Lec 12 and 13 - Flashcards
Smith study 2003 - association
Looking at young adults aged 19-21
Association study - found association between consuming breakfast and better mental health –Measures of ‘health’ included, depression, anxiety, cognitive failures and sleep duration.
Is only correlational and could be the result of confounding factors like home circumstances - these people will be less likely to have breakfast and more likely to have poorer health.
Including potential confounding factors in the analysis (e.g. smoking and alcohol consumption) reduced the statistical significance of the correlations between breakfast and health.
Brown et al 2013-cumulative meta analysis
- missing breakfast is assoicated with obesity - over time more and more evidence has accumulated looking at this association, the estimate of the odds haven’t really changed at all. What has changed, is the confidence intervals have got smaller (more evidence)
the Intervention studies do not clearly confirm or refute proposed effect of eating breakfast on obesity
Levitsky (2005) study - breakfast
Measure energy intake at lunch, snacks and dinner for people who have breakfast vs those who don’t..
If pp miss breakfast, they increase their intake at lunch only and by 135 kcal. But this doesn’t compensate for the missed breakfast (635kcal), so overall there is a decrease in daily energy intake. So this should result in lower body weight.
Your gut is relatively empty regardless of whether or not breakfast is consumed.
So where does the association between missing breakfast and obesity come from?
Obese people are perhaps more likely to miss breakfast. eg start the day by trying to limit intake, but this goal fails and you later consume more. By delaying eating, and eating later on, this gives you less appetite in the morning.
Pollitt et al 1981 - children and cog
Studied the effects of missing breakfast on cognitive performance in children
Children ate at 5pm in the evening and then either consumed breakfast at 8am or missed breakfast. Their cognitive function was assessed at 11am. Tests included matching familiar figures, continuous performance task and hagen central-incidental task
=Missing breakfast increased number of errors on matching familiar test, but only in those who had lower IQ than mean IQ of group
=On incidental recall test, there was a small effect of missing breakfast in which children had improved recall - memory is better for missing breakfast.
what are the issues with breakfast studies?
Blinding
Placebo for ‘no-breakfast’
Publication bias – no effects less likely to get publicated.
Meal size - A large meal acutely impairs performance
Perhaps a small meal is chosen at breakfast so as to avoid impairment (neutral effect)
Not eating breakfast leads to reduced daily energy intake
how much glucose is in the brain and blood?
Brain has a high metabolic rate -
oxidizes 120 g glucose daily, equivalent to about 20% of whole body’s daily energy expenditure
Glucose supplied from blood -
rate of blood supply to brain is high (10 x resting skeletal muscle and same as muscle during vigorous exercise)
Kennedy & Scholey (2000) - glucose
Tested between 9 am and noon, after overnight fast
On one occasion they had a 25g glucose drink, on the other they had a placebo. Tasks were then completed between 27 and 43 minutes after glucose consumption
Tasks included serial threes, serial sevens and word retrieval
=sig effect of glucose on cognitively demanding task only – serial sevens.
what is most amenable to the glucose memory facilitation effect?
verbal episodic memory
possibly suggesting the involvement of the hippocampus in glucose enhancement of memory,
what level is glucose at the start of the day?
4 / 5 mmo/l
blood glucose levels are constant, there are small spikes after eating.
what level of concentration causes glucose uptake to decrease?
Glucose supply to the brain is maintained even during prolonged fasting
Only when blood glucose concentration falls below 2 mmol/l does rate of glucose uptake decrease significantly
what happens to glucose in the body after eating?
Glucose supply to the brain is maintained even during prolonged fasting
-initially from food in the gut (up to 3 h) and glycogen in the liver (3-24 h), then gluconeogenesis (8 h to days )
what tasks is glucose most beneficial for?
high cognitively demanding tasks (Less so in participants with poorer glucose regulatory control (higher blood glucose for longer after a glucose load)
what is the name for high blood glucose? and where is this often seen?
hyperglycaemia
Type 2 diabetes and raised fasting blood glucose levels (hyperglycaemia) and are associated with cognitive impairment
what amino acid synthesises serotonin?
Tryptophan (consumed through protein) it has to be actively transported across blood brain barrier. The amount that gets into brain depends on ratio of blood and other amino acids. It has a fairly low concentraion compared to other amino acids.
what does serotonin effect?
influences satiety, food choice and in relation to mood and alertness/sleepiness, aggression and pain sensitivity.
what drug targets serotonin?
prozac
Carbs vs protein when consumed
and who provides evidence for these effects?
Tryptophan is an amino acid that we consume through protein foods, it has to be actively transported across blood brain barrier. The amount that gets into brain depends on ratio of blood and other amino acids. It has a fairly low concentraion compared to other amino acids. So a diet high in protein, reduces the amount of Tryptophan that enters the brain (due to competing amino acids).
