Curing Lyme Disease with Samento
by Dr. James Howenstine, MD
Lyme Disease was initially regarded as an uncommon illness caused by
the spirochete Borrelia burgdorferi (Bb). The disease transmission was
thought to be solely by the bite from a tick infected with this spirochete.
The Bb spirochete is able to burrow into tendons, muscle cells, ligaments,
and directly into organs. A classic bulls-eye rash is often visible in
the early stage of the illness. Later in the illness the disease can afflict
the heart, nervous system, joints and other organs. It is now realized
that the disease can mimic amyotrophic lateral sclerosis, Parkinson's
disease, multiple sclerosis, Bell's Palsy, reflex sympathetic dystrophy,
neuritis, psychiatric illnesses such as schizophrenia, chronic fatigue,
heart failure, angina, irregular heart rhythms, fibromyalgia, dermatitis,
autoimmune diseases such as scleroderma and lupus, eye inflammatory reactions,
sudden deafness, SIDS, ADD and hyperactivity, chronic pain and many other
conditions.
Dr. Paul Fink, past president of the American Psychiatric Association,
has acknowledged that Lyme Disease can mimic every psychiatric disorder
in the Diagnostic Symptoms Manual IV. This includes attention deficit
disorder (ADD), antisocial personality, panic attacks, anorexia nervosa,
autism and Ausperger's syndrome etc. It might be prudent in any person
suddenly found to have psychiatric symptoms to obtain a Q-RIBb blood test
to exclude Lyme Disease.
Biology professor, Lida Mattman, author of Cell Wall Deficient Forms:
Stealth Pathogens, has been able to recover live spirochetes of Bb from
mosquitos, fleas, mites, semen, urine, blood, and spinal fluid. A factor
contributing to making Bb so dangerous is that it can survive and spread
without having a cell wall (cell wall deficient CWD). Many valuable antibiotics
kill bacteria by breaking down the cell wall. These antibiotics often
prove ineffective against Bb.
Lyme Disease is now thought to be the fastest growing infectious disease
in the world. There are believed to be at least 200,000 new cases each
year in the US and some experts think that as many as one in every 15
Americans is currently infected (20 million persons). Dr. Robert Rowen
knows a family where the mother's infection spread to 5 of her 6 children[1]
all of whom recovered with appropriate therapy. It is difficult to believe
that these children were all bitten by ticks and seems more plausible
that person to person spread within the family caused this problem. Bacteriologist,
Dr. Lida Mattman, states "I'm convinced Lyme disease is transmissable
from person to person". In 1995 Dr. Mattman obtained positive cultures
for Bb from 43 of 47 persons with chronic illness. Only 1 of 23 control
patients had a positive Bb culture. Dr. Mattman has subsequently recovered
Bb spirochetes from 8 out of 8 cases of Parkinson's Disease, 41 cases
of multiple sclerosis, 21 cases of amyotrophic lateral sclerosis and all
tested cases of Alzheimer's Disease. The complete recovery of several
patients with terminal amyotrophic lateral sclerosis after appropriate
therapy shows the great importance of establishing the diagnosis of Lyme
Disease.
Some very important information has recently become available about
the spread and magnitude of the problem with Lyme Disease. The severity
of the Lyme illness is related to the spirochete load in the patient.
Few spirochetes produce mild or asymptomatic infection. A study from Switzerland
in 1998 pointed out that only 12.5 % of patients testing positive for
Bb had developed symptoms. A German boy developed Lyme arthritis 5 years
after his tick bite. Often mycoplasmal infections remain without symptoms
until the victim suffers a traumatic event (stress, injury, accident etc.)
These stressing events enable the mycoplasma to begin consumption of cholesterol
and symptoms may begin to present. The mechanism of this deterioration
is thought to be suppression of the immune system secondary to stress.
Many patients with LD have concomitant infections with other parasites
(Ehrlichia in white blood cells and Babesia in red blood cells) Some patients
have all 3 parasites. Each requires a different therapy with Babesia being
particularly difficult to eradicate. Recently, Artemisinin appears effective
in Babesia infections. All co-infections must be eliminated to obtain
a successful result.
