I took him to hospital, and the doctor on duty thought Chris had a gallbladder problem and prescribed painkillers, and said he would arrange for some tests in 10 days’ time. When I was told to take Chris home, I told the doctor I didn’t think my husband would last the night, so he gave us a second packet of painkillers.

I then decided to take Chris to the emergency department of another hospital and, within minutes of arriving, Chris was surrounded by doctors and nurses who said he was suffering a heart attack. One staff member told me that Chris had suffered an attack earlier that day.

After treatment, he was put on oxygen and I eventually left to go home. Almost as I walked through the door, the hospital phoned to say my husband was suffering yet another attack and was being rushed to a different hospital for an emergency angioplasty. Chris was also being given clot-busting drugs.

On the way to that hospital, my husband complained of headache and the ambulance crew suspected bleeding on the brain caused by the drugs. A CT scan revealed a cerebral haemorrhage.

For several days afterwards, Chris could not tolerate light or sound, and was paralysed down the whole of his left side. He could not sit unsupported and was unable to feed himself. He had also lost the sight in both of his eyes.

In all, my husband spent 56 days in hospital, and his weight fell from 11 st 9 lb to just 9 st 7 lb.

He has not worked since then, and he has been left with hearing loss, memory problems and poor eyesight. He now attends a day centre where he is learning furniture restoration. We still have the painkillers the doctor gave us at the first hospital. – JP, West Sussex

Avoid these troublesome foods:

Wheat based foods such as wheat bran, breakfast cereals, bread, crackers, biscuits, cakes, pastry and pies.

Cow’s milk.

Yeast.

Spicy foods such as chillies and curry.

Corn (maize) and corn products like corn syrup.

Rice syrup.

Anything that contains modified starch, often used as a fat replacing bulking agent.

Sugar and sugary foods.

Artificial additives, especially colourings and sweeteners. Sorbitol seems particularly

problematic, so do check labels.

Very hot or very cold foods.

Oranges and orange juice.

Beef and pork (lean lamb is usually well tolerated).

Tea and coffee, both of which tend to dry out the protective mucus lining of the gut.

The following foods are good for the gut:

Linseeds.

All kinds of fresh fruit aim for two to three pieces daily between meals.

All varieties of dried fruit.

All varieties of fresh vegetables and beans.

Fresh garlic (or a daily garlic capsule with your main meal).

Organic potatoes in their jackets.

Vegetable soups and juices: fresh carrot juice is particularly recommended.

Cereal foods (other than wheat).

Psyllium husks.

Water, four to eight glasses a day (preferably filtered).

Live bio yoghurt. Eat a small carton size daily, preferably an hour before bedtime.

Extra virgin olive oil.

Blackstrap molasses.

Manuka honey.

Aloe vera juice.

Unfortunately, the sharper the sword, the greater the risk you run of getting cut. The study that concluded that the drug was most effective for people with stable angina also admitted that 66 per cent of those in the trial had to stop treatment because the adverse reactions were so severe. Most complained of very bad headaches (Lancet, 2002; 359: 1269-75). By any reckoning, this is an astonishingly high failure rate.

Now, doctors at Aberdeen’s Royal Infirmary also suspect the drug can cause anal ulcers. They noticed that five patients suddenly developed the ulcers while taking the drug. The ulcers disappeared almost immediately after stopping treatment (Lancet, 2002; 360: 546-7).

Their findings tie in with an earlier discovery that nicorandil causes mouth ulcers. These were first noted in 1998, when 25 cases of severe ulcers were reported; in some cases, the ulceration was so bad that it affected eating and talking. Again, the ulcers disappeared when the drug was stopped.

Doctors should also be on the lookout if they are prescribing nicorandil with other heart drugs. Researchers at Addenbrooke’s Hospital in Cambridge have also found that it interacts badly with antidiabetic drugs, such as glibenclamide and glimepiride. The cocktail effect can cause serious reactions and makes it ineffective. A better choice with nicorandil is gliclazide, the researchers concluded.

Aside from headaches and ulcers, other reactions have included dyspepsia, nausea, vomiting, anorexia and dizziness. A fall in blood pressure and an increase in heart rate have been noted at high doses.

The GP took my blood pressure and prescribed Imigran (sumatriptan). On arriving home I had breakfast and took one. Nothing prepared me for what was to follow. I collapsed and came to some seven hours later, able to do very little. Breathing difficulties, a lack of appetite and a feeling of total lethargy followed for the next three days.

