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.
Guy: At this time I could find very few cases of trying carnivore for PD, actually none doing 100% carnivore.
According to Ronda Patrick below, Carnivore naturally includes caloric restriction, intermittent fasting, changes to the microbiome, low carb diet, and consuming more cholesterol those are 5 powerful tools which do not require a long term carnivore diet, which is a risk.
The one tool unique to a carnivore is eliminating all!! lectins (toxic molecules found in plants.
How significant is that in relation to the other tools and the diet outcome is yet to see.
another player to consider is MTOR high protein diet might shift it towards activation instead of deactivation
so, waiting for this to clear
In the following video, Dr. Ronda Patrick talks to Joe Rogan about the anecdotal evidence that suggests a carnivorous diet may be effective in alleviating the symptoms of autoimmune disorder, PD and other neurological conditions. She talks about her extensive 30-page work covering the trend towards a restrictive animal only diet. She discusses why someone would try this diet and how many immune disorder sufferers are trying low-carb high-protein diets because of the anecdotal reports they have heard.
Dr. Patrick talks about various studies related to high-protein diets and studies related to resetting your immune system through diet. This fascinating podcast brings up the anecdotal evidence and studies of various diets and their effect on autoimmune disorders and PD neurological conditions. She also discusses the effect of fasting, the potential damage of various diets, the modified Ketogenic diet, and the mechanisms that happen in the body when you restrict your diet or fast.
Michael E. McEvoy the founder of Metabolic Healing gives a summary of studies on the connection between cholesterol, Parkinson’s Disease, and statins. Cholesterol plays an important role in PD, yet it is very controversial for different reasons. A 2018 cohort study found higher total cholesterol and LDL was associated with a decreased risk of PD over time for men, but not for women. The 2008 Honolulu-Asia Aging study found PD incidence increased with decreasing LDL-C levels in a dose-dependent manner for men aged 71-75. A 2006 Rotterdam-based study found higher total cholesterol associated with a significantly decreased risk of PD in women only. A 2017 study of 2,322 PD patients found high cholesterol associated with lower PD risk. These studies establish that higher cholesterol is associated with lower PD risk.
Studies that have found statins were protective have been criticized for having significant population bias. As yet no study which has shown statin protection against PD has accounted for patients with hyperlipidemia (these studies have excluded patients with hyperlipidemia). A 2017 study investigating the possibility of statins used in association with PD suggested that statin use may facilitate the onset of pre-clinical PD.
Related research presented in the video
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).
good results in rats
keto vs low fat
both diets had good results, keto was better
some ways Keto help are not well understood
A research article published in Plos One in2018 looks at results of multiple observational studies focused on one or more cardio-metabolic risk factors in vegans and omnivorous diets. Macro-nutrient intake and cardio-metabolic risk factors were compared by dietary pattern. People on vegan diets and others on omnivorous diets were compared for energy, saturated fats, body mass index, lipoprotein cholesterol, triglycerides, glucose levels, blood pressure. The results support the idea that plant-based diets are likely to lower the risk of cardiovascular disease and diabetes.
In a 2019 systematic review article published on Frontiers in Nutrition, the link between vegetarian dietary patterns and various cardiovascular outcomes were examined. The aim was to update the European Association for the Study of Diabetes (EASD) clinical practice guidelines for nutrition therapy. Several prospective cohort studies were examined and the results considered. Although overall evidence was graded as “very low quality” there were indications that vegetarian dietary patterns are associated with reductions in CHD mortality and incidence but not with CVD and stroke mortality in individuals with and without diabetes.
A systematic literature review published on NCBI in July 2020 summarizes evidence from various publications in regard to the role of diet and nutrition as a cause of migraines and as migraine triggers. Data was gathered from primary literature sources from March 2019 to January 2000 in patients over 18 years old. A total of 43 studies were included in the review assessing diet patterns, diet interventions, and diet-related triggers. Among the diets assessed were low-fat, elimination diets, keto diet, and diet-related triggers such as alcohol and caffeine. The review concluded that there is limited high-quality randomized controlled trial data on diet patterns or diet-related triggers. Although many patients already reported avoiding personal diet-related triggers in their migraine management, further research is necessary.
An article published in the MDPI journal, Nutrients in June 2020 looks at the influence of dietary patterns and dietary triggers on migraines. Identifying these triggers is challenging because so many other factors such as age, genetics, sex, and individual immunological responses to food can influence migraines. If the triggers can be identified they can be avoided to prevent migraines. This review presents the current status of research into diet and migraines and how lifestyle changes may increase the quality of life of patients. The review examines elimination diets; migraine diets; epigenetic diets; the gut-brain axis and probiotics in relation to migraines. The review concludes that the selection of an appropriate diet and obtaining correct dietary counseling is recommended to ensure the biopsychosocial well-being of migraine patients, as strict food avoidance may result in stress and poor quality of life.