Dr. Joanne Whitaker relates that nearly every patient with Parkinson's
Disease (PD). has tested positive for Bb. Dr. Louis Romero reports that
3 patients with PD are 99 % better after TAO-free cat's claw (Uncaria
tomentosa) therapy. When Dr. Mattman cultured 25 patients with fibromyalgia
all subjects had positive cultures for the CWD Bb. which causes LD. She
relates that Bb can be found in tears and could thus easily appear on
the hands where touching could spread LD. Several families are now documented
where nearly every family member is infected. How sick the individual
patient becomes probably relates to their initial spirochete dose, immune
system, detoxification capability and stress levels.
Transmission of the disease has been clearly documented after bites
by fleas, mites mosquitoes and ticks. There is compelling evidence that
Lyme disease (LD) can be spread by sexual and congenital transfer. One
physician has cared for 5000 children with LD. 240 of these children were
born with the disease. Dr. Charles Ray Jones, the leading pediatric specialist
on Lyme Disease, has found 12 breast fed children who have developed LD.
Miscarriage, premature births, stillborn, birth defects, and transplacental
infection of the fetus have all been reported. Studies at the Univ. of
Vienna have found Bb in urine and breast milk of LD mothers.
Researchers at the Univ. of Wisconsin have reported that dairy cattle
can be infected with Bb hence milk could be contaminated. Bb can also
be transmitted to lab animals by oral intake such as food.
The Sacramento, California blood bank believes that LD can be spread
by blood transfusions. The CDC (Center for Disease Control) in Atlanta,
Georgia states that their data indicates that Bb can survive without detection
by the blood processing techniques used for transfusions in the US
Lyme Disease is the fastest growing epidemic in the world. LD is grossly
underreported so there may be far more than the 200,000 cases reported
annually in the US Dr. Harvey and Salvato estimate that 1 billion persons
in the world may be infected with LD. LD is thought to be a contributing
factor in 50 % of patients who have chronic illness.
Dr. Joanne Whitaker, a Lyme disease victim from childhood, has developed
a reliable test for the presence of Lyme disease. This test looks for
the Bb organism, not antibodies, and is able to identify the cell wall
deficient (CWD) form of the spirochete as well as the actual Bb organism.
The test is called Q-RIBb which stands for quantitative rapid identification
of Bb. Dr. Lida Mattman has confirmed that Dr. Whitaker's test is sensitive
because there has been a 100 % correlation between a positive culture
of Bb by Dr. Mattman's lab and a positive Q-RIBb test from Dr. Whitaker's
Laboratory.
Case Reports Illustrating The Critical Importance Of Establishing The
Diagnosis Of Lyme Disease
Case 1 Larry Powers, a former Mr. America in 1962,
became ill with the symptoms of Parkinson's Disease in 1990. Sinemet therapy
was taken for eight years but he gradually became worse. He became confined
to a wheel chair and required help with eating. After learning that Lyme
Disease might be causing his symptoms of PD he started taking TAO free
cat's claw (Uncaria tormentosa). Within three weeks he was out of his
wheelchair and fishing for 100 pound tarpon.
Case 2 Tom Coffey at age 34 developed diplopia, severe
hypertension uncontrolled by drugs, and impaired balance. A diagnosis
of amyotrophic lateral sclerosis was made. Surgery was performed to correct
the diplopia. By June 2001 he was unable to swallow saliva and feeding
tube nutrition was begun. His weight had fallen by 100 pounds. Nutritional
support from the tube feedings produced slow resolution of the swallowing
problem. Consultation with a Lyme expert uncovered the history of a bulls-eye
rash after a tick bite. Therapy with Rocephin led to complete recovery.
Case 3 A young male college student developed such
severe cognitive difficulties he was forced to drop out of school. A RIBb
test was positive for LD and he resumed a normal life after receiving
4 months of antibiotic therapy...
What Causes Neurone Death In Amyotrophic Lateral Sclerosis ALS?
One of the most insidious mimics for Lyme disease is ALS. The neurotoxins
released by the Bb organism are capable of causing neurologic dysfunction
in the central nervous system that produces symptoms typical of amyotrophic
lateral sclerosis. The pathological hallmark of ALS is motor neurone degeneration
and death.
Research performed by Dr. Harold Clark and Dr. Garth Nicholson and coordinated
by Donald W. Scott[2] has resulted in a breakthrough in our understanding
of amyotrophic lateral sclerosis.
