Parkinsons

[andyh]

Around 1986 a naturopath practicing on Hawaii, a participant in a seminar
series I was directing in California for PAHM, asked to give a short
presentation on use of Cycas circinalis in neurological diseases. He
probably presented only one case, (I forget the level of benefit) in (I
think the dx was Parkinsons).

Cycads are Sago Palms, a 300 million year-old group of nonflowering
plants possibly grazed by vegetarian dinosaurs and still widespread in
florida, central and south america. A cyanobacterium symbiotic with
cycads fixes nitrogen on its roots and also produces a neurotoxin which
the plant concentrates in the coat of its seeds to deter predators. Some
specie of (flying mammal) fruit bat or flying fox however seems to be
immune to the toxin, and moreover concentrates it further in some part of
its anatomy. In several pacific islands including Guam, a neurological
syndrome which may involve neural cross-fibrinization occurs, linked
especially to eating flying mammals there. Its pathogenesis is variable,
and encompasses the diseases ALS, Parkinsons, and Alzheimers. On Guam,
it is called Lytico-Bodig syndrome. People eating the starchy cycad
seeds alone (they use to make flour) don't seem to commonly develop the
diseases. But those eating a flying mammal feeding on these seeds, esp.
after acquiring guns during WW2 so able to better kill the bats – showed
a more reliable link between toxin and disease. Eating these bats caused
the syndrome to be the *leading* cause of native adult death on Guam
1940-1956. Hunting and a market for the bats for food eventually crashed
the population of them, causing one specie to go extinct, and the chronic
epidemic subsided by 1961. The plant seed toxin itself may be suitable
for a remedy, especially if first concentrated.

Helios pharmacy has Cycas circinatus up to 30C. However, in 1994, the
guam specie implicated in paralytic dementia syndromes was found to be
distinct from C. circinatus (this one is Cycas micronesica). The seed
cones (not sure if the male or the female seed cone or both) of Cycas
micronesica is thus the plant on which to focus homeopathic research.
The surviving bat species is extremely endangered, thus an individual is
unlikely to be available except perhaps from a researcher having tissue
samples. A further issue is which part of the bat is implicated, as the
entire animal was eaten (possibly even the wings).

http://en.wikipedia.org/wiki/Cycas_circinalis
Cycas circinalis, also known as the Queen Sago, is a type of cycad that
was thought to be linked with the degenerative disease Lytico-Bodig
disease on the island of Guam; however, the species native to Guam has
since been recognised as a separate species, Cycas micronesica, by K.D.
Hill in 1994. Cycas circinalis is the only gymnosperm species found among
native Sri Lankan flora.

------------------------------
Haloperidol, an allopathic psychiatric drug, may produce parkinson-like
syndrome (this is already a homeopathic preparation). Helios has
Haloperidol up to 50M.
-----------------------------
Another interesting factlet (UNCONFIRMED by me) with one mention from a
standard nosological research article below is that smoking cigarettes
seems to be a prophylactic to parkinsons. This may have to do with
nicotine tying up certain brain receptor sites which otherwise could be
involved in development of neuropathology. Following this train of
thought, it has elsewhere been proposed that juice of the Noni fruit (also
from Pacific area) is useful in quitting smoking, because it is supposed
to quickly tie up the same brain receptors that become habituated to
nicotine, aiding cold turkey after a few days of drinking a a few cups of
the juice daily for a few days. The latter Noni mechanism for dealing
with nicotine addiction has also NOT been tested yet with my clients.
Thus no idea if noni could possibly be a palliative for parkinsons.

------------------------------
Other candidates for neurological disease remedies include:

MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), a synthetic molecule
produced as an accidental byproduct by people attempting to manufacture
pethidine (meperidine), a mu-receptor opioid agonist, in their bathtub.
MPTP produces an irreversible, incapacitating paralysis in its victims
that closely resembles advanced Parkinson's disease. MPTP is oxidized to
MPDP+ in astrocytes by the enzyme monoamine oxidase type B, and then
spontaneously oxidizes to MPP+ (1-methyl-4-phenylpyridine) which then
kills dopaminergic neurons in the substantia nigra pars compacta. The
mechanism of MPP+ toxicity has not been definitively established, but may
be production of superoxide which reacts with nitric oxide in the cell.
After a single exposure to MPTP, the victims are permanently paralyzed.
Even with L-dopa treatment, many are unable to move normally for the rest
of their lives. The main difference between MPTP poisoning and true
Parkinson's disease is the absence of Lewy bodies, which are eosinophilic
inclusions in the neurons of Parkinson's disease patients.

Beta-carbolines, 1,2,3,4-tetrahydroisoquinoline and salsolinol.
Isoquinolines can be produced from phenylethylamine or dopamine itself by
condensation with acetaldehyde produced from ethyl alcohol. This is
interesting in view of the recent findings of mutations in the enzyme
alcohol dehydrogenase in some Parkinsons patients. Beta-carbolines are
nitrogen-containing molecules, sometimes found in food, that are
structurally similar to MPTP.

