Alzheimers

Peer-Reviewed Scientific Articles​

Ketone Bodies can provide Neuroprotection in Neurological Diseases

URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6581710/

Journal: Front Neurol

Publication Date: 05/2016

Summary: There is growing evidence that ketone bodies, which are derived from fatty acid oxidation and usually produced in fasting state or on high-fat diets have broad neuroprotective effects. Although the mechanisms underlying the neuroprotective effects of ketone bodies have not yet been fully elucidated, studies in recent years provided abundant shreds of evidence that ketone bodies exert neuroprotective effects through possible mechanisms of anti-oxidative stress, maintaining energy supply, modulating the activity of deacetylation and inflammatory responses. Based on the neuroprotective effects, the ketogenic diet has been used in the treatment of several neurological diseases such as refractory epilepsy, Parkinson’s disease, Alzheimer’s disease, and traumatic brain injury. The ketogenic diet has great potential clinically, which should be further explored in future studies. It is necessary to specify the roles of components in ketone bodies and their therapeutic targets and related pathways to optimize the strategy and efficacy of ketogenic diet therapy in the future.

Key Takeaways

Ketone bodies produced by fat burning metabolism likely have a protective effect on the brain. Ketogenic diets have been used in the treatment of neurologic diseases such as epilepsy, Parkinson's, Alzheimer's, and traumatic brain injury. The exact mechanism that ketones play in protecting the brain is still being studied, but the current evidence points to the ketone's ability to reduce oxidative stress, reduce inflammation, and maintain energy supply in the brain.

Ketones Protect The Brain From Injury and Degeneration

Nutrition and Alzheimer’s disease: The detrimental role of a high carbohydrate diet

URL: https://www.ejinme.com/article/S0953-6205(11)00004-5/fulltext

Journal: European Journal of Internal Medicine

Publication Date: 04/2011

Summary: Alzheimer’s disease is a devastating disease whose recent increase in incidence rates has broad implications for rising health care costs. Huge amounts of research money are currently being invested in seeking the underlying cause, with corresponding progress in understanding the disease progression. In this paper, we highlight how an excess of dietary carbohydrates, particularly fructose, alongside a relative deficiency in dietary fats and cholesterol, may lead to the development of Alzheimer’s disease. A first step in the pathophysiology of the disease is represented by advanced glycation end-products in crucial plasma proteins concerned with fat, cholesterol, and oxygen transport. This leads to cholesterol deficiency in neurons, which significantly impairs their ability to function. Over time, a cascade response leads to impaired glutamate signaling, increased oxidative damage, mitochondrial and lysosomal dysfunction, increased risk to microbial infection, and, ultimately, apoptosis. Other neurodegenerative diseases share many properties with Alzheimer’s disease, and may also be due in large part to this same underlying cause.

Key Takeaways

Excess carbohydrates in the diet play an important role in the development of Alzheimer's disease. Carbohydrates in the diet are broken down to sugars that when present in excessive quantities allows them to bind to proteins and impair their function. When these sugars bind to proteins essential for carrying fat, cholesterol, and oxygen to the brain, signaling mechanisms in the brain become impaired, which leads to inflammation, mitochondrial and lysosomal dysfunction, infection susceptibility, and cell death.

Are Carbohydrates Causing Alzheimer's Disease?

