||Meridian Institute News
RESEARCHING THE SPIRIT-MIND-BODY CONNECTION
For several years we have been exploring the therapeutic
potential of gold with regard to neuroprotective and healing properties
(see Meridian Institute News Vol 5, No 2 and Vol 6, No 4). We now
have some preliminary data on this topic from one of our basic science
projects that is being conducted by researcher Dorothy B. Spangenberg,
Ph.D., a faculty member of the Department of Pathology and Anatomy, Eastern
Virginia Medical School in Norfolk, Virginia. To date, the study
has been jointly funded by Meridian Institute and the A.R.E.
The project focuses on the use of tiny jellyfish
(Aurelia) to study damage to neurons in order to develop strategies to
prevent such damage. Neurons are cells which group together to form
nerves in humans. Common biochemical pathways lead to neuron degeneration
following head injuries, stroke, aging, and the development of neurodegenerative
diseases, such as Parkinson's, Alzheimer's, and Multiple Sclerosis.
Glutamate, a natural component of neurons, when present
in excess, can initiate degenerative changes which lead to the death of
neurons in humans. This study involves testing the effects of glutamate,
using monosodium glutamate, on the swimming and pulsing ability of jellyfish
to determine whether, at higher dosages, it causes neuron degeneration
in jellyfish as well.
The first step was to establish the toxicity level
of glutamate. By experimentation it was found that glutamate, given
for only 1 hour, can cause total inhibition of swimming ability, a lower
rate of pulsing, and pulsing abnormalities. In addition, glutamate causes
some of the jellyfish to curl-up or spread out physically. These effects
suggest that neurons of the neuromuscular system and sensory neurons (hair
cells) found in gravity sensing structures, are damaged by the glutamate.
Recovery to normal swimming and pulsing often does not occur in some jellyfish
even after being removed from the glutamate for 48 hours.
The next step was to explore the potential role of
gold chloride in preventing neuron damage in glutamate-treated jellyfish.
After establishing the dosage tolerance of the jellyfish to gold chloride,
a safe dosage was selected that was given to the jellyfish prior to, during,
and after exposure to glutamate.
One of the principle findings was that gold treatment
produced a neuroprotective effect. Simultaneous gold chloride and
glutamate treatment in conjunction with post-treatment with gold chloride
was the best method for overcoming swimming inhibition caused by glutamate.
Gold must be present simultaneously with the glutamate as well as post-glutamate
treatment for prevention and/or repair of the neuron damage. Jellyfish
not given glutamate pulsed and swam well throughout the time of the experiments.
The Next Stage of Research
The next phase of this project will involve testing
jellyfish given gold chloride pre-during-and post glutamate exposure to
achieve ultimate gold protection for the jellyfish neurons. The jellyfish
will be examined to determine whether their pulsing and swimming are normal
as compared to non-treated controls.
One hypothesis used to explain neuron damage in humans
following glutamate excess states that glutamate excess leads to the formation
of oxidants, called reactive oxygen species (ROS) in neurons which then
leads to neuron death. To test this hypothesis, Dr. Spangenberg will determine
whether jellyfish neurons form ROS following glutamate treatment.
She will give jellyfish glutamate and search for ROS using fluorescent
dyes and a special microscope, the confocal microscope. If she learns
that ROS forms in glutamate-treated jellyfish, she will give other jellyfish
gold chloride prior to and simultaneously with glutamate and determine
whether gold chloride prevents the formation of ROS. She will also determine
whether those organisms protected from ROS formation are able to pulse
and swim normally.
In humans, antioxidants have been identified that
protect against ROS damage. One of these is D-methionine, an amino acid
found in various proteins in neurons. The research protocol will call for
exposing jellyfish to this known antioxidant prior to and during exposure
to glutamate to determine whether the jellyfish are protected from neuron
damage as has been reported in mammals. If so, she will determine whether
ROS formation is prevented in these jellyfish.
