4 ways to reduce risk for Alzheimer’s Disease

4 ways to reduce risk for Alzheimer's Disease

Reviewed by Inna Krieger PhD.

Have you wondered, “What is my risk of getting Alzheimer’s disease?” Maybe you received the 23andMe DNA kit for Christmas and learned you have ApoE ε4. Now you want to know how to prevent Alzheimer’s disease.

In this article I’ll explain what are the odds of being diagnosed with Alzheimer’s disease given you have ApoE ε4, and then I will share four ways that anyone can reduce risk for Alzheimer’s disease.

Alzheimer’s is a neurodegenerative disease that causes progressive cognitive and functional impairment.1 Despite decades of intensive scientific study, this disease remains poorly understood. Usually, once symptoms appear the damage is too extensive to be fully reversed, and the best interventions merely slow down its progression.

Consequently research has focused on identifying early biomarkers that allow for prevention of the disease, rather than treating it. Do you know what is the earliest biomarker for Alzheimer’s disease today? It is a simple DNA test.

No single genetic factor is fully responsible for the condition, but one mutation in particular has been identified that is clearly associated with an elevated risk of the disease.  This DNA letter change in the ApoE gene is the strongest genetic risk factor for late onset Alzheimer’s disease.2,3 You can learn your genotype at this position with a DNA test. This information can empower you to make lifestyle decisions which may delay or even prevent this disease.

If you are homozygous (both copies of your gene contain the mutation) for ApoE ε4, you have a lifetime risk of 30-55% for developing Alzheimer’s disease.4  55% means 55 out of 100 individuals with the ApoE ε4/ε4 mutation will be diagnosed with Alzheimer’s disease in their lifetime. Your risk of Alzheimer’s disease is 8- to 15- times higher than the risk of someone without the ApoE ε4 mutation.4  The good news is the range 30-55% shows us that some individuals with this genotype have a much lower risk compared to others.

I will now share 4 ways you can reduce your risk for Alzheimer’s disease so that you are on the low end of that range even if you are ApoE ε4/ε4.  These recommendations are based off of the latest scientific research for Alzheimer’s disease.

1. Reduce autoimmunity

A recent study reported a strong association between Alzheimer’s disease and a primary or secondary diagnosis of autoimmunity.5  This is in agreement with previous studies that have reported links between Alzheimer’s disease and type 1 diabetes6, autoimmune thyroiditis7, rheumatoid arthritis8, and systemic lupus.9  The key step to reducing autoimmunity is healing leaky gut and balancing the immune system.  We are proud to partner with DayTwo a microbiome analysis company that has developed an algorithm for identification of specific foods that trigger aberrant glycemic responses which may result in obesity, diabetes, and autoimmunity.10  Many autoimmune diseases may also be caused by bacterial, viral, or fungal infections that have gone unidentified by routine medical testing.11  We can identify these sources of autoimmunity using deep sequencing through partnership with the company Aperiomics (see next paragraph).

2. Lower inflammation

Inflammation exacerbates the development of Alzheimer’s disease.12 Sources of neuron inflammation include traumatic brain injury,13 infections,14 viruses,15 and neurotoxic molecules.14 The brain tissue of Alzheimer’s disease patients is often infected with fungi and bacteria.11 One way that fungi and bacteria may find their way into the nervous system is by breaching the intestinal barrier.11 Another possibility is through the mouth and nasopharyngeal region.11 Regardless of how they get into the brain, often our immune system needs assistance in removing them. We partner with Aperiomics a company that performs deep sequencing of plasma, CSF, and tissue to identify stubborn fungal and bacterial infections so that they can be treated by qualified health providers before causing chronic inflammation. In parallel we use food as medicine to reduce your inflammatory response and rebuild your gut wall integrity.

3. Monitor cholesterol

High cholesterol has been implicated as an independent risk factor for Alzheimer’s disease.16 This might not come as a surprise if you have realized the function of the ApoE gene. Did you know ApoE is the most abundant transporter in the brain for cholesterol and lipids? ApoE also plays a critical role in neuron repair and glucose metabolism in the brain. ApoE ε4 binds cholesterol differently compared to ApoE ε3 and ApoE ε2.16 The result is that individuals who have the ApoE ε4 mutation are more likely to get atherosclerosis from high plasma cholesterol levels and LDL.16 Atherosclerosis results in inflammation which potentiates Alzheimer’s Disease.16 A personalized diet is critical for reducing cholesterol levels because everyone is a little different.

4. Address sleep disorders

Missing a single night of sleep causes increased accumulation of Amyloid beta (Aβ) a key pathology of Alzheimer’s disease.17 Aβ is a protein peptide that is secreted across neural synapses much like a neurotransmitter. Aβ is typically cleared by janitor microglia cells especially during sleep.17 Getting to the root cause of sleep disturbances is critical for management of Alzheimer’s disease risk as it has been estimated that 15% of Alzheimer’s disease occurrence may be attributed to disturbed circadian rhythms, shortened sleep, and poor quality of sleep.18 Often a multifaceted approach to insomnia is required including assessment of genetics, neurotransmitter pathways, and salivary cortisol levels.

