Does nutritional status play a role in the onset of dementia?

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Does nutritional status play a role in the onset of dementia?[edit]

Dementia, recognised as the most common form of cognitive impairment in the elderly (Salerno-Kennedy & Cashman 2005) increases in incidence and prevalence with age (Cereda et al 2008; Dauncey 2009; Gillette- Guyonnet et al 2007; Kivipelto & Solomon 2008). Recent Australian data reveals that dementia is the leading cause of burden of disease in individuals aged greater than 75 years, whilst amongst all ages it is the fifth highest identifiable cause of disease burden (Australian Institute of Health and Welfare [AIHW] 2010). Over the past two decades, there has been a 167.8% increase in the number of elderly people compared with a total population growth of 30.1% over the same period (Australian Bureau of Statistics [ABS] 2009). This ageing population and subsequent increase in the proportion of elderly (Pirlich & Lochs 2001) has resulted in an increasing prevalence of neurodegenerative diseases such as dementia in this population subgroup (Gillette-Guyonnet et al 2007; Kivipelto & Solomon 2008; Polidori & Nelles 2010). It is predicted that the number of individuals living with dementia will increase to almost 465,000 in Australia by 2031, a value more than double the current statistic of 200,000 (Access Economics 2005). Dementia is a condition characterised by progressive cognitive decline that affects thinking, memory, understanding and reasoning (AIHW 2010; Morley & Thomas 2007). It commonly exists in the form of two pathologically distinct subtypes, Alzheimer’s Disease (AD) and Vascular Dementia (VD) (Gonzalez-Gross et al 2001). AD, accounting for 50-70% of all dementias is a condition characterised by progressive degeneration and death of neurones in specific areas of the brain, namely the hippocampus while VD is an umbrella term for dementia associated with circulatory problems to the brain (Alzheimer’s Australia 2010). Despite the fact that AD and VD have a multi-factor origin, it has been recognised that they both share the same nutrition- related risk factors (Middleton & Yaffe 2009; Salerno-Kennedy & Cashman 2006). In spite of medical and technological advances, treatment options for dementia are still limited (Dauncey 2009; Middleton & Yaffe 2009; Steele et al 2006). Thus, the prevention of dementia through the identification and management of nutrition-related factors is of pivotal public health and research importance (Burgener et al 2008; Dauncey 2009). Scientific evidence which supports the role of nutrition-related factors in the prevention of dementia is limited to date (Gillette-Guyonnet et al 2007; Middleton & Yaffe 2009; Polidori et al 2010) yet some evidence exists to support the role of antioxidants, B vitamins, dietary fats, alcohol, the Mediterranean diet and caloric restriction in the prevention of the cognitive decline associated with dementia, thus and will now be discussed.

Evidence to support the role that nutrition plays in the prevention of cognitive decline is increasing.

