Cognitive decline refers to an age progressive process of cognitive deterioration which can eventually lead to a more serious recession into mild cognitive impairment (MCI) and then dementia. It is estimated that 15-20 percent of individuals aged 65 or above suffer from MCI in the UK and are at higher risk of developing Alzheimer's (AD) which accounts for the majority of dementia cases. MCI reduces health related quality of life by impairing crucial cognitive functions like memory, judgment and communication. Additionally, dementia will not only affect the patient but equally family and friends around them as relationships will change due to memory loss, change in behaviour and increase in dependability.
Thus, making this area of research vital for improving the life of the elderly, a population which is growing largely in many countries. Therefore, reducing the incidence of neurodegenerative diseases will allow people to work longer and reduce the number of dependents. Furthermore, as there are no high efficacy drugs for treatment of MCI or dementia, it is imperative to focus on the possible risk factors as a preventative measure. The UK spends 23.6 billion pounds on dementia yearly which includes both social and health care. Hence, research conducted on evaluating lifestyle risk factors leading to progressive cognitive decline can prove to reduce the financial burden on the health care system significantly. Highlighting the importance of preventative measures will allow adoption of healthier lifestyle choices such as a more nutritious diet and increased exercise which will reduce medical costs and promote a more productive population.
Immense research has been conducted in recent years suggesting various lifestyle factors contributing to cognitive impairment such as smoking, alcohol and exercise. One of the major risk factors amongst many affecting cognitive decline is diet and in particular the western diet which this review will be focusing on. Ever-growing research is being conducted on the effects nutrients can have on the brain, altering genes for synaptic plasticity, transferring energy to neurones for various cognitive functions and regulating neurotransmitter pathways. The diet has an immense impact on the body and its complex nature means altering one function can have multiple knock on effects downstream.
For example, diet can influence insulin levels which can promote diabetes leading to an increased risk of neurodegenerative diseases and other health problems. Previous studies have shown the detrimental effect the western diet can exert on cognitive function through its main constituents; red/processed meat, carbohydrates, saturated fats and sugars. This review will highlight the mechanisms by which these constituents impose their negative cognitive effects and the absence of neuroprotective dietary components in the western diet. Methods: Online databases used to obtain the research in this literature review were PubMed, Science Direct and Wiley online library.
To find suitable articles for this review the PubMed algorithm was used and Boolean factors such as 'AND', 'OR'. Search terms included western diet, Mediterranean diet, cognitive decline, MCI, dementia, used either alone or in combination. The search results were then condensed by applying appropriate filters such as; 'peer reviewed' and 'full free text' as well as by date using papers from the last 15 years. Using some review articles and their reference section, additional primary articles were found. Google search engine was used to facilitate my understanding of key words that was then narrowed by scientific resources through PubMed.
Discussion: Saturated Fats: Meats and dairy consist of the highest composition of saturated fatty acids which have been implicated to promote cognitive decline. Studies have shown a positive correlation between a higher intake of saturated/trans fats and an increased risk of developing both dementia and MCI. All studies focusing on the relationship between dementia and fat intake found that high consumption of saturated fats increased risk of developing dementia, but intake of unsaturated fats had a protective role. The follow up time was similar in most studies which was 4 years, however, in Latinen's study the follow up was 21 years which is much longer. The short duration of follow up time in studies allows for bias as poor diet could have been a result rather than a cause for dementia.
Most studies used a standardised questionnaire like the FFQ to obtain dietary data, a limitation to this method is that the FFQ accounts for the repeated intake of foods in one year and fails to include day to day variation which can alter results. Additionally, elderly men and women have shown to underreport caloric intake which could explain the low caloric intakes reported. Study accounted for other cofounding variables such as education levels by adjusting their models by years of education and observed no significant change in risk of developing AD. Morris didn't account for genetic variability, however the other studies depicted the risk of developing AD was greater in individuals carrying the APO E4 gene which is the major genetic determinant for AD and is involved in lipid transport.