After this experience I refused to take any more, preferring to suffer the pain of migraine, which I experience about once a year. J M, Newhaven, East Sussex.

A:As you know from the patient information leaflet you were given with your drug, Imigran, generically known as sumatriptan, is a new migraine drug, called a 5-HT agonist, which supposedly works by reducing the swollen blood vessels around the brain.

It is chemically related to 5-hydroxytryptamine, or serotonin, a chemical in the brain, and was developed after scientists revised their thinking about what causes migraine. Dr Frank Clifford-Rose of the Charing Cross Hospital, who helped coordinate many of the studies of sumatriptan, says that migraine, rather than being initiated by the blood vessels in the brain itself, is now believed to be a biological disease of the nervous system, and that serotonin plays a key role. It has long been known that 5-HT can cause headaches, and experiments have shown that 5-HT is released during migraine attacks.

Glaxo was the first to come up with a drug which was chemically related to 5-HT, but supposed to selectively block the receptors for this hormone, causing the blood vessels in the brain to constrict without affecting what could be as many as 15 other 5-HT receptors, which affect blood clotting, activity in the lungs and the gastrointestinal system in the central nervous system.

In 1991, Glaxo enthusiastically launched sumatriptan as “a revolutionary acute therapy in migraine” after a number of studies showed highly promising results in patients injected with the drug under the skin (the faster route) or given it in tablets.

In two studies testing sumatriptan against a placebo in a total of 1600

patients, within two hours, 81-86 per cent of patients had their headaches disappear or lessen to the point of being mild (N Engl J Med, 1991; 325: 316-21 and JAMA, 1991; 265: 2831-5).

In the wake of a great deal of noisy fanfare over what was thought to be one of the first real breakthroughs for migraine, medicine has begun to retrench, now that the reports are flooding in demonstrating that patients taking this drug may be trading one health problem for another or, indeed, making the problem worse.

The latest studies show that at least 5 per cent of users of sumatriptan experience chest pain. Because the drug works on blood vessels, it has always been assumed that the chest pain had to do with the heart. But a new study (The Lancet, 8 October 1994) shows that the pain may start in the esophagus (the canal from your mouth to your stomach). A double-blind study of 24 volunteers randomly injected with either sumatriptan or saline found that there were no electrocardiogram changes. However, studies of the esophagus showed that contractions of the esophagus were significantly increased by sumatriptan.

Five of the subjects (21 per cent) developed chest pain, lasting from two to 45 minutes, although there seemed to be no relation in time between onset of the pain and the abnormal recordings of movement of the esophagus.

A number of doctors writing from the Department of Medicine and Therapeutics, Western Infirmary, University of Glasgow, argued that the study results should be regarded with caution, particularly since the changes were seen only when three times the normal amount of the drug was given. They also point out that changes in the blood have been shown with the standard therapeutic dose of sumatriptan; blood pressure in the lungs and aorta rises by 40 per cent and 20 per cent, respectively, which could mean that the chest tightness arises from the veins in the lungs or those running the breadth of the body rather than in the esophagus (The Lancet, 26 November 1994).

Dr K M A Welch, from the Department of Neurology, Henry Ford Hospital and Health Sciences Center, in Detroit, Michigan, concluded that in rare cases heart arterial spasms have occurred (N Engl J Med, 329; 1476-83). A Lancet commentary (19 June 1993) added there is a small risk of poor blood flow to the heart, and a Dutch postmarketing study says that angiographies of patients showed that sumatriptan does indeed constrict arteries (BMJ, 6 November 1993).

The bottom line is that medicine doesn’t really have a clue what causes the chest pain or what it really means. What doctors do know is that one woman with no previous history of vascular disease suffered a fatal heart attack after injecting herself with sumatriptan (The Lancet 1993; 341: 861-2) and two patients developed serious irregular heartbeat (19 September 1992). Furthermore, in some the chest pressure or pain radiates out to the left arm and head, in the manner of angina (N Engl J Med, 11 November 1993).

The other problem is the possibility of rebound migraines, setting up increased dependence on the drug. The Gothenburg Migraine Clinic in Sweden found that 102 of 193 (53 per cent ) patients given sumatriptan by injection had recurrences of migraine within five to 10 hours after nearly every treated attack. Another study of 21 patients found that all but one had a headache the next day (The Lancet, 10 October 1992).

