[W7] - L7 Flashcards
The relevance of neuronutrition to SNP
Neuronutrition: Studying the impacts of food on the brain – what are the essential nutrients for the brain. Indeed, the brain is the organ that is most sensitive to damage as a result of a poor diet.
In children, neuronal development progresses rapidly, and so high rates of energy (obtained via food) are needed to fuel this process. It further relates to the importance of biological factors (not merely psychological). There are also some neuromyths about brain food and education. Plus, food habits begin in childhood.
Additionally, poor eating habits are often observed in children with neurodevelopmental conditions. They may be more sensitive to specific tastes, smells, textures – and reject certain foods as a result (i.e., child with FASD only likes crunchy foods)
What nourishment groups does the brain need?
- Water! – 80% of the brain is water.
- Fats – Lipids (e.g., omega 3 fatty acids)
- Proteins
- Sugars – carbohydrates.
- Vitamins/minerals.
FALSE Neuronutrition Neuromyths
- If pupils do not drink sufficient amounts of water (= 6-8 glasses a day) their brains shrink (but it can happen in older people – those with Alzheimer’s)
- It has been scientifically proven that fatty acid supplements (omega-3 [should be taken more] and omega-6) have a positive effect on academic achievement: not yet known for sure! The studies conducted had limitations with unnatural sources and low doses.
- Children are less attentive after sugary drinks and snacks (probably believed due to excessive movement observed in children)
- Reducing dietary intake of sugar or food additives is generally effective in reducing the symptoms of ADHD
TRUE Neuronutrition neuromyths
- The brain consists of 80% water (as opposed to 60% for the rest of the body)
- Water is necessary for all chemical reactions in the brain, e.g. for energy production, for the structure of the cells, and elimination of waste products.
- Dehydration causes many complaints including poor cognitive performance, brain fog and tiredness - sufficient water intake (1,5-2l /day) improves brain function by 30%.
- A diet low in omega-3 fatty acids relates to accelerated aging of the brain and increased risk for dementia (demonstrated only by correlational studies at this stage – given the ease with which this approach can be utilised in circumstances like this)
- A balanced diet with a ratio 2:1 omega-3 and omega-6 fatty acids fosters healthy aging and brain function (e.g., Mediterranean diet, Indian diet) - greater brain shrinkage at 50 for Western as opposed to Mediterranean diet!
- A diet high in refined sugar and saturated fat can increase the risk for ADHD or hyperactivity, whereas a healthy diet, characterized by high consumption of fruits and vegetables, would protect against it.
- Elimination diets can help reducing symptoms of ADHD but are in practice too restricted (too hard for children to adhere to a very strict diet, but some children have experienced benefits)
Neuronutritional Research with Children
Adequate nourishment from conception through infancy establishes the basis for lifetime brain function (including breast feeding in the first 6 months) – because of the rapid brain development/expansion that occurs in this period [25% of an adult’s brain volume at birth, 65% at 2, 90% at 5]
Children who are NOT adequately nourished are at risk for failing to reach their developmental potential in cognitive, motor, and socioemotional abilities. This strongly links to academic achievement.
Key risk factors for poor brain development are: severe acute malnutrition, chronic undernutrition, iron deficiency (anemia), and iodine deficiency.
Glucose and the Brain
Carbohydrates are the compound in foods that deliver glucose – which keeps us running. It is the main energy source for our organs.
The brain is the largest consumer of glucose in the body. It needs a 24/7 glucose influx to survive.
Glucose passes the blood-brain-barrier via ‘sugar gates. 3 tablespoons of honey is sufficient for one day of brain activity.
When glucose levels are low, the brain has a fallback system wherein it transforms fructose and lactose into glucose. Glucose cannot be stored as is, it must be consumed immediately. When this doesn’t happen, it can be transformed and stored as glycogen (energy for <24 hrs). The only back-up energy are ketone bodies – produced in the liver (if less than 50 g carbs are consumed per day)
The Three Forms of Glucose
- Sugars [sub-categorized as…]:
> Glucose (the type of sugar that travels in the blood stream)
> Fructose (fruit sugar)
> Lactose (milk sugar) - Starches (complex carbs, soluble fibers) - [essential for the function of microbiomes in the gut/digestion – and microbiomes help to extract vitamins/minerals]
- Fibers (complex carbs, insoluble fibers) - [essential for the function of microbiomes in the gut/digestion – and microbiomes help to extract vitamins/minerals]
Insulin and the Candy Bar Effect
The peak of one’s glucose spikes (blood sugar levels) depends on what you eat.
