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Keto For Parkinson’s Disease

Existing Literature On Nutritional Ketosis As Clinical Therapy In Parkinsons Disease

Keto Diet & Parkinson’s Disease with William Curtis

Phillips et al. addressed some of these knowledge gaps by comparing two randomized groups using a comparatively less stringent ketogenic diet vs. a low-fat diet. The diets were prescribed by meal plans, each by kilocalories approximately 18% protein and either 79% lipid/3.7% net carb or 23% lipid/59% net carb , the latter also with greater dietary fiber, stratified by estimated daily energy expenditure. The 8-week study involved daily participant ketosis monitoring by AM fasting beta-OHB levels using a validated fingerstick ketone meter. Dietary monitoring relied on participants to check off each meal from the plan outlined for the study period. Investigators reported reduced MDS-UPDRS-I scores , particularly urinary, pain/sensory disturbance, fatigue, daytime sleepiness, and cognitive impairment subscores. However, this study also had some limitations including infrequent data capture and diet monitoring relying upon self-report, which precludes correlative analysis between ketosis value and clinical rating scale that was performed only pre- vs. post-intervention. Another possible weakness was the relatively low mean beta OHB level in the KD group. It is probable that greater benefit could be seen with a greater degree of ketosis.

Table 1 Improvements in non-motor symptoms found in studies of ketogenic diet in Parkinsons disease

How Can Ketogenic Diet Treat Pd

The Ketogenic diet helps the brain cells to shift from glucose, its usual source of energy, to ketones, produced in the liver due to restricted carb intake.

Ketones are proven to boost antioxidant activity in the brain and control the production of free radicals. This further reduces the stress and damage to brain cells and its ability to produce dopamine.

Considering the impact of ketones on the mitochondrial function of brain cells, Ketogenic diet has been considered an alternative treatment to reduce the conditions associated with PD.

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Open Access License / Drug Dosage / Disclaimer

This article is licensed under the Creative Commons Attribution-NonCommercial 4.0 International License . Usage and distribution for commercial purposes requires written permission. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor. The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

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Neuroprotective Functions Of The Ketogenic Diet On Cognition In Neurological Disease

As mentioned, the ketogenic diet plays a major role at the metabolic and neuronal levels, whereby its therapeutic properties are relevant for certain diseases. According to scientific literature, important therapeutic evidence exists about this diet in certain diseases and, thanks to recent findings, evidence is also emerging about the ketogenic diet as applied to new neurological diseases, placing special emphasis on the cognitive benefits of this type of diet.

I Am Overweight What Can I Do

Keto Diet for Parkinson

Its easy to gain weight if you become less active but are eating the same amount of food.

If you are trying to lose weight, here are some tips to start with:

  • Dont eat fried food regularly grill, dry fry, microwave, bake, steam, poach or boil, without adding fat or oils. Instead, use marinades, adding extra herbs, stock and spices for flavour.
  • Use skimmed or semi-skimmed milk instead of full fat.
  • Try eating healthier snacks like diet yoghurts, nuts, fruit, crumpets or teacakes.
  • Have sugar-free, no added sugar or low-calorie drinks and use artificial sweetener instead of sugar.

If you have other health conditions as well as Parkinsons, such as circulation problems, high cholesterol, heart disease or diabetes, and are concerned about being overweight, speak to your GP, specialist, Parkinsons nurse or ask to see a registered dietitian.

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Where To From Here

If you have done your research and want to commence the keto diet, check with your doctor first as this dietary pattern may not be suitable for you. If you have diabetes and take insulin or oral hypoglycaemic agents, you may need your medications adjusted before initiating this diet. With diabetes, you should regularly monitor your blood glucose and blood ketone levels and liaise regularly with your doctor.

If you do decide to start the keto diet, trial it for a few months and closely observe your symptoms. Your doctor can monitor blood-work, including your blood lipid profile, and potential side effects.

You should also work with a Dietitian to ensure you follow a well-formulated keto diet containing nutrient dense foods. In addition, be sure to reduce your carbohydrate intake gradually and increase your fat intake gradually over several weeks. You can test your blood ketone levels using a device, such as this one, available online or from a pharmacy. Alternatively, urine testing strips can also indicate ketone levels.

If after giving it a go, you decide the keto diet is not right for you, transition back to your usual diet gradually and stay in contact with you doctor.

What Is The Keto Diet

The keto diet is a very high-fat, very low-carbohydrate, moderate protein diet that induces nutritional ketosis. Nutritional ketosis occurs when your body starts burning fat instead of carbohydrate for energy. Burning fat for energy produces ketones. Ketones are water-soluble compounds that can cross the blood-brain barrier to provide an alternative source of energy to the brain. Most people will need to eat less than 50 grams of carbohydrate per day to reach ketosis.

Researchers suggest the keto diet may help with diminished mitochondrial energy metabolism. In Parkinsons the potential support for the keto diet comes from a few human studies.

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Keto For Parkinsons Disease

A 12-week ketogenic diet alleviated cognitive symptoms and anxiety in participants with Parkinsons disease.


