Wednesday, December 7, 2022
Wednesday, December 7, 2022
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Keto Diet For Parkinson’s

There Are Several Ways The Ketogenic Diet Can Benefit Parkinsons Disease:

Ketosis & Parkinson’s Disease: Improving Symptoms with a Ketogenic Diet
  • Neuro-Protection

The ketogenic diet has largely been used to treat epilepsy. It has been recognized that there are strong neuroprotective effects with the diet.

Nerves are, in large part, made up of fat. When healthy fat intake increases immensely, the building blocks that the body needs to repair and protect the nerves are available to use.

Ketones themselves are also a part of the neuroprotection piece. Ketone bodies act on the nerve cells to protect them from degenerating. In animal models with Parkinsons disease, the ketogenic diet improved motor function and increased nerve cell survival in the substantia nigra of mice exposed to neurotoxins.

Glucose and the normal metabolism of glucose causes metabolic oxidation, or stress, on the cells. Ketones, however, have antioxidant activity and protect the body from oxidative damage.

Parkinsons disease has a key factor, which is oxidative damage to the substantia nigra. This oxidative damage contributes to the degeneration of the nerves, which then leads to Parkinsons symptoms. Since ketones themselves have antioxidant activity, they can help prevent continued oxidative damage to the brain and nerves.

  • Improved Energy Production

Ketones provide an efficient energy source for neurons. Ketones have the ability to bypass a part of the metabolic pathway that leads to stress in energy production. Therefore, ketones are an efficient way to fuel the body without adding to the stress that normal glucose metabolism can induce.

Putting It All Together

Many aspects of Parkinsons disease are still a mystery. The motor and non-motor symptoms make it a difficult disease to cope with, prevent, and reverse, but there are some ways to help.

For example, the use of the ketogenic diet in the treatment of Parkinsons disease appears to be very promising. There is a lack of clinical data, however, on the practical application of using the diet and ketone supplements for Parkinsons disease. That being said, there is now a lot of lab and animal work as well as case studies of people implementing the diet for themselves and experiencing powerful effects.

Because of the current state of the evidence, it is best to look at the ketogenic diet as an effective supplementary treatment for Parkinsons disease, used to complement current medications. The strictness of the diet doesnt seem to matter as much as getting into ketosis does. To find out how to follow the diet and get into ketosis within the next week, read through our comprehensive beginners guide to the ketogenic diet.

Once you are following the ketogenic diet in a way that works for you and your lifestyle, feel free to improve the results of your treatment even further by:

P.S. Have a look at the Keto Academy, our foolproof 30-day keto meal planner. It has all the tools, information, and recipes needed for you to succeed.

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Ketosis: What It Is And How It Works

It is beyond the scope of this brief review to describe the process of ketogenesis . In brief, ketosis is the metabolic state in which the body switches from using glucose as its primary energy source to using ketones as an alternative source of fuel. This metabolic state, as noted above, is achieved when one consumes a low-carbohydrate, moderate protein, high-fat diet or when one fasts for a few days or experiences starvation. Because of the need to maintain stable glucose levels, even in the context of little or no consumption of carbohydrates, glucose is supplied by gluconeogenesis . Since protein is the major substrate for GNG, it can be depleted quickly, representing the primary threat from starvation or prolonged fasting. The reduction in the hormone insulin, driven by the depletion of glucose, promotes lipolysis providing fatty acids as a major energy source. To reduce the potentially dangerous depletion of lean body protein, fatty acids provide ketone bodies which become a secondary fuel source that partially replaces the brain and CNSs demand for glucose.

Apart from fasting, KD is the most carbohydrate-restricted eating pattern. Therefore, KD keeps circulating insulin levels low which, in turn, gives access to fat stores to be burned as fuel. This explains why diets lower in carbohydrates tend to promote the greatest magnitude of selective depletion of body fat in the treatment of obesity .

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What Does The Future Hold

The study of synergies offers great hope that the therapies will work, given time and further research into other synergies. Perhaps synergies with ketosis will even work with cancer. There are many fields where scientists are beginning to comprehend that metabolic interventions may be needed to tackle treatment of the disease they study. The current thinking is that several interventions will be needed to suppress the cancer cells.

In Dr. Veechs lab, Dr. Robert Pawlosky, and Todd King, are busy making the measurements of potential energies of the great nucleotide coenzymes and producing ketone ester for animal studies for studies in Parkinsons, Alzheimers, heart disease and radiation mitigation to name the major collaborations.