Researchers at the Department of Neurology, University of Essen in Germany also reported on seven patients who after an average of nine months found that they had to use the drug nearly every day to prevent their headaches from recurring.

In another case, a patient who’d only suffered from migraines once a month began getting them every morning after he’d began taking sumatriptan (BMJ, 8 January 1994).

Glaxo denies that there is any evidence of dependence on the drug, and points out that the drug is only approved for short-term intermittent treatment of acute migraine attacks, and not for daily prevention.

Besides the problems mentioned, sumatriptan can cause dizziness, vertigo, malaise, fatigue, drowsiness and a feeling of heaviness.

In the Gothenburg Clinic, 70 per cent of patients experienced one or more side effects, including neck pain, chest symptoms, tiredness, tingling and a reaction at the injection site. The oral variety can also cause nausea and vomiting.

Besides this multitude of side effects a question mark hangs over sumatripan’s genuine effectiveness in times of need. Although as many as 90 per cent have responded to the drug over three treatment courses, only about 50-60 per cent will respond to it during any one attack (The Lancet, 23 January 1993).

As usual, medicine has rushed in shouting about its “breakthrough” far too early, without fully understanding what the role of serotonin is in the onset of migraine, what blocking could do to you or whether sumatriptan is as “selective” as first thought. (The not fully understood role of this hormone is also behind the many side effects reported with Prozac and cholesterol-lowering drugs). It also demonstrates that in studying the body microscopically and looking for a specific means to block the action in the body which specifically sets off the pain, medicine has once again missed the forest for the trees.

Without looking at the body as a whole, the approach fails to consider what exactly sets off the serotonin and the migraine pain in the first place.

The new drug was a combination of my other drug – felodipine [a calcium antagonist] (which had never given me any known problems) – and something called ramipril [an angiotensin-converting enzyme, or ACE, inhibitor].

During the course of the next two weeks, I had various problems, including chest pain, breathlessness, aches and pains, and a general feeling of `unwellness’. I was concerned that it may have been because of the ACE inhibitor, so I went to see my GP, who told me to persevere with the drug as I would eventually become more able to tolerate it.

A few days later, I was shopping with my sister when I felt a sudden pain in my chest. I felt very faint, and the pain became so bad, I had to phone for a taxi to take me home. My sister decided to take me to hospital, where I received all the usual ‘casualty’ treatment, including an ECG, and was told I had not had a heart attack, but a very bad attack of angina.

I was diagnosed with angina some years ago by my GP (who has since retired), but I have never suffered from angina pain since, so I have not needed to take the medication. Anyway, on the day described above, I had my medication with me, but it made no difference to my condition.

During my two-day hospital stay, I insisted that they take me off ramipril. Incidentally, on the leaflet that came with this combined felodipine/ramipril drug, among the long list of side-effects, was the phrase: “If you have the following conditions, do not take the drug but consult your GP”.

One of the conditions was angina. I don’t know why I forgot to point this out to my GP but, surely, she should not have given it to me in the first place.

It shouldn’t be up to patients to read the leaflets in drug boxes and to check whether or not they should be taking a drug. – Marion Aley-Parker, via e-mail

I am still awaiting the results from the diagnostic tests – an oesophageal echocardiogram and coronary angiography – but my doctors believe surgery is inevitable to have my mitral valve either repaired or replaced.

Are there any alternatives to surgery? If there are none, what are the risks and drawbacks of this operation? I am 55 years old, and both my parents also suffered from cardiac problems – my father had a slow heartbeat and needed two pacemakers, while my mother died from a heart condition. – Malcolm Linchis, London

A MVP is a common heart condition in which the two flaps of tissue (mitral valves) controlling the flow of blood from the upper to the lower left heart chambers stop working properly. As a result, blood is ‘regurgitated’ back into the upper chamber, causing a ‘heart murmur’.

While the symptoms of MVP are usually benign, with the majority of those affected continuing to lead normal lives, about a quarter of cases worsen with age. Progressive deterioration of the valves leads to more severe regurgitation, with the blood not only pushed back into the upper chamber, but also into the lungs. Symptoms such as breathlessness, fatigue and chest pain become more pronounced, as you’ve experienced and, in the worst-case scenario, congestive heart failure can ensue.

To prevent reaching such a dangerous stage, doctors recommend repairing your mitral valve or replacing it with a prosthesis, depending on the amount of damage. This essentially means open-heart surgery, and the risks are as high as you would expect for such an invasive procedure.

