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Video Presentations on the Dementia/Alzheimer's Disease and the Ketogenic Diet

019: How LOW CARB/KETO Can HELP Your BRAIN! (LOW CARB for NEUROSCIENCE PATIENTS) #ILCAW2023 - Dr. Don Agcopra

International Low Carb Awareness Week 2023

01-07 December 2023

In this presentation, I'll take you on an exciting journey through the fascinating realm of the low carbohydrate ketogenic diet (KD), exploring its medical and therapeutic applications, and its profound impact on patients in the fields of neurology and psychiatry. I will give you a captivating glimpse into the world of Metabolic Syndrome (MetS) and unravel its underlying mechanisms, dissect its potential connection to stroke, and discover how the innovative Therapeutic Carbohydrate Reduction (TCR) or Ketogenic Metabolic Therapy (KMT) serves as a powerful tool in my neurology practice, effectively addressing and preventing associated complications, with a special focus on stroke.

This presentation also tackles the important role of Ketogenic Metabolic Therapy (KMT) for patients with epilepsy, dementia/Alzheimer's disease (AD), Parkinson's disease (PD), Multiple Sclerosis (MS), migraine headache and neuropsychiatric/mental health problems.

Cognitive Improvement with Ketones in Mild Cognitive Impairment (MCI) - Dr. Stephen Cunnane, PhD

"Can Ketones Slow Down Alzheimer's?" - Dr. Stephen Cunnane, PhD

A diagnosis of Alzheimer’s disease (AD) strikes fear into everyone. But can AD be slowed down; can we do something to delay when it starts and how hard it strikes? There is growing evidence that a conscientious prevention approach can help one resist AD. The prevention approach to AD is the same as for what are called the ‘chronic Western diseases’ – hypertension, type 2 diabetes and obesity. The hormone insulin appears to play a key role in AD. Insulin tends to be less effective at controlling blood sugar (glucose) in older people, especially if they are sedentary. This in turn decreases the amount of fuel getting to the brain making it harder for brain cells to talk to each other so memories gradually slip away. Our research shows that it is difficult to increase glucose supply to the brain once it has declined in older people, even with exercise. Ketones are the brain’s back-up fuel and the brain of someone with AD can use ketones as well as the brain of a young adult. Moderate exercise helps get more ketones into the brain. Some older people may not be able to exercise but one can make a ketone drink made from medium chain triglyceride (MCT) in one’s kitchen. We are in the middle of a trial with an MCT drink in people at high risk of AD. The early results show a significant benefit for memory. There will be no miracle cures for AD but a prevention approach may delay and/or slow it down.

A major focus of Dr. Cunnane’s research over the past 30 years has been to develop a better understanding of the role of omega-3 fatty acids and ketones in human brain development and function. His team uses PET and MR imaging to study the impact of aging on brain structure and fuel metabolism. This information is applied to the development of keto-neurotherapeutic strategies for reducing the risk and progression of aging-associated cognitive decline and Alzheimer’s disease. He has published over 300 peer-reviewed research papers and five books. Two of his books highlight the concept that the key role of ketones for normal human brain development was of importance to overcoming the nutritional, metabolic and structural constraints on human brain evolution: Survival of the Fattest: The Key to Human Brain Evolution (World Scientific 2005), and Human Brain Evolution: Influence of Fresh and Coastal Food Resources (Wiley, 2010). Dr. Cunnane was elected to the French National Academy of Medicine in 2009. In Oct 2017, he received the Chevreul Medal from the French Society for the Study of Lipids for outstanding contributions in the area of omega-3 fatty acid metabolism and the role of ketones in optimal brain function during aging.

Can You Prevent or Reverse Cognitive Impairment and Early Dementia? -with Dr. Stephen Cunnane, PhD

Dr. Stephen Cunnane PhD discusses the beginnings of cognitive impairment and early reversible Alzheimer's. He makes very valid recommendations as to what you can do to reduce or reverse your cognitive impairment risk. We also discuss the importance of physical activity as a way to reduce the risk of dementia and the role of micronutrients. His findings are incredible. From childhood to senescence, what nutrition is optimal for the healthiest brain growth and development and which nutrient imbalances contribute to more rapid brain deterioration and brain cell dysfunction and death? Dr Cunnane is an incredible scientist willing to talk about what he knows but not willing to speculate like so many on the internet.

Know the scientific truth about how your body works. Ask and answer the right questions to optimize your health!

"Ketogenic Diets for Alzheimer's Prevention: Don't Push the ApoE4 Boulder" - Dr. Nicholas Norwitz, PhD

Dr. Nicholas Norwitz obtained his PhD in ketogenics and neurodegenerative diseases at Oxford University in just two years and is now pursing his MD at Harvard Medical School. His research expertise is ketosis and brain aging; however, he has published scientific papers on topics ranging from neuroscience to heart disease to gastrointestinal health to genetics to bone health to diabetes.