Mycoplasma were discovered in 1898. These are living particles of bacterial
nucleic acid which do not have a cell wall. In 1971 Rottem et al[3] learned
that most species of mycoplasma were absolutely dependent for their growth
on the consumption of pre-formed sterols including cholesterol obtained
from animal and human host cells. These mycoplasma live harmlessly in
host cells until they are stimulated to activity by a stressing traumatic
event (bullet wound, bad fall, injury from accident etc.). The growth
of the mycoplasma consumes the cell's cholesterol resulting in death of
the affected cell. Mycoplasma have been identified in ALS using high resolution
blood morphology. In the November 9, 2001 issue of Science Dr. Daniel
Mauch[4] et al revealed that the glial cells surrounding the motor neurone
supply the extra cholesterol needed to repair and replace aging synapses.
If the repair does not properly occur the motor neurone cells proceed
to die from overwork Glial cells are also heavily involved in gathering,
processing and storing glutamate. Elevations in glutamate have been found
in brain tissue in ALS.
A mycoplasma species, probably fermentans, which was harmlessly sequestered
in a glial cell becomes aroused by some traumatic stressful event. This
mycoplasma then consumes the glial cholesterol which makes up 40 % of
the glial cell membrane causing rupture and death of the glial cell. The
death of these glial cells releases large amounts of glutamate which becomes
elevated in brain tissue. Within the neurone some of the excess glutamate
accesses a urea molecule. The urea molecule gives up an ammonia ion which
converts a glutamate molecule into less dangerous glutamine. This leaves
the former urea molecule as a cyanate ion which damages the motor neurone's
mitochondria. One of the consequences of the damaged mitochondria is a
decrease in the energy output available to the neurone. This produces
the severe weakness and fatigue seen in patients with ALS. If the mitochondrial
injury is severe the neurone dies. The death of motor neurones stops message
delivery to muscle cells leading to atrophy of muscle tissue a universal
finding in ALS.
This avid consumption of cholesterol may also contribute to the endocrine
dysfunction seen in ALS because it decreases the amount of cholesterol
available to produce estrogen, testosterone, progesterone, hydrocortisone,
and aldosterone. Patients with ALS, fibromyalgia, and chronic fatigue
syndrome often have hypothalamic dysfunction which may result in adrenal
insufficiency, hypothyroidism, and gonadal failure.
Lyme Disease frequently exhibits neurologic abnormalities because the
Bb neurotoxins are drawn to the fatty tissue found in the brain and peripheral
nerves. As a consequence sudden deafness, Bells palsy, Parkinson's Disease,
Multiple Sclerosis, reflex sympathetic dystrophy, peripheral neuritis,
chronic pain, and a multitude of other neurologic disorders may appear.
The Influence of Toxins from Bb On The Symptoms and Course of Lyme Disease
Autopsy examinations of young persons (30s) dying from what appeared
to be Parkinson's disease PD have frequently failed to confirm the basal
ganglion damage that would be expected in the classic PD seen in the elderly.
Some patients with illnesses of many years duration misdiagnosed as Amyotrphic
Lateral Sclerosis, Multiple Sclerosis, and Parkinson's Disease have made
incredible recoveries within periods as short as 24 to 72 hours when placed
on TOA-free uncaria tormentosa (cat's claw) for LD.. This rapid response
could not rationally be attributed to improved immune function or bacteriocidal
effects on spirochetes. Bb is known to produce a group of neurotoxins.
The most sensible explanation for this recovery lies in turning off or
blocking the neurotoxic effects of Bb on the lipid containing structures
that the Bb neurotoxins are attracted to (central nervous system, peripheral
nerves, muscles, joints etc.). This sudden improvement appears to be the
result of blockage and inhibition of the neurotoxins[5]. The most important
example of a "Biotoxin Illness" appears to be Lyme Disease[6].
Patients with symptoms of Parkinson's Disease at a young age caused by
neurotoxins would not be expected to show permanent structural destruction
in the basal ganglia. These neurotoxins probably act at specific sites
such as neurotransmitters-pre- and- post synaptic membranes, altering
dopamine, serotonin, GABA, and acetylcholine molecules, thereby blocking
surface membrane receptors of various kinds which would interfere with
the proper action of enzymes, coenzymes and hormones. This is only one
of the damaging mechanisms of action of the neurotoxins.
