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Lyme disease : A leaky brain

MagazineApril 2009 (Vol. 20 Issue 1)Lyme disease : A leaky brain

The first cases of Lyme disease (LD) occurred in the US, but it's now acknowledged to be a worldwide problem

The first cases of Lyme disease (LD) occurred in the US, but it's now acknowledged to be a worldwide problem. Britain had its first official death due to LD in December 2005: "liver disease due to Lyme sepsis", according to the autopsy. In May of this year, a 38-year-old British pro-fessor committed suicide after developing dementia brought aboutby LD. It's particularly prevalent at this time of the year-late spring and early summer.

The number of diagnosed cases of Lyme disease are now rising-and not just because doctors are finally beginning to recognize it, but also possibly as a result of global warming. And, as with many new-disease discoveries, a whole raft of previously mysterious conditions are now being laid at the door of LD, including chronic fatigue (CFS/ME), multiple sclerosis (MS) and even autism. Could we be witnessing the start of a new epidemic? "Many of the diseases that are considered incurable by conven-tional medicine may have some kind of Lyme component," says American alternative practitioner Dr Lee Cowden.

What is Lyme disease? In essence, it's a kind of malaria, although it emerges not from the swampy jungle, but from temperate forests. Like malaria, the disease is transmitted by being bitten by a blood-feeding creature-in the case of LD, not by

an insect, but a tick, an arachnid, that lives on animals such as cattle, birds and even mice, but primarily deer.

Where it all began

Lyme disease first appeared more than 30 years ago as a mysterious disease outbreak in an American town called Lyme, in Connecticut. In the spring of 1975, there was a cluster of cases of what appeared to be juvenile arthritis. Children as young as 10 began to develop severe joint pain. Doctors from nearby Yale University were called in to investigate, and were puzzled by the appearance of odd rashes on the children's skin. Months of detective work finally led the doctors to connect the symptoms to a disease that had first been described in Europe almost a century before as 'sheep-tick fever'. After years of further detective work, researchers traced the illness to rogue spirochaetes bacterium in the patients' blood known as Borrelia burgdorferi-hence, the alternative name of 'Lyme borreliosis'. But where had it come from? Already alerted to the fact that it might be due to a tick bite, the scientists began a hunt among the local animal population. The Borrelia microorganism was finally tracked down to a tick of the genus Ixodes that lives on deer. This tiny arachnid-related to mites, spiders and scorpions, having eight legs-has a correspondingly tiny mouth, so its bite is rarely felt, which may be one reason why it was able to elude detection for so long. Ixodes is also cleverly able to inject its prey with a local anaesthetic, further disguising its attack. In fact, most victims of Lyme disease have no idea they were ever on the tick's hit list.

In fact, it's likely that Ixodes has to remain undetected because it's believed to be an inefficient feeder. It needs to be plugged in to its prey for hours to obtain sufficient nourish-ment. One indication of this is the probability that B. burgdorferi is not transmitted until the tick has been attached for at least 12 hours.

Initially, medicine treated the disease just like any other bacterial infection-with antibiotics. These appeared to work, and doctors patted themselves on the back for having put paid so easily to this novel disease. But the story hasn't turned out to be that simple.

Although this medical field is still relatively small, there is already a schism appearing among LD clinic-ians; indeed, some would call it a war. One army of experts believe that Lyme disease can be easily cured by a short course of antibiotics, whereas the opposing side says no, LD is a complex, potentially long-term illness (see box, page 6).

The problems begin with the diag-nosis. If LD is spotted early on, then antibiotics can prove helpful. But, in practice, LD turns out to be very diffi-cult to diagnose (see box, page 8), and the later stages of the disease are much harder to treat with the usual drugs.

What's more, these antibiotics can sometimes make things even worse. Any Borrelia bacteria that are not totally killed off by the drugs don't just develop resistance-which is bad enough-but also become what is referred to as 'cell-wall deficient'. This makes them very elusive as, without walls, they can hide inside of healthy cells, thereby avoiding direct attack by the drugs (Infection, 1996; 24: 218-26).

Lyme patients also find that the types of antibiotics used to treat them may actually exacerbate their symp-toms. This is thought to be the result of changes due to the drugs in the genetic sequencing of Borrelia, causing them to release toxins into the body. These toxins often get into the brain and nervous system, precipitatingwhat is called the Jarisch-Herxheimer reaction (named after Karl Herx-heimer, the German dermatologist who first observed it). J-H reactions can be life-threatening, and are seen in one in seven Lyme borreliosis patients treated.

The leaky brain

In fact, it has also been suggested that LD in itself-whether treated by antibiotics or not-may be neurotoxic. The idea is that Lyme disease creates ammonia in the brain, causing a 'leaky-brain syndrome'. Among the first to propose the idea was LD specialist Dr David Jernigan. As ammonia can alter permeability of the blood-brain barrier, he says, it would allow large molecules to reach the brain, causing 'cerebral allergies'. Jernigan believes that this may be a major cause of a variety of LD symptoms (Townsend Lett Docs, 2007; April: 141-8; online only).

Confirmation of this hypothesis has come from animal studies. Using adioactive tracers, researchers have shown that laboratory animals, when infected by Borrelia, lose the pro-tection of the blood-brain barrier after just two weeks (Schutzer SE, ed. Lyme Disease: Molecular and Immunologic Approaches, Series 6. Current Communications in Molecular and Cell Biology. Plainview, NY: Cold Spring Harbor Press, 1992)

How does Borrelia do this? It's thought that the bacteria burrow their way between the cells of the brain's outermost membrane, causing a localized inflammation that, in turn, releases proteins to fight against the bacterial invasion; this then results in holes in the cerebral membrane. It's much the same mechanism as seen in the leaky-gut syndrome but, in this case, it's potentially more serious as it involves the brain.

