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From: B. Harris)
Subject: Re: Bowel obsession !!!
Date: 19 Jun 1997

In <> (Rob Rowlands) writes:

>My father is 78 and appears to be showing signs of dementia. He is
>often confused and his memory is terrible.
>He recently had a scan and the conclusion was that he does not suffer
>from Alzeimers BUT...he is obsessed with his bowels!
>He is convinced he has a serious medical condition and is forever
>taking laxatives. No such problem exists and he is 'as regular as
>clockwork' - he just forgets he's been and panics.
>My poor mum is being driven round the bend. She's tried writing notes
>recording his visits to the loo;, witnesses tell him this is the 3rd
>trip in the last 15 minutes etc ...but nothing will stop him.
>Has anyone had similar experiences with elderly parents/relatives and
>could anyone please suggest a cure?

You can't rule out Alzheimer's with a scan.  You'll have much better
luck with a very simple cognative spacial test, such as having someone
but the 12 numbers in a clockface circle in a drawing, and then put in
hands showing the time "2:45" (I've yet to see an Alzheimer's patient
do this correctly, so it's pretty sensitive, albeit not perfectly

                                       Steve Harris, M.D.

From: B. Harris)
Subject: Re: Alzheimer's
Date: 26 Feb 1998 20:05:34 GMT

In <> (Peter H.
Proctor) writes:

>      At least part of it seems to be secondary to oxygen radical production
>by beta-amyloid. Maybe with a bit of peroxynitrite produced by the
>reaction of superoxide with nitric oxide thrown in. In fact, this seems
>to be the mechanism for a lot of age-related degenerative processes.
>Dr. P

   There's no doubt that amyloid makes oxygen radicals that kill
neurons in a dish.  And it's a good bet that this happens to some
extent in the actual Alzheimer brain, especially given the very mild
positive effects (albeit not yet replicated and confirmed) of vitamin E
on Alzheimer's progression.

   But, for all of that, vitamin E didn't stop Alzheimer's in its
tracks (far from it), and the simple oxidation theory doesn't explain
the good correlation between the disease and having apoE4 alleles of
cholesterol micelle proteins.  You can think of lots of blue sky
connections, but we've got a decade of research to go before we
understand any of them.

   As for free radicals being the cause of most aging pathology, that
of course has been the best single theory on the block for years.  It's
very attractive and I half-believe it, myself.  But I also remind
myself of reality, now and again.  The problems with the free radical
theory of aging include the fact that ANY tissue damage from anything
generates free radicals (it's part of the healing and immune cascade),
so you'd expect to see these things (all of our research results) with
aging, and aging damage, even if they *weren't* a primary causal
mechanism.  They're just along for the ride, like pain.  Moreover, if
free-radicals cause aging, how come we haven't been able to interfere
with the basic aging process much (increase max life span) by giving
antioxidants to mammals?  Antioxidants seem to affect "aging" only on
insects (to some minor degree).  But adult insects are post mitotic,
and nature didn't give them great repair resources, not expecting them
to be more than ephemeral.  If we improve that, it's not a big deal.

    Again, with both Alzheimer's and aging, until antioxidents really
bring the process to a halt, or slow it down GREATLY, it's very hard to
believe that oxidation plays THE major role in pathology for either of

                                            Steve Harris, M.D.

From: B. Harris)
Subject: Re: Alzheimer's
Date: 26 Feb 1998 23:13:15 GMT

In <> "Syd Baumel" <>

>My point was that we might be better able to understand, treat, and
>prevent AD if we start regarding it less as a specific disease and more
>as a special case of the general and highly nonspecific phenomenon of
>aging, decay, functional decline, and death of living tissue, in this
>case of certain types of brain tissue.
>I rest my case and eagerly await further insults -- and perhaps even
>meaningful comments.

   No insult intended, unless you want to take the remark that you
should examine the data more carefully before spinning theories, to be
an insult.

    Look, just because most (but not all! -- see below) "normal" aged
brains have SOME lesions indistinguishable from those seen in
Alzheimer's disease, doesn't mean that there's any good reason to
regard Alzheimer's as a special case of nonspecific aging.  One problem
with Alzheimer's is that the time course is just wrong.  With
Alzheimer's it's not unusual to go from normal function to complete
dementia (can't recognize your family) in a couple of years.  Often
less than five.  The loss of cells and brain metabolic rate parallels
that rapidity.  That doesn't look like the damage that happens to an
aging brain at all, unless you want to say that some people go along
with brains aging at a normal rate, and then suddenly their brains
start aging at 10 times normal rate.  But it escapes me how that
represents an advance in thinking.

