September is World Alzheimer’s Month and today, September 21st, is World Alzheimer’s Day. The goal of these special events is to raise awareness around, educate, encourage support of and demystify dementia.
World Alzheimer’s Day is an international campaign to raise awareness and highlight issues faced by people affected by dementia. It is an opportunity for people and organizations to demonstrate how to overcome these issues and help people live well with dementia. The Alzheimer’s Society, the organization behind these events, also encourages everyone to know the signs and symptoms of dementia, so they can get the right diagnosis and support as quickly as possible.
Studies show a variety of risk factors could be modified to lessen your chances of this insidious disease, including maintaining a healthy weight, eating a nutritious diet, and not smoking. We’ll talk about several of these in today’s blog, including a new study on omega-3 fatty acids and Alzheimer’s Disease (AD). But first, let’s talk about what this disease is all about and who is most at risk.
What is Alzheimer’s Disease and How Common Is It?
AD is the leading cause of dementia and the most common form of neurodegenerative disease in older populations. Prevalence rates of AD rise sharply from 3% in people over the age of 65 to nearly 50% in people over the age of 85.
The World Health Organization has projected that as the global population ages, the prevalence of AD will rise from 36 million to 115 million by 2050. Although AD is common among older populations, it is not a normal part of aging. We can control contributing factors to mitigate risk and improve our quality of life at any age.
AD is an irreversible neurodegenerative disorder characterized by progressive loss of memory, cognitive function, and behavioral changes that affect daily living. AD can only be definitively diagnosed postmortem, which is when doctors look for two things: neurofibrillary tangles (NFTs), and amyloid plaques.
NFTs are byproducts of the abnormal metabolism of tau protein, a protein normally found in brain cells that is known to promote cell stability when functioning properly. In AD, however, hyperphosphorlylation of tau protein transforms it from being a soluble asset to an insoluble hinderance that gradually aggregates and forms “tangles”. And these tangles contribute to neurodegeneration over time.
Amyloid plaques begin with another protein called amyloid-Beta (also commonly known as beta amyloid protein). This protein is normally produced and cleared within the brain, but when production and clearance are out of balance even a slight buildup of beta amyloid protein can lead to amyloid plaque and vascular deposits that disrupt neurobiology. Beta amyloid plaques have been found to increase pro-inflammatory cytokines, reactive oxygen species, and neurotoxic secretory products, ultimately leading to neuron death.
Although the exact etiology of AD is unknown, genetics seem to play a role in approximately 1-5% of AD cases known as familial AD, or early onset AD. For the other 95-99% of AD cases known as late onset AD, it is generally accepted that it is the result of complex interactions among aging, genetics, lifestyle, and environmental factors.
Who Is Most At Risk for AD?
The non-modifiable risk factors for AD include:
– Genetics: The apolipoprotein E type 4 allele (APOE-4) is a gene known to increase risk for AD. This allele gene is found in approximately 15% of the general population and is believed to be associated with earlier onset of AD.
– Family History: Offspring of parents with AD have been reported to have six times greater risk for developing the disease compared to those without a family history of AD.
– Age: Even though recent procedures have allowed us to better control our appearance of age, biological age cannot be stopped and is linked to increased risk for cognitive decline.
Even IF you have one or multiple non-modifiable risk factors, it doesn’t mean you’re destined to develop AD. Cases that are caused by genetics alone are thought to be restricted to early-onset cases in people less than 60 years old and account for only 1% of all cases. The truth is, there are more modifiable risk factors that play an even larger role in the development and progression of AD.
Twin studies demonstrate that even in people who are genetically identical, epigenetic forces can predispose an individual to disease while others are protected. Even APOE, the most established genetic risk factor for late onset AD, appears to be modified by several modifiable factors such as nutrition, alcohol consumption, exercise, antihypertensive treatment, and education.
So, let’s talk more about these modifiable risk factors that may protect you from cognitive decline later in life.
