Iceman, or Otzi, had a bad day. He had just gotten away from his chasers and stopped at the very top of the pass on the border of what is now Italy and Austria in 3200 BC. He had made it all the way to the top of the mountain and was now stopping for some lunch of ibex meat when a hidden assailant shot him in the back with an arrow. He likely died quickly, particularly after the blow to the back of his head dispatched him. His assailant pulled out the arrow shaft but left everything else behind, leaving us Europe’s oldest mummy, frozen in the snow to examine 5300 years later. When an autopsy was done this year and he was briefly thawed, samples showed that he had Lyme disease in addition to everything else. So, like tuberculosis, Lyme has been around awhile. It makes an illness that may not kill you, but sure slows you down until something else does.

Where do we get Lyme disease from? We thought it was just from ticks carried by deer. That’s the conventional thought. If you don’t have deer in your neighborhood, you are safe, right? Actually, wrong. In a paper presented at the International Lyme Conference in Toronto last month, John Scott presented a paper on the incidence of Lyme carrying ticks on birds in Canada. His paper caught my ear. 200 song birds that spend a fair amount of time on the ground were captured across Canada over the last three years with mist nets or from bird strikes against city buildings. The birds were then examined for the presence of ticks. The average bird carried two ticks, with one bird having 18. And when the 17 different kinds of ticks were examined, 29% of them were found to have B. burgdorferi in them. (That’s the Lyme bacteria) These birds migrate up into Canada from their winter homes. They cross virtually every state in the US. That means the average bird at your bird feeder may be pretty much the same, and have about a 30-50% chance of carrying the Lyme bacteria in a tick. Hmmm.

What are the symptoms of Lyme disease? How about something that feels like a cold that doesn’t go away, and then fatigue and malaise that doesn’t go away. Any new symptoms that wax and wane, you might think of Lyme. You don’t need to have a rash or a tick bite, as less than 50% of folks who have Lyme do. And the traditional Western Blot test may not be very accurate. The controversy about Lyme is unbelievable because there are those who believe you can cure Lyme with 30 days of antibiotic, and those who see patients who don’t get better until treated for Lyme for 1-2 years. I’ve heard too many stories from credible sources to believe the 30 day theory.

WWW. What Will Work for Me? I have a bird feeder and feed birds all winter. I will continue to do so. And I will look for ticks until we get a good hard frost when the risk of transmission seems to fall off. One thing winter is good for.

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 professor committed suicide after developing dementia brought about by 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 conventional 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 a 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 clinicians; 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.

The problems begin with the diagnosis. If LD is spotted early on, then antibiotics can prove helpful. But, in practice, LD turns out to be very difficult to diagnose, 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 symptoms. 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, precipitating what 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 radioactive 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 relapsing and resistant to treatment.

Incidentally, the spirochaetes bacterium that causes syphilis has a similar mode of action and can also lodge in the brain, potentially remaining active for years.

Brain abnormalities
The leaky-brain theory also accounts for some of the highly specific neurological 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 ‘neuropsychiatric 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 impairments” (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, chronically 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 response to 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 infection 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 borreliosis-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 chronically in 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 syndromes dramatically improved and, in some cases, resolved.”

Tony Edwards

In the August 2001 edition of The Doctor’s Prescription for Healthy Living, a US monthly magazine, it mentions that the average silver particle size of our Sovereign Silver products was 0.001 microns but, due to further developments, the size is now an average of 0.0008 microns (the smallest silver particle size available today).

We have a vested interest as the sole distributors in the UK of Sovereign Silver products, but our motive is to make the public aware of the benefits of colloidal silver. – Julian F. Byng, Natural-Immunogenics

In addition, other factors can interfere with the diagnosis when testing blood, including:

Recent infection before an immune response

The causal spirochaete bacteria may be encapsulated by host tissue

There may be no spirochaetes in the body fluid on the day of the test

The test only looks for one strain of B. burg dorferi, yet there are over 300 strains

Recent antibiotic or anti inflammatory treatment

Babesiosis co-infection (another tick borne disease) may cause immunosuppression

There may be other causes of immunosup pression (e.g. immunosuppressive drugs)

The lab test is not standardised to detect late stage disease

The lab may have a poor technical capability for detecting Lyme disease.