It is important that you consider very carefully if the benefits from surgery will outweigh the risks of the procedure. Once you have the results of your echo and angiographic tests, make sure the doctor explains to you as clearly as possible the severity of your condition and whether you really do need the surgery. Do not allow your doctor to wave away your questions and decide for you. Also, ask if there are any alternatives to surgery (see box on right).

If you do decide to opt for surgery, there seems to be a slight disparity between the success of mitral-valve repair vs replacement. Those who have undergone repair rather than replacement appear to have a slightly better chance of survival, and are less likely to need further surgery (J Cardiovasc Surg [Torino], 1999; 40: 93-9).

I have been on 50 mg of atenolol for four years; for the last two years, I have had an eczema problem that does not respond to any treatment and, for a year at least, a wheezing problem has continued and worsened, with increasing pain in my chest when breathing cold air.

This may be of interest to other readers of WDDTY. If you have to hand the number of other readers (if any) who may have written in with the same symptoms, I would appreciate being told the numbers, as I have to see my cardiologist soon and it may be of interest to her. – J.W. Brown, London

WDDTY replies: A well-known side-effect of atenolol, a beta-blocker, is wheezing and skin rashes. You may wish to ask your doctor if you can change to another drug or take a smaller dosage. It’s a great shame you’ve been suffering for so long.

Anywhere in the chest, behind the breast bone or in the throat, it could be simple indigestion, cramp caused by shallow breathing, hiatal hernia, heartburn or reflex oesophagitis.Inflammation and pain around the breastbone and upper abdomen, it could be a viral infection, which can cause inflammation and pain in a condition known as Bornholm disease. Like other viral infections, it will clear up with rest, relaxation, plenty of fluid, nourishing soups, extra vitamin C and so on.

In the chest, it should be taken seriously as it could be angina or the early signs of a heart attack especially if accompanied by pain in the arms.

Behind the shoulder blades, it could mean gall bladder trouble. If it strikes the upper right quadrant, consider gastroenteritis, gastritis, gallstones, ulcer or hiatus hernia.

In the upper left or lower left quadrant, it may be diverticular disease, constipation, ulcerative colitis or irritable bowel syndrome. The pain of hiatal hernia may also radiate to the lower left or right side under the ribcage.

In the lower right area of the abdomen, sharp pain could mean appendicitis whilst groaning discomfort could be Crohn’s disease or ulcerative colitis.

In the lower back or lower abdomen, it may indicate kidney problems, cystitis, diverticulis, pelvic inflammatory disease or period pains.

The pressure of trapped wind, it can be excruciating and deceiving. Not only does the discomfort move around, it can also be an amazing mimic, aping the pain of gallstones, appendicitis and a heart attack all within the space of an hour or two.

(1) Don’t smoke at home. Exposure to tobacco smoke, whether your own or someone else’s, increases your risk of developing lung cancer, bronchitis and heart attacks and your child’s risk of developing frequent colds, allergies, asthma, and recurrent ear infections.

(2) Remove shoes upon entering your home. In homes where people do not routinely remove their shoes, the house dust is loaded with lead and pesticides which are tracked in from outdoors. Carpeting holds up to a hundred times the amount of dust as bare flooring; the deeper the pile, the harder it is to remove the dust. Dr. David E. Camann of the Southwest Research Institute in San Antonio, Texas, isolated dangerous pesticides and wood preservatives from carpet dust five years or more after these had been sprayed outside homes.

House dust is the commonest source of chronic low-level lead exposure for children. A great deal of attention has been focused on old, lead-based paint, peeling and flaking from walls and ceilings, as a source of this contamination. It is less well-known that roadside soil is still poisoned with lead deposited by gasoline fumes emitted before the ban on leaded petroleum additives, or that the soil around houses becomes contaminated with lead during new home construction or home renovations. This lead is tracked into the house, elevating lead levels in air and dust. The lead levels in carpet dust often exceed levels requiring clean-up at Superfund sites. Toxins trapped in home carpets pose a particular hazard to crawling toddlers.

Taking shoes off upon entering the home, wet-mopping of all horizontal surfaces (including window-sills) and regular hand-washing markedly lowers the blood lead concentration of children living in homes with high lead exposure.

Although lead has been banned from house paint, it may still be used in printer’s ink, along with other toxic metals. Burning newspapers or magazines can liberate lead into the air.

