Nutrition and Alzheimer s Disease DR D A V I D W I L K I N S O N C O N S U L T A N T I N O L D A G E P S Y C H I A T R Y

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1 Nutrition and Alzheimer s Disease DR D A V I D W I L K I N S O N C O N S U L T A N T I N O L D A G E P S Y C H I A T R Y

2 Agenda Rethinking Alzheimer s disease Emerging specific nutritional needs for AD patients Interpretation of evidence A multi modal approach What does the future hold?

3 Rethinking Alzheimer s disease Since a cure for dementia is not yet available, finding effective preventive strategies is essential for a sustainable society in an aging world As dementia, cardiovascular diseases, stroke, and diabetes mellitus all major public health problems share several risk factors, public health efforts promoting a healthier lifestyle have the potential to enhance health status in advanced age Mangialasche et al. Alzheimers Res Ther 2012; 4 (1): 6

4 AD treatment 2014 and beyond Memantine, AChEIs, combination Other cognitive enhancers Improved and earlier diagnosis Patient segmentation (genetics ) Disease-modifying therapies Community-wide prevention initiatives (diet, exercise )

5 The brain requires nutrients to function The brain needs specific nutrients to build and maintain its structure 1 The brain is 60% fat 2 - the type of fat influences the physical properties of cell membranes 3 Nutritional deficiencies are associated with impaired brain function, for example: Omega 3 fatty acid levels affect mood, behaviour, stress, depression and dementia 1,4,5 Vitamin B deficiency is linked to neurologic disorders and psychological disturbances 1 The need to supply specific nutrients to the brain may be increased in neurological disease, such as AD 6 Enzymatic reactions in the brain are controlled by the local concentrations of their substrates, often nutrients that cross the BBB 7 1. Bourre. J Nutr Health Aging 2006a,b; 2. Nolte's The Human Brain, 6th Edition Youdim et al Bourre. J Nutr Health Aging 2005; 5. Phillips et al. Nutr Neurosci 2012; 6. van Wijk et al. J Alzheimers Dis ; 7. Wurtmann 2008.

