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Parkinson's - The Truth
Source: SPEAK.
Parkinson's disease (PD) is a terrible illness
which causes enormous human suffering. Supporters of the new Oxford
University animal lab claim that experimenting on animals will enable
advances in treating PD. We have always expected animal experimenters to
defend the proposed lab; their careers, reputation and future income
depend on projects such as this continuing. Unfortunately for them,
neither medical history nor science supports their
claims.
The reality is that there is no animal model of
PD, and all past advances in treating it have been made through human
study. In future, animals are of even less value as a research method –
for two reasons. One is that we are studying PD in greater details, and
the vague similarities between animal and human biology will be less
relevant. The other is the emergence of incisive technology which enables
the study of the human PD patient at levels we would hardly have believed
possible years ago.
The claim that animals have or will be helpful in
tackling the disease is hollow. Our opportunity to prove this is our
opportunity to take away the assertion that the Oxford animal lab has any
place at all in modern medical research. This means that we all need to
know why PD research fails in animals and how advances really have and
will be made.
We will therefore be looking at 5 specific
subjects in order to highlight the fraudulent arguments being made by the
pro vivisectionists:
THE VAGUENESS OF THE ANIMAL MODEL
| "…it is essential to understand that
animal models only represent an imperfect replica of human
disorders, and this is so for several reasons. First, animal
models are generally developed in beings (rodents, non-human
primates) that are subjects with behavioural repertoires and
anatomical characteristics very different from humans. These
species differences are known to play a critical role in the
clinical expression as well as in the cellular specificity of the
lesions. Second, in addition to these species differences, the time
source evolution of the nerve cell generation, which normally
evolves over several years in neurodegenerative diseases in humans
is for practical reasons being replaced over a much shorter period
of time in animal models. "[3] |
The cause of PD is specific – it's caused by degeneration
of a specific part of the brain. Animals don't get it, and the best animal
experimenters have managed to do is recreate some of the
symptoms.
The favourite way of doing this is to apply MPTP
(1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) to the brains of animals.
MPTP is a by-product of synthetic heroin. The problem with this method is
that it doesn't cause PD – it just causes illness which shares some of the
symptoms. Even the animal experimenters who practice it – usually experts
in blowing their own trumpets and exaggerating the value of their work –
criticise it and they don't claim animals with it have
Parkinson's.
Jay Schneider, one such experimenter, calls it
'parkinsonism', and writes: "Some monkeys had cognitive deficits and no
motor deficits. Other monkeys had full parkinsonism that was produced
after short-term high dose MPTP exposure, and some monkeys had full
parkinsonism after long-term low-dose MPTP exposure."[1]
Is this haphazard set of symptoms supposed to be a
scientific model? As if to add to the uselessness of the model, the animal
model recovers gradually – unlike the chronically afflicted human
patients. An expert explains that: "The best model of PD to date, is
the…(MPTP)-lesioned marmoset….unlike human PD, which is progressive, the
neurotoxic damage produced by MPTP is reversible." [2] The suggestion that
gradually recovering monkeys with a condition that causes variable
symptoms can be used to study the disease is clearly ludicrous.
A further problem which would render animals useless as a
method if they weren't already is that communication between animals and
human is so limited. Animals can't explain their symptoms, emotions,
difficulties in motor functions or what affects them in everyday
life.
In summary, the animal model is a failure
because:
- Animals don't get PD
- The 'best' animal model recovers and has some
similarities of symptoms – not PD
- Animals can't communicate well with humans, and have
different behaviour from humans
- The illness is induced quickly – unlike the slow
degeneration in humans.
Given that animals are a failed method, how has progress
been possible against PD? As for the overwhelming majority of illnesses,
progress has been due to a combination of study of patients, autopsy, the
use of technology and a helping of luck.
