With reference to the coconut oil earlier thread, it surprises me why ketogenic diet used effectively to treat epilepsy for the last 80 years, has been ignored by the medical establishment as a possible neuropretective method for PD and alzimer. but I shouldn't be surprised really!
Imad

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2367001/
One recently published clinical study tested the effects of the ketogenic diet on symptoms of Parkinson’s disease (VanItallie et al., 2005). In this uncontrolled study, Parkinson’s disease patients experienced a mean of 43% reduction in Unified Parkinson’s Disease Rating Scale scores after a 28-day exposure to the ketogenic diet. All participating patients reported moderate to very good improvement in symptoms. Further, as in Alzheimer’s disease, consumption of foods containing increased amounts of essential fatty acids has been associated with a lower risk of developing Parkinson’s disease (de Lau et al., 2005).

Animal models:
The most widely used animal model of Parkinson’s disease is based on the neurotoxin MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine). Exposure to MPTP causes degeneration of mesencephalic dopamine neurons, as in the human clinical condition, and is associated with parkinsonian clinical features. The ketogenic diet has not yet been studied in the MPTP or other animal models of Parkinson’s disease. As in epilepsy and Alzheimer’s disease models, however, caloric restriction has been found to have beneficial effects in MPTP models of Parkinson’s disease. This was first demonstrated in rats fed on an alternate-day schedule so that they consume 30–40% less calories than animals with free access to food. The calorie-restricted animals were found to exhibit resistance to MPTP-induced loss of dopamine neurons and less severe motor deficits than animals on the normal diet (Duan and Mattson, 1999). More recently, it has been reported that adult male rhesus monkeys maintained chronically on a calorie-restricted diet are also resistant to MPTP neurotoxicity (Maswood et al., 2004; Holmer et al., 2005). These animals had less depletion of striatal dopamine and dopamine metabolites and substantially improved motor function than did animals receiving a normal diet. In other studies in mice, caloric restriction has been reported to have beneficial effects even when begun after exposure to MPTP (Holmer et al., 2005).In addition to caloric restriction, several recent reports have indicated that β-hydroxybutyrate may be neuroprotective in the MPTP model. MPTP is converted in vivo to 1-methyl-4-phenylpyridinium (MPP +), which is believed to be the principal neurotoxin through its action on complex 1 of the mitochondrial respiratory chain. In tissue culture, 4 mmol/l β-hydroxybutyrate protected mesencephalic neurons from MPP + toxicity (Kashiwaya et al., 2000). Moreover, subcutaneous infusion by osmotic minipump of β-hydroxybutyrate for 7 days in mice conferred partial protection against MPTP-induced degeneration of dopamine neurons and parkinsonian motor deficits (Tieu et al., 2003). It was proposed that the protective action is mediated by improved oxidative phosphorylation leading to enhanced ATP production. This concept was supported by experiments with the mitochondrial toxin 3-nitropropionic acid (3-NP). 3-NP inhibits oxidative phosphorylation by blocking succinate dehydrogenase, an enzyme of the tricarboxylic acid cycle that transfers electrons to the electron transport chain via its complex II function. The protective effect of β-hydroxybutyrate on MPTP-induced neurodegeneration in mice was eliminated by 3-NP. Moreover, in experiments with purified mitochondria, β-hydroxybutyrate markedly stimulated ATP production and this stimulatory effect was eliminated by 3-NP. Thus, it seems likely that β-hydroxybutyrate is protective in the MPTP model of Parkinson’s disease by virtue of its ability to improve mitochondrial ATP production (Tieu et al., 2003). Whether the ketogenic diet would also be protective in Parkinson’s disease models as a result of increased β-hydroxybutyrate production remains to be determined. It is noteworthy that β-hydroxybutyrate is not anticonvulsant and is unlikely to directly account for the antiseizure activity of the ketogenic diet (Rho et al., 2002). Whether β-hydroxybutyrate contributes in some other way to the beneficial activity of the ketogenic diet in epilepsy therapy remains to be studied.