If she determines that the jellyfish respond to glutamate
in a manner similar to the known human response, she will be able to use
the jellyfish motility test system to screen therapeutic drugs and environmental
chemicals to detect those which cause glutamate-associated neuron damage
and to detect those which may prevent glutamate-associated damage. Such
treatments might ultimately be used to treat humans with neurodegenerative
diseases and neuron degeneration associated with aging, stroke, and head
TOPICAL CASTOR OIL APPLICATIONS
While doing the literature review for our castor
oil studies, we found the following two articles that relate to the external
application of castor oil. Researchers at the Department of Pharmacology,
Menarini Ricerche Spa in Pomezia Roma, Italy noted that observational studies
indicate that topical application of ricinoleic acid (RA), the main component
of castor oil, exerts remarkable analgesic and anti-inflammatory effects.
The pharmacology of RA has shown similarities between the effects of RA
and those of the herb capsaicin, suggesting a potential interaction of
this drug on sensory neuropeptide-mediated neurogenic inflammation. The
study assessed RA anti-inflammatory activities in comparison with capsaicin
in several models of acute and subchronic inflammation. The acute inflammation
was induced by intradermal injection of carrageenan in the mouse or by
histamine in the guinea-pig eyelid. Subchronic oedema was induced by complete
Freund's adjuvant injection in the ventral right paw of mice.
It was found that the acute topical application of
RA (0.9 mg/mouse) or capsaicin (0.09 mg/mouse) significantly increased
the mouse paw oedema induced by carrageenan, while an 8-day repeated topical
treatment with the same doses of both compounds resulted in a marked inhibition
of carrageenan-induced paw oedema matched by a reduction in SP tissue levels.
Similar effects were found against histamine-induced eyelid oedema in guinea-pigs
after acute or repeated application of RA or capsaicin. RA and capsaicin
given for 1-3 weeks reduced the established oedema induced by Freund's
adjuvant, a subchronic model of inflammation, particularly if given by
the intradermal route. Either in mouse paw or in guinea-pig eyelid, capsaicin
but not RA by itself produced a slight hyperemia and activation of a behavioral
response (e.g. scratching of the eyelids). On the basis of these results
the researchers recognized RA as a new capsaicin-like, non-pungent anti-inflammatory
agent suitable for peripheral application. This is a fascinating
finding for those of us are interested in the anti-inflammatory effects
of castor oil packs.
The other study we uncovered is more directly related
to a Cayce-based application of castor oil for healing plantar warts.
As you may recall, Edgar Cayce typically recommended applying a mixture
of castor oil and baking soda to remove plantar warts. In an article
that focused on the anti-inflammatory component associated with blackening
and subsequent regression of plantar warts, a case study was discussed
that involved a twelve-year-old girl who had four plantar warts on
her left foot for three or four months. Unknown to the girl's mother,
her grandmother had told the girl to rub castor oil onto the warts.
After applying the castor oil in this manner for approximately two months,
"little black dots" appeared in the warts. The attending physician
noted that the inflammatory process resembled the clinical picture of a
cellulitis with ascending lymphangitis. He suspected that the inflammation
was a healing response and did not treat it with antibiotics.
Thirteen days after the blackening of the warts was
noticed, all of the warts had disappeared. So the question is whether
the grandmother was an A.R.E. member who was aware of this Cayce remedy,
or was the intuitive Cayce tapping into a traditional use for castor oil
when he recommended it in his readings?
Meridian Institute will be completing another pilot
study on castor oil within the next couple of months. Stay tuned
for more on this intriguing therapy.
Vieira C, Evangelista S, Cirillo R, Lippi A, Maggi
CA, Manzini S. Effect of ricinoleic acid in acute and subchronic experimental
models of inflammation. Mediators Inflamm 2000;9(5):223-8
Berman A, Domnitz J.M., Winkelmann RK Plantar warts
recently turned black. Arch Dematol 1982;118:47-51.