UNDERSTANDING AND TREATING PD
PD was never really understood until 1960. An Austrian
team lead by Oleh Hornykiewicz performed autopsies on human PD patients at
the University of Vienna. The knowledge at this point – established by
autopsy - was that this very specific, human illness, was caused by a very
specific part of the human brain degenerating. The substantia nigra, part
of the brain found in the basal ganglia was badly affected. This was never
likely to be uncovered in animals, who don't have a comparable basal
ganglion. As an expert explains, animal models "do not reflect the
complexities of the human basal ganglion."[4]
The Austrian team discovered that the nigostriatial
pathway had degenerated and had very little dopamine. Dopamine regulates
movement and emotion, and normally carries most of the nerve signal.
[diagram]
This made perfect sense as PD does affect movement and
emotion, and led to tests on brain tissue from PD patients, which
confirmed the dopamine deficiency. They went on to discover that nerves
containing dopamine die, leaving a deficiency of dopamine. They soon gave
patients treatment intended to lead to dopamine production, which caused
immediate benefits. As well as revolutionising PD treatment, this enabled
better research into other neurological illnesses including epilepsy and
schizophrenia. As one expert put it, Hornykiewicz had "fundamentally
changed how neuropharmacology is practiced."[5]
Hornykiewicz was never awarded the Nobel Prize for this
work, although it was awarded to a team who had followed on from the work
pioneered by the Austrians. The award attracted disapproval: 250
neurologists criticised the decision and the decision not to reward
Hornykiewicz.[6]
This massive discovery is only a step on the way to
finding a cure for this terrible disease. The fact that the substantia
nigra dies is a symptom, not the cause of the disease, and further
knowledge of why it dies needs to be uncovered. For this reason why need
more studies into human patients on a detailed level studying the
interactions between the substantia nigra and the rest of the body.
Autopsies are now possible on a highly detailed level thanks to
improvements in microscope technology, and arguably provide the most
valuable of any single method in studying neurological illness.
Two pathologists wrote "In recent years, participants in
meetings of the American Association of Neuropathologists have heard
criticism about the increasing use of animal models to study human
neurologic disease…. A strong cadre of diagnostic and research
neuropathologists believe that only human material can provide relevant
answers to many problems about human central nervous system disease. In
fact, examination of the data bears out this contention. Of the 185
abstracts presented at the 1985 meeting of the American Association of
Neuropathologists, 115 (62%) were presentations of human neuropathology,
and an astounding 81 (43%) were based on investigations of human brains at
autopsy. Among these autopsy studies were seven presentations of either
the first complete description of a newly recognized human disorder, or
one of the first complete descriptions of an uncommon human neurologic
disease."[7]
Nevertheless, the Austrian discovery made a difference to
human patients, as it immediately enabled treatments to enhance dopamine
levels. Further human studies showed that Levodopa could be used to
stimulate dopamine levels.[8] This is imperfect and becomes less effective
over time – the reason for which is understood thanks to study of
patients. [9] Another method has been to use the nightshade plant, which
decreases levels of acetylcholine, which increases when dopamine is in
short supply.
Other effects have been discovered by accident – such as
the effect of ecstasy or the antiviral Amantadine.
Before the Hornykiewicz discovery, surgery was used to
control PD by removing both thalami. The thalamus is a two part brain
section. This had limited success, but it was in attempting these that a
more striking method was discovered.
DEEP BRAIN STIMULATION
[diagram]
To make surgery more accurate, high-frequency electrodes
were used to increase activity in neurons to aid the thalamotomy. By
chance, a doctor at Grenoble University Hospital in France used the wrong
frequency when doing this. Dr Bernabid found that the lower frequency
calmed the neurons, and tried applying them to other parts of the brain.
Reasoning that this may stop symptoms altogether, he tried to do so, and
was successful.
He soon was presented with a patient on whom he couldn't
perform a thalamotomy, so tried implanting the electrodes permanently. It
was successful, and led to more research, and the eventual approval of the
technique around the world.[10]
Bernabid's discovery was a victory for surgical technique,
human study, and observation. It owes nothing to animal experiments. This
same technique is the one used by Tipu Aziz, an outspoken supporter of the
Oxford University animal lab. Aziz has in the past claimed that the
treatment of deep brain stimulation given to Parkinson sufferers owes
everything to his research on monkey brains and could not have been made
in any other way. It is the technique demonstrated by PD patient Mike
Robbins. We can be absolutely clear that this technique has nothing to do
with animal experiments, and everything to do with the technology,
clinical medicine and observation SPEAK and the scientific
anti-vivisectionist movement has supported. Deep Brain Stimulation was not
discovered by experimenting on non-human animals as the vivisectors would
like you to believe.