(3) Control Moisture. People who live in housing that is damp or shows visible mildew have a higher rate of sickness than people whose housing is free of dampness or visible mold growth. These problems are not dependent upon smoking habits, occupation or income; they occur because dampness encourages the growth of mold and of dust mites, microscopic insects that live in dust and secrete enzymes that damage the respiratory lining. Heavy exposure to dust mites and mold in childhood increases the rate at which allergy develops. Exposure to airborne or food-borne mold toxins increases the incidence of cancer. Because high humidity encourages mold and mite growth, you should maintain a relative humidity of 3 5% to 45% in each room of your house. Relative humidity can be measured with an inexpensive meter, available in hardware stores. Detailed advice on measures for controlling excess humidity and its attendant ills is presented in my book, The Four Pillars of Healing.

There is surprisingly little evidence to implicate lack of humidity as a source of sickness. If the relative humidity is less than thirty per cent, dryness of the skin and irritation of the nose and throat may occur. Before you rush out to buy a humidifier, however, try lowering the thermostat a few degrees. The hotter you keep your home, the more moisture you need in the air. Humidifiers are dangerous breeding grounds for mold and bacteria. Anti-foulants added to the water in a humidifier are worthless in controlling bacterial growth and themselves pose a health hazard if inhaled. Medical advice to humidify the air for improving respiratory problems has little evidence to support it. Only humidify your home air if you notice a definite improvement in pre-existing respiratory complaints; otherwise the risks outweigh the benefits. If you must use a humidifier, use a cool mist or ultrasonic room unit that is not connected to your central heating system. It will be much easier to clean. Use only distilled water in the reservoir and drain the unit daily, cleaning it with hydrogen peroxide diluted one-to-one with distilled water.

(4) Check appliances and sources of combustion. Stoves, heaters and dryers that burn fuel of any kind may generate carbon monoxide and nitrogen dioxide. If the appliance is improperly maintained or vented, carbon monoxide poisoning can occur. Acute carbon monoxide exposure can cause death by asphyxiation, heart attacks, headache, lethargy, hyperactivity, irritability, confusion, bizarre behavior, shortness of breath, chest pain, nausea, blackout spells and seizures. Acute poisoning may be followed by evidence of brain damage two to four weeks later. The delayed symptoms include memory loss, unclear speech, visual disturbances, unsteady gait and personality changes. Chronic low grade exposure may cause subtle deterioration in mental function and hearing loss. Sometimes the first signs of carbon monoxide toxicity in the home are morning headache or dizziness and difficulty concentrating. Information on low-cost carbon monoxide detectors is available from the Consumer Products Safety Commission (800-638-2772).

Nitrogen dioxide is a respiratory tract irritant that can cause sore throat or cough and increase the rate at which allergies develop. It has been shown to increase the spread of cancer in experimental animals. Its main indoor sources are appliances that burn natural gas and kerosene space heaters. Nitrogen dioxide emissions in homes are greatly reduced by venting appliances to the outside and by the electrical ignition of gas stoves rather than the use of a pilot light.

(5) Reduce formaldehyde levels. Because of the extensive use of building materials and furnishings which release it, formaldehyde exposure is almost inescapable in modern indoor environments. The greatest levels are given off by the glue which holds together fiberboard, particleboard, and plywood panelling. New houses with particle board sub-flooring and mobile homes are loaded with formaldehyde. Although formaldehyde emission eases with time, high humidity or moisture disintegrates the glue and increases formaldehyde release. Formaldehyde is used to stiffen fabrics of all types, so that new clothing, carpeting and upholstered furniture may off-gas considerable formaldehyde for days or weeks. Other sources of formaldehyde in household air are foam insulation, urea-formaldehyde finish coatings on furniture and flooring, fresh latex paint, space heaters, new paper or plastic products of any type, and cosmetics (including nail polish, skin creams, and hair sprays).

Acute exposure to low doses of formaldehyde may cause burning of the eyes, nose and throat, tearing, nausea, dizziness, cough, chest pain and shortness of breath. Chronic exposure has been causally associated with headache, drowsiness, memory loss, menstrual irregularities and two types of human cancer.

Testing for formaldehyde in home air should be done when all doors and windows are closed and heat and humidity are high, to eliminate false negative readings. When the source of formaldehyde cannot be removed (e.g. in mobile homes), surface treatments to seal pressed-wood sources may significantly reduce emissions.

