Week 7-Diabetes Flashcards

1
Q

Neuronutrition

A

Essential foods for your brain
Not just what we eat, also the bacteria we have in our gut

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2
Q

Neuronutrition and school neuropsychology

A

-Rapid neuronal development requires high energy rates and nutrients
-Biological factors matter
-There are neuromyths about brain food in education that need tackling
-School policies: Food habits start in childhood

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3
Q

Poor eating and neurodevelopmental conditions

A

Poor eating common in neurodevelopmental conditions
Picky eaters may have specific tastes they dislike

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4
Q

Functions of starches and fibres

A

Essential for functioning of microbiome
Play important role of processing foods
Make new nutrients that are important

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5
Q

When glucose is low

A

Brain transforms fructose and lactose into glucose

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6
Q

“Candy bar effect”

A

How glucose behaves in the body
-Fluctuates during the day
-Fluctuation levels depend on what you eat
-Foods with high GI cause blood sugar to peak very fast
-Body produces insulin to make blood sugar go down

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7
Q

Glycemic Index (GI)

A

Low GI (55 or less): Fruit and veg, beans, grains, low fat dairy foods, nuts
Moderate GI (56 to 69): Potatoes, corn, white rice, couscous, wheat breakfast cereals
High GI (70 or higher): White bread, rice cakes, crackers, bagels, cakes, doughnuts, croissants, packaged breakfast cereals

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8
Q

Consequences of high carb/ high GI diets

A

-Burns out the pancreas (because it constantly has to produce insulin)
-Insulin resistance
-Leads to type 2 diabetes
-Fat accumulation/obesity
-Cardiovascular diseases
-Eventually can lead to brain inflammation/dementia

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9
Q

High blood glucose levels

A

-Increases risk for developing dementia
-Accelerates the aging process of the brain
-Shrinks hippocampus
-Reduces memory performance

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10
Q

T1D

A

Autoimmune disease- Body attacks cells in the pancreas
Pancreas doesn’t produce insulin

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11
Q

Metabolic disorders

A

-Rare genetic disorders
-Body cannot turn food into energy
-Caused by deficits in specific proteins (enzymes) that help break down parts of food
-Food product that is not broken down into energy can build up in the body and cause a wide range of symptoms
-Several inborn errors of metabolism cause developmental delays or other medical problems if they are not controlled
-700 metabolic disorders in total

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12
Q

Types of metabolic disorders

A

Wilson’s disease- Defect in copper excretion
Phenylketonuria- Break down of the protein phenylalanine
Galactosemia- Break down of the simple sugar galactose
T1D- Take up of glucose into cells to produce energy

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13
Q

Differences between T1D and T2D

A

T1D: Insulin is missing, glucose cannot enter cells, glucose levels rise
T2D: Insulin is present, cells are locked, glucose cannot enter cells, glucose and insulin levels rise

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14
Q

Environmental triggers of T1D

A

Vitamin D deficiency
Viral infections
Early exposure to cows milk

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15
Q

Hyperglycaemia

A

-High blood glucose levels (above 140mg)
-Toxicity/oxidative stress
-Can be a result of poor metabolic control (diet/ insulin injection)
-In the worst case can lead to Diabetic Ketoacidosis (DKA)

Symptoms:
-Stomach pain
-Irritability
-Very thirsty
-Need to urinate often

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16
Q

Euglycaemia

A

Acceptable levels of blood glucose
70-140mg

17
Q

Dysglycaemia

A

Fluctuating levels of blood glucose

18
Q

Hypoglycaemia

A

Excessively low blood glucose levels
Below 70 mg
Due to:
-Overdoses of insulin
-Omitting food
-Strenuous physical activity
-Stress/emotions

19
Q

2 neurocognitive phenotypes in T1D

A

Majority
-Onset after age 7
-Lower intelligence and academic achievement
-Lower psychometric speed
-Intact learning and memory

Minority
-Onset before age 7
-Poor performance in all cognitive domains
-Poor learning and memory
-Significant clinical impairments
-Abnormalities visible within 1 or 2 years after onset

20
Q

Academic outcomes of T1D

A

-Lower school grades
-Poorer academic achievement
-Less years of schooling/ less employment
-Verbal IQ 3-5 points lower
-Declining IQ in young adulthood
-Relates to disease duration (Early onset= more chance of decline in intelligence)
-Early metabolic insults
-Poor metabolic control
-History of hypoglycaemia

21
Q

Grooved pegboard test

A

Predictive of long-term poor metabolic control
Test for psychomotor speed
Indicative for psychomotor slowing
Early marker of T1D related brain abnormalities
Predicts long-term poor metabolic control
Compare score to typical score for children their age

22
Q

Brain structure abnormalities in T1D

A

Subtle abnormalities in gray matter volume (MRI measures) in posterior brain regions and cerebellum
-They are stronger with hyperglycaemia and longer disease duration
Potential improvement in adolescence
Subtle microstructural abnormalities (DTI measures)

23
Q

Neurodevelopmental effects of hypers and hypos

A

Hypers:
-Default mode network
-EF’s

Hypos:
-Gating info & memory and learning
-Integration of info & language
-TOP association areas

24
Q

LT risk of hypers

A

Toxic effects on blood vessels
Risk for cardiovascular disease
Risk for hypertension
Microvascular damage

25
Q

Microvascular brain damage in adulthood

A

› The brain relies on an intricate network of small blood vessels
› Damage accelerates the ageing process
› Cognitive impairments
 Slow information processing
 Mental flexibility
› Those with retinopathy more impaired (proxy for microvascular damage in brain)

26
Q

Hormonal changes in puberty

A

New balance
Increased insulin resistance