After a peak, the body produces insulin to combat/bring down the peak. The larger the peak, the more insulin that is produced. The peak is then followed by a sharp dip - the candy bar effect.
What is a Glycaemic Index?
The Glycaemic Index of a food/carbohydrate has an impact on how it is digested.
- Low glycemic index (GI of 55 or less): Most fruits and vegetables, beans (Brand-Miller calls beans “star performers”), minimally processed grains, pasta, low-fat dairy foods, and nuts.
- Moderate glycemic index (GI 56 to 69): White and sweet potatoes, corn, white rice, couscous, breakfast cereals such as Cream of Wheat and Mini Wheats.
- High glycemic index (GI of 70 or higher): White bread, rice cakes, most crackers, bagels, cakes, doughnuts, croissants, most packaged breakfast cereals - these foods will give you a quick and high spike in blood glucose levels/insulin
The Consequence of a high Carbs/Glycaemic Index Diet
- Burns out the pancreas.
- Insulin resistance (energy from glucose cannot be used in cells, blood glucose levels rise)
- Type 2 diabetes.
- Fat accumulation / obesity.
- Cardiovascular diseases (through wearing out your cardiovascular systems)
- Brain inflammation / dementia
The impacts of high blood glucose levels
High blood glucose levels accelerate the ageing process of the brain (increases the risk for developing dementia)
High glucose levels have also been correlated with lower hippocampal volume and reduced memory performance.
Define Metabolic Disorders
Rare genetic (inherited) disorders in which the body cannot properly turn food into energy.
They are caused by defects in specific proteins (enzymes) that help break down (metabolize) parts of food. A food product that is not broken down/metabolized 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, and there are 700 metabolic disorders in total.
Some examples:
- Type 1 Diabetes -> take-up of glucose into cells to produce energy/autoimmune disease: body attacks insulin cells in the pancreas.
- Wilson’s Disease -> defect in copper excretion.
- Phenylketonuria (PKU) -> defect in the break-down of the protein phenylalanine.
- Galactosemia -> defect in the break-down of the simple sugar galactose.
The Prevalence of T1D
Type 1 Diabetes is a common childhood disease. Incidence in Europeans 1.7/1000 (peak in puberty).
Every year the prevalence is inexplicably increasing (2-5% increase). The age of onset is also trending younger (under age 5) - so it has a higher impact on neurodevelopment. T1D affects cognition and academic performance.
There are higher incidences of type 1 diabetes in children in northern/colder countries or in countries with niqabs – perhaps relating to a vitamin d deficiency? (other environmental triggers may be viral infections or early exposure to cow’s milk)
Type 1 Diabetes vs. Type 2 Diabetes
Insulin is like a key, that enables glucose to enter the body’s cells.
In T1D: insulin is missing, glucose cannot enter cells, so blood glucose levels rise.
In T2D: insulin is present, cells are locked, glucose cannot enter cells, blood glucose and insulin levels rise.
Hyperglycaemia (hypers)
Excessively high blood glucose levels (> 140 mg/dl; > 7.8 mmol/dl)
Such levels can be toxic because the cells do not have enough oxygen as a result/experience oxidative stress. The long-term effects of “hypers” are worse than “hypos” (better to be on the low side than the high side).
Characterized by: irritability, stomach pain, thirst, need to urinate etc.
Results from: poor exogenous metabolic control (diet / insulin injection).
Diabetic Ketoacidosis (DKA)
DKA results from hyperglycaemia. It is characterized by:
- Back-up energy needing to be produced in the liver (ketones) – acidic blood.
- Organ damage.
- Cerebral oedema (leading cause of death in T1D).
- Coma.
- Death.
Euglycemia vs Dysglycemia
Acceptable levels of blood glucose (70-140 mg/dl; 4-7.8 mmol/dl). - very hard to achieve with T1D but it is the goal.