(6) Volatile Organic Compounds (VOCs). These are invisible gases which are emitted from paints, adhesives, carpeting, wall coverings, new furniture, building materials, solvents, cleaning solutions, copy machines, and laser printers. Studies using experimental chambers have shown that VOCs can cause irritation of the respiratory system in humans and animals at levels which are one hundred times weaker than the World Health Organization Indoor Air Guidelines. Controlled experiments with people who suffer from Sick Building Syndrome confirm that VOC exposure can also cause headache, fatigue and difficulty concentrating. Dozens of VOCs have been identified in residential air. Some of the VOCs found in indoor air, such as benzene derivatives, may promote cancer in humans. Concern over the safety of cleaning solutions and VOCs has created a demand for less toxic alternatives. Information about these products can be obtained from sources in listed in the appendix of The Four Pillars of Healing. Good dust control (as described in section 2 above) will lower VOC levels, because dust particles absorb VOCs and increase their concentration in the air.

(8) Purify your water. Chlorination of municipal water supplies was first introduced in Jersey City, New Jersey, in 1908. It dramatically reduced the death rate from typhoid fever, a bacterial infection which is spread through drinking water. But chlorination has drawbacks. Chlorine reacts with organic matter dissolved in water to form cancer-promoting substances like the trihalomethanes (THMs), of which the best known is chloroform. Drinking chlorinated water increases the risk of developing cancer of the rectum or the bladder, the risk increasing the more water is drunk. THMs are volatile; they evaporate from water during cooking or when showers are running and contaminate the air in homes. A preventive solution: filter your tapwater through activated charcoal, which removes the vast bulk of chlorinated compounds, before you boil it. Shower-head filters that remove chlorine will help to prevent the release of chloroform gas during hot showers.

(9) Refresh the air in your home/office. Laser printers, copiers and fax machines all release VOCs into the air when they operate. Maintain a source of fresh air, like an open window, and run an exhaust fan or an air purifier that contains a charcoal filter. Ordinary air purifiers remove dust and pollen but not chemicals. Don’t make yourself a victim.

The signs of vascular disease appear on the legs as loss of hair, thinning and atrophy of the skin, non-healing sores, or even blackened toes from gangrene, and pain on exercise. In the heart, the signs are pain or pressure in the chest, shortness of breath or unusual fatigue. It can also affect the brain, causing loss of memory and confusion, momentary lapses of consciousness (sometimes called a TIA, or transient ischemic attack), or eventually strokes.

One of the most effective treatments for arteriosclerosis is being ignored and even maligned by mainstream practitioners. This treatment is known as chelation therapy, and it has been a successful treatment for over forty years. What is chelation therapy all about?

EDTA (Ethylene diamine tetra acetic acid) is a synthetic amino acid which has the ability to attach itself to metals and minerals, forming a particular kind of bond called a chelate, from the Greek word for claw. Heavy metals have a great affinity for EDTA and form strong bonds.

In the 1950’s, EDTA was found to be an effective treatment for lead toxicity. In many cases, patients who coincidentally had symptoms of heart disease, such as angina, improved while undergoing treatment. Since that time, a number of studies have confirmed the effectiveness of chelation therapy for blood vessel disease, including improved blood flow to the heart, the legs and the brain. They have been published in reputable journals by experienced physicians and medical researchers.

Two events slowed down the growing use of EDTA in traditional medical settings. The patent on EDTA expired in the 1960’s. Drug companies no longer had incentives to pursue or finance studies on the drug. The development of the heart-lung machine allowing open-heart surgery paved the way for more mechanical solutions to heart disease. Coronary artery bypass surgery has become a multi-billion dollar industry, including numerous unnecessary procedures. Estimates are that 50-75% of the surgery being done is unnecessary. Other studies show that non-surgical treatment is better than surgery.

The exact action of EDTA in improving blood vessel disease is not clear, and it probably works by several mechanisms. One effect of EDTA is to bind calcium in the blood stream, and alter the intracellular balance of calcium with magnesium. Calcium accumulates inside the cells with age, and this excess can disrupt enzyme systems. Pushing more magnesium into cells allows them to relax, and this opens up the circulation. There are also several other potential mechanisms of action.