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Is The Keto Diet Right For Me

Ketogenic Diet and Parkinson

The keto diet can cause appetite suppression and as seen in all 3 studies weight loss. For some people with Parkinsons who are carrying extra weight this may be appropriate but for many struggling with poor appetite and unplanned loss of weight this dietary pattern may not be suitable.

If not well formulated the keto diet can lack fibre. A lack of dietary fibre can lead to or exacerbate constipation. to learn how to get an adequate amount of fibre on a keto diet.

The keto diet is very high in fat. If you suffer from gastroparesis or slow stomach emptying consuming very high-fat meals can cause symptoms such as nausea, stomach pain and bloating. As fat empties more slowly from the stomach this dietary pattern may not be suitable.

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Existing Literature On Nutritional Ketosis As Clinical Therapy In Parkinsons Disease

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

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Ketone Body Metabolism: Ketogenesis And Ketolysis

The classic ratio of fat to carbohydrate plus protein in the KD is 3:1 or 4:1, in which 8090% of total calories comes from fats, 4% from carbohydrates and 6% from proteins. Modifications of the diet to increase palatability and improve compliance are common, although may complicate drawing comparisons among different studies. These modifications include varying the relative amounts of macronutrients, the nature and sources of the fats and duration of the diet, while maintaining the appropriate fat to carbohydrate ratio. The general goal of classic and modified KDs is to achieve ketosis, a state in which levels of ketone bodies are elevated in the blood. Ketone bodies are chemically related water-soluble molecules that are generated by normal physiological metabolism of fatty acids by -oxidation. The most well-known ketone bodies are beta-hydroxybutyrate , acetoacetate and acetone. Typical circulating levels of ketone bodies within the blood are 100250 M, whereas physiological or nutritional ketosis leads to elevated ketone body levels in the range of 0.55 mM. In contrast, blood levels of ketone bodies in pathological ketoacidosis can reach up to 1525 mM. Levels of blood and urine ketones are often measured to assess adherence to the diet, although ketone concentrations do not always correlate with better outcomes .

Parkinsons And Weight Gain

Keto Diet & Parkinson’s Disease with William Curtis

Parkinsons medication does not tend to make people gain weight, but a small number of people may experience impulsive and compulsive behaviour. This is a side effect of some Parkinsons medication, particularly dopamine agonists and, in some cases, levodopa.

Impulsive behaviour is when a person cant resist the temptation to carry out certain activities. These are often activities that give an immediate reward or pleasure, such as gambling, hypersexuality and overeating.

So, someone may eat large amounts of food in a short period of time because they cant control their appetite, and as a result, they gain weight.

If you think youre experiencing this behaviour, speak to your GP, specialist or Parkinsons nurse.

We dont advise anyone to stop taking or to change their Parkinsons medication without the advice of their specialist or Parkinsons nurse.

Any changes have to be made slowly and gradually, and should always be carried out and reviewed by a specialist, because of the risk of side effects and withdrawal symptoms.

Someone experiencing impulsive or compulsive behaviour may not realise they have a problem. So its important that their carer is aware of these side effects.

Deep brain stimulation and weight gain

Some people with Parkinsons may put on weight quickly after having deep brain stimulation, a surgery sometimes used to treat the condition.

If you think youre experiencing this behaviour, speak to your GP, specialist or Parkinsons nurse.

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Other Ways To Improve Parkinsons Disease

As of now, the most promising research for reducing symptoms and improving the quality of life of Parkinsons patients is on ketones, the ketogenic diet, and specific medications nothing else. There are, however, some other simple strategies you can use to make life easier if you are struggling with Parkinsons disease:

Ketone Supplements And Parkinsons Disease

Ketones have powerful effects in the brain, and they seem to be the main reason for the benefits that many people with Parkinsons, Alzheimers, and epilepsy have experienced while following the ketogenic diet.

Although it is best to follow the ketogenic diet, you dont have to restrict your carbs to raise your ketone levels. Coconut oil, MCT oil, ketone salts and ketone esters can all be used to reliably increase ketones and potentially improve the condition of Parkinsons patients. The reason why I say potentially is because there is not enough clinical evidence to support ketone supplements as a treatment for Parkinsons disease. However, the existing evidence is promising.

For example, one particular study on mice that were administered the exogenous ketone, beta-hydroxybutyrate , for 7 days found that BHB protected against the structural and functional effects that occur in Parkinsons Disease. What is also interesting to note is that the animals presented with improvements of the disease even with ketone levels as low as 0.9 mmol/L. Many other lab-based studies also have demonstrated that BHB administration protects neurons and helps to correct the defects seen in the mitochondria that are thought to increase the progression of Parkinsons disease.

A recent case study report looked at the use of ketone salts that were given to an individual who has had Parkinsons Disease for the past 20 years.