!ALyme disease is common throughout most of the world. There are now more than 10,000 medical papers on Lyme. But even as the knowledge surrounding this infection by the Borrelia burgdorferi spirochete (one of a family of corkscrew shaped bacterium) increases, there remain many unanswered questions about this disease. Lyme is spread by the bite of infected ticks of the genus Ixodes. Host animals include deer, mice and other mammals as well as birds.

The symptoms of Lyme mimic over 200 other conditions and it is often misdiagnosed as rheumatoid arthritis, fibromyalgia, lupus, chronic fatigue syndrome (CFS) and even some psychiatric disorders.

Blood tests for Lyme are notoriously unreliable (JAMA, 1992; 268: 891-5; Ann Intern Med, 1991; 115: 533-9), and a negative test cannot fully rule out infection. A better diagnosis can probably be made on the basis of careful assessment of symptoms and patient history (Arch Intern Med, 1990; 150: 761-3; Clin Courier, 1991; 9: 5-8). But even here you should not necessarily let yourself be satisfied by an “all clear” or an alternative diagnosis. In a small, informal study by the American Lyme Disease Alliance, 90 per cent of those diagnosed with CFS actually had Lyme disease.

Initially, it was thought that 75 per cent or more of those with Lyme would initially produce a round red rash. Now we know that the rash neither has to be red nor round and that the figure is closer to 50 per cent. In one study in Finland, only 16 per cent had the rash (Ann Med, 1993, 25: 349-52).

The most common and disturbing symptoms are those which affect the nervous system. Hands, fingers, feet and toes may twitch or go numb again and again, even though they may appear to be normal on examination. Vision can become blurred, and sharp electric pains may suddenly rip through the body.

The most common treatment, with long term antibiotics, has other implications for an already compromised immune system (WDDTY vol 8, no 1) and is unreliable. The FDA has not approved any drug for the treatment of Lyme disease and the dose and type of antibiotic which you are likely to receive varies wildly from physician to physician.

Several studies have shown that the Lyme disease bacteria can be present, without producing symptoms, in the spinal fluid of individuals who have been “cured” by aggressive antibiotic treatment (Infection, 1989; 17: 355-8; J Clin Microbiol, 1993; Aug: 61-63) and that symptoms can persist even after therapy (Ann Intern Med, 1994; 121: 560-7; Antimicrob Agents Chemother, 1995; 39: 1127-33; Clin Infect Dis, 1995; 21: 380-9; J Am Acad Dermatol, 1993; 28: 312-4; Eur Neurol, 1995; 35: 113-7).

Another problem with antibiotic treatment is that a two week course of oral antibiotics, given for instance on a just in case basis, is thought to be enough to cause a Lyme positive patient to test false negative for the rest of his or her life.

One question which has not been asked is why some become symptom free even if the spirochete remains in their bodies and others don’t. It seems reasonable that genetic factors and the overall health of the immune system play an important part. So while there are no specific alternative remedies for Lyme disease, you can help yourself greatly by supporting your immune system, especially with supplements of copper, evening primrose oil, vitamin C and pycnogenol and by increasing your garlic intake. Herbal remedies which enhance immunity include echinacea, golden seal, alfalfa, dandelion root, Oregon grape and milk thistle.

WDDTY panellist Patrick Kingsley also recommends that a homeopathic treatment with Borrellia burgdorferi may be of benefit but cautions that, as with antibiotics treatment, improvement will often be slow and treatment may need to last for 40-60 days. In addition, aconite is indicated when your symptoms include fever; rhus tox for rheumatic symptoms; and ledum for joint and muscular pain

Cannabis: One reader agrees with last week’s article that cannabis is an effect, and not a cause of social problems, but prolonged use will cause its own problems, and so it is better to seek out and treat the original problem. . .

Warts revisited: your responses still come in, but one gentleman was particularly animated because we did not include his therapy. His simple solution is iodine, which should be applied after first pricking the wart with a sterilized needle so that a small amount of blood appears, and then soak the area in iodine.

