Alzheimer’s and Dementia: Stacking the Odds in Your Favour
Neurodegenerative diseases are among the most common conditions that humans suffer from as we age. These include Alzheimer’s and Parkinson’s diseases, as well as other dementias. In Canada, it is estimated that 733,040 people are currently living with dementia, and by 2030, nearly 1 million Canadians will be diagnosed with the disease.[1] These numbers are staggeringly high, which raises both concern and interest in research regarding the prevention and reduction of the onset of these cognitive diseases. There is a particular interest in the link between nutrition, nutraceuticals, lifestyle, and the rate of cognitive decline in Alzheimer’s and dementia patients. Strong evidence highlights specific nutrients that decrease the pathologies associated with neurodegenerative diseases, such as increased oxidative stress, beta-amyloid plaque formation, and cerebral inflammation. This begs the question: What can we do to stack the odds in our favour?
What Are Alzheimer’s Disease and Dementia?
Alzheimer’s disease is a specific kind of dementia, which is an umbrella term for various brain disorders that affect mental processes severely enough to impact normal activities. Alzheimer’s disease accounts for about 60–80% of all dementia patients.[2] Alzheimer’s is characterized by the gradual loss of brain cells, leading to a decline in memory, reasoning, and other cognitive abilities over time. In Alzheimer’s disease, parts of the brain start to shrink, and the connections between the brain cells get weaker. Those affected might forget little things, like where they put their keys or what they had for breakfast. Over time, they might forget important things, like recognizing loved ones. They can also get confused easily, have personality changes, and get frustrated.
Memory difficulties, particularly with recalling recent events and experiences, are often among the initial signs of Alzheimer’s disease. Other indicators include a decline in the ability to remember spoken words, challenges with solving problems, a decrease in motivation, depressive states, and issues with sleeping. In later phases, there is a continued decline in memory and thinking skills, leading to significant impairment and loss of physical coordination, alongside notable changes in personality and behaviour.
Who Is at Risk?
Genetic factors, like having a parent or sibling with Alzheimer’s, increase the risk. Specific genes, like the APOE e4 allele, are associated with a higher risk of developing Alzheimer’s. People that have this gene have twice the risk of developing Alzheimer’s disease.[3] As we age, especially after 65, certain factors can increase the risk of Alzheimer’s disease. Conditions such as hypertension, high cholesterol, obesity, and diabetes can pose significant risks to heart health, which in turn may elevate the risk of developing Alzheimer’s. Additionally, experiencing serious head injuries, including concussions that result in loss of consciousness, may also heighten the likelihood of developing Alzheimer’s.
How to Stack the Odds in Our Favour
Diet and Lifestyle
The Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet is an eating paradigm designed to be neuroprotective and reduce the rate of cognitive decline in the aging population. The MIND diet utilizes dietary antioxidants and brain-supporting foods that reduce the accumulation of reactive oxidative species (ROS) that can lead to cellular damage and inflammation, especially as they accumulate with age.[4] The MIND diet is modelled after the Mediterranean diet and the Dietary Approaches to Stop Hypertension (DASH) diet, used to increase cardiovascular health and decrease systolic blood pressure, respectively.[5], [6] It is an evidence-based approach that nourishes the body to promote a healthy mind. It highly encourages the consumption of healthy omega‑3 fatty acids, mainly in the form of docosahexaenoic acid (DHA) found in fish, as well as antioxidant vitamins like dietary tocopherols (vitamin E) found in olive oil, nuts, and seeds; vitamin C; and carotenoid- and flavonoid-rich berries. Additionally, it emphasizes the importance of B vitamins like folate, derived from vegetables and whole grains. The MIND diet restricts red meat, processed food, dairy, and fast foods.
