From: sbharris@ix.netcom.com(Steven B. Harris)
Newsgroups: sci.med.nutrition
Subject: Re: Alzheimers
Date: 24 Apr 1998 05:48:08 GMT

In <6hmqth$2pm$1@news.ptialaska.net> "Mark Sixbey"
<msixbey@ptialaska.net> writes:
>
>I've been under the impression that it's a genetic disease. Like your
>height and eye color, there is virtually little you can do to either
>prevent or cause this disease by even drastically altering your
>lifestyle.
>
>If your father had it, you'll get it. Not because he drank from aluminum
>beer cans, or wrapped his sandwiches in foil, but because that's the way
>genes go. There's nobody to blame in that situation. The aluminum buildup
>in the brain is only in people who are genetically prone to accumulation
>of aluminum.
>
>That's what I thought, anyway.


    First of all, Alzheimer's disease (AD) has little to do with
aluminum.  Maybe nothing.  People who once got demented on renal
dialysis because there was too much aluminum in the blood, didn't get
pathology in their brains that looked anything like AD.  If AD was due
to aluminum, they certainly should have.

   Attempts to get anything in Animals which looks like AD by feeding
them aluminum, have been abject failures.  You can inject aluminum
directly into the brains of animals and make them demented, but now
we're into a model which isn't exactly close to that your problems and
mine.  Alzheimer's does correlate with prior histery of head trauma.
Having somebody drill a hole in your skull and poke a needle in,
qualifies, wouldn't you say?  It's not exactly a reason not to drink V8
from cans...

    Also, although there is clearly a genetic component to AD
(especially in people who get it young), it's a small one.  Too small
to use to predict very well who will be demented by death, and who
won't.
                                     Steve Harris, M.D.

From: sbharris@ix.netcom.com(Steven B. Harris)
Newsgroups: sci.med.nutrition
Subject: Re: No link of aluminium and Alzhemiers disease
Date: 27 Apr 1998 12:36:55 GMT

In <3447D7F0AFD4D011AE0400608C14CE5604C3F17C@pfs01.ex.nus.edu.sg>
Durairaj Ponraj <phydp@nus.edu.sg> writes:

>Hi
>Our lab is researching on this aluminium and Alzheimers disease. We
>found no aluminim in any of the fresh human brain tissue that were
>analyzed. We have used the technique of nuclear microscopy for even
>looking into damaged neurons of Alzheimers patients. This theory
>probably evolved due to previous analysis of chemically (eg Osmium)
>fixed brain tissues. So don't worry on aluminium as a causative agent.
>
>Cheers
>Dr Raj
>Research Center for Nuclear Microscopy
>NUS, Singapore


   Well, Duh, if that's the case, shouldn't it have been obvious to
people from their control samples?  I mean, if the fixation technique
brings in aluminum, and you fix everything you look at, everything
should have the same amount of alumnium in it, right?  You won't be
able to find brain withouth aluminum.  But the data that has started
the theories has to do with MORE aluminum in diseased brains than non
diseased ones.  Perhaps damaged brains take up more fixative?

From: sbharris@ix.netcom.com(Steven B. Harris)
Newsgroups: sci.med.nutrition
Subject: Re: Aluminum
Date: 28 Apr 1998 02:50:49 GMT

In <3447D7F0AFD4D011AE0400608C14CE5604C8711A@pfs01.ex.nus.edu.sg>
Durairaj Ponraj <phydp@nus.edu.sg> writes:

>	Hi, what you said is right. So we find more aluminum in control
>as well as experimental samples of fixed tissues. So what we actually
>did was to get fash frozen samples without any fixation  or staining.
>Sectioned them and charecterised them for senile plaques by
>immunohistochemistry, then the adjasunt sections (unfixed,unstained,
>freez dried) were scanned using the nuclear microscope (using 2mev
>proton beam). We found no aluminum in any of these samples. It must be
>noted that the senstivity (all elements including aluminum) is higher in
>proton beam than electron beam. If you need further reference I can
>give you our recent publication in neuroscience letters and a previous
>one published in nature.
>
>Raj



