According to the Alzheimer’s society, there are currently around 800,000 people with dementia in the UK and these figures are expected to rise to over one million by 2021 (www.alzheimers.org.uk). Dementia, the umbrella term used to describe a syndrome that can have many different causes, is characterised by a gradual decline in cognitive abilities and neuropsychiatric symptoms. Alzheimer’s is by far the most common and most recognised form of dementia, but other forms include vascular dementia, frontotemporal dementia, Lewy body dementia, Korsakoff’s syndrome, Huntington’s disease and Parkinson’s disease.
Whilst some memory loss can happen as we age, the onset of neurodegenerative disease should not be considered as a prerequisite to the normal ageing process; indeed, it can be, in some cases, prevented. Yet, sadly, it is a common fallacy that the onset of dementia is simply a normal part of ageing and therefore, to some degree, accepted as inevitable. Dementia actually begins to damage the brain many years before symptoms become apparent, thereby causing a progressive decline in functioning as more of the brain becomes damaged. Knowing that the onset of dementia can occur early in life, and as prevalence rates climb, the focus is shifting from treatment to prevention, with factors such as diet and lifestyle becoming key targets for intervention.
For many of us, sitting at a desk for 6-7 hours a day, five days a week, is not uncommon. Making time to include activity, whether walking, running, cycling or spending a couple of hours at the gym a few times a week can seem daunting, given our busy schedules. We know that inactivity is linked to the increase in obesity figures, but the consequences of leading a sedentary lifestyle do more than just increase our risk of piling on the pounds. Significant lack of activity can double the risk of cardiovascular diseases, diabetes and obesity, as well as increase the risks of colon cancer, high blood pressure, osteoporosis, lipid disorders, depression and anxiety. As such, we are actively encouraged to spend 30 minutes, 5 times a week, on some form of physical activity. When it comes to the health of our brains, an increasing body of evidence strongly suggests that exercise, specifically aerobic exercise, may also attenuate cognitive impairment and reduce dementia risk.  Recent findings from the Caerphilly Cohort Study reporting the health habits of 2,235 men over a 35-year period found that taking regular exercise, not smoking, keeping a low body weight, and adopting a healthy diet with limited alcohol intake to be the top five healthy behaviours for reducing overall disease risk. This may seem like common sense but, interestingly, individuals who consistently followed four or five of these behaviours experienced a 60% decline in dementia and cognitive decline, with exercise being the strongest mitigating factor. 
The majority of us spend about one third of our life asleep. Ensuring we get a good night’s sleep is vital to overall wellbeing and studies show us that when people fail to get enough sleep, concentration, coordination, memory and mood all suffer. Indeed, studies show that long working hours in midlife are associated with a decline of cognitive function, and possibly dementia. Both shift work and long work hours reduce sleep time and quality, and can lead to sleep disturbances, with an overwhelming detrimental impact on nervous system function. For example, evidence is emerging that the sleep-wake cycle directly influences brain levels of amyloid-β; in experimental models, sleep deprivation increases the concentration of soluble amyloid-β and results in chronic accumulation whereas sleep extension has the opposite effect. An excess level of amyloid-β peptide within the brain is considered to be the hallmark of Alzheimer’s disease, with accumulation initiating a cascade of key events in the pathogenesis of the disease.
Exposure to various forms of stress is a common daily occurrence in the lives of most individuals, with both positive and negative effects on brain function. The impact of stress is strongly influenced by the type and duration of the stressor and, in its acute form, stress may be a necessary adaptive mechanism for survival. Exposure to severe and/or prolonged stress (such as induced by job loss or divorce) can cause over-activation and dysregulation of the hypothalamic pituitary adrenal (HPA) axis. This in turn causes detrimental changes in both brain structure and function and stress is one of the most potent environmental factors known to suppress adult neurogenesis.
Our modern eating habits have seen an overwhelming increase in obesity levels throughout the UK. Foods high in fat and sugar are typical of a Western style diet and contribute to obesity by increasing overall energy consumption. It is known that being obese or even carrying excessive weight increases the risk of developing Western-style diseases, such as type II diabetes and cardiovascular disease, but research indicates that poor dietary choices can also impact negatively on neural functions in brain systems involved in memory and cognitive processing. Regarding fat intake, understanding how types of fat impact on brain structure and function is vital for making the correct dietary choices when it comes to reducing dementia risk. Increasing fish intake, rich in omega-3 fatty acids, may be good advice for those looking to improve cognitive function and ward off dementia. Epidemiologic studies have shown that regular fish consumers have a decreased risk of dementia and better cognitive performance. [6, 7] The Mediterranean diet, for example, is well documented for its high fish content and low omega-6 to omega-3 ratio, both of which contribute to its cardiovascular health benefits. Adherence to the Mediterranean diet also appears to affect not only risk for developing dementia, but also subsequent disease course. 
The omega-6 to omega-3 ratio
The protective effect of fish consumption has been attributed to its high content of long-chain omega-3 polyunsaturated fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).A diet that is rich in omega-3 supports cognitive processes and up-regulating genes that are important for maintaining synaptic function and plasticity, support cognitive function and reduce dementia risk.The role of omega-3 in neuronal growth, survival and maintenance, improved neurotransmission and reduced oxidative stress is well documented.  The physiological roles of omega-3 in the brain include regulation of cell membrane fluidity, dopaminergic and serotonergic transmission, influencing membrane-bound enzymes and cellular signal transduction. They are also involved in brain glucose metabolism, eicosanoid synthesis, gene expression, cell growth and protection from apoptosis.