Rather than assisting scientific research in finding cures
for human diseases, the use of animals is actually hampering it. We are
now in the 21st Century. We have the technological capacity to send space
probes to Mars. However, some scientists are still involved in the crude
and barbaric practice of vivisection, a practice which dates as far back
as the 1600's. The following section will deal with the new forms of
technology that are available to us. These new and innovative types of
technology are our best hope in finding cures for human disease.
TECHNOLOGY IN THE MODERN
LABORATORY
fMRI (functional Magnetic Resonance Imaging)
This technique identifies the role of different areas of
the brain. It does this by detecting higher and lower magnetic
susceptibilities in the blood, which indicate whether the blood is newly
oxygenated or not. Real time scans are possible which aid treatments
such as surgery and are of great value as a diagnostic tool.
See http://www.fmrib.ox.ac.uk/fmri_intro/brief.html for more or http://www.dcn.ed.ac.uk/bic/research/structural.asp for a British University applying the
technique.
MagnetoEncephaloGraphy (or MEG)
Detects the magnetic fields associated with brain
activity without using X-rays. It sends no signals into the brain so is
entirely safe. It enables a functional image of the brain to be shown.
This helps show what activity the brain is undertaking, and where in the
brain this comes from. It helps show where problems (eg epilepsy or
migraine) is coming from.
See http://www.magres.nottingham.ac.uk/meg/index.phtml for a UK university working at the forefront of this technology.
Or see http://www.aston.ac.uk/lhs/research/facilities/meg/faq.jsp and see http://www.aston.ac.uk/lhs/research/groups/nrg/nrg_projects.jsp for some of their valuable work in humans.
EIT (Electrical Impedance Tomography)
EIT is mobile and cheap. It registers electrical
resistance in disease-affected areas. The main benefit is therefore to
trace the movement of blood and other fluids. Developments will
hopefully lead to this being a cheap, portable method of imaging the
brain in full 3-D detail.
See http://dnl.ucsf.edu/users/tferree/docs/IEEE2002.pdf for the detailed interpretation of info from EIT and http://www.mdx.ac.uk/hssc/research/groups/biomedical/g_biomodel.htm
SPECT (Single Photon-Emission Computed
Tomography)
Enables doctors to build 3D images of the brain by
detecting details about the flow of blood. This shows brain function and
is vital for detection of illnesses. This is done by radioactive
labelling blood.
See more at: http://www.amershamhealth-us.com/patient/diaguide/spect.html and http://www.answers.com/topic/single-proton-emission-computed-tomography
PET (Positron emission tomography)
Scans detect radiation from positrons, and enable a
detailed picture of the illness to be constructed. This is vital for
patients with brain dysfunction for which the cause has not been
determined.
See more at http://www.radiologyinfo.org/en/info.cfm?pg=pet&bhcp=1 OR http://www.chm.bris.ac.uk/webprojects2002/wrigglesworth/brainimaging.htm
MRS (Magnetic Resonance Spectroscopy)
Enables chemical analysis of the brain without surgery,
by distinguishing the chemical nature of the part of the brain being
scanned. This is done by detecting the magnetic resonance in that part
of the brain and analysing the data this shows.
See more at http://www.ness-foundation.org.uk/Magnetic-Resonance-Spectroscopy.htm. Used in: http://www.qrd.alzheimers.org.uk/researchdetail.asp?GrantsID=65
EROS
Uses lasers which can pass through the skull, to image
the brain. They are fired from dozens of different directions at once,
and the technique measures differences in the way they reflect. The
differences are caused by the fluid in the brain cells, and reveal vital
information about the condition of the different parts of the brain.
http://www.sciencentral.com/articles/view.php3?