The ketogenic diet as a treatment paradigm for diverse neurological disorders

URL: https://www.frontiersin.org/articles/10.3389/fphar.2012.00059/full

Journal: Frontiers in Pharmacology

Publication Date: 04/2012

Summary: Dietary and metabolic therapies have been attempted in a wide variety of neurological diseases, including epilepsy, headache, neurotrauma, Alzheimer disease, Parkinson disease, sleep disorders, brain cancer, autism, pain, and multiple sclerosis. The impetus for using various diets to treat – or at least ameliorate symptoms of – these disorders stems from both a lack of effectiveness of pharmacological therapies, and also the intrinsic appeal of implementing a more “natural” treatment. The enormous spectrum of pathophysiological mechanisms underlying the aforementioned diseases would suggest a degree of complexity that cannot be impacted universally by any single dietary treatment. Yet, it is conceivable that alterations in certain dietary constituents could affect the course and impact the outcome of these brain disorders. Further, it is possible that a final common neurometabolic pathway might be influenced by a variety of dietary interventions. The most notable example of a dietary treatment with proven efficacy against a neurological condition is the high-fat, low-carbohydrate ketogenic diet (KD) used in patients with medically intractable epilepsy. While the mechanisms through which the KD works remain unclear, there is now compelling evidence that its efficacy is likely related to the normalization of aberrant energy metabolism. The concept that many neurological conditions are linked pathophysiologically to energy dysregulation could well provide a common research and experimental therapeutics platform, from which the course of several neurological diseases could be favorably influenced by dietary means. Here we provide an overview of studies using the KD in a wide panoply of neurologic disorders in which neuroprotection is an essential component.

Key Takeaways

The ketogenic diet has been shown to be neuroprotective and used in the treatment of epilepsy. The exact mechanisms of how the diet is protective against epilepsy is unclear, but it is thought that energy regulation plays a major role. Because the ketogenic diet does not rely on continuous inputs of carbohydrates, blood sugar levels remain constant. Without these large fluctuations in blood sugar, the energy supply to the brain is stable resulting in a reduction in seizures. Additionally, ketone bodies produced by burning fat are neuroprotective in their own way through a variety of actions. This dietary approach has been shown to be helpful in treating other neurologic conditions such as headache, neurotrauma, Alzheimer disease, Parkinson disease, sleep disorders, brain cancer, autism, pain, and multiple sclerosis.

Is The Ketogenic Diet The Best Treatment For Neurologic Diseases?

Dietary ketosis enhances memory in mild cognitive impairment

URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3116949/

Journal: Nuerobiology of Aging

Publication Date: 02/2012

Summary: We randomly assigned 23 older adults with Mild Cognitive Impairment to either a high carbohydrate or very low carbohydrate diet. Following the six-week intervention period, we observed improved verbal memory performance for the low carbohydrate subjects (p = 0.01) as well as reductions in weight (p < 0.0001), waist circumference (p < 0.0001), fasting glucose (p = 0.009), and fasting insulin (p = 0.005). Level of depressive symptoms was not affected. Change in calorie intake, insulin level, and weight were not correlated with memory performance for the entire sample, although a trend toward a moderate relationship between insulin and memory was observed within the low carbohydrate group. Ketone levels were positively correlated with memory performance (p = 0.04). These findings indicate that very low carbohydrate consumption, even in the short-term, can improve memory function in older adults with increased risk for Alzheimer’s disease. While this effect may be attributable in part to correction of hyperinsulinemia, other mechanisms associated with ketosis such as reduced inflammation and enhanced energy metabolism also may have contributed to improved neurocognitive function. Further investigation of this intervention is warranted to evaluate its preventive potential and mechanisms of action in the context of early neurodegeneration.

Key Takeaways

Low carbohydrate ketogenic diets showed improved memory, weight loss, blood sugar, and fasting insulin in adults with mild cognitive impairment. Further research is needed to determine whether the improvement is due to correction of high insulin levels, or the reduction in inflammation brought about by the ketosis.

Ketogenic Diet Improves Memory in Adults With Cognitive Impairment

Intermittent fasting from dawn to sunset for 30 consecutive days is associated with anticancer proteomic signature and upregulates key regulatory proteins of glucose and lipid metabolism, circadian clock, DNA repair, cytoskeleton remodeling, immune system and cognitive function in healthy subjects