– Cardiovascular Disease: Hypertension and elevated serum cholesterol levels in midlife increase the risk of developing AD decades later. Mounting evidence suggests that microvascular brain damage caused by high blood pressure is often part of the neuropathology of cognitive impairment. Additionally, elevated cholesterol appears to play a role in the formation of amyloid plaques.
– Type 2 Diabetes: People who have type 2 diabetes have a 50-65% increased risk of suffering from AD. Insulin resistance in the brain has been shown to compromise survival of neurons, metabolism, and neuroplasticity, and is also implicated in the formation of the amyloid plaques. Research has found that type 2 diabetes before the age of 65 corresponds with a 125% increased risk for AD.
– Low Mental Stimulation: Several observational studies demonstrate that education and complex mental activities are the most established risk factors for dementia. People who have higher rates of education have lower rates of AD and all cause-dementia compared to those with less education.
– Sedentary Lifestyle: One study reported that individuals participating in leisure-time physical activity at least twice a week had 60% lower odds of AD compared with those in the sedentary group.
– Diet: Studies have found that people who eat a Mediterranean diet have thicker cortical brain regions, lower levels of beta-amyloid protein, reduced rates of AD, and substantial slowing of cognitive decline compared to those who do not.
Unfortunately, at the time of clinical diagnosis of AD, neurodegeneration is well underway and significant brain damage has already occurred. Therefore, prevention of AD through the identification and modification of risk factors is currently the most efficacious approach available.
What’s the Connection Between Omega-3 & Alzheimer’s?
The relationship between omega-3 fatty acids (particularly DHA) and brain health has been studied for several years. Approximately 60% of fatty acids in the neuronal cell membranes consists of DHA. Moreover, it has been confirmed that AD patients have reduced brain and serum DHA levels compared with age-matched healthy controls, suggesting that a DHA deficiency could play a role in AD development.
A case-cohort study found that both plasma and dietary DHA levels appear to protect against dementia. The researchers in this study found that those who had plasma DHA in the highest tertile had a 65% reduction in odds of all cause-dementia and a 60% reduction in odds of AD. Further, those with dietary DHA in the highest tertile were associated with 73% reduced odds of all-cause dementia and 72% reduced odds of AD.
Omega-3s May Decrease Risk for AD Through Multiple Pathways:
- Research has found that DHA reduces beta-amyloid protein generation not by modulating multiple cellular functions at once. One study found that DHA-enriched diets significantly reduced total beta-amyloid by >70% compared to low-DHA or controlled diets.
- The hippocampus is the brain area involved in memory and spatial orientation. This is why when the hippocampus cells die as a result of AD, memory loss and disorientation follow. DHA has been found to promote hippocampus neurogenesis (new neuron growth), which may help maintain and improve hippocampus survival throughout aging.
- DHA is incorporated into the plasma membranes, which increases membrane fluidity and has a significant impact on neural membrane function and efficiency.
- DHA enriched diets have been found to increase levels of brain-derived neurotrophic factor (BDNF). BDNF is one of the most widely distributed neurotrophins in the brain and plays a critical role in the development, maintenance, and plasticity of neurons.
It is important to note that nutritional intervention with omega-3 fatty acids appears beneficial before cognitive impairment sets in, or in the earlier stages of cognitive impairment. Controlled studies on patients with well-established AD have not shown improvement with high doses of omega-3 fatty acids. Optimizing intake of omega-3 fatty acids as a preventative measure is encouraged earlier rather than later in life to stave off dementia and AD.
How to Optimize Diet to Reduce Risk of AD
Nutrition can affect the brain throughout the lifecycle with implications on brain structure and function, mental health, and degenerative disease. While it’s well known that specific nutrients can support brain health, let’s discuss a long-living dietary lifestyle that has been proven time and time again to support not only brain health, but also overall healthy aging.
