What Were The Most Surprising Results From The Pilot Study
To tell the truth, I anticipated a few of the variables improving, but I never imagined that every single variable we tested would improve significantly over 12 weeks! Every one! This, in my experience, is rather unheard of, even for a small, short-term study like this one.
All biomarkers, and I mean all of them, improved significantly . Of course, I knew these would improve somewhat but did not expect them to show statistically significant changes in 12 weeks.
More surprisingly were the changes in the UPDRS scores. The UPDRS is a scale used to assess symptoms of PD. There were significant improvements in Behavior, Mentation, and Mood scores in 12 weeks. Additionally, improvements in scores on the Depression and Anxiety scales were also seen in 12 weeks, even in the midst of COVID isolation. This was surprising.
Many of my 16 participants reported improvements in quality of life including increased willingness to socialize with others. Persons with PD often isolate themselves due to feelings of embarrassment over their symptoms or speech difficulties. Many said they were more willing to get out into society and participate . They reported improvements in cognition and a reduction in brain fog, which is a common complaint in PD.
How The Ketogenic Diet Can Boost Brain Health
Theres substantial research proving ketogenic diets are quite beneficial in tackling certain brain dysfunctions. The presence of ketone bodies has a neuroprotective effect on the brain. In addition, ketone bodies enhance the function of mitochondria, the powerhouses of the cell, and reduce inflammatory chemicals in the blood, acting to maintain good brain function.
The brain disorders helped by the ketogenic diet are conditions such as Alzheimers Disease, epilepsy, and Parkinsons Disease.
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.
Recommended Reading: Does Rls Lead To Parkinson’s
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!
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 .
Don’t Miss: Ok Google Parkinson’s Disease
Why Do You Think There Isnt Much Evidence Yet With Using Kd For Neurodegenerative Diseases What Else Needs To Happen For Other Practitioners To Adopt This Treatment Modality
This is a really good question and one that baffles me. With PD and Alzheimers Disease on the rise in our world, why are there very few research studies or talks online regarding the effects of TCR and KD on persons with neurodegenerative diseases? This, in my opinion, is a large gap. I have kept track, and for all the conferences on the LCHF/KD lifestyle I have attended in the past five years, there has not been one talk on the management of neurodegenerative diseases using this approach. Why is this? It seems the focus has been largely on diabetes and cardiovascular diseases, which is good to establish the benefits. However, Pringsheim estimates that 50 million people worldwide suffer from neurodegenerative diseases , and that by 2050 this figure will increase to 115 million people . This is in comparison with type 2 diabetes where according to an article by Khan , the author estimates that Globally, an estimated 462 million individuals are affected by type 2 diabetes , corresponding to 6.28% of the worlds population .
I sincerely appreciate the work of Dr. Matthew Phillips in New Zealand who encouraged me in the design of my study and allowed me to use some of his patient materials with my participants. His work in PD is ongoing and I consider him to be one of the few experts on the use of TCR and KD with PD.
Effects Of Nutritional Ketosis On Parkinsons Disease Evidence And Theories
One of the key correlates of both aging and insulin resistance is the reduced cerebral metabolic rate of glucose as defined by positron emission tomography fluorodeoxyglucose tracer . Cerebral metabolic rate can be gauged indirectly via functional magnetic resonance imaging blood oxygen level-dependent signal. One measure, the amplitude of low-frequency fluctuations , is correlated with cerebral blood flow and studied as a possible index of regional network stability over time. As described by reviews on fasting NK , there are benefits associated with fasting in rodent models of learning and memory associated with PI3K via cyclic AMP response element binding protein and brain-derived neurotrophic factor pathways activated in this state as an evolutionary adaptation for homeostasis and survival. Such pathways provide a mechanistic theory for learning and memory involving brain network stabilization, which may be a target for NK therapy. Evidence for a similar benefit was found via insulin administration, and similarly by fasting, ketogenic diet, and exogenous ketone ester drink, as described below.
