Nutrition-related factors and the development of dementia

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Nutrition-related factors and the development of dementia[edit]

Mental health continues to pose a major challenge in the twenty-first century. Mental disorders such as dementia, depression, bipolar disorder, and schizophrenia outrank diseases such as cancer and cardiovascular disease as the major contributors to non-communicable global burden of disease (Prince et al 2007). The leading cause of years of life lost to disability (YLDs) in Australia is depression, followed closely by dementia (Henderson & Jorm 1998). However, dementia is predicted to be the leading cause of disability by 2016 (Access Economics 2005). In addition to negatively impacting on quality of life and sense of well-being, mental illness, especially dementia, can significantly impair a person’s level of functioning, including in the social, occupational and self-care domains (Prince et al 2007). A core component of self-care is adequate nutrition. Dementia is strongly age-related and is associated with a poor nutritional status (Gillette-Guyonnet et al 2007; Scheltens 2009). Australia’s ageing demographics are driving a need to prioritize mental health, especially dementia, both now and in the future. In this essay, the association between nutrition-related factors and the development of dementia will be discussed bi-directionally. Firstly, the evidence relating to whether poor nutritional status increases the risk of developing dementia in the older person will be explored. Secondly, the evidence for the occurrence of nutritional deficiencies as a consequence of developing dementia will be examined.

The Australian population is ageing (AIHW 2010). In 2007, 13% of the population was over the age of sixty-five and this is forecast to almost double by 2056 (ABS 2008). Dementia is common in the older person. Increasing age is the most consistent risk factor for dementia (Morris 2009). The prevalence of Alzheimer’s Disease (AD), the commonest form of dementia, doubles every five years after the age of sixty, increasing from a prevalence of 1% among those aged sixty to sixty-four years 30% of those aged eighty years (Ritchie & Lovestone 2002). It is estimated that by 2051, 2.8% (730,000) of the Australian population will have dementia. Therefore, in Australia, with our ageing population, dementia is a national health priority (Access Economics 2005). Dementia can be conceptualized as a multi-faceted cognitive decline that impairs daily living (Sachdev, Brodaty & Looi 1999). Impairment of memory is generally regarded as a core feature of dementia but there is also decline in one or more other cognitive domains. These include aphasia (language difficulties), apraxia (inability to carry out purposeful motor activities, such as using a fork while eating) and agnosia (difficulty recognizing things, including food), and executive dysfunction (difficulty with planning and organization, including food preparation) (Sachdev, Brodaty & Looi 1999). There are four main sub-types of dementia: AD, vascular dementia, dementia with Lewy Bodies and fronto-temporal dementia. In addition, there are several medical disorders associated with dementia syndromes including Huntington’s Disease, HIV-AIDS, Creutzfeld-Jakob Disease and corticobasal degeneration (Draper 2007).

Dementia is common in the elderly

This discussion will focus principally on AD and vascular dementia, as these dementia sub- types are common and have the most evidence supporting a link with nutrition-related factors (Gillette-Guyonnet et al 2007). The epidemiological evidence for this link comes mainly from prospective cohort studies, which is Level III-2 within the hierarchy of evidence (NHMRC 2008). As yet there is limited Level II evidence, with only a small number of randomised controlled trials (RCTs) (Gillette-Guyonnet et al 2007; Del Parigi et al 2006). In addition to nutritional status being a possible risk factor for dementia (Scheltens 2009), there are multiple other putative risk factors that may also influence both how a person’s brain ages, as well as the potential risk of developing dementia, such as smoking, hypertension, physical inactivity, and genetic factors, especially the apolipoprotein E ε4 allele (Morris 2009). These factors are potential confounders, which may impact on the validity of epidemiological studies exploring a relationship between nutrition and development of dementia (Luchsinger and Mayeux 2004). The reliability of food frequency questionnaire data is a dependent on the memory and cognitive ability of the participants and this may be subject to bias in a person with dementia (Del Parigi et al 2006).

