mmm
1 1
Created on November 2, 2021
Over 30 million people build interactive content in Genially.
Check out what others have designed:
COUNTRIES LESSON 5 GROUP 7/8
Presentation
BLENDED PEDAGOGUE
Presentation
WORLD WILDLIFE DAY
Presentation
FOOD AND NUTRITION
Presentation
2021 TRENDING COLORS
Presentation
HISTORY OF THE CIRCUS
Presentation
LETTERING PRESENTATION
Presentation
Transcript
The impact of dietary macronutrient intake on cognitive function and the brain
conclusion
Mechanisms underlying the effects of macronutrients on the brain
Macronutrients on cognitive function
Dietary macronutrient intake and cognitive function
Dietary macronutrient intake and cognitive function
- A balanced diet plays a role in the prevention of preventable diseases such as cardiovascular disease, cancer, and type 2 diabetes mellitus .
- the WHO recommends a carbohydrate intake of 55 - 75%, a protein intake of 10 - 15%, and a fat intake of 15 - 30%
- Accumulating evidence suggests that psychological and mental health is also affected by inadequate dietary intake and can be linked to a higher risk of depression, dementia, and cognitive decline.
- Evidence from experimental manipulation of macronutrient compositions, such as changing the ratio of carbohydrates to protein in a single meal, has been shown to acutely affect cognitive functions.
Macronutrients on cognitive function
Carbohydrates and cognitive function:
- Complex carbohydrates, such as starches and fibers, in plant whole meals all must be broken down into their constituent sugars. Processed foods, such as snack foods and sweets, give simple sugars that have already been broken down and produce mono- and disaccharides that are readily available.
- Simple carbohydrates and added sugar & fructose are associated with worse global cognition, as assessed by cognitive test batteries that assess multiple cognitive functions.
- For example, each 60 g of daily sugar intake lowered the Mini-Mental State Examination score by as much as 10 additional years of life.
- memory function negatively correlated with total sugar intake.
- sugar intake is negatively correlated with executive control, working memory, attention and visual-spatial processing.
- diets rich in fibre are associated with better cognitive outcomes. A longitudinal study provided evidence for an association between regular higher fibre intake (29 g/day) and successful ageing 10 years later.
But wait! These effects could be different among individuals .
Write a subtitle here
Lorem ipsum dolor sit amet, consectetuer adipiscing elit. Aenean commodo ligula
Write a title
- non-diabetic individuals with impaired fasting glucose performed significantly poor on a declarative memory task following a meal rich in carbohydrates in comparison with individuals with normal fasting plasma glucose levels.
- memory performance improved with the concurrent intake of at least 6 g of fibre in individuals with poor glucose tolerance.
- glucoregulation and carbohydrate availability also play a role in selective attention in older, but not in young adults.
- In middle-aged and older adults with good glucoregulation, a low glycemic index meal led to superior sustained attentional performance using visual stimuli in contrast to a high GI meal both in accuracy and reaction time.
- above-average sugar intake is associated with adverse neural outcomes such as increased amyloid burden, reduced cortical thickness (in older adults), and impaired global cognition.
6. Malnutrition with insufficient carbohydrate intake also correlates with poor cognitive scores in elderly adults as shown in longitudinal studies using the MMSE and the short portable mental state questionnaire.7. Fibre-rich diets are associated with optimal cerebral glucose metabolism and ultimately better long-term outcomes, i.e., successful ageing over 10 years in adults aged 49 and older.8. variations on the cholesterol regulator gene apolipoprotein E (APOE) may modulate cognitive performance following carbohydrate intake. (Carrying the epsilon allele (ε4) is linked to higher cognitive decline per year compared to non-carriers while cognitively healthy ε4 carriers seemed to benefit from a high GI meal in terms of memory performance on the contrary cognitively impaired ε4 carriers and people without ε4 while ε4 carriers showed poorer attention following high carbohydrate intake).
Dietary fatty acids and cognitive function:
- Diets rich in PUFAs have been linked to improved memory and faster psychomotor processing speed.
- omega-3 is beneficial for memory functions such as spatial memory, semantic, learning and short-term memory and recall in older adults and memory function generally in middle-aged to old adults.
- PUFA intake with none of the other fatty acids predicts delayed story recall performance using the East Boston memory task in adults aged 60 years and above.
