Lyme disease is the fastest growing disease in the
by Dr. James Howenstein
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 U.S. 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 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
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
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
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
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 beleives 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
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 U.S. 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 postive culture of Bb by Dr. Mattman’s lab and a postive Q-RIBb test from Dr. Whitaker’s
Case Reports Illustrating The Critical Importance Of Establishing
The Diagnosis Of Lyme Disease:
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.
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.
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
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 has resulted in a breakthrough in our understanding of amyotrophic lateral
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 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 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
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
The Influence of Toxins from Bb On The Symptoms and Course of Lyme
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 . The most important example of a “Biotoxin Illness” appears to be Lyme Disease . 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
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
anti-microbial 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 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
Favorable Therapeutic Results With TAO-Free Cat’s Claw In Lyme
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, anerobic 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.