   Please do!  This is a NEAT piece of research, and if and when
properly confirmed by others, will pretty much wipe out an entire
subgroup of Alzheimer's theories.  Good progress.  There are a lot of
people out there putting a lot of good time and energy into reducing
aluminum in their diets, who might profitably do something else with
it.  I am in mind of one Sikh-guru M.D. in particular, who wears a
turban (of course) and runs a whole program for anxious people who are
afraid they might be getting Alzheimer's disease.  As suspected, he
doesn't have as many of the answers as he thinks he does-- par for the
course in too much of "alternative" medicine.  "It ain't the things you
don't know that hurt you, so much as the things you know, that just
ain't so!" (Josh Billings).  Gosh, orthodox doctors are so stupid they
don't even know that aluminum causes Alzheimer's disease.  How many
times have I heard this?

   Now, if you can just do the same for mercury, and save a lot of
people a lot of dental pain?  If we're going to be using alternative
medicine for Alzheimer's prevention, it might just as well be the right
alternative medicine.   Perhaps vitamin E, B6, folate, B12, and a diet
high in soy?  Too soon to tell for sure, but my money goes there at the
moment.  It's a guess, and you're welcome to it (we do know that
vitamin E helps.  And selegiline.  And NSAIDS and estrogen).  But I'm
willing to say it's a guess, and I'm not running any retreats where
anxious people spend thousands of dollars to hear me say I've got the
answer.

                                    Steve Harris, M.D.

From: cam@holyrood.ed.ac.uk (Chris Malcolm)
Newsgroups: sci.med.nutrition
Subject: Re: Aluminum
Date: 28 Apr 1998 08:04:33 GMT

sbharris@ix.netcom.com(Steven B. Harris) writes:

>If we're going to be using alternative
>medicine for Alzheimer's prevention, it might just as well be the right
>alternative medicine.   Perhaps vitamin E, B6, folate, B12, and a diet
>high in soy?  Too soon to tell for sure, but my money goes there at the
>moment.  It's a guess, and you're welcome to it (we do know that
>vitamin E helps.  And selegiline.  And NSAIDS and estrogen).  But I'm
>willing to say it's a guess, and I'm not running any retreats where
>anxious people spend thousands of dollars to hear me say I've got the
>answer.

The UK national press has recently discussed some recent research in
mice which been artificially predisposed to develop the amyloid
plaques charac. of Alzheimers. It has been found that a diet low in
cholesterol reduces the rate of formation, and high in cholesterol
increases formation drastically. It was suspected that this might be
the case, because the gene which predisposes to Alzheimers is
concerned with tranporting cholesterol to needed sites in neurones,
and the bad (Alz) variant is not so good at delivering, and dumps it
in the neurone body. If too much is dumped there, a function of blood
levels, the plaques develop.

It would be wise too to take account of the research which shows that
a good indicator of age of onset of dementias of all kinds is the
previous brain insult history, i.e., the more often you get knocked
out by a blow to the head, an anaesthetic, recreational drugs, or
drink, the earlier you are likely to develop dementia. I'm rather
startled by how many health and fitness fanatics, who spend lots of
money and time ensuring the good health of their bodies, seem quite
happy to regularly poison their brains for a bit of weekend fun.

In other words, if you want your brain to last, be nice to it.
--
Chris Malcolm    cam@dai.ed.ac.uk         +44 (0)131 650 3085
Department of Artificial Intelligence,    Edinburgh University
5 Forrest Hill, Edinburgh, EH1 2QL, UK                DoD #205
www.dai.ed.ac.uk/daidb/people/staff/Christopher_Malcolm.html

From: sbharris@ix.netcom.com(Steven B. Harris)
Newsgroups: sci.med.nutrition
Subject: Re: References against aluminium theory
Date: 29 Apr 1998 12:04:52 GMT

In <3447D7F0AFD4D011AE0400608C14CE5604D20236@pfs01.ex.nus.edu.sg>
Durairaj Ponraj <phydp@nus.edu.sg> writes:

>Hi Harris
>Here are some references published by our group:
>
>1.Landsberg J P, McDonald and Watt. Absence of aluminium in neuritic
>plaque cores in Alzheimer's disease. Nature. 360 (1992) 65-67.
>
>2. J Makjanic, B McDonald and F Watt, Nuclear microscopy study of
>neurofibrillary tangles in Alzheimers disease. Nucl Instr and Meths B130
>(1977) 439-444.
>
>3. J Makjanic, B McDonald, CPL-H Chen and F Watt. Absence of Aluminium
>in Neurofibrillary Tangles in Alzheimer's disease. Neurosci. Lett. 240
>(1998) 123-126.
>
>Certainly these findings are strongly against aluminium theory which
>still some belive!!
>
>Dr Ponraj
>Research Centre for Nuclear Microscopy
>NUS, Singapore




   Cool.  Now, what about mercury?

