Researchers from the London School of Hygiene and Tropical Medicine have confirmed an earlier study that the drug can be dangerous. However, they wouldn’t go as far as to say, as the earlier study did, that it increased the risk of death by 50 per cent.

The research team had been asked by the Medicines Control Agency, which monitors drug safety, to investigate the drug, following alarming findings made by the Parkinson’s Disease Research Group.

The group had found the mortality rate increased by 50 per cent in patients treated with selegiline and levodopa, compared with patients treated only with levodopa.

The new research team investigated the records of 12,621 patients who had been prescribed an anti parkinsonian drug.

In all, 1,720 of the patients died, and there was a “non significant” 11 per cent increase in the risk of death among patients taking selegiline with or without levodopa.

This risk increased among patients younger than 80 years, and who were taking selegiline alone (BMJ, 1998; 317: 252-4).

This investigation had some grounding in human experience. In the 1980s, a number of heroin users developed irreversible symptoms of Parkinson’s after injecting themselves with a batch of MPTP contaminated heroin.

MPTP acts in a similar way to rotenone it inhibits complex I (the NADH de-hydrogenase complex), an enzyme involved in the development of Parkinson’s.

More study is needed, but the researchers note that, within 24 hours of the study results being made public, they were contacted by two Parkinson’s patients who had also been exposed to rotenone on a regular basis (Lancet, 2000; 356; 1659).

Researchers from Harvard School of Public Health found that men who ate 2.9 or more servings of dairy products a day had a far higher risk of developing Parkinson’s than those who ate less than one serving a day. The link gets stronger over time, and seems to peak after six years of eating dairy. (Source: Annals of Nuerology, 2002; 52: 793-801).

Another supplement that may slow Parkinson’s is the coenzyme Q10. It was tested at a daily dose of 300, 600 and 1,200 mg against a placebo and, perhaps not surprisingly, the highest dose was the most effective at slowing the disease.

Those in the placebo group saw their disease worsen by 12 points, as measured on a rating scale, over 16 months, while those taking 300 mg of Q10 saw their score worsen by 8.8 points, the 600 mg group by 10.8 points, but the 1,200 mg group by just 6.7 points, nearly half that of the placebo group.

It would be interesting to see the effect of combining Q10 with vitamins C and E – provided we can buy the potency.

(Source: Archives of Neurology, 2002; 59: 1541-50).

A:Typically, doctors aren’t happy unless they’re engaged in major life-

and-death solutions. In Parkinson’s, a group of cells in the brain degenerates. These cells are responsible for producing dopamine, a brain chemical which transmits instructions from the brain to nerves controlling movement. As the cells degenerate and dopamine levels fall, so movement becomes more involuntary and difficult. Attempts have been tried by many international research teams to implant tissue containing dopamine neurons in the brains of patients with Parkinson’s disease, demonstrating moderate improvement in studies reported in 1987. However, subsequent studies showed that the grafted material didn’t survive well in humans, although it did so in animals.

Late last month, scientists were aflutter with the publication of a study of the successful implantation of dopamine producing cells from aborted fetuses in a 59-year-old man with Parkinson’s disease (New Eng J of Med, April 27, 1995). The man received implants from seven fetal donors during two operations (48 fetal grafts in all). Between one and three months later, clinical improvement in motor behaviour was noted and continued up to 15 months. Advanced scanning techniques showed not only that the graft had survived but also that regions of the brain had new cells. Although the patient died from a pulmonary blood clot 18 months after the operation (no one bothered to ask if there might be a connection), the pathology report showed that the grafts had survived and that brain tissue had grown normally.

Besides our ignorance over whether grafts can last longer or prove safe, we also don’t know if the grafts can prevent the progression of the disease or if they will eventually succumb as well. It’s also important to note that although patients with transplants were able to reduce their medication, thus far, no patient had been able to come off it entirely. This all signals that surgeons are very much at the drawing board stage with this experimental operation.

Besides messing around with fetal tissue (with its ethical implications), researchers at King’s College in London have been experimenting with such solutions as engineering the herpes virus to make dopamine, because of its ability to last indefinitely. At the moment, scientists have a long way to go, as the engineered virus is potentially fatal.

The orthodox possibilities for Parkinson’s victims are no less grim. Because dopamine derives from L-dopa, an amino acid, the standard treatment is to give patients L-dopa, or levadopa, which tends to restore dopamine levels to normal and lessens parkinsonian symptoms. However, this improvement also has its price; patients on L-dopa develop nausea or vomiting, postural hypotension (fainting on getting up), sweating attacks, psychotic symptoms like hallucinations, delusions and confusion, and, most ironically, motor difficulties and involuntary movements the very thing they’re being treated for! For all these reasons, the latest advice is that levodopa be delayed until a patient is over 70 (BMJ, March 4, 1995). (See drug of the Month, p 7.)

A popular choice for early Parkinson’s are the anticholinergic drugs (benzhexol and orphenadrine). These drugs, which are more mild than L-dopa, are more effective for tremor, rather than other symptoms, although patients can worsen considerably if the drugs are suddenly withdrawn. The side effects include blurred vision, dry mouth, constipation, retention of urine and possibly worsening of some of the movement disorders (BMJ, March 4, 1995).