Conclusion

You can learn your risk for Alzheimer’s disease by doing a simple DNA test. Knowledge of your risk can empower you to prioritize preventive strategies early in life. We would love to help you learn about your risk and discuss how you can reduce that risk in an individual way informed by targeted testing. Click here to set up an appointment with Nutriplexity today!

References

  1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (DSM-5®). American Psychiatric Pub; 2013.
  2. Tzioras M, Davies C, Newman A, Jackson R, Spires‐Jones T. Invited Review: APOE at the interface of inflammation, neurodegeneration and pathological protein spread in Alzheimer’s disease. Neuropathology and Applied Neurobiology. 2019;45(4):327-346. doi:10.1111/nan.12529
  3. Corder EH, Saunders AM, Strittmatter WJ, et al. Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer’s disease in late onset families. Science. 1993;261(5123):921-923.
  4. Qian J, Wolters FJ, Beiser A, et al. APOE-related risk of mild cognitive impairment and dementia for prevention trials: An analysis of four cohorts. PLoS Med. 2017;14(3):e1002254.
  5. Li X, Sundquist J, Zöller B, Sundquist K. Dementia and Alzheimer’s disease risks in patients with autoimmune disorders. Geriatr Gerontol Int. 2018;18(9):1350-1355.
  6. Huang C-C, Chung C-M, Leu H-B, et al. Diabetes mellitus and the risk of Alzheimer’s disease: a nationwide population-based study. PLoS One. 2014;9(1):e87095.
  7. Tan ZS, Beiser A, Vasan RS, et al. Thyroid function and the risk of Alzheimer disease: the Framingham Study. Arch Intern Med. 2008;168(14):1514-1520.
  8. Ferraccioli G, Gremese E. Rheumatoid Arthritis and Alzheimer Disease: Possible Cellular and Molecular Links. Journal of Gerontology & Geriatric Research. 2012;01(02). doi:10.4172/2167-7182.1000104
  9. D’Andrea MR. Add Alzheimer’s disease to the list of autoimmune diseases. Medical Hypotheses. 2005;64(3):458-463. doi:10.1016/j.mehy.2004.08.024
  10. Suez J, Shapiro H, Elinav E. Role of the microbiome in the normal and aberrant glycemic response. Clinical Nutrition Experimental. 2016;6:59-73. doi:10.1016/j.yclnex.2016.01.001
  11. Alonso R, Pisa D, Fernández-Fernández AM, Carrasco L. Infection of Fungi and Bacteria in Brain Tissue From Elderly Persons and Patients With Alzheimer’s Disease. Frontiers in Aging Neuroscience. 2018;10. doi:10.3389/fnagi.2018.00159
  12. Kinney JW, Bemiller SM, Murtishaw AS, Leisgang AM, Salazar AM, Lamb BT. Inflammation as a central mechanism in Alzheimer’s disease. Alzheimers Dement. 2018;4:575-590.
  13. Ebert SE, Jensen P, Ozenne B, et al. Molecular imaging of neuroinflammation in patients after mild traumatic brain injury: a longitudinal 123 I‐CLINDE single photon emission computed tomography study. European Journal of Neurology. 2019. doi:10.1111/ene.13971
  14. Glass CK, Saijo K, Winner B, Marchetto MC, Gage FH. Mechanisms underlying inflammation in neurodegeneration. Cell. 2010;140(6):918-934.
  15. Koyuncu OO, Hogue IB, Enquist LW. Virus infections in the nervous system. Cell Host Microbe. 2013;13(4):379-393.
  16. Xue-Shan Z, Juan P, Qi W, et al. Imbalanced cholesterol metabolism in Alzheimer’s disease. Clin Chim Acta. 2016;456:107-114.
  17. Website. TED. 2017. “What You Can Do to Prevent Alzheimer’s | Lisa Genova.” Youtube. May 19, 2017. https://www.youtube.com/watch?v=twG4mr6Jov0. Accessed September 9, 2019.
  18. Bubu OM, Brannick M, Mortimer J, et al. Sleep, Cognitive impairment, and Alzheimer’s disease: A Systematic Review and Meta-Analysis. Sleep. 2017;40(1). doi:10.1093/sleep/zsw032

1 thought on “4 ways to reduce risk for Alzheimer’s Disease”

  1. Reading this article is rather frightening to me as my wife many of these conditions. She is Bi-polar manic depressant (diagnosed in 1999) and currently takes Lithium Carbonate, Carbamazepine and Olanzapine along with Lorazepam as treatment. She is also (at this time) obese (5’5″ @ 215lb) at 66 years old and, of course wants to loose weight. Add to that, for about 6 years now her sleep has been anything but normal. She goes to bed at 10 and then is up by 10:30 back at 11 back up by 12 (all numbers are relative) then up and down all night long and a 2 hr nap fro 1pm to 3pm. We are both retired on fixed incomes and Medicare but she does have a Medicare Supplement, however, I do have other funds available if cost become significant. Can you assist with sleep and weight and/or even the Bipolar?
    p.s. Her Dr,s. are Don and Lisa Regier whose daughter is Mary, a researcher at UW in Seattle. Small world!

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