Based On Your Experience How Are The Current Protocols For Treating Parkinsons Disease Symptoms Missing The Mark In Terms Of Improving Anxiety And Depression Symptoms
Well, I could really write a book here! The most common treatment we have for PD is the administration of a Carbo-Levodopa medication to replace the missing dopamine neurochemical. Unfortunately, this medication has many side effects, a short half-life, variability with interference from dietary ingredients, and the schedule for dosing vary from day to day. I also feel the treatment of anxiety and depression in PD uses all the common medications used for patients who do not have PD but have depression or anxiety diagnoses. Therefore, these medications often exacerbate the symptoms and cause severe side effects like lethargy, suicidal ideation, loss of appetite, etc. There has to be a better way!
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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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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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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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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
What Closes Or Opens The Gate That Lets Pyruvate Into The Mitochondria Energy Process
Four different enzymes start to close the pyruvate dehydrogenase complex gate and two enzymes can open it once partly closed. These enzymes regulate the opening and closing of the gate to let pyruvate into the mitochondria. The control of these enzymes is complex, but we know the gate is often closed in degenerative disease, infections, and trauma.
Dr. Veech knew HB does not go through the PDC to fuel the mitochondria. There are no gates to stop HB from making ATP once it reaches the mitochondria. This means HB can overcome a lack of energy found when the PDC switch turns off the flow of pyruvate fueling the mitochondria.
Dr. Veechs mentor at Harvard, George Cahill, had demonstrated that the brain could use HB for fuel when a person is fasting. Dr. Veech reasoned that HB could help people who have diseases where the gate that lets pyruvate into the mitochondria has been shut down. This includes many degenerative diseases such as Alzheimers and Parkinsons disease.
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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.
What Lead You To Become A Certified Metabolic Health Practitioner
I was so excited to see the formation of the Society of Metabolic Health Practitioners. Finally, an organization where those of us practicing TCR with our patients can have a home. We can receive ongoing support, training, and recognition as we seek to support each other along with encouraging ongoing research endeavors addressing the need to fill the gaps in research and add to the body of evidence for the use of TCR in chronic disease.
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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.
Can The Ketogenic Diet Help Parkinsons
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Emerging evidence supports the use of the ketogenic diet against a variety of neurological disorders including multiple sclerosis and Alzheimers. But what about Parkinsons? Is there a potential place for the ketogenic diet and could following this pattern of eating improve symptoms of Parkinsons and your quality of life? Before looking at the evidence lets first take a closer look at the ketogenic or keto diet.
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I Am Overweight What Can I Do
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.
Use Of Kd By Seniors: Risks
Among the elderly, malnutrition is a particularly common problem, caused by comorbidities, poor nutrition, and the aging process. Patients with dementia are more likely to develop it than healthy individuals . Malnutrition is associated with an inadequate and/or insufficient supply of nutrients, which can affect the loss of muscle mass and also contribute to poorer health, including the potential for premature death .
People diagnosed with PD are more likely to be malnourished and have a lower BMI compared to healthy individuals. The cause of this phenomenon is not fully understood. This is believed to be influenced by factors such as the severity of the condition, the presence of seizures, dyskinesia, and limited food intake among PD patients. Some patients are diagnosed with taste and smell disorders that may be related to dietary changes .
People suffering from AD are significantly more likely to develop sarcopenia compared to healthy individuals. The use of classic 4:1 and 3:1 KDs may exacerbate malnutrition and loss of muscle mass due to the reduced calorific value of the diet and low protein supply . The authors of some studies suggest that KD can prevent muscle atrophy, but other studies do not support this .
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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.
Various Foods That Are Easier To Consume
Because PD causes a loss of control of bodily motor function, chewing and swallowing can become very difficult. Thus, foods that dont require chewing and are easier to swallow are quite helpful for those suffering from PD. Some relatively healthy and easy to eat options you can try include: Unsweetened applesauce and strawberry jams, cream cheese or cottage cheese, soups, avocado or tahini dips, unsweetened fruit or vegetable smoothies and soft, well cooked sweet potatoes.
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Unplanned Weight Loss Or Weight Gain
The medications that people with Parkinsons disease usually take can cause the side effects of either loss of appetite or an increase in hunger . This can then lead to unintentional weight gain or weight loss both of which can cause issues to health.
As well as looking at the specific macronutrient distribution of the ketogenic diet, one must also be mindful of the calorie content.
Furthermore, as ketone bodies increase, they can elicit a natural appetite suppressing effect so further care must be taken to ensure adequate calories are consumed.
Feel free to use our keto calculator to find out how much you need to eat to maintain, lose, or gain weight.
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A proof of concept trial that recruited 14 people with PD and mild cognitive impairment, randomized to a standard western diet or a KD , reported a between-group improvement in aspects of cognitive performance in the KD group, without a difference in motor function
Krikorian R, Shidler MD, Summer SS, et al. Nutritional ketosis for mild cognitive impairment in Parkinsons disease: a controlled pilot trial. Clin Parkinsonism Relat Disord. 2019 1:4147.
The largest study was performed by Matt Phillips and his group in Hamilton, New Zealand. They conducted a pilot randomized, controlled trial to compare the plausibility, safety, and efficacy of a low-fat, high-carbohydrate diet versus a ketogenic diet in a hospital clinic of PD patients. The trial had 47 patients, of which 44 commenced the diets and 38 completed the study .
Both diet groups significantly improved their MDS-UPDRS scores over the 8-week diet intervention. Both diet groups improved in Part 1 , but the ketogenic group improved more every single patient in the ketogenic group improved in Part 1, resulting in a substantial 41% reduction in baseline Part 1 scores over the 8-week diet intervention.
Phillips M, Murtagh D, Gilbertson L, et al. Low-fat versus ketogenic diet in Parkinsons disease: a pilot randomized controlled trial. Mov Disord 2018 33:13061314.
ADDITIONAL REFERENCES
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Telomere Shortening Is Linked To Cellular Redox Status And Metabolism
The work of Hayflick and Moorhead pointed out that shortening of the telomeres set a limit to the number of divisions cells in culture could undergo before senescence occurs. Expression of the telomerase enzyme in certain germ and progenitor cells provides a solution to replicate the ends of linear chromosomes, so that the chromosomes do not become shorter with each new round of DNA replication. Telomeres are lengthened by starvation and shortened by ROS damage . These observations are consistent with aging being a function of reactive oxygen and its reversal a function of the increasing redox potential of the NADPH system brought about by caloric restriction. The FOXO protein FOXO1 was shown to be essential for the calorie restriction-mediated increase in telomerase subunit expression . As cells approach their Hayflick limit, the expression of the FOXO genes FOXO1 and FOXO4 have also been shown to decline , which would lead to decreased SOD2 and catalase expression. Senescent cells and tissues not only show decreased function but also acquire a senescence-associated secretory phenotype , a pro-inflammatory, pro-aging state. Mitochondrial dysfunction that increases ROS/RNS production also induces a cellular senescence program with a modified SASP .
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.
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