joe the tick

November 14, 2009

Under the Eightball

In 1951 at Fort Detrick, Maryland, construction crews built a hollow metal sphere four stories high. Inside germ weapons were to be exploded, creating mists of infectious aerosols for testing on animals….and people. Employees called it the eight ball.

In the summer of 2006 my sister Lori was afflicted with an illness that, ten months later, has yet to be definitively diagnosed. Less than one year ago she had full function of her body, regularly riding bicycles, swimming and gardening with her son Jackson. One day, while helping Jackson onto his bicycle her leg gave way beneath her and she collapsed. Although it felt no different it just wouldn’t respond.

She quickly sought treatment for what she thought was simply a pinched nerve. However, after seeing a specialist she was told that due to the quickly lost muscle function Guilian Barre Syndrome, a rare autoimmune disease, could be the culprit. She was started on a rigorous and extremely expensive course of intravenous immunoglobulin, or IVIG, which boosts antibodies to help the good guys fight the bad guys. But why after a month of treatments, when improvements should be seen in a few weeks, was Lori not getting better but getting worse?

Countless hours and myriad visits to Munson Medical Center in Traverse City, University of Michigan in Ann Arbor and other traditional and homeopathic specialists only fueled confusion and frustration. Lori soon lost function in her other leg and motion in her hands deteriorated. Finally, after months of testing, poking, scraping, and analyzing, the diagnoses began arriving. They seemed forced and without tangible evidence, some symptoms conflicting with others: Guilian Barre Syndrome, Multiple Sclerosis, Lupus, Lyme disease, Lou Gehrig’s disease, then Lyme disease again, Lou Gehrig’s disease again. Once being told by her neurologist that “Everyone dies”.

During one visit to the doctor’s we crossed paths with a friend who had recently been diagnosed with Multiple Sclerosis. What were the odds that two people who knew each other would contract similar disease in such a short time? we began to dig a little deeper. Lori realized that she knew of five people in her neighborhood that had been diagnosed with MS, ALS, fibromyalgia or a similar degenerative disease. This could not be a coincidence.

Two diagnoses took rein: Lou Gehrig’s disease or ALS, incurable and fatal, and Lyme disease, an easily treatable and often durable ailment.

At the time my knowledge of Lyme was the same as others –What’s Lyme? A disease — How do you get it? Ticks – What does it do? Makes you sick. Right? – Well, Lyme disease can be hard to diagnose with its vague flu-like symptoms. However, when Lori described a bite she had that was surrounded with Lyme’s trademark round red rash, commonly called a “bulls-eye”, why didn’t doctors start her on a routine regimen of antibiotics? If untreated Lyme’s can cause debilitating arthritis and joint swelling, meningitis, blindness, fatigue, droopy eyes and other serious conditions. Why wouldn’t doctors prescribe the harmless antibiotics?

We were all very scared at what was happening to Lori and we had discovered, but even more frightening was the possibility that this was something that could have been prevented…. or worse that it was intentional in the name science and National Security… I had questions… many questions. And I’d be damned if they went unanswered.

October 26, 2009

Alzheimer’s & Lyme Disease: Is there a connection?

Alan MacDonald discuses with the Lyme Disease Research Database founder his research looking into a connection between Alzheimer’s and Lyme disease.

October 23, 2009

Activated protein C therapy slows ALS-like disease in mice by transcriptionally inhibiting SOD1 in motor neurons and microglia cells

Filed under: Lyme Disease, Lyme Disease News — Tags: , , — joethetick @ 4:12 pm

Activated protein C (APC) is a signaling protease with anticoagulant activity. Here, we have used mice expressing a mutation in superoxide dismutase-1 (SOD1) that is linked to amyotrophic lateral sclerosis (ALS) to show that administration of APC or APC analogs with reduced anticoagulant activity after disease onset slows disease progression and extends survival. A proteolytically inactive form of APC with reduced anticoagulant activity provided no benefit. APC crossed the blood#x02013;spinal cord barrier in mice via endothelial protein C receptor. When administered after disease onset, APC eliminated leakage of hemoglobin-derived products across the blood#x02013;spinal cord barrier and delayed microglial activation. In microvessels, motor neurons, and microglial cells from SOD1-mutant m…