   Worse, it's not even true.  Not all aged people who come to autopsy
have brains with Alzheimer's type lesions (plaques and tangles).  Most
do, but there are a small minority of people that have NONE.  In these,
at the age of 80 you cannot tell their brains, either grossly or
histologically, from the brain of a 20 year old.  Shocking, but true.

   To me, that's the real problem.  "Aging," whatever else it is, must
be UNIVERSAL.  If there are any processes that some people escape, they
aren't aging.  What are they?  Perhaps it's fair to call them diseases.
Perhaps, in a sense, they are late-life appearing genetic diseases from
the results of genes with negative pleiotropy.  There is lots of
indirect evidence that most people die from this kind of thing in old
age, and only people who survive into their late 90s and beyond enter
the realm where mortality rate is truely controlled by aging, rather
than by genes with negative pleiotropy.

   You either have to believe that, or else believe that the aging
process itself slows up at about 95, as the time dependence of the
increase in the mortality function becomes less severe (which it does--
a great undiscussed mystery in gerontology presently).  I think the
latter (slowdown in aging) is the least likely scenario, as it seems
silly to imagine that people age more slowly when they get REALLY old.
Boy, how could that be explained mechanistically?

   Although, to be sure, this question is partly semantic, rather than
scientific.  It all depends on what you want to LABEL aging.  There's
substantial agreement that the process we label "aging" needs to be
universal, time-dependent, degenerative (increasing risk of death), and
irreversable.  There's much less agreement that it needs to have a
relatively constant *rate* over time.

                                       Steve Harris, M.D.

From: B. Harris)
Subject: Re: Alzheimer's
Date: 7 Mar 1998 11:09:24 GMT

In <> John Scudamore <>

>Blood and urine levels aren't a useful indicator.  Brain levels would
>be more like it. Presumably these dentists knew that.

   Look, there's no great evidence that brain levels of mercury
correlate with Alzheimer's either.  So far we've seen one paper for,
one against.  And these Alzheimer's-- brain metal correlations are (as
Syd points out) correlations which might run either way, so far as
cause and effect.  We know very well that when the brain is damaged by
any mechanism (even trauma) the blood brain barrier breaks down and all
kinds of environmental stuff leaks in.  Including metals.  That doesn't
mean that metals cause the damage.  In a lot of degenerative brain
diseases, the damage clearly causes the metals to accumulate.

    ONCE AGAIN, in science, correlative studies are useful, but you
need to know how to use them.  Don't take them for more than they are
worth.  Studies which correlate a disease with an environmental factor
are not usually very useful, in and of themselves, because there are
too many reasons for the correlation to occur and not be causal.  Far
more useful are epidemiologic studies which show LACK of correlation
between putative causes, and a disease.  These negative studies are
much more powerful, since it is quite difficult to have a cause which
does NOT correlate with effect.  On the other hand, "effects" correlate
with markers which aren't causes, all the time.  In that case, proof
takes more.

    To that end, we simply need to note that lots of studies looking
for environmental causes of Alzheimers have turned up negative.  If
it's caused by mercury or aluminum, we *ought* to see people who work
with these things industrially get more Alzheimer's.   We MUST see
this, or the theory is shot.  Problem: they don't.  The same with a
host of other suggested toxic causes.  There may be environmentally
caused brain diseases, but so far the evidence is lacking that
Alzheimer's disease is one of them.  As for many specific toxins, there
is specific evidence AGAINST a number of agents.  If some environmental
agent DOES causes Alzheimer's, it's not one we've suspected and looked
at, yet.  It certainly isn't anything as simple as a heavy metal or a
common industrial solvent.

   On the other hand, certain things show up in Alzheimer's studies
again and again.  Anti-inflammatory drugs seem to be protective.
Smoking seems to be partly bad.  It's not that the studies aren't
sensitive enough not to see ANY effects or correlations.  It's just
that those that the "alternative medicine" or "clinical ecology" types
assume should be there, aren't.

    Do try to read a few of these abstracts and educate yourself,
Scudamore.   Very few people have the luxury of getting medical
knowledge spoon-fed to them, so show a little appreciation to people
like Syd and Runswim and Rind and the others around here who try to
capture knowledge and pass it on.  Medicine is not one of those
disciplines where you can figure out the truth by scratching your head
and thinking about what sounds good to you.  Rather, it takes study of
the evidence, and it takes critical thinking.  Get off your lazy butt
and do some of it.  Most of the rest of the people on this forum trying
to hold discussions about this, at least are trying.