6 study Agarwal '10 Anello '04 Asita De Silva '05 Cascalheira '09 Clarke '98 Dominguez '05 Faux '11 Galimberti '08 Galluci '04 Hogervorst '02 Irizarry '05 n control mean control sd study control Agarwal 30.1 '10 32 Anello 5.9 '04 Asita 9.7 De Silva 23 '05 Cascalheira 1.7 '09 19 Clarke 10.0 '98 Dominguez 9.0 '0529 Faux 12.7'11 Galimberti 6.2 '0829 Hogervorst 11.3 '0266 Lower nutrient status in AD Independent of nourishment status nfolate mean n sd mean AD Galluci 11.1 ' Irizarry 32.9 ' ADcontrol AD control folate sd control n AD mean study AD 15.0 Ahlskog ' Baldeiras ' Bourdel-Marchasson ' Ciabattoni ' Feillet-Coudray 7.2 ' Glaso ' Mangialasche ' Polidori ' sd AD Polidori ' folate n control mean control sd n mean sd n mean mean weight mean Vitamin E control study AD AD AD control control difference (95% CI) (%) difference (95% CI) (-8.03, Ahlskog 6.61) ' (-2.60, -0.20) 13.4 Baldeiras ' (-9.24, 1.54) Bourdel-Marchasson ' (-4.03, 0.85) 13.0 Ciabattoni ' (-7.80, -2.80) (-16.51, Feillet-Coudray -6.89) 25 ' (-3.12, Glaso 1.24) ' (-13.91, -8.47) 5.5Mangialasche 168' (-6.01, 1.01) 10.2 Polidori ' (-12.99, -5.13) 5.2Polidori ' (-13.00, 2.40) (-8.03, ) (-2.60, -0.20) (-9.24, 1.54) (-7.80, -2.80) (-16.51, ) (-3.12, ) (-13.91, -8.47) vitamin E (-4.03, 0.85) (-6.01, 1.01) (-12.99, -5.13) (-13.00, 2.40) sd control (%) weight n AD mean AD sd AD vitamin E mean difference (95% CI) (-8.91, 1.23) Similar results for plasma levels of vitamins B12 and C (-13.55, -2.65) (-12.41, -2.59) (-24.87, ) 1.73 (-4.21, 7.67) (-19.07, -5.73) (-6.70, -4.92) (-15.45, -9.35) (-13.79, -9.61) weight (%) mean difference (95% C (-8.91, (-13.55, (-12.41, (-24.87, (-4.21, 7.67) (-19.07, (-6.70, (-15.45, (-13.79, -9 Joosten ' Joosten 3.2 ' Sinclair ' (-2.14, Sinclair 0.78) ' (-2.14, ) (-5.63, -4.17) (-5.63, Karimi ' Karimi 8.6 ' Zaman ' (-4.37, 1.65) 12.0 Zaman ' (-4.37, 1.65) (-17.11, -5.65) (-17.11, -5 Koseoglu ' Koseoglu 3.4 ' Unadjusted Overall (REML, I-squared=90%, P<0.001) (-8.28, -5.08) (-8.28, -5.08) Unadjusted Overall (REML, I-squared=90%, P<0.001) (-11.59, -5.52) (-11.59, -5.5 Unadjusted Overall (REML, I-squared=87%, P<0.001) Unadjusted Overall (REML, I-squared=87%, P<0.001) (-6.42, -2.27) (-6.42, -2.27) Age adjusted Overall (REML meta-regression, P=0.001) Age adjusted Overall (REML meta-regression, P=0.001) Age adjusted Overall (REML meta-regression, P<0.001) Age adjusted Overall (REML meta-regression, P<0.001) (-7.26, -2.02) (-7.26, -2.02) (-13.27, -6.15) (-13.27, AD lower AD lower AD AD higher lower AD higher lower higher AD lower AD higher AD higher AD lower AD higher 4.35 ( ); P < ( ); P = Lopes da Silva et al, Alzheimers Dement, 2013 Unadjusted overall mean difference (95% CI) Age-adjusted overall mean difference (95% CI) 8.56 ( ); P < ( ); P = 0.001

7 DHA (nmol/g) Impaired liver conversion of ALA 1 to DHA 2 in AD Total mrna Reduced liver biosynthesis of DHA Reduced peroxisomal D-bifunctional protein expression Control AD Control AD p = p = Astarita et al. PLoSOne α-linolenic acid 2 docosahexaenoic acid

8 Choline Creatine Ratio Change After Choline Intake Impaired nutrient uptake and absorption: choline Brain Uptake of Choline Decreases With Aging 0.6 Older men Older women Younger men Younger women 0.2 p < for younger vs older subjects Age (y) Choline intake increases plasma levels similarly in younger and older adults Brain choline shows lower increase after choline intake in older compared with younger adults 1. Cohen et al. JAMA. 1995

9 High Homocysteine levels reduce availability of DHA and choline High HCy levels in AD inhibit the activity of methyltransferases like PEMT involved in DHA and choline production Normal levels of HCy PEMT PATHWAY PHOSPHATIDYLETHANOLAMINE (enriched in DHA) Met PEMT B12 FO Via PEMT, high homocysteine levels negatively impact DHA and choline availability HCy CYSTEINE B6 PHOSPHATIDYLCHOLINE (enriched in DHA) liver-derived lipoproteins Choline DHA

10 Lower nutrient levels in AD brain/csf compared to healthy controls Nutrient Number of studies Significant lower Lower Higher Significant higher DHA EPA 1 2 Choline Folate Vitamin B Vitamin C 3 1 Vitamin E Selenium 3 5 3

