For many people approaching retirement, dementia and Alzheimer’s are mysterious and concerning possibilities. For many years, the cause of this disease and risk factors were not well-known. However, we’ve made significant progress in assessing risk and treatment.
While there is not yet a cure for Alzheimer’s or dementia, certain behaviors, lifestyle choices, and other factors can increase the likelihood of developing this disease.
Here are 13 risk factors for Alzheimer’s that you should know.
What causes Alzheimer’s disease?
The cause of Alzheimer’s disease has been the source of study for many years. Traditionally, the direct cause is considered to be the accumulation of amyloid-beta plaque and tau tangles (or neurofibrillary tangles). However, new information points more and more toward inflammation as a cause of dementia.
Essentially, these amyloid plaques build up between nerve cells in the brain and inhibit communication between them. This can cause symptoms like memory loss, confusion, and other cognitive function impairments.
These brain cells begin to die as mental decline continues. But is plaque the ultimate culprit and risk factor for Alzheimer’s and dementia?
Strangely, medications that clear plaque from the brain do not actually cure the disease, often worsening the condition. More recent research suggests that inflammation may be the root cause, opening up more possibilities for preventing and treating Alzheimer’s disease (AD).
The plaque and tangles associated with Alzheimer’s may be a protective response to inflammation, and once they are cleared, inflammation can cause even more damage. It’s becoming clear that plaque isn’t the only risk, nor potential cause, to address in treating AD.
Most drugs manufactured to treat it have little effect in slowing the symptoms, and the disease is currently considered incurable. Thankfully, knowing the risk factors can help with prevention and even slowing the progression of this disease.
Bredesen’s “Holes in the Roof:” A Prevention-Based Approach
Over 4 decades, Dr. Dale Bredesen sought a cure for Alzheimer’s in a laboratory. Instead, he discovered at least 36 possible contributors (a number that has grown to over 50+ factors).
These lifestyle factors take patients down a path toward amyloid-beta plaque buildup, leaving them at a higher risk of Alzheimer’s.
Bredesen explains these factors as “holes in the roof,” places where the risk of developing Alzheimer’s can seep in. This integrative medicine approach highlights areas where preventative care can help patch potential holes and lower risk factors.
He found that most people he saw with dementia had between 20-25 of these 36 holes he identified. This led him to believe that his prevention-driven approach could help “patch up the roof” and even reverse or slow symptoms.
While this protocol is not a cure for Alzheimer’s, most cases treated this way see improvements in brain function and memory, preserving precious years with family members and caregivers.
Much of Bredesen’s “holes in the roof” approach can be examined using Dr. Bredesen’s 6 subtypes to classify Alzheimer’s disease cases.
6 Subtypes of Alzheimer’s Disease
Alzheimer’s is the most common out of all of the types of dementia, and its characteristics can be far-ranging. When looking for root causes, it’s helpful to break the disease down into subtypes according to Dr. Bredesen’s approach.
The second word in quotes found in each subtype comes from Ayurvedic medicine, which has touched on these points for many years.
Bredesen describes the 6 subtypes of Alzheimer’s as follows:
- Type 1: Inflammatory, or “hot.” This subtype may be triggered by inflammation due to underlying conditions like leaky gut, poor oral hygiene, or an unhealthy diet. It typically presents as forgetfulness in patients and is likely to have genetic components.
- Type 2: Atrophic, or “cold.” This variety often is linked with hormonal imbalances and nutritional deficiencies. Long-term memory and daily tasks may remain relatively normal, but processing new information may be challenging.
- Type 1.5: Glycotoxic, or “sweet.” This subtype combines characteristics of type 1 and 2, often involving both insulin resistance and inflammation.
- Type 3: Toxic, or “vile.” The toxic subtype is often triggered by external issues like stress, depression, or exposure to environmental toxins or pathogens. This can affect more areas of the brain than other subtypes and often occurs in the early 50s.
- Type 4: Vascular, or “pale.” The vascular subtype of Alzheimer’s disease is not to be mixed up with vascular dementia. Cardiovascular issues like heart disease are the main contributors to this type, which can also be associated with the atrophic subtype.