                                         Steve Harris, M.D.

Alzheimer Dis Assoc Disord 1997 Mar;11(1):21-27
Occupational risk factors for Alzheimer disease: a case-control

Gun RT, Korten AE, Jorm AF, Henderson AS, Broe GA, Creasey H,
McCusker E, Mylvaganam A

Department of Community Medicine, University of Adelaide,

There is evidence to support the role of a number of environmen-
tal factors in Alzheimer disease (AD). This study examines the
role of chemical and physical exposures in the occupational
environment. The sample included 170 patients with AD and 170
medical-practice-based controls, matched for age and sex, who
were assessed for histories of occupational exposures to a range
of chemical and physical agents, including hydrocarbon solvents,
lead, mercury, organophosphates, aluminum, asbestos and other
silicates, vibration, and physical underactivity. Occupational
histories were obtained from informants for both patients and
controls. Exposure was assessed by a panel of occupational
hygienists, blinded to the case or control status of each
subject, using the occupational histories and the Job-Exposure
Matrix of the U.S. National Institute for Occupational Safety and
Health. No statistically significant associations were found
between any of the exposures and the occurrence of AD, either in
the overall study group or in patients with a family history of
AD. The findings suggest the absence of any occupational
cause for AD.

PMID: 9071441, UI: 97225068


Neurology 1990 Nov;40(11):1698-1707
A case-control study of Alzheimer's disease in Australia.

Broe GA, Henderson AS, Creasey H, McCusker E, Korten AE, Jorm AF,
Longley W, Anthony JC

University of Sydney, Department of Geriatric Medicine,
Repatriation General Hospital, Concord, NSW, Australia.

We conducted a case-control study of clinically diagnosed
Alzheimer's disease (AD) on 170 cases aged 52 to 96 years, and
170 controls matched for age, sex and, where possible, the
general practice of origin. Trained lay interviewers naive to the
hypotheses and to the clinical status of the elderly person
carried out risk-factor interviews with informants. Significant
odds ratios were found for 4 variables: a history of either
dementia, probable AD, or Down's syndrome in a 1st-degree relati-
ve, and underactivity as a behavioral trait in both the recent
and more distant past. Previously reported or suggested associ-
ations not confirmed by this study include head injury,
starvation, thyroid disease, analgesic abuse, antacid use
(aluminum exposure), alcohol abuse, smoking, and being

PMID: 2146525, UI: 91043542


Br J Psychiatry 1996 Feb;168(2):244-249
A case-control study of Alzheimer's disease and aluminium

Salib E, Hillier V
Winwick Hospital, Warrington.

BACKGROUND: We examined clinically diagnosed Alzheimer's disease
patients and controls, and collected information from informants,
to examine the association between Alzheimer's disease and
aluminium occupation. METHOD: An unmatched case-control study
comparing 198 cases of Alzheimer's disease (ADRDA-NINCDS
diagnostic criteria), to selected controls (164 other dementias
and 176 nondementing group) in respect of their occupational
history. The subjects included all patients referred to and seen
by the first author during a 2 year study period. RESULTS:
Twenty-two of 198 patients with Alzheimer's disease
(11.1%) reported having an aluminium occupation at some stage in
their working life compared with 39 of 340 controls (11.5%), odds
ratio 0.98, 95% Cl 0.53-1.75, P > 0.05. Aluminium workers
reported to have worked in direct contact with aluminium dust and
fumes did not appear to be at any greater risk than other workers
who were employed at the same factory, odds ratio 1.19, 95%
Cl, 0.64-4.18, P > 0.05. CONCLUSION: There is no evidence to
support an association between having previously worked in an
aluminium factory and the risk of Alzheimer's disease later in


Neurology 1994 Nov;44(11):2073-2080
The Canadian Study of Health and Aging: risk factors for
Alzheimer's disease in Canada.

