The keto diet is a high-fat, low-carbohydrate diet where the body’s blood sugar and insulin levels are lowered putting your body into a metabolic state called ketosis. During ketosis, your body doesn’t have enough insulin to turn sugar into energy so it uses fat instead. The liver turns the fat into ketones, a type of acid, and sends the ketones into the bloodstream. The standard keto diet (SKD) is very low-carb, moderate protein, and high fat; the high protein keto diet is similar to SKD but with higher protein intake; the cyclical keto diet (CKD) involves periods of ketogenic days followed by high carb days and the targeted keto diet (TKD) includes carb intake around workouts. Intermittent fasting may help you enter ketosis. The ketogenic diet may be useful in weight loss; reducing diastolic blood pressure and triglyceride levels; lowering blood sugar levels; improving insulin sensitivity and may be useful in treating neurological diseases. The keto diet may improve risk factors for epilepsy, heart disease, cancer, Alzheimer’s, and PD.
elevation of lymph ketone body levels by a high-fat, low-carbohydrate ketogenic diet or by administration of the ketone body β-hydroxybutyrate increases lymphangiogenesis – www.nature.com/articles/s42255-019-0087-y
Many studies show that low-carb and ketogenic diets can lead to dramatic weight loss and improve most major risk factors for heart disease and diabetes. Also, repeatedly shown (but not always) to help with or reverse PD and other neurologicsal conditions
Low carb diets (LCDs starting at a young age are associated with an increased risk of subsequent coronary artery calcification (CAC) progression, particularly when animal protein or fat are chosen to replace carbohydrates.
Mike Mutzel from High Intensity Health (author of Belly Fat Effect) talks to Frank Llosa of KetoneAid. KetoneAid produces a Ketone Ester (raw beta-hydroxybutyrate (BHB) ketone) supplement that can get you into a deep state of ketosis within 30 minutes. You would have to fast or go on an intense ketogenic diet to reach the same ketosis state. There are different types of Keto testing, blood glucose testing, and different types of exogenous Ketones. Ketosis is influenced by BHB salts; Ketone supplements. There have been many discussions about the link between PD and the ketogenic diet. In one study PD patients were put on a ketogenic diet for a month and the results showed a 43% improvement in the Unified Parkinson’s Disease rating scale. There is no doubt that PD is affected by diet and nutrition so the ketogenic diet may offer relief from some symptoms.
Mike Mutzel from High-Intensity Health (author of Belly Fat Effect) talks to William Curtis about his PD journey and how a ketogenic diet changed his life. Curtis suffered from PD for over 17 years before he started exercising, fasting, and following a low-carb, ketogenic diet that remarkably improved his PD symptoms. Through trial and error, Curtis found the right balance in his diet. The William Curtis’ program for easing PD symptoms is not appropriate for everyone. For example, PD patients that have balance problems could do more harm to themselves if they followed Curtis’ diet. After 12 hours of fasting through the night, Curtis has a bulletproof coffee in the morning prepared with butter, heavy cream, coconut oil, and Stevia. This helps his PD symptoms and increases the ketone D-betahydroxybutyrate (BHB).
This 2019 report in the National Library of Medicine (National Center for Biotechnology Information) looks at lifestyles and dietary habits associated with PD. A fasting mimicking diet (FMD), fasting 3 days followed by 4 days of refeeding for three 1-week cycles, which accelerated the retention of motor function and attenuated the loss of dopaminergic neurons in the substantia nigra in 1-methyl-4-phenyl-1,2,3,6-tetrathydropyridine (MPTP)-induced PD mice. Levels of brain-derived neurotrophic factor (BDNF), known to promote the survival of dopaminergic neurons, were increased in PD mice after FMD, suggesting the involvement of BDNF in FMD-mediated neuroprotection. The findings showed that FMD also inhibited neuroinflammation and modulated the shifts in gut microbiota composition.
A 2018 study published in NCBI aimed to compare the plausibility, safety, and efficacy of a low‐fat, high‐carbohydrate diet versus a ketogenic diet in PD patients. Primary outcomes were within‐ and between‐group changes in MDS‐UPDRS Parts 1 to 4 over 8 weeks. 47 patients were randomized, of which 44 commenced the diets and 38 completed the study (86% completion rate for patients commencing the diets). The ketogenic diet group maintained physiological ketosis. Both groups significantly decreased their MDS‐UPDRS scores, but the ketogenic group decreased more in Part 1 (−4.58 ± 2.17 points, representing a 41% improvement in baseline Part 1 scores) compared to the low‐fat group (−0.99 ± 3.63 points, representing an 11% improvement) (P < 0.001), with the largest between‐group decreases observed for urinary problems, pain and other sensations, fatigue, daytime sleepiness, and cognitive impairment. The trial found that It is plausible and safe for PD patients to maintain a low‐fat or ketogenic diet for 8 weeks. Both diet groups significantly improved in motor and nonmotor symptoms; however, the ketogenic group showed greater improvements in nonmotor symptoms.
A review focused on the role of ketogenic diets in neurodegenerative diseases (including PD) was published in the MDPI journal Nutrient in 2019. The goal of the review was to assess the effectiveness of ketogenic diets as part of therapy for neurodegenerative diseases. In PD, dopaminergic neurons in the substantia nigra are affected by a degeneration process leading to motor and non-motor disturbances. The available results of research projects dealing with the use of the KD and ketone bodies in neurodegenerative diseases are fairly promising. At the same time, the majority of studies reviewed were employed in vitro or by using animal models. The number of studies with human participation is rather small, and those that exist feature relatively short therapy duration periods.
high-fat, low-carb keto diet. Being in ketosis, the state where your body uses fat instead of glucose for energy, increases the NAD+ to NADH ratio. You want higher NAD+, because it protects cells from oxidative stress — an imbalance between free radicals and antioxidants in your body that contributes to aging.
Practice intermittent fasting. Restricting your eating increases NAD+ levels. Though calorie-restriction diets and periods of fasting will do it, those aren’t sustainable for the long term. Intermittent fasting is, if you do it right. Here’s how to get started with intermittent fasting.
Take oxaloacetate. A higher ratio of NAD+ to NADH helps you make more energy and makes your cells work better. Oxaloacetate activates the longevity pathway in a similar way that calorie restriction does. It converts to malate, which raises your NAD+ to NADH ratio, which makes more NAD+ available for your cells to use. Try: KetoPrime, a highly bioavailable form of oxaloacetate.
…What are the benefits of Ketosis?
Achieving a state of ketosis can have many benefits from treating chronic illnesses to optimizing performance. While the benefits are well documented, the underlying mechanism of action is not entirely known. The diet seems to enhance the ability of mitochondria, the power plants of our cells, to deliver our bodies’ energy needs in a manner that reduces inflammation and oxidative stress. Through optimizing the way our body uses energy, we fortify our bodies’ ability to take on the ever-growing stressors of our modern way of living.
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