11 Lower nutrient intakes due to poor food choices in early AD Lower intake from food sources of DHA vitamin B-6 vitamin B-12 Folate vitamin C vitamin E Lower intake of Fruits Nuts Seeds Fish Higher intake of Sugars & Snacks Shatenstein et al., J Am Diet Assoc, 2007 Phillips et al., Nutr Neurosci, 2012; Hart et al., Nutr Soc, 2013

12 Altered nutrient intake in AD: potential causes 12 Preclinical stage Changes in regulation of appetite Hypometabolism of hypothalamus, Hippocampal atrophy, impairment of olfaction and taste Genetic predisposition Metabolic changes: increase TNF-alpha levels Early stage of AD Memory and attentional deficits Reduced intake, unbalanced nutrient choice Increased energy requirements Restless, wandering Co-morbid medical illness Late stage of AD Reduced food intake Apraxia, dependency Dysphagia Medication side effects 1. adapted from Wirth 2012

13 AD is a multi-faceted disease requiring a multi-domain approach Multiple pathologies occur in AD, including neuroinflammation, neurovascular pathology and neurodegeneration Approaches that have targeted single pathologies, such as amyloid aggregation or inflammatory responses, or individual nutrients have had limited success A multi-modal approach may therefore be required, as has been effective in other conditions such as heart failure 1 The Finger study 1. Gillete-Guyonnet et al. Br J Clin Pharmacol. 2013;75:

14 Midlife AD risk profile, 20 years prediction CAIDE Dementia Risk Score Age, years < 47 0 Education, years > Sex Women Men Systolic BP, mmhg BMI, kg/m 2 Cholesterol, mmol/l 140 > > > % SCORE Physical activity Active Inactive 0 1 Kivipelto et al., Lancet Neurology 2006

15 Diet and AD risk Epidemiological data has shown an association between certain dietary patterns and a lower risk of AD, e.g. 1 Regular intake of fish (providing PUFAs) 2,3 Mediterranean diet 4,5 Adherence to nutritional recommendations in middle-age adults is associated with future memory performance 6 BUT we do not eat specific foods or nutrients in isolation, so supplementation of single nutrients is likely to yield mixed results. These data suggest that supplementation with specific combinations of nutrients is more effective in improving cognitive performance than single nutrient supplementation 1.Salerno-Kennedy et al. Int J Vitam Nutr Res Kalmijn. J Nutr Health Aging Barberger-Gateau et al. BMJ Solfrizzi et al. Expert Rev. Neurother Martínez-Lapiscina et al JNNP Kesse-Guyot et al. Am J Clin Nutr 2011

16 Single nutrient interventions in AD/MCI: in general no beneficial effects on cognition Nutrient Author Journal n3 PUFAs Quinn 2010 Freund-Levi 2006 JAMA Arch Neurol #Subjects/ Duration months months Outcome DHA compared with placebo did not slow the rate of cognitive and functional decline in mild-moderate AD patients. Administration of n3pufa in mild -moderate AD patients did not delay the rate of cognitive decline according to the MMSE or the cognitive portion of the ADAS. However, positive effects were observed in a small group of patients with very mild AD (MMSE>27) Aisen 2008 JAMA months This regimen of high-dose B vitamin supplements does not slow cognitive decline in individuals with mild to moderate AD. B-vitamins McMahon 2006 N Eng J Med months The results of this trial do not support the hypothesis that homocysteine lowering with B vitamins improves cognitive performance. Vitamin E / Antioxidants Dysken 2014 Petersen 2005 JAMA N Eng J Med 304 Mean f-up 27 months months Among patients with mild to moderate AD, 2000 IU/d of alpha-tocopherol compared with placebo resulted in slower functional decline. Vitamin E had no benefit in patients with mild cognitive impairment. Galasko 2012 Arch Neurol weeks However, this treatment (vitamin E + vitamin C plus α-lipoic acid) raised the caution of faster cognitive decline Vitamin D2 Stein 2011 J Alz Disease 32 8 weeks We conclude that high-dose vitamin D provides no benefit for cognition or disability over low-dose vitamin D in mild-moderate AD Ginkgo biloba DeKosky 2008 JAMA 3069 median f-up 6.1 Y Ginkgo biloba at 120 mg twice a day was not effective in reducing either the overall incidence rate of dementia or AD incidence in elderly individuals with normal cognition or those with MCI.

