It is likely that someone you know has Parkinson's disease. If not, it's likely you will, as it's a condition on the rise. PD is now the second-most-common neurodegenerative disorder in the United States. Currently, PD affects approximately 500,000 people in the U.S., with 50,000 new cases diagnosed each year.
Most afflicted individuals are older, with onset usually occurring in one's late 50s to early 60s. In fact, symptoms of PD are seen in up to 15 percent of men and women age 65 to 74, and almost 30 percent of those age 75 to 84.
Although conventional treatments tend to improve symptoms in the early stages of the disease, they generally lose their effectiveness over time and can also have significant side effects.
To understand what can be done to prevent and possibly treat PD with natural therapies, it helps to know a bit more about the disease itself. PD is defined as a progressive movement disorder. Its hallmark symptoms are tremors (particularly at rest), rigidity, slowed movements and, eventually, difficulty walking and accomplishing various activities of daily living. These changes occur because certain brain cells (dopaminergic neuronal cells located in the substantia nigra area of the brain) that control these functions die. The reasons for the death of these neurons are not completely understood, but multiple factors appear to be involved, most likely a combination of environmental toxins in genetically susceptible individuals.
It appears that some people, because of an inherited trait, are more sensitive to low levels of certain toxins. Over time, the toxin destroys more and more of these specific dopaminergic neurons. Because it is cumulative damage, the longer we live, the more likely we are to develop this disease. PD is therefore sometimes called a long-term latency disease. The processes that cause this destruction involve inflammation and oxidative stress. Studies show that nutritional therapies that decrease these processes help reduce PD.1
Environmental risk factors in Parkinson's disease
There is little question that environmental toxins increase the likelihood of PD. Exposure to toxins in well water and pesticides are two of the most probable sources. Animal evidence suggests pesticides can selectively injure the neurons of the dopaminergic system.2 Living in rural areas is also a risk factor, probably because it increases exposure to these toxins. A meta-analysis performed a few years ago calculated environmental risks for PD, and showed independent correlations for several factors. In the U.S., the highest risk was for individuals living in rural areas for more than 40 years; they had almost five times the risk, likely indicating that cumulative exposure to toxins over time is required to develop the disease. The odds for developing PD were almost 1.5 times higher for those who drank well water. For chronic pesticide exposure, the risk for PD was doubled. The longer the exposure to pesticides, the greater the risk; however, no specific type of pesticide has been clearly identified as posing a risk for PD.3, 4 A history of exposure to heavy metals may increase the risk of PD as well.5
Dietary influences in Parkinson's disease
Dietary influences appear to play a significant role in the development of PD. Because oxidative stress and free-radical generation appear to be an underlying cause of PD1, some researchers have suggested that dietary antioxidants may provide protection. Confirming this, however, has been a controversial and complicated task. A study 10 years ago first suggested that a high intake of dietary vitamin E may protect against the occurrence of PD.6 A more recent meta-analysis confirmed that dietary sources of vitamin E have a protective role; however, dietary levels of vitamin C and beta-carotene did not seem to have any protective effect.7 (While vitamin E in the diet may be important, as we will see later, supplemental vitamin E studies have been disappointingly negative).
If some antioxidants afford protection, it would make sense that pro-oxidants—substances that increase free-radical generation—may have a deleterious effect. A recent case-controlled study suggested just that. Individuals with PD were matched to those without. The subjects with the highest iron intake were 1.7 times more likely to have PD compared with those who had the lowest intake. Too much iron is widely understood to produce free radicals. There was an apparent joint effect of iron and manganese (another pro-oxidant at high levels); above-average dietary intake for both together conferred a nearly doubled risk for PD compared with lower intakes of each nutrient.8
Another study examined the relationship between milk and calcium intake and the risk of PD. After adjustment for other factors, there was a 2.3-fold increased risk of PD in the group with the highest intake of milk (more than 16 oz per day) versus those who consumed no milk. Calcium from other dairy and nondairy sources had no apparent relation with the risk of PD.9 High intake of carbohydrates also seemed to increase the risk of PD; however, a diet higher in polyunsaturated fats appeared protective.10
Other dietary factors may be at work as well. A long-term observational study on males suggested that body fat and constipation were also risk factors.10 Being overweight is associated with increased inflammation,11 which is a PD trigger. The researchers in this study found that after adjustment for various other risk factors in PD, men with less than one bowel movement a day had a 2.7-times higher risk of PD versus men with one bowel movement daily. And compared with men who had two bowel movements daily, those who had fewer than one a day had a four times greater risk of PD.12
Perhaps the most interesting work on dietary factors in PD are the studies looking at caffeine. There is good evidence that people who consume caffeinated beverages have a decreased risk of PD. Similar relationships were observed with total caffeine intake and caffeine from noncoffee sources. When the researchers looked at coffee, it appeared the mechanism was related to caffeine intake and not to other nutrients or phytochemicals contained in coffee.13
For men, the effects seem to be dose-related. Men consuming between 400 mg and 2,800 mg of caffeine (from any source) on a daily basis seem to have the greatest reduction in risk. However, even drinking 100 mg to 200 mg a day had a positive effect. A 5 oz cup of coffee contains an average of 65 mg to 115 mg of caffeine, according to the International Coffee Organization. In women, the association with caffeine seems dependent on postmenopausal estrogen use. It appears that caffeine reduces the risk of PD, but that effect may be prevented by use of estrogen replacement therapy.14 One study looked to quantify the amount of caffeine, and suggested that drinking 3 cups of coffee or tea daily for 10 years would lead to a 22 percent to 28 percent risk reduction of PD.5 So while caffeine often gets a bad rap—and some people, such as pregnant women, should avoid excessive caffeine, there is a positive side as well.
