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The case for environmental triggers

MagazineSeptember 2003 (Vol. 14 Issue 6)The case for environmental triggers

Parkinson's disease (PD) is found throughout the world and is thought to affect one or two people in every 1000

Parkinson's disease (PD) is found throughout the world and is thought to affect one or two people in every 1000. It is named after William Parkinson, who first described it as 'the shaking palsy' in 1817.

So it's been around a long time, and critics of claims that environmental triggers, such as pesticides, play a crucial role in its onset have used this as their reason. The suspected pesticides were mostly not available in the past or were used on a smaller scale than today.

So what is the basis for the idea that 21st-century environmental triggers are involved?

PD mostly develops late in life. It affects 0.4 per cent of people aged 40-plus, and 1 per cent of those 65 and over (Merck Manual of Diagnosis and Therapy, 1999; section 14, chapter 179). Pope John Paul II is a high-profile example in this category.

But about 10 per cent of cases are in those in their late 20s and early 30s, like film actor Michael J. Fox and boxer Mohammed Ali, raising concern to new levels.

Although not a disease of childhood, many researchers believe that this could be when it first begins, with early exposures to 'environmental intoxicants' that continue throughout life (Lancet, 1986; ii: 1067-70).

It is worth noting that these 'environmental intoxicants' don't only mean pesticides, but also anything from ingested foods and liquids to the build-up of toxins from long-term medications to viral infections and air pollutants.

Yet, despite numerous studies of environmental factors in PD, as yet there is no definitive proof of a causal relationship.

What is known is that only 5 per cent of cases have an inheritance pattern suggesting a genetic defect. Work with pairs of twins has found that, while genetic factors may influence early-onset PD, where symptoms arise before age 50, they don't play a major overall role in causing the disease (JAMA, 1999; 281: 341-6).

The consensus is that, for the most part, PD develops over time if an inherited susceptibility meets continued environmental exposure to a toxin together with cell damage caused by toxic free radicals in the body, and possibly with accelerated ageing.

The big question is, which toxin or - more likely - toxins? And what are the mechanisms in the body that come into play?

Researchers from the US National Institute of Environmental Health Sciences are currently setting up a retrospective/prospective case-controlled study of 1200 people, including 400 with newly diagnosed idiopathic PD (where the cause is unknown), in three rural California counties.

The aim is to test whether susceptibility genes, such as those coding for the cytochrome P-450 superfamily, start changing form in individuals as a result of interaction with agricultural pesticides in the environment. The study started in September 2000 and should be completed by September 2005 (see www.clinicaltrials.gov/ct/gui/show/NCT00044590?order=28).

The findings should throw fresh light on earlier work strongly suggestive of an environmental involvement. Three studies stand out in particular.

In one, it was found that people living in farming communities who drink water from wells, and have a history of exposure to pesticides and herbicides (though fungicides were given the all-clear), are more likely to develop PD (Neurology, 1998; 50: 1346-50).

It has also been revealed that those who die of PD have higher levels of organochlorine pesticides in the brain compared with the general population.

Moreover, in the early 1980s, a group of young people who had injected the illegal designer drug MPTP developed Parkinson-like symptoms. MPTP interferes with dopamine-producing mitochondria in the brain, and has a structure similar to some herbicides and pesticides; the structure of its metabolite is also similar to the herbicide paraquat (Science, 1983; 219: 979-80; Ann Neurol, 1999; 46: 598-605).

It's not only agricultural-use pesticides that have been investigated. A keynote study at Emory University in Atlanta, Georgia, looked at the effect of intravenous doses of rotenone (derris root), repeated for up to five weeks, on rats and found that the animals not only developed the characteristic symptoms of PD - trembling and loss of muscle control - but also acquired the specific microscopic fibrous tangled deposits in the brain known as Lewy bodies, considered a sure sign of the disease (Nature Neurosci, 2000; 3: 1301-6).

True, the researchers accept that feeding rats intravenous rotenone is not exactly how humans handle the poison - so these findings cannot be directly applied to people - but it does confirm the likelihood that low levels of chronic exposure to a common pesticide can reproduce the range of features seen in PD.

