What if you are cognitively healthy now but worried that dementia might be in your future? Perhaps you have relatives that have developed Alzheimer’s disease (AD) or another type of dementia. Is there a way to prevent it?
Alzheimer’s disease is the most common type of dementia, accounting for 60% to 80% of all cases. AD develops as a result of multiple factors such as age, genetics, environment, lifestyle and coexisting medical conditions. No successful medications against AD have been found and the disease is inevitably fatal. However, there is emerging consensus that certain lifestyle choices and the management of other chronic health conditions may help to prevent the onset of from 30% to 50% of AD cases. (1,30)
The evidence for AD prevention began with the research showing that addressing risk factors for heart disease can prevent and even reverse diseases of the heart. (2) Recent investigations are demonstrating that the same processes that are involved in the development of heart disease are also implicated in cognitive dysfunction. In other words, damage to blood vessels in the brain is linked to the development of dementia. (1,29)
In 2014, researchers looked at seven conditions that cause damage to blood vessels and also have consistently shown an association with the onset of AD. These conditions include diabetes, mid-life hypertension, mid-life obesity, physical inactivity, depression, smoking and low levels of education. Many of these risk factors are modifiable. After revealing that the combined influence of these conditions on the development of AD could be attributed to about a third of AD cases worldwide, the researchers noted that modifying the risk factors for these conditions through taking such steps as choosing to eat healthier foods, stopping smoking and/or increasing physical activity has the potential to reduce the incidence of AD. (1)
Science indicating that vegetarians and vegans are less likely to develop dementia than meat eaters has existed from the 1990s on and the evidence continues to build. (3,4) In 2015, the MIND diet arrived on the scene, combining two previous diets that had shown brain protective effects, the DASH (Dietary Approaches to Stop Hypertension) diet and the Mediterranean diet. The DASH diet emphasizes reducing saturated fats, meats (including fish) and sugar-sweetened foods. The Mediterranean diet advises the restriction of dairy products and the consumption of beans and nuts. Along with this guidance, further recommendations of the MIND diet include eating natural plant-based foods and, in particular, to eat green leafy vegetables at least six times a week, to focus on berry consumption over other fruits and to reduce the intake of fried foods and other fast foods to less than once a week (5). Adhering to the MIND diet was positively associated with many aspects of cognition including a 53% lower risk of developing AD for those most closely following the MIND diet and a 35% reduction for those in the mid-range of MIND diet scores compared with those with the lowest scores. (5,6)
In 2019, Dr. Dean Sherzai and Dr. Ayesha Sherzai, both physicians, neurologists and co-directors of the Alzheimer’s Prevention Program at Loma Linda University in California, published a paper on the urgent need to address the problem of cognitive aging. They tackle the prevailing myths about dementia; that AD is exclusively a genetic disease and an inevitable result of aging. On the contrary, there is strong data illustrating that AD is not simply due to getting old. Nor is it likely the result of the simple formation of ß-amyloid plaques and neurofibrillary tangles. The Sherzais maintain that, though these two molecules are involved at some level, they don’t appear to be the driving force behind AD development. (7)
Note: The appearance of β-amyloid plaques and neurofibrillary tangles have long been postulated to be one of the causes of AD. The theory was that these plaques and tangles were involved in the death of neurons (brain cells) and the loss of synapses (brain cell connections) which contribute to cognitive decline in a progressive manner. Unfortunately, the lack of efficacy on AD from drugs aimed at reducing levels of these possible threats has cast doubt on this hypothesis. (8,9)
AD is linked to a multitude of genetic, epigenetic and environmental factors that interact with each other. Considering genetics, the APOE gene is the most common gene linked to the development of AD. It occurs in three forms that are associated with differing risks for AD. These are APOEe2, APOEe3 and APOEe4. APOEe2 appears to significantly reduce the risk of AD, APOEe3 has a neutral effect and APOEe4 is associated with increased risk. Inheriting an APOEe4 gene from one parent increases AD risk four-fold. Receiving an APOEe4 gene from both parents raises the risk of AD by up to 12 times. However, in the United States, only 2% of the population have 2 copies of the APOEe4 gene and these people don’t necessarily develop AD. In fact, 50% of them do not develop dementia at all. Additionally, there is an apparent paradox in Nigeria. A 2001 study of the Nigerian population found very high rates of the APOEe4 gene but extremely low rates of AD. This is thought to be due to the low cholesterol levels in their diet because of the very small amount of animal fat it contains. The Sherzais maintain that, in almost all cases of AD, genes provide a risk range, but it is lifestyle that ultimately determines at which point in that range disease will manifest. (7,10)
The Sherzais lay out the central causes of AD, taken from both their own work and a comprehensive review of the literature. These causes are;
- Energy dysregulation
- Lipid dysregulation
- Inflammation
- Oxidation
Certain lifestyle factors can have an immense influence on the central causes of AD and can even interrupt pathological pathways early in the formation of the disease. Such lifestyle factors are nutrition, exercise, stress management, restorative sleep and optimizing mental and social activities. (7).