OBJECTIVE: To study risk factors for Alzheimer's disease (AD)
based on data from the Canadian Study of Health and Aging.
DESIGN: Population-based case-control study. SETTING: Communities
and institutions in 10 Canadian provinces. PARTICIPANTS: Two
hundred fifty-eight cases clinically diagnosed with probable AD,
with onset of symptoms within 3 years of diagnosis, and 535
controls, frequency matched on age group, study center, and
residence in community or institution, clinically confirmed to be
cognitively normal. MAIN OUTCOME MEASURE: Odds ratios (ORs) were
calculated using unconditional logistic regression for previously
hypothesized and potential risk factors for AD. RESULTS: The OR
for family history of dementia was significantly elevated
(2.62; 95% confidence interval [CI], 1.53 to 4.51) and increased
with the number of relatives with dementia. Those with less
education were at higher risk of AD, with an OR of 4.00 (95% CI,
2.49 to 6.43) for those with 0 to 6 years, in comparison with
those with 10 or more years. Head injury achieved borderline
significance. A history of arthritis resulted in a low risk of AD
(OR = 0.54; 95% CI, 0.36 to 0.81), as did a history of use of
nonsteroidal anti-inflammatory drugs. Initial analyses showed an
increased risk of AD for occupational exposure to glues as well
as to pesticides and fertilizers; the increased risk was greater
in those with less education. CONCLUSION: This study
confirmed a number of previously reported risk factors for AD,
but provided little support for others. A new finding was an
increased risk for those with occupational exposure to glues as
well as pesticides and fertilizers, but this needs further study.

  Comment in: Neurology 1995 Aug;45(8):1635

PMID: 7969962, UI: 95059994


From: B. Harris)
Subject: Re: Diagnosing Alzheimers
Date: 9 Aug 1998 03:48:49 GMT

In <6qiprg$jeg$> writes:

>Is there any way to diagnose if a person has the beginning stages of
>alzheimers? There must be some way to diagnose it once a person has it,
>since they definately say a person has the disease. Am curious to find
>out if there is a test to determine if a person has it. Am really not
>very informed about this at all. Please respond to me privately also.
>Thanks, Terry

    Actually there isn't.  A long battery of clinical tests plus some
testing of apoE4 alleles may get you to 90% certainty, but no farther.
Short of an autopsy the best you can do to do better than that is a PET
scan.  These are available only at a few places, such as UCLA, since a
cyclotron is needed to make the short-lived positron emitting isotope
of fluorine (F-18).  Some other places might be willing to do a SPECT
scan for you, which isn't as good as PET, but measures many of the same
things, and may improve the diagnosis.

   Ultimately, though, a demented person is a demented person.  Once
they're on aspirin and vitamin E, there's not a lot you can do for them
if they don't have some mass lesion on CT scan.  Differentiating
Alzheimer's from the other dementing illnesses is not that useful.

                                      Steve Harris, M.D.

From: B. Harris)
Subject: Re: Diagnosing Alzheimers
Date: 15 Aug 1998 23:34:28 GMT

In <6r3vdb$> (guidonospam) writes:

>  wrote
>> On 10 Aug 1998 19:47:24 GMT,
>(guidonospam) wrote: >
>> >     Dr. Harris is quite wrong.  It is important to diagnose dementia
>> >appropriately, because unlike alzheimers, many dementias are easily and
>> >rapidly reversed.
>> >
>> >     Surely Dr. Harris has heard of dementias due to vitamin B12
>> >defficiency, myxedema comas, pneumonias, carotid strictures,
>> >toxic psychoses, and pseudotumor cerebris to mention just a
>> >few which are easily and rapidly reversed, frequently fully reversed.


    There is, FYI, a difference in terminology between dementia and
delerium.  No, for the record I have not heard of dementias caused by
carotid strictures, pneumonia, and pseudotumor cerebri.  Could you be
so kind as to educate this gerontologist with some literature
references to this?  And if not, stop acting so superior?

   Quite frequently, "Alzheimer's disease" is improperly made as a
diagnosis of exclusion, after "reversible" causes of long term
cognative dysfunction have been ruled out.  We all look for UTIs, draw
B12s and TSH's and do a CT to look for posssible subdural or NPH, and
so forth.  But you know what?  Rarely do they show anything that does
anybody any good, when somebody comes in with a history of significant
cognitive dysfunction in several areas, lasting 6 months or a couple of
years (very often the presentation).  If you find something to treat,
really demented patients get a little better, but stay demented
(lightly demented, but to become more severely demented again soon).
This is because they are in the early phase of an irreversible
dementing illness anyway, and have simply been pushed into an area of
social dysfunction by an additional stress.  When you fix this, you
haven't "cured" or "reversed" the dementia, you've just fixed an acute
delerium or episode of confusion, and delayed the inevitable by a few
months, much like the honeymoon phase in early diabetes type I.

