http://www.curedisease.net/faqs/faq03.shtml
Technically humans are animals, so what's the big difference?
Whereas all animal cells have properties in common - a nucleus,
mitochondria and so on - we now know that even smaller idiosyncrasies
distinguish the way the cells of different species react to food,
environment and medicines. Failed animal experimentation has
irrevocably proven that tiny differences can prevent disease in one
species or enable it in another. The smallest biological differences
between humans and animals lead to lethal errors when applying animal
data to humans. White blood cell surface receptors, for example, leave
humans uniquely vulnerable to AIDS. Even the animal experimenters'
bible, The Handbook of Laboratory Animal Science, states:
"It is impossible to give reliable general rules for the validity of
extrapolation from one species to another. [This] can often only be
verified after the first trials in the target species [humans].
Extrapolation from animal models. . . will always remain a matter of
hindsight."[3]
3: Handbook of Laboratory Animal Science ,Volume II: Animal
ModelsSvendensen and Hau (Eds.) CRC Press 1994 p6.
What about the argument that animal experimentation is indispensable
as our only model of intact metabolic systems?
This assertion suggests that in vitro research methodologies, though
valuable, cannot predict what will happen in a whole living system,
which is true. But history has proven that results in lab animals are
even more inadequate - predicting results solely for the animal
tested, not humans.
Given that metabolic processes differ greatly between species,
information garnered in animal experiments has no predictive value and
is wholly unscientific when applied to humans. Very often substances
that have proven effective in animals demonstrate no curative value
for humans, sometimes even causing harm.
By using in vitro research and new technology we can simulate the
living intact human far better than a lab animal can. All drugs must
eventually be tested on humans, and those humans are every bit the lab
creatures that animals are. These "clinical phases" of drug testing,
as they are called, submit human volunteers to what are at first very
incremental dosages, monitor their reactions, and slowly increase
dosage.
Clinical testing and subsequent non-animal methods, such as
epidemiology and post-marketing drug surveillance, provide what lab
animals cannot - 100% accurate measures of the human metabolic
processes.
How can we know that medicines will not cause birth defects without
testing them on animals?
The medical principle called Karnofsky's Law states that any substance
can be teratogenic (cause birth defects) if given to the right
species, at the right stage in development, and in the right dose.
Common table salt or even water can be teratogenic to some species in
certain circumstances! Therefore, science has already told us that any
medication can cause birth defects in some creatures. [4]
In addition, agents that are teratogenic to some species may have
little or no teratogenic affect in others.[5] Of 1,200 chemicals that
caused birth defects in animals, only 30 were proven to affect humans.
[6] As the book, Chemically Induced Birth Defects records:
"In approximately 10 strains of rats, 15 strains of mice, 11 breeds of
rabbits, 2 breeds of dogs, 3 strains of hamsters, 8 species of
primates and in other such varied species as cats, armadillos, guinea
pigs, swine and ferrets in which thalidomide has been tested,
teratogenic effects have been induced only occasionally."[7]
Rats, popular lab animals, have been shown to get birth defects from
almost every chemical that causes birth defects in humans. But they
also get birth defects from hundreds of drugs that are safely used by
humans! If chemicals that harm rat offspring do not cause birth
defects in humans, the animal tests are meaningless and
non-predictive.
So what is teratogenicity-testing in animals good for and why does it
continue? As obstetrics professor Dr. D. F. Hawkins points out:
"The great majority of perinatel toxicological studies seems to be
intended to convey medical and legal protection to the pharmaceutical
houses and political protection to the official regulatory bodies,
rather than produce information that might be of value in human
therapeutics."[8]
As Karnofsky's Law postulates, researchers can eventually inflict
birth defects on a species with substances that are teratogenic in
humans. But to what purpose? Non-predictive animal experiments are of
no human value. They only deplete valuable research funding that might
otherwise be of true medical value.
Didn't the polio vaccine come from animal experimentation?
Animal experimentation actually delayed this much-needed vaccine
throughout the first half of the 20th century.
When polio first appeared around 1835, it rapidly paralysed and killed
its victims. In 1908, a virus was suspected and scientists began
working on a vaccine. Note: In developing vaccines, it's crucial to
determine how the infection enters the body. Luckily, pathologists
discovered the polio virus in human intestines as early as 1912,
suggesting entrance through the digestive tract.
Meanwhile, researchers successfully infected monkeys with polio. But
because monkeys contract polio nasally rather than orally, this
"triumph" only postponed the development of an effective vaccine for
decades. Incredibly, the scientists working on the vaccine chose to
ignore the human digestive data in favour of the monkey data!
It is true that a "vaccine" was derived from animal experimentation.
But manufactured from monkey tissue, this "cure" resulted in six human
deaths and 12 cases of paralysis.[9] It was abandoned. Further animal
experimentation led to the development of a nasal treatment, which
only caused permanent olfactory damage to the children tested. [10-11]
In 1941, Dr. Albert Sabin studied human autopsies to finally disprove
the nasal theory. He found the virus confined to the gastrointestinal
tract, as had been documented nearly 30 years earlier.
Sabin later denounced the monkey model blunder:
"... prevention was long delayed by the erroneous conception of the
nature of the human disease based on misleading experimental models of
the disease in monkeys."[12]
Finally, in 1949, Nobel Prize winner John Enders paved the way for a
vaccine by growing the virus in tissue cultures.[13] Though the
vaccine could have been produced from human tissue, convention
prevailed and manufacturers opted to use monkey tissue instead.
Containing the live virus, the animal-based vaccine infected 204
people with polio and resulted in 11 documented deaths. It also
resulted in at least one virus (SV4O) jumping the species barrier and
infecting humans.
Because of that, the polio vaccine is now grown in human diploid-cell
culture rather than animal tissue.
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