The Impact of Obesity on Alzheimer’s Disease

by Brooklin White MS, RDN, LDNNews
Feet on a scale

The prevalence of overweight and obese individuals in America is skyrocketing. Currently, 71.6% of Americans are overweight with 42.4% of them being obese (1). It is no surprise to find that the rate of chronic diseases, including Alzheimer’s disease, are also accelerating.

We live in a country where there is an abundance of food around us, all of the time. Although fast food restaurants and easy-to-make processed meals are efficient, they often contain the highest amounts of calories, saturated fats, and refined carbohydrates. Unfortunately, these empty calories don’t satiate the body’s need for nutrients, so it often leaves us consuming more calories than we need. Many big food companies such as Nestlé, Coca-Cola, PepsiCo, Kraft and Frito-Lay actually hire scientists at labs such as the Monell Chemical Sciences Center, to create the best tasting potato chip, soda, cereal, ice cream etc., which explains our innate desire to consume these foods. Michael Moss wrote an excellent book called Salt, Sugar, Fat that describes this deception in more detail but essentially, these big food companies have worked with hundreds of physiologists, chemists, neuroscientists, biologists and geneticists to create the perfect combination of flavors that literally trigger centers in our brain responsible for addiction – leaving us, of course, always wanting for more (2).

Americans are eating more calories than ever before. Unfortunately, these extra calories often go unnoticed, turn into pounds and eventually lead to an individual being overweight or obese. It is clear that this increase in processed foods and extra calories have led our country into a state of disease, but the conversation surrounding these diet changes and the prevalence of Alzheimer’s Disease is less discussed.

Obesity as a risk factor for AD

An increasing number of studies have linked the elevated intake of saturated fats and simple sugars to an increased occurrence of Alzheimer’s Disease (3)(4)(5). For instance, several epidemiological studies have shown that people with a higher body mass index (BMI) during midlife have a greater risk for developing Alzheimer’s Disease (6)(7)(8). A higher BMI also seems to accelerate the reduction of brain volume in frontal, temporal, parietal, occipital lobes of those with Alzheimer’s Disease and Mild Cognitive Impairment (9). A decrease in white and grey matter has been detected in cognitively normal persons who are obese (10) and a high saturated fat diet that induced obesity in male mice, was shown to create impaired learning, synaptic plasticity and loss in Long-Term Potentiation (LTP) (11). In humans, increased energy intakes via western diets have been associated with neurophysiological changes such as impaired glucose regulation, reduced neurotrophins (such as BDNF that support the functioning of neurons), increased neuroinflammation, and the loss of structural integrity of the BBB (12)(13).

The Western Diet, Obesity and the Brain

Researchers have begun to recognize the relationship between diet induced obesity, the blood-brain barrier and neurodegeneration. The brain controls what travels in and out of it through something called the blood brain barrier (BBB). The BBB serves as protection for the brain and central nervous system by shielding it from neurotoxic substances found circulating in the blood. The BBB functions as the brain's first line of defense and is only permeable to certain molecules, such as water, glucose, carbon dioxide, hormones and oxygen. The breakdown and increased permeability of the BBB is associated with normal aging, however, it is worsened in those with mild cognitive impairment. Post-mortem tissue analysis has indicated there is extensive BBB damage in Alzheimer’s Disease brains (14).

In addition to aging, diet induced obesity has also been shown to increase the permeability of the blood-brain barrier. This BBB breakdown leads to the accumulation of neurotoxic blood-derived molecules that can damage neurons and lead to impairments in learning and memory (14)(12). A diet high in simple sugars and saturated fat contributes to high blood sugar and insulin resistance which can impact the integrity of the BBB and therefore impair glucose transport through the BBB. Neurons have the highest energy demand for glucose and thus require continuous delivery of it from the blood. The down regulation of a certain glucose transporter (GLUT1) which is associated with high blood sugar and insulin resistance therefore, has been linked to the progression of cognitive decline (15)(16). As noted in our ketone testing blog post, permitting ketone bodies to supply a portion of the brain’s required energy compensates for this deficiency in glucose metabolism (17).

Insulin resistance is found in nearly 80% of obese individuals which indicates the integrity of these brains are being impacted – and often times, go unnoticed until later in life. Early Alzheimer’s research was geared towards developing a drug to reverse the pathophysiology of the disease. However, we are now realizing that the complexity of the brain requires much more than a single pill could provide and that focusing on the prevention of the disease with a functional medicine approach could be the most impactful. The Bredesen Protocol incorporates a diet focused on nutrient rich foods that helps maintain the integrity of the BBB and appropriate glucose control. To learn more and set up an individualized plan to prevent or reverse your cognitive decline, sign up for our Cognitive Health Program today.