The TOA free form of cat's claw (Samento) may have three direct beneficial
effects in humans with LD:
- Immune modulation (correcting immune dysfunction)
- Direct broad spectrum antimicrobial effect on spirochetes. Quinovic
acid glycosides found in TAO-free cat's claw are similar to the quinilones
widely used as antibiotics.
- Blocking the adverse neurotoxic effects on cells, enzymes, and hormones
Whether the serious lack of energy and fatigue seen in LD are similar
to the cyanate[7] induced damage to the mitochondria's ability to produce
energy in the motor neurone found in amyotrophic lateral sclerosis or
is due to failure of proper calcium channel function is not clear.
Favorable Therapeutic Results With TAO-Free Cat's Claw In Lyme Disease
A pilot study treated 28 patients with Advanced Chronic Lyme Disease
with TOA-free Uncaria tomentosa (cat's claw). Conventional cat's claw
contains TOA alkaloids that interfere with the desired immune modulation.
The 14 person control group was given antibiotic therapy. At the study's
termination 85 % of those receiving the cat's claw preparation no
longer had positive blood tests for Bb. All 28 persons had experienced
a dramatic improvement in their clinical condition. No significant changes
were seen in the control group.
Currently it is believed that nearly all adults are infected with stealth
organisms (Borrelia burgdorfi, yeast, fungi, mycoplasma, anaerobic bacteria,)
and have picked up toxic metals (mercury, lead, cadmium, aluminum, fluoride,
aluminum etc.) both of which lead to detrimental effects on health. Samento
may be of great value in eliminating some of these infectious (certainly
Bb) and has also proven very effective in cancer therapy.
The Prima Una de Gato can be obtained from Allergy Research Group 800-545-9960,
Nutramedix (product name Samento Plus) 561-745-2917, Farmacopia at 800-896-1484
and from Natural Health Team 800-416-2806. Dr. Whitaker's lab can be reached
by Internet at www.bowen.org or by calling 727-937-9077 to arrange blood
Bb testing. Improving nutrition, detoxifying and improving mental health
all contribute to good results in treating Lyme Disease. Removal of mercury
amalgams and treatment of heavy metals may be needed.
There is convincing evidence that the Lyme Disease epidemic may have
originated from the bio-warfare laboratory in Plum Island off the coast
of Lyme, Connecticut. This, however, would require a lengthy discussion
not relevant to this article.
Much of this information about LD was obtained from Lyme disease: Nutraceutical
Breakthrough Using TOA-Free Cat's Claw published in Focus by Allergy Research
Group (October 2003) and from the November and December 2003 issues of
Dr. Robert Rowen's Second Opinion.
Footnotes:
1. Rowen Robert If you have ANY chronic debilitating disease, you could
be the victom of a Monster Epidemic! Second Opinion Vol X111 No. 11 November
2003
2. Scott, D.W.,Crusador P.O. Box 618205, Orlando, Fl. 32861-8205 October-November
2002 pg.26-32 Also see Scott, D.W. and Scott, W.L.C. Amyotrophic LateralSclerosis:
The Probable Cause; A possible Cure 233 Government St., Suite 6 E, Victoria,
B.C. Canada V*T 4P4 TOLL FREE 1-888-232-4444 ISBN 1-55395-214-6
3. Rottem, Pfend, Hayflick Sterol Requirements Of T-strain Mycoplasmas
Journal Of Bacteriology 1971
4. Daniel Daniel H., Nagler, Goritz, Muller, Otto, Pfrieger. CNS Synaaptogenesis
Promoted By Glia-Derived Cholesterol. Science Nov. 9, 2001
5. Romero, Louis M.D. Ph.D Neurotoxins Focus Allergy Research Group Newsletter
pg. 10 Oct. 2003
6. Shoemaker, C. M.D., Hudnall, Kenneth, Ph.D.Focus ,Allergy Research
Group Newsletter pg. 10 Oct 2003
7. Scott, Donald W. Lou Gehrig's Disease is Not a Mystery Anymore Crusader
pg. 31 Oct-November 2002
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