- High intake of SFA leads to worsening of different cognitive functions, such as prospective memory performance, visuospatial learning, and verbal memory performance in young adults.
- habitual intake of processed foods high in trans fats predicted poorer visuospatial learning and verbal memory performance in young women.
- The effects of cholesterol and MUFA intake on cognitive functioning are less clear; both have been shown to correlate with better performance on memory tasks, global cognitive function, as well as decreased risk for Alzheimer's and mild cognitive impairment.
- Poor performance on the Concept Shifting task, the Stroop test, and a visual-verbal learning task were related to higher cholesterol intake in both middle-aged and older adults, and high MUFA intake was predictive of mild cognitive impairment in middle-aged adults.
- A cross-sectional study showed that former athletes who consumed high amounts of SFA did not suffer from self-reported cognitive difficulties wheres diet and exercise jointly affect energy homeostasis and synaptic plasticity as evidenced by human and animal studies.
- The benefits of docosahexaenoic acid (DHA belonging to omega-3 fatty acids) intake are further increased by concurrent exercise, exercise can ameliorate the negative effects of a high-fat diet on synaptic plasticity via brain-derived neurotrophic factors as shown in rodents.
- Carriers of ε4 may not benefit from PUFAs the way that non-carriers do whereas higher PUFA intake (20-30 g/day) in carriers was associated with higher, potentially detrimental, levels of cerebral glutamate, which is necessary for learning and memory but is neurotoxic at high concentrations.
- People with the ε4 allele seemed to benefit from medium intake (0.07 g/day) of omega-3 PUFAs DHA and eicosapentaenoic acid from seafood higher intake of the plant-based omega-3 alpha-linolenic acid.
Protein and cognitive function
- tryptophan and tyrosine: both play key roles in cognitive functioning as they are precursors to dopamine and serotonin.
- Results from a 21-day high protein dietary intervention (3 g/kg bodyweight of animal-derived protein per day compared to usual protein intake) revealed benefits for inhibition on the go/no go task following the intervention period as well as for reaction times on a relatively demanding task that requires cognitive control to withhold undesired responses but not on a less demanding sustained attention task. These results suggest that protein may boost task performance on more complex tasks.
- tyrosine levels via protein intake were significantly correlated with fluid intelligence and working memory in both old and young people.
- A negative association between high protein intake and digit subtraction has also been reported in older adults likely due to a concurrent increase in fibrinogen.
- A positive relationship between protein intake and episodic memory tasks such as the face-profession task and scene encoding in young and old people while there was no association between protein intake and semantic memory due to the high correlation of tryptophan with tyrosine levels.
- Both amino acids have been shown in depletion studies to play a role in long-term memory: tryptophan is involved in declarative memory consolidation whereas tyrosine plays a role in spatial memory.
- B vitamins may confound findings and account for protein cognition improvement.
- Cognitive difficulties in the elderly may in part be due to inadequate protein consumption.
- Most studies found a positive correlation between protein intake in the elderly and global cognitive functioning, whereas other studies reported null findings.
- Habitual protein intake as a protective factor seems to attenuate cognitive decline in old age and to reduce the incidence of mild cognitive impairment or dementia together with PUFA intake.
- evidence that the average daily intake of tyrosine in older adults was 2.8 g, which is significantly below the WHO recommendation. Overconsumption of protein may be as detrimental as insufficient intake.
- High protein intake in older adults is associated with an increased incidence of mild cognitive impairment compared to individuals with normal protein intake (15% and below) which corresponds to the protein intake goal recommended by the WHO.
- excessive tyrosine intake, which increases with greater protein intake, correlated with decreased working memory performance as measured by the 3 back tasks (but not with lower working memory loads) in older adults.
Mechanisms underlying the effects of macronutrients on the brain
Glucose and insulin metabolism
- Glucose and insulin metabolism are tightly linked and are known to act in the brain as neuromodulators.
- Cerebral insulin is involved in many important functions such as gene transcription, neuroendocrine function, neurotransmitter regulation such as norepinephrine, as well as serotonergic and dopaminergic signalling.
- rising levels of insulin can trigger the release of striatal dopamine.
- Cerebral insulin plays a role not only in homeostatic maintenance but also in cognitive functions like memory, learning, mood and reward processing.