Vascular dementia is diagnosed if significant cerebrovascular disease is present and is assessed to be causally relevant to the cognitive impairment (Sachdev, Brodaty & Looi 1999). Stroke is a major determinant of vascular dementia (Sachdev, Brodaty & Looi 1999). Over 30% of older people who suffer a stroke develop vascular dementia within three years (Henon et al 2001). Therefore, vascular dementia and stroke share the same risk factors (Sachdev, Brodaty & Looi 1999). These include smoking, hypertension, hyperlipidemia, diabetes mellitus type 2, sedentary life style, obesity, metabolic syndrome and family history (ie genetic loading) (Grand, Caspar & MacDonald 2011; Querfurth & LaFerla 2010). Many of these common risk factors are nutrition-related including hyperlipidemia, obesity, hypertension and diabetes mellitus type 2, and therefore are potentially modifiable. There is robust evidence to demonstrate the relationship between dietary intervention and minimising the risk of vascular disease (Van Horn et al 2008). Hypertension is the greatest risk factor for stroke (Ezzati et al 2005) and may be contributed to by a number of nutrition-related factors such as a high saturated and trans-fat diet, an energy dense diet and a high dietary intake of salt in those predisposed with a salt sensitivity (Obarzanek et al 2001; Margerison et al 2004). A diet high in saturated fat and trans-fat has been found to be associated with vascular dementia risk (Kalmijn et al 1997; Ferland, Greenwood & Shatenstein 2011). In addition, a high kilojoule diet in the absence of adequate energy expenditure may lead to obesity with a consequent increase in the risk of type II diabetes mellitus. Hence, modification of nutrition- related factors may mitigate the risk of developing vascular dementia, as well as lowering the risk for coronary artery disease (Morris 2009). There is strong epidemiological evidence demonstrating that adoption of a Mediterranean diet is associated with increased longevity, reduced risk of cardiovascular and cancer mortality, and reduced risk of neurodegenerative disease (Trichopoulou et al 2003; Sofi et al 2008; Knoops et al 2004). A Mediterranean diet rich in monounsaturated fatty acids, omega-3s, vitamins B12 and folate, anti-oxidants such as vitamin E, carotenoids and flavonoids, and a moderate amount of alcohol, may be protective against dementia (Feart et al 2009). A prospective cohort study with a long follow-up period (16.4 years) found an association between adherence to a Mediterranean diet and lower risk of AD and mild cognitive impairment (Scarmeas et al 2009) independent of physical activity. A strength of this study was that it controlled for physical activity as a potential confounder, as physical activity has been associated with higher educational-socioeconomic status and healthier eating habits (Scarmeas et al 2009). In contrast, another prospective cohort study found that adherence to a Mediterranean diet was not associated with risk for incident dementia (Feart et al 2009). However, a methodological limitation of this study was its comparatively short follow-up period (5 years) making it less likely to detect a beneficial effect of a Mediterranean diet on dementia risk (Feart et al 2009).

With respect to the development of AD, there is growing epidemiological evidence to support an association with the following dietary risk factors: anti-oxidants (vitamin E, C, beta- carotenes and selenium), fish and omega-3 fatty acid intake, dietary fats and vitamin Bs involved in homocysteine metabolism (vitamin B12, B6 and folate) (Morris 2009). However, due to the paucity of RCTs there is inconclusive evidence for a causal relationship between dietary variables and the development of AD (Gillette-Guyonnet et al 2007). Furthermore, even results of RCTs examining pharmacological interventions that target the reduction in amyloid protein and plaque accumulation have proved inconclusive (Mangialasche et al 2010). This is consistent with the complex pathophysiology of AD and possibly intervention strategies, including nutrition-related factors, should begin in a younger cohort such as fifty years olds. There is evidence suggesting a long asymptomatic phase of AD where elevated homocysteine levels, inflammatory variables and oxidative stress may be biochemical markers predictive of the eventual development of clinical features of AD (Scheltens 2009; Colyer 2011).

The evidence for antioxidants (especially vitamin E, C, beta-carotene and selenium) as protective factors against the development of AD is mixed (Morris et al 2002; Luchsinger et al 2003; Engelhart et al 2002). The brain is vulnerable to oxidative stress due to its high metabolic activity. In laboratory studies free radicals, secondary to oxidative stress and inflammation, have been found to lead to neuronal cell death and therefore may be implicated in the pathogenesis of AD (Morris 2009). In particular, when beta-amyloid (a core biochemical feature of AD) accumulates in the brain it produces an inflammatory response, free radicals and neurodegenerative effects (Devore et al 2010). Vitamin E, a fat-soluble vitamin, may mitigate these effects. The Chicago Health and Aging Project (Morris et al 2002) found that a higher intake of vitamin E, but not vitamin C or beta-carotene, was associated with a significant reduction in AD risk over two years. The Rotterdam study (Engelhart et al 2002) revealed a lower risk of AD in participants with a higher dietary intake of both vitamin E and vitamin C over six years of follow-up. In contrast, another prospective cohort study, the Washington Heights-Inwood Columbia Aging Project, which was conducted over a four-year period, found no association with the intake of vitamin E or C or beta-carotenes and the risk of developing AD (Luchsinger et al 2003). A possible reason for the negative finding in this study may be the significantly lower doses of these nutrients ingested compared to the Chicago Health and Aging Project and the Rotterdam studies. The Rotterdam study, which had a follow-up period of ten years, found that higher dietary intake of vitamin E, but not vitamin C or beta-carotene, was associated with a decreased risk of dementia, including AD (Devore et al 2010). Interestingly, clinical trials have shown no benefit of anti-oxidant supplements in reducing the risk for the development of AD (Devore et al 2010). For instance, Petersen et al 2005 conducted an RCT extending over a fifty-eight month period which showed no association between vitamin E (2000IU/day) supplementation and the progression to AD among older people with mild cognitive impairment (which is usually 10-15% per year) (Petersen et al 2005). These results suggest that protective effects against the development of dementia may be contingent on obtaining anti-oxidants from a natural diet rather than from supplementation. Another differentiating factor may be that in vitamin E supplements only α-tocopherol is provided, which excludes the anti-inflammatory and anti-oxidant effects of the other forms of tocopherol, especially gamma-tocopherol (Gillette-Guyonnet et al 2007). Only one prospective cohort study has investigated the relationship between selenium and cognitive decline and risk of AD (Gillette-Guyonnet et al 2007). It found that low plasma selenium levels were associated with accelerated decline in cognition and premature death (Neve 1991).