Exercise has been widely recognized for its general health benefits, but it also has specific advantages when it comes to Alzheimer’s disease prevention and management. Engaging in regular physical activity has been shown to offer a range of benefits that may help reduce the risk of developing Alzheimer’s disease.[7] Exercise can improve cardiovascular health, which is important in the development of Alzheimer’s. Regular physical activity can help manage these risk factors by keeping blood vessels healthy and ensuring good blood flow to the brain.[8] It is a beneficial practice for maintaining overall brain health and functionality, especially as one ages. Moderate- to high-intensity exercise for at least 75–300 minutes per week can be protective.[9] An easy way to monitor your exercise intensity is through your heart rate. Adding in just 10 minutes of intense aerobic activity like cycling, Tabata training, or running a few times per week can make a difference.[10]
Supplements
Citicoline
Citicoline is a brain chemical that occurs naturally in the body. It has a role in the synthesis of phosphatidylcholine, an important component of brain tissue. It may also help to repair brain-cell membranes and potentially improve neurodegenerative diseases. Citicoline is thought to work by increasing the levels of certain neurotransmitters in the brain, protecting neural tissues from damage, and reducing the buildup of harmful substances in the brain that are associated with cognitive decline.[11]
Omega‑3s
Omega‑3 fatty acids are found in fish oil and are known to be anti-inflammatory and neuroprotective. There is strong evidence that the consumption of fish, mainly those high in the omega‑3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), has been shown to lower brain inflammation and have benefits associated with improved brain function.[12] DHA is an omega‑3 fatty acid that is vital for brain growth and cognitive function. DHA is concentrated in areas of high metabolic activity like the cortex, neuronal synapses, and mitochondria,[13], [14] and is important for the structure and function of the brain. Increasing DHA levels in the brain supports mitochondrial function and structural components in the brain. Animal studies have shown that increasing DHA in the diet, through the consumption of fish and high‑DHA omega‑3 supplements, increases DHA levels in the brain. This may in turn increase antioxidant enzyme functions and decrease the levels of damage and oxidation in the brain.[15]
B Vitamins
B vitamins, especially folic acid, B₆, and B₁₂, have been shown to decrease the risk of Alzheimer’s disease and decrease brain aging. A prospective study that analyzed the link between folate intake and Alzheimer’s disease found that adequate folate intake (400 mcg or more per day) decreased the incidence of Alzheimer’s disease by 60%.[16] This decrease may be credited to the fact that increased folate intake is related to decreased levels of serum homocysteine. Homocysteine is related to vascular disease, impaired neuronal DNA repair, and oxidative stress, all contributing to the development of Alzheimer’s disease.[17]
Nicotinamide Riboside
Nicotinamide riboside is a form of vitamin B₃ that functions as a precursor to nicotinamide adenine dinucleotide (NAD+), a coenzyme involved in cellular metabolism. Some evidence suggests that increasing NAD+ levels may help to protect against neurodegenerative diseases. NAD+ plays a key role in energy production, DNA repair, and the regulation of circadian rhythms, all of which are important in the maintenance of neuronal health.[18] Nicotinamide has been shown to influence certain neuronal pathways that are involved in oxidative stress and regulation of apoptosis and autophagy. Autophagy is the cell’s way of cleaning out and recycling its damaged parts, while apoptosis is the cell’s programmed self-destruction when it is damaged or no longer needed. These are all critical for cellular health and survival.
Clinical studies have shown that supplementation with nicotinamide riboside can elevate NAD+ levels, which has been linked to potential therapeutic effects on metabolic and age-related diseases.[19] It is well-tolerated in healthy middle-aged and older adults and can effectively increase levels of NAD+ in peripheral blood mononuclear cells, indicating its potential for clinical use.
Conclusion
Alzheimer’s and dementia represent a significant and growing challenge. Adopting strategies to mitigate the risks and slow the progression of these neurodegenerative diseases is crucial. Research suggests that a proactive approach encompassing the MIND diet, rich in antioxidants and brain-healthy nutrients, combined with regular exercise and specific supplements like citicoline, nicotinamide riboside, omega‑3 fatty acids, and B vitamins, could be effective in supporting cognitive health and potentially delaying the onset of Alzheimer’s and dementia. These lifestyle and dietary changes, along with an understanding of risk factors, provide a hopeful avenue for individuals to influence their neurological health positively.
Dr. Dasha Leneva, ND
A naturopathic physician based in British Columbia helping people understand their bodies so they can be more confident about their health, she believes that even small practical habits can make astounding differences in people’s lives.
[1] Dementia numbers in Canada. Alzheimer.ca. Updated 2024‑02‑01. Consulted 2024‑04‑26. Available from https://alzheimer.ca/en/about-dementia/what-dementia/dementia-numbers-canada.
[2] Dementia. World Health Organization. Updated 2023‑03‑15. Accessed January 20, 2024. https://www.who.int/news-room/fact-sheets/detail/dementia.
[3] Gal, J., Y. Katsumata, H. Zhu, S. Srinivasan, J. Chen, L.A. Johnson, W.‑X. Wang, et al. “Apolipoprotein E Proteinopathy Is a Major Dementia-Associated Pathologic Biomarker in Individuals with or without the APOE Epsilon 4 Allele.” The American Journal of Pathology, Vol. 192, No. 3 (2022): 564–578.
