Difference between revisions of "Blood Sugar"

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While the brain does indeed need glucose, it doesn’t want too much of it.  A person doesn’t need to eat sugar to provide glucose to the brain.  Such foods are known as high glycemic, they are typically carbohydrates and sugar.  But  even people who follow a zero carb/zero sugar diet (a type of ketogenic diet not advocated for ApoE4s) are able to maintain acute mental clarity, this is because the body, primarily the liver, can make its own glucose, a process called gluconeogenesis.  So eating glucose isn’t necessary to provide fuel the brain, in fact too much glucose is detrimental to the brain (discussed below).   
While the brain does indeed need glucose, it doesn’t want too much of it.  A person doesn’t need to eat sugar to provide glucose to the brain.  Such foods are known as high glycemic, they are typically carbohydrates and sugar.  But  even people who follow a zero carb/zero sugar diet (a type of ketogenic diet not advocated for ApoE4s) are able to maintain acute mental clarity, this is because the body, primarily the liver, can make its own glucose, a process called gluconeogenesis.  So eating glucose isn’t necessary to provide fuel the brain, in fact too much glucose is detrimental to the brain (discussed below).   


 
== I eat sugar and carbohydrates and my blood sugar levels are fine, so why worry?  ==
It’s hard to discuss blood glucose without including insulin.  The body wants blood glucose levels to be just right (metabolic homeostasis).  Insulin is the hormone that works to keep blood sugar levels steady, neither too high (hyperglycemia) nor too low (hypoglycemia).  But when insulin has been overworked, being asked to keep blood glucose levels under control for too long (a period of many years), insulin eventually “gives up,” blood glucose levels subsequently raise dramatically and that, very simplistically, is Type II Diabetes. 





Revision as of 10:18, 3 March 2019

Introduction

Blood sugar is also known as (aka) blood glucose (BG), the two terms are used interchangeably.

The body, in particular the brain needs glucose. The brain needs glucose constantly, 24 hours a day, the brain can’t burn fatty acids like other cells in the body. The brain can use ketones as a source of fuel, it’s cleaner and more efficient than glucose, which is why metabolic flexibility (the ability to easily switch from burning glucose to ketones) or ketosis (when the body is almost completely fueled by fat/ketones) is often recommended for ApoE4s, see Ketosis and Ketogenic Diet. But the brain has special cells, glutaminergic cells, that can only burn glucose. So the brain cannot run on ketones alone. Under the best of circumstances, ketones can only provide about 2/3rds of what the brain needs to work properly.

While the brain does indeed need glucose, it doesn’t want too much of it. A person doesn’t need to eat sugar to provide glucose to the brain. Such foods are known as high glycemic, they are typically carbohydrates and sugar. But even people who follow a zero carb/zero sugar diet (a type of ketogenic diet not advocated for ApoE4s) are able to maintain acute mental clarity, this is because the body, primarily the liver, can make its own glucose, a process called gluconeogenesis. So eating glucose isn’t necessary to provide fuel the brain, in fact too much glucose is detrimental to the brain (discussed below).

I eat sugar and carbohydrates and my blood sugar levels are fine, so why worry?

It’s hard to discuss blood glucose without including insulin. The body wants blood glucose levels to be just right (metabolic homeostasis). Insulin is the hormone that works to keep blood sugar levels steady, neither too high (hyperglycemia) nor too low (hypoglycemia). But when insulin has been overworked, being asked to keep blood glucose levels under control for too long (a period of many years), insulin eventually “gives up,” blood glucose levels subsequently raise dramatically and that, very simplistically, is Type II Diabetes.


Why it is important for ApoE4s

1) "Individuals with both type 2 diabetes and the APOE epsilon4 allele had an RR of 5.5 (CI 2.2-13.7) for AD compared with those with neither risk factor. Participants with type 2 diabetes and the epsilon4 allele had a higher number of hippocampal neuritic plaques (IRR 3.0 [CI 1.2-7.3]) and neurofibrillary tangles in the cortex (IRR 3.5 [1.6-7.5]) and hippocampus (IRR 2.5 [1.5-3.7]), and they had a higher risk of cerebral amyloid angiopathy (RR 6.6, 1.5-29.6)." [1]

2) In contrast, the Kungsholmen project ([2]) reported no interaction between diabetes and the APOE ε4 genotype, as described in [3]. These authors stated that “These differences could be due to chance or differences in ethnicity and sex distribution in the populations.”

3) “Unexpectedly, memory-impaired epsilon4+ subjects showed poorer recall following insulin administration on one test of memory.” [4]. However, a 2013 study showed that the response might be dose related. [5]

4) "Among AD individuals with DM2, those who are ApoE ε4 carriers had significantly greater neuropathology than those who do not carry an ApoE ε4 allele. Positive DM2 status appears to exacerbate AD neuropathology in the presence of ApoE ε4." [6]


Strategies for controlling blood sugar

Doctors tend to overlook testing for blood glucose levels in Alzheimer's patients. When recruiting people for a resveratrol study to study glucose effects in patients with Alzheimer’s, a Georgetown neurologist was “shocked” by how many had pre-diabetes. [7]

For strategies, check out the Insulin Resistance page.


The Science

- Epidemiological studies.

1) Glucose levels and risk of dementia. (2013) PubMed ID:23924004

2) Diabetes mellitus and risk of Alzheimer disease and decline in cognitive function. (2004, full text) PubMed ID:15148141

3) Type 2 diabetes, APOE gene, and the risk for dementia and related pathologies: The Honolulu-Asia Aging Study. (2002, full text) PubMed ID:11916953

4) Risk of Dementia among Persons with Diabetes Mellitus: A Population-based Cohort Study (1997, full text) PubMed ID:9329716

5) Increased Alzheimer's disease neuropathology is associated with type 2 diabetes and ApoE ε.4 carrier status. (2013) PubMed ID:23627755


- Other studies.

1) Intranasal Insulin as a Treatment for Alzheimer’s Disease: A Review of Basic Research and Clinical Evidence (2013, full text) PubMed ID:23719722


- Animal studies.

1) Increased Susceptibility to Amyloid-β Toxicity in Rat Brain Microvascular Endothelial Cells under Hyperglycemic Conditions. (2013) PubMed ID:23948922

2) Amyloid-β and tau pathology of Alzheimer's disease induced by diabetes in a rabbit animal model. (2012) PubMed ID:22785400

3) Epigenetic mechanisms linking diabetes and synaptic impairments. (2013) PubMed ID:24154559


Proposed mechanism(s)

1) Insulin plays an important role in the formation of memories. Abnormal insulin and insulin receptor levels and activities are seen in Alzheimer's dementia, whereas administration of insulin significantly improves the cognitive performance of these patients. ([8]) Increased blood glucose increases amyloid beta “oligomer” assemblies in the brain, which bind to hippocampal neurons and cause insulin receptors to be eliminated from the surface membranes, contributing to insulin resistance in the brain. ([9])

2) Diabetes may induce epigenetic modifications in the brain. Elevation of HDAC IIa in the brains of diabetics coincide with altered expression of synaptic proteins. [10]


Related SNPs

SNPs associated with Type II Diabetes: List

SNPs associated with HbA1c levels : Article