- Impaired insulin metabolism is linked to mitochondrial dysfunction and micro-structural aberrations in the brain, and downregulated dopamine signalling as well as depressive-like symptoms in rodents. Impaired glucose metabolism is linked to oxidative stress and inflammation as well as macrostructural changes.
- dysfunctional glucose and insulin metabolism leads to a cascade of detrimental consequences that play into the vicious cycle linking metabolic dysfunction and cognitive impairment.
- Dietary fat intake also impacts peripheral glucose tolerance and insulin regulation in the short- and long term. A prolonged high-fat diet, typically rich in saturated and trans fats, reduces the expression of the glucose transporter GLUT1, responsible for cerebral glucose uptake, which induces memory impairments in rodents.evidence for worsened speed of retrieving memories in humans following a short-term high-fat diet intervention.
- PUFA intake is associated with improved insulin sensitivity and is associated with improved memory and processing speed.
- fatty acids also act directly on brain glucose metabolism, which is predictive of Alzheimer's disease development.
- Omega-3 and omega-6 intake was positively associated with glucose metabolism in the medial, inferior, and lateral frontal cortex.
- saturated fat intake was negatively associated with glucose metabolism in the middle and inferior temporal cortex bilaterally, right frontal cortex, and left parietal cortex.
- It has been debated whether a high or low protein diet can improve glucoregulation.
Neurotransmitter actions
- carbohydrate to protein ratio, as well as the type of protein acutely affect the balance of amino acids in the blood and brains of rodents.
- A high protein intake impacts social decision-making via tyrosine metabolism. A meal with a high protein/carbohydrate ratio reduced rejection rates to unfair offers in the ultimatum game. The reduction of rejection rates could be predicted by the enhanced tyrosine/LNAA ratio manipulated by meal composition (high protein versus low protein meals).
- Fat intake can also directly influence serotonin levels in the brain via tryptophan synthesis, and indirectly via insulin.
- eicosapentaenoic acid (EPA; contained in omega-3 fatty acid) regulates serotonin release from presynaptic neurons by reducing prostaglandins.
- docosahexaenoic acid (DHA) regulates serotonin receptor function by increasing membrane fluidity and thereby serotonin receptor accessibility in postsynaptic neurons.
- Rodents on high-fat diets showed reduced dopamine transporter receptor binding density and turnover in the nucleus accumbens and striatum, which is a subcortical structure.
- Different amino acids can acutely affect cognitive functions distinctly. For instance, faster reaction times on a complex attention task were driven by increased branched-chain amino acids as well as plasma tyrosine and phenylalanine concentration (a tyrosine precursor), which are crucial for dopamine and norepinephrine synthesis.
- Protein intake is implicated in regulating monoamine oxidase (MAOB) which breaks down dopamine.
- Zellner observed a 26% decrease of MAOB expression following a 21-day high protein diet. The authors discussed the possibility that both an increase in dopamine synthesis due to higher phenylalanine availability and a lower metabolic rate of dopamine attributed to decreased MAOB activity may have caused the boost in reaction time on a cognitively demanding but not on a simple task.
- tyrosine counteracts performance decrements under physically and mentally taxing conditions by recharging exhausted brain catecholamine levels.
- There are dose-dependent effects of protein whereby optimal habitual dietary tyrosine intake seems to be beneficial in older people and may be mediated by downregulated MAOB expression, which is involved in dopamine breakdown.
- Cognitive determinants due to insufficient protein intake in an older population could be explained by the depletion hypothesis: older people may be particularly vulnerable to inadequate protein consumption due to decreased brain dopamine receptor and transporter binding. In contrast, performance declines due to excessive protein consumption may be accounted for by the overdose hypothesis, postulating that detriments may be caused by increased dopamine synthesis capacity in the elderly.
- Other neurotransmitters are also affected by macronutrient intakes, such as glutamate, the major excitatory neurotransmitter that plays an important role in memory and learning.
- High PUFA intake may be protective from future cognitive decline and is associated with lower cerebral glutamate, which may be neurotoxic.
Oxidative stress and inflammation
- Reactive oxygen species (ROS, or free radicals) are a by-product of Oxidation and excessive amounts cannot be neutralized by antioxidants and cause oxidative stress to the brain, further leading to cellular degeneration predicting cognitive decline over 4 years.
