The Effect of Socioeconomic Status on Alzheimer’s Disease

by Brooklin White MS, RDN, LDNNews
small plant growing out of a glass filled with coins

Research has indicated that living in a low socioeconomic community has the largest effect on life expectancy. In fact, it has been estimated that poverty alone accelerates aging by 20 years (1). This metric is astonishing and can be attributed to a lack of financial resources, health education, health resources, stress, poor air quality, limited access to health care, lack of affordable and available health foods and a lack of clean and safe areas to exercise. There is no doubt therefore that individuals who are poorer and have less education have a greater prevalence of chronic diseases such as obesity, type 2 diabetes, cardiovascular disease and hypertension (2)(3)(4). There is increasing research that indicates being in a low socioeconomic bracket with limited education also increases the risk of developing Alzheimer’s disease. For instance, if an individual has less than 7 years of education, his or her risk of getting Alzheimer’s Disease is doubled every year after the age of 40 of those who have a college degree (1).

The founder of Functional Medicine, Dr. Jeffrey Bland, brings up the concept of organ reserve as it relates to aging and disease states. Organ reserve is the notion that our organs are exceptional at clearing out toxins and maintaining health when we are young, but slowly start to lose their vigor as we age (5). The rate at which we lose this reserve is what shapes our individual aging processes, and it has been proved that individuals lose organ reserve at different rates and thus, age differently (6). Healthy choices in food, moderate exercise, minimal stress and plenty of sleep for example, are all ways to maintain organ reserve, healthspan and longevity. Unfortunately, low SES communities are repeatedly unable to sustain these healthy practices and thus lose their organ reserve more rapidly, leading to chronic diseases such as Alzheimer’s Disease.

Functional Medicine + Alzheimer’s Disease

Diet and cognition: Low SES communities are often found in dense, urban areas where it can be difficult to find and afford fresh foods. This often leads to a high consumption of processed meats, saturated-fats and sugars and a low consumption of nutrient rich foods. The components of a typical western diet are directly linked to the high prevalence of chronic disease we see in these communities, including Alzheimer’s Disease. Dr. Suzanne Craft, a neuropsychologist and professor at Wake Forest has done extensive research on the link between poor control of blood sugar and higher incidences of Alzheimer’s disease. Her research indicates that a high sugar diet impacts the concentrations of amyloid-beta, lipoproteins, oxidative stressors and insulin (7). A recent systematic review on obesity suggests there is a positive association between obesity in midlife and later dementia (8). For instance, if an individual has a BMI of 30 at midlife, their age of Alzheimer’s Disease onset is lower than those with a midlife BMI of 20. (9). Individuals with the ApoE4 allele are particularly susceptible to the dangers of a diet high in sugar, saturated fats and a sedentary lifestyle (10). Too many saturated fats, omega-6 unsaturated fats and sugars can increase inflammatory markers such as CRP, Interleukin-6 and Homocysteine which creates an increased risk for Alzheimer’s Disease (11)(12).

Diet isn’t the only environmental factor that leads to higher amounts of Alzheimer’s Disease in low SES communities. Lack of exercise, sleep and stress management have also been linked to the prevalence of Alzheimer’s Disease.

Exercise on cognition: In addition to diet, exercise is considered one of the most beneficial things individuals can do to maintain cognition. Unfortunately, most low SES communities lack clean and safe areas to exercise. Older adults who engage in consistent, moderately intense exercise have been shown to have higher levels of cognitive functioning, as compared to sedentary adults (13)(14). Exercise has also been associated with increased neurogenesis and long-term potentiation (15).

Stress management on cognition: Although higher education and consistent problem solving are associated with the strengthening of synapses and better cognition later in life, chronic stress throughout life is severely detrimental. Low SES communities are often faced with various stressors such as living from paycheck to paycheck, having enough food for the entire family, access to healthcare, safety, being a single parent, and managing going to school while having a full-time work schedule. Participants from the Framingham Heart Study who had high cortisol levels, as compared to those with normal cortisol levels, had worse visual perception, memory and global cognitive function. These individuals were also shown to have lower total cerebral brain, occipital and frontal lobe gray matter volumes (16).