6-hydroxydopamine (6-OHDA). Although 6-hydroxydopamine cannot cross the
blood-brain barrier, it can be formed spontaneously in the brain by
reaction of dopamine with iron and hydrogen peroxide. This is consistent
with the association of Parkinson's disease with physical brain trauma,
which exposes neurons to iron from blood that is released during injury.
However, the molecular sites affected during 6-OHDA poisoning are not
exactly the same as those affected in Parkinson's disease.

======================================
The purpose of this post is thus to encourage others to investigate this
information further in a homeopathic sense, as it is likely that a
useful remedy for some cases of several problematical neurological
diseases may exist:

n --in a homeopathic preparation of a concentrate of the neurotoxin
isolated from seeds of the types of cycads that grow on pacific islands.
n --the remedy haloperidol already in the homeopathic mm.
n --other chemicals being investigated by biochemists trying to understand
if an environmental toxin is involved may also provide clues for creating
remedies.
General Background Cycad Plant Info:
Cycad overview: http://en.wikipedia.org/wiki/Cycad
Gymnosperm reproduction:
http://botany.suite101.com/article.cfm/ ... ymnosperms

=====================================
Illustrative source articles with links are presented below:

http://www.intelihealth.com/IH/ihtIH/WS ... 71823.html
Study Links Bats, Parkinson's In Guam
November 11, 2003HONOLULU (AP) -- Bats with a wingspan of up to four feet,
boiled in coconut cream and eaten whole, are linked to the exceptionally
high rate of a form of Parkinson's disease on Guam, a new scientific study
confirms. Scientists have long suspected a link between Guamanians'
consumption of the bats known as flying foxes and their high rate of a
form of Parkinson's. The study being published Tuesday in the Proceedings
of the National Academy of Sciences confirms that the neurotoxic
non-protein amino acid BMAA, found in Chamorros with Parkinson's, is
contained in the cycad tree, whose seeds the winged mammals eat. Dr. Paul
Cox, the director of the National Tropical Botanical Garden on Kauai and
the leader of the study, said analysis shows that the seeds must be eaten
by the bats before the neurotoxin transfers to humans. Eating foods made
from cycad seeds, including tortillas popular in Guam, would require
massive amounts to be dangerous, Cox said. The same neurotoxin, however,
has been found in brain tissue from two Canadians who died of Alzheimer's
and have no connection to Guam. It is the first time BMAA has been found
outside of the cycad tree, Cox said. But Cox said no conclusions can be
drawn yet from the Canadian discovery. "Although we think we have
established a link between a dietary neurotoxin and the disease among the
Chamorro," Cox said, "we have only opened a door that other scientists
will need to go through in a long path to coming up with a therapy." For
more than a decade, Cox and other researchers have been trying to find out
why the incidence of neurological disease ALS-parkinsonism dementia
complex among Guamanians from the 1940s to 1970s was 100 times higher than
elsewhere. Previous studies by Cox, an ethnobiologist, and Oliver Sacks,
the inspiration for the neurologist in the movie "Awakenings," found
evidence that the native Chamorros were exposed to the neurotoxin by
eating the bats -- brains, fur, wings and all -- at traditional feasts.
The new study examined victims of neurological disease in Guam and
compared them to a group of 15 Canadians. The study found the neurotoxin
originating in the cycad tree in the brain tissue of people who died with
Parkinson's or Alzheimer's but not in those who were healthy. Among the
Canadians, the neurotoxin was found only in the two who died of
Alzheimer's. Cos said the study confirms that the neurotoxin was working
its way up the food chain and, through a process of biomagnification,
exposing humans to neurodegenerative diseases such as Parkinson's and
Alzheimer's. "It really shows that this molecule magnifies at each step of
the food chain in increasing concentrations," he said. ALS-parkinsonism
dementia complex, called lotico-bodig on Guam, is similar to a number of
ALS-like conditions, such as Parkinson's and Alzheimer's diseases.
Copyright 2003 The Associated Press. All rights reserved.
http://en.wikipedia.org/wiki/Cycas_micronesica
Cycas micronesica
Conservation status

Endangered (IUCN 3.1)
Scientific classification
Kingdom: Plantae
Division: Cycadophyta
Class: Cycadopsida
Order: Cycadales
Family: Cycadaceae
Genus: Cycas
Species: C. micronesica
Binomial name
Cycas micronesica
K.D. Hill, 1994