The increased consumption of foods that are rich in omega-6 fatty acids, including vegetable oils, cereal-based products and grain-fed animal products, has displaced omega-3 fats, leading to an increased risk of dementia through suppression of many of the aforementioned processes and there is a growing body of evidence that shows a positive association between the omega-6 to omega-3 ratio and the risk of Alzheimer’s disease.
Blood levels of omega-3 fatty acids have been shown to be inversely related to the risk of dementia. A 2012 meta-analysis of 10 studies (including 2,280 subjects) showed reduced levels of EPA and total omega-3 in patients with dementia. Furthermore, levels of EPA, but not DHA, were significantly lower in patients with pre-dementia syndrome, implying that low EPA may act as a disease-state marker AND a risk factor for cognitive impairment. The benefits of pure EPA have been demonstrated in neurodegenerative disorders such as Huntington’s  and may even outweigh EPA and DHA blends for cognitive performance in general. Whilst consistent changes in neurochemical substances, brain electrical activity, cerebral metabolic activity and brain oxygenation are observed following omega-3 supplementation, EPA intake has been found to be more advantageous than DHA in reducing ’brain effort’ relative to cognitive performance. [11, 12] EPA competes with arachidonic acid (AA), the main inflammatory omega-6 fatty acid; increasing EPA intake has a favourable effect on the omega-6 to omega-3 ratio (specifically the AA to EPA ratio). EPA has several neuroprotective roles in the brain, up-regulating gene expression concerned with neurogenesis, improving neurotransmission and connectivity and endothelial nitric oxide generation, and decreasing inflammatory cytokine levels.[13, 14]
Evidence has accumulated to support the involvement of oxidative stress, stress hormones and inflammation in the onset of cognitive dysfunction leading to dementia. Reducing or coping with stress, ensuring adequate sleep and making good dietary choices, whilst keeping the mind ‘active’ can all help to reduce the risk of developing dementia.
- Ahlskog JE, Geda YE, Graff-Radford NR, Petersen RC: Physical exercise as a preventive or disease-modifying treatment of dementia and brain aging. Mayo Clinic proceedings 2011, 86:876-884.
- Elwood P, Galante J, Pickering J, Palmer S, Bayer A, Ben-Shlomo Y, Longley M, Gallacher J: Healthy lifestyles reduce the incidence of chronic diseases and dementia: evidence from the Caerphilly cohort study. PloS one 2013, 8:e81877.
- Virtanen M, Singh-Manoux A, Ferrie JE, Gimeno D, Marmot MG, Elovainio M, Jokela M, Vahtera J, Kivimaki M: Long working hours and cognitive function: the Whitehall II Study. American Journal of Epidemiology 2009, 169:596-605.
- Ju YE, Lucey BP, Holtzman DM: Sleep and Alzheimer disease pathology–a bidirectional relationship. Nature reviews Neurology 2014, 10:115-119.
- Scarmeas N, Luchsinger JA, Mayeux R, Stern Y: Mediterranean diet and Alzheimer disease mortality. Neurology 2007, 69:1084-1093.
- Loef M, Walach H: The omega-6/omega-3 ratio and dementia or cognitive decline: a systematic review on human studies and biological evidence. Journal of nutrition in gerontology and geriatrics 2013, 32:1-23.
- Kanoski SE, Davidson TL: Western diet consumption and cognitive impairment: links to hippocampal dysfunction and obesity. Physiology & behavior 2011, 103:59-68.
- Hsu TM, Kanoski SE: Blood-brain barrier disruption: mechanistic links between Western diet consumption and dementia. Frontiers in aging neuroscience 2014, 6:88.
- Lin PY, Chiu CC, Huang SY, Su KP: A meta-analytic review of polyunsaturated fatty acid compositions in dementia. The Journal of clinical psychiatry 2012, 73:1245-1254.
- Puri BK, Bydder GM, Counsell SJ, Corridan BJ, Richardson AJ, Hajnal JV, Appel C, McKee HM, Vaddadi KS, Horrobin DF: MRI and neuropsychological improvement in Huntington disease following ethyl-EPA treatment. Neuroreport 2002, 13:123-126.
- Bauer I, Hughes M, Rowsell R, Cockerell R, Pipingas A, Crewther S, Crewther D: Omega-3 supplementation improves cognition and modifies brain activation in young adults. Human psychopharmacology 2014, 29:133-144.
- Bauer I, Crewther S, Pipingas A, Sellick L, Crewther D: Does omega-3 fatty acid supplementation enhance neural efficiency? A review of the literature. Human psychopharmacology 2014, 29:8-18.
- Salvati S, Natali F, Attorri L, Di Benedetto R, Leonardi F, Di Biase A, Ferri F, Fortuna S, Lorenzini P, Sanchez M, et al: Eicosapentaenoic acid stimulates the expression of myelin proteins in rat brain. Journal of neuroscience research 2008, 86:776-784.
- Salvati S, Natali F, Attorri L, Raggi C, Di Biase A, Sanchez M: Stimulation of myelin proteolipid protein gene expression by eicosapentaenoic acid in C6 glioma cells. Neurochemistry international 2004, 44:331-338.