Manipulating Brain Inflammation May Help Clear Brain Of Amyloid Plaques, Researchers Say

Filed under: Lyme Disease, Lyme Disease News — Tags: , , , — joethetick @ 3:48 pm

In a surprising reversal of long-standing scientific belief, researchers have discovered that inflammation in the brain is not the trigger that leads to buildup of amyloid deposits and development of Alzheimer’s disease. (Source: ScienceDaily Headlines)

Apathy is a prominent neuropsychiatric feature of radiological white-matter changes in patients with dementia

The objective was to study the relationships between WMCs on MRI/CT and neuropsychiatric symptoms and vascular factors in patients with cognitive impairment. One hundred and seventy-six patients with Alzheimer’s disease, vascular dementia, mixed dementia, and mild cognitive impairment were included. All patients underwent a standardized examination including medical history, clinical examinations, laboratory tests and brain imaging (CT or MRI). The identification and severity degree of WMCs was assessed blindly to clinical findings, using a semi-quantitative scale. For statistical analyses, patients were grouped based on absence or presence of WMCs. Significant variables in bivariate analyses were included as predictors in stepwise multiple logistic regression analyses.updated hourly from thousands of authoritative health and news sources./p/div

October 17, 2009

Olive oil compound linked to Alzheimer’s

CHICAGO, Oct. 17 (UPI) — A compound in olive oil targets and blocks toxic proteins that damage brain cells and cause memory loss in Alzheimer’s disease victims, U.S. researchers said.

The compound, oleocanthal, alters the structures of the proteins, ADDLs, said William L. Klein of Northwestern University and Paul A.S. Breslin of Monell Chemical Senses Center.

“Binding of ADDLs is thought to be a crucial first step in the initiation of Alzheimer’s disease,” Klein said in a statement. “Oleocanthal alters ADDL structure in a way that deters the protein from binding to synapses that allow the nervous system to connect.”

ADDLs bind within the synapses of the brains of Alzheimer’s patients and are believed directly to disrupt nerve cell function, eventually leading to memory loss, cell death and global disruption of brain function, the researchers said.

Klein and colleagues identified ADDLs in 1998, leading to a major shift in thinking about the causes, progression and treatment of Alzheimer’s disease. ADDLs are structurally different from the amyloid plaques that accumulate in brains of Alzheimer’s patients.

Future studies are needed to identify more precisely how oleocanthal changes ADDL composition. Such insights could provide discovery pathways related to disease prevention and treatment, the researchers said.

The findings are published in the journal Toxicology and Applied Pharmacology.

September 29, 2009

Hope in Lyme disease battle

New bill would protect physicians who prescribe long-term therapy
by Debra Neutkens
Staff Writer
Published: Tuesday, September 29, 2009 8:53 PM CDT

St. PAUL — Those who suffer chronic, debilitating Lyme disease have only a handful of doctors, maybe three in the state, willing to treat them.

There are probably more, but those physicians are forced to fly under the radar when it comes to aggressive treatment for the tick-bite malady.

Legislation introduced at the Capitol recently by Sen. John Marty, DFL-Roseville, and Sen. Ray Vandeveer, R-Forest Lake, hopes to change that.

Senate Bill No. 1631 allows a doctor to treat chronic Lyme disease without fear of disciplinary action by the state Board of Medical Practice. The legislation is based on a Connecticut law allowing physicians to use their best clinical judgment when treating Lyme disease.

Three states, Connecticut, Rhode Island and California, have passed similar bills to protect physicians.