Sleep on cognition: A 2019 study on sleep found that a decrease in sleep quantity throughout aging, specifically through the 50s to 70s, was associated with higher levels of amyloid and tau proteins later in life. (17). Additionally, various cross-sectional studies have shown that reported sleep duration is linked to greater amyloid-beta accumulation (18)(19). Among other issues, many in low SES communities are forced to work multiple jobs to make ends meet, reducing the time left for restorative sleep.

These are just additional indicators that genes in themselves don’t control the manifestation of Alzheimer’s Disease, but rather decide how they are expressed based on environmental and lifestyle factors.

Looking Forward

Functional medicine leaders such as Dr. Dale Bredesen and Dr. Jeffrey Bland understand the crucial importance of treating the root cause of a disease rather than the symptoms. It is becoming more widely understood that a shift in lifestyle behaviors, such as proper nutrition, exercise, sleep and stress management habits contribute to a long and healthy life. Unfortunately, low SES communities are not offered the opportunity to consistently engage in these healthful lifestyle habits. Dr. Dariush Mozaffarian, cardiologist and Dean at the Friedman School of Nutrition Science and Policy at Tufts University is working hard to establish systemic changes to our food system. For example, his team at Tufts is working to establish cost-effective policies that would improve diet quality in the US and globally. The subsidization of farmers who grow fruits, vegetables and tree nuts, for example. Changing our food system would create a healthier country, reduce diet related health disparities, preserve our natural resources, and reduce healthcare costs. Shifting our food system and healthcare policies to focus on disease prevention, rather than disease maintenance would make healthy food sustainable and affordable and would reverse the increasing rates of all chronic disease, including Alzheimer’s disease in low SES communities. The government should be encouraging and incentivizing nutrition, equity and sustainability as it would not only be beneficial for low SES communities, but the country as a whole.

“Policy without science is dangerous, and science without policy is merely stale knowledge” - Dr. Dariush Mozaffarian


