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“That’s fatal, isn’t it?” This is how my mom responded to the doctor when she was told she had Alzheimer’s. As a teenager in 1979, I had never heard of this strange disease, but my mom knew enough to understand that it was a death sentence. Sadly, more than four decades later it still is. “Alzheimer’s disease is the sixth leading cause of death in the United States, and the only one of the top 10 causes of death that has no cure or disease modifying treatment.” Read that again—no cure or no disease modifying treatment. Not only is there no cure, but the disease can’t even be slowed down. I think this is why we fear it so much.
Shortly after my mom’s diagnosis, Alzheimer’s Disease (AD) research began to focus on the amyloid plaques found in the brains of AD patients. Unfortunately, this narrow focus has led to almost forty years of faulty research.[i] The Alzheimer’s Associations reported that “By 2017, 146 drug candidates for treating Alzheimer’s disease had been deemed unsuccessful. Only four drugs had been approved, and they treated the symptoms of the disease, not its underlying pathology. The results were so disappointing that in 2018, Pfizer pulled out of Alzheimer’s research.”[ii] The amyloid plaque theory may not be completely wrong, but researchers are finally admitting that it is an insufficient cause of AD. However, the benefit of time has been lost since the majority of the tens of billions spent on research since the mid-80’s has been focused on this one area.
Though there is a strong genetic link to AD, genetics is not determinative. The most common gene associated with AD is the APOe4 gene. About 25 percent of people carry one copy of APOEe4, and 2 to 3 percent carry two copies.[iii] Recently, actor Chris Hemsworth was told that he has two copies of the APOe4 gene, which increases a person’s risk of AD by about 15%.[iv] “Researchers estimate that between 40-65% of people diagnosed with Alzheimer's have the APOE-e4 gene.”[v] [vi]
There is also strong correlation between AD and diabetes, so much so that many refer to AD as “type 3 diabetes.”[vii] Type 1 diabetics are 93% more likely to develop dementia.[viii] One study showed that 81% of AD patients had either type 2 diabetes or impaired fasting glucose.[ix] Furthermore, a younger age at onset of diabetes was significantly associated with higher risk of subsequent dementia.[x] If you are diagnosed with type 2 diabetes at age 70, your risk of developing dementia only increases by 11%. But if you are diagnosed at age 60, your risk increases by 77%.[xi] The rate of new cases of type 2 diabetes in children is 5%[xii] which only increase their risk of other diseases like AD.
While a cure has not yet been found, there is tremendous hope in the form of prevention. When faced with a frightening disease like Alzheimer’s, we need to understand that reducing our risk lies within our control. Our lifestyle choices can literally turn on or turn off genes for Alzheimer’s. Epigenetics is the process of lifestyle and environmental factors that work “upon” (‘epi’-genetics) our genes. The genes that you inherit can be likened to the 88 keys on a piano. You can’t control which 88 keys you receive from your parents, but you can have a tremendous influence over which keys are played. For example, even if you inherit 2 copies of the APOe4 gene, your lifestyle choices could turn off this gene which could effectively prevent you from developing AD.
One powerful area of prevention-oriented epigenetics is in the gut-brain axis. The vagus nerve connects the nervous system in the gut directly with the brain. Remarkably, most of the communication travels from the gut to the brain, mostly in the form of neurotransmitters. For example, at least 90% of the serotonin in your body is produced by gut bacteria and then sent to your brain along the vagus nerve.
There are also gut brain connections through the bloodstream. What is often called a “leaky gut” occurs when the tight junctions in the epithelial cells that line your colon open and allow contents of your colon to enter the bloodstream. This could include bacteria and toxins that gram-negative bacteria produce, called lipopolysaccharides (LPS). Once in the bloodstream, LPS can travel throughout the body and cause chronic inflammation in any organ system.
Image source[xiii]
By itself, LPS can open tight junctions and create a leaky gut.[xiv] LPS has two weapons—it has the ability to create a leaky gut and then it can take advantage of these openings to travel throughout the body. The resulting chronic inflammation is a cause of most metabolic and many autoimmune diseases. Moreover, LPS can travel to the brain and open the tight junctions in the endothelial cells separating the bloodstream from the brain tissue, known as the blood-brain barrier (BBB).[xv] Researchers had long thought that the BBB was very difficult to pass through, which served as a protective barrier for the brain. However, research is showing that this BBB can be “leaky” in almost the same way that the gut can be leaky. LPS has been found lodged in many parts of brain tissue, which increases the risk for developing AD.[xvi] Therefore, the health of your gut microbiome directly impacts whether or not you will develop a leaky gut or a leaky brain—or both.