The following is an overview of the research supporting the role of lifestyle changes in lowering the risk for AD. (7)
Nutrition:
In 1993, a group from Loma Linda University Health looked at the relationship between meat consumption and dementia among Seventh Day Adventists. Results illustrated that those who consumed meat, including poultry and fish, had twice the risk of developing dementia compared with vegetarians (3).
In 2002 a study based in Finland demonstrated that the risk of AD from treatable factors such as elevated total cholesterol and blood pressure appeared to be greater than the genetic risk from the APOEe4 gene. (11)
The Chicago Health and Aging Study from 2003 discovered that high intake of saturated fats increased the risk of AD by 2.2 times and high intake of hydrogenated fats (trans-fats) increased the risk of AD by 2.4 times compared with those eating low amounts. Inversely, intake of omega-3 polyunsaturated fats and monounsaturated fats were associated with lower risk of AD (12).
In 2009, Kaiser Permanente in Northern California revealed that their patients who had high cholesterol levels during midlife had a 57% higher risk of developing AD later in life. They found that even borderline high cholesterol levels increase AD risk by 23% (13).
The Women’s Health Study from 2010 followed almost 6000 women for over 4 years and observed that higher saturated fat intake was linked to negative effects on cognition. Moreover, memory declines happened 70% faster in those eating higher levels of saturated fats (14).
In 2019, data was collected from over 12,000 participants of the Tzu Chi Vegetarian Study in Taiwan. The findings show that vegetarians have 38% lower risk of dementia compared to non-vegetarians after adjusting for age, sex, education, marital status, high blood pressure, diabetes, hyperlipidemia, ischemic heart disease, physical activity, smoking, and alcohol consumption. (15)
A 2021 study took the unusual route of measuring the level of the metabolites of certain nutrients in the blood. (Metabolites are the products of metabolism, the chemical process of breaking down and building up molecules in living organisms as they convert foods and drinks into energy.) In this way, inconsistencies in data due to the misreporting of food intake on food surveys can be prevented. Study participants were free of dementia at the start of this trial. Researchers discovered that some nutrients were protective against cognitive decline and some were associated with increasing dementia. Protective metabolites came from polyphenol-rich foods like cocoa, mushrooms, blueberries, apples, coffee and red wine while harmful metabolites came from unhealthy dietary components such as artificial sweeteners and alcohol. In addition, it is interesting that most of the brain protective metabolites resulted from actions of the microbes in the microbiome. We know that including more plants in the diet promotes a healthier microbiome. This study found that eating more plants is also associated with less cognitive decline. (16)
A systematic literature search performed in 2022 examined the relationship between a plant-based diet and both AD and diseases of the small blood vessels in the brain. Results pointed to plant-based diets, especially those containing berries, vegetables and plenty of fiber, along with limiting saturated fat, refined carbohydrates and alcohol, as a healthy choice for memory and brain health. (17)
Exercise:
It turns out that the exercise needed to boost brain health is a bit more strenuous than a sedate walk or pulling weeds in a garden.
The Framingham Longitudinal Study found that daily brisk walks can lower the risk of AD by 40% (14).
A meta-analysis of previous studies included almost 34,000 people without dementia who were followed for between 1 and 12 years. Those who regularly participated in a high level of physical activity had a 38% lower risk of cognitive decline; those undergoing low to moderate exercise had more modest benefits. (18).
At Wake Forest University, a group of participants with strong genetic risk for AD and already diagnosed with MCI (Mild Cognitive Impairment) were placed on an exercise program which consisted of 45 minutes a day of either stretching or intensive exercise on 4 days a week for 6 months. Those in the intensive exercise group showed increased blood flow to the frontal lobe of the brain, improved executive function and protection against cognitive decline. Those in the stretching groups displayed worsening of their dementia, brain shrinkage and decreased executive function. (19)
Note: Executive function includes a set of cognitive skills that help an individual plan, monitor and successively meet their goals and includes attentional control, working memory, inhibition and problem-solving.