  1. Crimmins, E. M., Kim, J. K., & Seeman, T. E. (2009). Poverty and Biological Risk: The Earlier “Aging” of the Poor.The Journals of Gerontology Series A: Biological Sciences and Medical Sciences,64A(2), 286–292.
  2. World Health Organization. (2020).Chronic diseases and health promotion Part Two. The urgent need for action Chapter Two. Chronic diseases and poverty. WHO | World Health Organization. Retrieved July 10, 2020, from
  3. Hayward MD, Crimmins EM, Miles TP, Yu Y. The significance of so- cioeconomic status in explaining the racial gap in chronic health con- ditions.Am Sociol Rev. 2000;65:910–930.
  4. L. Letenneur, J. Launer, K. Andersen, M. E. Dewey, A. Ott, J. R. M. Copeland, J-F. Dartigues, P. Kragh-Sorensen, M. Baldereschi, C. Brayne, A. Lobo, J. M. Martinez-Lage, T.
  5. Fries JF. Aging, natural death, and the compression of morbidity.N Engl J Med. 1980;303(3):130-135. doi:10.1056/NEJM198007173030304
  6. Bland, J. S. (2014).The disease delusion: Conquering the causes of chronic illness for a healthier, longer, and happier life. HarperCollins.
  7. Bayer-Carter, J. L., Green, P. S., Montine, T. J., VanFossen, B., Baker, L. D., Watson, G. S., Bonner, L. M., Callaghan, M., Leverenz, J. B., Walter, B. K., Tsai, E., Plymate, S. R., Postupna, N., Wilkinson, C. W., Zhang, J., Lampe, J., Kahn, S. E., & Craft, S. (2011). Diet Intervention and Cerebrospinal Fluid Biomarkers in Amnestic Mild Cognitive Impairment.Archives of Neurology,68(6), 743–752.
  8. Pedditizi, E., Peters, R., & Beckett, N. (2016). The risk of overweight/obesity in mid-life and late life for the development of dementia: A systematic review and meta-analysis of longitudinal studies.Age and Ageing,45(1), 14–21.
  9. Chuang, Y.-F., An, Y., Bilgel, M., Wong, D. F., Troncoso, J. C., O’Brien, R. J., Breitner, J., Ferruci, L., Resnick, S. M., & Thambisetty, M. (2016). Midlife Adiposity predicts earlier onset of Alzheimer’s dementia, neuropathology and presymptomatic cerebral amyloid accumulation.Molecular Psychiatry,21(7), 910–915.
  10. Berkowitz, C. L., Mosconi, L., Rahman, A., Scheyer, O., Hristov, H., & Isaacson, R. S. (2018). Clinical Application of APOE in Alzheimer’s Prevention: A Precision Medicine Approach.The Journal of Prevention of Alzheimer’s Disease,5(4), 245–252.
  11. Enos, R. T., Davis, J. M., Velázquez, K. T., McClellan, J. L., Day, S. D., Carnevale, K. A., & Murphy, E. A. (2013). Influence of dietary saturated fat content on adiposity, macrophage behavior, inflammation, and metabolism: Composition matters.Journal of Lipid Research,54(1), 152–163.
  12. Shivappa, N., Hébert, J. R., Rietzschel, E. R., De Buyzere, M. L., Langlois, M., Debruyne, E., Marcos, A., & Huybrechts, I. (2015). Associations between dietary inflammatory index and inflammatory markers in the Asklepios Study.The British Journal of Nutrition,113(4), 665–671.
  13. Cassilhas RC, Viana VA, Grassmann V, Santos RT, Santos RF, Tufik S, Mello MT (2007) The impact of resistance exercise on the cognitive function of the elderly. Med Sci Sports Exerc 39, 1401–1407.
  14. Dustman RE, Ruhling RO, Russell EM, Shearer DE, Bonekat HW, Shigeoka JW, Wood JS, Bradford DC (1984) Aerobic exercise training and improved neuropsychological function of older individuals. Neurobiol Aging 5, 35–42.
  15. Farmer J, Zhao X, van Praag H, Wodtke K, Gage FH, Christie BR. Effects of voluntary exercise on synaptic plasticity and gene expression in the dentate gyrus of adult male Sprague-Dawley rats in vivo. Neuroscience. 2004;124:71–79.
  16. Echouffo-Tcheugui, J. B., Conner, S. C., Himali, J. J., Maillard, P., DeCarli, C. S., Beiser, A. S., Vasan, R. S., & Seshadri, S. (2018). Circulating cortisol and cognitive and structural brain measures: The Framingham Heart Study.Neurology,91(21), e1961–e1970.
  17. Winer, J. R., Mander, B. A., Helfrich, R. F., Maass, A., Harrison, T. M., Baker, S. L., Knight, R. T., Jagust, W. J., & Walker, M. P. (2019). Sleep as a Potential Biomarker of Tau and β-Amyloid Burden in the Human Brain.Journal of Neuroscience,39(32), 6315–6324.
  18. Spira AP, Gamaldo AA, An Y, Wu MN, Simonsick EM, Bilgel M, Zhou Y, Wong DF, Ferrucci L, Resnick SM (2013) Self-reported sleep and beta- amyloid deposition in community-dwelling older adults. JAMA Neurol 70:1537–1543.
  19. Sprecher KE, Bendlin BB, Racine AM, Okonkwo OC, Christian BT, Koscik RL,SagerMA,AsthanaS,JohnsonSC,BencaRM (2015) Amyloidbur- den is associated with self-reported sleep in nondemented late middle- aged adults. Neurobiol Aging 36:2568 –2576.