One theory of aging and degenerative disease is the “free-radical theory.” Free radicals are highly active molecular fragments formed during the production of energy in the cells. They have high energy, like sparks in a fireplace, and this energy can be used by the body, when properly handled. However, if these free radicals get out of control they can cause damage to surrounding tissues, just as sparks that get out of the fireplace can cause the rug to catch fire. Excess free radicals contribute to the obvious signs of aging such as wrinkling and loss of elasticity of the skin, and the deposition of age pigment (commonly called liver spots). Internal damage, such as heart disease and cancer, is less visible but even more serious.

In addition to the formation of free radicals in the body, you are exposed to them in the environment. They are found in cigarette smoke in high amounts, and also in polluted air. (Large numbers of people who do not smoke have been found to have significant levels of cotinine, a nicotine derivative, in their blood, in most cases even if they do not live with a smoker. ) Free radicals are produced by radiation and rancid oils, by hydrogenated oil such as those found in margarine and shortening, and by ultraviolet light, and many therapeutic drugs increase metabolism and the action of liver enzymes that can increase free radicals.

Heavy metals cause direct toxicity to tissues, poisoning enzyme systems and especially affecting the nervous system. One of the most interesting properties of EDTA is the removal of lead and other metals. Iron is a transition metal, and it accumulates in the body with age and dietary excess, especially from meat. Excess accumulation of iron leads to the production of free radicals. Heavy metals are directly toxic. Removal of iron and heavy metals with chelation is thought to help prevent and reverse the tissue damage of a variety of diseases, including vascular disease.

Free radicals, with their high energy levels, are thought to contribute to the development of heart disease, cancer, arthritis, and certain immune system disorders. A study in Zurich, Switzerland showed a markedly lower incidence of cancer among patients who had received chelation therapy. This makes a strong case for chelation inhibiting free radicals.

For protection from free radicals, your body has a number of defenses. You produce enzymes that are free radical scavengers, such as superoxide dismutase, glutathione peroxidase, and catalase. These require trace mineral cofactors such as zinc, manganese, selenium, and copper. Many other nutrients are also anti-oxidant free-radical scavengers. These include vitamins C and E, beta-carotene, bioflavonoids and other plant pigments, coenzyme Q10, and sulfur-containing amino acids such as cysteine and methionine. These protect you from aging and degeneration. A comprehensive approach to treatment is more effective than any one treatment alone. This includes diet, exercise and stress management, as well as dietary supplements.

The nutritional components of a treatment program using EDTA chelation play several roles. One is the above-mentioned supportive role in the free-radical scavenging activity of chelation. Other nutrients act to help with vascular disease in different ways. For example, the B-vitamins folic acid, pyridoxine (B6), cobalamin (B12), and betaine help to lower blood levels of homocysteine, a metabolite implicated in higher rates of vascular disease. Coenzyme Q10 also helps directly with heart muscle function and lowering blood pressure. Hawthorne berry extracts act similarly. Supplements of the amino acid taurine help to increase the strength of the heart muscle.

Another role of dietary supplements is to replace those that are removed by the chelation itself. Because EDTA binds with minerals, it removes some of those that you want to keep. Chelation treatments remove large amounts of zinc and manganese, and these need to be replaced with supplements in order to assure the safety of chelation treatment. Chelation reduces vitamin B6 levels, and supplements help are essential.

Although most patients are treated with chelation for vascular disease, it has many other benefits, as well as a value as preventive medicine. Specific benefits are found in diabetic arterial disease, macular degeneration, decreased mental function from vascular disease, osteoporosis, intermittent claudication (leg pain on exercise), scleroderma, and other conditions.

There have been no serious side effects from EDTA-chelation treatment since the 1950’s, when it was first being administered. We have learned much about the treatment since then, and it is now safely administered by physicians trained by the American College for Advancement in Medicine (ACAM). There is a specific, safe protocol for EDTA-chelation administration.

Doctors critical of chelation therapy are usually unfamiliar with the literature and have no experience with the treatment in practice. Studies are in the design and production phases to further document the value of chelation for these controversial uses. A protocol sanctioned by the FDA was being conducted at army hospitals but for a variety of reasons it was stopped. Other studies have also been mysteriously blocked when they were well on their way to implementation.

