Dr. Doni reviews the facts about Alzheimer’s Disease, including some of the current research connecting it to oxidative stress.
Part 3 of Dr. Doni’s Series on Oxidative Stress
In my life, my grandfather died of Alzheimer’s disease in 1983 when he was 87 years old after 7 years of at-home care. I remember visiting him, listening to his stories, and also dodging cherry pits as he spat them straight out (instead of into a bowl). It was sad to watch him forget his home, family, and everything he had lived for in his life. I also often hear from patients who are caring for aging parents with dementia or Alzheimer’s disease—about how difficult it is to observe a loved one deteriorate. It can lead to years and years of worry, sadness, sleepless nights, guilt, and even anger as the change in behavior and loss of memory impacts daily life and activities, not to mention the financial cost. A recent report showed that the costs associated with care for Alzheimer’s patients exceeds that for heart disease and for cancer, much of which is not covered by insurance.1 With all of this, care for the caregiver increases in importance and is demonstrated in studies to be beneficial.2
After such experiences, it’s not uncommon to start worrying about getting Alzheimer’s ourselves. Unfortunately, this is not simply an unfounded fear: it is expected that the prevalence of Alzheimer’s disease will increase by 40% in the next 10 years.3
However, the scariest part is that, although a lot of people talk about it and worry about getting Alzheimer’s, it isn’t actually that well understood in the medical community. Doctors don’t even know exactly why or how some people get it and others don’t. Also, at present, medical researchers have yet to discover a biomarker (something we can easily test in blood or urine) to help us identify whether someone has the disease, so it is mainly identified by cognitive decline. And to top it off, there is not yet a treatment to stop the disease, although researchers are studying it at a rapid pace in hopes of finding a cure.
What the researchers are finding is that the underlying medical reason for Alzheimer’s is probably a combination of factors. It’s partially down to genetic influences that predispose some people towards it (and at an earlier age), but more and more research is showing that diet, lifestyle, and environmental factors also play a role in whether or not we are susceptible to the disease. That, in my opinion, is where the solution lies. My grandfather, for example, smoked for over 40 years. His lifelong career was farming, where he was often exposed to pesticides (and was actually hospitalized twice for pesticide toxicity).
Even though I do not have the same degree of exposure to toxins as my grandfather, I sometimes find myself wondering whether low level exposure over a lifetime could also increase my own risk. It appears that researchers are looking at that same question. This is because we now know we can influence the way our genetics play out by addressing our exposure to stress, including dietary, physical, emotional, and environmental stresses—a field called “epigenetics.”
NOTE: You can read more about genetic testing and how the information can be used to benefit your health in my blog series on genetics.
Alzheimer’s Disease and Oxidative Stress
It turns out that many of the same diet, lifestyle and environmental factors that affect our genes also contribute to our exposure to oxidative stress. So when it comes to preventing Alzheimer’s disease, addressing oxidative stress is the way to go. In this article and the two to follow it in this series, I’ll be showing you how oxidative stress plays a part in Alzheimer’s, and what kinds of things you can do to minimize your risk of contracting the disease and alleviate symptoms if you or someone in your life has already developed it.
If you are unfamiliar with oxidative stress, you may want to start by reading this article which explains how oxidation inside our cells damages them and leads to many common health issues.
Today, I’ll start by explaining what we do and don’t know about Alzheimer’s, as well as a few of the many misconceptions people have about the disease.
The Facts about Alzheimer’s Disease
Let’s begin by reviewing a few facts:
- Alzheimer’s is a neurodegenerative disease that damages brain cells. It begins by causing short-term memory loss (not being able to remember something you just learned or heard) and later causes long-term memory loss.
- The damage caused by Alzheimer’s disease falls into three categories:
- Plaques. “Plaques” are sticky clumps of amyloid proteins that surround the nerve cells in the brain. When they develop, it makes it difficult for the cells to communicate with each other. These “crossed wires” cause messages between cells to be misdirected which can lead to confusion and disorientation.
- Tangles. “Tangles” occur with when a protein called tau gets twisted inside the nerve cells of the brain. When tau functions correctly, it acts like a railroad track moving nutrients inside the nerve cells. But when it gets twisted, the tangles prevent much-needed nutrients getting to where they are supposed to go. As a result, the nerve cells die.
