The ageing brain and dementia
As people age, they often expect to experience cognitive decline: memory problems and slower thinking. Some, however, suffer a form of dementia, such as Alzheimer’s disease. Dementia poses a major public health challenge. At present, though drugs like Aricept can sometimes slow progression, no clear treatment has emerged.
What causes dementia? We do not know, although risk factors such as age, genetic profile, smoking, high blood pressure, obesity and cardiovascular disease have been identified. Research has also found brain abnormalities. Brain scans of Alzheimer’s patients show shrinking brain tissue, especially in areas of the brain associated with memory and reasoning. Postmortem studies have shown that two proteins, called beta-amyloid and tau, build up in the brain tissue of patients with Alzheimer’s disease, damaging brain cells and their connections – although scientists are not yet sure whether the abnormal proteins are causes or results of the disease process.
Epidemiological studies show that people who take anti-inflammatory medicines are at lower risk of dementia, suggesting that excessive, chronic inflammation may be involved. Inflammation is also linked to other risk factors for dementia, like cardiovascular disease. Modern Western diets are high in omega-6 unsaturated fats, saturated fats, and sugar, which have pro-inflammatory effects in the human body. Some researchers have therefore proposed that the food we eat may contribute to many illnesses, including dementia, and that changes in diet might reduce the risk of dementia.
Since dementia is currently incurable, public health strategies have focused on prevention, for example by encouraging healthier lifestyle choices. Dietary changes are an attractive target, not least because they are cheap compared with drug treatments and care costs. There is thus great interest in identifying anti-inflammatory ‘nutriceuticals’.
The best-known and most-studied of these are the omega-3 fatty acids, which have been repeatedly linked to better heart and brain health. Research suggests that in the body, omega-3 fats compete with omega-6/saturated fats 1, so that consuming more of the former reduces the latter’s pro-inflammatory effects. Thus raising dietary levels of omega-3 fats, while reducing omega-6 and saturated fat, might reduce the risk of inflammation, lower the chance of getting Alzheimer’s, and perhaps even preserve healthy brain function for longer.
Circumstantial evidence supports this hypothesis. Omega-3 fatty acids are found in many foods considered part of a healthy diet, such as oily fish, nuts and seeds, and green leafy vegetables, whereas omega-6 fatty acids and saturated fats are common in fast food. (One Big Mac, for example, contains half the recommended daily allowance (RDA) of saturated fat, while adding a large latte and portion of fries would provide the entire RDA in a single meal.1)
Obtaining scientific evidence for the hypothesis, however, has not proved easy. Clinical trials of nutriceuticals typically involve either dietary change or taking micronutrient supplements, both of which can change many variables at once, especially if supplements are taken in tandem with other treatments like drugs or exercise. Dietary intake and blood biochemistry are not always strictly monitored. Large, long-term samples are needed to tease out the complex mechanisms involved, especially when RCTs, the best way of determining causation, are used (since these require both a treatment and a control group). Drawing conclusions about whether dietary changes can reduce the risk of dementia is thus not easy. It is also very expensive.
Nonetheless, more and better-quality research is urgently needed, as shown by a 2012 Cochrane review 2 of whether polyunsaturated fatty acids (PUFAs) can prevent cognitive decline and dementia2. The authors’ criteria were that participants were over 60 and without cognitive impairment or dementia at the trial’s start. Trials had to be RCTs in which the method of randomisation was described, the intervention was ‘for 26 weeks or 180 days or longer’, and participants were given either omega-3 capsules (or placebo) or ‘a strictly enforced or provided dietary intervention (meals) including omega-3 PUFA supplemented foods in specific portions’. After de-duplication, 1424 records were identified. Yet only three studies (albeit each generating several publications) met the criteria.
The review found no evidence that omega-3 supplementation had any beneficial effect. However, the participants showed little sign of cognitive decline during the studies, so this is hardly surprising. Dementia can take many years to be diagnosed, hence the need for large, long-term studies.
In short, the evidence at present hints strongly at a crucial role for diet. To confirm that role, however, requires much more long-term, good-quality research.
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