The recent (1994) study from New Zealand on chelation and peripheral vascular disease does not discredit chelation therapy, although that was the conclusion of the authors. In that small study, which was mainly of smokers with severe disease, the “placebo” group actually received effective intravenous chelating agents-vitamin B1 and vitamin C–although weaker than EDTA. Sixty per cent of both groups improved. That is a large number for placebo effect, and argues that the control group received some effective agents. In five of the evaluations, the EDTA group did significantly better than the control group after only 20 treatments-too few for smokers with severe disease. None of the tests were better in the control group. Even the conservative Harvard Heart Letter said that “this study is unlikely to lay the chelation controversy to rest,” and rightly so, since the results showed benefits from chelation. (Statistically, there was one “outlier” in the control group. Removing his aberrant results from the evaluation, shows that the EDTA group did remarkably better than the controls.)

For further information, I recommend Bypassing Bypass by Elmer Cranton, MD, an in depth look at chelation with a chapter on free radical theory. My own booklet on the subject is shorter but still gives a good overview. It will be a Good Health Guide published by Keats Publishing when it comes out in June of 1998.

Heart disease is the number one killer in America. Bypass surgery is expensive and risky, and has not been shown to be of clear benefit for the majority of patients who have bypasses. It is important to consider the value of chelation therapy, which has so many direct and side benefits with so few negative side effects. If you have vascular disease, it would be worthwhile to look for a doctor who does chelation therapy as part of a comprehensive approach to treatment. You can find one through the American College for Advancement in Medicine (800-532-3688, or on the web at http://www.acam.org).

Michael Janson, M.D. is the Past President of both the American College for Advancement in Medicine (ACAM), and the American Preventive Medical Association (now the American Association for Health Freedom), and he is a charter member of the American Holistic Medical Association. He is the author of The Vitamin Revolution in Health Care (1996, Arcadia Press), Chelation Therapy and Your Health, All About Saw Palmetto and Prostate Health, and Dr. Janson’s New Vitamin Revolution. He publishes a
monthly newsletter, Dr. Michael Janson’s Healthy Living, available for free by Email (newsletter@drjanson.com). Dr. Janson is an international professional speaker on the subject of health and nutrition, dietary supplements and alternatives in medicine.
He practices in Arlington, Massachusetts (781-641-1901). You can find more information at his website: http://www.drjanson.com.

2 Meltzer LE; Ural E; Kitchell JR. The Treatment of Coronary Artery Heart Disease with Disodium EDTA, Metal-Binding in Medicine, 132, Seven MJ (Ed), 1960, JB Lippincott Philadelphia.

3 Cranton EM; Frackelton JP. Current Status of EDTA Chelation Therapy in Occlusive Arterial Disease, J Adv Med, Spring/Summer 1989, 2(1/2):107-19.

4 Chappell LT, Stahl JP. The correlation between EDTA chelation therapy and improvement in cardiovascular function: a meta-analysis. J Adv Med 1993; 6: 139-160.

5 Olszewer E, Carter JP. EDTA chelation therapy in chronic degenerative disease. Med Hypoth 1988; 27:41-49.

6 Casdorph HR. EDTA chelation therapy: efficacy in arteriosclerotic heart disease J Hol Med 1981; 3:53-59.

7 Graboys TB, Biegelsen B, Lampert S, Blatt CM, Lown B. Results of a second-opinion program for coronary artery bypass grafting surgery. JAMA 1987; 258: 1611-1614.

8 CASS principal investigators, et al., Coronary Artery Surgery Study (CASS): Circulation, Nov 1983; 68(5);939-950

9 Cranton EM, Frackelton JP. Free radical pathology in age-associated diseases: treatment with EDTA chelation, nutrition and antioxidants. J Hol Med 1984; 6: 6-37.

10 Pirkle JL, et al. Exposure of the US population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey, 1988 to 1991. JAMA, 1996 Apr 24; 275(16):1233-40

11 Blumer W, Cranton EM, Ninety percent reduction in cancer mortality after chelation therapy with EDTA. J Adv Med 1989; 2:183

12 Selhub J, et al. Association between plasma homocysteine concentrations and extracranial carotid-artery stenosis. N Engl J Med 1995 Feb 2;332(5):286-91

13 Langsjoen P, et al. Treatment of essential hypertension with coenzyme Q10. Mol Aspects Med 1994;15 Suppl():S265-72

14 Fujita T, Sato Y, The hypotensive effect of taurine. J Clin Invest 1988 Sep;82(3):993-7

15 Cranton EM; ed: A textbook on EDTA chelation therapy. J Adv Med 1989; 2: 1-416.

16 Ibid.

17 van Rij AM, et al., Chelation therapy for intermittent claudication. A double-blind, randomized, controlled trial. Circulation, 1994; 90:1194-1199