type=article&article_id=218392783
TMS (Transcranial magnetic stimulation)
Stimulates or calms parts of the brain using magnetic
impulses. Higher frequencies stimulate, lower ones calm. This enables
doctors to calm brain areas and assess the affect on symptoms, therefore
identifying brain areas linked with specific illnesses. Long-term
imbalances in the brain can be identified.
http://www.psy.ox.ac.uk/xmodal/TMS-for-volunteers.htm
http://www.ccni.gla.ac.uk/index.php?option=com_content&task=view&id=24&Itemid=41
Autopsies
Without autopsies, the progress in neurology would be
almost non existent. This method has focused on real patients and the
real nature of their brains, and full records of their condition have
been compared with the findings. As microscopes become more powerful,
the method becomes more effective.
In vitro study
Involves studying human brain tissue and understanding
the chemical interactions and detailed information about the biology of
it. It also compares healthy tissue with unhealthy tissue to show the
difference, and has already helped enormously with development of
treatments.
Computer modelling
Computer modelling is becoming more advanced each year.
With the information from autopsy, in vitro studies and technological
imaging, knowledge of the brain and activity in it is more detailed than
ever. The healthy brain, and the brain afflicted by illnesses can now be
modelled and the complex interactions can be
modelled.
The human brain is unlike any other, with additional
areas, different proportions, and is organised differently. The only way
the function of the human brain has been understood has been through
clinical (human) study.
Studies have shown that the same areas in different animal
and human brains play different roles as well: damage to the corresponding
parts of monkey and human brains has been shown do cause different
symptoms.[11]
In the early 1800s the speech centres of the brain were
located through autopsies and observing patients – work which would have
been impossible through vivisection as animals lack the same speech
process more obviously than they lack other processes.[12]
Research into human brain function is only really possible
through studying humans – either in life or at post mortem. As a
recognised neurologist explains:
"The study of the brain, if it is to bear fruit, must be
made on man, i.e. at the bedside and in the post-mortem theatre; …The
utmost that can be learned from experiments on the brains of animals is
the topography of the animal's brain, and it must still remain for the
science of human anatomy and clinical investigation to enlighten us in
regard…of our own species; and in fact, it is from the department of
clinical investigation and post-mortem study that so far all of our best
brain localizations have been secured."[13]
OTHER ILLNESSES AFFECTING THE
BRAIN
Human illness cannot be researched by using animals. The
evidence that proves this played a major part of the decision not to build
a similar lab in Girton, attached to Cambridge University. The evidence
was written by a doctor and can be viewed by going to: http://www.vivisection-absurd.org.uk/xprimate.html and selecting 'part 2'.
Some of the other illnesses of the brain are also claimed
to be advanced through animal study, but as with PD, progress has only
been possible through human study.
Multiple Sclerosis
MS is caused by the immune system attacking itself, and
the cause is not yet known.
Animal models have misled experimenters about how MS
progresses[14] and have symptoms and patterns of damage to the brain
that are not at all in line with human experience.[15] They have also
failed to provide treatments of value.
