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Omega-3 May Help Deter Parkinson's Disease
12/3/2007
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Study in mice indicates possible protective power of DHA vs. Parkinsonís disease; full picture of Parkinsonís suggests limits on the promise of stem cell therapy
by Craig Weatherby


Parkinsonís disease is the second most common neurodegenerative disease, after Alzheimerís disease.

The National Parkinson Foundation estimates that 1.5 million Americans suffer from Parkinson's disease, and that 60,000 new cases are diagnosed annually. The disease affects roughly equal numbers of men and women.

The immediate cause of Parkinson's disease is damage to dopamine-producing neurons (brain cells), which are concentrated in a part of the brain called the substantia nigra. Dopamine is required for proper muscle function and body movement.

Key Points
  • Parkinsonís disease is characterized by loss of dopamine-producing cells, which are concentrated in a specific part of the brain.

  • Diets high in omega-3s protected mice injected with a chemical that kills dopamine-producing cells where they are most abundant.

  • The actual cause of damage to dopamine-producing cells in Parkinsonís patients remains uncertain, so the new results are intriguing but inconclusive.
Symptoms include tremors, muscle rigidity, poor balance, cramped handwriting, stiff facial expression, shuffling walk, muffled speech, and depression. And the signs donít usually manifest until some 80 percent of the dopamine-producing cells are already destroyed or damaged.

Parkinson's disease usually develops after the age of 65, but about 15 percent of cases occur in people younger than 50. The actor Michael J. Fox is perhaps the best-known younger patient. He developed Parkinson's symptoms at age 30, and has become a leading advocate for research.

Other high profile patients include Booth Gardner, the former governor of our companyís home state, Washington, and Time magazine columnist Michael Kinsley.

Kinsley joins Fox in calling for unfettered stem cell research in the hope that it might produce implantable dopamine-producing neurons, while Gardner is campaigning to legalize suicide for people with Parkinsonís and other crippling, currently incurable conditions: a fight covered in last Sundayís edition of The New York Times Magazine.

There is a family history of Parkinsonís disease in about 10 percent of patients, and researchers suspect that the disease results from a combination of genetic factors and unknown environmental toxins.

Epidemiological research links higher risk of Parkinsonís to rural living, well water, herbicide use, and exposure to pesticides. Contamination of well water by pesticides such as atrazine is common in farming states.

No known treatment can slow or stop the progression of Parkinson's. The primary medicines
óL-dopa and similar drugs, called dopamine agonistsóeither replace dopamine or mimic its effects, to partial extents.

Have hopes for stem cell therapy been raised too high?
The available evidence indicates that loss of dopamine-producing neurons, which produces some of the symptoms of Parkinsonís, is only one of many kinds of brain damage caused by the disease.

In fact, the brain's dopamine-producing neurons are affected only later in the course of the disease. And some of the disabilities seen in Parkinsonís do not even involve dopamine deficiencies.

Accordingly, as the author of one recent evidence review observed, ďWe have reached the point of diminishing therapeutic returns with drugs acting on dopamine systems...Ē (Ahlskog JE 2007)

And these findings led him to sound a pessimistic note concerning the hope that transplanted dopamine-producing neurons produced by stem cell research could prove curative: "the benefits from transplantation surgeries aimed at restoring dopaminergic neurotransmission [by implantation of healthy neurons] will be limited...Ē (Ahlskog JE 2007)

As with other diseases, the greatest benefits may flow from discovering any environmental causes of the disease, and finding drugs or nutrients that might delay or deter its development.
  • Mouse chow supplemented with omega-3 DHA.

  • Normal mouse chow, which is relatively low in omega-3s and high in omega-6 fatty acids.
They injected both groups with an opiate chemical called MPTP. After entering the brain, MPTP is converted to another opiate called MPP+, which kills dopamine-producing neurons in the substantia nigra (Two other groups of mice, which did not receive MPTP, served as controls).

The results were striking, and favored the omega-3-rich diet:
  • The mice fed the omega-3-rich diet suffered no ill effects.

  • The mice fed an ordinary, omega-6-rich diet developed symptoms of Parkinson's disease after losing 31 percent of their dopamine-producing neurons and half their dopamine production.
The researchers determined that DHA was the likely protective factor in the fish oil used to supplement the animalsí diet, for two reasons:
  • DHA displaced omega-6 fatty acids in the animalsí brain cell membranes.

  • The concentrations of EPA Ė the other omega-3 that occurs in animal and human brain-cell membranes Ė remained the same in both groups of mice.
And the US-Canadian team concluded that brains overabundant in omega-6 fatty acidsóa description that fits the average Americanómay be more vulnerable to Parkinsonís and suffer a more rapid decline in dopamine production.

