Re: [Marxism] Junk science alert: Human Mad Cow, variant CJD may be wide-spread in USA

[Andy Coates <esquincle@xxxxxxxxxxx>]

Having reached and proven the diagnosis of CJD in several patients (recent
years), after following Prusiner's (controversial) Nobel-prize-winning prion
theory closely (and attending his and other lectures on the subject), after
teaching medical students and residents about dementias...

there remains the enormous scientific chasm yawning open between "the bench" and
"the bedside."  (Thanks for that to capitalism, and a growing failure of its
education system-- medicine included.)

That the true number of cases of CJD, let alone those of its variant (related to
BSE), is not known in the U.S. is hardly the fault of the CDC.  Much more it is
the fault of the entire profit-driven, craven and degenerating system of medical
care and research-- a system predicted to be on the precipice of total failure
by the recent past editor of the New England Journal of Medicine (Marcia 
Angell).

I doubt sincerely that a majority of primary care physicians in the United
States possess the clinical knowledge or intellectual space and wherewithal to
consider routinely the diagnosis of CJD at the bedside.  And if you can't
consider it you're not going to push for a brain biopsy!  Sure, a very young
patient (<50 years) with rapid-onset dementia will get referred to a
neurologist, who will hopefully consider the diagnosis.  But what of the 70
year-old working person who presents with dementia?  "Alzheimer's."  (Which is
also a diagnosis proven only by brain-biopsy or autopsy, in either case unlikely
to be done.)

On top of memory and behavior disturbance, findings of myoclonus (generalized
muscle twitching like those little jumps you get when you're falling off to
sleep, the sole (yet rather weak) distinguishing clinical sign of CJD, yet found
in other conditions), and eventually onset of seizures, will be lost as the
continuity of care fragments and the patient moves from home to hospital to
nursing home.

As a resident I was actively discouraged on several occasions from pushing for a
comprehensive work-up of the cause of dementia.  Take the example of tertiary
syphilis, one of the causes.  How would you like to announce that to the
assembled family of the 84 year old man?  "Don't order that test unless you're
going to take responsibility for its results."  (One of my teachers recounted
guiltily how he had shaken an elderly widow profoundly with that very news.)

Additionally, dementias tend to be practically irreversible, whatever the cause
(like many neurologic diagnoses) and so bear also the 'doctorly' prejudice that
it's merely "diagnose and adios" -- in other words giving the disease a name
will not change its course or outcome.  (Against this I have held out hope for
my patients that diagnosis-- hence prognosis-- can be itself therapeutic.)

Is there more CJD than officially recognized?  Certainly.  Is there a way to
estimate that?  I doubt it.  Not while a small minority control the scientific
resources.

Finally, Jose Perez (whose posts I read closely) seems to know more statistics
than most physicians I've worked with (an uplifting or scary thought?).  Jose
offered in anticipation several useful criticisms of studies which he did not
have in hand.  (Of course Louis posted a link to the abstracts only 12 minutes
later!)  The statistic Jose hammered on was that as much of 13% of dementias are
actually CJD -- the first article in Louis' link.  The article in question was a
case series of 46 patients whose brain tissue remained on hand to review at
Yale.  It is a not only a small number, it was a case series -- a very weak way
to demonstrate the prevalence of a disease, frought with potential biases.  On
an internet list one of the authors of that study is quoted:

http://www.ualberta.ca/htbin/lwgate/PATHO-L/archives/patho-l.archive.1998-06/Author/article-122.html

"As I remember these AD cases were not selected in any way...just a routine
reasonably consecutive sampling from our cases with the diagnosis. I would have
to check the time frame of the cases (if I can still find it as the lists were
kept by Elias who is now deceased). At the same time, because Yale is a large
referral center, some somewhat atypical cases may be preferentially seen here.
Nonetheless, the clinical neurologists were very competent and the clinical
impression was AD. Cases thought to be CJD were excluded. Because we had a very
active autopsy service at that time and good relations with clinicans who
routinely sought autopsy permission, a "selection" for autopsy is not obvious.
Perhaps now with BSE there is more consideration of CJD diagnostically in
academic centers.  Hope this helps.  Laura Manuelidis"

The theory of prion disease transmission appears well-founded (in my mind it is
grounded in the primoridal natural phenomenon of molecular self-reference.)  An
increasing incidence of variant CJD also seems plausible, given the contemporary
use of ground animal products as a protein source in cow feed, considering the
disease examples of scrapie and kuru.  Overall there is surely a greater
prevalence of CJD than previously recognized.  But how prevalent?  Presently
unknown.

Andy Coates




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