  1. Centers for Disease Control and Prevention. (2020, February 27).Obesity is a common, serious, and costly disease.
  2. Moss, M, 1955-. (2013). Salt, sugar, fat : how the food giants hooked us. New York : Random House
  3. Berrino F. Western diet and Alzheimer's disease. Epidemiol Prev 2002;26:107–15. [PubMed: 12197047]
  4. Grant WB, Campbell A, Itzhaki RF, Savory J. The significance of environmental factors in the etiology of Alzheimer's disease. J Alzheimers Dis 2002;4:179–89. [PubMed: 12226537]
  5. Pasinetti G, Eberstein J. Metabolic syndrome and the role of dietary lifestyles in Alzheimer's disease. J Neurochem 2008;106:1503–14. [PubMed: 18466323]
  6. Fitzpatrick, A.L., Kuller, L.H., Lopez, O.L., Diehr, P., O’Meara, E.S., Longstreth, W.T., Jr, Luchsinger, J.A., 2009. Midlife and late-life obesity and the risk of dementia: Cardiovascular Health Study. Arch. Neurol. 66, 336–342
  7. Whitmer, R.A., Gunderson, E.P., Quesenberry, C.P., Jr, Zhou, J., Yaffe, K., 2007. Body mass index in midlife and risk of Alzheimer disease and vascular dementia. Curr. Alzheimer Res. 4, 103–109.
  8. Kivipelto, M., Ngandu, T., Fratiglioni, L., Viitanen, M., Kareholt, I., Winblad, B., Helkala, E.L., Tuomilehto, J., Soininen, H., Nissinen, A., 2005. Obesity and vascular risk factors at midlife and the risk of dementia and Alzheimer disease. Arch. Neurol. 62, 1556–1560.
  9. Ho, A. J., Raji, C. A., Becker, J. T., Lopez, O. L., Kuller, L. H., Hua, X., Lee, S., Hibar, D., Dinov, I. D., Stein, J. L., Jack, C. R., Weiner, M. W., Toga, A. W., & Thompson, P. M. (2010). Obesity is linked with lower brain volume in 700 AD and MCI patients.Neurobiology of Aging,31(8), 1326–1339.
  10. Raji, C. A., Ho, A. J., Parikshak, N. N., Becker, J. T., Lopez, O. L., Kuller, L. H., Hua, X., Leow, A. D., Toga, A. W., & Thompson, P. M. (2010). Brain structure and obesity.Human Brain Mapping,31(3), 353–364.
  11. Hwang, L.-L., Wang, C.-H., Li, T.-L., Chang, S.-D., Lin, L.-C., Chen, C.-P., Chen, C.-T., Liang, K.-C., Ho, I.-K., Yang, W.-S., & Chiou, L.-C. (2010). Sex Differences in High-fat Diet-induced Obesity, Metabolic Alterations and Learning, and Synaptic Plasticity Deficits in Mice.Obesity,18(3), 463–469.
  12. Kanoski, S. E., & Davidson, T. L. (2011). Western Diet Consumption and Cognitive Impairment: Links to Hippocampal Dysfunction and Obesity.Physiology & Behavior,103(1), 59–68.
  13. Davidson TL, Kanoski SE, Walls EK, Jarrard LE. Memory inhibition and energy regulation. Physiol Behav 2005;86:731–46. [PubMed: 16263144]
  14. Montagne, A., Barnes, S. R., Sweeney, M. D., Halliday, M. R., Sagare, A. P., Zhao, Z., Toga, A. W., Jacobs, R. E., Liu, C. Y., Amezcua, L., Harrington, M. G., Chui, H. C., Law, M., & Zlokovic, B. V. (2015). Blood-Brain Barrier Breakdown in the Aging Human Hippocampus.Neuron,85(2), 296–302.
  15. Koppel, S. J., & Swerdlow, R. H. (2018). Neuroketotherapeutics: A Modern Review of a Century-Old Therapy.Neurochemistry International,117, 114–125.
  16. De la Monte, S. M. (2017). Insulin Resistance and Neurodegeneration: Progress Towards the Development of New Therapeutics for Alzheimer’s Disease.Drugs,77(1), 47–65.
  17. Broom, G. M., Shaw, I. C., & Rucklidge, J. J.(2019). The ketogenic diet as a potential treatment and prevention strategy for Alzheimer’s disease.Nutrition,60, 118–121.