Ask Dr. Casey: alzheimer’s Disease
Hi Dr. Casey,
I have a family history of Alzheimer’s disease on my mother’s side. What can I do to prevent the same fate for myself and enhance my brain’s abilities for the long term?
- Hailey P.
Hailey, what a loaded question you have proposed! Alzheimer’s disease (AD) is such a layered topic with a lot of research on both slowing progression and prevention. From nutrition, lifestyle, microbiome (of both the gut and the mouth), environmental factors, supplementation, pharmaceuticals, infections, genetics … I could write an entire response on each of those factors individually. I’ll give a broad overview of primary prevention before disease starts.
While genetic testing is an amazing tool for better understanding risks, genes do not entirely guide our destiny for disease. To borrow an old saying, genes may load the gun, but lifestyle can pull the trigger. ApoE/E4 is the genetic testing most considered with a first degree relative with Alzheimer’s. If this test returns positive, it does not mean AD is your fate, but rather an invitation for more vigilance on modifiable risk factors. Some labs I consider running in patients with a family history of AD include folate, homocysteine, hemoglobin A1C and CRP. All of these labs are modifiable with diet, lifestyle and supplementation, and also serve as a conduit for highlighting ways you can take action in prevention.
Let’s begin with folate. Folate first became of known importance relating to AD with what became known as the Nun Study. Initiated in 1986 by researcher David Snowdon, this longitudinal study has tracked over 500 nuns to better understand healthy aging and dementia. A surprising finding was lower folate levels correlated to higher risk for AD (1). Folate, also known as B9, is well known for its importance in the neural tube formation in fetuses. Turns out, it could continue to have an important neurologic impact for the entirety of our lives. Coming from the root word foliage, folate can be found in dark green leafy vegetables - a key missing ingredient in many diets. Folate is also ubiquitously supplemented, usually alongside other B vitamins, and is most bioavailable in a methylated form. A 2021 review study by Zhang confirmed the findings by stating, “folate deficiency/possible deficiency increases the risk for AD, while sufficient intake of folate is a protective factor against AD” (2). I personally like to see folate levels at least twelve in my patients for replete stores. In my mind, this folate finding relates to unprocessed, whole-foods nutrition as a way to help prevent AD.
Next up, homocysteine is a type of amino acid that can be measured with a blood test. Traditionally, elevated levels of homocysteine (> 10 micromol/L) are correlated with higher rates of cardiovascular disease, as well as a long list of other undesirable chronic diseases. The Framingham study analyzed homocysteine levels in relation to cognitive performance and found an inverse relationship: the lower the homocysteine levels, the better the cognitive performance - especially after age 60 (3). Supplementation with B6, folate and B12 can help bring higher homocysteine levels down. To my point above with folate, don’t forget that food is medicine, too. A short two week change of those consuming a focused Mediterranean-style diet intervention decreased homocysteine by 19%, and also increased HDL cholesterol (4).
Another lab to monitor at least once yearly is hemoglobin A1C (A1c). This is an average measure of blood glucose levels over three months and is generally used to diagnose and track prediabetes and diabetes. Considering that professor at Brown Medical School, Suzanne de la Monte, began labeling AD as Type 3 Diabetes in 2005, there is a highly correlative relationship to metabolic health, glucose regulation and insulin resistance. In addition to modifying eating habits to include more fiber and vegetables, exercise is another key in glucose regulation. What’s more, there is a known protective correlation between regular exercise and dementia. Walking an hour three times weekly can increase gray matter in the brain - exactly the part that shrinks in AD. For my patients, an ideal A1C we discuss is 5.5% and lower. If indicated, we may also decide to test insulin as well to have a deeper picture of possible insulin resistance.
Lastly, an additional marker you can ask your doctor to run is c-reactive protein (CRP). CRP is a generalized inflammation marker that is a confirmed risk factor in cardiovascular disease, among others. I have also seen it markedly elevated in active infection, untreated sleep apnea, amongst other conditions. Increased levels have been shown in longitudinal studies to put individuals at higher risk for AD (5). Treating sleep apnea, caring for cardiovascular health and living a general anti-inflammatory lifestyle through balanced nutrition and exercise are important for reducing elevations in CRP, and possibly AD. There is a well-known link between neuroinflammation and risk of AD. Some supplements that have been shown to reduce levels of neuroinflammation, including curcumin. A constituent of the culinary spice turmeric, curcumin is eaten in generous quantities in India as food-based preparation. Of note, India has markedly lower rates of dementia compared to the US.
Hailey, I hope this has been helpful with some actionable tests you can seek out to better modify your own risk for AD. Keeping your brain engaged with brain exercises and possibly even learning a new language are some things I didn't even touch on, but are of importance. While there are many supplements indicated for AD at early onset, the best early prevention is with your own daily choices. In my reading of brain health and neurodegeneration, these processes can begin thirty years prior to actual diagnosis at age 60+. While genes are important, in this case, it may not mean your fate if you maintain a focus on regular health habits that contribute to your overall well being, and brain health, too. .
Citations
Snowdon DA; Nun Study. Healthy aging and dementia: findings from the Nun Study. Ann Intern Med. 2003;139(5 Pt 2):450-454. doi:10.7326/0003-4819-139-5_part_2-200309021-00014
Zhang X, Bao G, Liu D, et al. The Association Between Folate and Alzheimer's Disease: A Systematic Review and Meta-Analysis. Front Neurosci. 2021;15:661198. Published 2021 Apr 14. doi:10.3389/fnins.2021.661198
Elias MF, Sullivan LM, D'Agostino RB, et al. Homocysteine and cognitive performance in the Framingham offspring study: age is important. Am J Epidemiol. 2005;162(7):644-653. doi:10.1093/aje/kwi259
Mietus-Snyder ML, Shigenaga MK, Suh JH, et al. A nutrient-dense, high-fiber, fruit-based supplement bar increases HDL cholesterol, particularly large HDL, lowers homocysteine, and raises glutathione in a 2-wk trial. FASEB J. 2012;26(8):3515-3527. doi:10.1096/fj.11-201558
Schmidt R, Schmidt H, Curb JD, Masaki K, White LR, Launer LJ. Early inflammation and dementia: a 25-year follow-up of the Honolulu-Asia Aging Study. Ann Neurol. 2002;52(2):168-174. doi:10.1002/ana.10265