Marty, who is chair of the Senate health committee, acknowledged a lack of consensus on Lyme treatment in a statement released last month. Even doctors in other states feel they will face severe repercussions for treating patients, he said after a lawmaker’s meeting with state and national Lyme health experts.

One of those experts was Dr. Betty Maloney, a family practice physician from the Forest Lake area who advocates for the Minnesota Lyme Action Support Group.

“It is a principle of medical ethics that patients hear treatment options, including risks and benefits of alternative treatments to make a choice,” Maloney told the Press. “Now patients with persistent Lyme disease hear only strategies advanced by the Infectious Diseases Society of America (IDSA). They don’t learn the alternatives – longer antibiotic therapy or combinations of antibiotics – to make an informed choice.”

Marty and Vandeveer’s bill would make it possible for physicians to prolong administration of antibiotics longer than the recommended 28-day treatment course by removing concerns about medical board interference, noted Maloney. She attended a July IDSA hearing in Washington, DC, to discuss current guidelines for treating Lyme disease, submitting more than 80 pages of research analyses on behalf of the International Lyme & Associated Diseases Society. The 2006 IDSA guidelines state there is no evidence long-term antibiotics cure chronic Lyme.

The issue is complicated because the disease is complicated, Maloney said. “I am not trying to promote a particular agenda beyond wanting patients to get the care they need. I want the science to speak. In some instances, we have lost track of the science and become political on this issue. I’m not sure why it’s political, but if the disease is defined in very narrow fashion, insurance companies have the right to deny care.”

A medical ethicist was asked to submit guidelines for selecting review panel members, according to Maloney. Anyone who made $10,000 related to care and treatment of Lyme patients was omitted from the panel. “Essentially all physicians who treat Lyme were eliminated,” Maloney pointed out. “That was ludicrous. So no one on the panel really understands nuances of treating a Lyme disease patient; who understands the importance of treating co-infecting organisms. The panel doesn’t understand the level of fatigue in Lyme patients and how sick they are — fatigue like ‘I can’t get out of bed.’ Lyme patients aren’t working. They have cognitive issues. The spectrum is wide.”

After review of written submissions and hearing transcripts, the IDSA panel is expected to make a decision on whether guidelines need revision by the end of year.

Meanwhile Lyme disease cases are dramatically increasing in Minnesota, which is considered a hot spot for tick-borne illness. Anoka, Washington and Chisago County are all included on maps of high-risk areas for tickborne disease.

According to Maloney, tick numbers change season to season and by zip code. Pockets of infection have to do with trees, especially oak trees, which attract rodents.

The primary host for the blacklegged, or deer, tick is not deer, but mice. The first stage of its life cycle, the larvae, becomes infected with the bacteria responsible for Lyme disease, Borrelia burgdorferi, after feeding on diseased mice. The next stage is the poppy-seed-sized nymph, the stage that causes the most human cases. Nymphs live in leaf litter under oak trees. Woodpiles are another source of infestation because mice nest there.

Left untreated, Lyme disease can cause a multitude of problems, including paralysis, arthritis, flu-like illness, irregular heartbeat, and loss of ability to concentrate, according to the Minnesota Department of Health. It can infect any organ, including the brain, heart, joints and nervous system. It has also been called the “Great Imitator” because it can look like other diseases. Many sufferers have been misdiagnosed with conditions such as fibromyalgia or chronic fatigue. If the brain is infected, the misdiagnosis might be MS, ALS or Parkinson’s.

If the Marty/Vandeveer legislation passes, will doctors who treat Lyme be confident they won’t be investigated? “Employers might still mandate how physicians treat Lyme, but it is one more obstacle to access removed,” replied Maloney. “I want physicians and patients to go back to relationships. The bill helps that. It allows physicians to more fully enter into a relationship with Lyme patients.”

For more articles on Lyme disease, access Press Publications archives at www.presspubs.com.