- Type 5: Traumatic, or “dazed.” This subtype can be traced to head trauma or brain injury, perhaps due to an accident or playing sports.
Many patients ask: what is the most common cause of dementia? The most common cause of dementia is likely inflammation, but many underlying triggers compound on one another to lead to the development of this disease.
Various triggers from head injuries to insulin issues can contribute to an increased risk of dementia, and it’s common for patients to fall into more than one subtype.
Factors That Increase Your Risk for Alzheimer’s Disease
After reading through the subtypes, you’re aware there are many facets to assessing risk and type of Alzheimer’s.
What are the risk factors of Alzheimer’s disease? The 14 most well-known risk factors of Alzheimer’s disease include:
- Advanced age
- Genetic predisposition and family history
- Chronic diseases associated with vascular injury
- Inflammatory diet
- Heavy metal toxicity
- Chronic stress
- Sleep issues
- Sedentary lifestyle
- Hormone imbalances
- Head injury
- Dysbiotic gut microbiome
- Gum disease
- Female gender
- Cellular function problems
Patients with one or more of these risk factors are at a higher odds of developing Alzheimer’s or dementia. Here are the details on each category.
Who is at high risk for dementia? Patients over 65 are at increased risk for dementia compared to the younger generation. While advanced age is undoubtedly a risk factor for Alzheimer’s and dementia, that doesn’t mean that this debilitating disease is a natural part of your golden years.
Less than 5% of all patients have early-onset Alzheimers, which is usually linked to a genetic predisposition. In other words, 95% of Alzheimer’s patients are senior citizens, and their risk increases even more as they continue to age.
Though Alzheimer’s may be one of the leading causes of death, both in the USA and across the world, it may be possible to slow its spread or practice prevention.
Genetic Predisposition and Family History
While it’s true that genetics are a known risk factor for Alzheimer’s disease, it’s not an inevitability. It is extremely rare to carry a chromosome or mutation that directly causes Alzheimer’s or dementia, known as a “deterministic” gene.
The most common genetic predisposition is the APOE-e4 allele (Apolipoprotein E), which increases a person’s risk of developing late-onset Alzheimer’s disease but does not guarantee it. Only 14% of people worldwide carry this gene.
It’s also unfortunate that people with Down Syndrome develop Alzheimer’s at a much higher rate than the general population, with earlier onset than is typical in other groups.
Family history also plays a role: children or siblings of Alzheimer’s patients have a higher relative incidence of the disease. However, these genetics don’t guarantee a person will develop Alzheimer’s. Only 1% of cases come from deterministic genes, so don’t despair.
Chronic Diseases Associated with Vascular Injury
Chronic diseases associated with vascular injury can link into subtype 4, or vascular Alzheimer’s. These may include:
- Heart disease (cardiovascular disease)
- High blood pressure (hypertension)
- High cholesterol
Research continues to point toward inflammation as an underlying cause of Alzheimer’s, particularly subtype 1. An inflammatory diet has the following traits:
- High in simple carbohydrates/sugars. The brain loses the ability to burn sugars as the disease progresses, and they’re known to feed inflammation. A high sugar diet may also lead to insulin resistance and prediabetes, seen in subtype 2.
- Constant eating and snacking. A fasting window of 12 hours allows your cells to enter autophagy, the body’s routine “cleaning” process for cells. Without this break, your body is literally not “taking out the trash” that is created by cell turnover, contributing to inflammation.
- Deficiencies in vitamin B12, D3, and zinc. These help the body function properly and fight off inflammation. Additionally, a vitamin B12 deficiency causes high homocysteine levels, which are associated with Alzheimer’s.
- Limited antioxidant intake. Antioxidants can help remove free radicals and fight inflammation in the body.
What is the Bredesen diet? The Bredesen diet is an anti-Alzheimer’s way of eating that emphasizes whole foods, healthy fats and lean proteins, fasting, and mild ketosis to reduce inflammation. It’s also known as the KetoFLEX 12/3 diet.