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Impact On Parkinsons Disease

The small uncontrolled study demonstrated a 46% reduction in the UPDRS scale in 5 of the 7 individual who participated in the study. The participants followed the ketogenic diet for 28 days.

However, as this is a very small and uncontrolled study we cant be sure this was not due to the placebo effect.

Animal studies demonstrate protection against MPTP induced cell damage by protecting the mitochondria. Other studies report anti-inflammatory effects of ketones providing neuroprotection in MPTP models of Parkinsons disease.

Another mechanism that can be explored is the impact of the ketogenic on the microflora of the digestive tract in patients with Parkinsons disease. As more research supports the gut brain connection as an important factor in the development of this condition it becomes reasonable to wonder if regulating this microflora through diet could also regulate the condition itself.

The Deanna Protocol For Als

Pin on Keto

Most neurologists agree on three general facts about ALS and neurodegenerative diseases such as Parkinsons disease:

  • Cells lack energy
  • Glutamate, an excitatory neurotransmitter, accumulates.
  • The Deanna Protocol was developed by a determined physician, Dr. Vincent Tedone whose daughter Deanna was diagnosed with ALS. He teamed up with Dr. Dominic DAgostino and other researchers and they developed a protocol to address the third factor of excess glutamate accumulation.

    Their work focused on the actions of two normal enzymes necessary to breakdown glutamate:

  • GDH which breaks down glutamate to Alpha Keto Glutaric Acid a ketone molecule
  • GAD which breaks down glutamate into Gamma Amino Butyric Acid an inhibitory neurotransmitter.
  • AKG is an important substrate for the TCA/Krebs cycle which drives cellular energy processes. A lack of AKG stops the Krebs cycle and the affected cell dies. Low levels of GABA contribute to muscle spasticity and stiffness. Mainstream medicine teaches that GABA cant cross the blood brain barrier so its of no use to supplement with it. However, in ALS the BBB isnt working so well, and when given GABA, Deannas symptoms improved. Providing AKG as a supplement added to that improvement.

    Eventually, the team developed a protocol for treating Deanna which resulted in a marked improvement in her symptoms. It included supplementation with

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    Effects On Energy Metabolism

    As noted above, ketone bodies, including -hydroxybutyrate, that are produced during consumption of the ketogenic diet may serve as an alternative source of energy in states of metabolic stress, thus contributing to the neuroprotective activity of the diet. In fact, -hydroxybutyrate may provide a more efficient source of energy for brain per unit oxygen than glucose . Recently, using microarrays to define patterns of gene expression, made the remarkable discovery that the ketogenic diet causes a coordinated upregulation of hippocampal genes encoding energy metabolism and mitochondrial enzymes. Electron micrographs from the dentate/hilar region of the hippocampus showed a 46% increase in mitochondrial profiles in rats fed the ketogenic diet. Thus, the ketogenic diet appears to stimulate mitochondrial biogenesis. Moreover, there was a greater phosphocreatine : creatine ratio in the hippocampal tissue, indicating an increase in cellular energy reserves, as expected from the greater abundance of mitochondria. In sum, during consumption of the ketogenic diet, two factors may contribute to the ability of neurons to resist metabolic stress: a larger mitochondrial load and a more energy-efficient fuel. In combination, these factors may account for the enhanced ability of neurons to withstand metabolic challenges of a degree that would ordinarily exhaust the resilience of the neurons and result in cellular demise.

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    Tribute To Dr Richard Veech

    Sometimes it takes a prediction coming true to prove a hypothesis. Einstein predicted the gravity of the sun would bend the light from stars. He had to wait for Edington to take pictures of stars in the background of the sun. These stars are normally hidden by the suns light. A shift in position of those stars would indicate that those beams of light were bent as they raced past the nearby sun into Edingtons camera during the 1919 total eclipse demonstrating Einsteins prediction and changing the scientific paradigm. Dr. Veech made a bold hypothesis in several papers in 2002 and 2003 that ketones would be important in medicine. An examination of his lifes work leads one to ask, Is there evidence of these predictions? Are ketones becoming important in medicine?

    His friends and colleagues called him Bud. Everyone who worked in his lab, Martin Kemper, Robert Pawlosky, Todd King, Calvin Crutchfield, Yoshihiro Kashiwaya and many, many others called him Dr. Veech out of respect. Those who worked closest with him held him in highest esteem. Perhaps this was because Dr. Veech understood biochemistry from a different perspective, one that was not taught in books. Rather one that came from having ones work guided by annual reviews and direction from Hans Krebs, Albert Lehninger and others of that stature.

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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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