Resistance exercises are just as effective as aerobic exercise when it comes to preserving brain health. A study from 2017 placed 100 older adults (over 55 years of age) with diagnosed MCI on a resistance training program 2 or 3 times a week for 6 months. Not only did they increase their upper, lower and whole-body strength but 47% of them achieved normal cognitive scores after the exercise program and sustained this improvement for at least 18 months afterwards. The researchers also noted that increasing lower body strength was particularly effective at improving cognitive performance. (20)
Stress Management:
Stress can affect every part of the body. A stressful situation sends nerve and hormonal signals that cause the adrenal glands to release hormones such as adrenaline and cortisol. Adrenaline raises blood pressure and increases the heartbeat. Cortisol raises the level of glucose (sugar) in the bloodstream and slows functions that are not needed in a situation of danger such as the digestive system, the reproductive system, the cardiovascular system, the respiratory system, the nervous system and immune responses. If a stress resolves, hormones return to normal levels and the systems of the body normalize as well. But when stressors are constant, the stress response system remains active. On-going high levels of cortisol and other stress hormones disrupt bodily processes, causing muscle tension, rapid breathing and shortness of breath, increased heart rate and stronger contractions of the heart muscle and higher blood pressure. This in turn leads to dysbiosis of the gut microbiome, increased acid reflux, along with interference with mood, memory and cognition and even reductions in the size of critical areas of the brain such as the hippocampus. (7,21,22) Stress management activities such as mindfulness and meditation have been associated with greater neuroplasticity, reduced shrinkage of the brain and improved cognition. (7)
Note: Neuroplasticity is the ability of the brain to learn, adapt and grow in response to new experiences and demands.
Restorative Sleep:
Sleep is essential for optimal brain health. During sleep our experiences, thoughts and memories are organized and the important ones filed away with the ability to access them in the future. But, more importantly, it is during our sleep that the brain washes away inflammatory, oxidative and waste by-products. (7)
Studies have discovered that long-term night-shift workers have lower cognitive performance, specifically on verbal memory and speed performance, than those who have never worked shifts. In addition, memory performance tended to decrease with increasing duration of shiftwork. However, four years after stopping shift work, cognitive performance increased in these shift workers. (23).
Research shows that sleep deprivation is linked to increased levels of markers of inflammation like cytokines, interleukin-6 and C-reactive protein. This may be because when blood pressure drops during sleep, blood vessels relax; but when there is no drop in blood pressure due to unrestful sleep, inflammation within the blood vessel walls may be triggered and the body’s stress response system activated. In addition, the lack of good sleep interferes with the glymphatic system, the brain’s cleansing system which, during deep sleep sends cerebrospinal fluid flushing through the brain, clearing away waste products of the brain’s daily activities as well as reducing ß-amyloid build-up. Although ongoing sleep loss is related to decreases in brain size and function, even one night of lost sleep results in higher levels of ß-amyloid. This could explain why people who sleep poorly are at higher risks of developing AD disease, cardiovascular disease, high blood pressure, diabetes and other chronic conditions. (24)
A review and meta-analysis of seven studies from 2015 reported that sleep apnea increases the risk of AD by 70%. (25)
Other Matters:
Other issues, some not so preventable, that can increase the risk for the development of dementia including AD are smoking, excessive consumption of alcohol, hearing loss and traumatic brain injury. (7)
Optimizing Mental and Social Activities:
Each brain cell has the capability to form thousands of connections with other cells. The more connections the cells form, the more routes accessible for the transfer of messages. The availability of multiple connection points between brain cells allows brain signals to be sent through alternate pathways in the case of damage to the brain. Research has revealed that some patients with disease of the blood vessels of the brain or significant ß-amyloid build-up in the brain display no symptoms of AD. This suggests that some brains have cognitive reserves, other connections between brain cells that can be employed to complete a task, providing protection in an aging or damaged brain. This is optimization of the brain. (7)
Many life activities can help in the goal of brain optimization. Challenging jobs, learning a language or taking up a musical instrument have all been linked to the increased ability of the brain to withstand damage from cerebrovascular disease, allowing impaired brains to perform at a similar cognitive level as healthier brains of their peers. (26) The Active Study from 2016 provided cognitive training to older adults and indicated that those taking speed of processing training were 33% less likely than controls to develop dementia over 10 years. (27) Results from a trial in which individuals with MCI received multiple types of training (including lifestyle changes) showed small to moderate increases in cognition. (28)
Summing Up Possible Steps for Decreasing the Risk of Cognitive Decline (7,31):
- Eat more plants of all kinds but especially greens and beans
- Eat lots of fruits, especially berries
- Eat fewer animal-sourced foods (meat, dairy, cheese)
- Eat fewer fats, especially saturated fats
- Eat less processed sugar and artificial sweeteners
- Reduce salt intake
- Perform regular and fairly intensive aerobic exercise most days of the week
- Move the body regularly throughout the day
- Do leg strengthening exercises
- Reduce bad stress (prolonged stress which does not go away) through stress management programs such as mindfulness and meditation
- Increase good stress (temporary stress which is oriented towards desired goals)
- Aim for 7 to 8 hours of sleep per night that involves reaching the different sleep phases of REM sleep, deep sleep and light sleep several times
- Go to bed and get up in the morning around the same time every day, weekends included
- Follow the same routine before going to bed each night (29);
Allow 30 minutes for winding down through activities such as reading, relaxation exercises, soft music and light stretching.