- recurrent postprandial hyperglycemia can cause inflammation due to an overproduction of reactive free radical molecules and the response of inflammatory cytokines which affects behaviour, e.g., depressive and sickness behaviour.
- peripheral and neuroinflammation have commonalities and can exacerbate one another, they are considered distinct processes. Hypothalamic inflammation is implicated in insulin and leptin resistance in the arcuate nucleus, and disrupts metabolic feedback, thereby promoting hyperphagia and weight gain.
- Other brain structures, including the hippocampus, cortex, cerebellum, and amygdala are also affected by diet-induced neuroinflammation, linking diet-induced metabolic diseases with cognitive deficits.
- inflammation and oxidative stress are affected by dietary intake and play a pivotal role in long-term cognitive outcomes and successful brain ageing. For instance, it has been shown that poor glucose and insulin regulation contribute to neuroinflammation and oxidative stress in the brain leading to neurodegeneration, dementia, depression, and mild cognitive impairment.
- Poor glucose and insulin metabolism are associated with structural changes. Structural changes in the brain are linked to dementia risk and there is strong evidence that an unhealthy diet is linked to vascular damage.
- A study on non-diabetic elderly participants found that macro-structural damage (including atrophy) correlated with higher fasting glucose, and micro-structural aberrations correlated with measures indicating reduced insulin sensitivity.
- High intake of sugar fosters inflammation and oxidative stress via cerebral accumulation of Advanced Glycation Endproducts (AGEs) . while low intake of high GI foods reduces inflammation due to the absence of glycemic spikes which induce oxidative stress.
- Possible pathways by which fibre intake might decrease inflammation are: (1) increased lipid oxidation and (2) short-chain fatty acids produced by fermentation of fibre in the gut.
- Dietary fats also affect cognition via pro- or anti-inflammatory processes by activating microglia. Short-chain fatty acids produce inflammatory mediators such as cytokines and reactive oxygen species.
- Omega-3 fatty acids such as EPA and DHA play an important role in the inflammatory response. They are precursors for the formation of pre-resolving mediators such as resolving, protectins and maresins, which actively resolve inflammation found in the brain, significantly influencing neuroinflammation.
- saturated fatty acids and monounsaturated fatty acids are pro-inflammatory.
- Inflammatory responses can be very quickly induced: a three-day high-fat diet was shown to foster transient inflammation in a mouse model, while a long-term high-fat diet leads to prolonged inflammation that fosters cellular stress and induces apoptosis of hypothalamic neurons.
- The link between central inflammation and cognition has been substantiated by evidence from animal studies.
- Inflammation due to high protein intake negatively affects cognition. Plant protein was associated with better global cognition in the elderly and, unlike protein from heme (iron-rich protein, often referred to as ‘red’) meat, not associated with adverse neural consequences due to systemic low-grade inflammation.
- Over 95% of the amino acid tryptophan is converted to kynurenine in the gut, a neuroactive substance that regulates immune function and inflammation. Importantly, the metabolites of kynurenine can be neuroprotective or neurotoxic depending on physiological conditions.
- Elevated levels of neurotoxic metabolites have been linked to cognitive difficulties, mood disorders and schizophrenia.
- Inflammation affects dopamine synthesis, release, and/or reuptake, thereby plausibly affecting cognition negatively in the long term.
- fibrinogen, an inflammatory biomarker, is associated with a ‘Western lifestyle’ and decreased following a low protein diet in nephrotic patients. In an elderly sample, fibrinogen likely moderated the negative association between age and protein intake on digit subtraction.
- Dietary patterns high in heme meat correlate with high saturated fatty acid intake, which is also associated with negative effects on diverse cognitive functions such as global cognitive function and memory.
- Inflammation and oxidation may lead to structural changes: intake of the anti-inflammatory fatty acid omega-3 was associated with larger cortical thickness, higher grey matter volume and white matter integrity.
- intake of saturated, trans fats, and cholesterol was inversely correlated with grey matter volume.
- impaired metabolism of macronutrients can also affect autophagy. Impaired autophagy plays a central role in the development of neurodegenerative diseases and life span regulation and the ageing process more generally. Both decreased and increased autophagy can lead to neuronal damage due to difficulties maintaining axonal homeostasis and synaptic activity.
