Diet and mental performance


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Diet and mental performance

  1. 1. Pilar Riobó MD, PhDJefe A. Endocrinología yNutrición.Hospital Jiménez Díaz-CapioMadrid. Spain.
  2. 2. Today discussion points  Dehydration  Exercise induced Hyponatremia  Caloric restriccion  N3-PUFA  Vitamins  Caffeine  Physical activity and exercise
  3. 3. Decline in function resulting from dehydration
  4. 4. Role of dehydration in heat stress-induced variations in mental performanceA battery of tests was performed to assess the effect of various degrees of dehydration on mental performance, n=11 soldiers of IndiaAfter 1, 2, 3, 4% dehydration induced by exercise in heat:  Short-term memory impaired at 2% or more dehydration  Visual-motor tracking impaired at 2% or more  Attention impaired at 2% or more dehydration  Arithmetic ability impaired at 2% or more Gopinathan PM. Arch Environ Health 43:15–17, 1988
  5. 5. Role of hydration on cognitive function Cognitive test battery was administered prior and 30 min post- intervention (exercise or heat – induced dehydration) 2.8% dehydration by exercise or climatic heat:  Increased perception of fatigue  increased tracking errors,  increasedreaction time to making a decision,  decreased short-term memory impaired  Long-term memory : Impaired recall, especially following exercise Cian C, J Psychophysiology 14:29–36, 2000
  6. 6. Dehydration Performance in physical and cognitive tasks is impaired. Fluid ingestion during exercise can decrease the sensation of fatigue when exercise > 40 minutes A high core temperature, especially a high brain temperature, seems to be associated with the onset of fatigue in endurance exercise in warm environments Changes in brain neurotransmiters, (dopamine) and alterations of cerebral blood flow appear to be responsible for fatigue when exercising in the
  7. 7. Significant dose-related effects of dehydration Symbol substitution test effects were observed at the 3% level of dehydration (p < .05), Eye-hand coordination effects were observed at all three levels of dehydration Sharma VM, Sridharan K, Pichan G, Panwar MR: Influence of heat-stress induced dehydration on mental functions.Ergonomics29 :791,1986
  8. 8. “How sore does your head feel now?” “How well can you concentrate just now?” Changes in body mass over time for fluid restriction and euhydration conditions Subjects reported feelings of headache during the trial andtheir ability to concentrate and their alertness were reduced.
  9. 9. Decrements in psychomotor, andcognitive performance can occur when> 2% of body weight is lost due to water restriction, heat, and/or physical exertion A major limitation of most studies conducted to date is the inability to determine the effects of dehydration independent of the effects of thermalstress, physical stress, and/or fatigue.
  10. 10. Mild dehydration impairs cognitive performance and mood Randomised, single-blind, trial (N= 26)  exercise-induced dehydration plus a diuretic  exercise-induced dehydration plus placebo  exercise while maintaining euhydration , plus placebo A cognitive test battery, mood states and symptom questionnaire (headache, concentration and task difficulty) was administeredDehydration degraded aspects of cognitive performance:  errors increased on visual vigilance  visual working memory response latency slowed  Fatigue and tension/anxiety increased  Plasma osmolality increased but resting temperature was not altered Even mild dehydration without hyperthermia induced adverse changes in vigilance and working memory, and increased tension/anxiety and fatigue. Ganio, MS. Br J Nutr. 2011;106(10):1535-43
  11. 11. Today discussion points Dehydration Exercise induced Hyponatremia Caloric restriccion N3-PUFA Vitamins Caffeine Physcal activity and exercise
  12. 12. Exercise-associated hyponatraemia The first reports of hyponatraemic encephalopathy in athletes, army personnel, and hikers appeared shortly after the new dictum: “drink the maximal amount that can be tolerated”. To date at least seven fatalities and more than 250 cases have been described in the medical literature. Presumably reported cases represent only a small proportion of all such cases.
  13. 13. Hyponatraemic encephalopathy is a potentially life threateningcondition, with cerebral oedema causing vomiting, headache,confusion, coma, seizures and pulmonary oedema
  14. 14. hyponatremia (Na<135 mmol/l) in 13% participants0.6% critical hypona (<120 mmol/l). Predictors: • weight gain while running • Long racing time, • BMI extreme
  15. 15. 1,319 collapsed runners. Hypernatremia waspresent in 366 (27.7%) ; hyponatremia in 63 (4.8%).