From: sbharris@ix.netcom.com(Steven B. Harris)
Newsgroups: sci.med.nutrition
Subject: Re: No link of aluminium and Alzhemiers disease
Date: 30 Apr 1998 01:18:18 GMT

In <6i7vgp$r6t@news.ww.co.nz> molab@ww.co.nz (R Molony) writes:

>Maybe alzhiemers is a syndrome which can be caused by a number of
>different initiators. Only those cases which were initiated by
>aluminium would be likely to show an elevated aluminium level.
>Remember that aluminium toxicity is a proven cause of an alzhiemers
>like disease in kidney patients and in babies fed contaminated milk
>formula.
>bob


   That is exactly wrong.  Such aluminum poisonings cause brain damage
and dementia, but the pathology and damage at the micro level in the
brain doesn't look anything like Alzheimer's.  That was one of the
things that made me first doubt the model!

                                      Steve Harris, M.D.

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: misc.kids.health,sci.med,misc.health.alternative,uk.people.health
Subject: Re: A Glimpse into the Scary World of Vaccine Adjuvants
Date: 9 Nov 2005 16:50:25 -0800
Message-ID: <1131583825.588458.116250@g43g2000cwa.googlegroups.com>

Vaccine-man wrote:
> Well, since you think metal mercury is in thimerosal, you must also
> believe that metal aluminum is in aluminum hydroxide. Have you had
> *any* chemistry? Misleading.

COMMENT:

In fairness I don't think he mentions aluminum metal.

While it is true that aluminum ion Al+3 is neurotoxic, it is also true
that only the dose makes the poison. Aluminum is very common in the
environment and in food--- if it was that toxic, we'd all have
dementia. Aluminum ion in the blood is rapidly excreted through the
kidneys, and that is why aluminum salts have caused human neuro
symptoms only in kidney patients and neonates who don't have great
renal function, and have gotten large amounts IV. And in doses far, far
higher than you'd ever get from less than a milligrams of alum adjuvant
per month (you get less than 4 mg in the first 6 mo of life, if you get
all your shots).

The aluminum adjuvant in DT is indeed probably responsible for a
certain amount of the redness, swelling, and pain caused by this
vaccine (which isn't much). Otherwise, worse reactions have been looked
for, but not found. Interestingly, in monkeys the adjuvant clearly
causes a macrophage response in the muscle at the point of vaccine
entry. This is the immune response that no doubt is responsible for the
adjuvent's effect.

Perhaps in future we'll learn to give kids DT subcutaneously, in order
to enhance the immune response by getting killed vaccine to skin
dentritic cells, so we don't have to stir up deep tissue macrophages
with alum crystals. Whatever it is, It can always be done better.

SBH

Lancet Infect Dis. 2004 Feb;4(2):84-90.

Comment in:
    Lancet Infect Dis. 2004 Jun;4(6):324; discussion 325.

Adverse events after immunisation with aluminium-containing DTP vaccines:
systematic review of the evidence.

Jefferson T, Rudin M, Di Pietrantonj C.

