

> 1. The Dean-Fowkes article doesn't tell readers that the *only*
> tentative hypothesis that the Parkinson's Disease Research Group put
> forward concerning the high death rates in their study concerned
> deprenyl alone - and not deprenyl only when it is used conjunctively
> with levodopa. The Parkinson's Group acknowledged that the precise cause
> of the high death rates wasn't known.

You mean they didn't talk about "tentative hypothesis" in reports they weren't
talking about? How odd!

I could go on, but why waste bandwidth. I tell you what Mr. Farmer. State
that you'll stake your reputation and job on the conclusion you find so self-
evident: That uncontaminated deprenyl, in and of itself, causes high death rates
in people with Parkinson's disease. Do this in a legally binding manner and
you won't hear another word from me commenting on your emotional, illogical
tirades. Fair enough?


Please Steve, please, tell everyone one the URL for your new website

Marcus E Engdahl

unread,
Jun 17, 1996, 3:00:00 AM6/17/96
to

In article <31C36A...@fishnet.net>,
Paul Anacker <xtra...@fishnet.net> wrote:

>I could go on, but why waste bandwidth. I tell you what Mr. Farmer. State
>that you'll stake your reputation and job on the conclusion you find so self-
>evident: That uncontaminated deprenyl, in and of itself, causes high death rates
>in people with Parkinson's disease. Do this in a legally binding manner and
>you won't hear another word from me commenting on your emotional, illogical
>tirades. Fair enough?

Gambling has absolutely nothing to do with science and neither does
majority vote. Since you probably live in the one country where old ladies
may earn millions by spilling hot coffee on themselves, you are probably
more than willing to recommend Deprenyl (for life-extension as well as
treating Parkinson's disease. Am I correct?

Marcus
---
Marcus E Engdahl meng...@beta.hut.fi
http://www.hut.fi/~mengdahl/index.html


cosmic sales

unread,
Jun 18, 1996, 3:00:00 AM6/18/96
to

I think you have been watching too much of the O.J. Simpson travesty!
--
gk

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