Alzheimer's and Dementia
Some are now referring to Alzheimer's Disease as Type 3 Diabetes. Is it possible that excess carbohydrates could be the cause of some of our dementia? Scientific discussion article here.
More detailed scholarly article here at the Western Price organisation website.
Georgia Ede writes about Alzheimer's.
The major hallmarks of Alzheimer’s Disease—neurofibrillary tangles, amyloid plaques, and brain cell atrophy—can all be explained by insulin resistance. A staggering 80% of people with Alzheimer’s Disease have insulin resistance or full-blown type 2 diabetes. The connection between insulin resistance and Alzheimer’s Disease is now so firmly established that scientists have started referring to Alzheimer’s Disease as “Type 3 Diabetes.”
High Low-Density Lipoprotein Cholesterol Inversely Relates to Dementia in Community-Dwelling Older Adults: The Shanghai Aging Study
Vitamin D and the risk of dementia and Alzheimer disease
"Our results confirm that vitamin D deficiency is associated with a substantially increased risk of all-cause dementia and Alzheimer disease. This adds to the ongoing debate about the role of vitamin D in nonskeletal conditions."
More detailed scholarly article here at the Western Price organisation website.
Georgia Ede writes about Alzheimer's.
The major hallmarks of Alzheimer’s Disease—neurofibrillary tangles, amyloid plaques, and brain cell atrophy—can all be explained by insulin resistance. A staggering 80% of people with Alzheimer’s Disease have insulin resistance or full-blown type 2 diabetes. The connection between insulin resistance and Alzheimer’s Disease is now so firmly established that scientists have started referring to Alzheimer’s Disease as “Type 3 Diabetes.”
High Low-Density Lipoprotein Cholesterol Inversely Relates to Dementia in Community-Dwelling Older Adults: The Shanghai Aging Study
Vitamin D and the risk of dementia and Alzheimer disease
"Our results confirm that vitamin D deficiency is associated with a substantially increased risk of all-cause dementia and Alzheimer disease. This adds to the ongoing debate about the role of vitamin D in nonskeletal conditions."
High carbohydrate diets and Alzheimer's disease.
Alzheimer's disease (AD) is a common, progressive, neurodegenerative disease that primarily afflicts the elderly. A well-defined risk factor for late onset AD is possession of one or more alleles of the epsilon-4 variant (E4) of the apolipoprotein E gene. Meta-analysis of allele frequencies has found that E4 is rare in populations with long historical exposure to agriculture, suggesting that consumption of a high carbohydrate (HC) diet may have selected against E4 carriers. The apoE4 protein alters lipid metabolism in a manner similar to a HC diet, suggesting a common mechanism for the etiology of AD. Evolutionarily discordant HC diets are proposed to be the primary cause of AD by two general mechanisms. (1) Disturbances in lipid metabolism within the central nervous system inhibits the function of membrane proteins such as glucose transporters and the amyloid precursor protein. (2) Prolonged excessive insulin/IGF signaling accelerates cellular damage in cerebral neurons. These two factors ultimately lead to the clinical and pathological course of AD. This hypothesis also suggests several preventative and treatment strategies. A change in diet emphasizing decreasing dietary carbohydrates and increasing essential fatty acids (EFA) may effectively prevent AD. Interventions that restore lipid homeostasis may treat the disease, including drugs that increase fatty acid metabolism, EFA repletion therapy, and ketone body treatment.
Alzheimer's disease (AD) is a common, progressive, neurodegenerative disease that primarily afflicts the elderly. A well-defined risk factor for late onset AD is possession of one or more alleles of the epsilon-4 variant (E4) of the apolipoprotein E gene. Meta-analysis of allele frequencies has found that E4 is rare in populations with long historical exposure to agriculture, suggesting that consumption of a high carbohydrate (HC) diet may have selected against E4 carriers. The apoE4 protein alters lipid metabolism in a manner similar to a HC diet, suggesting a common mechanism for the etiology of AD. Evolutionarily discordant HC diets are proposed to be the primary cause of AD by two general mechanisms. (1) Disturbances in lipid metabolism within the central nervous system inhibits the function of membrane proteins such as glucose transporters and the amyloid precursor protein. (2) Prolonged excessive insulin/IGF signaling accelerates cellular damage in cerebral neurons. These two factors ultimately lead to the clinical and pathological course of AD. This hypothesis also suggests several preventative and treatment strategies. A change in diet emphasizing decreasing dietary carbohydrates and increasing essential fatty acids (EFA) may effectively prevent AD. Interventions that restore lipid homeostasis may treat the disease, including drugs that increase fatty acid metabolism, EFA repletion therapy, and ketone body treatment.
APOE ε4, the door to insulin-resistant dyslipidemia and brain fog? A case study
Conclusion
Ketogenic protocols seem to exert powerful modulatory effects on the most treatment-resistant conditions including obese carriers of the APOE ε4 variant who suffer from comorbid mild cognitive impairment and T2DM. Previous clinical trials have demonstrated the neurological efficacy of the KD. The significant improvements in memory, executive function, MetS pathologies, and cerebral metabolic rate demonstrated in this case study are reproducible and could be easily translated to a general population of MetS patients with self-reported impairments in cognition. The novel approach of nutritional modulation to halt brain atrophy and restore cognitive functionality warrants further investigation.
Conclusion
Ketogenic protocols seem to exert powerful modulatory effects on the most treatment-resistant conditions including obese carriers of the APOE ε4 variant who suffer from comorbid mild cognitive impairment and T2DM. Previous clinical trials have demonstrated the neurological efficacy of the KD. The significant improvements in memory, executive function, MetS pathologies, and cerebral metabolic rate demonstrated in this case study are reproducible and could be easily translated to a general population of MetS patients with self-reported impairments in cognition. The novel approach of nutritional modulation to halt brain atrophy and restore cognitive functionality warrants further investigation.