[treated with an insulin pump which acts as an external pancreas – and the device can guide how much insulin needs to be injected (PDA)]
vs.
Fluctuating levels of blood glucose
Hypoglycaemia (“hypos”)
Excessively low blood glucose levels (<70 mg/dl; <4 mmol/dl).
Characterized by: anxiety, weakness/fatigue, dizziness, headache, blurry vision, shakiness, irritability/hunger etc.
Causes:
› an overdose of insulin
› Omitting food
› Strenuous physical activity
› Stress/ emotions.
Results:
› Altered conscious state
› Seizures (epileptic)
› Coma
› Death (in prolonged cases).
The two neurocognitive phenotypes of T1D
Onset after age 7 (Majority):
- Lower intelligence and academic
achievement
- Lower psychomotoric speed
- Intact learning and memory
Onset before age 7:
- Poor performance in all cognitive
domains
- Poor learning and memory
- Significant clinical impairments
- Abnormalities visible within 1 or 2 yrs
post-onset
Academic Outcomes and T1D
- Lower school grades
- Poorer academic achievement
- Less years of schooling /less employment
- Verbal IQ 3-5 points lower
- Declining IQ in young adulthood (with rate of decline relating to disease duration (early onset carrying greater risk); early metabolic insults; poor metabolic control; history of hypos)
[The size of these effects are small to medium on average!]
Structural brain abnormalities related to T1D
- Subtle abnormalities in grey matter volume (MRI measures) (particularly in posterior brain regions like the cerebellum) – Greater/stronger with hyperglycaemia and longer disease duration.
- Potential improvement in adolescence has emerged – likely as a result of the brain’s “growth spurt” helping to compensate in this period) (Perantie et al., 2007)
- Subtle microstructural abnormalities (DTI measures) (which are greater/stronger with more hyperglycaemic periods, poorer metabolic control, earlier onset, longer disease duration)
Grooved Pegboard Test and T1D
Doing poorly on this test suggests poor psychomotor speed and it predicts long-term poor metabolic control.
It is indicative of psychomotor slowing and can be an early marker of T1D related brain abnormalities.
It is performed with one hand at a time, but both hands are tested.
The differential effects of the glycemic extremes in childhood
[It is difficult to disentangle these effects because children typically experience both – although hypers appears to be more damaging]
Hypers: Affects the Default Mode Network and Executive functions. Can have toxic effects on blood vessels and increase risk for cardiovascular disease, hypertension, and microvascular damage.
Hypos: Affects gating information &
memory and learning; and integration of information &
language. The risks of hypos are less understood – perhaps because it often goes unnoticed as children are more quiet – it appears to impact upon memory/learning/verbal intelligence; but perhaps because children are just less receptive to learning in this state.
However, an 18-year follow up study found no long term relations to neuropsychological outcome. Perhaps this is because of the body’s compensatory mechanisms (i.e., Back-up energy system (ketones)).
T1D and Puberty
T1D requires constant management (never a day off), and people with T1D often have other autoimmune conditions as well (like coeliac disease).
So, how is it to make the transition from managing a disease in childhood and then in adolescence? Hormonal changes also call for a need to establish a new balance. Puberty often coincides with a period of poorer metabolic control (increased insulin resistance, more risk taking, spontaneity etc.,)
Poor treatment adherence leads to more hypers; leads to reduced attention/executive functions; leads to…
Summarizing Lecture 7
Neuronotrition:
› Highly controversial topic
› Adequate nourishment from conception through infancy
establishes the basis for lifetime brain function (water; fats - lipids; proteins; sugars - carbohydrates; vitamins and minerals)
› Glucose keeps the body and the brain running
› Glucose is essential for brain function
› High blood sugars fasten the ageing process of the brain
(high carbohydrate intake + high GI foods)
T1D:
› Metabolic disorders = rare genetic (inherited) disorders
in which the body cannot properly turn food into energy
› T1D as example = lack of insulin
- Common childhood disease
- Increasing incidence, decreasing age
› T1D causes global cognitive impairments that are mild
- Metabolic control is essential (prevent insults)
- Long-term effects of “hypers” are worse than “hypos”
- Younger age and more insults predict worse outcome