Oxidative stress in the brain may facilitate the pathogenesis of dementia by increasing a number of its risk factors (Barberger-Gateau et al 2007; Cereda et al 2008; Devore et al 2010; Gillette-Guyonnet et al 2007; González-Gross et al 2001; Gray et al 2008; Middleton & Yaffe 2009; Morris et al 2009; Salerno-Kennedy & Cashman 2006). Subsequently, it has been proposed that a high dietary intake of antioxidants, namely vitamins E, C, carotenes and polyphenols (flavenoids) may lower the risk of dementia and slow cognitive decline (Gillette-Guyonnet et al 2007; Middleton & Yaffe 2009; Salerno-Kennedy & Cashman 2006) by protecting neurones from the oxidative damage caused by free radicals and reactive oxygen species (ROS), apoptosis, protein oxidation, lipid peroxidation, cell membrane damage and beta-amyloid toxicity or deposition (Floyd & Hensley 2002; Perry et al 2002). It is well acknowledged that oxidative damage increases with increasing age (Cereda et al 2008; Gillette-Guyonnet et al 2007; Morris et al 2009) and has been linked to vascular disease which can increase the probability of suffering a stroke, a common vascular dementia risk factor (Cereda et al 2008). Further, it has been suggested that oxidative stress is associated to the pathogenic lesions in the brain of AD patients (Christen 2000; Markesbery et al 1997). Two recent meta- analyses conducted by Gonzalez-Gross et al (2001) and Esposito et al (2002) have identified support for the protective role of these antioxidants in protecting neurons from oxidative damage, though both groups agree that further research into this area is required. However, a more recent review by Luchsinger & Mayeux (2004) has concluded that there is insufficient evidence to warrant specific antioxidant dietary recommendations for the prevention of AD. The relationship between antioxidant intake and dementia risk has been studied in both observational studies and RCTs with varying conclusions produced. Two separate observational studies by Masaki et al (2000) and Morris et al (2002) have suggested that vitamin E offers a protective effect against the cognitive decline seen in AD, while a prospective cohort study by Engelhart et al (2002) identified that high intakes of both vitamin C and vitamin E are associated with a lower risk of AD. In all of these studies, the beneficial effect was a result of vitamin E containing foods, with no association found between supplementation and reduced risk of cognitive decline. The results of an RCT conducted by Yaffe et al (2004) support this conclusion, whereby no association with any effect on cognitive function was found in the antioxidant supplement group compared to the placebo group. In fact, a recent meta-analysis of 19 RCTs conducted by Miller et al (2005) identified a dose-response relationship between vitamin E supplementation of >400 IU/day and total mortality. This relationship, along with treatment via β-carotene and vitamin A were also identified in a recent meta-analysis (Bjelakovic et al 2007) to increase mortality. Thus, future work needs to be diverted to the development of epidemiological and RCT studies which ascertain the extent of these associations (Gillette-Guyonnet et al 2007).

Elevated homocysteine (Hcy) levels, caused by inadequate dietary intake of folate, vitamins B6 and B12 can increase the risk of Hcy toxicity (Gillette-Guyonnet et al 2007; Salerno-Kennedy & Cashman 2006) and regional brain atrophy (Smith et al 2010), with a resultant effect of cognitive decline. These B vitamins act as co-factors for the methylation of Hcy, a metabolic pathway that is essential for brain function (Gillette- Guyonnet et al 2007). Deficiencies of the B vitamins result in disturbed methyl-action and redox potentials which can promote calcium influx, amyloid and tau protein accumulation, apoptosis and neuronal death (Ho et al 2003; Kruman II et al 2000; Kruman II et al 2002; Lipton et al 1997). Inadequate dietary intake can also result in hyperhomocysteinemia, a risk factor for atherosclerosis, a condition which has recently been associated with increased cognitive decline, including both AD and VD (Joosten 2001). Current research detailing folate, vitamin B6 and B12 and its relationship to cognitive decline and AD is inconsistent. Only two prospective studies by Kado et al (2005) and Tucker et al (2005) have found an association between low folate intake and AD, with another study (Morris et al 2005) concluded that high folate intake (>400 ug/day) is associated with more rapid cognitive decline. A longitudinal study by Wang et al (2001) identified that subjects with low levels of vitamin B12 or folate had two times greater risk of developing AD. However, a longitudinal cohort study by Crystal et al (1994) determined that there was no association between the risk of dementia and low levels of vitamin B12, a conclusion that was similarly produced in a prospective study by Seshadri et al (2002). To date, four RCTs have been conducted where the effects of supplementation with one or more of folic acid, vitamin B6 or vitamin B12 on cognitive decline have been trialled, with no association determined (Bryan et al 2002; Clarke et al 2003; Fioravanti et al 1997; Sommer et al 1998). Accordingly, no dietary recommendations can be made regarding the dietary intake of B vitamins as epidemiological evidence for protective associations are still limited. In the future, it has been suggested that greater prospective studies be conducted which control for dietary confounders inclusive of carotenoids, niacin, dietary fats, and indicators of vitamin B12 deficiency such as methylmalonic acid (Gillette-Guyonnet et al 2007) be undertaken so as to determine the association between B vitamins and dementia. However, one very recent RCT (Smith et al 2010), has identified that the accelerated brain atrophy (a result of inadequate folate, vitamins B6 and B12 and subsequent elevated Hcy) can be reduced via the treatment of homocysteine-lowering B vitamins, namely folic acid, vitamins B6 and B12 in elderly patients. It is well acknowledged that brain atrophy is accelerated in AD patients (Bradley et al 2002; Fox et al 1999; Jack et al 2004; Smith 2002). However, Smith et al (2010) suggests that future RCTs are required to determine if the same treatment is capable of delaying AD.