In a balanced diet, the ratio between omega-6 and omega-3 fatty acids should be 4 to 1, say the Université Laval team. However, the average Western diet contains ten to 20 times more omega-6s than omega-3's.

Lead author Frederic Calon made this key comment: ďIn North America, the average consumption of DHA is approximately 60 to 80 mg per day, whereas the experts recommend consuming at least 250 mg. Our results suggest that this [DHA] deficiency is a risk factor for Parkinson's, and that it would be worth the effort to evaluate the potential of omega-3s for the prevention and the treatment of this disease in humans.Ē (Hamann J 2007)

Note: The study was funded by the Parkinson Society of Canada, one of whose major sponsors is Burnbrae Farms, which markets eggs higher in omega-3s (DHA) than standard commercial eggs.

Intriguing results in mice remain inconclusive
The sources of the neuronal damage underlying Parkinsonís remain uncertain. One hypothesis is that Parkinson's disease may be caused by repeated exposure to minute amounts of an opiate-class compound called MPP+.

MPP+ targets the substantia nigra, where it interferes with the energy centers (mitochondria) in brain cells: an effect that kills the dopamine-producing neurons concentrated in this region, and generates free radicals that damage more neurons.

MPP+ is produced in the brains of humans and monkeys exposed to a close opiate-class cousin called MPTP. This was the chemical used in the new study to produce a Parkinsonís-like condition in mice, which was prevented by feeding the animals omega-3 DHA.

Researchers discovered that MPTP causes Parkinsonísí symptoms in 1973, when a chemistry graduate student erred in his attempt to make a synthetic opiate drug called MPPP.

The grad student injected the result and developed symptoms of Parkinson's disease within three days.  Investigators found traces of MPTP in his lab, and determined that the human body converts MPTP in to MPP+, which damages dopamine-producing neurons and quickly produces the symptoms of Parkinsonís disease.

Ever since then, researchers have used MPTP to produce Parkinsonís disease in animals, and (hypothetically) aid the hunt for drugs that might protect the brainís dopamine-producing neurons from MPP+ or related chemicals.

Although many toxins and neurological insults can damage the part of the brain that contains most of its dopamine-producing neurons, MPP+ is the only chemical known to target those neurons specifically, so it is a leading suspect as a proximate cause of Parkinsonís.

The brain produces various opiate-class compounds naturally. It could be that exposing animals to MPTP mimics an unknown dysfunction that causes other, as yet undiscovered, opiate precursors to MPP+ to accumulate in the brain.

We cannot be sure that the actual cause(s) of Parkinsonís disease in humans is MPP+, or a closely related chemical whose damaging effects on neurons would also be blocked by increasing oneís intake of omega-3 DHA.

Thus, while the intriguing new finding in mice may point toward possible causes or cures, we are a long way from knowing whether DHA can deter or alleviate Parkinsonís disease, in which the loss of dopamine-producing neurons is just one of several forms of brain damage.


Sources
  • Ahlskog JE. Beating a dead horse: dopamine and Parkinson disease. Neurology. 2007 Oct 23;69(17):1701-11. Review.

  • Bousquet M, Saint-Pierre M, Julien C, Salem Jr. N, Cicchetti F, Calon F. Beneficial effects of dietary omega-3 polyunsaturated fatty acid on toxin-induced neuronal degeneration in an animal model of Parkinsonís disease  FASEB J. Published online before print November 21, 2007 as doi:10.1096/fj.07-9677com

  • Burnbrae Farms. Naturegg Omega 3. Accessed online November 30, 2007 at http://www.burnbraefarms.com/consumer/our_products/shell_naturegg_omega3.htm

  • Hamann J. Les oméga-3 protégeraient contre le parkinson: Líeffet protecteur de ces acides gras, démontré chez la souris, mérite díÍtre exploré chez líhumain, estime Frédéric Calon. Accessed online November 30, 2007 at http://www.aufil.ulaval.ca/articles/les-omega-protegeraient-contre-parkinson-3392.html

  • Hirsch EC. Animal models in neurodegenerative diseases. J Neural Transm Suppl. 2007;(72):87-90.

  • Lang AE, Obeso JA. Challenges in Parkinson's disease: restoration of the nigrostriatal dopamine system is not enough. Lancet Neurol. 2004 May;3(5):309-16. Review.

  • The Parkinsonís Disease Foundation. What causes Parkinson's? Accessed online November 30, 2007 at http://www.pdf.org/AboutPD/causes.cfm
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