  16. 16. Exercise-associated hyponatraemia  Thought to be due to overconsumption of hypotonic fluid  inability to suppress antidiuretic hormone during exercise or to mobilise adequate sodium from osmotically inactive internal stores.  Non-specific symptoms- difficult to diagnose on site without the assistance of Na measurement,  Any delay in treatment of patients with encephalopathy can prove fatal.  Mainstays of treatment include fluid restriction, hypertonic saline, loop diuretics and mannitol. Editorial. Overconsumption of fluids by athletes BMJ 2003;327:113-114
  17. 17. Risk factors of EAH  military personnel,  female  marathon runner,  gains weight during exercise because  she drinks excessively To prevent it, the advice is “ drinking according to the personal dictates of thirst”(fluid intake 400- 800 ml/hour)Wijdicks EFM. Noncardiogenic pulmonary Edema in Marathon Runners. Ann Intern Med, 2000; 133(12): 1010 - 1011.SiegelAJ. Noncardiogenic Pulmonary Edema in MarathonRunners. Ann Intern Med, 2000; 133(12): 1010
  18. 18. 44 years old patient admitted with serum Na 121 mmol/L & oxigen saturation 66% Ayus, J. C. et. al. Ann Intern Med 2000;132:711-714
  19. 19. Plasma AVP concentrations weremarkedly elevated after a marathon despiteunchanged plasma (Na). Pathogenesis of EAH1. voluntary fluid intake exceeds urinary and sweat water losses.2. inability to maximally suppress (AVP)P during exercise as a result of nonosmotic stimulation of AVP secretion
  20. 20. Chronic hyponatremia: potomany associated with eating disorders Overzealous correction of chronic hyponatremia can lead to central pontine myelinolysis, with permanent neurologic deficits The initial rate of sodium correction with hypertonic saline should not exceed 1 to 2 mmol per L per hour Correction of chronic hyponatremia should be kept at a rate less than 10 mmol/L in any 24-hour period
  21. 21. Today discussion points Dehydration Exercise induced Hyponatremia Caloric restriccion N3-PUFA Vitamins Caffeine Physcal activity and exercise
  22. 22. Healthy elderly subjects, 3 groups:1. caloric restriction (30% reduction)2. increased intake of UFAs (20%, unchanged total fat),3. controlBefore and after 3 months of intervention, memorywas assessed under standardized conditions. Witte A V et al. PNAS 2009;106:1255-1260
  23. 23. Percentage changes in weight, BMI , and unsaturated-to-saturated fatty acids ratio after caloric restriction (group 1), UFA enhancement (group 2), and control condition. Witte A V et al. PNAS 2009;106:1255-1260
  24. 24. Significant increase in verbal memory scores after caloric restriction (mean 20%), which was correlated with decreases in plasma levels of insulin and CRP Mechanisms: higher synaptic plasticity and stimulation of neurofacilitatory pathways in the brain because of improved insulin sensitivity and reduced inflammation
  25. 25. Beneficial effect of CR or RSV supplementation onspecific cognitive functions in a primate. RSV could be a good candidate to mimic long- term CR effects
  26. 26. Cognition Leptin ?Caloric restriccion longevity
  27. 27. Today discussion points Dehydration Exercise induced Hyponatremia Caloric restriccion N3-PUFA Vitamins Caffeine Physcal activity and exercise
  28. 28. Evidence has accumulated suggesting that thebeneficial effect of fish is due to its content in omega- 3 polyunsaturated fatty acids (n-3 PUFAs) 2 kinds of omega-3 fatty acids: plant-derived (α-linolenic acid) and marine-derived (eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA])
  29. 29. N-3 polyunsaturated fatty acids (PUFA) 1. α-linolenic acid: long-chain, 18-carbon atom with 3 double bonds 2. Eicosapentaenoic acid (EPA): 20 carbon atoms and 5 double bonds 3. Docosahexaenoic acid (DHA): 22 carbon atoms and 6 double bondsn-3 PUFA are "essential“: we cannot make them in our bodies and they are needed for normal growth, development, and optimal function of brain, heart, and other systems
  30. 30. N3-PUFA Important during early brain development, with low intake resulting in poor neurological development and low IQ (Innis SM. Dietary omega 3 fatty acids and the developing brain. Brain Res. 2008;1237:35–43) Such associations may extend through adolescence (Aberg MA. Fish intake of Swedish male adolescents is a predictor of cognitive performance. Acta Paediatr. 2009;98:555–60). In late life, low fish intake predicts greater age-related cognitive dysfunction and elevated risk for Alzheimers dementia (Morris MC. Fish consumption and cognitive decline with age in a large community study. Arch Neurol. 2005;62:1849–53)
  31. 31. 280 volunteers, 35 - 54 y.o. Distributed by quintiles of DHA intake Higher DHA (mol %) was related to better performance on tests of nonverbal reasoning and mental flexibility, working memory, and vocabulary (P ≤ 0.05).Muldoon MF. Serum phospholipid docosahexaenonic acid is associated withcognitive functioning during middle adulthood. J Nutr. 2010;140(4):848-53.
  32. 32. Chicago Health and Aging ProjectAnnual rate of change in cognitive score (standardized units per year [SU/y]) by number of fish meals per week 3718 persons , > 65 years: •cognitive testing were conducted (basal & 3 years) • self-administered food frequency questionnaire (FFQ) were conducted (basal & 3 years) Fish consumption may be associated with slower cognitive decline with age Morris, M. C. et al. Arch Neurol 2005;62:1849-1853.