It is the largest of the spirochaetesIt has a superefficient internal propulsion system, which allows it to swim quickly through blood and tissue

It is covered with a clear gel like coat of glycoproteins, sometimes called the slime layer, or S-layer. This coating acts like a deflector shield, protecting the bacteria from attack by the immune system and antibiotics

It replicates slowly. Bacteria replicate by a process of division and most only take 20 minutes to divide. The division time of B. burgdorferi is 12-24 hours. This is important since most antibiotics can only kill bacteria while they are dividing. A slow doubling time means that B. burgdorferi is less exposed to antibiotics. While most bacteria are killed in 10-14 days by antibiotic treatment, for a Lyme spirochaete to get the same amount of lethal exposure, the antibiotic would have to be present 24 hours a day for one and a half years!

The Lyme spirochaete can remain in the body for years in a state of suspended animation. Since it does not divide during this time, antibiotics will not kill it. A Lyme spirochaete in this state will wait for conditions to be right before releasing itself into the blood stream to cause new symptoms or a relapse of old ones

The Lyme spirochaete appears to be selective and able to enter ‘safe’ human cells, and hide in the body, evading the immune system and medication. For instance, the spirochaete can enter human fibroblasts (the cells that make scar tissue). In this situation, the bacteria remain protected from the immune system and can thrive without assault. Laboratory tests have shown that, even when these fibroblast cultures were flooded with massive doses of antibiotics, they still yielded live spirochaetes after two weeks.

For details of how to obtain a copy of Grier’s book, write to: The Lyme Disease Survival Manual, 902 Grandview Avenue, Duluth, MN 55812-1146, USA.

More than 10 years ago, I had two similar episodes, each about two years apart, but a load of tests, including an MRI scan, could find nothing wrong.

These episodes never occurred before I contracted Lyme disease 12 years ago. A year after that, I had my first attack. Since then, I have had an irregular and rapid heartbeat, and I am susceptible to everything going, including every type of flu.

Before the TIA, my doctor wanted to put me on beta-blockers to regulate my heartbeat but, according to tests, my heart is fine. He believes there is no imminent danger of a stroke as I have no family history of it, although my grandmother did have a stroke at age 26.

I don’t have high blood pressure or drink and, at 33, I’m probably too young for hardened arteries. My only other symptom is general fatigue, which means I often live on coffee. What should I do?- MM, Maidstone

A Transient ischaemic attacks are mini-strokes, when the blood supply to parts of the brain is temporarily interrupted or blocked. A stroke can be due to lack of blood (thus lack of oxygen) to the brain which, in turn, is caused by atherosclerosis, a ruptured blood vessel or a blood clot from elsewhere in the body which travels to the brain. During a proper stroke, there is brain damage and even death.

While stroke damage can persist for weeks or permanently, a TIA lasts only a few minutes or, at most, an hour, and there is no permanent damage.

It’s a shame you weren’t seen promptly as you need to be medically evaluated within 60 minutes of the attack to determine whether you suffered a genuine stroke or only a TIA.

In our view, your doctor is remiss in dismissing TIAs as just part of your makeup, a typical and now outdated attitude. In a new study (J Am Med Assoc, 2000; 284: 2901-6), only 14 per cent of patients with TIAs were hospitalised and 8 per cent received no subsequent treatment whatsoever to protect them from a serious stroke later.

TIAs should be considered a major warning of a future full-blown stroke, and all possible causes should be ruled out. The same study showed that 10 per cent of those who had TIAs went on to have a major stroke within the next 90 days. Indeed, half the strokes occurred within two days of the TIA.

This makes it imperative that your doctor run the gamut of routine tests on you as a matter of urgency to find out if your episode had any cause – a blockage, clot or haemorrhage – which could lead to a full-blown stroke later. These tests include Doppler ultrasound of your carotids (the neck arteries feeding blood to the brain) and other arteries to see if there is any minor or major blockage. Often, in stroke, both arteriosclerosis (hardened arteries) and arterial occlusions (clots) are present since platelet thickening may occur due to a damaged arterial lining. You should also undergo all the usual tests to determine your risk of stroke.