Nick’s passion for Food as Medicine is founded a personal history. At eighteen years old, he developed severe osteoporosis, a bone disease that crippled his promising running career. Next, Nick developed ulcerative colitis, an inflammatory bowel disease so severe as to cause him to lose twenty percent of his body weight in weeks and end up in the palliative care ward of a hospital with a heart rate in the twenties.

Through scientific self-study, Nick discovered his salvation in a ketogenic diet. He reversed his osteoporosis and colitis and is thriving! But Nick is grateful for his apparent misfortunes. In his words, “The most remarkable part of my story is that it’s not unique. The healthcare system isn’t built to address metabolic diseases. For that, we need metabolic medicine rooted in nutrition. My lifelong goal is to help reform the system and educate people. Plus, I’d like to think being a patient has made me a more compassionate person.”

"Treating and Preventing Dementia - How Diet Can Work When Drugs Fail" - Dr. Paul Mason

Dr Paul Mason obtained his medical degree with honours from the University of Sydney, and also holds degrees in Physiotherapy and Occupational Health. He is a Specialist Sports Medicine and Exercise Physician.

Dr Mason developed an interest in low carbohydrate diets in 2011. Since then he has spent hundreds of hours reading and analysing the scientific literature.

For a number of years, Dr. Mason has been applying this knowledge in treating metabolic and arthritis patients who have achieved dramatic and sustained weight loss and reductions in joint pain.

This presentation was recorded for 'Low Carb International All Stars – Online Conference' held in June 2020.

"Ketone Effects on the Brain: ApoE4, Vascular Dementia, Ischemia and Epilepsy" - Dr. Dominic D'Agostino

Elevated levels of ketone bodies, such as beta-hydroxybutyrate, can have beneficial effects on several brain-related diseases. Research suggests that ketone bodies can increase blood flow in the brain by 30 to 40 percent, which may have profound effects for patients with brain injury or vascular dementia. By studying ischemic wounds, which are analogous to an aged brain or clogged arteries, researchers observed increased blood flow when ketone levels were elevated. Nutritional ketosis may also reduce neural inflammation which may be a predictor of seizure in epilepsy. In this clip, Dr. Dominic D'Agostino describes the positive effects that ketones can have on the brain.

Keto Helps with Symptoms of Alzheimer's Disease

Could a ketogenic diet be the solution for Alzheimer's we have been waiting for? A new study shows that a ketogenic diet is better than a low-fat diet for quality of life and activities for daily living in those with Alzheimer's disease. For a devastating condition with few if any helpful treatments, this could be the start of a revolution in Alzheimer's care.

Ketones Improve Cognitive Function

A new study shows ketones improve cognitive function. This could have huge implications for treating those with early dementia.

Can Alzheimer's Be Treated with the Keto Diet? - Dr. Mary Newport, MD

Does a keto diet help with Alzheimer's? Alzheimer's Disease expert Dr. Mary Newport discusses her personal discovery of the ketogenic diet as an effective treatment for her husband's Alzheimer's symptoms.

Keto Diet In Human Trials For Mild Cognitive Impairment & Parkinson's - with Dr Mary Newport

In this video Dr Newport talks about some of the trials which are using MCT and ketogenic diets to address mild cognitive impairment and Parkinson's.

How Insulin Resistance Destroys Your Brain and Causes Alzheimer's Dementia - Dr. Ben Bikman, PhD

Nearly six million individuals live with Alzheimer’s disease in the U.S., and the numbers continue to rise. After 30 years of encountering dead ends while addressing Alzheimer’s disease as a problem of brain plaques, researchers are looking at other contributing factors. 

There is a growing body of evidence that indicates a strong correlation between Alzheimer’s disease and a disrupted metabolic state, where the brain can’t get enough energy.

On today’s episode of The Dhru Purohit Podcast, Dhru sits down with Dr. Benjamin Bikman, a renowned metabolic research scientist, and a popular speaker on human metabolism and nutrition. Backed by years of research, Dr. Bikman’s mission is to help the world appreciate the prevalence and relevance of insulin resistance. He is the author of, Why We Get Sick, which offers a thought-provoking yet real solution to insulin resistance and how to reverse pre-diabetes, improve brain function, shed fat, and prevent diabetes. Dr. Bikman has a Doctor of Philosophy in Bioenergetics from East Carolina University, a Master of Science in Exercise Physiology, and a Bachelor of Science in Exercise Science from Brigham Young University.