When carbohydrates are consumed, the opposite happens. Large amino acids are taken out of blood into muscle, apart from Tryptophan which remains in blood because it doesn’t dissolve and doesn’t get taken into muscles. Therefore there is an increase in Tryptophan to the brain after carbs.
Liberman et al 1986 study provides evidence of this
Lieberman et al. (1986) study- Pp fed a high protein meal or high sugar meal or high starch meal – they measure ratio of …
Pp fed a high protein meal or high sugar meal or high starch meal – they measure ratio of Tryptophan to amino acids after consumption (measure every hour)
These were extreme meal manipulations (eg 160g of sugar)
=they demonstrate expected effects of trypotophan: LNAA, protein causes decline in ratio relative to starch and sugar which increase it. This isn’t an immediate increase it happens between 1 and 2 hours
Spring et al 1982- Higher Carb meal in males vs females
Higher Carb meal which increases serotonergic activity, increases sleepiness in females but found opposite in males.
Higher protein had higher sleepiness in males.
Performance is impaired in older people in the afternoon in people who had a higher carb meal
Pivonka & Grunewald. (1990) effect of sugar
Consumption of water versus low calorie drink versus 50g sucrose drink
=there is a small but reliable effect of sugar increasing sleepiness after consumption within 30 minutes.
This is not in line with Liberman’s carb craving findings, perhaps the mechanism for this behaviour is therefore something else.
Wurtman & Wurtman. (1989) = carbohydrate-craving obesity’
Proposed circle relationship between mood, food intake and brain serotonin in ‘carbohydrate-craving obesity’
having low mood as a result of vulnerability to depression (under-functioning serotonergic system) can be relieved if one consumes carbohydrates. Or perhaps low mood causes you to crave carb – they don’t say whether this is conscious or not.
Liberman 1986 - carb cravers
Measured mood before and 2 h after consumption of a high-carbohydrate lunch in obese ‘carbohydrate cravers’ and obese non-carbohydrate cravers
=noncarbohydrate cravers reported feeling considerably less alert and more fatigued and sleepy, while carbohydrate cravers described little or no change.
=noncarbohydrate cravers experienced an increase in depression, while carbohydrate cravers reported feeling less depressed.
markus et al 2000 - high stress proneness
Subjects with high stress proneness or low stress proneness participated in a controllable- and uncontrollable-stress experiment during either a protein-rich- carbohydrate-poor diet (40% CHO, 26% protein) or carb-rich and protein poor (66% CHO, 4% protein).
= feelings of depression became higher under the protein-rich carb-poor diet condition in high stress prone
=dep was lower in carb-rich PP group
Young et al. (1985) - Used homeless men
Used homeless men so their depressed moods were
Probably quite high because of their situation
3 conditions:
Fed participants pure amino acids in a drink
1) The amino acid mixture had all but tryptophan
2) control drink which is used to balance amino acid
3) drink had addition of typtophan.
A cognitive task was used to measure if mood was effected. They performed this under diff levels of distractibility.
5 hours after treatment
=Tryptophan depletion caused higher depression scores and these people had lowest plasma tryptophan (24% below baseline)
=when they are depressed participants were more distracted by the dysphoric theme (heard things congruent with low mood)
=when tryptophan was added, they perform better on dysphoric theme condition than low and high distraction
what are rich sources of the n-3 fatty acids and what is another name for them
and what are two compound examples
Fish, sea food and particularly oily fish and cod liver oil
AKA Omega-3 fatty acids
Eicosapentaenoic acid (EPA) and Docosahexaenoic acid (DHA)) These are long chain fatty acids
DHA - 22:6n-3 -is a long chain polyunsaturated fatty acid. (22 means is that 22 carbon atoms in chain, the 6n means it has 6 double bonds which is why it is unsaturated. Any fatty acid that has more than 1 double bond it is a polyunsaturdated bond. The 3 is because the first double bond occurs 3 bonds away from omega molecule
The n-6 and n-3 are families of polyunsaturated fatty acids
linoleic vs alpha-linolenic acid - origins of consumption?
The alpha-linolenic acid – n-3 is grape seed.
The origin of consumption for linoloeic n6 is through sunflower and palm oil which are primary saturated acid but also has linoleic acid.
n3 - EPA then DHA - the rate of alpha-linolenic acid (ALA),to DHA is slow
n6- Arachildonic acid then DPA
The amount of n-6 can influence synthesis of n-3 because they use same enzymes
The ratio of n6 to n3 is important in our diets.