- Inflammation. This refers to inflammatory processes in and around nerve cells. Over time, chronically inflamed cells become damaged. Inflammation (and the cytokines associated with it) are triggered by the plaques and cell damage caused by tangles. Inflammation (and even auto-immune antibodies) in the brain is also triggered by neurotoxins if/when they are able to pass through a compromised blood-brain barrier (BBB), a selectively permeable membrane that should only allow nutrients into the brain.4 Ultimately, all of this results in, and is a result of oxidative stress.
All three kinds of damage contribute to the loss of communication between the nerves, making it difficult for messages to travel between brain cells. This makes it difficult for the cells to communicate with each other. So if you’re trying to remember something and the cells that contain that memory can’t get the message through, it shows up as memory loss.
- Alzheimer’s is the most common type of dementia. It is more common in women, and although the average age of onset is over 65 years old, up to 5% of people with the disease have “early onset” in their 40s or 50s.
- As the disease progresses, generally over three to nine years (but sometimes longer), it is common to experience loss of motivation, mood changes, disorientation, difficulty speaking, and eventually an inability to complete daily tasks, loss of bodily functions, and ultimately, death.
- In the 1990s, researchers first associated Alzheimer’s with a gene (APOE e4) and plaque build-up. Then, in October 2015, they made another discovery—that another gene (IL1RAP), which influences cytokines, inflammation and the brain’s “garbage disposal system” (or microglia) is even more associated with plaque.5,6
- While there is not yet any solid evidence that the degeneration caused by Alzheimer’s can be reversed, some research has shown that the degeneration can, in some cases, be prevented and/or slowed down.
- The best way to prevent Alzheimer’s from developing is to make lifestyle and environmental changes (such as the ones we’ll be looking at in the next article). These changes protect your nervous system and the cells of your body from oxidative stress.
- Current research indicates that oxidative stress plays a major role in the progression of Alzheimer’s disease.7, 8, 9, 10, 11
- There is not yet a cure for Alzheimer’s.
Is the Connection Between Alzheimer’s and Aluminum a Myth?
In the 1960s and 70s, it was thought that the main cause of Alzheimer’s Disease was over-exposure to aluminum. In fact, many people were left thinking that cooking in aluminum pots and pans, and drinking from aluminum cans was the biggest risk factor. Then studies lead researchers to think that aluminum was not actually a major cause, and not the only cause, so they kept searching for answers.
It has taken decades, but now research is indicating that the cause of Alzheimer’s Disease is much bigger and more pervasive than simply exposure to aluminum (although metal exposure does play a role). It is now thought that oxidative stress is the prime suspect, which is increased by many potential sources, including:
- stress 12
- high blood sugar levels 13
- neurotoxins, such as glyphosate, leaking through the blood-brain barrier 14
- leaky gut and dysbiosis (imbalanced microbiome – bacteria in the digestive tract), and 15, 16
- over-exposure to metals, like aluminum, and toxins.17
When you think about it, we are often exposed to toxins and metals at low levels throughout the day, every day. That’s the problem. These toxins accumulate in our bodies and increase oxidative stress. If we can take steps to reduce oxidative stress then that will surely reduce our risk of Alzheimer’s.
Up Next: Looking at Key Risk Factors and Changes You Can Make
Now that we have a better sense of what Alzheimer’s is, and what it isn’t, we are ready to look at the key risk factors for oxidative stress, diet and environment, and some changes you can make to reduce your exposure to them. That’s what I’ll be covering in Part 2 of this mini-series on Alzheimer’s and its connection to oxidative stress. In that article, I’ll go into depth about two of the major sources of oxidative stress in our daily lives: high blood sugar and environmental toxins.
Then, in Part 3 of this mini-series, I’ll talk about supplements, herbs, and nutrients that can actually prevent Alzheimer’s disease. To be sure you receive the next article in this series, please sign up to receive my e-newsletter, Weekly Wellness Wisdom.
If you or someone in your family has Alzheimer’s, and you are interested in natural solutions for alleviating symptoms or for preventing it from developing in the first place, contact me at https://doctordoni.com/appointment to set up a free five-minute consultation to discuss my Oxidative Stress Solutions Package. When you send your request, be sure to mention that Alzheimer’s is your primary concern.