In addition, there is now laboratory evidence that Borrelia can "attach to or invade human cortical neuronal cells", say researchers at the National Center for Infectious Diseases in Colorado, part of the US Centers for Disease Control and Prevention (CDC). This makes the bacteria difficult to kill by the immune system (Microbes Infect, 2006; 8: 2832-40). It also helps to explain why Lyme disease can be both relaps-ing and resistant to treatment.

Incidentally, the spirochaetes bac-terium that causes syphilis has a similar mode of action and can also lodge in the brain, potentially remain-ing active for years.

Brain abnormalities

The leaky-brain theory also accounts for some of the highly specific neur-ological abnormalities found in Lyme patients-including Bell's palsy, lymphocytic meningitis, meningo-encephalitis and cranial neuritis-not to mention the less specific CFS/ME and 'brain fog'.

"The neurological and psychiatric manifestations of Borrelia are so numerous that it is called the 'new great imitator'," says Dr Frederic Blanc, of the University of Strasbourg, France. "Every part of the nervous system can be involved: from central

to peripheral nervous system, and even muscles" (Med Mal Infect, 2007; Mar 8; Epub ahead of print).

In fact, as long as 10 years ago, LD was firmly characterized as a 'neuro-psychiatric illness'. Reviewing the whole history of the disease, a team of psychiatrists at New York's Colum-bia University found Lyme disease to be responsible for "a broad range of psychiatric reactions", including paranoia, dementia, schizophrenia, bipolar disorder, panic attacks, major depression, anorexia nervosa and obsessive-compulsive disorder (Am J Psychiatry, 1994; 151: 1571-83). Since then, tests have discovered reduced blood flow in the brains of chronic LD sufferers, explaining the impaired mental functioning that afflicts so many victims of the disease (Neuro-psychiatry Clin Neurosci, 2003; 15: 326-32).

The autism connection

The most dramatic mental condition thought to be caused by Lyme disease is autism. A rare condition 50 years ago, autism now affects one in every 150 American children, according to the latest figures from the CDC.

But why should Lyme disease be implicated? One of the first clues was that the psychological symptoms of LD are similar to those of autism.

Six years ago, the above-mentioned Columbia University psychiatrists found that children with Lyme disease have "significantly more cognitive and psychiatric disturbances . . . resulting in psychosocial and academic impair-ments" (J Neuropsychiatry Clin Neurosci, 2001; 13: 500-7).

There are other clues, too. As already mentioned, syphilis, which is caused by a similar spirochaetes as in LD, in the womb is known to cause autism. Furthermore, autistic children are known to have many metabolic dysfunctions which are shared by victims of LD, in particular, chronic-ally low counts of CD57 natural-killer (NK) cells.

Of course, scores of theories have been proposed for the cause of autism, among which vaccine damage is perhaps the best known. But LD may be involved there, too. "It is possible that the two are conjoined in damage, and the long-term effects of Borrelia could hamper the body's ability to mount a significant, timely responseto vaccines," says Dr Geoffrey Radoff, of the Alternative Medical Care Center of Arizona. "This could explain the higher incidences of adverse reactions to vaccinations in children with autism (Townsend Lett Docs, 2007; April: 78-81; online only).

However, some children appear to be born with autism, so how could Lyme disease be involved there? Although the research has yet to be done in humans, studies of farm animals have shown that Borrelia can pass through the placental barrier into the womb and even into breast milk. This makes it possible for an infected mother to pass on the disease to her newborn child, in whom it could present as autism.

Do the numbers stack up? With autism now so widespread, is it likely that so many children-or their mothers-could have been bitten by a relatively uncommon tick?

One answer is that ticks, it appears, are not the only cuplrits. Mosquitoes, fleas and lice may also carry Borrelia (Agric Environ Med, 2002; 9: 257-9), thus vastly increasing the risk of infection. Another theory is that there may be a 'Borrelia-related complex' whereinthe bacteria pass unnoticed from generation to generation, and only present when the immune system is under stress. Autistic children are known to suffer from a plethora of autoimmune and metabolic disorders (J Autism Dev Disord, 2000; 30: 475-9), and these could turn latent Borrelia infect-ion into a full-blown attack-with no tick in sight. Such theories were recently aired at a January 2007 meeting of the newly formed Lyme-Induced Autism Foundation, held in San Diego. Texas physician Dr William Harvey reported that he had many patients who tested positive for Borrelia, and yet, "our part of Texas is not an endemic region of Lyme disease", he said. "No patient had the typical skin rash, but most had been ill for many years, with similarly ill family members."

Other delegates agreed. "There may be two forms of Borrelia infection: Lyme disease and epidemic borrelio-sis-disease spread directly between humans," said fellow LD physician Dr Radoff. "It is quite possible that the prevalence of autoimmune disorders found in families with autism is an infection that has existed chronicallyin the body for years, if not decades."

Dr Warren Levin, another LD practitioner, has reported that, in the 10 children with autism he has seen, all tested positive for Lyme disease.

Predictably, medicine's knee-jerk reaction to such findings has been to dismiss them, but one group of researchers is taking them seriously. Yet again, that pioneering team of psychiatrists at Columbia University, led by Dr Brian Fallon, has already taken up the challenge and embarked on a huge epidemiological study of Lyme disease and autism.

Fallon believes that two things will emerge from his study: that regions with very high rates of Lyme disease will also have higher-than-normal rates of autism; and that at least some of those autistic children will respond to LD therapy.

"In our work with children with LD, we have encountered a few children with autistic-like disorders," says Dr Fallon. "When they received intensive antibiotic therapy, the autistic syn-dromes dramatically improved and, in some cases, resolved."

Tony Edwards


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