Cycas micronesica is a type of cycad found in Micronesia , the Marianas
Group and the western Caroline Islands. The species, previously lumped
with Cycas rumphii or Cycas circinalis, was described in 1994 by Ken
Hill.[1] It is linked with the human degenerative disease Lytico-Bodig
disease, which is similar to Amyotrophic lateral sclerosis (ALS) through a
neurotoxin in the seeds, which were a traditional food source on Guam
until the 1960s.[2]

Cycas micronesica is threatened by an introduced insect pest, the
diaspidid scale Aulocapsis yasumatsui, first recognised in Guam in
December 2003.[3] Because of this the species is considered to be
Endangered.[4]
[edit] References

1. ^ Hill, K.D. (1994). Cycas micronesica. Australian Systematic Botany
7: 554-556.
2. ^ Sacks, Oliver. (1996). The Island of the Colour-blind. Pan
Macmillan Australia: Sydney. ISBN 0-330-35887-1
3. ^ Terry, Irene; & Marler, Thomas. (2005). Paradise Lost? Tipping the
scales against Guam’s Cycas micronesica. The Cycad Newsletter 28(3-4):
21-23.
4. ^ Marler, T.; Haynes, J.; & Lindstrom, A. (2006). Cycas micronesica.
In: IUCN 2006. 2006 IUCN Red List of Threatened Species. [1].
Downloaded 12 August 2007.

http://plantnet.rbgsyd.nsw.gov.au/cgi-b ... icronesica
The Cycad Pages
Cycas micronesica
Cycas micronesica K.D. Hill, Austral. Syst. Bot. 7: 554-556, fig 10
(1994). H�NSW
TYPE: Guam, Anderson Air Force Base, T.L. Turner NSW 270411, 1992 (holo
NSW; iso CANB, NY, K). [NSW] [NSW] [NSW]

Etymology: From the endemic occurrence of this species in Micronesia.
Literature: Schuster 1932 (as C. rumphii), Kanehira 1938 (as C. rumphii),
Stone 1970 (as C. circinalis), Fosberg & Sachet 1975 (as C. circinalis),
Fosberg et al. 1982 (as C. circinalis).
Illustration: Hill 1994c, fig. 10.
Historical notes: Nomenclature of this taxon has been unstable, with the
name C. circinalis L. frequently applied (Stone, 1970; Fosberg & Sachet,
1975; Fosberg et al., 1982). Schuster (1932) made the combination C.
circinalis forma undulata, and included material from Micronesia
thereunder (together with other clearly different material from Asia).
Kanehira (1938) realised the affinities with C. rumphii, and corrected the
error he had perceived in Schuster by making the combination C. rumphii
forma undulata. He was, however, still misapplying the concept of C.
undulata, which is a synonym of C. circinalis. Stone (1970) returned to
use of Schuster's combination, with no mention of Kanehira.
Distinguishing features: Distinguished by the broad, hard, glossy leaflets
with some but interrupted laminar hypodermis and adaxial mesophyll
interrupted at the broad, low midrib, the relatively long, usually
spine-free petiole, and the broad megasporophyll lamina with few (16-20)
lateral spines and a short apical spine (10-15 mm long). A broad zone to
the south of Guam has no cycads, until the New Britain region is reached.
No evidence of intergradation with the more southern species (C. rumphii,
C. apoa, C. bougainvilleana) is known. Taxonomy is complicated further to
the west, with several recognisable and different taxa that require
further study occurring in the region of Yap, Palau and the Philippines.
Distribution and habitat: Micronesia, the Marianas Group and the western
Caroline Islands. This species does not extend west into the Philippines,
but is replaced by related species in comparable habitats (Amoroso 1986).
This species occurs in closed forest country on coral limestone or coral
sand, or occasionally on volcanic soils on islands where these occur.
Conservation status:
Description:
Stems arborescent, to 8-12 m tall, 14-25 cm diam. at narrowest point.
Leaves deep green, highly glossy, 160 cm long, flat (not keeled) in
section (opposing leaflets inserted at 180° on rachis), with 130-140
leaflets, with white and orange tomentum shedding as leaf expands; rachis
usually terminated by a spine 4 mm long. Petiole 35-40 cm long (20-25% of
total leaf), petiole glabrous, unarmed. Basal leaflets not gradually
reducing to spines.
Median leaflets simple, strongly discolorous, 260 mm long, 16.5 mm wide,
inserted at 80° to rachis, decurrent for 9 mm, narrowed to 5.5 mm at base
(to 30-35% of maximum width), 18.5 mm apart on rachis; median leaflets
section flat; margins slightly recurved; apex acute, not spinescent;
midrib flat above, raised below.
Cataphylls linear, pungent, pilose, persistent.
Pollen cones fusiform, orange, 40 cm long, 8 cm diam.; microsporophyll
lamina firm, dorsiventrally thickened, 40 mm long, 22 mm wide, fertile
zone 30 mm long, sterile apex 10 mm long, level, apical spine rudimentary,
sharply upturned.
Megasporophylls 30 cm long, yellow-tomentose; ovules 2-6, glabrous; lamina
ovate, 45-50 mm long, 38-40 mm wide, shallowly pectinate, with 18-20
pungent lateral spines 2-6 mm long, apical spine distinct from lateral
spines, 12-15 mm long.
Seeds flattened-ovoid, 60 mm long, 50 mm wide; sarcotesta orange-brown,
not pruinose, 6 mm thick; fibrous layer absent; sclerotesta apically
crested. Spongy endocarp present.
http://en.wikipedia.org/wiki/Lytico-Bodig_disease
Lytico-Bodig disease
Lytico-Bodig disease, sometimes spelt Lytigo-bodig[1] is a neurological
disease that exists on the island of Guam.
It resembles both Amyotrophic lateral sclerosis (ALS) (more commonly known
as Lou Gehrig's disease) and Parkinson's Disease. First reports of the
disease surfaced in 3 death certificates on Guam in 1904. These death
certificates made some mention of paralysis. The frequency of cases grew
amongst the Chamorro people on Guam until it was the leading cause of
death between 1940 and 1956. The symptoms range from strongly resembling
ALS to those resembling Parkinson's Dementia Complex (PDC). The symptoms
tend to show themselves between the ages of 25 and 40. Many victims aren't
able to speak of their own accord but they can speak coherently and
fluidly when spoken to. It is commonly thought that the disease is caused
by toxins in the Cycad trees which are prevalent on Guam.
The neurologist Oliver Sacks detailed this mysterious condition in his
book Island of the Colourblind. Sacks wrote that a local species of fruit
bat, which is now largely extinct due to over-hunting, had been feeding on
Cycads and concentrating the poison in its body fat. Some researchers
believe that consumption of the fruit bat transferred sufficient
quantities of the poison to lead to long term toxicity,[2] although this
is not accepted by all researchers on Lytico-Bodig.[3]
[edit] See also
· β-Methylamino-L-alanine (BMAA)
[edit] References
1. ^ Elsevier
2. ^ Lytico-bodig
3. ^ Miller, Greg (2006). "Guam's Deadly Stalker: On the Loose
Worldwide?". Science 313: pp. 428 - 431.
[edit] External links
· Details at National Parkinson's Foundation