Heavy Metal Toxicity
This risk factor of heavy metal toxicity often plays into subtype 3 of AD. Heavy metals like lead, cadmium, and manganese can be stored and transported throughout the body, accumulating over time. These can come in the form of food, medicines, containers and cookware, and more.
As these environmental toxins build up, these neurotoxicants are associated with cognitive decline and impaired cognitive function in adults. People with regular exposure to these metals are at a higher risk for dementia like Alzheimer’s.
Chronic stress and depression are known to contribute toward the buildup of amyloid-beta proteins in the brain, playing a potential role in the pathogenesis of Alzheimer’s.
People with high-stress lifestyles or jobs may run a greater chance of developing Alzheimer’s down the road, particularly subtype 1 or 3.
Sleep issues earlier on in life may create problems with mild cognitive impairment later down the road. Regularly getting poor sleep, which many Americans admit to, can trigger the beginnings of Alzheimer’s.
Poor sleep means not getting 7-8 hours a night or getting poor quality sleep (limited deep sleep and REM). The most common causes of this are sleep-disordered breathing, a high-stress lifestyle, sleep apnea, and a poor diet (especially too much alcohol or caffeine late at night).
A sedentary lifestyle is a major risk factor for Alzheimer’s, including a lack of stimulation for both mind and body.
People who don’t get enough physical activity (at least 30 minutes daily) are more likely to develop the disease. Even a 30-minute walk can be effective in getting active.
Additionally, a sedentary mind can contribute to the issue. Not getting enough social engagement and no longer learning new skills or solving new problems can spell trouble. Be a lifelong friend and learner; keep the mind active as well as the body!
Interestingly, sedentary behavior may also contribute to inflammation, which is all the more reason to get moving.
Unbalanced hormones can create havoc within the body in many systemic ways, and the risk of Alzheimer’s and dementia is no exception. Changes to estrogen levels, in particular, seem to affect cognition, as estrogen both protects the brain and helps it to grow.
Insulin, another hormone, can influence inflammation as well as other hormones, often playing a part in subtypes 1, 2, and 1.5.
A head injury can usually be directly linked to subtype 5, with a moderate or severe head injury doubling the chances of developing Alzheimer’s or other forms of dementia later on in life.
Children who play contact sports and those who have been in car accidents are especially susceptible.
Dysbiotic Gut Microbiome
A dysbiotic gut microbiome may play tricks on bacterial balances in other areas of the body, including the brain. This can happen in the absence of probiotics, after a course of antibiotics, and an inflammatory diet.
When pathogenic bacteria run rampant, they are a risk factor for Alzheimer’s on their own and contribute to issues like obesity, type 2 diabetes, and inflammation.
Your oral microbiome has a lot more to do with your brain health than you might expect. For years, scientists have understood that periodontal disease (periodontitis or gum disease) increases the risk of developing Alzheimer’s disease.
The bacterial culprit for gum disease, P. gingivalis, can make its way to the brain. There, it builds up over time, inducing inflammation and causing amyloid-beta deposits on the brain.
In a 2019 study, researchers found evidence that P. gingivalis in the brains causes the development of compounds called gingipains. This groundbreaking discovery strongly suggests a rare causal link, not just a correlation, between P. gingivalis bacteria and Alzheimer’s disease.
Translation: The study postulates that gum disease may literally cause Alzheimer’s disease in certain patients.
Sadly, being a woman is a risk factor that puts you at a greater likelihood of developing this disease.
Female patients make up approximately ⅔ of those diagnosed with Alzheimer’s disease.
However, it’s important to remember another statistic: Roughly 30% of people will develop Alzheimer’s by age 90. Considering that aging is the most well-known risk factor and that women live longer, there may be some overlap to account for here.
Cellular Function Problems
Specific cellular function problems may raise the odds of developing Alzheimer’s, particularly:
- Limited mitochondrial function
- Limited SirT1 gene function
- Low nerve growth factor (NGF) levels
These issues with the inner workings of your cells can affect your body’s functioning and impact long-term neurological health.
The Key to Alzheimer’s Prevention: Fixing the Roof
Knowing the range of risk factors and how they can link to Alzheimer’s is critical, as is catching and preventing Alzheimer’s early.