The third main category are dopamine agonists (bromocriptine and pergolide), which act on the dopamine receptors of the brain. They can prevent nausea (although initially they cause it), but also have worse psychotic side effects than L-dopa and cause sudden lowering of blood pressure, which poses a considerable risk of hip fracture in a patient who is unstable at the best of times.

Selegiline is one of a number of enzymes which help to metabolize L-dopa and have it last longer, although, again, it makes psychiatric and movement side effects worse. Risperidone has been suggested as a drug to take care of some of the psychiatric side effects of L-dopa (The Lancet, May 28, 1994).

Given this line-up of debatable options, nutritional doctors like WDDTY panel member Melvyn Werbach offer a better approach. He notes that since L-dopa must compete with other amino acids for transport from the blood to the brain, it makes sense to limit protein, from which amino acids are derived, to lessen the competition. In several studies, he says, protein restriction has made L-dopa more effective and lessened the “on-off” effect, where people do better at certain times of the day.

Dr Werbach suggests that you restrict your daily intake of protein to 0.12 oz per lb of body weight, and serve 90 per cent of this with your evening meal.

Other suggestions include supplementing with folic acid (a deficiency can cause Parkinson’s disease), niacin, B6, vitamin C, vitamin E, iron,

omega-6 fatty acids (and watching for excessive intake of manganese).

L-tryptophan, another amino acid, prevents some of the side effects of L-dopa, or you can use L-tyrosine as a substitute for L-dopa when side effects are severe.

Also check for mercury or other industrial heavy-metal poisoning, which has been implicated in Parkinson’s disease (Movement Disorders, 1993, 8(1): 87-92).

A:As you know, Parkinson’s disease is a nervous system disorder in which sufferers have trouble controlling or initiating movement. It’s due to degeneration of that part of the brain that controls movement, causing a disorder in the production of dopamine, one of the brain chemicals used to transmit messages which works in balance with another chemical message transmitter, acetylecholine.

The drugs used to treat parkinsonian symptoms like Sinemet contain levodopa, a substance the body uses to make dopamine. Modern treatment therefore seeks to replace dopamine in the body, which suppresses parkinsonian symptoms, but doesn’t cure the disease.

The problem with taking levadopa orally is that this conversion process happens too quickly in the body, before it can get to the brain. Consequently, some modern drugs like Sinemet combine levadopa with carbidopa, to inhibit the speed of the conversion process. The benefit of this kind of drug is that it reduces the ordinarily high dosage of levadopa necessary to do the job. But whether taken in high or lower dosages, levadopa has a number of extremely harmful side effects; indeed, a majority of people taking the drug develop some side effects; Du Pont Pharmaceuticals, which manufactures the drug in Britain, recommends in the Data Sheet Compendium that patients should be carefully monitored and the dosage adjusted until they stop having side effects.

The most common side effects of Sinemet are, ironically, dyskinesias, or involuntary movements the same problems the drug is trying to cure! If your husband developed these symptoms or the usual problems of nausea and vomiting, this would be an early alert that he was being given too much drug.

According to Peter Parish, author of Medical Treatments: the Benefits and Risks (Penguin, 1991) , patients taking this drug over time should be given regular tests for liver and kidney function, blood counts, ECG and other medical checkups, particularly since the dosage can be tailored to individual needs. Therefore, your doctor was remiss in not monitoring your husband more carefully, before he developed hepatitis. We’re also surprised that your doctor didn’t recommend an anticholinergic drug (which reduces the level of the acetylcholine chemical).

One suggestion is for him to try a nutritional approach. Patients with Parkinson’s disease can improve with supplements of vitamin B6.

So how do you then treat the drug induced psychosis? With drugs of course! Researchers tested the antipsychotic drug clozapine on a group of 60 Parkinson’s patients who, at daily doses of 50 mg, saw their psychoses improve.

Of course, clozapine doesn’t come without its own side effects, such as weight gain and agranulocytosis, an acute blood disorder. So all we need now is a drug that successfully treats agranulocytosis. . .

They have discovered that smokers are 50 per cent less likely to develop Parkinson’s than non smokers. And the same is true of people who drink alcohol or coffee.

But medicine isn’t about to rewrite the rulebook on healthy lifestyles. Smoking and drinking are indicative of addictive behaviour, and it is higher levels of endogenous dopamine which triggers addictions and act as a preventative to Alzheimer’s and Parkinson’s, Patricia Willems-Giesbergen, from Erasmus University in Rotterdam, told delegates at the Annual Meeting of the American Academy of Neurology.

It also suggests that life, even at the end, is kind. If you’ve had a boring life, you won’t remember it. . .

Twelve patients with advanced Parkinson’s, whose disabilities cannot be controlled any longer by drugs such as levodopa, were given the transplants in a trial overseen by the Boston Medical Center in the USA.

One year after the transplants, the patients have been recording an average 19 per cent improvement on a Parkinson’s rating.

Rumours, however, that they also enjoy rolling in straw and have replaced dinner plates with a trough have been discounted (Neurology, 2000; 54: 1042-50).