Countless studies have investigated the relationship between dietary fats, specifically polyunsaturated fatty acids (PUFAs) and dementia, with mixed results produced (Van Dyk & Sano 2007). A prospective study by Kalmijn et al (2004) has indicated that diets high in cholesterol, trans-unsaturated and saturated fats are positively associated with an increase in cognitive decline, a belief supported by other prospective studies by Huang et al (2005), Morris et al (2003), Morris et al (2004) and Solfrizzi et al (2006). PUFAs have been proposed to play a pivotal role in brain function (Alan et al 2006; Cole & Frautschy 2010; Kroger et al 2009); specifically they have a modulating effect on inflammation, have anti-thrombotic properties and play a role in the composition and fluidity of neuron membranes in the brain, thus have been promoted as protective against cognitive decline (Cereda et al 2008; Gillette-Guyonnet et al 2007). Longitudinal studies have identified a positive relationship with a high dietary PUFA content and dementia, whereby regular fish consumption (at least weekly) is associated with reduced risk of cognitive decline (Barberger-Gateau et al 2007; Kalmijn et al 1997; Morris et al 2003; Morris et al 2004). However Barberger-Gateau et al (2007) identified that studies such as these fail to control for confounders such as fruit and vegetables (antioxidants) and alcohol; foods which have been also been identified as plausible in the prevention of dementia. A prospective cohort study and RCT has failed to produce the positive conclusions identified in these longitudinal studies. The Rotterdam study, a prospective cohort study concluded that there is no association between n-3 PUFAs and the risk of dementia (Engelhart et al 2002). To date, one RCT has been published which examines the effect of n-3 supplementation on cognitive functioning in mild to moderate AD sufferers (Freund-Levi et al 2006). Unfortunately, this study failed to identify any change in cognitive functioning in mild to moderate sufferers, though a positive effect was evident in very mild AD sufferers. At present there are three RCTs being conducted on n-3 fatty acids and cognitive decline in the elderly (Alan et al 2006; Van de Rest et al 2006; Yurko-Mauro et al 2006) with results yet to be published. Until the results of these RCTs are made available, little recommendations can be made regarding PUFA intake in the prevention of dementia despite the conclusions reached by prospective studies that diets high in PUFA are protective against cognitive decline (Gillette-Guyonnet et al 2007).

Some suggest that moderate alcohol consumption protects against cognitive decline.

Despite different methodological approaches in study design, many prospective studies have concluded that moderate alcohol consumption (1 to 3 servings/day or 15-30g ethanol/day) offers a protective effect against cognitive decline (Stampfer et al 2005). This VD protective effect can be attributed to alcohols association with large and medium-sized HDL particles, which have been identified as cardioprotective, reduced brain infarcts and the associated reduced risk of stroke (Cereda et al 2008) Whilst many of these studies note the beneficial effects of moderate consumption irrelevant of the type of alcohol consumed (Anttila et al 2004; Ruitenberg et al 2002; Stampfer & Kang et al 2005;), others where the type of alcohol was reported note that the advantage of wine in the prevention of both VD and AD is attributed to the antioxidants (polyphenols) it contains which other beverages such as beers and spirits fail to comprise (Belleville 2002; Zern & Fernandez 2005). A longitudinal study by Ganuli et al (2005) identified that mild to moderate drinking, compared to not drinking, was associated with less average decline in cognitive domains over the same time period. This positive cognitive outcome was also identified in the Nurses’ Health Study; a prospective cohort study undertaken in 2005 where it was asserted that up to one drink per day may decrease the risk of cognitive decline (Stampfer et al 2005). However whilst the moderate consumption has been identified as protective, this does not warrant consumption in abstainers. Further, heavy alcohol consumption (>4 servings/day or >35g ethanol/day) has also been associated with increased risk of dementia (Edelstein et al 1998; Nutt 1999; Ruitenberg et al 2002), though results are not statistically significant in this case. To date, there have been no RCTs conducted on the beneficial effect of alcohol on cognitive function, thus no specific recommendations can be made regarding its consumption (Cereda et al 2008; Morley & Thomas 2007).