http://www.itg.be/itg/DistanceLearning/ ... ntsp12.htm

12 Lytico-bodig

* 12.1 Guam, history
* 12.2 Evolution of the disease
* 12.3 Other geographical areas
* 12.4 Clinical aspects
* 12.5 Aetiology
* 12.6 Brain pathology
* 12.7 Cycads
* 12.8 Toxin
* 12.9 Fruit Bats
* 12.10 Cyanobacteria

Back to top
12.1 Guam, history

Guam is the largest of the Mariana Islands in the Western Pacific. In
March 1521, the Portuguese sailor Magelhaes was the first Western explorer
to land on Guam. Pigafetta, the writer aboard Magelhaes’ ship, made a
short description of the island and its native people, the Chamorro. Guam
was occupied by the Spanish in 1565. In 1668 a near-genocide was started
and by 1710 most Chamorros had disappeared. In 1819, an extensive
description of the island and its surviving inhabitants was made by
Jacques Arago, an artist aboard the French expedition corvette Uranie.
Leprosy and other illnesses were described, but he made no mention of a
severe paralysis. At the end of the Spanish-American war in 1898, the
island was handed over to the US government. After the Second World War,
the island was retaken from the Japanese by American Forces. There has
been a dramatic improvement of the Chamorro standard of living after World
War II.

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12.2 Evolution of the disease

During the long period of foreign occupation, not one explorer, missionary
or colonist mentioned a fatal paralysis among the Chamorro. This healthy
state of affairs continued till the beginning of the 20th century. Even in
1902, the American vice-governor William Safford reported that the
Chamorro were "remarkably free from disease and physical defects, and
lived to a great age". However, in1904, three death certificates mentioned
some form of paralysis. The number of cases grew, until by 1940,
neurological disease was the leading cause of death among adult Chamorro.
After the second World War, Harry Zimmerman, a US Navy doctor, described
that a special neurological disease was very common among adult Chamorro.
In some patients the symptoms were similar to those of amyotrophic lateral
sclerosis, and in others, the disease resembled Parkinson’s disease ±
dementia. It became known as ALS/PDC (amyotrophic lateral sclerosis and
Parkinson-dementia complex). The local names were lytico and bodig. Lytico
referred to a progressive paralysis which resembled amyotrophic lateral
sclerosis. Bodig resembled parkinsonism, sometimes with dementia. Between
1940 and 1965, lytico-bodig became the leading cause of death for adult
Chamorro. In the remote village of Umatac, the incidence was the highest
of all.

