A new look at fish oil
 

The essential fatty acids EFA and DHA contained in fish oil and walnuts have long been recognized as both potent against inflammation and as a main building block in the brain. Now it seems as if they are much more. If you have dyskinesias or if you take ldopa, take a look at these recent studies:

First, it seems to be able to reduce dyskinesias, at least for monkeys. If you wonder why, read on to the second abstract.
1: Ann Neurol. 2006 Feb;59(2):282-8.

Docosahexaenoic acid reduces levodopa-induced dyskinesias in
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine monkeys.

Samadi P, Gregoire L, Rouillard C, Bedard PJ, Di Paolo T, Levesque D.

Centre de recherche en Neurosciences, Centre Hospitalier Universitaire de Quebec
(CHUQ), Ste-Foy, Quebec, Canada.

OBJECTIVE: The objective of the present study was to investigate the effect of
docosahexaenoic acid (DHA), a polyunsaturated fatty acid (omega-3), on
levodopa-induced dyskinesias (LIDs) in parkinsonian
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys. METHODS: We
explored the effect of DHA in two paradigms. First, a group of MPTP monkeys was
primed with levodopa for several months before introducing DHA. A second group
of MPTP monkeys (de novo) was exposed to DHA before levodopa therapy. RESULTS:
DHA administration reduced LIDs in both paradigms without alteration of the
anti-parkinsonian effect of levodopa indicating that DHA can reduce the severity
or delay the development of LIDs in a nonhuman primate model of Parkinson's
disease. INTERPRETATION: These results suggest that DHA can reduce the severity
or delay the development of LIDs in a nonhuman primate model of Parkinson's
disease. DHA may represent a new approach to improve the quality of life of
Parkinson's disease patients.

PMID: 16437566 [PubMed - indexed for MEDLINE]
*

As to why, there's a good bet that ldopa is chewing up our brains while it keeps us going. Extra fish oil is a very reasonable attempt to counter that. And if you read on down to the last abstract, you'll see there's even a bonus....
1: Neurochem Int. 2006 Apr;48(5):404-14. Epub 2006 Jan 26.

Postmortem brain fatty acid profile of levodopa-treated Parkinson disease
patients and parkinsonian monkeys.

Julien C, Berthiaume L, Hadj-Tahar A, Rajput AH, Bedard PJ, Di Paolo T, Julien
P, Calon F.

Molecular Endocrinology and Oncology Research Centre, Centre Hospitalier de
l'Universite Laval Research Centre (CHUL), Que., Canada.

Fatty acids play a critical role in brain function but their specific role in
the pathophysiology of Parkinson disease (PD) and levodopa-induced motor
complications is still unknown. From a therapeutic standpoint, it is important
to determine the relation between brain fatty acids and PD because the brain
fatty acid content depends on nutritional intake, a readily manipulable
environmental factor. Here, we report a postmortem analysis of fatty acid
profile by gas chromatography in the brain cortex of human patients (12 PD
patients and nine Controls) as well as in the brain cortex of monkeys (four
controls, five drug-naive MPTP monkeys and seven levodopa-treated MPTP monkeys).
Brain fatty acid profile of cerebral cortex tissue was similar between PD
patients and Controls and was not correlated with age of death, delay to autopsy
or brain pH. Levodopa administration in MPTP monkeys increased arachidonic acid
content (+7%; P < 0 .05) but decreased docosahexaenoic acid concentration (-15%;
P < 0.05) and total n-3:n-6 polyunsaturated fatty acids ratio (-27%; P < 0.01)
compared to drug-naive MPTP animals. Interestingly, PD patients who experienced
motor complications to levodopa had higher arachidonic acid concentrations in
the cortex compared to Controls (+13.6%; P < 0.05) and to levodopa-treated PD
patients devoid of motor complications (+14.4%; P < 0.05). Furthermore, PD
patients who took an above-median cumulative dose of levodopa had a higher
relative amount of saturated fatty acids but lower monounsaturated fatty acids
in their brain cortex (P < 0.01). These results suggest that changes in brain
fatty acid relative concentrations are associated with levodopa treatment in PD
patients and in a non-human primate model of parkinsonism.

PMID: 16442670 [PubMed - indexed for MEDLINE]
*

While not actually new, this last one just adds icing to the cake.
1: Lipids. 2001 Sep;36(9):937-44.

Polyunsaturated fatty acids and cerebral function: focus on monoaminergic
neurotransmission.

Chalon S, Vancassel S, Zimmer L, Guilloteau D, Durand G.

INSERM U316, Laboratoire Biophysique Medicale et Pharmaceutique, Universite
Francois Rabelais, 37200 Tours, France. chalon@univ-tours.fr

More and more reports in recent years have shown that the intake of
polyunsaturated fatty acids (PUFA) constitutes an environmental factor able to
act on the central nervous system (CNS) function. We recently demonstrated that
the effects of PUFA on behavior can be mediated through effects on the
monoaminergic neurotransmission processes. Supporting this proposal, we showed
that chronic dietary deficiency in alpha-linolenic acid in rats induces
abnormalities in several parameters of the mesocortical and mesolimbic
dopaminergic systems. In both systems, the pool of dopamine stored in
presynaptic vesicles is strongly decreased. This may be due to a decrease in the
number of vesicles. In addition, several other factors of dopaminergic
neurotransmission are modified according to the system affected. The
mesocortical system seems to be hypofunctional overall [e.g., decreased basal
release of dopamine (DA) and reduced levels of dopamine D2 (DAD2) receptors]. In
contrast, the mesolimbic system seems to be hyperfunctional overall (e.g.,
increased basal release of DA and increased levels of DAD2 receptors). These
neurochemical changes are in agreement with modifications of behavior already
described with this deficiency. The precise mechanisms explaining the effects of
PUFA on neurotransmission remain to be clarified. For example, modifications of
physical properties of the neuronal membrane, effects on proteins (receptors,
transporters) enclosed in the membrane, and effects on gene expression and/or
transcription might occur. Whatever the mechanism, it is therefore assumed that
interactions exist among PUFA, neurotransmission, and behavior. This might be
related to clinical findings. Indeed, deficits in the peripheral amounts of PUFA
have been described in subjects suffering from neurological and psychiatric
disorders. Involvement of the monoaminergic neurotransmission function has been
demonstrated or hypothesized in several of these diseases. It can therefore be
proposed that functional links exist among PUFA status, neurotransmission
processes, and behavioral disorders in humans. Animal models are tools of choice
for the understanding of such links. Improved prevention and complementary
treatment of neurological and psychiatric diseases can be expected from these
studies.

PMID: 11724466 [PubMed - indexed for MEDLINE]

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