Cochrane Vaccines Field and Health Reviews Ltd, Rome, Italy.
toj1@aol.com

We have reviewed evidence of adverse events after exposure to
aluminium-containing vaccines against diphtheria, tetanus, and
pertussis (DTP), alone or in combination, compared with identical
vaccines, either without aluminium or containing aluminium in different
concentrations. The study is a systematic review with meta-analysis. We
searched the Cochrane Vaccines Field Register, the Cochrane Library,
Medline, Embase, Biological Abstracts, Science Citation Index, and the
Vaccine Adverse Event Reporting System website for relevant studies.
Reference lists of retrieved articles were scanned for further
studies. We included randomised and semi-randomised trials and
comparative cohort studies if the report gave sufficient information
for us to extract aluminium concentration, vaccine composition, and
safety outcomes. Two reviewers extracted data in a standard way from
all included studies and assessed the methodological quality of the
studies. We identified 35 reports of studies and included three
randomised trials, four semi-randomised trials, and one cohort study.
We did a meta-analysis of data from five studies around two main
comparisons (vaccines containing aluminium hydroxide vs no adjuvant in
children
aged up to 18 months and vaccines containing different types of
aluminium vs no adjuvants in children aged 10-16 years). In young
children, vaccines with aluminium hydroxide caused significantly more
erythema and induration than plain vaccines (odds ratio 1.87 [95% CI
1.57-2.24]) and significantly fewer reactions of all types (0.21
[0.15-0.28]). The frequencies of local reactions of all types, collapse
or convulsions, and persistent crying or screaming did not differ
between the two cohorts of the trials. In older children, there was no
association between exposure to aluminium-containing vaccines and onset
of (local) induration, swelling, or a raised temperature, but there was
an association with local pain lasting up to 14 days (2.05
[1.25-3.38]). We found no evidence that aluminium salts in vaccines
cause any serious or long-lasting adverse events. Despite a lack of
good-quality evidence we do not recommend that any further research on
this topic is undertaken.

Publication Types:
    Meta-Analysis
    Review

PMID: 14871632 [PubMed - indexed for MEDLINE]

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: misc.kids.health,sci.med,misc.health.alternative,uk.people.health
Subject: Re: A Glimpse into the Scary World of Vaccine Adjuvants
Date: 9 Nov 2005 18:56:25 -0800
Message-ID: <1131591385.103366.165960@f14g2000cwb.googlegroups.com>

PeterB wrote:
> The fact that such exposures are even diminutively toxic is evident in
> the study abstract you posted, otherwise such reactions wouldn't occur.


COMMENT:

That doesn't follow. Or if so, it's a bizzare definition of "toxicity".
Is sunlight toxic? How about frostbite? Asbestos?  Injury is not
necessarily toxicity, or else we wouldn't have two different words for
them.  The local and limited damage/irritation from adjuvants is more
like that of a splinter or some mechanical object. Indeed, it reminds
me of asbestos, except there's no evidence it causes local cancer. This
kind of irritation does not imply some neurological effect after the
chemical crystals have all been dismantled and their constituents
distributed elsewhere in another from.

>  That the study authors did not see evidence for more serious,
> long-term harm, is not evidence that such harm doesn't occur over time.
>  The closing comment by the study author is rather bizarre: "Despite a
> lack of good-quality evidence we do not recommend that any further
> research on this topic is undertaken."  Sounds like a pharma-sponsored
> study to me, one designed to arrive at a pre-determined conclusion.  As
> for your recitation that only the dose makes the poison, it's more
> accurate to say that only the dose makes the poison by degree.  Even a
> small amount of toxin can have a harmful affect in human physiology,
> and if exposure is constant over time, that damage can be difficult to
> measure.

COMMENT:
No, it's more accurate to say that the dose makes the poison. There's
not a single chemical element in the environment your body doesn't
contain in some degree, including all the heavy metals. Your faith that
there is damage, but damage difficult to measure, is just that---
faith. It's much more rational to imagine that below some threshhold,
none of it matters. To imagine not is to go back to homeopathy.

SBH

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: misc.kids.health,sci.med,misc.health.alternative,uk.people.health
Subject: Re: A Glimpse into the Scary World of Vaccine Adjuvants
Date: 10 Nov 2005 13:48:08 -0800
Message-ID: <1131659288.704834.104460@g44g2000cwa.googlegroups.com>

john wrote:
> >While it is true that aluminum ion Al+3 is neurotoxic, it is also true
> >that only the dose makes the poison. Aluminum is very common in the
> >environment and in food--- if it was that toxic, we'd all have
> >dementia.
>
> Surely you are not admitting aluminium can cause dementia??
>
> That must have been a slip of the tongue,  forked tongues and all that


Dialysis dementia from aluminum is a well-known medical phenomenon
(albeit a historical one).  Recognizing this is not to say that any
large fraction of modern dementia (dementia is a syndrome like anemia,
NOT a specifc disease), is due to aluminum. That's still a subject of
intense debate. Aluminum is neurotoxic without doubt. The brains of
animals with aluminum toxicity and dialysis patients with the same,
resemble Alzheimer's disease, but not *perfectly.* (for example, there
are tangles, but not as many). Alzheimer brains have more aluminum in
them than normal brains and it's associated with the areas of damage,
but that may only be because the damged areas pick it up. It's very
hard to prove causation.

