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Environmental/nutritional risk factors

Prevention of dementia

Alcohol drinking

Cognitive impairment is frequently observed in heavy drinkers and visuomotor capacity, memory or abstract thinking is affected in those individuals. Excessive alcohol consumption can lead to alcohol-related brain damage and severe loss of short-term memory, and is responsible for alcoholic dementia, also named Korsakoff’s syndrome. This disease is associated with the lack of vitamin B1, frequently associated with malnutrition in heavy drinkers. It is assumed that light to moderate alcohol consumption may lower the risk of cognitive decline and dementia. The health benefit may be mediated by a protective effect against vascular disease, as moderate alcohol consumption lowers the risk of stroke as well as subclinical infarcts and white matter disease on brain imaging. Binge drinking in midlife is associated with an increased risk of dementia. There is evidence that risk of dementia increased with rising alcohol consumption for those people who carried the ApoE e4 allele. One possible explanation could be that individuals with the e4 allele have less effective neural repair mechanisms and thus would be more susceptible to the deleterious effects of alcohol. On the other hand, resveratrol, a polyphenol may partly be responsible for the beneficial effects of wine, especially of red wine. It has complex physiological effects via gene modulation: antioxidative, cytoprotective and anti-inflammatory. The impact of alcohol consumption on the incidence of MCI and its progression to dementia has been studied recently. Patients with MCI who were moderate drinkers, i.e. those who consumed less than 1 drink/day (approximately 15g of alcohol), had a lower rate of progression to dementia than abstainers.

There seems to be a J-shaped association between alcohol intake and a variety of adverse health outcomes, including coronary heart disease, diabetes, hypertension, congestive heart failure, stroke, dementia, Raynaud's phenomenon, and all-cause mortality. Light to moderate alcohol consumption (up to 1 drink daily for women and 1 or 2 drinks daily for men) is associated with cardioprotective benefits, whereas increasingly excessive consumption results in proportional worsening of outcomes. Other studies have shown that a history of heavy drinking or alcohol abuse might be associated with an increased occurrence of dementia and Alzheimer’s disease.

There is insufficient evidence to promote alcohol to nondrinkers as a means of reducing dementia risk. As there is still debate whether the positive effects of moderate alcohol consumption are due to methodological artefacts, e.g. the fact that people who do not drink at all are more ill in general. Abstinent people might have deliberately stopped alcohol consumption due to severe chronic illness like past alcohol addiction.


The interaction between smoking and dementia is complex. Smoking is a clear risk factor for cardiovascular disease and stroke. In prospective population based cohort studies like the Rotterdam study, smoking was a risk factor for AD. Overall in this study, smoking doubled AD (relative risk 2.3). The risk was much higher in individuals without an APOE4 allele. A recent collaborative population-based study in Europe confirmed that smoking is associated with higher rates of cognitive decline in elderly subjects without dementia; higher cigarette-year consumption was correlated with a significantly higher rate of decline. Older family and case-control studies have found that smoking has a protective effect against developing Alzheimer’s disease. In contrast, others have argued that the results reported by case-control studies were a consequence of survival bias rather than a true protective effect of smoking. Thus, any lower rates of Alzheimer’s disease among smokers may have little or nothing to do with any protective quality of smoking. Interestingly, findings from several studies have shown that there is an increased risk of dementia and Alzheimer’s disease associated with smoking in those without an APOE e4 allele.

Mediterranean diet

Adherence to a so-called “Mediterranean diet”, i.e. a diet containing more fish than (red) meat, more vegetables and fruit than carbohydrates and moderate amounts of wine, (MeDi) may affect not only risk for Alzheimer’s disease (AD) but also subsequent disease course: Higher adherence to the MeDi is associated with lower mortality in AD. The gradual reduction in mortality risk for higher adherence to this diet suggests a possible dose-response effect.

W-3 fatty acids and fish intake

Elderly people who eat seafood or fish at least once a week are at lower risk of developing dementia. Daily consumption of fruit and vegetables was associated with a decreased risk of all cause dementia. Weekly consumption of fish seems to be associated with a reduced risk of all cause dementia but only among ApoE epsilon 4 non-carriers Regular use of omega-3 rich oils seems to be associated with a decreased risk of borderline significance for all cause dementia. Regular consumption of omega-6 rich oils not compensated by consumption of omega-3 rich oils or fish seems to be associated with an increased risk of dementia among ApoE epsilon 4 noncarriers. Frequent consumption of fruit and vegetables, fish, and omega-3 rich oils may decrease the risk of dementia and Alzheimer’s disease, especially among ApoE epsilon 4 non-carriers.