Parkinsons disease is a neurodegenerative disease characterized by the loss of dopamine-producing cells in the brain. Because ketogenic diets cause the brain to use ketone bodies instead of glucose for fuel, they are sometimes used to alleviate neurological disorders such as PD.

The study

This single-group pilot study assessed the role of a low carbohydrate/high fat ketogenic diet on PD symptoms, anxiety, depression, and general health biomarkers in 16 adults with PD. For 12 weeks, the participants followed a LCHFKD consisting of 1,750 calories per day .

The authors monitored participant compliance by assessing food logs and weekly fasting blood glucose and ketones. The participants received educational materials on the diet throughout the intervention.

At baseline and the end of the study, the authors assessed the following outcomes:

  • PD severity, via the United Parkinson’s Disease Rating Scale Parts 14

  • Anxiety, via the Parkinson’s Anxiety Scale

  • Depression, via the Center for Epidemiologic Studies Depression Scale Revised-20

  • Blood markers .

  • Body weight

Primary And Secondary Outcomes

Ketosis & Parkinson’s Disease: Improving Symptoms with a Ketogenic Diet

Primary outcomes were within and betweengroup changes in MDSUPDRS Parts 1 to 4 from the mean of the two baseline clinical visits to week 8 after commencing the diet intervention. Secondary outcomes were within and betweengroup changes in metabolic parameters, including weight, BMI, HbA1C, triglycerides, HDL, LDL, total cholesterol, urate, and CRP.

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Am I A Candidate For The Ketogenic Diet

While the short answer is yes for the majority of people consuming a western diet, we urge you to consult your general practitioner prior to making the switch to Keto. The Charlie Foundation will provide you with the information and tools necessary to adopt the diet, and partnering with your doctor during this process will ensure the most therapeutic outcome. We also suggest that you connect with a diet professional who can help you form a plan in collaboration with your doctor, who may be less familiar with the diet.

The Impact Of Nutritional Ketosis On Parkinsons Disease Functional Domains

Studies showed ADAS-Cog score improvement in the APOE4 negative subgroup only on post-hoc analysis . APOE4 is associated with low-density lipoprotein receptors, cerebral amyloid angiopathy, and formation of astrocyte lipid core formation with less transfer of cholesterol to neurons , thus suggesting a pathobiological risk that is distinct from brain insulin resistance and glucose hypometabolism. It is known that insulin resistance, as in metabolic syndrome and type 2 diabetes mellitus, is associated with hippocampal atrophy, particularly in the dentate gyrus with atrophic spine arborization. Therefore, promoting insulin sensitization, whether or not strictly ketogenic, may be beneficial with regard to encoding and recall, mood, and other related cognitive processes. Furthermore, a more stable energy source may be beneficial for fatigue, pain and other non-motor symptoms.

Fig. 2

a Benefits attributed to reduced carbohydrate intake similar to increased activity levels include improved cognition and mood. b Benefits attributed to a ketogenic diet in PD may relate to increased dopamine synthesis and availability

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Patient Flow And Baseline Characteristics

Information About the Ketogenic Diet

Details of patient flow, including all study exclusions and withdrawals, are shown in Figure . We randomized 47 patients, of which 44 commenced the diets and 38 completed the study 6 patients withdrew for reasons unrelated to the diets and 3 patients withdrew as a result of dietrelated difficulties. Randomized patient baseline characteristics are shown in Table . There were no significant betweengroup differences in any baseline characteristics.

Except for % variables, values are presented as mean┬▒standard deviation.

Baseline values were obtained by averaging the two baseline clinical visits 1 patient withdrew postrandomization, several hours before their scheduled second baseline visit, so the first visit was used as the baseline value.

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Types Of Ketogenic Diets

There are a variety of diets that will allow you to get into ketosis. The major differentiating factor between them all is the amount of calories that come from protein, carbs and fat, which are what we call macronutrients, or nutrients in our food that have a caloric value. The three macronutrients differ in many ways, namely, their caloric values, as well as how the body uses them. Fat is the most calorically dense macronutrient, having 9 calories per gram, compared to 4 calories per gram for both carbs and protein. In a homeostatic state, the body utilizes fat and carbs for energy production, while it uses protein to rebuild the cells of our body. While this is generally the case, an overconsumption of protein can lead the body to break down the excess protein into glucose

Food Aversions To Popular Keto Foods

Some individuals with Parkinsons Disease have also reported that they have developed specific food aversions to proteins such as meats, dairy, and eggs. This could make the selection of foods a little bit trickier. Sometimes a change in the way that the protein is cooked has been shown to help with this. However, if changing how the food is prepared doesnt work, you can find other keto-friendly suggestions in our guide to the vegan ketogenic diet.