The brain is composed of 50-60% lipids, of which 35% are phospholipids containing long chain poly-unsaturated fatty acids (PUFAs), predominantly docosahexaenoic acid (DHA) (Assisi et al 2006). DHA accumulates in the brain during growth. It is also found in dendrites during memory formation (Innis 2005). DHA is best obtained from the diet (fish oils), as their conversion (desaturation and elongation) from α-linolenic acid is not very efficient in the brain (Seo, Blanar & Deckelbaum 2005). Omega-3 fatty acids, particularly DHA, are believed to protect neurones due to their anti-amyloid, anti-oxidant, anti-inflammatory and anti-atherogenic properties (Bourre 2004). DHA content was found to be decreased in the brain and plasma of patients with dementia (Schaefer et al 2006). This is suggestive of a role for omega-3 fatty acids in maintaining cognitive functioning in older people. Many prospective cohort studies have suggested a protective role for increased fish and omega-3 fatty acid intake in reducing the risk of AD (Morris 2009). However, more RCTs are needed before a causal relationship between amount of fish and omega-3 fatty acid consumed, and reduced risk of dementia, can be made (Morris 2009; Issa et al 2006). A limitation of much of the research is failure to adjust for potentially confounding variables. The following factors have been found to be associated with either a reduced or an increased risk of dementia and therefore need to be controlled for in examining the link between diet and dementia: socioeconomic status and educational attainment, intake of fruit and vegetables, alcohol intake, hypertension, past stroke and depression (Barberger-Gateau et al 2005).

Some suggest that eating fish once a week decreases the risk of developing Alzheimer's Disease

The Chicago Health and Aging Project (CHAP) showed that older people who consumed less than one fish meal per week had a 12% increase risk of cognitive decline compared to those who consumed just one fish meal or more a week (Bienias et al 2003). Similarly, Morris et al (2003b) found that the consumption of one fish meal a week in older people was associated with a 60% decrease in the risk of developing AD. However, the Rotterdam study, which initially reported a 70% risk reduction of AD after two years of weekly fish consumption (Kalmijn et al 1997), after six years found no association between fish and omega-3 fatty acid intake and the risk of AD (Engelhart et al 2002). The Framingham study, a prospective cohort study of 899 participants over 9.1 years who were dementia-free at base-line, found that those with higher levels of baseline plasma DHA (upper quartile) were significantly less likely to have developed any type of dementia (47% less likely than those in the lower 3 quartiles of base line plasma DHA levels). In addition, this group were 39% less likely to have developed AD specifically (Schaefer et al 2006). However, an RCT (Dangour et al 2010) has shown no difference in cognitive decline and risk of dementia while taking DHA supplements for 2 years. The Three-City cohort study of 8085 older people without dementia conducted over a four-year period was carried out in Bordeaux, Dijon and Montpellier in France. Similar to the Framingham Study, the Three-City cohort study found a positive association with weekly consumption of fish and omega-3 fatty acid intake and reduced risk of AD (35%) and all cause dementia (54%) (Barberger-Gateau et al 2002). As with vascular dementia, a diet high in saturated and trans-fats has been found to be associated with an increased risk of AD in some studies (Morris et al 2003; Kalmijn et al 1997). The most compelling evidence for the association of high saturated fat intake and increased risk of developing AD in the general population was shown in a Chicago prospective cohort (Morris et al 2003). In this study, ingestion of trans-fat was associated with a 2-3 times increased risk of developing AD. In contrast, the Rotterdam study, with a six year follow-up period, found no association with the increased risk of developing AD and higher intakes of saturated fat, trans-fat or cholesterol (Engelhart et al 2002). Cholesterol may play a significant role in the generation and accumulation of beta-amyloid plaques in the cerebral cortex, especially for people with the genetic risk factor of the apolipoprotein E (APOE)-€4 allele, the main regulator of fat transport in the blood and brain (Morris 2009). Therefore, a high intake of saturated fatty acids may be implicated in dementia due to its association with serum cholesterol levels (Mensink & Katan 1992). In fact, elevated blood cholesterol levels in midlife have been shown to be associated with three times the risk of developing AD in older age (Notkola et al 1998). People with the APOE4 gene are also at greater risk of higher serum triglyceride levels and amyloid precursor protein, which accumulates in the brains of AD sufferers (Mahley, Weisgraber & Huang 2006) and therefore may have a higher risk of developing AD.