[4] Cherian, L., Y. Wang, K. Fakuda, S. Leurgans, N. Aggarwal, and M. Morris. “Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) Diet Slows Cognitive Decline After Stroke.” The Journal of Prevention of Alzheimer’s Disease.” Vol. 6, No. 4 (2019): 267–273.
[5] Soldevila‑Domenech, N., A. Boronat, K. Langohr, and R. De La Torre. “N‑of‑1 clinical trials in nutritional interventions directed at improving cognitive function.” Frontiers in Nutrition, Vol. 6 (2019): 110.
[6] Saneei, P., A. Salehi‑Abargouei, A. Esmaillzadeh, and L. Azadbakht. Influence of Dietary Approaches to Stop Hypertension (DASH) diet on blood pressure: A systematic review and meta-analysis on randomized controlled trials.” Nutrition, Metabolism, and Cardiovascular Diseases, Vol. 24, No. 12 (2014): 1253–1261.
[7] Dominguez, L.J., N. Veronese, L. Vernuccio, G. Catanese, F. Inzerillo, G. Salemi, and M. Barbagallo. “Nutrition, Physical Activity, and Other Lifestyle Factors in the Prevention of Cognitive Decline and Dementia.” Nutrients, Vol. 13, No. 11 (2021): 4080.
[8] Thomas, B.P., T. Tarumi, M. Sheng, B. Tseng, K.B. Womack, C.M. Cullum, B. Rypma, R. Zhang, and H. Lu. “Brain Perfusion Change in Patients with Mild Cognitive Impairment After 12 Months of Aerobic Exercise Training.” Journal of Alzheimer’s Disease, Vol. 75, No. 2 (2020): 617–631.
[9] Müller, P., Y. Duderstadt, V. Lessmann, and N.G. Müller. “Lactate and BDNF: Key Mediators of Exercise Induced Neuroplasticity?” Journal of Clinical Medicine, Vol. 9, No. 4 (2020): 1136.
[10] Cammisuli, D.M., A. Innocenti, F. Franzoni, and C. Pruneti. “Aerobic exercise effects upon cognition in mild cognitive impairment: A systematic review of randomized controlled trials.” Archives Italiennes de Biologie, Vol. 155 (2017): 54–62.
[11] Gareri, P., A. Castagna, A.M. Cotroneo, S. Putignano, G. De Sarro, and A.C. Bruni. “The role of citicoline in cognitive impairment: Pharmacological characteristics, possible advantages, and doubts for an old drug with new perspectives.” Clinical Interventions in Aging, Vol. 10 (2015): 1421–1429. ERRATUM in Clinical Interventions in Aging, Vol. 10 (2015): 1625.
[12] Devassy, J.G., S. Leng, M. Gabbs, M. Monirujjaman, and H.M. Aukema. “Omega‑3 polyunsaturated fatty acids and oxylipins in neuroinflammation and management of Alzheimer disease.” Advances in Nutrition, Vol. 7, No. 5 (2016): 905–916.
[13] Calon, F., G.P. Lim, F. Yang, T. Morihara, B. Teter, O. Ubeda, P. Rostaing, et al. “Docosahexaenoic acid protects from dendritic pathology in an Alzheimer’s disease mouse model.” Neuron, Vol. 43, No. 5 (2004): 633–645.
[14] Lim, G.P., F. Calon, T. Morihara, F. Yang, B. Teter, O. Ubeda, N. Salem, S.A. Frautschy, and G.M. Cole. “A diet enriched with the omega‑3 fatty acid docosahexaenoic acid reduces amyloid burden in an aged Alzheimer mouse model.” Journal of Neuroscience, Vol. 25, No. 12 (2005): 3032–3040.
[15] Calon et al. op. cit.
[16] Corrada, M.M., C.H. Kawas, J. Hallfrisch, D. Muller, and R. Brookmeyer. “Reduced risk of Alzheimer’s disease with high folate intake: The Baltimore Longitudinal Study of Aging.” Alzheimer’s & Dementia, Vol. 1, No. 1 (2005): 11–18.
[17] Corrada et al. op. cit.
[18] Campbell, J.M. “Supplementation with NAD+ and Its Precursors to Prevent Cognitive Decline across Disease Contexts.” Nutrients, Vol. 14, No. 15 (2022): 3231.
[19] Yulug, B., O. Altay, X. Li, L. Hanoglu, S. Cankaya, S. Lam, H.A. Velioglu, et al. “Combined metabolic activators improve cognitive functions in Alzheimer’s disease patients: A randomised, double-blinded, placebo-controlled phase‑II trial.” Translational Neurodegeneration, Vol. 12, No. 1 (2023): 4.