Editor’s Note: Dr. Maloney has just published an article on “The Need for Clinical Judgment in the Diagnosis and Treatment of Lyme Disease,” in the Journal of the Association of American Physicians and Surgeons, www.jpands.org. Find it at

http://www.jpands.org/vol14no3/maloney.pdf.

March 14, 2008

Cannabis Based Treatments Could Improve Memory Loss

This week at a symposium of cannabis experts hosted by the Royal Pharmaceutical Society of Great Britain (RPSGB) where the scientists from Israel and Spain said that a compound present in cannabis significantly slows memory problems caused by Alzheimer’s disease.

Ten years ago the RPSGB launched its protocols to demonstrate the therapeutic effectiveness of cannabis which led to Government-funded trials in Britain to explore the benefits for patients with multiple sclerosis and in the treatment of severe pain.

Professor Tony Moffat, chairman of the Symposium says progress has been made in the last ten years but more research is needed as there is considerable interest in the medical benefits of cannabis and related compounds for a range of conditions including arthritis, multiple sclerosis and neurological pain.

Alzheimer’s disease is the commonest form of dementia, which affects an estimated 24.3 million people worldwide. Most of us reading this blog is well aware that most cases of Alzheimers are actually Lyme Disease..

February 20, 2006

Plaques of Alzheimer’s disease originate from cysts of Borrelia burgdorferi, the Lyme disease spirochete

Elsevier Health Journal
Alan B. MacDonald

St. Catherine of Siena Medical Center, Department of Pathology, 50 Rte 25 A, Smithtown, NY 11787, USA
Received 20 February 2006; accepted 23 February 2006

Download PDF

Summary Here is hypothesized a truly revolutionary notion that rounded cystic forms of Borrelia burgdorferi are the
root cause of the rounded structures called plaques in the Alzheimer brain. Rounded ‘‘plaques’ in high density in brain
tissue are emblematic of Alzheimer’s disease (AD). Plaques may be conceptualized as rounded ‘‘pock mark-like’’ areas
of brain tissue injury. In this century, in brain tissue of AD, plaques are Amyloid Plaques according to the most up to date
textbooks. In the last century, however, Dr. Alois Alzheimer did not require amyloid as the pathogenesis for either the
disease or for the origin of its plaques. Surely, amyloid is an event in AD, but it may not be the primal cause of AD. Indeed
in plaques, amyloid is regularly represented by the ‘‘congophilic core’’ structure which is so named because the waxy
amyloid material binds the congo red stain and is congophilic. However an accepted subset of plaques in AD is devoid of a
congophilic amyloid core region (these plaques ‘‘cotton wool’’ type plaques, lack a central congophilic core structure).
Furthermore, there is ‘‘plaque diversity’’ in Alzheimer’s; small, medium and large plaques parallel variable cystic
diameters for Borrelia burgdorferi. Perturbations of AD plaque structure (i.e. young plaques devoid of a central core
and older plaques with or without a central core structure) offer room for an alternate pathway for explanation of
ontogeny of the plaque structures. If amyloid is not required to initiate all of the possible plaques in Alzheimer’s, is it
possible that amyloid just a by product of a more fundamental primal path to dementia? If a byproduct status is assigned
to amyloid in the realm of plaque formation, then is amyloid also an epiphenomenon rather than a primary pathogenesis
for Alzheimer’s disease. In the ‘‘anatomy is destiny’’ model, cysts of borrelia are always round. Why then not accept
roundness as a fundamental ‘‘structure determines function’’ argument for the answer to the mystery of why Alzheimer
plaques are always round? Parataxis causality, a concept borrowed from philosophy, is the error that comes from linking
two events, which occur contemporaneously or in close proximity to one another with a cause and effect relationship.
Parataxis tells us that what appears to be cause and effect in the couplet ‘‘amyloid plaque’’ merely by a proximity
relationship may be ‘‘spurious causality’’ which is a cognitive dead end.

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