"Time after time, researchers have discovered new ways
to cure laboratory rats of experimental induced encephalomyelitis, the
murine model of MS, only to face obstacles in bringing the treatment to
humans."[16]
Treatments developed on animals include Tumor necrosis
factor (which has the opposite effect in humans) [17], Copaxone (which
came with numerous side effects)[18], and injected immunoglobins, which
were no more effective than placebos [19]. Peptide ligand formulas
trials were abandoned as patients nearly died.[20]
Most research into MS has been based on clinical
research and culture work using T-cell lines and cells taken from
individual patients.[21]
Alzheimer's Disease
Dr Alois Alzheimer first identified AD using microscopes
and autopsy. The lack of mental function is caused by protein becoming
uncontrolled and forming protein deposits in the brain now known as
neurofibrillary tangles.[22] The particular protein involved (tau) was
identified in mice, but altering the mouse's tau did not even cause any
symptoms similar to AD, despite enormous efforts and
resources.[23]
The first major breakthrough was the discovery that AD
patients lacked acetylcholine, which helps neurons communicate. This was
discovered through autopsy.[24]
Animal models have proved frustrating and
unproductive:
"The full spectrums of the biochemical and pathological
abnormailities characterized by AD have not been found to occur
spontaneously in any animal species other than human…"[25]
Another explains: "There is no good animal model for the
disease process characterized by a loss of cognitive functions and
memory decline."[26]
While human studies have enabled advances, especially in
the knowledge of the genetic implications of AD, a medical journal
editorial criticising animal models points out that the first discovered
characteristic of AD is not present in animal models:
"More problematically, these animals do not develop
neurofibrillary tangles or show significant
neurodegeration."[27]
Epilepsy
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In a speech at the International
Symposium of April 25 1987, Zurich, Dr Med. Bernhard Rambeck,
Director of the Biochemistry Department of the Society for
Epilepsy Research in Bielefield-Bethel, West Germany
stated:
"As a scientist, I am of the opinion
that animal experiments bring no progress in the diagnosis and
therapy of epilepsies. I have a well-founded suspicion that
similar facts apply in other areas of medicine."[29]
Unsurprisingly, animal experiments
are seen as a poor method of studying human illness and are
rapidly becoming less respected. As two pathologists
explain:
"In recent years, participants in
meetings of the American Association of Neuropathologists have
heard criticism about the increasing use of animal models to study
human neurologic disease…. A strong cadre of diagnostic and
research neuropathologists believe that only human material can
provide relevant answers to many problems about human central
nervous system disease. In fact, examination of the data bears out
this contention. Of the 185 abstracts presented at the 1985
meeting of the American Association of Neuropathologists, 115
(62%) were presentations of human neuropathology, and an
astounding 81 (43%) were based on investigations of human brains
at autopsy. Among these autopsy studies were seven presentations
of either the first complete description of a newly recognized
human disorder, or one of the first complete descriptions of an
uncommon human neurologic disease."
[35] |
The first accurate description of epilepsy was by John
Hughlings Jackson. Long before electroencephalograms (EEGs) he correctly
described the illness as one caused by abnormal electrical discharges in
the brain. This was based on observing patients, although now, MRIs can
show which part of the brain is causing the seizures and how the illness
is progressing.
Progress has enabled types of epilepsy to be
identified:
"The detailed models for focal interictal discharges
arose largely from experiments on brain slices in vitro [studied after
death], combined with computer simulations." [28]
An evaluation of modern epilepsy research by vivisection
supporters recently identified the most important methods as:
- Brain imaging methods, especially MRI
- Surgical technique and the ability to detect
opportunities for surgery
- Molecular genetics
Animal experiments were not mentioned.[30]
Attempts to cause an animal model by inducing birth
defects in animals were based on the discovery that substance abuse in
humans is linked to epilepsy. It didn't work.[31]
The discovery of treatments has been mainly due to
discovering the effects medicines have had on epilepsy when intended for
another condition. "Overwhelmingly, discovery of the old and a number of
the new AEDs [antiepileptic drugs] came from serendipity
[chance]."[32]
The idea that animal models would enable this is
dismissed: "In other words, a potent new drug against NMDLA ot
NMDA-induces seizures [animal models of epilepsy] is not necessarily a
useful drug for therapy of drug-resistant epilepsy (in humans) as
demonstrated by the disappointing data from clinical studies with NMDA
antagonists in patients with refractory epilepsy."[33]
Although dogs can naturally develop epilepsy, comparing
human and dog patients is not viable due to the way the drugs are
handled by the bodies. Vigabatrin treats epileptic dogs, but when given
to human was related to severe vision damage and has led to large court
cases.[34]
The claim by animal experimenters that their practice has
been invaluable is false. It is also a claim which other researchers feel
is detrimental to the advancement of science. Concern about the
preoccupation with animal research is becoming more prevalent.
The evidence that animal experiments are bad science and
hamper the progress of human medicine is overwhelming and more doctors are
coming to the conclusion that vivisection is a deeply flawed scientific
practice. Vivisectors want to continue with animal experiments not because
it's the best form of research but because it keeps them in their chosen
career. It's vitally important that for those people suffering from
terrible illnesses, that the fraud is stopped now.
See the following websites for more
information:
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back
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