Nevertheless, the data are useful. The researchers suspect that mitochondria, the energy-producing components of every cell in the body, produce toxic waste in the form of free radicals as they generate this energy, and that these free radicals move throughout the body, wreaking havoc as they go. Free radicals have been implicated in a number of diseases such as cancer, heart disease and neurodegenerative disorders, including Lou Gehrig's disease (amyotrophic lateral sclerosis) and Alzheimer's dementia as well as chronic degenerative disorders like arthritis, hypertension and diabetes.

There's also a shock element within the findings. Powdered derris root, from a tropical plant, was used on an industrial scale from the mid-19th century onwards and, in some countries, for even longer. Today, it is thought of as a traditional insecticide and a natural plant extract, but 'natural' doesn't always mean safe.

Even insecticides for indoor plants may be implicated in PD. According to research carried out at Stanford University, California, individuals exposed to sprayed insecticides in the home were more than twice as likely to develop PD than those who were not exposed. There is also a small, but still increased, risk due to exposure to herbicides in the garden. However, garden insecticides and fungicides did not appear to be associated with PD (paper presented at the Annual Meeting of the American Academy of Neurology, San Diego, May 2000).

There may also be an added risk when two or more chemicals, used for different purposes, interact, as so often happens in the real world. A study at the University of Rochester, New York, examined the effects on mice of the widely used agricultural herbicide paraquat and the fungicide maneb, both of which are applied to millions of acres of farmland around the world each year, and already known to affect the neurotransmitter network in these animals.

It was found that moderate exposure to each chemical on its own had little effect. But, in combination, they produced a pattern of brain disorders similar to that seen in PD sufferers (J Neurosci, 2000; 20: 9207-14).

The findings prompted the lead author, Deborah Cory-Slechta, to suggest that the ongoing environmental investigations on the health effects of pesticides also include the potential hazards of exposure to combined pesticides - incredibly, something that the US EPA (Environmental Protection Agency) has never done.

Some studies are looking at the role of human gene proteins, such as alpha-synuclein, in the brain. This is a major component of the Lewy bodies characteristically found in the brain of people with PD.

One group at the University of California, San Diego, used mice that were genetically manipulated and bred to express this protein. Subsequent generations of these mice consistently developed PD-type symptoms (www.sciencemag.org, February 2000).

Another study from Virginia found that exposure to tiny amounts of the insecticide permethrin, used to treat clothing to repel and kill ticks and mosquitoes, was sufficient to reduce dopamine levels in the brain and increase production of alpha-synuclein. However, although the mice showed PD-like symptoms, none went on to develop the full-blown disease (paper presented at a meeting of the American Chemical Society, March 2003).

Evidence is also mounting that what we eat may act as an environmental trigger. Researchers at the University of Hawaii have found a link between high consumption of fruit and fruit juice, and PD in middle-aged men. Those who ate more than three servings a day had a 70 per cent higher risk of PD, while those consuming one or more servings a day had an increased risk of 55 per cent. However, there was no increased risk for men with a high vitamin C intake from their diet or supplements.

The researchers emphasise that it is unlikely that fruit per se is the problem but, rather, the increased risk may be a marker of exposure to residual pesticides. Also, these findings were based on data starting from 1965, when pesticides were more persistent than those used nowadays. So, continue eating fruit - just make sure it is thoroughly washed, and only drink juice from organic sources (paper presented at the Annual Meeting of the American Academy of Neurology, Honolulu, April 2003).

Besides pesticides, other chemical substances have been linked to PD, including aspartame. This artificial sweetener is found in 6000 processed food products, such as hydrolysed vegetable protein and carbonated soft drinks, and is also used as a low-calorie sugar substitute (NutraSweet) in coffee and tea. A dipeptide, it is made up of L-phenylalanine
(50 per cent) and aspartic acid (40 per cent) plus methanol
(10 per cent).

It has been characterised as an excitotoxin by campaigners in the US such as Betty Martini of Mission Possible International. Excitotoxins (usually amino acids) act upon certain receptors in the brain so as to cause damage to certain brain cells. It is well known that excitotoxins like glutamate and aspartate can cause irreversible brain damage in animals (J Neuropathol Exp Neurol, 1972; 31: 464-88; Neurobehav Toxicol Teratol, 1980; 2: 125-9).