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12.3 Other geographical areas

Lytico-bodig was though to be unique for Guam, but in 1962, Carleton
Gajdusek (discoverer of the prion disease kuru) discovered a disease which
resembled lytico-bodig, among the Jakai and Auyu people in the southern
coastal plain in western Papua New Guinea. Kiyoshi Kimura and Yoshiro Yase
discovered in Japan a third focus on the Kii peninsula (Honshu, Japan).

Back to top
12.4 Clinical aspects

The disease has a wide spectrum of symptoms ranging from ALS-like muscle
degeneration and weakening to Parkinson-like tremor and catatonia as well
as dementia. Parkinson-dementia complex (PDC) refers to a disorder that
combines the tremor of Parkinson's disease with the memory loss of
Alzheimer's. The disease has a late onset and generally appears between
the ages of 25-40 years old. In general, patients with bodig tend to be
about 10 years older than lytico patients. They can have difficulties in
taking initiatives, e.g. waiting for a question to be asked in order to
answer, but not starting a sentence without being asked. Severe dementia,
speaking and swallowing problems, spasticity of arms and legs, sometimes
with contractures, characterise some patients. A loss of sense of smell is
common. Many have memory problems. The akinesia which mimics catatonia
with extreme lack of movement, with little tremor or stiffness, and with
an immobility which can suddenly disappear, resembles encephalitis
lethargica (Von Economo's disease). The parkinsonism is characterized by
disturbed sleep, stupor, mental and physical slowing and immobility. Some
have tremor and stiffness, others have increased salivation and sweating.
About 50% of patients with lytico-bodig have strange, curly tracts on the
retina (visible with indirect ophthalmoscopy). About 20% of the Chamorro
older than 50 years have these lesions. Treatment is based on
physiotherapy. L-dopa became available in 1967. Patterns on the ground or
music can help in walking. Especially the acceptance and care provided by
the family is of major importance.

Back to top
12.5 Aetiology

The disease itself is dramatically clear, but the cause was a mystery. In
Guam, ALS/PDC wasn't found among non-natives. Among the Chamorro, it runs
in families, especially in those with a traditional lifestyle. The three
main hypotheses which were put forward were toxins (organic or mineral),
viruses (postencephalitis, slow virus or prions) and genetic mutations.
Ciguatera neurotoxins which are common in Guam, were a suspect, as was
Japanese encephalitis. Other forms of Parkinson’s disease are caused by
manganese intoxication (in Chili), the drug MTTP, postinfectious, genetic
or unknown. The lack of superoxide dismutase (SOD1) gene defects in Guam
contrasts with the findings in ALS in the Western World, where defects of
this enzyme are associated with familial forms of the disease.
Lytico-bodig resembles to a certain extent neurolathyrism. Could both
diseases have a similar cause? In 1963, the anthropologist Marjorie
Whiting made an in depth investigation into the local cuisine, and she
concluded that consumption and medicinal use of cycads were linked to the
disease. Cycads contain a large amount of starch in roots, stem, seeds as
well as many bioactive compounds. Fadang or federico is the name Chamorro
give to the cycad flour. The people of Guam depended heavily on flour made
from the starch extracted from cycad seeds, particularly when there were
food shortages during and after World War II. Flour made from cycad nuts
contains the neurotoxic beta-methylamino-L-alanine (BMAA). However,
processing the flour reduced the concentration of the toxin to very low
levels. The toxin was discovered in the brain of people who died of
ALS/PDC with concentrations of around 7 microgram/gram. If this scenario
would be true, then why did the disease not exist in earlier times? In the
Kii peninsula, cycads were used in phytotherapy, where fresh seeds were
used on open wounds. In Irian Jaya, a different species of cycad is used
by the people.

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12.6 Brain pathology

One of the pathological features of the Guamian ALS-PD include
neurofibrillary tangles, which are found in damaged nerve cells and are a
hallmark of many neurodegenerative diseases, such as Alzheimer's disease
and progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome).
The histological and cytological characteristics of progressive
supranuclear palsy, Von Economo’s disease and lytico-bodig were very
similar. Alzheimer plaques are not present in lytico-bodig. Mid 1970’s,
the pathologists Frank Andersen and Leung Chen discovered that brains from
traffic accident victims born before 1940 showed clear pathological
abnormalities. People born between 1940 and 1950 had few neurofibrillary
tangles and people born after 1950 never had any tangles. Prominent
cerebral atrophy, especially of the temporal lobes, was observed. The
substantia nigra and locus ceruleus were atrophied and depigmented. In
general, Lewy bodies and senile plaques were absent.