In our experience, the sooner the diagnosis, the better the outcome.
In fact, these risk factors are generally the ones used in the Bredesen Protocol and other prevention approaches to AD, stopping Alzheimer’s progression in its tracks– or even before it starts.
In the Group Medical Visit program, created by PrimeHealth, we integrate your unique risk factors and the pioneering Bredesen Medical Protocol. We want to help you prevent Alzheimer’s or slow the symptoms based on your labs and the lifestyle factors that apply to you.
Each prevention program offers 10-15 people to learn alongside virtually. Set up a phone consultation with us to find out if our program is right for you.
- Wyss-Coray, T., & Rogers, J. (2012). Inflammation in Alzheimer disease—a brief review of the basic science and clinical literature. Cold Spring Harbor perspectives in medicine, 2(1), a006346. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3253025/
- Kinney, J. W., Bemiller, S. M., Murtishaw, A. S., Leisgang, A. M., Salazar, A. M., & Lamb, B. T. (2018). Inflammation as a central mechanism in Alzheimer’s disease. Alzheimer’s & Dementia: Translational Research & Clinical Interventions, 4, 575-590. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6214864/
- Casey, D. A., Antimisiaris, D., & O’Brien, J. (2010). Drugs for Alzheimer’s disease: are they effective?. Pharmacy and Therapeutics, 35(4), 208. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2873716/
- Gustafson, C. (2015). Dale E. Bredesen, md: Reversing cognitive decline. Integrative Medicine: A Clinician’s Journal, 14(5), 26. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4712873/
- Bredesen, D. E., Sharlin, K., Jenkins, D., Okuno, M., Youngberg, W., Cohen, S. H., … & Braud, M. (2018). Reversal of cognitive decline: 100 patients. J Alzheimers Dis Parkinsonism, 8(450), 2161-0460. Full text: https://www.researchgate.net/profile/Kenneth-Sharlin/publication/329063941_Reversal_of_Cognitive_Decline_100_Patients/links/5d965c00458515c1d391b494/Reversal-of-Cognitive-Decline-100-Patients.pdf
- Van Giau, V., Bagyinszky, E., Yang, Y. S., Youn, Y. C., An, S. S. A., & Kim, S. Y. (2019). Genetic analyses of early-onset Alzheimer’s disease using next generation sequencing. Scientific reports, 9(1), 1-10. Abstract: https://pubmed.ncbi.nlm.nih.gov/31182772/
- Liu, C. C., Kanekiyo, T., Xu, H., & Bu, G. (2013). Apolipoprotein E and Alzheimer disease: risk, mechanisms and therapy. Nature Reviews Neurology, 9(2), 106-118. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3726719/
- Schupf, N. (2002). Genetic and host factors for dementia in Down’s syndrome. The British Journal of Psychiatry, 180(5), 405-410. Abstract: https://pubmed.ncbi.nlm.nih.gov/11983636/
- Jarvik, L., LaRue, A., Blacker, D., Gatz, M., Kawas, C., McArdle, J. J., … & Zonderman, A. B. (2008). Children of persons with Alzheimer disease: what does the future hold?. Alzheimer disease and associated disorders, 22(1), 6. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3377487/
- Williamson, J., Goldman, J., & Marder, K. S. (2009). Genetic aspects of Alzheimer disease. The neurologist, 15(2), 80. Abstract: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3052768/
- Gottesman, R. F., Albert, M. S., Alonso, A., Coker, L. H., Coresh, J., Davis, S. M., … & Knopman, D. S. (2017). Associations between midlife vascular risk factors and 25-year incident dementia in the Atherosclerosis Risk in Communities (ARIC) cohort. (10), 1246-12JAMA neurology, 7454. Abstract: https://pubmed.ncbi.nlm.nih.gov/28783817/
- Iadecola, C. (2015). Sugar and Alzheimer’s disease: a bittersweet truth. nature neuroscience, 18(4), 477-478. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4731873/
- Glick, D., Barth, S., & Macleod, K. F. (2010). Autophagy: cellular and molecular mechanisms. The Journal of pathology, 221(1), 3-12. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2990190/