Describe how n-3 fatty acids could influence mood and behavioural
Consumption of high amounts of n3 fatty acids means there are more incorporated into cell membrane. The nature of those fatty acids can in turn effect cell membrane function and hormone neurotransmitter function through influencing receptors embedded in cell membrane.
how has consumption of n3 and n6 or omega 3 and 6 changed over time?
declining dietary intakes of omega-3 fatty acids relative to omega-6 intake
DHA - 5 facts
DHA is the most abundant n-3 fatty acid in the human brain.
present in fish and sea foods (and poultry and eggs are also significant sources) and especially alpha-linolenic acid (ALA), which is present in soybean, rapeseed (canola) and flax oils, and some nuts
Concentration can affect neural membrane function (and thereby speed of signal transduction, and neurotransmission)
DHA is involved in neurogenesis, and metabolites of DHA have neuroprotective activity
Rate of synthesis of DHA from ALA is generally low and is higher in women and during pregnancy - DHA is present in breast milk and concentration is influenced by the amount of DHA in the mother’s diet
n-3 fatty acid nutrition has been investigated in relation to:
Cognitive development Visual acuity Cognitive decline, including Alzheimer’s disease ADHD Dyspraxia / DCD Dyslexia Asperger’s syndrome and autism Aggression and impulsivity Schizophrenia Depression, including postpartum depression
DHA and cognitive development
Breast milk has higher levels of DHA than raw cows milk and is therefore better for us.
Rate of increase in DHA in the brain (relative to brain weight) is greatest during foetal development and early infancy
Cognitive function better at 6-23 months of age in children who were previously breast fed
but the research doesn’t show a clear effect of DHA on its own
The ‘Oxford-Durham’ orginal study - Richardson et al 1999
Children, aged 5-12 years, with developmental co-ordination disorder (DCD) given either
558 mg EPA, 174 mg DHA, 9.6 mg vitamin E per day or
Placebo, olive oil
Outcome at 3 months :
=Motor skills, no difference between fish oil and placebo
=Performance on reading and spelling tests, and teacher ratings of ADHD symptoms improved more for those receiving fish oil
Addition of vitamin E could have influenced results
Also had specialized sample so not generalisable to all children
Also - they did not match pp at baseline, the real difference is at baseline – the fish oil group by chance was lower. Therefore could be regression to the mean effect – the groups could be quite similar.
DOLAB study Richardson et al 2012
Looked at baseline reading score, 33rd centile, 20th centile and 10th centile
= found benefit gained over 16 week period in terms of reading ability for those performing the worst (worst 10% in study showed benefit)
But when you include all of the children (33rd) there is no sig effect
So if the worst performing children are getting a benefit, but as group they aren’t, then this group must be doing slightly worse on placebo so there could be a neg effect of consuming fish oil for top-performing 80% of the population
what is the relationship between seafood consumption and prevalence rates of bipolar spectrum disorder (‘manic-depression’)
the more fish eaten, the lower rates of depression (eg iceland eat more and have less depression) - however cant infer cause.
Stoll et al. (1999) depressed patients
Patients with bipolar disorder whose conventional treatment was proving uneffective so they were treated with fatty acids. They were treated with their normal treatment too
=found clear evidence of positive outcome when given huge amounts of fatty acids relative to normal diet
=2 out of 4 outcomes were sig - these were hamilton rating scale for dep and clinical global impresssion scale
Appleton et al. (2006) review
18 trials on fish oil supplementation and depression
used Duration of supplementation 28 to 180 days
Supplement given alone or as adjunctive treatment
And range of measures for depression
when put into forest plot, there is a small, just significant benefit of fish oil supplementation
findings were influenced by one large study in which Pp were told to increase fatty acids in diet and primary outcome was heart disease. But dep was also measured. If this study is removed, the effect size would be bigger in favour of fatty acids.
Rogers et al 2008 - supplement study
General population was of interest, not clinically depressed just moderately dep. They supplemented levels of EPA and DPA that is equivalent to diet just slightly higher in ratio of what is consumed.
these were the groups:
EPA, DHA, EPA+DHA, olive oil, vitamin e, orange oil
recieved either with EPA+DHA or placebo
primary outcome measure was DASS - self-report depressed mood at 4 and 12 weeks
=found a small effect of the supplement
=No effect of supplementation in people who started with higher depressed mood
=no effect on Beck Depression Inventory
concluded where benefits were found the participants had more severe depression, but these findings were small
therefore was a null effect and no benefit
what are some common breakfast myths?
Children who eat a healthy breakfast are more likely to do well in assessment
Unhealthy foods have no positive effect
A direct link has been found between breakfast quality and educational attainment
Tryptophan depletion lowers mood in vulnerable individuals
true or false?
true
who created the forest graph?
Appleton