   There are a lot of myths associated with dementia, and a biggie is
the idea that a lot of elderly dementias can be fixed, if only you find
that the thyroid is low, or something (you can find this one even in
some textbooks, making me wonder who writes this stuff).  A practicing
gerontologist will tell you this is baloney, mostly.  Low thyroid makes
people slow, but it does not make them forget who their grandchildren
are.  Ditto with low B12s and low folates and carotid strictures and
depression and dysorientation due to hospital admission, and so on.  I
wish it weren't so, but it is.  There are a FEW reversible causes of
severe cognative dysfunction in basically cognatively intact people,
but nearly all of them present with a very short history (infection is
the main culprit here).  Dementia is of course the wrong word for them,
by definition.

                                     Steve Harris, M.D.

From: B. Harris)
Subject: Re: Diagnosing Alzheimers
Date: 19 Aug 1998 07:02:47 GMT

In <6rclid$> (guidonospam) writes:

>August 18, 1998
>Dear Dr. Harris:
>     I use the term "Dr." loosely, only because you claim to be
>one. Nothing in what you have written convinces me of this.
>     No offence, but your writing reads like that of a 13 year
>old who got onto his Dad's net account without permission.  You
>sound like you got your medical knowledge from watching Doogie
>howser, M.D.
>     You have a lot of gall asking the readers of to
>accept your idiosyncratic views on the medical zeitgeist without
>so much as a wave of your hands at any medical references, and
>then demand footnotes from anyone who disagrees with you.

Comment: This has been fixed below.  Enjoy.

>     Are you any sort of licensed medical professional at all
>even a nurse?     Did you graduate college anywhere?  Or even
>attend any medical school let alone graduate from one?  Did you
>buy a medical school diploma at one of those $250 diploma mills?
>Did you take any boards at all let alone pass them?  And did you
>have any practice at all anywhere?

<More of the same snipped, but also answered below>

>The treatable dementias are not rare.  Just less common than the
>untreatable ones.

>     But still, among the older folks, many dementias may be due
>to medication reactions that do not affect younger folks.  And
>typically, some of these present with months of problems, as do
>most of the endocrine disorders in older folks.  Which keep the
>treatable dementias very common, including those I mentioned

>Janice Guidotti, M.D.


Dear Dr. Guidotti:

   I wonder why I subject myself to people such as yourself
trying to teach their grandmothers to suck eggs, as it were.
Unlike yourself, I use the term "Dr." with regard to you in full
confidence, because you do indeed write with the arrogance of a
doctor.  Alas, in this case you are writing about something you
really know little about.  I'm hearing nothing from you but the
urban myths of dementia, and not hearing about anything real
(at least, not in geriatrics).

   Yes, there has been a craze in recent years about identifying
reversible causes of dementia.  I am aware that there is also
a lot of unsupportable pap circulating in throw-away journals about
reversible causes of dementia, and how "common" they are.
Actually, they've never been common.  The main question today in
geriatrics is: how rare are they?

   As I've said, when studies are actually done and the numbers
counted up (something which everyone in their enthusiasm for
curing dementia forgot to do, for a long time), it turns out it's
rare (1%) to find fully reversible true dementia in geriatrics.
What you find instead are mostly "Gee, whiz, look what we did for
this guy!" case reports.   However, when statistics are actually
done, fractions of greater than 1% full reversibility of dementia
are generally due to lax definitions of dementia, and/or reliance
on inpatient populations of people under acute stress of rather
severe disease (in which "dementia" is impossible to diagnose
anyway, due to the short clinical course).  The practicing
gerontologist will see very little reversible dementia in an
outpatient practice.  It's more common to see new cognitive
dysfunction in inpatients, but (again) there it's not correct to
call it dementia.  All that's not only my own experience, but
it's also borne out by every recent study in geriatrics I can
find in which numbers are actually used.  Below is an example.
Following it is a meta-analysis of a number of such studies by
the same group, coming to basically the same conclusion.

   If you want to argue this point, I'm willing to read your
arguments.  To get figures for fractions of reversible dementia,
I suggest you start looking at the literature and posting
citations of papers which come to different conclusions than mine
(you can use the second paper below for a pretty good
bibliography).  No pap reviews by optimists, please, which don't
say anything quantitative.  Stick to numbers if you want to argue
numbers.  If the meta-analysis below is flawed, for instance, I'm
sure we'd all like to know how and why.