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12.7 Cycads

The Kingdom of plants is divided in bryophytes (mosses, liverworts and
hornworts) and vascular plants. Among the vascular plants there are
seedless vascular plants (e.g. horsetails, ferns, lycophytes) and seed
plants [(1) gymnosperms ["naked seeds"], such as cycads, ginkgo,
gnetophytes and conifers; and (2) angiosperms, such as dicotyledons and
monocotyledons]. Cycads are also known as sago palms. Do not confuse
cycads with true palm trees. True palms are monocot angiosperms and cycads
are gymnosperms. Cycads are among the most primitive living seed-plants
found today. Cycads do not have flowers. The plants always have separate
sexes, so that male and female cones are present on different plants. Male
cones are warm, because of heat produced via the break down of lipids and
starch. They produce massive amounts of pollen. These pollen were once
suspected of causing the disease. The pollen produce gigantic sperm cells
with many flagelles (higher plants do not have motile sperm). The female
cones contain very large egg cells. Female seeds are as large as plums.
The seeds are enclosed by a brightly colored soft layer (sarcotesta).

*

There are almost two hundred cycad species, divided into 11 families. The
Guam tree was initially known as Cycas circinalis, which was later changed
into Cycas micronesica. Some botanic experts state that C. circinalis s.s.
only occurs in Sri Lanka and India. C. celebica is another name which was
proposed for the Guam tree. The etymology of Cycas circinalis refers to
the Latin circinus, a spiral, in reference to the inrolled leaflets in
developing leaves.

Cycads form symbioses with nitrogen-fixing cyanobacteria (formerly known
as the blue-green algae). These cyanobacteria are endosymbionts, living
within the roots. They provide fixed carbon and a stable environment for
the cyanobacteria in exchange for nitrogen. In addition to normal roots,
cycads develop specialized organs at a young age called precoralloid
roots. These roots grow upward toward the surface of the soil, instead of
downward. Upon successful colonization by cyanobacteria, precoralloids
begin an irreversible transformation into coralloid roots, so named for
their resemblance to coral. Within the coralloid root is a cyanobacterial
zone, which is the region inhabited by cyanobacteria.

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12.8 Toxin

Cycads are often highly toxic, containing both neurotoxins and
carcinogenic compounds. George Rumphius was a botanist working as an
officer for the Dutch East Indian Company, working mainly in Southeast
Asia and India. He described the first cycad in Malabar. He wrote that the
juice obtained from cycad seeds was used to kill young children in
Celebes. In Honduras, Zamia roots were used to kill enemies or criminals.
Members of Cook’s expedition became sick after eating cycad seeds in
Australia and members of the La Pérousse expedition became ill after
eating Macrozamia communis seeds in Botany Bay, Australia. Cycad poisoning
in sheep is well known. Either gastrointestinal disturbances with liver
damage is seen, or else paralysis of the hind limbs and death due to
starvation. In Australia, this paralysis is known as 'zamia staggers' and
results from cattle grazing on cycad leaves. In the affected animals nerve
cell death is seen in the spinal cord.

*

Cycasin is a glycoside and was isolated form cycads in 1950. Large amounts
provoke liver failure; small amounts are carcinogenic. Methazoxymethanol
is derived from cycasin and is neurotoxic. Another toxin is BMAA, an
aminoacid which resembles BOAA, beta-N-oxalylamino-L-alanine (see
lathyrism). Pete Spencer, a neurotoxicologist, discovered that large doses
of BMAA provoked a neurological syndrome in cynomolgus monkeys after 8
weeks of administration. Very high doses provoked an ALS-like syndrome,
and somewhat lower doses provoked a Parkinson’s disease-like syndrome
similar to lytico. The symptoms were acute, non-progressive and
dose-related (as opposed to the human disease). But neurotoxins usually
act fast, in a matter of days or weeks, not years.

Back to top
12.9 Fruit Bats

In 2002, neurologist Oliver Sacks and etnobotanist Paul Cox (director of
the National Tropical Botanical Garden in Kalaheo, Hawaii), suggested that
BMAA could still be the cause of lytico-bodig. Besides eating tortillas
made from cycad flour, people also ate the local flying foxes. Cycad seeds
were part of the animals’ diet. If BMAA would accumulate in the tissues of
the bats, people could be exposed to damaging doses. Since flying foxes
feed on the seed sarcotesta it is important to understand the distribution
of BMAA in the various tissues of the cycad. BMAA is concentrated in cycad
reproductive organs, with the highest concentrations being found in the
outmost layer of the sarcotesta. This finding is consistent with the
putative evolutionary role of BMAA as an antiherbivory compound, as well
as the accumulation of the compound in flying foxes that ingest the seed
sarcotesta. Since the bats feed on cycads and eat twice their body weight
every night, their tissues accumulate levels of toxin much higher than
those in cycad flour.

