BASICS
- Dementia is on the increase.
- Associated with Type 2 Diabetes and Cardiovascular Disease.
- Link with Uric Acid inhibition of Nitric Oxide effect on circulation.
- Increased risk with obesity.
- Increased risk with an elevated Blood Glucose level.
IDEAS
The brain is no different to any other organ of the body in that it can succumb to chronic inflammation and poorer blood supply.
The consumption of Sugar and Polyunsaturated Seed Oils combine in our diet to create inflammation in every blood vessel wall and in every tissue in every organ of the body. The inflammatory process makes everything susceptible to damage and disease.
- Poorer cognitive performance in children in all age groups tested from 3 years through to teenage years.
- Childhood obesity looks to be a predictor of longer term cognitive problems.
- Breakfast is a VERY important predictor of cognitive function, attention and memory in children.
- Obesity as an adult is associated with poorer cognition and a greater risk of Dementia.
- Diabetes and Metabolic Syndrome increase the likelihood of poorer cognition and Dementia.
- Obesity in middle age is associated with a more rapid decline in cognition and Dementia.
- Obesity and hypertension in aging males was a poor predictor.
- Several rat experiments point towards fructose and sucrose but not glucose affect memory, object recognition and cognition. One human study supported this.
- ‘Added sugar’ in the diet rather than fruit and vegetable sourced fructose was implicated.
- Simple rather than complex carbohydrates may impair memory performance.
- Omega 3 Fatty Acids may have a protective effect on the fructose effect on cognition in rats.
- Human consumption of fish once per week reduced the risk of Alzheimer’s Disease.
Inflammation may be the mechanism of action which fits completely within the NoFructose model of Fructose, Polyunsaturated Fats and Processed Grains creating the ‘Perfect Storm’ of inflammation in every organ of the body.
MORE INFORMATION
Dementia is associated with cardiovascular disease as well as Type II diabetes. The link again appears to be related to uric acid having an inhibition of nitric oxide. At the brain it has the potential of being two-fold. There is a specific neuronal nitric oxide synthase which is unique to the brain and may be involved in maintenance of blood supply.
The second effect of uric acid inhibition of nitric oxide is that associated with cardiovascular disease and the inhibition creating a vasoconstrictive effect on blood vessels, relative hypertension and over time atherosclerotic disease and reduced blood supply to an end organ.
The brain is no different to any other organ of the body in that it can succumb to chronic inflammation and poorer blood supply.
Read about the Damage Process
Read about the Metabolism
Read about the Health Issues
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ARTICLES
Type 3 Diabetes – Alzheimer’s Disease
http://www.westonaprice.org/modern-diseases/type-3-diabetes-metabolic-causes-of-alzheimers-disease/
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Dietary ketosis enhances memory in mild cognitive impairment
Robert Krikorian et al
Glucose levels and risk of dementia.
BACKGROUND:
Diabetes is a risk factor for dementia. It is unknown whether higher glucose levels increase the risk of dementia in people without diabetes.
METHODS:
We used 35,264 clinical measurements of glucose levels and 10,208 measurements of glycated hemoglobin levels from 2067 participants without dementia to examine the relationship between glucose levels and the risk of dementia. Participants were from the Adult Changes in Thought study and included 839 men and 1228 women whose mean age at baseline was 76 years; 232 participants had diabetes, and 1835 did not. We fit Cox regression models, stratified according to diabetes status and adjusted for age, sex, study cohort, educational level, level of exercise, blood pressure, and status with respect to coronary and cerebrovascular diseases, atrial fibrillation, smoking, and treatment for hypertension.
RESULTS:
During a median follow-up of 6.8 years, dementia developed in 524 participants (74 with diabetes and 450 without). Among participants without diabetes, higher average glucose levels within the preceding 5 years were related to an increased risk of dementia (P=0.01); with a glucose level of 115 mg per deciliter (6.4 mmol per liter) as compared with 100 mg per deciliter (5.5 mmol per liter), the adjusted hazard ratio for dementia was 1.18 (95% confidence interval [CI], 1.04 to 1.33). Among participants with diabetes, higher average glucose levels were also related to an increased risk of dementia (P=0.002); with a glucose level of 190 mg per deciliter (10.5 mmol per liter) as compared with 160 mg per deciliter (8.9 mmol per liter), the adjusted hazard ratio was 1.40 (95% CI, 1.12 to 1.76).
CONCLUSIONS:
Our results suggest that higher glucose levels may be a risk factor for dementia, even among persons without diabetes.
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The ketogenic diet as a treatment paradigm for diverse neurological disorders.
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.