Source:Migraine and Diet
In this Goop podcast chief content officer at Goop, Elise Loehnen talks to Valter Longo, author of the longevity diet, as part of a series on detox, nutrition, and resetting the body. Longo is also one of the world’s leading experts on fasting. During the interview, they tackle questions such as “Is intermittent fasting the key to health?” Longo proposes fasting as one of the elements that contribute to longevity and to a healthy life, avoiding the diseases that often plague the elderly. The podcast also addresses the research surrounding the connection between fasting and preventing autoimmune diseases and cancer as well as the idea of making fasting part of standard cancer treatment. Longo discusses clinical trials including seven clinical trials supporting FMD (Fasting Mimicking Diet).
The blood-thinning medication, warfarin decreases the chance of harmful blood clots by blocking the effects of vitamin K which helps blood-clotting proteins form in the liver. Your warfarin dose is determined by your PT or INR measurements that show how long it takes for your blood to form clots.
A document published by ImpactTeam looks at how your diet affects warfarin and how the amount of vitamin K in your diet will determine the warfarin dose needed to prevent bleeding. Warfarin may have possible interaction with cranberry juice, mango juice, grapefruit juice, caffeine, charbroiled foods, alcohol, garlic, soy, ginger, and green tea. In addition, there is potential interaction of dietary supplements with warfarin.
Source: Warfarin and your Diet
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.
Source: Low‐fat versus ketogenic diet in Parkinson’s disease: A pilot randomized controlled trial (© 2018 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.)
If you’re dealing with a chronic disease or you know someone who is then Chris Kresser’s Health Solutions Library can provide you with resources. Among the resources are books and ebooks that cover preventing and reversing chronic illness and guides for living a healthier life. There are also courses you can take in health care and articles focused on health written by leading specialists. Kresser offers an easy-to-use index to help you find the resources for your particular ailment.
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.
A review published in the Current Neuropharmacology journal in 2018 looked at the impact of dietary fats on brain function. It also examined gut-brain communication through microbiota; the impact of probiotics and prebiotics on brain functions; SCFA’s, microbiota, and neuroinflammation. It reviewed lipid sensing, satiety, and processing of hedonic food; the impact of diet on the hypo-thalamic control of reproduction; neuroprotective effects of N-3 PUFAs; dietary PUFAs, brain PUFAs and the role of PUFAs. The results of this review revealed that dietary fats are both friends and foes for brain functions. However, dietary manipulation for the treatment of brain disorders is not just a promise for the future, but a reality. In fact, the clinical relevance of the manipulation of dietary lipids, as for KDs, is well-known and currently in use for the treatment of brain diseases.
Source: Impact of Dietary Fats on Brain Functions
LGIT safe (see 305)
A review by Caldwell B. Esselstyn published in the Journal of Geriatric Cardiology in 2017 covered the connection between a plant-based diet and coronary artery disease. Caldwell states that in ignoring diet as a cause of CVD there is no hope for a cure as patients continue to consume the foods that destroy them. He discusses studies conducted using WFPBN in patients ill with CAD. The results showed that WFPBN can halt and reverse CVD. In summary, current palliative cardiovascular medicine consisting of drugs, stents, and bypass surgery cannot cure or halt the vascular disease epidemic and is financially unsustainable. WFPB can restore the ability of endothelial cells to produce nitric oxide, which can halt and reverse disease without morbidity, mortality, or added expense.
A study by Caldwell published by the NIH set out to show that plant-based nutrition helps prevent coronary artery disease in a large group of patients. 198 patients with CVD were followed and given counseling on how to convert from a regular diet to plant-based nutrition. Results showed that 89% adhered to the diet and in the group of adherent participants major cardiac events recurred at a rate of 0.6%. This was significantly less than reported in other similar studies where a smaller group was used. Of the non-adherent participants, 62% experienced adverse events. Caldwell concludes that patients with CVD respond to intense counseling and when on a sustained plant-based diet for a mean 3.7 years they experience a low rate of cardiac events. Plant-based nutrition has the potential for a large effect on the CVD epidemic.
Source: A Way to Reverse CAD?
Supporting Articles: Evidence listed by Coldwell to support a low-fat vegan diet:
- Chriss Kresser’s ebook on debunking diet-heart hypothesis + Grain brain by Perlmuter etc … high-fat low carb advocates
Will use Michel Greger and Ronda Patrick video’s as references, corresponding research to back up the claims, shows in the video background or on the website
Reduce meat increase plant-based foods,, especially cruciferous
boost liver enzymes with solphorofane (supplement or broccoli sprouts
see post here
go vegan-Greger on cancer
- 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.