The work of neurosurgeon Russell L. Blaylock, an expert on brain and nervous system toxins, has contributed to the theory of aspartame's effect on the brain. Blaylock argues that high daily intake of aspartame nowadays results in very high levels of aspartate, a part of the aspartame molecule that acts as an excitatory neurotransmitter. Not only can this damage the blood-brain barrier, designed to protect the brain from toxins, but also aspartate, along with glutamate, can actually open the barrier, he says.

Within the brain, Blaylock continues, high intakes of food excitotoxins, including aspartate, can overwhelm the glutamate-transport system, which stores these molecules in special cells. As a result, excitotoxins accumulate in the brain and generate large numbers of free radicals that damage brain and nerve cells. And, of course, free radicals are associated with PD. The effects are not dramatic, but accumulate over time.

In the main, the evidence for a possible role of aspartame in PD is circumstantial and anecdotal. It is primarily based on animal studies as well as on the testimonials of many PD patients who have themselves observed an association between a high ingestion of the sweetener and the severity of their symptoms.

Many patients post stories online at both Mission Possible and the Aspartame Toxicity Information Center, claiming that once they gave up the sweetener, their condition improved. 'I was in the habit of taking my levodopa and washing it down with artificially sweetened blackcurrant .. . . I switched to the sugar-sweetened variety and all my PD symptoms were diminished - in some cases to the point of eradication,' wrote one.

Although hard evidence of this association has yet to be seen, there is research to suggest a possible role of aspartame in causing the disease, worsening its effects or interfering with medication.

Besides Blaylock's concept of excitotoxins, another theory of a possible link between aspartame and PD relates to the methanol component of aspartame, which is metabolised to formaldehyde. Chronic exposure to formaldehyde at even low doses can cause immune and nervous system changes (J Occup Med, 1983; 25: 896-900).

Yet a third theory for an effect of aspartame on PD is that levodopa, the amino acid deficient in PD patients and given as a drug, is carried to the brain on the same pathway as phenylalanine. High levels of the latter could be blocking passage of the drug. Furthermore, the phenylalanine from aspartame is not bound to any protein, so causing blood levels of phenylalanine to dramatically spike upwards (J Pediatr, 1986; 190: 668-71; Metabolism, 1987; 36: 507-12).

One study of nerve cell cultures has shown that aspartame can cause severe cell damage (Neuroreport, 1995; 6: 318-20).

A study examining whether aspartame interferes with levodopa uptake involved 18 PD patients given, on alternate days, either large doses of aspartame or a placebo. Though their blood levels of phenylalanine did significantly increase, there was no effect on motor performance. The conclusion was that, even at huge doses, aspartame had no adverse effect on PD patients (Neurology, 1993; 43: 611-3).

Critics point to the fact that the study lasted only a few days whereas the neurological effects of the sweetener only appear after medium- or long-term use (J Appl Nutr, 1988; 40: 85-94). They also claim that the doses given were low (only 20-40 per cent of FDA acceptable daily limits) and supplied via capsules, which don't cause the sudden spiking of phenylalanine seen when taken as a sweetener.

This divided opinion only underscores the ongoing questions raised according to who is doing the testing. Ralph G. Walton, chairman of the Center for Behavioral Medicine at the Department of Psychiatry in Northeastern Ohio Universities College of Medicine, examined the source of funding of all studies examining the safety of aspartame. Of the studies considered relevant, he writes, 74 were funded by the aspartame industry and 92 were independent. Of the industry-sponsored studies, he found that every single one concluded that aspartame was safe. In contrast, of the non-industry studies, 84 of the 91 (92 per cent) concluded that aspartame may pose a health problem. As Walton himself understatedly noted: 'The clear split in the literature, with outcome correlated so closely to funding source, is deeply troubling' (www.dorway.com/peerrev.html).

Clearly, what is needed is an independent analysis of the effects of aspartame on the brain.

In the meantime, it may be prudent for anyone with a history of nervous system disorders in the family to steer clear of artificial sweeteners and pesticides - sensible advice for all the rest of us as well.
Deanna Wilson
with additional reporting by Lynne McTaggart and Megan McAuliffe


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