Vitamin B12 deficiency is common with older age, occurring in more than 20% of persons sixty-five years and older (Gillette-Guyonnet et al 2007; Morris et al 2002). Deficiency of vitamins B12, folate and B6 is associated with significantly raised serum homocysteine levels. Hyperhomocysteinaemia is a risk factor for vascular disease and is likely to play a role in the development of vascular dementia and AD (Seshadri et al 2002; Ravaglia et al 2005; Gonzalez-Gross et al 2001). One RCT (Smith et al 2010) found that an accelerated rate of brain atrophy in people over seventy years old with mild cognitive impairment could be delayed with supplements of folic acid, vitamin B12 and vitamin B6. A prospective cohort in the Framingham study, carried out over an 8-year period, found an association between hyperhomocysteinemia and increased risk of developing dementia (Del Parigi et al 2006). However, Cochrane reviews have concluded that there are insufficient grounds for a definitive relationship between folic acid, vitamin B12 and vitamin B6 supplementation, and reduced risk of developing dementia, including AD (Malouf, Grimley & Areosa 2003).

Dementia is not a part of normal aging but rather a neurodegenerative disease resulting in the progressive destruction of neuronal cells in the brain (George et al 2009). However, even in the absence of dementia, increasing age is independently associated with poor nutritional status (Forster & Gariballa 2005). Epidemiological studies consistently demonstrate that older people have higher rates of nutritional deficiency, in particular B vitamins, especially B6, B12 and folate; vitamin D and K; the anti-oxidant nutrients beta-carotene, vitamin C, E and selenium; and the minerals zinc, calcium and iron (Gillette-Guyonnet et al 2007; Mcreynolds & Rossen 2004). These changes in nutritional status are likely to represent a risk factor for developing dementia, especially AD and vascular dementia (Gillette-Guyonnet et al 2007; Mayeux 2003).

In addition to be being a possible risk factor for the onset of dementia, malnutrition may be associated with the development of dementia, by being a consequence of this mental disorder (Gonzalez-Gross et al 2001; Grand, Caspar & MacDonald 2011). The characteristic cognitive deficits in dementia and the frequent accompanying behavioural and psychological features (confusion, apathy, agitation, anxiety and depression) often have a major impact on eating habits and nutritional status (Draper 2007). The nutritional implications include: inability to verbally express food preferences (aphasia); reduced interest in food (apathy, which is the commonest mood change in dementia); forgetting having eaten (short term memory loss); not recognizing the need to eat; easily distracted from eating; refusal to eat; inability to recognise food (agnosia); reduced ability to plan and prepare meals (executive dysfunction); inability to manipulate eating utensils or food; difficulties chewing and swallowing: and appetite regulation (Norberg & Athlin 1989; Draper 2007). Even with the most active nutrition intervention, it is challenging to maintain energy and protein requirements, and weight loss often results (Nowson 2009). Nowson (2009) has shown that 50-80% of older people living in long term residential care suffer from malnutrition, and 32% of these have dementia (ABS 2006).

In conclusion, nutritional status is an integral component of mental and physical health, and quality of life in old age (Nowson 2009). Dementia has been associated with poor nutritional status in the older person (Gillette-Guyonnet et al 2007; Scheltens 2009). There is growing but mixed evidence for a link between nutrition-related factors and the development of dementia, particularly vascular dementia and AD. Early dietary intervention may play an important role in minimising the risk of malnutrition and possible related development of dementia later in life. Finally, given the robust evidence for poor nutritional status as a consequence of developing dementia, dietary assistance for those with this disorder is a core component of their overall management.

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Acknowledgements[edit]

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

See also[edit]