Among the many dietary patterns there are in society today, evidence shows that higher adherence to a Mediterranean-type diet is associated with slower cognitive decline, reduced risk of AD, and decreased all-cause mortality in AD patients. While the precise definition of the Mediterranean diet differs, it generally consists of high intakes of vegetables, fruits and nuts, legumes, cereals, fish (high in omega-3 fatty acids) and monounsaturated fatty acids; relatively low intakes of meat and dairy products; and moderate consumption of alcohol.
A 2013 review reported a 28-48% reduced risk of developing AD in response to a higher level of adherence to a Mediterranean-type diet. These findings were confirmed by another study that found a gradual reduction in AD risk in a dose-dependent manner, where each additional Mediterranean Score Group (zero to nine point scale with higher scores indicating higher adherence to the diet) was associated with a 9-10% less risk for development of AD. This dietary lifestyle is believed to play a role in multiple mechanisms in the pathogenies of AD, including oxidative stress and inflammation.
Turns out even moderate red wine consumption, a well-known component of a traditional Mediterranean diet, has been found to support brain health. In fact, one study found that among 922 older subjects, those who drank no more than one to two glasses of wine each day had lower risk for developing AD compared to those who abstained. Researchers believe that the antioxidant and anti-inflammatory properties of resveratrol and melatonin, which are prominent in red wine, offer neuroprotective effects.
High adherence to the Mediterranean diet is associated with lower incidence of chronic disease, including cognitive decline, and lower physical impairment in old age due to the synergistic actions of different nutritional elements of the dietary choices.
What Else Can You Do to Reduce Your Risk of AD?
- Exercise regularly. The most thoroughly researched behavioral intervention for cognitive functioning is physical activity. In addition to modifying other associated risk factors with AD, such as cardiovascular disease and the APOE gene, physical activity has also been found to increase levels of BDNF,a molecule known to play a role on synaptic plasticity. Aerobic exercise, in particular, has been found to attenuate progression of neurodegenerative processes and age-related loss of brain matter and neuroplasticity. Studies show that physical activity, particularly midlife physical activity, decreases risk of dementia and AD later in life.
- Prioritize quality sleep. Research has found that Beta-amyloid plaque deposition, a biological marker of AD, is associated with poor sleep quality. The same study found that frequent napping was also associated with amyloid deposition. During wakefulness, there is increased neuronal activity leading to increased production of Beta-amyloid protein. During sleep, neuronal activity decreases, as does Beta-amyloid production. Based on this information, chronically insufficient sleep leads to increased neuronal activity and excess Beta-amyloid build up.
- Get social. It’s well documented that those who have more extensive social interactions are less susceptible to cognitive decline than those with reduced social networks. Moreover, social activity and support are associated with decreased risk for AD. Don’t stress if you are living alone or are an only child, participation in any socially engaging leisure activities such as visits with friends, going to the movies, clubs, community centers, places of worship, and volunteering are all associated with reduced risk of dementia.
- Participate in cognitive training programs and mentally stimulating activities on a regular basis. This is considered to be one of the most effective non-pharmacological therapeutic interventions to reduce risk of AD and cognitive decline. Studies indicate that intellectual activity in middle adulthood influences AD risk more than it does in early adulthood, so it’s vital to continue this practice throughout your life. This doesn’t mean you have to go get another degree (of course you can if you’d like), but you can simply learn a new skill, a new language, a new instrument, or you can participate in games and puzzles that challenge your brain power.
- Manage stress. High levels of perceived stress are associated with higher risk for developing AD. While still under investigation, it is believed that the stress hormones and neuroinflammatory mechanisms induced by stress can cause neuronal dysfunction that can contribute to the development and progression of AD. Stress management is imperative for long-term health and wellbeing. Meditation, Tai Chi, Mindfulness, and Breathing Techniques all have a role to play here.
There are many modifiable risk factors for AD that can be addressed at any point in life. Don’t wait until it’s too late. Make changes now to reduce your risk of cognitive decline later.