You also need to check your blood pressure, as high blood pressure can sometimes lead to an aneurysm, where a section of the arterial wall balloons out and bursts, causing a haemorrhage in the brain.

In a sense, you were lucky to have the TIA before taking beta-blockers, as these are just one of a large number of drugs which can cause a stroke in susceptible individuals. Others include sumatriptan, taken for migraines (Intensive Care Med, 1995; 21: 82-3); all hormones, including HRT and the Pill (Acta Neurol Belg, 1992; 92: 45-7); phenylpropanolamine, present in OTC drugs for weight loss, cold preparations and nasal decongestants (Am J Emerg Med, 1987; 5: 163-4); nifedipine, a calcium-antagonist type of antihypertensive (BMJ, 1992; 305: 693); and any sort of nasal decongestants used excessively (J Neurol Neurosurg Psychiatry, 1989; 52: 541-3). Ironically, even drugs used to prevent stroke – such as anticoagulants, streptokinase, heparin and recombinant tissue-type plasminogen activators – can cause a stroke (Circulation, 1991; 83: 448-59; Arch Neurol, 1985; 42: 1033-5).

Even thrombolytics, the drugs used to dissolve blood clots after a cerebral infarction, or blockage of a vessel in the brain, can bring on another stroke – this time, by haemorrhage.

We’re frankly mystified at the suggestion to take beta-blockers for a rapid heartbeat. Certain beta-blockers, like Sotacor, can cause torsade de pointes, or an unusually rapid heartbeat of more than 100 beats per minute, according to Sortacor’s manufacturer, Bristol-Myers Squibb (Physicians’ Desk Reference).

So if you are taking any sort of medication, even for migraine, you might consider this a possible cause of your TIAs.

Ordinarily, if there are one or more risk factors for stroke, a doctor may suggest either drug therapy or surgery to reduce your risk. The gold standard of preventative stroke therapy is antiplatelet therapy – taking aspirin. Aspirin supposedly ‘works’ by thinning the blood and lowering blood pressure, and is a first-line treatment for TIA patients. The bottom line is that aspirin has never been proven to prevent stroke in low-risk patients with no history of cardiovascular disease (N Engl J Med, 1992; 327; 175-81).

Furthermore, aspirin is given in daily dosages of 5-325 mg/day but, at this level, it can act paradoxically – by increasing the risk of a burst blood vessel in the brain by 21 per cent, even in low-risk patients (Drugs Ther Bull, 1994; 32: 1 – 3).

One of the problems in using long-term just-in-case medicine like aspirin is that it depletes the body of many vital nutrients, which may be essential for protecting your heart and blood vessels.

In a study comparing patients taking aspirin with those taking warfarin and still others left untreated, there was no significant difference in low-risk patients between doing something and doing nothing; in high-risk patients, the differences between the three groups were large enough to be statistically significant, but not enough to be meaningful in terms of survival (J Am Med Assoc, 1995; 274: 1839-45).

The only other usual treatment for stroke is an operation to scrape away fatty deposits in your carotid arteries, which is unlikely in your case, given your age.

>From what you say, you don’t have any of the obvious causes for a TIA – high cholesterol, smoking, diabetes or alcohol abuse – although with your grandmother’s circumstance, there is a possibility of a genetic propensity to stroke.

Although you don’t give much information about your general health, one detail is highly significant: you had Lyme disease, caused by a bite from a tick which spreads Borrelia burgdorferi, a spiral-shaped bacteria). Although this disease is most prevalent in the US, it is being seen in increasing numbers in the UK. If left untreated, symptoms can come and go for years.

Numerous studies show that untreated Lyme disease can cause different neurological problems that imitate true stroke and TIAs. Indeed, the evidence suggests that Lyme borreliosis may be a more common cause of these puzzling episodes than medicine has previously thought.

In a study of patients with cerebral thrombosis or TIAs without a thrombosis, 24 of the 281 patients – nearly 9 per cent – had an immune-system response to B. burgdorferi, suggesting the presence of the bacteria in their blood. The researchers concluded that the symptoms of Lyme borreliosis may often masquerade as stroke (Stroke, 1993; 24: 1393-6).