The real difficulty is that this problem is like trying to prove
cigarettes cause lung cancer in emphysema, in a population where
EVERYBODY smokes. Aluminum is a prime ingredient in dust and dirt. It's
everywhere. All animal life evolved in a soup of aluminum compounds.
Humans don't particularly get more if than cats or dogs or rats.  But
we're the species that gets Alzheimer's. So it's not a simple causal
problem, even if aluminum is somehow involved.

SBH

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: misc.kids.health,sci.med,misc.health.alternative,uk.people.health
Subject: Re: A Glimpse into the Scary World of Vaccine Adjuvants
Date: 10 Nov 2005 21:45:19 -0800
Message-ID: <1131687919.134419.179080@z14g2000cwz.googlegroups.com>

Christopher J. Henrich wrote:
> In article <1131659288.704834.104460@g44g2000cwa.googlegroups.com>,
> Steve Harris <sbharris@ix.netcom.com> wrote:
>
> >  Alzheimer brains have more aluminum in
> > them than normal brains and it's associated with the areas of damage,
> > but that may only be because the damged areas pick it up. It's very
> > hard to prove causation.
> I seem to recall reading that the detection of Aluminum in Alzheimer
> brains was dubious: only one lab found the result, other labs couldn't
> replicate it.  Is my info out of date or mistaken altogether?


No, the finding and failure to replicate pendulum has been swinging
back and forth on the subject for 20 years. It all comes down to whose
papers and techniques you believe. Plus, perhaps you can "explain away"
the negative results by suggesting a buildup of aluminum in very small
and specific neurons and areas, which gets overwhelmed by analysis of
larger bulk tissue samples. In the end, I don't know how it wil come
out.  My sense is that there is too much smoker here for there not to
be some fire. But the direction of causality is still up for grabs.

Also, again, if this was THE main cause of Alzheimer's, you'd expect a
clearer signal. The idea of an "aluminum trigger" again gets us nearly
back to homeopathy. That would be very hard to prove, even if true. As
I say, aluminum is everywhere. As well come up with a hypothesis of a
"glucose trigger."


1: J Alzheimers Dis. 2005 Aug;7(4):273-84.

Brain aluminum, magnesium and phosphorus contents of control and
Alzheimer-diseased patients.

Andrasi E, Pali N, Molnar Z, Kosel S.

Institute of Inorganic and Analytical Chemistry, L. Eotvos University,
Budapest, Hungary. anal@para.chem.elte.hu

A study was undertaken to determine Al, Mg and P concentrations in 5
different brain regions of 3 control and 3 Alzheimer-diseased patients.
One of the aims of this work was to evaluate the performance of applied
analytical techniques. The digested samples were analyzed by inductively
coupled plasma atomic emission spectrometry for Al, Mg and P. The dried
samples were measured by instrumental neutron activation analysis for Al
and Mg. The determination of human brain Al levels is complicated by the
interfering reaction of P. We have previously worked out an analytical
method which can eliminate this interference.  The accuracy of the
measured data was investigated by the analysis of biological standard
reference materials. Our second goal was to study the possible elemental
concentration changes in Alzheimer-diseased patients.  Significantly
higher Al and lower Mg and P values were found in some AD brain regions
compared to the controls.

PMID: 16131728 [PubMed - in process]

2: Ann Neurol. 1993 Jan;33(1):36-42.

Comment in:
    Ann Neurol. 1993 Sep;34(3):413-5.

Laser microprobe analysis of brain aluminum in Alzheimer's disease.

Lovell MA, Ehmann WD, Markesbery WR.

Department of Chemistry, University of Kentucky, Lexington 40536-0230.