In this episode, we dive into:  

 - Why Alzheimer’s disease is increasingly being referred to as insulin resistance of the brain or Type 3 diabetes (7:30)

 - How the brain runs on different fuel sources (10:24)

 - Why insulin prevents the production of ketones (15:59)

 - Early signs of potential cognitive decline (27:02)

 - Common foods that drive insulin resistance (37:50)

 - The role insulin resistance plays in migraine headaches and epilepsy (52:22)

 - Where to get your carbohydrates from (1:02:25)

 - Foods that fuel your body and brain (1:05:40)

 - How seed oils wreak havoc on our health (1:13:43)

 - What you can do today to reduce your risk for Alzheimer’s disease (1:24:19)

Could Fructose Be Driving Alzheimer's Disease? - Dr. Richard Johnson & Dr. Robert Lustig

Fructose and its byproduct uric acid may play a role in the development of Alzheimer’s, thanks to an evolutionary adaptation hijacked by the modern diet. Fructose can be directly consumed, or the body can convert high-glycemic carbohydrates and other foods to fructose. Fructose suppresses some cognitive functions. Dr. Richard Johnson and Dr. Rob Lustig discuss a new study, of which Johnson was an author, on how fructose may be a potential driver in Alzheimer’s, and they hypothesize about fructose’s potential connection to the development of other conditions.

Scholarly Articles on Brain Insulin Resistance

Insulin Resistance in Brain and Possible Therapeutic ApproachesAlthough the brain has long been considered an insulin-independent organ, recent research has shown that insulin has significant effects on the brain, where it plays a role in maintaining glucose and energy homeostasis. To avoid peripheral insulin resistance, the brain may act via hypoinsulinemic responses, maintaining glucose metabolism and insulin sensitivity within its own confines; however, brain insulin resistance may develop due to environmental factors. Insulin has two important functions in the brain: controlling food intake and regulating cognitive functions, particularly memory. Notably, defects in insulin signaling in the brain may contribute to neurodegenerative disorders. Insulin resistance may damage the cognitive system and lead to dementia states. Furthermore, inflammatory processes in the hypothalamus, where insulin receptors are expressed at high density, impair local signaling systems and cause glucose and energy metabolism disorders. Excessive caloric intake and high-fat diets initiate insulin and leptin resistance by inducing mitochondrial dysfunction and endoplasmic reticulum stress in the hypothalamus. This may lead to obesity and diabetes mellitus (DM). Exercise can enhance brain and hypothalamic insulin sensitivity, but it is the option least preferred and/or continuously practiced by the general population. Pharmacological treatments that increase brain and hypothalamic insulin sensitivity may provide new insights into the prevention of dementia disorders, obesity, and type 2 DM in the future.
Insulin Resistance in Peripheral Tissues and the Brain: A Tale of Two SitesThe concept of insulin resistance has been around since a few decades after the discovery of insulin itself. To allude to the classic Charles Dicken’s novel published 62 years before the discovery of insulin, in some ways, this is the best of times, as the concept of insulin resistance has expanded to include the brain, with the realization that insulin has a life beyond the regulation of glucose. In other ways, it is the worst of times as insulin resistance is implicated in devastating diseases, including diabetes mellitus, obesity, and Alzheimer’s disease (AD) that affect the brain. Peripheral insulin resistance affects nearly a quarter of the United States population in adults over age 20. More recently, it has been implicated in AD, with the degree of brain insulin resistance correlating with cognitive decline. This has led to the investigation of brain or central nervous system (CNS) insulin resistance and the question of the relation between CNS and peripheral insulin resistance. While both may involve dysregulated insulin signaling, the two conditions are not identical and not always interlinked. In this review, we compare and contrast the similarities and differences between peripheral and CNS insulin resistance. We also discuss how an apolipoprotein involved in insulin signaling and related to AD, apolipoprotein E (apoE), has distinct pools in the periphery and CNS and can indirectly affect each system. As these systems are both separated but also linked via the blood–brain barrier (BBB), we discuss the role of the BBB in mediating some of the connections between insulin resistance in the brain and in the peripheral tissues.

