Although the death rate from stroke is declining, it is rising for other neurologic diseases such as Alzheimer disease and Parkinson disease (PD). Unlike in Alzheimer’s, we can pinpoint the abnormality in the brain that leads to PD, a substantial destruction of the dopamine-producing neurons in the substantia nigra. By the time an individual has lost 50%-70% of the dopamine-producing neurons in this region, the symptoms of PD, such as tremor, slowness of movement, rigidity, and impaired balance and coordination, are already apparent. You might think that simply giving dopamine would resolve the symptoms, but any of the initial benefits of dopamine soon erode, leaving the patient trapped in a body that is increasingly less responsive. We also know that PD is associated with neuroinflammation. Therefore, we need a therapy known to both increase dopamine and reduce neuroinflammation. Does any such therapy exist? Yes, and it comes from therapeutic levels of omega-3 fatty acids. I say “therapeutic,” because if you give placebo levels of omega-3 fatty acids to patients with PD, you get placebo effects.
Omega-3 fatty acids have the unique ability to cross the blood-brain barrier that most drugs don’t have. They are also known to increase dopamine levels and reduce neuroinflammation in the brain.[1,2] Furthermore, the omega-3 fatty acid eicosapentaenoic acid (EPA) has been shown to reduce the motor impairments and neuroinflammation in animal models in which the symptoms of PD can be rapidly induced by a drug known as MPTP.
Why don’t we see any clinical trials using high-dose omega-3 fatty acids? Previous trials have all used placebo doses of omega-3 fatty acids — in particular, EPA. I know this because I have published many peer-reviewed articles on the use of high-dose omega-3 fatty acids rich in EPA in the treatment of attention-deficit/hyperactivity disorder (ADHD), major childhood depression, and age-related macular degeneration (AMD).[4-6] Once you give a therapeutic dose of omega-3 fatty acids, especially EPA, you get therapeutic effects. The common reason given for not using high-dose omega-3 fatty acids is the mistaken belief that the patients will bleed to death. That is simply not true, especially if you monitor the ratio of arachidonic acid (AA) to EPA in the blood. As long as the AA/EPA ratio remains above 1.5 (as it is for the Japanese population, whose diet is rich in omega-3 fatty acids through fish consumption), you are not going to have any bleeding problems. But as you get closer to that AA/EPA ratio, you start to see dramatic improvements in neurologic function.
Another problem with human trials is that you have to treat the patients like lab rats. That is, you have to control their entire diet and in particular the levels of omega-6 fatty acids that they are consuming. Whereas omega-3 fatty acids are anti-inflammatory, omega-6 fatty acids are proinflammatory. In fact, increased intake of AA (an omega-6 fatty acid) appears to be correlated with an increased incidence of PD. Another recent study indicated that if you simultaneously reduce omega-6 fatty acids while increasing the omega-3 fatty acids in the diet, the clinical results are significantly improved.[8,9] Maybe that’s asking too much for patients with PD or any patient with a neurologic problem. As a result, we simply continue to look for a “magic drug” that allows patients to eat whatever they want. I don’t think that this is a productive research route for treating PD, let alone other neurologic diseases such as Alzheimer’s, ADHD, AMD, or even chronic headaches.
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