Although consumption of lean fried fish doesn’t seem to have a protective effect, consumption of fatty fish more than twice per week is associated with a reduction in risk of dementia by 28% in comparison to those who eat fish less than once per month. This effect seems to be selective to those without the epsilon4 allele.

However, until data from randomised trials become available for analysis, there is no good evidence to support the use of dietary or supplemental omega 3 PUFA for the prevention of cognitive impairment or dementia.

Homocystein, Folate (Folic Acid) and Vitamin B12

Plasma total homocysteine has emerged as a major vascular risk factor. Homocysteine is a sulfur amino acid in the blood whose metabolism is closely related to that of the vitamins folate, B6, and B12. Too much of it can damage blood vessels and it has also been linked with dementia. Folate and other B vitamins, including vitamins B6 and B12 help process and lower levels of homocysteine. Fortified cereals, green leafy vegetables, orange juice, yeast extract and liver are all good sources of folate. There is evidence that having too little folate may contribute to the cognitive impairment of some older people’s brains. This may result in reversible damage or possible increase in the risk of AD and vascular dementia. Low levels of folate and vitamin B12 might be related to an increased risk of Alzheimer’s disease. The results from a prospective, observational study indicated that an increased plasma total homocysteine level is an independent risk factor for the development of dementia and AD. But there is no evidence currently that folate or vitamin B12 deficiency is associated with the neuropathologic hallmarks of AD. It is not yet known whether increasing your intake of folate either through diet or by taking supplements will reduce the risk of developing dementia.

Antioxidants/Vitamin C and E

One hypothesis that accounts for both the heterogeneous nature of AD and the fact that ageing is the most obvious risk factor is that free radicals are involved. The probability of this involvement is supported by the fact that neurons are extremely sensitive to attacks by destructive free radicals. Free radicals are a by-product that occurs when the body uses oxygen. They are harmful and can cause damage inside the cells of the body. Environmental factors such as cigarette smoke or pollution can increase the level of free radicals in the body. Antioxidants are the body’s defence system against free radicals, as they mop up these destructive molecules. The danger from free radical damage increases with age. Some researchers think that the destructive effect of free radicals may be one of the causes of brain cell death in Alzheimer’s disease. This has led to interest in whether increasing antioxidant intake through diet or vitamin supplements could provide any protection against Alzheimer’s disease.It seems that patients taking vitamin E supplement might have a slower progression of AD than patients taking placebo. In studies, neither supplemental dietary nor total intake of carotens and vitamin C and E was associated with a decreased risk of AD. In the Honolulu-Asia Aging Study (HAAS), men had been followed for research purposes for more than 30 years. It showed that midlife dietary intake of beta-carotene, falvonoids, and vitamin E and C was not related to the incidence of dementia and its subtypes in late life. Others have investigated the association between the intake of antioxidants from food and the risk of AD. The results from a population-based cohort study with a mean follow-up period of six years suggested that high intake of vitamin C and vitamin E from food might be associated with a lower incidence of Alzheimer’s disease. They found that those who had the highest intake of vitamin E had a 43% lower risk of developing Alzheimer’s disease compared with the people who had the lowest intake. There was a slight association between high intake of vitamin C and risk of Alzheimer’s disease. The results from the Chicago Health and Aging project showed that those with the highest intake of vitamin E from food, but not from vitamin supplements, had a 70% lower risk of developing Alzheimer’s disease. This reduced risk was only found in those people who did not have the ApoE e4 gene. Vitamin C did not seem to offer any protection.



Last Updated: Thursday 08 October 2009


  • Acknowledgements

    The EuroCoDe project received financial support from the European Commission. Neither the European Commission nor any person acting on its behalf is responsible for any use that might be made of the following information. Alzheimer Europe also gratefully acknowledges the support it received from Fondation Médéric Alzheimer for this project.
  • European Union
  • Fondation Médéric Alzheimer