Scholarly Articles on Brain AGE/RAGE

Scholarly Articles on Dementia/Alzheimer's Disease and the Ketogenic Diet

Randomized crossover trial of a modified ketogenic diet in Alzheimer’s disease - Alzheimer's Research & TherapyBackground Brain energy metabolism is impaired in Alzheimer’s disease (AD), which may be mitigated by a ketogenic diet. We conducted a randomized crossover trial to determine whether a 12-week modified ketogenic diet improved cognition, daily function, or quality of life in a hospital clinic of AD patients. Methods We randomly assigned patients with clinically confirmed diagnoses of AD to a modified ketogenic diet or usual diet supplemented with low-fat healthy-eating guidelines and enrolled them in a single-phase, assessor-blinded, two-period crossover trial (two 12-week treatment periods, separated by a 10-week washout period). Primary outcomes were mean within-individual changes in the Addenbrookes Cognitive Examination - III (ACE-III) scale, AD Cooperative Study - Activities of Daily Living (ADCS-ADL) inventory, and Quality of Life in AD (QOL-AD) questionnaire over 12 weeks. Secondary outcomes considered changes in cardiovascular risk factors and adverse effects. Results We randomized 26 patients, of whom 21 (81%) completed the ketogenic diet; only one withdrawal was attributed to the ketogenic diet. While on the ketogenic diet, patients achieved sustained physiological ketosis (12-week mean beta-hydroxybutyrate level: 0.95 ± 0.34 mmol/L). Compared with usual diet, patients on the ketogenic diet increased their mean within-individual ADCS-ADL (+ 3.13 ± 5.01 points, P = 0.0067) and QOL-AD (+ 3.37 ± 6.86 points, P = 0.023) scores; the ACE-III also increased, but not significantly (+ 2.12 ± 8.70 points, P = 0.24). Changes in cardiovascular risk factors were mostly favourable, and adverse effects were mild. Conclusions This is the first randomized trial to investigate the impact of a ketogenic diet in patients with uniform diagnoses of AD. High rates of retention, adherence, and safety appear to be achievable in applying a 12-week modified ketogenic diet to AD patients. Compared with a usual diet supplemented with low-fat healthy-eating guidelines, patients on the ketogenic diet improved in daily function and quality of life, two factors of great importance to people living with dementia. Trial registration This trial is registered on the Australia New Zealand Clinical Trials Registry, number ACTRN12618001450202 . The trial was registered on August 28, 2018.
Study of the ketogenic agent AC-1202 in mild to moderate Alzheimer's disease: a randomized, double-blind, placebo-controlled, multicenter trial - Nutrition & MetabolismBackground Alzheimer's disease (AD) is characterized by early and region-specific declines in cerebral glucose metabolism. Ketone bodies are produced by the body during glucose deprivation and are metabolized by the brain. An oral ketogenic compound, AC-1202, was tested in subjects with probable AD to examine if ketosis could improve cognitive performance. Methods Daily administration of AC-1202 was evaluated in 152 subjects diagnosed with mild to moderate AD in a US-based, 90-day, randomized, double-blind, placebo-controlled, parallel-group study. Subjects were on a normal diet and continued taking approved AD medications. Primary cognitive end points were mean change from Baseline in the AD Assessment Scale-Cognitive subscale (ADAS-Cog), and global scores in the AD Cooperative Study – Clinical Global Impression of Change (ADCS-CGIC). AC-1202 was compared to Placebo in several population groups, including: intention-to-treat (ITT), per protocol, and dosage compliant groups. Results were also stratified by APOE4 carriage status (a predefined analysis based on the epsilon 4 (E4) variant of the apolipoprotein E gene). This trial was registered with ClinicalTrials.gov, registry number NCT00142805, information available at http://clinicaltrials.gov/ct2/show/NCT00142805 Results AC-1202 significantly elevated a serum ketone body (β-hydroxybutyrate) 2 hours after administration when compared to Placebo. In each of the population groups, a significant difference was found between AC-1202 and Placebo in mean change from Baseline in ADAS-Cog score on Day 45: 1.9 point difference, p = 0.0235 in ITT; 2.53 point difference, p = 0.0324 in per protocol; 2.6 point difference, p = 0.0215 in dosage compliant. Among participants who did not carry the APOE4 allele (E4(-)), a significant difference was found between AC-1202 and Placebo in mean change from Baseline in ADAS-Cog score on Day 45 and Day 90. In the ITT population, E4(-) participants (N = 55) administered AC-1202 had a significant 4.77 point difference in mean change from Baseline in ADAS-Cog scores at Day 45 (p = 0.0005) and a 3.36 point difference at Day 90 (p = 0.0148) compared to Placebo. In the per protocol population, E4(-) participants receiving AC-1202 (N = 37) differed from placebo by 5.73 points at Day 45 (p = 0.0027) and by 4.39 points at Day 90 (p = 0.0143). In the dosage compliant population, E4(-) participants receiving AC-1202 differed from placebo by 6.26 points at Day 45 (p = 0.0011, N = 38) and 5.33 points at Day 90 (p = 0.0063, N = 35). Furthermore, a significant pharmacologic response was observed between serum β-hydroxybutyrate levels and change in ADAS-Cog scores in E4(-) subjects at Day 90 (p = 0.008). Adverse events occurred more frequently in AC-1202 subjects, were primarily restricted to the gastrointestinal system, and were mainly mild to moderate in severity and transient in nature. Conclusion AC-1202 rapidly elevated serum ketone bodies in AD patients and resulted in significant differences in ADAS-Cog scores compared to the Placebo. Effects were most notable in APOE4(-) subjects who were dosage compliant.