   As to your long and boring attacks on my credentials, you can
look me up if you like.  I practice geriatrics in Salt Lake City.
I teach geriatrics for the Family Practice Program (resident
training), and also the physician's assistants program, at the
University of Utah School of Medicine, where I'm a clinical
instructor.  I trained in geriatrics at UCLA, graduating the
geriatric medicine fellowship there in 1989.  I'm board certified
in geriatrics (1990).  And internal medicine also, 1986.  I'm
licenced to practice medicine in California and Utah.  I've been
licenced since 1984, so while I'm not a grey eminence, I'm not
exactly Doogie, either.  I've also published a number of papers
in experimental gerontology.

   Following your erudite (and, of course, heavily referenced)
refutation of what you call my "idiosyncratic" ideas, I will
expect to see YOUR qualifications in regard to what you're talking
about--since you asked for mine.  You want to play this game?
I'll play.  Let me repeat from my last message:

   "I do this for a living.  Prey tell, where did you do your
fellowship in geriatrics, and your boards, and how many patients
with new dementia do you work up in the average week?  In other
words, give me a reason to believe you're not some gung ho
internist straight out of The House of God, with limited clinical
experience and a really big ego relating to what you can fix in
the demented elderly."

   And don't forget to tell us when you were licenced, and what
your clinical experience has been in geriatrics, that you figure
you can tell both me and the quantitative studies to go to hell.
How many years did you say?  Must be at least 50, for you to be
so wise <g>.  Though you write like somebody still in residency,
and figuring your hospital experience is the whole world.

                              Steven B. Harris, M.D.


J Neurol 1997 Jan;244(1):17-22
Reversible dementia in elderly patients referred to a memory

Walstra GJ, Teunisse S, van Gool WA, van Crevel H

Department of Neurology, University of Amsterdam, The

Dementia has a reversible cause in some cases, and these should
be diagnosed without over-investigating the many patients with
irreversible disease. We prospectively studied the prevalence of
reversible dementia in a memory clinic, determined the added
value of investigations compared with clinical examination
and assessed the outcome of treatment of potentially reversible
causes by measuring (1) cognition, (2) disability in daily
functioning, (3) behavioural changes and (4) caregiver burden.
Two hundred patients aged 65 years and over were examined, using
the CAMDEX-N. If they were demented, the probable cause
was diagnosed clinically and confirmed or excluded by a standard
set of investigations, which were done in all patients. Of the
patients, 170 (mean age 79.2 years) were demented; 31 were
treated for potentially reversible causes. At follow-up after 6
months, no patients showed complete reversal of dementia.
Five patients improved on clinical impression, but only one on
clinical measurement. Thirty patients were cognitively impaired,
but not demented; seven were treated. Judged clinically, three
patients improved, but on assessment only one did so; she recove-
red completely. Blood tests often produced diagnostic results
that were not expected clinically, but electroencephalography and
computed tomography of the brain did not. None of the
investigations had an effect on outcome of dementia after
treatment. We conclude that in elderly patients referred to a
memory clinic, the prevalence of reversible dementia is of the
order of 1%, if outcome after treatment is assessed by a
standardized measurement. We recommend blood tests in all
patients, to detect not only metabolic causes of dementia but
also co-morbidity possibly worsening the dementia. Other
investigations can be performed on clinical indication. Clinical
evaluation remains the mainstay of diagnosis in

PMID: 9007740, UI: 97160224


J Neurol 1995 Jul;242(7):466-471
Reversible dementia: more than 10% or less than 1%? A
quantitative review.

Weytingh MD, Bossuyt PM, van Crevel H

Department of Neurology, Academic Medical Center, Amsterdam, The

Dementia is reversible in some cases and these should be
diagnosed without over-investigating the many others with
irreversible disease. To estimate how often dementia can be
reversed, we carried out a quantitative review of studies
reported between 1972 and 1994 in which reversible dementia was
diagnosed and outcome after treatment was assessed. We found 16
studies comprising 1551 patients. The percentages of reversed
dementia varied widely: from 0 to 23% for partial and from 0 to
10% for full reversal. Depression and drug intoxication were the
most frequent causes of reversible dementia, followed by
metabolic and neurosurgical disorders. The percentage of both
partial and full reversal of dementia has fallen in recent years,
to less than 1% for both in the four most recent studies. This
decrease could be associated with the change from an inpatient to
an outpatient setting and the use of stricter diagnostic methods.
We conclude that reversible dementia is very rare in an
outpatient setting when using strict diagnostic methods. This has
important implications for the diagnostic strategy in patients
with dementia: major procedures should be performed selectively.
In patients with clinical characteristics of Alzheimer's
disease, CT of the brain is unlikely to detect a treatable cause
of dementia.