  33. 33. DHA May Prevent Age-Related Dementia DHA acts at multiple steps to reduce the production of the β- amyloid 1. moderates some of the kinases that hyperphosphorylate the τ- protein, a component of the neurofibrillary tangle. 2. help suppress neuroinflammation, and oxidative damage that contribute to synaptic loss and neuronal dysfunction 3. increases brain levels of neuroprotective brain-derived neurotrophic factorAD pathways targeted by DHA. Cole G M , Frautschy S A J. Nutr. 2010;140:869
  34. 34. Today discussion points Dehydration Exercise induced Hyponatremia Caloric restriccion N3-PUFA Vitamins Caffeine Physcal activity and exercise
  35. 35. Hyperhomocystenemia and B12 deficiency Evidence is convincing that hyperhomocysteinemia is a risk factor for dementia (leukoaraiosis ) B12 deficiency manifestations include abnormal psychiatric, neurological, gastrointestinal, and hematological findings (pernicious anemia) Subclinical deficiencies exit (metformin¡¡) Assessing serum B12 : <200 pg/ml Patients with B12 deficiency and mild cognitive impairment or dementia, might show cognitive improvement with supplemental B12 treatment.
  36. 36. SAM Aceptor ATPReceptor Metionina Ser SAHomocis THF Aden Gly Homocys metilen THF B12 B6 Ser metil THF Cistationina B6 K-butirato Cys
  37. 37. Folic Acid Low levels of folate are associated with high blood levels of homocysteine which has been linked with the risk of arterial disease, dementia and Alzheimers disease long-term folic acid supplements appear to improve cognitive function of healthy older people with high homocysteine levels There is a risk that folate supplementation can delay the diagnosis of B12 deficiency, which can cause irreversible neurological damage. So, folic acid supplementation must associate vitamin B12
  38. 38. Today discussion points Dehydration Exercise induced Hyponatremia Caloric restriccion N3-PUFA Vitamins Caffeine Physical activity and exercise
  39. 39. A case-control studyCases were 54 patients with probable ADControls ,54 persons, cognitively normal, matched Patients with AD had an average daily caffeineintake of 73 mg during the 20 years that precededdiagnosis of AD, whereas the controls had anaverage daily caffeine intake of 198.7 +/- 135.7 mgCaffeine intake was associated with asignificantly lower risk for AD, independentlyof other possible confounding variables Maia & de Mendonça. Eur J Neurol 2002 9:377
  40. 40. Cardiovascular Risk, Aging and Dementia(CAIDE Study) After an average follow-up of 21 years, 1409 individuals (71%) aged 65 to 79 completed the re-examination in 1998. A total of 61 cases were identified as demented Coffee drinkers at midlife had lower risk of dementia and AD later in life adjusted for demographic, lifestyle and vascular factors, apolipoprotein E epsilon4 allele and depression The lowest risk (65% decreased) was found in people who drank 3-5 cups per day. Coffee drinking at midlife is associated with a decreased risk of dementia/AD later in life. This finding might open possibilities for prevention of dementia/AD Eskelinen, M et al. Midlife Coffee and Tea Drinking and the Risk ofLate-Life Dementia: A Population-Based CAIDE Study . J Alzheimer Dis 16 (2009) 85-91
  41. 41. Caffeine Epidemiological studies have found an association betweencoffee consumption and improved cognitive function in ADpatients and in the elderly.Long-term administration of caffeine (non-selective adenosineantagonist) in animals showed a reduced amyloid burden inbrain with better cognitive performance.Adenosine receptors play important roles in the modulation ofcognitive function. Antagonists of adenosine A2A receptorsmimic the beneficial effects of caffeine on cognitive function.The adenosinergic system constitutes a new therapeutic targetfor AD, and caffeine and A2A receptor antagonists may havepromise to manage cognitive dysfunction in AD
  42. 42. Today discussion points Dehydration Exercise induced Hyponatremia Caloric restriccion N3-PUFA Vitamins Caffeine Physical activity and exercise
  43. 43. Mean Differences in Change in CognitiveFunction Scores by Quintile of Physical Activity*. higher levels of physical activity, including walking, are associated with better cognitive function and less cognitive decline Weuve, J. et al. JAMA 2004;292:1454-1461
  44. 44. Clear and strong associations between greater physical activityand reduced cognitive decline in women with vascular disease Adjusted global cognition composite score during the cognitive follow-up period (1998-2005) by quintile of total physical activity at baseline (n = 2809) Vercambre, M.-N. et al. Arch Intern Med 2011;171:1244-1250.
  45. 45. AEE as 90% of total energy Cognitive function was assessed atexpenditure (assessed using doubly baseline and 2 or 5 years laterlabeled water) minus resting metabolic using the Modified Mini-Mentalrate (measured using calorimetry) State Examination In this study, older adults with higher objectivelymeasured total daily activity had a lower incidence of cognitive impairment
  46. 46. PRCT, randomized to a high-intensity aerobic exercise (45 to 60 min/d, 4 d/wk for 6months) vs control. Results Six months of high-intensity aerobic exercise had effects oncognition Mean values representing the change from baseline for cognitive measures Baker, L. D. et al. Arch Neurol 2010;67:71-79.
  47. 47. These studies showed that systematized physical activity contributed to at least improve temporarily some cognitive functions of patients with Alzheimersdisease, particularly, attention, executive functions and language Coelho et al. Rev Bras Psiquiatr.2009 ;31(2):163-70.
  48. 48. Thank you very much for your attention