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Synergism Of Ketosis And Nicotinamide Riboside Food Supplements

In some of the Alzheimers experiments it appears that the HB is needed for nicotinamide riboside to have any results. In other words, unless the HB makes NADPH available to provide electrons, eating the nicotinamide riboside precursor of NADPH has no effect, but when the precursor is added to HB the results are synergistic. This can be easily explained if one understands the math behind the redox potential. Both the Nernst redox potential and the Gibbs free energy derived equations Dr. Veech used had terms where the concentration of products over the concentration of the reactants were used to determine the redox potential. In this equation the concentration of the pair of nucleotides cancels out. That means the redox potential at any given steady state or near equilibrium is only proportional to the ratio of to . It is not affected by the number of the total of NADP plus NADPH. In fact, when Dr. Veech or anyone else measured the Gibbs free energy or the redox potential of the great controlling nucleotides, they only had to calculate the ratio of the low energy form to the high energy form.

Study 1 Vanitallie Et Al

Parkinson and Keto – The Journey begins

The first study, conducted in 2005, assigned 7 participants with Parkinsons to the keto diet for 4-weeks to determine if symptoms could improve on this diet. 5 participants completed the study. Urine ketones were measured daily. The macronutrient breakdown as a percent of total calories was 90% fat, 2% carbohydrate and 8% protein.

Outcomes: Unified Parkinsons Disease Rating Scale scores improved in all 5 participants. Among symptoms that improved were resting tremor, freezing, balance, gait, mood and energy level. Although 2 participants did not follow the diet as strictly as others, they were still able to achieve ketosis and improve UPDRS scores. All participants had a body mass index above 28 and lost an average of 6.1 kg during the study period.

Limitations: the assigned diet was inadequate in protein which may have improved levodopa absorption making it difficult to determine if the observed improvements were due to this or due to the effects of the diet. In addition, there was no control group, a very small sample size was followed for a short duration and the potential of a placebo effect must be kept in mind when interpreting these outcomes.

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Ketogenic Diet Positively Impacts Parkinsons Disease

Parkinsons disease is a chronic disease that affects a part of the brain called the substantia nigra, the nerves, and the nervous system. Anything that can protect or add health to the brain, the nerves, and nervous system can benefit individuals diagnosed with Parkinsons disease.

In a study of a small sample of Parkinsons disease patients, there was a 43% improvement in the Unified Parkinsons Disease rating scale following 1 month of implementing the ketogenic diet.

Interview With Bill Curtis

This is an excellent interview with William Curtis. I met Mr. Curtis at the Tripping Over the Truth conference in November 2017. Mr. Curtis was diagnosed with Parkinsons in 2010 and has been keeping his symptoms in check using what he calls intermittent ketosis and exogenous ketones. He also has a website. The video is well worth watching if you have or care for someone with Parkinsons.

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Genetic Mechanisms Of Life Span Extension

There are marked heritable differences in median life span between species: from less than 3 weeks in C. elegans, between 2 and 3 years for the mouse or rat, 10 to 15 years for the dog, around 70 years for humans, and up to over 400 years in a bivalve mollusk Artica islandica. This observation makes it clear that life span has a heritable component.

The first genetically induced increase in life span in C. elegans was reported for a mutation in age-1, encoding a catalytic subunit of the of phosphatidylinositol 3-OH kinase of the insulin/insulin-like growth factor receptor signaling pathway . The Kenyon laboratory insightfully took experimental advantage of the short life span of C. elegans to identify mutations in the abnormal dauer formation-2 insulin/IGF-1 receptor gene of the IIS pathway that led to a twofold increase in C. eleganslife span . This life span extension was found to be predominately caused by the decreased phosphorylation and nuclear translocation of the DAF-16/FOXO transcriptional regulator leading to expression of over 200 genes including those involved in metabolism, proteostasis, and antioxidant defenses , . Activation of other factors such as the SKN-1/Nrf2 transcriptional regulator also contributes to the longevity effects of reduced IIS under certain experimental conditions . The increased life span of the daf-2 mutant could be further increased by dietary restriction indicating at least partially distinct mechanisms of action .

Figure 1

Measuring The Potential Energy Of The Great Controlling Nucleotide Coenzymes


Figure 1. The great nucleotide coenzymes. illustration by Sam Lally, grandson of Richard L. Veech.

Although pathways are important, it is just as important to know what role is played by these 3 to 5 letter abbreviations of coenzymes that magically appear over and over along those paths. These great nucleotide coenzymes work like a group of circus acrobats jumping from a platform onto a teeter board. The acrobats convert potential energy to kinetic energy when they jump down. Standing on the downside of the teeter board is an acrobat that will be hurled spinning into the air and land in a seat. The coenzymes provide chemical potential energy needed to drive the metabolic pathways. Acrobats must carefully measure the heights and mass and know the formula for the conversion of potential energy to kinetic energy. Potential energy of the launching acrobats that jump from a platform determines if a stunt is likely to succeed. In the same way the potential energy of the great controlling nucleotides determines the likelihood of all the chemical reactions in the metabolic pathways.

Josiah Willard Gibbs provided the thermodynamic equation describing chemical potential. It is known as the Gibbs free energy equation. It is a measure of the energy found in the chemical bonds and a measure of energy related to changes in entropy. Apparently, it takes energy to organize things. Dr. Veech would use this equation along with a close variant proposed by Walther Nernst.

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