*

The disease appeared early in the 20th century, reached a peak around 1940
and then began to decline. No one born since 1961 has developed the
disease. This rise and fall mirrors the consumption of flying foxes. Fruit
bats, boiled in coconut milk and then consumed from head to toe, were a
meal usually reserved for special occasions. The traditional way of
catching the bats was to net them in the bread fruit trees where they
roost. This is however easier said than done. Flying foxes tend to notice
hunters and fly away. However, after the American take over, the Chamorro
began to acquire guns, making it much easier to kill flying foxes. At the
same time, the island acquired a cash economy, allowing hunters to sell
their bats. Consumption of flying foxes soared, and so did the number of
cases of ALS/PDC. Demand eventually outstripped supply. By the mid-1970s,
steady hunting and consumption had nearly extinguished the bats, and Guam
began importing bats from Samoa, where there are no indigenous cycad
trees. One of two native species of flying fox became extinct. The second,
Pteropus mariannus, survived, but today, only a small colony (less than
100 animals) survives on the US strategic air command base.

*

In cycads, the toxin is concentrated in the seeds and its protective coat,
which on average contains 9 microgram per gram of tissue. The
concentration in live bats could not be tested, but in 2003, researchers
managed to test 50-year-old museum specimens. They contained almost 400
times as much as the cycad’s seed coat. It is now thought that a constant
low level of toxins in the brain is enough to kill neurons.

Back to top
12.10 Cyanobacteria

In 2002, Cox, Banack and the Canadian biochemist Susan Murch discovered
that BMAA is actually produced by a cyanobacterium that lives inside the
cycad’s corraloid roots, which grow up through the soil and form clumps at
the surface. The micro-organisms fix nitrogen, providing the cycad with an
important nutrient. The cycad divert the BMAA to its seeds, possibly as a
protection from herbivores. The cyanobacterial origin of the toxin might
explain the existence of ALS/PDC in other places where there are cycads or
bats are not a staple food, such as in the people of the Kii peninsula of
Japan and the Auyu and Jakai people of Irian Jaya. It is possible that the
toxin could find its way into the diet via other routes.

http://www.cababstractsplus.org/abstrac ... 0053122635
(abstract)

Title: Cycad consumption and neurological disease.
Personal Authors: Schulz, J. D., Hawkes, E. L., Shaw, C. A.
Author Affiliation: Graduate Program in Neuroscience, University of
British Columbia, Vancouver, British Columbia, Canada.
Editors: Preedy, V. R., Watson, R. R.
Document Title: Reviews in food and nutrition toxicity. Volume 4

Abstract:
Amyotrophic lateral sclerosis-parkinsonism dementia complex (ALS-PDC) has
been termed the "Rosetta Stone" of neurological disease, due to its
component amyotrophic lateral sclerosis, Parkinson's disease, and
Alzheimer's disease symptomatology and neuropathology. The largest and
most studied geographic focus of ALS-PDC is that of the island of Guam in
the South Pacific. The consumption of the seeds of a local, indigenous
species of cycad, Cycas micronesica, is thought to play a causal role in
the development of ALS-PDC. Cycad contains many toxins, and traditional
processing methods have therefore been developed with the aim of removing
them. Water-soluble, cycad-specific toxins such as cycasin, macrozamins,
and β-methylamino-L-alanine are removed by washing the cycad. This
refutes early cycad theories of ALS-PDC that these toxins are causal in
the development of ALS-PDC. Since cycad consumption still appeared to be
linked to ALS-PDC, our laboratory has reexamined the cycad hypothesis. By
feeding mice with processed cycad flour, we have created a valid mouse
model of ALS-PDC. This model allows us to analyse ALS-PDC in four
dimensions: its behavioural deficits, biochemical changes, and
morphological or pathological outcomes through time. Our time course
project is an attempt to delineate the rate, type, and extent of disease
progression as the subjects move from normal central nervous system state,
through preclinical neurological damage, to clinical diagnosis, and,
ultimately, arrive at the end state. This information, in conjunction with
data on the effects of various genetic conditions, sex, and age, will
allow us to template-match our findings against the human experience of
ALS-PDC. This will allow us to distinguish between the disease's causal,
coincidental, and compensatory (successful or failed) components, and
thus, provide us with targeted therapeutics with which we can move from
palliative to preventative care for patients suffering from ALS-PDC, as
well as those diagnosed with amyotrophic lateral sclerosis, Parkinson's
disease, or Alzheimer's disease.

Publisher: Taylor & Francis
http://brneurosci.org/reviews/parkinsons.html (book review)

Neurotoxic Factors in Parkinson's Disease and Related Disorders Kluwer
Academic / Plenum, 2000, 340 pages A. Storch and M. A. Collins, ed.