Avoid bright lights to encourage the body’s production of melatonin, a hormone that facilitates sleep.
Limit screen time during the hour or so before you go to bed. Avoid electronics such as cell phones, tablets, computers and television as they stimulate the brain making it hard to shut off. In addition, screens emit blue light that can decrease the production of melatonin.
If sleep hasn’t come after 20 minutes or so, get up and stretch, read or do another calming activity in low light before going back to bed.
- Don’t smoke
- Limit alcohol intake
- Wear a helmet when participating in sports that have the potential to damage the brain (for example, soccer, football and rugby)
Conclusions:
It is now demonstrable that lifestyle changes can be significantly effective in maintaining a healthy brain and reducing the risk for developing dementia and AD, some of the most dreaded diseases worldwide. But there’s more to this than just warding off one disease. The same lifestyle choices can also prevent and reverse heart disease, a leading causes of death in Canada. (32). In addition, many other chronic health conditions, including diabetes, obesity, autoimmune diseases, liver and kidney disease and some cancers, respond to the same recommended healthy actions for longevity. To top it all off, an often-overlooked benefit of eating a plant-based diet is that it is the best way to reduce the carbon footprint of your diet, making a larger difference than how far the food has travelled or how much packaging it has. (33) With so many advantages resulting from just the single choice of eating mostly plants, you might find more than enough motivation to do it. And you might be surprised at the resulting improvement in both your health and your outlook on life.
SOURCES:
1 Norton, S., Matthews, F.E., Barnes, D.E., Yaffe, K., Brayne, C. Potential for primary prevention of Alzheimer’s disease: an analysis of population-based data. Lancet Neurol. 2014 Aug;13(8):788-94. doi: 10.1016/S1474-4422(14)70136-X. Erratum in: Lancet Neurol. 2014 Nov;13(11):1070. PMID: 25030513.
2 Ornish, D., Scherwitz, L.W., Billings, J.H., Brown, S.E., Gould, K.L., Merritt, T.A., Sparler, S., Armstrong, W.T., Ports, T.A., Kirkeeide, R.L., Hogeboom, C., Brand, R.J. Intensive lifestyle changes for reversal of coronary heart disease. JAMA. 1998 Dec 16; 280(23): 2001-2007. Doi: 10.1001/jama.280.23.2001. Erratum in: JAMA 1999 Apr 21;281(15):1380. PMID: 9863851.
3 Giem, P., Beeson, W.L., Fraser, G.E. The incidence of dementia and intake of animal products: preliminary findings from the Adventist Health Study. Neuroepidemiology. 1993;12(1):28-36. Doi: 10.1159/000110296. PMID: 8327020.
4 Morris, M.C., Tangney, C.C. Dietary fat composition and dementia risk. Neurobiol Aging. 2014 Sep;35 Suppl 2:S59-64. Doi: 10.1016/j.neurobiolaging.2014.03.038. Epub 2014 May 15. PMID: 24970568; PMCID: PMC4107296.
5 Morris, M.C., Tangney, C.C., Wang, Y., Sacks, F.M., Bennett, D.A., Aggarwal, N.T. MIND diet associated with reduced incidence of Alzheimer’s disease. Alzheimers Dement. 2015 Sep;11(9):1007-14. Doi: 10.1016/j.jalz.2014.11.009. Epub 2015 Feb 11. PMID: 25681666; PMCID: PMC4532650.