Cigarette smoking also appears to have an upside in this regard. This same study linked smoking three packs of cigarettes a day for 10 years with a 62 percent decreased risk of PD.5 Other studies have confirmed this.15 However, in this case, the benefit doesn't come close to canceling out the potential risks.
Supplementation in Parkinson's disease
Antioxidants. Three primary antioxidant supplements have been studied for use in the prevention or treatment of PD: tocopherol (vitamin E), Coenzyme Q10 and glutathione.
While there were high expectations that vitamin E supplementation could be a powerful neuroprotective agent in PD, the results have been disappointing. In a large, well-controlled trial, 2,000 IUs of alpha tocopherol taken for more than a year showed no beneficial effect on progression of PD.16 While there could be many reasons for this failure, and much has been written about it, the idea that vitamin E alone is of some help seems to have been abandoned.17
Glutathione has shown some promise. Several studies demonstrated a deficiency in glutathione (also known as gamma-glutamylcysteinylglycine, or GSH) in the substantia nigra of patients with PD. In a small, non-placebo-controlled trial, patients who received intravenously administered GSH had a 42 percent decline in PD-related disability. Once GSH was stopped, the therapeutic effect lasted for two to four months.18 It is unlikely, however, that oral glutathione would be sufficiently absorbed to create the same serum levels.
Co-Q10 is a potent antioxidant that has been shown to partially recover the function of dopaminergic neurons, and has been found to protect animals that have been subjected to toxins that injure those neurons.19 Additionally, PD patients have been found to have lower levels of Co-Q10 than those without PD. The initial human study looked at 80 subjects with early-stage PD who did not require drug treatment. They were randomly assigned to a placebo or Co-Q10 at dosages of 300, 600 or 1,200 mg a day. They were studied for 16 months or until they developed disability requiring treatment with levodopa (an amino acid used in PD drugs). The study found that less disability developed in subjects who took Co-Q10 than in those who took a placebo, and the benefit was greatest in subjects receiving the highest dosage of Co-Q10. While the study showed Co-Q10 was safe and well-tolerated at dosages of up to 1,200 mg a day, the improvements were quite modest.20
A recent study analyzing the PD-preventive effects of nanoparticular Co-Q10, which is thought to be more readily absorbed, was disappointing. Supplementing with 100 mg of this Co-Q10 formulation three times a day for three months did not result in significant changes compared with a placebo.21 It could be that the trial was not long enough. An additional question is how much Co-Q10 is optimal. In a new, high-dose study, subjects were given escalating dosages of Co-Q10: 1,200, 1,800, 2,400 and 3,000 mg per day (with a stable dosage of vitamin E at 1,200 IU per day). The researchers found that the plasma level of Co-Q10 plateaued at the 2,400 mg dosage, suggesting that future studies might choose that as the appropriate highest dosage to be studied.22
Creatine. Creatine appears to exert some neuroprotective effects in animals with PD. Some evidence shows that taking 10 g of creatine a day can decrease the rate of disease progression compared with placebo in patients with early symptoms of PD.23 In patients with advanced PD, who are taking medications for the condition, supplementing with 20 g a day of creatine for six days, followed by 2 g a day for six months and then 4 g daily for 18 months, did not decrease overall progression of symptoms. However, it did appear to improve patient mood and led to a smaller dose increase of other medications.24 New trials with creatine are planned.25
NADH. Reduced nicotinamide adenine dinucleotide is a nutritional supplement that seems to boost production of dopamine, a neurotransmitter. While some older, uncontrolled trials initially showed promise, nothing recently has been published and no placebo-controlled trial has shown clear benefit. While NADH may yet prove to be beneficial, recommendations at this point seem premature.26
Cowhage. A legume that grows wild in the tropics, cowhage has been used traditionally in Ayurvedic medicine to treat PD.27 Cowhage appears to contain significant amounts of the PD-treatment compound levodopa. So while there is basis for its effect, it works by the same mechanism as the levodopa drug and therefore does not offer much of an improvement over levodopa effects such as gastrointestinal upset, dizziness, difficulty speaking or decreased attention.
Clearly, a number of factors lead to the development of PD. It is a slow, progressive disorder that likely results from years of exposure to toxins, along with certain lifestyle habits. While there appear to be a few promising natural treatments, the best medicine is early awareness of what can be done over the long term.
Dan Lukaczer, N.D., has a private practice in Fife, Wash., and is associate director of medical education at the Institute for Functional Medicine, a nonprofit teaching institution in Gig Harbor, Wash.
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