17 Why have single nutrient supplements failed? Cognition poorly assessed or assessed post hoc Populations too heterogenous Level of supplementation is very variable 1 Variable dietary intake confounds total nutrient levels May be that multiple nutrient combinations are more effective by being more physiological 1. Barnes et al. Nutr Rev 2014

18 What correlates best with severity of dementia? Synapse loss/neurone loss Neurotransmitter loss acetylcholine Neurofibrillary tangles Amyloid plaques

19 Alzheimer s disease is not primarily a nutritional disorder but age-related nutritional deficiencies occur Age-related reduced uptake of choline by brain Reduced plasma levels folate, Vit B12, Vit C, Vit E Reduced synthesis of uridine monophosphate Increased homocysteine Reduced CSF and brain levels of omega-3 (DHA/EPA)

20 Methodologies in nutrition studies

21 Assumptions are dangerous Choline uptake across BBB decreases with age Transport across BBB Metabolism of long chain fats in liver decreases in AD Microbiome? Metabolism Absorption Digestion Vitamin B12 digestion and absorption decreases with age

22 The need to take a broad view of the evidence Take preclinical studies into consideration for likely MOA Look at trends, doses, comparators, intakes in: Epidemiology Prospective cohorts Observational studies Population based studies RCTs but interpret results with caution 1 as nutrition trials do not lend easily to RCT formats 1. Blumberg et al 2010

23 So where is there good evidence? Nutrition for optimal brain health 1 Vitamin E DHA Folate & B12 Ratio of saturated to unsaturated fats Some aspects of Alzheimer s disease 2 Neuroinflammation Glucose dysregulation Homocysteine Neuronal loss These disease elements can be influenced with nutrition 1. Morriss JAMA Ferreira et al Alz Dem 2014

24 Advice from Royal College of Psychiatry Depression Bipolar Schizophrenia ADHA Epilepsy Eat diet rich in omega 3 Eat diet rich in omega 3 Eat diet rich in omega 3 No clear advice Eat ketogenic diet Selenium Selenium Calcium Folate Tryptophan Vitamin D S-adenosylmethionine St John s Wort Folate Tryptophan Vitamin D S-adenosylmethionine St John s Word No advice on AD or dementia yet advice on nutrition for other major organ failures like heart, kidney and liver are common place and accepted. RCGP website

25 Dietary guidelines for AD prevention The seven guidelines to reduce risk of Alzheimer s disease 1 Minimise your intake of saturated and trans fats 2 Eat plant-based foods vegetables, legumes, fruits & wholegrains should replace meat and dairy products as primary staples of the diet 3 Consume 15 mg of vitamin E from foods daily. Healthful food sources incl nuts, seeds, green leafy veg and wholegrains 4 Take a vitamin B12 supplement : 2.4 micrograms per day for adults 5 Avoid multivitamins with iron and copper 6 Choose aluminium free products (?) 7 Exercise for 120 minutes each week A Special Report, Physicians Committee for Responsible Medicine, July 2013

26 Whats the future for nutrition in AD Dietary correction earlier in disease course Nutrient combinations preferable to single nutrient supplementation Dietary pattern adoption instead of single food recommendations Better trial development to what works best for nutrition Nutrition in combination with other lifestyle factors Higher doses may be needed in diseased populations

27 Nutrition and Alzheimer s Disease DR D A V I D W I L K I N S O N C O N S U L T A N T I N O L D A G E P S Y C H I A T R Y

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