The Mediterranean diet, a diet based around the consumption of cereals, legumes, fresh fruit and vegetables, fish, olive oil and the occasional red wine is ‘opening new insights’ (Cereda et al 2008) into the role whole foods and dietary patterns influence dementia (Scarmeas et al 2006a; Scarmeas et al 2006b). The diet has been associated with risk reduction (Cereda et al 2008) due to its high antioxidant, PUFA and monounsaturated fatty acid (MUFA) content which has a favourable effect on oxidative damage, reducing inflammation and influencing lipoprotein levels respectively (Burgener et al 2008; Cereda et al 2008). Polidori et al (2010) further suggests that the Mediterranean diet is effective in reducing the risk of diabetes, cardiovascular disease and obesity; chronic conditions which are risk factors for vascular disease and thus VD (Kopman 2009). Hughes & Ganguli (2009) also identify that a high adherence to the Mediterranean diet is associated with a decreased risk of AD. Scarmeas et al (2006) supports this assertion, further identifying that a dose-response effect exists. A review undertaken by Panza et al (2004) has attributed a greater dementia reduction in population samples with great intakes of MUFA (>2400kJ/day) in the form of olive oil (>100g/day); though whether the protective effect is a result of the MUFA content or the concomitant presence of tocopherol and polyphenols as antioxidants needs to be further investigated (Panza et al 2004)). However, these findings were not considered plausible in a more recent literature review conducted by Solfrizzi et al (2005). In their review, which contained an RCT it was concluded that based on the body of evidence available, that no recommendations based on dietary consumption of unsaturated fat, fish or vegetables can be made for the prevention of AD because of a lack of causative evidence (Solfrizzi et al 2005).

Caloric restriction and its association to dementia has been the subject of a large number of studies (Mattson et al 2002). Both Lee et al (2000) and Mattson et al (2000) argue that caloric restriction is associated with an increase in the expression of neurotrophic factors in the brain and a decrease in neuronal death, as well as a greater capacity for neuroplasticity and both prevention and repair in neurodegenerative disorders such as dementia, a belief supported by Mattson et al (2002). In their review of 125 studies in a well-designed meta- analysis, Mattson et al (2002) identified that the neurons are capable of repairing themselves after damage, offering hope to nutrition-related factors such as caloric restriction which has proved capable of increasing plasticity and repair. Another review by Mattson (2000) which contained an RCT identified that caloric restriction provides a neuroprotective role to the brains neurones, preventing them from damage by ROS by reducing the quantity of neurotoxic substances in the brain. Mattson (2000) goes on further to suggest that a quantity of 1800-2200 calories/day can dramatically decrease the incidence and severity of AD. A meta- analysis and follow-up on rodents conducted by Pasinetti et al (2007) identified that a high energy intake associated with high saturated fat content promotes AD type β-amyloidosis, while a low energy intake associated with a low carbohydrate intake can delay the onset of AD. However, despite this evidence from prospective studies, no dietary recommendations concerning caloric restriction can be drawn until future RCTs which support this causative evidence are conducted.

The evidence to support the role that nutrition-related factors plays in the prevention of cognitive decline is increasing and has great implications for the prevention of dementia. However, due to the lack of high level evidence and inconsistent results produced from the literature, it appears that antioxidants, B vitamins, dietary fats, alcohol, the Mediterranean diet and caloric restriction play an elusive role in the prevention of dementia. Whilst many epidemiological studies have produced evidence to support the employment of these dietary strategies as a means to prevent dementia, there are few RCTs with humans as subjects. Future research into these specific nutrition related factors and dietary patterns needs to be conducted before definitive dietary recommendations can be made and intervention strategies be developed with the intention of dementia prevention.

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Acknowledgements[edit]

The original version of this essay was by Lara Hannah Gillbert and was a prize winner NSW/ACT Dementia Training Student Centre essay competition, 2011.

See also[edit]