6 Morris, M.C., Tangney, C.C., Wang, Y., Sacks, F.M., Barnes, L.L., Bennett, D.A., Aggarwal, N.T. MIND diet slows cognitive decline with aging. Alzheimers Dement. 2015 Sep;11(9):1015-22. Doi: 10.1016/j.jalz.2015.04.011. Epub 2015 Jun 15. PMID: 26086182; PMCID: PMC4581900.
7 Sherzai ,D., Sherzai, A. Preventing Alzheimer’s: Our Most Urgent Health Care Priority. Am J Lifestyle Med. 2019 May 9;13(5):451-461. Doi: 10.1177/1559827619843465. PMID: 31523210; PMCID: PMC6732875.
8 Kocahan, S., Doğan, Z. Mechanisms of Alzheimer’s Disease Pathogenesis and Prevention: The Brain, Neural Pathology, N-methyl-D-aspartate Receptors, Tau Protein and Other Risk Factors. Clin Psychopharmacol Neurosci. 2017 Feb 28;15(1):1-8. Doi: 10.9758/cpn.2017.15.1.1. PMID: 28138104; PMCID: PMC5290713.
9 Zhang, Y., Chen, H., Li, R. et al. Amyloid β-based therapy for Alzheimer’s disease: challenges, successes and future. Sig Transduct Target Ther 8, 248 (2023). Doi.org/10.1038/s41392-023-01484-7.
10 Sepehrnia, B., Kamboh, M.I., Adams-Campbell, L.L., Bunker, C.H., Nwankwo, M., Majumder, P.P., Ferrell, R.E. Genetic studies of human apolipoproteins. X. The effect of the apolipoprotein E polymorphism on quantitative levels of lipoproteins in Nigerian blacks. Am J Hum Genet. 1989 Oct;45(4):586-91. PMID: 2491016; PMCID: PMC1683508.
11 Kivipelto, M., Helkala, E.L., Laakso, M.P., Hänninen, T., Hallikainen, M., Alhainen, K., Livonen, S., Mannermaa, A.,Tuomilehto, J., Nissinen, A., Soininen, H. Apolipoprotein E epsilon4 allele, elevated midlife total cholesterol level, and high midlife systolic blood pressure are independent risk factors for late-life Alzheimer disease. Ann Intern Med. 2002 Aug 6;137(3):149-55. Doi: 10.7326/0003-4819-137-3-200208060-00006. PMID: 12160362.
12 Morris, M.C., Evans, D.A., Bienias, J.L., Tangney, C.C., Bennett, D.A., Aggarwal, N., Schneider, J., Wilson, R.S. Dietary fats and the risk of incident Alzheimer disease. Arch Neurol. 2003 Feb;60(2):194-200. Doi: 10.1001/archneur.60.2.194. Erratum in: Arch Neurol. 2003 Aug;60(8):1072. PMID: 12580703.
13 Solomon, A., Kivipelto, M., Wolozin, B., Zhou, J., Whitmer, R.A. Midlife serum cholesterol and increased risk of Alzheimer’s and vascular dementia three decades later. Dement Geriatr Cogn Disord. 2009;28(1):75-80. Doi: 10.1159/000231980. Epub 2009 Aug 4. PMID: 19648749; PMCID: PMC2814023.
14 Tan, Z.S., Beiser, A.S., Au, R., et al. Physical activity and the risk of dementia: the Framingham study. Alzheimers Dement. 2010;6(suppl):S68. Doi: 10.1016/j.jalz.2010.05.203.
15 Lin, M.N., Chiu, T.H., Chang, C.E., Lin, M.N. The Impact of a Plant-Based Dietary Pattern on Dementia Risk: A Prospective Cohort Study. Innov Aging. 2019 Nov 8;3(Suppl 1):S734. Doi: 10.1093/geroni/igz038.2691. PMCID: PMC6846186.
16 González-Domínguez, R., Castellano-Escuder, P., Carmona, F., Lefèvre-Arbogast, S., Low, D.Y., DuPreez, A., Ruigrok, S.R., et al. Food and Microbiota Metabolites Associate with Cognitive Decline in Older Subjects: A 12-Year Prospective Study. Mol. Nutr. Food Res. 2021, 65, 2100606. https://doi.org/10.1002/mnfr.202100606.