Publication Types:
PMID: 7595679, UI: 96021384

From: B. Harris)
Subject: Re: About Alzheimer's Dementia: do you use Aricept?
Date: 21 Aug 1998 02:34:52 GMT

In <> (Scott
Goodman) writes:
>Being a 4th-year medical student (going into Neurology), and being
>brand new to the newsgroup (I have tired myself of
> and am looking for more meaningful discourse;
>OK actually now I read both  NG's :-)), I must say that I have found
>the arguments about dementia to be very amusing.
>All of the education I have received at my school, and all of my
>recent research into dementia, leads me to agree completely with Dr.
>Harris on all of his points.  I won't bother to point out the
>shortcomings of Dr. Guidotti's arguments, as Dr. Harris has already
>done that.
>Enough of that.  I have a question, for Dr. Harris and for anybody
>else who takes care of Alzheimer's patients: what do you think of

   Big advance over Tacrine, which was hardly worth using.  It's a
symptom-relief drug, not a treatment for the disease itself, but some
of my patients like it very much.

>I am preparing a presentation on the efficacy of Aricept as
>symptomatic treatment for dementia.  I have read (or at least
>surveyed) most of the research on the subject (including recent
>studies on donepezil and metrifonate in J Neuro and Arch Int Med,
>1998).  Having little clinical experience myself, I am seeking
>opinions from more experienced clinicians about how useful the drug is
>in real practice.
>* Do you uniformally prescribe Aricept to all of your patients with
>mild to moderate dementia?

  I recommend it to all who want to spend the money ($2/day here if you
prescribe it as the 10 mg pill, which is about the same price as the 5
mg pill, and have your patients/caregivers cut it in half as best they
can, taking the two halves of each pill on sucessive days), and who
complain about the memory problems (occasionally you find a person who
doesn't care that they can't remember, and their caregivers don't

>* In your experience, have you found Aricept to result in a clinically
>meaningful beneficial outcome?

  For some, yes.  For others, no.  I haven't kept stats, but I'd
estimate that maybe one person in 3 who tries it, stays on it more than
a few months.  It's always a question of whether or not the benefits
are worth money (and, rarely, the side effects-- mostly loose bowels
and GI problems in few takers).

>* What is the extent of this benefit and does it justify the cost of
>the drug?

   Depends on the person. A few will rave,and say they their memories
back.  Others, you have to ask the caregiver if they've noticed changes
in behavior (not asking the same question again and again,etc). It
varies.  Note that of course the responses of each patient and family
are TOTALLY subjective and non-scientific.  I'm unable to say how much
is placebo effect, since the drug is always open-label for my patients
(or their caregivers-- whoever will be making the report of effect to
me).  So I don't pretend I'm doing science here. I just hope the
science done by the drug company was good.  It *seems* to be.  But the
placebo effect is SO powerful, that I can't say for SURE.  Even
demented patients have good days and bad days, and sometimes I see
really good days that might be the drug, or might be just normal
variation in the disease.  The drug is NOT so powerful that it wouldn't
get lost in the noise of a non-blinded study.

>* What do you feel are the disadvantages to Aricept therapy?  What are
>the arguments *against* treatment?

   Only money and the occasional GI problem (which can be gotten
around, usually, but using even lower doses and working up).  There's
not much additional benefit to going over 5 mg, if you look at the
company's own literature.

    Occasionally the GI effects will make somebody very sick (this is
rare, but happens), and in that case you risk only having your patients
lose their trust in your treatments.  Adeqate warnings, and
"permission" to stop the drug at the first sign of trouble, usually
adequately mitigate this.

   BTW, I expect Aricept to work much better as an adjunct for people
trying to quit smoking, than Wellbutrin (sorry, "Zyban") does.  For
obvious reasons.  In the days before Aricept I had a few Alzheimer's
patients who responded to nicotene patches.  It was a LOT less risky
than Tacrine.

                                     Steve Harris, M.D.