Multiple mechanisms have been proposed explaining how a high fat diet can progress to dementia, for example an animal study observed neuroinflammation and cognitive decline in mice fed a high fat diet. This can lead to various issues like Increased levels of inflammatory cytokines like LPS which can alter gut bacteria responsible for stimulating the innate system. Subsequently this can then increase inflammatory cytokines in the brain which affect cognitive performance. Additionally, research has suggested that neuroinflammation can decrease levels of anti-inflammatory commensal gut bacteria which have shown to lead to a characteristic of cognitive decline in mice by particularly impairing spatial memory. Future studies should aim to clarify if the total amount of fat consumed or the ratio of saturated fat to unsaturated holds a greater effect on the development of dementia.
Dietary patterns with high consumption of red/processed meats that contain large amounts of fats have shown to accelerate cognitive decline in the elderly through inflammation aswell. Inflammation can lead to an increase in amyloid beta plaques, one of the major hallmarks for the pathology of AD and to an increase of IL-6 which is a proinflammatory cytokine linked to AD. Therefore, diet induced inflammation can indirectly promote the development of AD through altering other biological mechanisms in the body. Carbohydrates and Sugars: Fructose is an isomer of glucose and is naturally found in fruit but now is used in the western diet as sweeteners especially as an additive in sweetened beverages. A recent study implied a sugar rich diet (where 21% energy came from sugars) was linked to a decreased cognitive function assessed by an MMSE test amongst Puerto Rican participants. This relationship was restricted to added sugars only and not natural fructose which showed to have no significant difference in cognitive function.
However, a major limitation of this study was that language barriers and the educational levels of the participants was not accounted for and could have explained the poor cognitive performance in the tests. On the other hand, although there is a lack of population-based research in linking long term effects of sugar intake to cognitive decline, many mice models have proven to support this theory. Animal studies have depicted that rats fed fructose syrup performed worse in the Morris water maze which assesses hippocampus dependent memory. Additionally, research depicted that rats fed sucrose solutions showed memory impairment by not exploring novelty objects in the novel object recognition task. A longitudinal study carried out by Roberts on the elderly found that a high percentage carbohydrate accompanied by a low protein was associated with MCI. Consuming a diet rich in sugars and carbohydrates in the elderly can damage glucose and insulin metabolism.
Other studies found a similar relationship demonstrating that individuals carrying the APOE ϵ4 allele coupled with a high caloric dietary pattern (by eating less protein and more sugars) had an increased risk of AD. The Western diet has been found to increase insulin resistance, reducing the frequency of insulin signalling in the hippocampus which regulates synaptic plasticity and cognitive ability. Various mechanisms have been proposed for the neurological role of insulin such as its function in promoting long term potentiation (essential for long term memory formation), reducing neuroinflammation by increasing level of IL-1beta which is an anti-inflammatory cytokine and improves spatial memory in rats. Contrastingly, a study has suggested that carbohydrate containing foods can enhance cognition whilst simultaneously not effecting plasma glucose.
It was found that an optimum amount of 50 grams of carbohydrates in the form of glucose, potatoes or barley improved cognition in those who had poor be call function through increased performance in verbal declarative memory and visuomotor tests. This study inferred that individuals with poor glucose regulation are susceptible to the cognitive enhancing benefits of glucose. Similarly, Ortega found that diet rich in carbohydrates, vitamins and fibers improved cognitive function. However, in this case carbohydrates played an enhancing role with other nutrients and not solely, so the positive cognitive effects can't be fully attributed to the consumption of carbohydrates but rather as a combinational dietary pattern. Antioxidants and the Mediterranean diet: Antioxidants (vitamins A, C and E) found naturally in fruits and vegetables play a protective role by preventing free radical damage on cells.
When reviewing the detrimental effects of the western diet on cognition it is as important to look at components lacking in the diet that could enhance cognition as much as existing components that exert harm. Hence, the typical characteristic of a low intake of fruit and vegetables in a western diet induces a lower consumption of antioxidants, a nutrient shown to play a role in slowing the progression of cognitive decline (ref1,2,3). Studies focusing on vitamin E intake have depicted that consumption may lead to lower risk of AD. Study 2 observed the positive effects vitamin E supplements had on cognition, a limitation to this study is that results can differ from antioxidant intake through supplementation rather than naturally from foods. This is because supplement users can have more of a health seeking behaviour which could cause bias and that differences in absorption exist between the two methods of intake.