17 Lempiäinen, J. How diet affects Alzheimer’s disease and small vessel disease. Lifestyle Med. 2022; 3:e36. https://doi.org/10.1002/lim2.57.
18 Sofi, F., Valecchi, D., Bacci, D., Abbate, R., Gensini, G.F., Casini, A., Macchi, C. Physical activity and risk of cognitive decline: a meta-analysis of prospective studies. J Intern Med. 2011 Jan;269(1):107-17. Doi: 10.1111/j.1365-2796.2010.02281.x. Epub 2010 Sep 10. PMID: 20831630.
19 Baker, L.D. Exercise and memory decline. Alzheimers Dement. 2016;12:P220-P221. Doi: 10.1016/j.jalz.2016.06.2371
20 Mavros, Y., Gates, N., Wilson, G.C., Jain, N., Meiklejohn, J., Brodaty, H., Wen, W., Singh, N., Baune, B.T., Suo, C., Baker, M.K., Foroughi, N., Wang, Y., Sachdev, P.S., Valenzuela, M., Fiatarone, Singh, M.A. Mediation of Cognitive Function Improvements by Strength Gains After Resistance Training in Older Adults with Mild Cognitive Impairment: Outcomes of the Study of Mental and Resistance Training. J Am Geriatr Soc. 2017 Mar;65(3):550-559. Doi: 10.1111/jgs.14542. Epub 2016 Oct 24. PMID: 28304092.
21 https://www.mayoclinic.org/healthy-lifestyle/stress-management/in-depth/stress/art-20046037
22 https://www.apa.org/topics/stress/body
23 Rouch, I., Wild, P., Ansiau, D., Marquié, J.C. Shiftwork experience, age and cognitive performance. Ergonomics. 2005 Aug 15;48(10):1282-93. Doi: 10.1080/00140130500241670. PMID: 16253945.
24 https://www.health.harvard.edu/healthbeat/how-sleep-deprivation-can-cause-inflammation
25 Bubu, O.M., Utuama, O., Umasabor-Bubu, O.Q., Schwartz, S. Obstructive sleep apnea and Alzheimer’s disease: a systematic review and meta-analytic approach. Alzheimers Dement. 2015;11(suppl):P452. Doi: 10.1016/j.jalz.2015.06.458.
26 Boots, E.A., Schultz, S.A., Oh, J.M., Racine, A.M., Koscik, R.L., Gallagher, C.L., Carlsson, C.M., Rowley, H.A., Bendlin, B.B., Asthana, S., Sager, M.A., Hermann, B.P., Johnson, S.C., Okonkwo, O.C. (2016), IC-P-178: Occupational Complexity, Cognitive Reserve, and White Matter Hyperintensities: Findings from The Wisconsin Registry for Alzheimer’s Prevention. Alzheimer’s & Dementia, 12: P130-P130. https://doi.org/10.1016/j.jalz.2016.06.209.
27 Edwards, J.D., Xu, H., Clark, D., Ross, L.A., Unverzagt, F.W. (2016), S2-01-02: The Active Study: what we Have Learned and what is Next? Cognitive Training Reduces Incident Dementia Across Ten Years. Alzheimer’s & Dementia, 12: P212-P212. https://doi.org/10.1016/j.jalz.2016.06.373.
28 Sherman DS, Mauser J, Nuno M, Sherzai D. The Efficacy of Cognitive Intervention in Mild Cognitive Impairment (MCI): a Meta-Analysis of Outcomes on Neuropsychological Measures. Neuropsychol Rev. 2017 Dec;27(4):440-484. doi: 10.1007/s11065-017-9363-3. Epub 2017 Dec 27. PMID: 29282641; PMCID: PMC5754430.
29 https://www.sleepfoundation.org/sleep-hygiene
30 Ornish, D., Madison, C., Kivipelto, M., et al. Effects of intensive lifestyle changes on the progression of mild cognitive impairment or early dementia due to Alzheimer’s disease: a randomized, controlled clinical trial. Alz Res Therapy. 2024:16(122). Doi:10.1186/s13195-024-01482-z.
31 https://www.ornish.com/zine/9-steps-you-can-take-to-ward-off-dementia/
32 https://www150.statcan.gc.ca/n1/daily-quotidien/231127/t001b-eng.htm
33 https://ourworldindata.org/less-meat-or-sustainable-meat
Incredibly well researched, well-written and understandable! Thanks Deb!