The Link Between Lyme Disease and Alzheimer’s
One of the unfortunate realities of Lyme disease is that it can create susceptibility to other illnesses and conditions, such as diabetes, metabolic syndrome, cancer, and Alzheimer’s, just to name a few. This is because Lyme disease interferes with a multitude of biochemical processes in the body; it damages cells, causes inflammation and toxicity and other unfavorable issues that can become a setup for other problems.
Since Lyme disease is first and foremost a neurological disease that affects the brain and nervous system (although it affects every system of the body), perhaps one of the most important diseases that people with Lyme disease are at an increased risk for is Alzheimer’s dementia. Indeed, research shows that some chronic infections are linked to Alzheimer’s, including spirochetal infections such as Borrelia, one of the primary infections of Lyme disease.
Authors Thomas J. Lewis, PhD and Clement L. Trempe, MD, describe the correlation between Alzheimer’s and Lyme disease in their 2014 book, The End of Alzheimer’s: A Differential Diagnosis Toward a Cure. They cite Dr. Judith Miklossy, a pioneering doctor who has extensively researched the connection between infection and Alzheimer’s. In a 2011 research paper entitled, “Alzheimer Disease—A neurospirochetosis?” Dr. Miklossy states, (as cited in The End of Alzheimer’s), “It is established that chronic spirochetal infection can cause slowly progressive dementia, brain atropy and amyloid deposition in neurosyphiis. Recently it has been suggested that various types of spirochetes, in an analogous way to Treponema palladium could cause dementia and may be involved in the pathogenesis of Alzheimer’s disease.”
Borrelia burgdorferi has been shown to be similar to the syphilis spirochete, but Dr. Miklossy also goes on to say, “Borrelia burgdorferi was detected in the brain in 25.3% of AD [Alzheimer’s dementia] cases analyzed and was 13 times more frequent in AD compared to controls.” Even more interesting, she notes that the common dental spirochete Treponema has been observed in over 90% of people with Alzheimer’s. Thus, spirochetal infections have been shown in multiple studies to be linked to Alzheimer’s.
Borrelia is thought to cause chronic inflammation and corticol atrophy and to play a role in amyloid deposition. These are all factors which lead to Alzheimer’s. Corticol atrophy refers to degeneration of the outer layer of the brain, which consists of six folded layers of connected neurons. Amyloid deposition refers to the plaque deposits on the brain that are found in Alzheimer’s patients. In The End of Alzheimer’s, Dr. Miklossy is quoted as saying, “Bacteria and their degradation products may initiate a cascade of events leading to cell death, neurodegeneration and amyloid deposition in Alzheimer’s disease.”
What’s more, a meta-analysis on the relationship between spirochetal infections and Alzheimer’s, published in 2015 in Journal of Alzheimer’s Disease revealed that there is a tenfold increased occurrence of Alzheimer’s when there is evidence of a spirochetal infection, including Borrelia.
Fortunately, by understanding the connection between Lyme and Alzheimer’s, people with Lyme disease can be empowered to heal more completely from the illness and prevent the onset of Alzheimer’s. The obvious first step is to eliminate the infections. Beyond that, there are things that people with Lyme disease can do to improve cognitive function, prevent neurological degeneration and lower inflammatory markers.
One of the most important of these is to take Omega-3 essential fatty acid (EFA) supplements from fish oils. Omega-3 essential fatty acids have been shown in studies on thousands of people to lower inflammation and prevent or reduce symptoms of Alzheimer’s. They are responsible for maintaining the integrity of neuronal cell membranes, and since the brain is comprised of 80% fat, consuming omega-3 EFAs can help to prevent degradation of brain tissue.
In The End of Alzheimer’s, Authors Thomas J. Lewis, PhD and Clement L. Trempe, MD cite additional nutrients that have been shown in studies to help prevent Alzheimer’s. These include Vitamin D and magnesium, both of which lower inflammation and which have shown to be specifically helpful for people with Alzheimer’s. The authors note that deficiencies of zinc and Vitamin K have also been associated with Alzheimer’s, so supplementation with these nutrients may also be helpful.
Diet also plays a crucial role in staving off Alzheimer’s. Because inflammation has been linked strongly to Alzheimer’s, avoiding inflammatory foods in the diet is essential for people with chronic Lyme. This includes any food that the body perceives as an allergen, including food additives, genetically modified food, and foods that may seem to be healthy but which the body may prefer to avoid because they are not natural. High-carbohydrate diets have been particularly linked to Alzheimer’s, because they cause blood sugar imbalances and high insulin levels, which have been linked to Alzheimer’s. Many Lyme-literate doctors have found Paleo diets, which are rich in animal protein, healthy fats like olive and coconut oil, fruits and green veggies, to be generally healthful diets for people with Lyme disease and for keeping inflammation at bay.
Finally, keeping the brain engaged and active, and connecting with others socially can help to prevent dementia. Working in a stimulating or mentally challenging job or having a mentally stimulating hobby, and interacting with others on a regular basis, all encourage brain health.
Further Reading and References
Bu XL et al. “A study on the association between infectious burden and Alzheimer’s disease.” Eur J Neurol. (2014 Jun 9). doi: 10.1111/ene.12477.
Lewis, T. and Clement Trempe. (2014). The End of Alzheimer’s: A Differential Diagnosis Toward a Cure. TJLPHD, LLC.
Maheshwari P1, Eslick GD. Bacterial infection and Alzheimer’s disease: a meta-analysis. J Alzheimers Dis. 2015;43(3):957-66. doi: 10.3233/JAD-140621.
Miklossy J. “Alzheimer’s disease – a neurospirochetosis. Analysis of the evidence following Koch’s and Hill’s criteria.” J Neuroinflammation. (2011 Aug 4);8:90. doi: 10.1186/1742-2094-8-90.