Your tachycardia (rapid heartbeat) may also be related to Lyme myocarditis (heart inflammation due to the Lyme spirochaete) rather than a structural problem. In one case study, Lyme myocarditis had all the hallmarks of tachycardia (J Cardiovasc Electrophysiol, 1997; 8: 323-4).

Animal studies have shown that B. burgdorferi has a predilection for cardiac connective tissue, especially near the aorta (Am J Trop Med Hyg, 1992; 47: 249-58).

Carditis is seen in 4-10 per cent of all cases of Lyme disease. Its symptoms usually include various types of atrioventricular block, or abnormalities in the electrical conduction tissue between the chambers of the heart, leading to disturbances in heart rhythm if left untreated (Ugeskr Laeger, 1993; 155: 2147-50).

In some cases, a pacemaker may be necessary (J Cardiovasc Electrophysiol, 1997; 8: 323-4). According to the researchers of one study, when serious arrhythmias are present and a cause can’t be found, Lyme disease should be one of the first possibilities considered, particularly among young people (Ugeskr Laeger, 1993; 155: 2147-50).

Although Lyme disease is often difficult to diagnose and treat, aggressive treatment with a strong antibiotic like ceftriaxone can often do the job. In six patients with Lyme carditis treated with antibiotics, echocardiograms and exercise tests showed that symptoms resolved up to seven years after the acute disease (Scand J Infect Dis, 1997; 29: 153-7). There is controversy over whether a short- or long-term course of antibiotics will truly kill this intractable bug (see WDDTY, vol 12 no 3) and also whether it can be completely eradicated after being in the system for so long – in your case, 12 years.

There is increasing evidence that colloidal silver is effective against B. burgdorferi. You may also wish to augment any type of antimicrobial treatment with vitamins and minerals that counter heart disease and stroke; this includes consuming a wholegrain diet rich in fruits and vegetables, supplementing with magnesium, coenzyme Q10 and antioxidants, and taking regular exercise. Just taking regular supplements of vitamin E, for instance, can decrease blood platelet stickiness by 80 per cent (Blood, 1989; 73; 141-9).

Alternative medicine has not been proven particularly successful at treating chronic and severe Lyme disease. However, there are several things you can do to support your system as it fights the infection while taking conventional treatment.Watch out for Candida. Patients being treated with antibiotics can develop a yeast overgrowth. To combat this, take two high quality probiotics after each meal and follow a strict anti Candida diet, which contains no sugars. If you can tolerate dairy, you may include live yoghurt daily in your diet

Avoid caffeine, alcohol and smoking, all of which put your immune system under greater stress

Sleep as and when you need to

Supplements are a must, although improvement may not be noticeable for a few weeks. A good quality multivitamin and mineral supplement should be augmented by extra magnesium, 400-800 mg daily (helpful for tremors, headaches, twitches and cramps), and vitamin B-complex, at least 50-100 mg daily (to help combat neurological symptoms)

Increase essential fatty acid intake. To get a good balance, Dr Burrascano recommends 1000 mg of cod liver or other fish oil, or flaxseed (linseed) oil (rich in omega-3) four times daily, and 1000 mg of borage, evening primrose or blackcurrant seed oil (rich in omega-6) four times daily

Try coenzyme Q (Q10 or ubiquinone) to deal with symptoms related to poor heart function, stamina and immune response. Lyme patients need around 200-300 mg daily of standard brands, or 90 mg daily of pharmaceutical quality brands, divided into two daily doses

Treatment with homoeopathic nosodes made from Borrelia burgdorferi may be of benefit, says WDDTY panellist Patrick Kingsley. He cautions, however, that as with antibiotics improvement may be slow and, often, treatment is needed for as long as 40-60 days. Similarly, deer antler, cultivated and used throughout China and Russia, has been suggested as a possible therapy for Lyme disease (Townsend Lett Docs, 1991; 91/2: 154-5)

Whatever treatment you take, give it time to work. The Jarish-Herxheimer, or Herx, reaction is not uncommon in the treatment of Lyme disease. As the spirochaetes die during antibiotic therapy, they give off toxins, causing you to feel worse before you feel better. The Herx reaction is a normal and good result, and a sign that the treatment is working.