Aluminum (Al) levels were measured in the cytoplasm and nucleus of 241
neurofibrillary tangle (NFT)-bearing neurons, in 217 NFT-free neurons and
adjacent neuropil from 7 autopsy-confirmed Alzheimer's disease (AD)
patients, and in 316 normal neurons from 5 control subjects, by laser
microprobe mass spectrometry. Grand mean Al levels (dry weight basis) in
AD samples were 2.93 +/- 1.24 micrograms/gm for NFT-bearing neuron
cytoplasm, 3.54 +/- 1.39 micrograms/gm for NFT-bearing neuron nuclei,
2.31 +/- 1.09 micrograms/gm for NFT-free neuron cytoplasm, and 3.23 +/-
1.09 micrograms/gm for NFT-free neuron nuclei. Control values were 1.85
+/- 0.78 micrograms/gm for cytoplasm and 2.01 +/- 0.93 micrograms/gm for
nuclei. The differences between corresponding regions of AD NFT-bearing,
AD NFT-free, and control neurons were not significant (p > 0.05, analysis
of variance). Al levels in neuropil were identical for AD and control
samples at 2.16 +/- 0.93 micrograms/gm. In contrast to some literature
reports, we found very few (< 2.5%) extremely high Al values (> 20
micrograms/gm, dry weight) on a cellular basis in AD samples. AD neurons
did exhibit a higher number of Al values (9.6-14.3%) that were > 3 sigma
above the corresponding control means, than did control neurons
(1.3-1.6%), indicating that small elevations of Al may exist in patients
with AD. Our data suggest that any Al accumulation in patients with AD is
small and generalized in both NFT-free and NFT-bearing neurons and that
analyses of large bulk brain samples are likely to have AD/control
differences masked by the large amount of unaffected neuropil sampled.

PMID: 8257483 [PubMed - indexed for MEDLINE]

3: Alzheimer Dis Assoc Disord. 1996 Fall;10(3):171-4.

Content of brain aluminum is not elevated in Alzheimer disease.

Bjertness E, Candy JM, Torvik A, Ince P, McArthur F, Taylor GA, Johansen
SW, Alexander J, Gronnesby JK, Bakketeig LS, Edwardson JA.

Section of Epidemiology, Institute of General Practice and Community
Medicine, Oslo, Norway.

Several studies have reported that the bulk aluminum (Al) concentration
is increased in the brain in Alzheimer disease (AD), while other studies
have failed to demonstrate an increase. Most of these investigations have
had one or more methodological deficiencies, including lack of adequate
neuropathological assessment; failure to age-match the control samples;
small sample sizes, lacking statistical power; and geographical
heterogeneity in the AD and control populations. The present
population-based study of 92 clinically and histopathologically diagnosed
AD patients and normal elderly nursing home residents was designed to
avoid these potential biases. When a subsample of AD cases with the most
severe brain pathology was compared with controls having no or minimal
pathology, no statistically significant differences were found in the
bulk aluminum concentration measured by graphite furnace atomic
absorption spectrometry in frontal cortex (1.8 +/- 0.7 vs. 1.7 +/- 0.7
micrograms/g dry wt), temporal cortex (1.4 +/- 0.3 vs. 1.5 +/- 0.5
micrograms/g dry wt), liver (2.0 +/- 1.3 vs. 2.0 +/- 1.2 micrograms/g dry
wt), or head of femur (2.4 +/- 1.6 vs. 2.2 +/- 1.0 micrograms/g ash wt).
Within the whole series of 92 cases, there was no difference in the bulk
aluminum concentration of the frontal cortex between individuals
diagnosed as definite, probable, and possible cases of AD using the CERAD
(Consortium to Establish a Registry for Alzheimer's Disease) criteria.
The density of senile plaques and neurofibrillary tangles in frontal and
temporal cortex showed no correlation with the bulk aluminum
concentration.  Logistic regression analyses, which controlled for age
and sex, did not influence outcome for any of the comparisons. The data
show conclusively that in AD, bulk aluminum concentration is not
increased in two cortical brain regions that are selectively vulnerable
to the neuropathological changes associated with this disorder.

PMID: 8876778 [PubMed - indexed for MEDLINE]