4th December 2015
- Amy S. Kelley, MD, MSHS; Kathleen McGarry, PhD; Rebecca Gorges, MA; and Jonathan S. Skinner, PhD. The Burden of Health Care Costs for Patients With Dementia in the Last 5 Years of Life. Annals of Internal Medicine. Ann Intern Med. 2015;163(10):729-736. http://annals.org/article.aspx?articleid=2466364
- Mausbach BT, Chattillion EA, Ho J, Flynn LM, Tiznado D, von Känel R, Patterson TL, Grant I. Why does placement of persons with Alzheimer’s disease into long-term care improve caregivers’ well-being? Examination of psychological mediators. Psychol Aging. 2014 Dec;29(4):776-86. http://www.ncbi.nlm.nih.gov/pubmed/25133414″>http://www.ncbi.nlm.nih.gov/pubmed/25133414
- Alzheimer’s Association. Alzheimer’s disease facts and figures. Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association. 2015;11(3):332 – 384. http://www.alzheimersanddementia.com/article/S1552-5260(15)00058-8/abstract
- D’Andrea MR. Med Hypotheses. Add Alzheimer’s disease to the list of autoimmune diseases. 2005;64(3):458-63. http://www.ncbi.nlm.nih.gov/pubmed/15617848
- Andre Altmann, Lu Tian, Victor W. Henderson, et al: Sex modifies the APOE-related risk of developing Alzheimer disease. Annals of Neurology, April 14, 2014.
- Vijay K Ramanan, et al. GWAS of longitudinal amyloid accumulation on 18F-florbetapir PET in Alzheimer’s disease implicates microglial activation gene IL1RAP. Brain. 2015; 138(10):3076 – 3088. http://brain.oxfordjournals.org/content/138/10/3076
- Yan Zhao and Baolu Zhao. Oxidative Stress and the Pathogenesis of Alzheimer’s Disease Oxidative Medicine and Cellular Longevity. 2013, Article ID 316523, 10 pages. http://www.hindawi.com/journals/omcl/2013/316523/
- Sochocka M, K. E. Vascular Oxidative Stress and Mitochondrial Failure in the Pathobiology of Alzheimer’s Disease: New Approach to Therapy. CNS Neurol Disor Drug Targets. 2013 Feb 27.
- George Perry, Adam D. Cash and Mark A. Smith. Alzheimer Disease and Oxidative Stress. J Biomed Biotechnol. 2002; 2(3): 120– http://www.ncbi.nlm.nih.gov/pmc/articles/PMC161361/
- Markesbery WR. Oxidative stress hypothesis in Alzheimer’s disease. Free Radic Biol Med. 1997;23(1):134-47. http://www.ncbi.nlm.nih.gov/pubmed/9165306
- Jennifer Madeo* and Chris Elsayad. The Role of Oxidative Stress in Alzheimer’s Disease. Department of Medicine, Nassau University Medical Center, 2201 Hempstead Turnpike, East Meadow, New York 11554, USA http://www.omicsonline.org/the-role-of-oxidative-stress-in-alzheimers-disease-2161-0460.1000116.pdf
- Baglietto-Vargas D1, Chen Y2, Suh D1, Ager RR1, Rodriguez-Ortiz CJ1, Medeiros R1, Myczek K1, Green KN1, Baram TZ2,3, LaFerla FM1. Short-term modern life-like stress exacerbates Aβ-pathology and synapse loss in 3xTg-AD mice. J Neurochem. 2015 Sep;134(5):915-26. http://www.ncbi.nlm.nih.gov/pubmed/26077803
- de la Monte SM1. Type 3 diabetes is sporadic Alzheimer׳s disease: mini-review. Eur Neuropsychopharmacol. 2014 Dec;24(12):1954-60. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4444430/
- Weekman EM, Wilcock DM. Matrix Metalloproteinase in Blood-Brain Barrier Breakdown in Dementia. J Alzheimers Dis. 2015 Nov 21. http://www.ncbi.nlm.nih.gov/pubmed/26599057
- Leblhuber F, Geisler S, Steiner K, Fuchs D, Schütz B. Elevated fecal calprotectin in patients with Alzheimer’s dementia indicates leaky gut. J Neural Transm (Vienna). 2015 Sep;122(9):1319-22. http://www.ncbi.nlm.nih.gov/pubmed/25680441
- Surjyadipta Bhattacharjee and Walter J. Lukiw. Alzheimer’s disease and the microbiome Front Cell Neurosci. 2013; 7: 153. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3775450/
- Christopher Exley and Thomas Vickers. Elevated brain aluminium and early onset Alzheimer’s disease in an individual occupationally exposed to aluminium: a case report. Journal of Medical Case Reports 2014, 8:41. http://www.jmedicalcasereports.com/content/8/1/41/abstract