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.

Imad,

This study doesn't point out that the diet in the PD trial was for hyperketogenic diet...meaning it was almost 90% fat based. Yes, participants still lost weight but the food seemed really unappealing, and I can't see how anyone could sustain that long term. I read somewhere one dish described as ground beef swimming in a mix of oil run off from meat and heavy cream. That triggered my gag reflex. I know it sounds sily, but I feel like our quality of life already takes a hit, so I won't start eating really unappealing foods until they prove it is neuro-regenerative. We lose dopamine...not our taste buds!

Still, this study was conducted five years ago! Frustrated by how long everything seems to take. Of course, I get it...research advances at the same pace as PWP move when off meds. It happens in bradykinetic time...ha ha.

On a side note, caloric restriction seems key to helping us too. Interestingly, research shows that intermittent eating helps immensely to quell inflammation. That is, research shows it is more beneficial to fast every other day, while on eating days, you eat twice as much to make up for it. Weird as it is, this supposedly is even better than reducing calories over all.
Don't have the citation handy- will try to add.

Laura

Laura

The use of medium chain triglycerides (MCT) with a modified Atkins or paleolithic diet is a promising compromise.

Rick,

This is exactly what I want to try but modified to allow some of the mitochondrial friendly diet in to- I'd have to up the carbs a bit tof it in 9 cups of vegetables a day


I can't seem to get started as I'm rather freaked by throwing out all processed foods from our pantry.

Laura

Hi Laura

I am knew here and I am intersted in any ideas anybody has regarding ketogenic diets. right now I am on one ( not for Parkinsons) and my dad is on one (for Parkinsons).

Kindest regards

joanne

Hi, all. I have been ketogenic for almost six months now, (not for Parkinson's) and I enjoy how much better I feel.

I follow Dr. Kurt Harris' "Get Started" page, at his blog, PaleoNu.

Reading Dr. Richard Bernstein's book, The Diabetes Solution, made such a strong impression on me about the damaging effects of CHO, that I knew I would stay on a very low CHO diet for life.

Dr. Mary Newport's blog, "Coconut Oil and Ketones", about Alzheimer's and what has helped her husband, who has AD, convinced me of the need to stay ketogenic. I started taking expeller-pressed coconut oil, and have noticed a marked improvement in overall well being.

There are some on low carb, Paleo, and Carnivore forums who espouse ketogenic diets, but I have not read posts related to improvements in things specifically related to brain and neurological health.

I found this thread through a search for ketogenic diet and Alzheimer's.


I'd be interested in reading what iimprovements others have found, in staying ketogenic.

I have PD and have been very interested in trying ketogenic diet.
Since 10 weeks ago I started reducing carbo foods drastically, take two table spoons of coconut oil daily and obtain most of my calories from meat, vegtables and little fruits. So it is a far shot from strict ketogenic diet but never the less I noted a remarkable improvement in energy and mood. however, my main PD complain which is tremor did not improve at all.
wish you good health and companionship in our forum
Imad

Imark, I'm glad you have noticed improvement. I have been ketogenic for almost six months. I do not have Parkinson's, but other health challenges.

I notice improvements every few weeks. I eat no sweet fruits and keep my carbs under 20 per day. I know several who eat fewer than 10 carbs per day. We count total carbs, not net. I eat meat, meat fat, egg yolks, wild salmon, liver, a few herbs and low starch vegs, butter and cream (mostly as yoghurt).

Are you increasing your CO intake, or staying at 2 tablespoons?

When I can get grass-fed beef and pastured butter, I notice that helps me a good deal.

Best wishes to all.

Yes. First thing in the morning I take 2 table spoons CO, 1 tea spoon of creatine and 2 table spoons whey protin. Then I hard exercise for over an hour burning at least 500 calories followed by hot and freezing cold shower for about 10 minuits. Then I am ready to start my day ! very heavy breakfast, sinemet and supplements.
My other daily activity is wii games with my 6 years grand son and taichi/attemp at meditation.
these are glimpses from my personal life at 67. my other hobbies are music listening, film watching and of course, the internet.
I feel more free since I was diagnosed with PD.
Cheers
Imad

Imad, thanks for your post. Hope your Tai Chi is going nicely. I have a morning and evening routine I do of Callanetics, yoga and ballet exercises. I do them slowly and take rests between exertions.

Playing the games with your grandson sounds delightful.


Hope you are doing well.

All the best to you.