Fig. 1
Press and pulse model for neurometabolic degenerative disease. Hypothetical intervention begins at week 4 in the home with ketone meter, BP cuff and weekly lab testing, showing improved metabolic syndrome parameters. Instructions to fast and/or exercise produces episodically elevated ketosis
Also Check: Can Parkinson’s Go Away
Ketogenic Diet Neuroprotective Activity
In neurodegenerative diseases, it has so far not been possible to propose any causative therapy, since the atiology of the diseases is still not well-understood. The goal of neuroprotection is then either a slowing down or a complete stop of the processes, which leads to neuronal death in the CNS .
Increased production of ketone bodies by the liver and reduction in blood glucose concentration are key factors of significance for the therapeutic effects of KD. An increased concentration of ketone bodies is largely a consequence of fatty-acid oxidation. Oxidative stress and mitochondrial dysfunction are highlighted as central features of brain degenerative diseases. Oxidative stress, a condition that occurs due to an imbalance in oxidant and antioxidant status, has been known to play a vital role in the pathophysiology of neurodegenerative diseases, including AD and PD. Although reactive oxygen species play a pivotal role in several cellular and signaling pathways at physiological concentrations , excessive generation of ROS leads to several harmful effects, including DNA, lipid, and protein damage. Mitochondrial dysfunction and enhanced apoptosis, accompanied by a poor antioxidant status, are the mechanisms of AD pathogenesis. The pathology of PD is characterized by the gradual and selective loss of dopaminergic neurons in the substantia nigra pars compacta. Imbalance in dopamine metabolism due to oxidative stress has been recognized as a contributor to this disease .
More On Fasting And Keto For Individuals With Pd
Its slightly too early to claim that the ketogenic diet dramatically improves Parkinsons disease and Alzheimers. But this approach, as well as fasting, is quickly showing some strong potential. Since its outside the realm of drugs and medications, its a very gentle method that is gaining attention.
Both diets rely on our bodies switching to an alternate energy source ketone bodies. Keto diet for Parkinsons patients can increase ketones fourfold, whereas fasting has been shown to increase ketones by up to twentyfold.
Researchers assume that the positive effects seen in mice could be rooted in evolution. The transition from hunter-gatherer to agricultural societies meant that people no longer had to go long periods without eating. However, back then, our bodies favored those who could survive with long breaks between meals.
Our bodies are dependent on glucose as an energy source that we receive from carbohydrates in foods. It lasts for about 12 hours after we eat, and then our bodies switch to ketones. These chemicals also fuel our organs, including the brain. Higher ketone production has been linked to improved thinking, learning, and memory.
Other reasons Parkinsons and Alzheimers patients are recommended fasting are:
Read Also: How To Improve Balance In Parkinson’s Disease
Metabolic Changes Associated With The Use Of The Ketogenic Diet
In the course of the KD, the body modifies its metabolism to its fasting-related form. In the initial stage of the KD, blood glucose concentration lowers, and the insulin-to-glucagon ratio is decreased. A higher glucagon concentration leads to mobilization of glucose acquisition from its resources in the liver . Following two or three days of fasting or after a drastic reduction of carbohydrate supplementation in the diet , glycogenesis is suppressed and glucose reserves begin to be insufficient for the normal course of fat oxidation through the supply of oxaloacetate in the Krebs cycle , as well as to meet the demands of the Central Nervous System . Since CNS uses glucose as a primary energy source, after 23 days of fasting it has to identify an alternative source of energy, which is provided by the ketone bodies acetoacetate, 3-hydroxybutyrate, and acetone. The process of their production is called ketogenesis, and occurs mainly in the mitochondrial matrix of hepatic cells .
A Ruledme Keto Diet Vs A Low
In this randomized controlled trial, 47 patients were selected and 38 of them completed the 8-week dietary protocol. 20 of the patients who completed the study were on the low-fat diet, and 18 followed the keto diet.
Each diet plan was designed to provide similar calorie and protein content. The primary differences between the two diets were in carb, fat, and fiber content.
To give you a better idea of each diet, heres a chart with the average macronutrient and calorie intake of each group:
| Low-fat Diet | |
| 33 | 11 |
However, this was not a controlled feeding trial where every piece of food was measured precisely before consumption, so it is highly unlikely that the subjects ate the recommended amount.