For example, Vitamin E supplement is at a higher concentration whereas from food it is taken alongside other nutrients. Overcoming this methodological limitation, study 3 also looked at vitamin E intake from food and found that the highest quintile of vitamin E intake corresponded to a decrease in age of 8-9 years. Oxidative stress is caused by an increased generation of reactive oxygen species (free radicals) which cause neurological toxicity through protein misfolding, mitochondrial dysfunction and apoptosis. Hence, the Mediterranean diet has been increasingly studied in recent years as a promoter for healthier cognition in later age due to its richness in antioxidants, unsaturated fats and plant-based foods. Despite contradicting results, multiple studies have suggested that a greater adherence to the Mediterranean slows the rate of cognitive decline.
Possible explanations for the results of studies suggesting otherwise could be the shorter duration of follow up time and smaller sample sizes. Additionally, the chosen populations of these studies came from an educated background and reported in questionnaires they thought their health was good/very good. This healthier lifestyle factor could explain why the experimental group failed to significantly perform better in cognitive tests compared to the control group as both groups would have had a comparable healthy diet and lifestyle. In order to truly evaluate the extent of the neurological protective function the Mediterranean diet holds and compare it to the detrimental effects of the western diet, future studies should focus particularly on components of the diet that differ. Secondly, research should be conducted to investigate if the effects of the western diet are reversible by using the Mediterranean diet as a 'treatment' intervention.
This will provide indication for quantifying period of adherence to the Mediterranean diet that is required to significantly reduce the risk of an individual developing MCI or dementia. The blood brain barrier (BBB) is a membrane separating blood from cerebrospinal fluid and acts as a barrier to larger molecules and cells (refg). Many studies have suggested that a high caloric diet leading to higher BMI is linked to disruption of the BBB. Furthermore studies depict that damage to the BBB is correlated to developing AD and MCI(2). Kanoski investigated the effects a western diet had on the membrane permeability of the BBB and on expression of tight junctions. The western diet fed to rats had decreased expression of the tight junctions which function to control permeability.
This further strengthens the ideology of the extent the western diet can damage the hippocampal region and elicit cognitive impairment. Disruption to the permeability of the BBB could lead beta amyloid entering from the blood to the brain which would induce the formation of AD inducing plaques. Similarly, a study linked the obesity promoting western diet to the deterioration of hippocampal memory formation through disruption of the BBB. Although all the studies had promising significant results, future research needs to be conducted to see the effect dietary patterns have on the BBB in humans rather than rodents. This could be carried out by investigating post mortem tissue samples of individuals with higher BMIs compared to healthier weighted individuals.
The evidence presented here shows that the western diet has a role in both accelerating the rate of cognitive decline and increasing risk of MCI/AD in the elderly. Despite discrepancies in research most studies have suggested that the main components of the western diet; saturated fats, carbohydrates, sugars, lack of antioxidants and vitamins coupled with the high caloric intake promote the development of dementia. Many studies have focused on investigating the mechanisms allowing these macronutrients to exert their negative effects on cognition leading to MCI and dementia. suggesting key roles for glucoregulation, inflammation, oxidative stress and meta amyloid plaque formation. Recent growth in this field has been impressive but there's a large scope for research to be completed on the effects dietary patterns hold on cognition. With many studies looking at effect of singular components rather than the dietary pattern as a whole, results have to be taken with caution.
Additionally, future work would benefit with adopting uniform standards when assessing dietary intake and cognition to strengthen the significance of relationships across studies. Reliability of FFQs used to assess food consumption need to be strengthened by accounting for longer periods of time and ensuring change in dietary patterns in longitudinal studies is accounted for. The meaningful evidence provided by research in this field will play a vital role in maintaining a healthier elderly population which is crucial for minimising the burden on health care systems and the economy. With no cure for dementia and only medication reducing the extent of the symptoms but not inhibiting them fully, this can serve as a reminder for the demand for continued research.
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