June is Alzheimer's Awareness Month
Updated: Jul 14, 2021
Currently, there are more than six million people living with Alzheimer’s in the US. It is projected that by 2025 there will be 40,000 Nebraskans living with this debilitating disease. There is not one specific cause of Alzheimer’s but a multitude of factors that play a role in the development of this disease. Some of these factors include genetics, lifestyle factors, and concurrent health issues such as cardiovascular diseases. Alzheimer’s hallmark sign is amyloid beta protein deposits in the brain which is neurotoxic. Oxidative stress, extracellular acidity, and metabolic acidosis are additional triggers for the development of this disease (Alzheimer's Association).
There is growing research in the prevention of Alzheimer’s which is encouraging! The standard American Diet delivers more than enough sodium but not enough dietary potassium to balance out the excess intake of sodium. Studies show that switching to a paleolithic diet can increase dietary potassium levels while balancing out extracellular pH in the body. While on the subject of diet, it may be a large contributor to metabolic acidosis in the body, which contributes to chronic diseases such as Type 2 Diabetes and Hypertension. Metabolic acidosis breaks down proteins in the body and increases oxidative stress. Dietary changes such as increasing intake of antioxidants by consuming more fresh fruits and vegetables can be sufficient in preventing disease (Veurink, G. 2020).
Specific antioxidant supplementation can prove beneficial as well. Molecular hydrogen (H₂) is one antioxidant that has been shown to reduce inflammation and modulate the immune pathways, as it is the smallest molecule that easily enters cells to reduce free radicals and beta amyloid. Glutathione is another antioxidant that is neuroprotective against Alzheimer’s, it specifically protects against oxidative stress, reduces inflammation and detoxes metals. Vitamin B9 and B12 are crucial at reducing high homocysteine levels in the body. Homocysteine is an amino acid that is produced when proteins are broken down and is a generalized inflammation marker. B9 and B12 break down homocysteine (Veurink, G. 2020).
Physical activity has also been shown to reduce one's risk of developing Alzheimer's. One study stated that those who exercised regularly had a decreased risk of developing the disease by 45% (Silva, M. 2019). Sleep deprivaton is another important factor in development of AD. One single night of disturbed sleep showed increased amyloid beta plaques in the brain in rodent studies (Havekes, R. 2019). Working on sleep hygiene and getting restful sleep is important in the prevention of this neurodegenerative disease.
Testing for individuals at risk of developing Alzheimer’s is now available. As a provider for Vibrant labs as well as Cyrex labs we can offer these services in the office. The Vibrant Neural Zoomer has 11 markers that are linked to Alzheimer’s disease development. Cyrex Lab’s Alzheimer’s Linx looks at not only brain proteins but also pathogens, chemicals and foods that are cross reactive to amyloid beta to identify individuals at greater risk for developing Alzheimer’s. If you are interested in learning more about testing or preventative measures call our office to set up a free consultation.
Call or text 402-769-6624 to schedule.
Veurink, G., Perry, G., & Singh, S. K. (2020). Role of antioxidants and a nutrient rich diet in Alzheimer's disease. Open biology, 10(6), 200084. https://doi.org/10.1098/rsob.200084
Silva, M., Loures, C., Alves, L., de Souza, L. C., Borges, K., & Carvalho, M. (2019). Alzheimer's disease: risk factors and potentially protective measures. Journal of biomedical science, 26(1), 33. https://doi-org.uws.idm.oclc.org/10.1186/s12929-019-0524-y
Havekes, R., Heckman, P., Wams, E. J., Stasiukonyte, N., Meerlo, P., & Eisel, U. (2019). Alzheimer's disease pathogenesis: The role of disturbed sleep in attenuated brain plasticity and neurodegenerative processes. Cellular signalling, 64, 109420. https://doi-org.uws.idm.oclc.org/10.1016/j.cellsig.2019.109420