The study followed a more realistic dietary change protocol including 4week diet plans including weekly shopping lists, daily menus, and simple, satisfying recipes. Along with the diet plan, each subject received tips on how to stay on the diet and troubleshoot common issues.
To help them craft a legitimate keto diet plan that is both satisfying and healthy, the researchers reached out to us, and we provided them with some of our most popular Ruled.me keto recipes and other diet tips, which they used as the basis for their keto diet meal plan.
In essence, the researchers created an abridged version of our Keto Academy for their Parkinsons disease patients. If youd like to take a look at the keto meal plan and information that each subject received, follow this link.
Read Also: Can Stress Cause Parkinson’s
Low Or Restricted Protein
A low-protein diet involves eating less high protein foods including dairy products, eggs, beans, pulses, fish, and meat, and eating more low-protein food such as cereal products , fruit, and vegetables.
What does the research say?For some people with Parkinsons, protein seems to interfere with how well levodopa is absorbed by the body and can cause fluctuations in symptoms. As a result, a large number of studies have investigated whether reducing protein intake or controlling when people eat protein in the day may be helpful for those people.
A recent review of all these studies found that low protein or redistributed protein diets can be beneficial for people with Parkinsons who experience fluctuations in the effectiveness of their medication due to dietary protein. However, there can be side effects including increasing dyskinesia and weight loss which need to be carefully monitored.
How Do You Educate Patients With Parkinsons To Adopt A Lchf Diet What Has Been Your Biggest Challenge
I have not found a website with more educational materials and videos for my patients and participants needing to adopt the TCR lifestyle than the Keto-Mojo website. I use thevideos on the website for training on blood glucose and ketone testing to teach my participants and patients how to use the Keto-Mojo meter. I find the resources to be incredible and direct my patients to the site to answer any questions they might have.
My biggest challenge in PD is the apathy associated with reductions in dopamine levels as the disease progresses. It is difficult to encourage patients with PD to initiate and follow-through, especially on dietary changes that reduce the sugar, something they use to self-medicate, if you get my meaning. Many persons with PD struggle with sugar in their diet. So little in their experience gives them the highs they crave and sugar often fits the bill.
Another challenge with the ketogenic diet is the abundance of meat in the diet. Many persons with PD have issues with chewing and swallowing so adjustments need to be made to be able to keep the high fats and moderate proteins without sacrificing safety when eating.
Recommended Reading: Can You Be Tested For The Parkinson’s Gene
Keto And Parkinsons: Is The Ketogenic Diet Useful For Parkinsons Disease
Research suggests that damage to a specific mitochondrial complex may cause the death of dopaminergic neurons. This leads to impairments in energy production, causing neurons to starve. Since the uptake of ketone bodies utilize a completely different transport system, as compared to glucose, they may be able to provide neurons with an alternative fuel source.
Furthermore, research suggests ketones improve mitochondrial health and may help protect from further damage. Studies show that supplementation with exogenous ketones may also improve symptoms of Parkinsons disease.
For more information about the therapeutic benefits of a ketogenic diet for Parkinsons disease, check out the Parkinsons disease Doctors Guide in Keto Club.
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.
You May Like: Leaky Gut And Parkinson’s
The Impact Of The Ketogenic Diet On Pd
Several studies examined the potential impact of the KD on PD. In an 8-week clinical trial conducted in New Zealand, Philips et al. randomized participants to follow either a low-fat diet or a KD . Both diet plans provided participants with the same amount of protein and included a weekly shopping list, daily menu sets, and recipes . While both intervention groups experienced significant improvements in MDS-UPDRS Part I, Part II, and Part III scores, only the KD group experienced a significant improvement in MDS-UPDRS Part IV scores . As a result, the study by Philips et al. indicates that short-term use of either a low-fat diet or KD could alleviate PD symptoms. Because data was not collected on the effect of either diet post-intervention, more research is needed to examine the long-term implications of a low-fat diet or KD after diet cessation in PD. The occurrence of weight loss among participants in both diet groups and exacerbated tremor or rigidity among patients in the KD group also highlights the need for more research on the safety of long-term adherence to a KD in individuals with PD .