>I want my presentation of this controversial subject to be balanced,
>presenting cohesive arguments both in favor of and against treatment.
>I am having difficulty forming arguments against treatment, as the
>literature is not concerned with that question, and I don't have the
>personal clinical experience to present my own opinions.
>Any opinions on these matters would be appreciated!
>Scott Goodman, M4
>KU Medical School

From: B. Harris)
Newsgroups: soc.history.what-if,sci.physics,,,
Date: 26 Aug 1998 22:34:09 GMT

In <> Carey Gregory <>

>jwwright wrote:
>> so you would go into the after life with no recollection of what
>> happened in your lifetime.
>I always find it interesting when people make scientific arguments to
>support or refute the mystical. If you assume an afterlife, then why
>assume that memories depend on the functioning of mere flesh?
>Carey Gregory


   On the other hand, it's always been darned hard for me to figure out
how people can assume that memories are NOT just stored in "flesh" (but
also somewhere else, like in your "soul,") and at the same time still
explain all the memory disorders we know about.

   Example: I've had Alzheimer's patients who could not tell me what I
was holding in front of them, when I held up my wristwatch.  Dialog
would be as follows:

"What's this?"
"I don't know."
"It's a watch."
"Oh, yes, it's a watch."
"Good!  Okay, now what is it again?"
"<pause>. I don't know."
"It's a watch"
"Oh, yes.  It's a watch."
"Good, now say it again."
"Say what?"
"What is this?"
"I don't know."
It's a watch."
"Oh, yes, it's a watch."
"Good.  Now tell me what it is again."
"I don't know."

   You can go on like this with some patients for as long as you have
the patience and the heart for it.  I must have done this for 10
minutes with one patient, and got no progress AT ALL.  She knew the
word and could repeat it, but could not retrieve it.  If it was stored
in her "soul," then what in the world was happening here?

  Many religions believe that there is a metaphysical part of humans
which has both memory and processing capability.  They assume dementia
and brain damage are simply a communications breakdown.  But no
communications breakdown with a normally intelligent person (say, a bad
phone connection) could possibly mimic dementia.  It would mimic
hearing loss, perhaps, but that's about it.  The conversation above is
not hearing loss.

                                        Steve Harris, M.D.

From: B. Harris)
Subject: Re: New Subscriber with a BIG Question
Date: 2 Sep 1998 16:55:12 GMT

In <6sjed7$>  (Ron
Gibson) writes:

>>Catherine: Yeah, stick the old folks in homes. Me. Me. Me. One of the
>>saddest things about all of this was I remember promising my Mother
>>that I would make sure that she never had to be in a home and that I
>>would offer her the same care and love in her "dotage" that I got in
>>my infancy-

   Bad promise.  Demented adults are 10 or more times more massive than
babies, and can be more difficult to take care of by an order of magnitude
also.  And it can last for a lot longer than it takes a child to get
potty trained.  I've seen previous mothers of four go nuts trying to
take care of a demented parent.  And, of course, trying to do BOTH
(which can happen also) is especially bad.

   I'm not saying it can't be done, mind you.  But skilled nursing
facilities don't exist only for childless people, and people with
children who don't care.  They exist because of reality.

                                  Steve Harris, M.D.

From: "Steve Harris" <>
Subject: Re: Lecithin?
Date: Wed, 16 May 2001 10:10:20 -0700

James Michael Howard wrote in message <>...
>A person exhibiting dementia probably also has neural death.  No supplement
>can aid a dead neuron.  For the effects of lecithin (choline) to be really
>examined, the subjects should be young and healthy.
>James Michael Howard

Well, if you lose some cholinergic neurons, you can make up for it
a bit by making the others overactive, or adding the chemical
they make. Rather as in the treatment of Parkinson's disease.
It's a little like putting nitromethane in a jalopy which is misfiring
on one cylinder, but it's better than nothing. Cholinergics DO
have a modest effect on early Alzheimer's disease symptoms.
No, they don't influence the underlying pathology.

But then, neither does the chemical treatment of Parkinson's, by and


From: "Steve Harris" <>
Subject: Re: Lecithin?
Date: Wed, 16 May 2001 10:13:49 -0700

James Michael Howard wrote in message <>...
>A person exhibiting dementia probably also has neural death.  No supplement
>can aid a dead neuron.  For the effects of lecithin (choline) to be really
>examined, the subjects should be young and healthy.

Lecithin doesn't work on Alzheimer's, but not because the idea
isn't sound. Some other cholinergic drugs of one sort or another
do have positive effects on Alzheimer's symptoms. Lecithin
either doesn't happen to get enough choline where it needs to
be, or else getting it there is ineffective at getting more
acetylcholine made.


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