URL: https://www.sciencedirect.com/science/article/pii/S1874391920300130

Journal: Journal of Proteomics

Date of Publication: 04/2020

Summary: Murine studies showed that disruption of circadian clock rhythmicity could lead to cancer and metabolic syndrome. Time-restricted feeding can reset the disrupted clock rhythm, protect against cancer and metabolic syndrome. Based on these observations, we hypothesized that intermittent fasting for several consecutive days without calorie restriction in humans would induce an anticarcinogenic proteome and the key regulatory proteins of glucose and lipid metabolism. Fourteen healthy subjects fasted from dawn to sunset for over 14 h daily. Fasting duration was 30 consecutive days. Serum samples were collected before 30-day intermittent fasting, at the end of 4th week during 30-day intermittent fasting, and one week after 30-day intermittent fasting. An untargeted serum proteomic profiling was performed using ultra high-performance liquid chromatography/tandem mass spectrometry. Our results showed that 30-day intermittent fasting was associated with an anticancer serum proteomic signature, upregulated key regulatory proteins of glucose and lipid metabolism, circadian clock, DNA repair, cytoskeleton remodeling, immune system, and cognitive function, and resulted in a serum proteome protective against cancer, metabolic syndrome, inflammation, Alzheimer’s disease, and several neuropsychiatric disorders. These findings suggest that fasting from dawn to sunset for 30 consecutive days can be preventive and adjunct therapy in cancer, metabolic syndrome, and several cognitive and neuropsychiatric diseases.

Key Takeaways

14 hour daily fasting from daw to sunset for 30 days showed upregulation of metabolic proteins, DNA repair enzymes, immune function, cognitive function, and circadian rhythm. This fasting regimen was also associated with protective effects against cancer, metabolic syndrome, inflammation, Alzheimer's disease, and psychiatric disorders.

Daily 14 Hour Fasting Provides a Host of Health Benefits

Menaquinone-4 Suppresses Lipopolysaccharide-Induced Inflammation in MG6 Mouse Microglia-Derived Cells by Inhibiting the NF-κB Signaling Pathway

URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6540242/

Journal: International Journal of Molecular Sciences

Publication Date: 05/2019

Summary: Alzheimer’s disease is associated with glial inflammation. In a rat model, MK-4, a subtype of Vitamin K2, reduced the inflammatory response of glial cells to LPS exposure.

Key Takeaways

Vitamin K2 is a nutrient found only in animal foods that reduced brain inflammation in rat models.

Vitamin K2 May Reduce Brain Inflammation, Where Can I Get It?

Ketogenic diet rescues cognition in ApoE4+ patient with mild Alzheimer’s disease: A case study

URL: https://www.sciencedirect.com/science/article/abs/pii/S1871402118306684?via%3Dihub

Journal: Diabetes & Metabolic Syndrome: Clinical Research & Reviews

Publication Date: 03/2019

Summary: The significant results in both MetS biomarkers and the MoCA score suggest that a ketogenic diet may serve to rescue cognition in patients with mild AD. The results of this case study are particularly compelling for ApoE4 positive (ApoE4+) subjects as ketogenic protocols extend hope and promise for AD prevention.

Key Takeaways

ApoE4 is a genetic marker that is thought to increase one's risk for Alzheimer's disease. A ketogenic diet showed improvement in cognitive performance in ApoE4 positive patients with mild cognitive impairment.

Do You Have The ApoE4 Gene? Try Switching To a Ketogenic Diet For Alzheimer's Prevention

Nutrition and Alzheimer’s disease: The detrimental role of a high carbohydrate diet

URL: https://people.csail.mit.edu/seneff/EJIM_PUBLISHED.pdf

Journal: European Journal of Internal Medicine

Publication Date: 04/2011

Summary: A review of the role of an excess of dietary carbohydrates and deficiency of dietary fats and cholesterol in the development of Alzheimer’s disease.

Key Takeaways

Eating too many carbohydrates and not enough fats and cholesterol can lead to the development of Alzheimer's disease.

High Carbohydrate Low Fat Diets Are Risky For Alzheimer's Development

Hyperinsulinemia and risk of Alzheimer disease

URL: https://www.ncbi.nlm.nih.gov/m/pubmed/15477536/

Journal: Neurology

Publication Date: 11/2004

Summary: Observational study of 683 American men >65 years old without dementia at baseline. Hyperinsulinemia is associated with a higher risk of AD and decline in memory.

Key Takeaways

After studying 683 Americans above the age of 65, there was an association between high insulin levels and risk of Alzheimer's disease and decreased memory.

Alzheimer's Disease: Sometimes Called Type 3 Diabetes Due To Its Association With High Insulin

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