- Altered carbohydrate and lipid metabolism has been implicated in disturbing autophagy processes For instance, insufficient glucose activated autophagy in the cerebral cortex in mice and glycogen accumulation in the brain interfered with autophagy flux.
- Interestingly, intermittent fasting has been implicated as an enhancer for autophagy and thereby positive for certain diseases (e.g., cancer).
- caloric restriction has also been studied in the context of psychological benefits such as healthy ageing. For example, memory improved following a 3-month period of caloric restriction (reducing energy intake by 30%) in middle-aged and elderly adults.
Gut-brain axis
- SignallingSignaling between the gut, gut microbiota and brain runs via neuronal pathways involving the central and enteric nervous systems as well as the circulatory system.
- SCFA acts as an energy source, promotes glucose homeostasis and regulates inflammation by promoting blood-brain barrier (BBB) integrity.
- A compromised BBB is more likely to let pro-inflammatory cytokines. A weakened BBB lets these cytokines pass through to the brain where they can alter mood and behaviour negatively.
- experimental studies could show the link between probiotics on butyrate-producing bacteria with anxiety-lowering effects in rats, higher stress tolerance in humans and a reduction in anxiety in individuals suffering from chronic fatigue syndrome.
- A diet high in fat decreases macrobiotic diversity and reduces the presence of Bifidobacteria and Bacteroidetes while increasing Firmicutes thereby increasing central inflammation. In mice, this pathway has been linked to symptoms of anxiety, schizophrenia-type and reduced learning and memory in an anxious mouse strain
- supplementing a high fat-low fibre diet with microbiota accessible carbohydrates in mice ameliorated cognitive deficits, prevented gut dysbiosis and suppressed inflammation in the hippocampus.
- Fermentation of amino acids and proteins in the gut generates metabolites with toxic potentials, such as branched-chain fatty acids and hydrogen sulfide. A randomized controlled crossover trial examined whether eating a high protein diet affected the microbiota of healthy older women finding relative stability of the microbiota profile.
- The precise ways in which the gut microbiota affect the brain remain to be established. However, some mechanisms have already been established such as actions via 1) short-chain fatty acids, 2)branched-chain fatty acids, 3) glucose metabolism, and 4)inflammation. Most studies on cognitive effects and behaviour are limited to mice models at the moment, thus it remains to be seen what impact they have on human brain function.
- Fibre intake is associated with better cognitive performance wheres high sugar or simple carbohydrate intake is linked with impaired cognitive functions.
- glucoregulation mediates the impact carbohydrate intake has on individuals.
- Memory performance is highly sensitive to food-induced glucose changes.
- Advanced age inherently increases the risks for suboptimal glucoregulation.
- APOE ε4 genotype, involved in fat metabolism modifies the impact carbohydrate intake has on memory and attention.
conclusion
- SFA, trans fat, and cholesterol are largely associated with impaired functioning while MUFA and PUFA intake are generally beneficial for executive function, memory, and overall cognitive performance.
- In the elderly, high fat intake is related to dementia risk whereas PUFA and MUFA intake may act protectively
- protein intake selectively enhances working memory and episodic memory (but not semantic memory), primarily when task demands are high.
- Especially in advanced age, adequate protein intake is crucial as both insufficient and excessive protein intake has been associated with adverse outcomes.
conclusion
- glucose and insulin metabolism can have profound influences on brain activity, notably, through modulation of neurotransmitter signalling which affects cognition.
- Impaired glucose and insulin metabolism are linked to oxidative stress and inflammation in the brain as well as structural aberrations.
- dietary macronutrient intake affects cognitive functions and behaviour via neurotransmitters directly, and in the case of serotonin indirectly via insulin metabolism.
- effects on dopaminergic and serotonergic pathways via tyrosine and tryptophan.
- Dose-dependent effects of tyrosine point to the importance of adequate protein intake, especially in old age.
conclusion
- all three macronutrients appear to impact glucose and insulin metabolism and neurotransmitter actions,
- the role of protein in glucose metabolism remains debated.
- Of major importance appears to be the quality of the macronutrients themselves (e.g., SFA versus PUFA).
- Diets high in sugars and SFA foster oxidative stress and neuroinflammation, leading to neurodegeneration over time.
- diets high in nutrients such as fibre and PUFA act neuroprotective by keeping structural integrity.
conclusion
Sarah Abdulrhman Almatrafi
Thank you!