- Bakulski, K. M., Seo, Y. A., Hickman, R. C., Brandt, D., Vadari, H. S., Hu, H., & KyunPark, S. (2020). Heavy metals exposure and Alzheimer’s disease and related dementias. Journal of Alzheimer’s Disease, (Preprint), 1-28. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7454042/
- Dong, H., & Csernansky, J. G. (2009). Effects of stress and stress hormones on amyloid-β protein and plaque deposition. Journal of Alzheimer’s Disease, 18(2), 459-469. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2905685/
- Shokri-Kojori, E., Wang, G. J., Wiers, C. E., Demiral, S. B., Guo, M., Kim, S. W., … & Volkow, N. D. (2018). β-Amyloid accumulation in the human brain after one night of sleep deprivation. Proceedings of the National Academy of Sciences, 115(17), 4483-4488. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5924922/
- Yan, S., Fu, W., Wang, C., Mao, J., Liu, B., Zou, L., & Lv, C. (2020). Association between sedentary behavior and the risk of dementia: a systematic review and meta-analysis. Translational psychiatry, 10(1), 1-8. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7174309/
- Cheng, S. T. (2016). Cognitive reserve and the prevention of dementia: the role of physical and cognitive activities. Current psychiatry reports, 18(9), 1-12. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4969323/
- Edwards, M. K., & Loprinzi, P. D. (2018). Systemic inflammation as a function of the individual and combined associations of sedentary behaviour, physical activity and cardiorespiratory fitness. Clinical physiology and functional imaging, 38(1), 93-99. Abstract: https://pubmed.ncbi.nlm.nih.gov/27781404/
- Janicki, S. C., & Schupf, N. (2010). Hormonal influences on cognition and risk for Alzheimer’s disease. Current neurology and neuroscience reports, 10(5), 359-366. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058507/
- Gottlieb, S. (2000). Head injury doubles the risk of Alzheimer’s disease. BMJ, 321(7269), 1100. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1173459/
- Jiang, C., Li, G., Huang, P., Liu, Z., & Zhao, B. (2017). The gut microbiota and Alzheimer’s disease. Journal of Alzheimer’s Disease, 58(1), 1-15. Abstract: https://pubmed.ncbi.nlm.nih.gov/28372330/
- Poole, S., Singhrao, S. K., Chukkapalli, S., Rivera, M., Velsko, I., Kesavalu, L., & Crean, S. (2015). Active invasion of Porphyromonas gingivalis and infection-induced complement activation in ApoE-/-mice brains. Journal of Alzheimer’s Disease, 43(1), 67-80. Abstract: https://pubmed.ncbi.nlm.nih.gov/25061055/
- Ishida, N., Ishihara, Y., Ishida, K., Tada, H., Funaki-Kato, Y., Hagiwara, M., … & Matsushita, K. (2017). Periodontitis induced by bacterial infection exacerbates features of Alzheimer’s disease in transgenic mice. NPJ aging and mechanisms of disease, 3(1), 1-7. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5673943/
- Dominy, S. S., Lynch, C., Ermini, F., Benedyk, M., Marczyk, A., Konradi, A., … & Potempa, J. (2019). Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors. Science advances, 5(1), eaau3333. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6357742/
- Mielke, M. M. (2018). Sex and gender differences in Alzheimer’s disease dementia. The Psychiatric times, 35(11), 14. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6390276/
- Alzheimer’s Association. (2017). 2017 Alzheimer’s disease facts and figures. Alzheimer’s & Dementia, 13(4), 325-373. Abstract: https://www.sciencedirect.com/science/article/abs/pii/S1552526017300511
- van der Flier, W. M., & Scheltens, P. (2005). Epidemiology and risk factors of dementia. Journal of Neurology, Neurosurgery & Psychiatry, 76(suppl 5), v2-v7. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1765715/
- Santos, R. X., Correia, S. C., Wang, X., Perry, G., Smith, M. A., Moreira, P. I., & Zhu, X. (2010). Alzheimer’s disease: diverse aspects of mitochondrial malfunctioning. International journal of clinical and experimental pathology, 3(6), 570. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2907118/