“With no practical treatment for AD yet in development, the control of gram-negative bacteria and their LPS may be an excellent strategy to prevent the onset and progression of AD.”[xvii] In other words, if a person can reduce the number of LPS producing bacteria in their gut, they directly reduce the odds of developing a leaky gut or a leaky brain.
This is where lifestyle choices come into play. A diet rich in fiber is proven to increase beneficial gut bacteria while a diet of sugar and simple carbs is proven to increase harmful, LPS-producing bacteria. With the myriads of diets out there, one simple way to begin is with the Fiber-Fueled book by Will Bulsiewicz. It is an excellent overview that explains the gut microbiome and how it can be greatly improved by your diet.
Prebiotics like HMO also decrease LPS producing bacteria by feeding beneficial/probiotic bacteria. In one example, adding a daily dose of HMO reduced the amount of LPS producing bacteria to a mere 3.4%.[xviii] (Watch the video below)
By comparison, according to the data gathered by Biomesight.com, the average number of gram-negative bacteria in an adult microbiome is 46%. The added benefit is that any changes that lower your risk for AD will also lower your risk for cancer, diabetes, heart disease, stroke and more.
Lifestyle and epigenetic influences to reduce the risk of AD and metabolic diseases. To summarize:
I believe that if my mom knew then what we know now and was able to put it into practice, it is doubtful she would have ever developed Alzheimer’s disease.
Written by: Rich Maurer, BS, MT (ASCP), MDiv
Rich worked as a board-certified Medical Technologist for eight years before serving as an ordained pastor for thirty years. He has developed a hobby of learning about the microbiome and helping others to improve their health through microbiome testing and lifestyle changes.
[i] https://www.quantamagazine.org/what-causes-alzheimers-scientists-are-rethinking-the-answer-20221208/?fbclid=IwAR05LPDHSOJwOUpM5hWC002yGhFjWhuqGpL08G7SEHXn9hJ-6EZicEwn7Xk
[ii] https://www.quantamagazine.org/what-causes-alzheimers-scientists-are-rethinking-the-answer-20221208/?fbclid=IwAR05LPDHSOJwOUpM5hWC002yGhFjWhuqGpL08G7SEHXn9hJ-6EZicEwn7Xk
[iii] https://www.nia.nih.gov/health/alzheimers-disease-genetics-fact-sheet
[iv] https://www.webmd.com/alzheimers/news/20221230/chris-hemsworth-alzheimers-risk-what-to-know-apoe4-gene#:~:text=Hemsworth%20learned%20that%20he%20has,of%20genes%20in%20Alzheimer's%20disease.
[v] https://www.alz.org/alzheimers-dementia/what-is-alzheimers/causes-and-risk-factors/genetics?utm_source=google&utm_medium=paidsearch&utm_campaign=google_grants&utm_content=alzheimers&gclid=Cj0KCQiA6LyfBhC3ARIsAG4gkF_T6VrIivRL5P--x0lyD7twqQ2vief011fQFutzKSqAtKXW8vHJiwEaAqnCEALw_wcB
[vi] https://www.cell.com/neuron/fulltext/S0896-6273(17)30791-2
[vii] https://www.alzra.org/blog/what-you-should-know-about-alzheimers-and-type-3-diabetes/
[viii] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8302147/
[ix] https://diabetesjournals.org/diabetes/article/53/2/474/11453/Increased-Risk-of-Type-2-Diabetes-in-Alzheimer
[x] https://jamanetwork.com/journals/jama/article-abstract/2779197
[xi] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7246646/
[xii] https://www.cdc.gov/diabetes/research/reports/children-diabetes-rates-rise.html#:~:text=The%20rate%20of%20new%20cases,of%20CDC's%20Morbidity%20and%20Mortality
[xiii] https://www.frontiersin.org/articles/10.3389/fimmu.2020.594150/full
[xiv] https://pubmed.ncbi.nlm.nih.gov/34200555/
[xv]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8599158/?fbclid=IwAR2tKeK5PUMF1vXXoqIoTtPi2PZRCvkBZbuL0Y593BsL1j7Cw5j1nxO-X-g
[xvi] https://translationalneurodegeneration.biomedcentral.com/articles/10.1186/s40035-021-00273-y
[xvii] https://translationalneurodegeneration.biomedcentral.com/articles/10.1186/s40035-021-00273-y
[xviii] https://www.youtube.com/watch?v=mkdp4BIbtVI
