Sample keto dinner for Parkinson’s


We had friends of friends round to supper the other day. They were interested (as Veech is) in ketosis as a tool to try and modify the progress of Parkinson’s disease. So we had a baked mushroom each, filled with bacon and melted soft cheese with a smidge of fried onions and a micro smidge of spinach then topped with half a round of goat cheese for starters, belly pork goulash with soured cream, broccoli and asparagus for main course and Optimal ice cream (minimal dose of honey, no sugar) with a few raspberries for desert. Coffee and double cream. Modest red wine portions. The funniest part was trying to explain to them that serious researchers/nutritionists genuinely explained away the reduced appetite on LC diets as being due to either boredom or lack of palatability.

Read the rest HERE

Parkinson’s and Keto

LACIE via comments at HYPERLIPID:

There has been very little recent research on ketones and PD, but Veech, Vanitallie, and D’Agostino all believe there’s overlap between ALS, Alzheimer’s, Huntington’s, MS, and PD. I ended up at Deanna Tedone’s site, where D’Agostino helped her father develop a multi-supplement protocol (Deanna Protocol) for ALS patients.
Not all of those supplements are effective for PD, but my partner takes the 18g of Primaforce AAKG and liposomal or IV glutathione. He tried MCT oil and coconut oil per Dr. Mary Newport’s work with her husband:
but the AAKG is much easier to digest and accommodates higher dosing.

Treatment of Parkinson disease with diet-induced hyperketonemia: a feasibility study.


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Ketones may bypass the defect in complex I activity implicated in Parkinson disease (PD). Five of seven volunteers with PD were able to prepare a “hyperketogenic” diet at home and adhere to it for 28 days. Substituting unsaturated for saturated fats appeared to prevent cholesterol increases in four volunteers. Unified Parkinson’s Disease Rating Scale scores improved in all five during hyperketonemia, but a placebo effect was not ruled out.

Ketoacids? Good medicine?

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D-beta-hydroxybutyrate, the principal “ketone” body in starving man, displaces glucose as the predominating fuel for brain, decreasing the need for glucose synthesis in liver (and kidney) and accordingly spares its precursor, muscle-derived amino acids. Thus normal 70 kg. man survives 2-3 months of starvation instead of several weeks, and obese man many months to over a year. Without this metabolic adaptation, H. sapiens could not have evolved such a large brain. Recent studies have shown that D-beta-hydroxybutyrate, the principal “ketone”, is not just a fuel, but a “superfuel” more efficiently producing ATP energy than glucose or fatty acid. In a perfused rat heart preparation, it increased contractility and decreased oxygen consumption. It has also protected neuronal cells in tissue culture against exposure to toxins associated with Alzheimer’s or Parkinson’s. In a rodent model it decreased the death of lung cells induced by hemorrhagic shock. Also, mice exposed to hypoxia survived longer. These and other data suggest a potential use of beta-hydroxybutyrate in a number of medical and non-medical conditions where oxygen supply or substrate utilization may be limited. Efforts are underway to prepare esters of beta-hydroxybutyrate which can be taken orally or parenterally to study its potential therapeutic applications.

Ketone bodies, potential therapeutic uses.

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Ketosis, meaning elevation of D-beta-hydroxybutyrate (R-3hydroxybutyrate) and acetoacetate, has been central to starving man’s survival by providing nonglucose substrate to his evolutionarily hypertrophied brain, sparing muscle from destruction for glucose synthesis. Surprisingly, D-beta-hydroxybutyrate (abbreviated “betaOHB”) may also provide a more efficient source of energy for brain per unit oxygen, supported by the same phenomenon noted in the isolated working perfused rat heart and in sperm. It has also been shown to decrease cell death in two human neuronal cultures, one a model of Alzheimer’s and the other of Parkinson’s disease. These observations raise the possibility that a number of neurologic disorders, genetic and acquired, might benefit by ketosis. Other beneficial effects from betaOHB include an increased energy of ATP hydrolysis (deltaG’) and its linked ionic gradients. This may be significant in drug-resistant epilepsy and in injury and anoxic states. The ability of betaOHB to oxidize co-enzyme Q and reduce NADP+ may also be important in decreasing free radical damage. Clinical maneuvers for increasing blood levels of betaOHB to 2-5 mmol may require synthetic esters or polymers of betaOHB taken orally, probably 100 to 150 g or more daily. This necessitates advances in food-science technology to provide at least enough orally acceptable synthetic material for animal and possibly subsequent clinical testing. The other major need is to bring the technology for the analysis of multiple metabolic “phenotypes” up to the level of sophistication of the instrumentation used, for example, in gene science or in structural biology. This technical strategy will be critical to the characterization of polygenic disorders by enhancing the knowledge gained from gene analysis and from the subsequent steps and modifications of the protein products themselves.


Blunt, reverse and possibly prevent Neurologic Disease

“As an alternative to glucose, the brain can draw energy from ketones, a group of metabolites synthesized from fatty acids in the liver. Interestingly, the addition of ketones as an alternative fuel source for the brain attenuates the progression of Alzheimer’s in a mouse model of the disease.4

“Because the mammalian brain does not metabolize fatty acids, a secondary metabolite, such as ketones, could be responsible for the beneficial effect of the high-fat diet. Indeed, ketones increase the life span of a short-lived nematode model of Cockayne syndrome. Ketones also ameliorate mitochondrial changes in models of Cockayne syndrome and have recently been shown to have life span-extending properties in wild-type C. elegans. Interestingly, ketogenesis, the production of ketones as a result of fatty acid breakdown, can be induced by fasting, suggesting that ketones could play a central role in the increased longevity effects of caloric restriction observed in the lab. ”

“We are, however, getting closer to an understanding of fundamental aspects of neurological aging, and we may soon be able to intervene in the aging process as a whole, perhaps with the benefit of preventing Alzheimer’s, Parkinson’s, and other age-associated neurological diseases. Increasing the level of circulating ketones, through dietary interventions or exogenous ketone sources, may be one relatively easy way to intervene, and could be efficacious either alone or in combination with other targeted interventions.”


What can reverse or blunt most modern disease? Keto Can.

Ketogenic Diets: From Cancer To Mitochondrial Diseases And Beyond

study LINK via pubmed

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The employment of dietary strategies such as ketogenic diets, which force cells to alter their energy source, has shown efficacy in the treatment of several diseases. Ketogenic diets are composed of high fat, moderate protein and low carbohydrates, which favor mitochondrial respiration rather than glycolysis for energy metabolism.


This review focuses on how oncologic, neurologic and mitochondrial disorders have been targeted by ketogenic diets, their metabolic effects, and the possible mechanisms of action on mitochondrial energy homeostasis. The beneficial and adverse effects of the ketogenic diets are also highlighted.


Although the full mechanism by which ketogenic diets improve oncologic and neurologic conditions still remains to be elucidated, their clinical efficacy has attracted many new followers, and ketogenic diets can be a good option as a co-adjuvant therapy, depending on the situation and the extent of the disease.