Parkinson's disease is a progressive degenerative disease characterized by
loss of dopamine-synthesizing cells in the substantia nigra, a region in
the brain that uses the neurotransmitter dopamine to send signals to the
caudate nucleus. The symptoms of Parkinson's disease are tremor, rigidity,
slow movement, and gait freezing which slowly progresses to eventual
paralysis.
Many scientists suspect that an environmental factor may be responsible
for Parkinson's disease because its geographical distribution is not
uniform. Parkinson's disease is slightly more common in rural areas than
cities. There is also a very high prevalence of amyotrophic lateral
sclerosis-parkinsonism-dementia complex (ALS-PDC) among Japanese residents
of the Kii peninsula in Japan and in Guam. This appears to be caused by
ingestion of cycad, a natural plant that contains methylazoxymethanol, a
naturally-occurring molecule that attacks the DNA of its victims to
produce a syndrome closely resembling Parkinson's disease.
Another important clue about Parkinson's disease is MPTP
(1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), a synthetic molecule
produced as an accidental byproduct by people attempting to manufacture
pethidine (meperidine), a mu-receptor opioid agonist, in their bathtub.
MPTP produces an irreversible, incapacitating paralysis in its victims
that closely resembles advanced Parkinson's disease. MPTP is oxidized to
MPDP+ in astrocytes by the enzyme monoamine oxidase type B, and then
spontaneously oxidizes to MPP+ (1-methyl-4-phenylpyridine) which then
kills dopaminergic neurons in the substantia nigra pars compacta. The
mechanism of MPP+ toxicity has not been definitively established, but may
be production of superoxide which reacts with nitric oxide in the cell.
After a single exposure to MPTP, the victims are permanently paralyzed.
Even with L-dopa treatment, many are unable to move normally for the rest
of their lives. The main difference between MPTP poisoning and true
Parkinson's disease is the absence of Lewy bodies, which are eosinophilic
inclusions in the neurons of Parkinson's disease patients.
A third interesting molecule is 6-hydroxydopamine (6-OHDA). Although
6-hydroxydopamine cannot cross the blood-brain barrier, it can be formed
spontaneously in the brain by reaction of dopamine with iron and hydrogen
peroxide. This is consistent with the association of Parkinson's disease
with physical brain trauma, which exposes neurons to iron from blood that
is released during injury. However, the molecular sites affected during
6-OHDA poisoning are not exactly the same as those affected in Parkinson's
disease.
Many other substances, including haloperidol, can induce parkinson-like
syndromes, while smoking appears to protect against it. Much research has
focused on searching for molecules in Parkinson's disease brains that are
absent in normal brains. The holy grail is to find something in food or in
the environment that not only selectively kills dopaminergic cells, but
also produces Lewy bodies.
This book is a collection of scientific articles on these and other toxins
including beta-carbolines, 1,2,3,4-tetrahydroisoquinoline and salsolinol,
as possible causes of Parkinson's disease. Isoquinolines can be produced
from phenylethylamine or dopamine itself by condensation with acetaldehyde
produced from ethyl alcohol. This is interesting in view of the recent
findings of mutations in the enzyme alcohol dehydrogenase in some
Parkinsons patients. Beta-carbolines are nitrogen-containing molecules,
sometimes found in food, that are structurally similar to MPTP. Some of
the articles are review papers, and others are short BBRC-style research
papers. The intended audience is researchers and graduate students
familiar with neuroanatomy, biochemistry, and the pathology of Parkinson's
disease. The writing style is typical scientific writing--precise and
functional technical prose full of abbreviations.

[muthu kumar]

Thanks Andy- that is very informative. MPTP is itself the recreational drug seems like

Potentized Haloperidol is a good suggestion.

I have used Haloperidol lots of times in my residency in psychiatry almost 2 decades ago - this is the night duty doctor's answer to all violent patients, give a shot for every new admission being brought in to hold them till morning - by morning the patient will become immobile like a statue
There are a bunch of allopathic drugs that can cause a Parkinsonian like syndrome.
Drugs such as phenothiazines, butyrophenones ( Haloperidol is in this group) , metoclopramide, reserpine etc can cause Parkinson.

Manganese is supposed to cause this too.
--- In minutus@yahoogroups.com, andyh@... wrote:

[Tanya Marquette]

thank you all for this information. such a generous and knowledgeable group that we are
tanya

[Carol Orr]

"however, after the American take over, the Chamorro
began to acquire guns, making it much easier to kill flying foxes. At the
same time, the island acquired a cash economy, allowing hunters to sell
their bats. Consumption of flying foxes soared, and so did the number of
cases of ALS/PDC."
Regarding above paragraph....all interesting in light of old studies done in
past about the huge amt of native people on guam who had MS. "Their"
theory..without any of the above knowledge...was that native people started
eating food eaten by the military...as they worked on the bases...and that it
was the change in their native diet that made them sick. But, aha..it was the
guns. This was all part of a big theory that ms came from moving from one's
native place and eating a new diet. Like southeners who moved north(from most
anywhere in the world)

[Tanya Marquette]

follow the money, follow the guns, and follow the poisons!
same old formula for demise of health and genocide!!!
tanya