Numerous medical studies have supported the idea that gut inflammation can lead to problems of mood and memory as well as other neurologic symptoms including Alzheimer’s Disease and dementia. In many of our articles, we have shown recent studies that a healthy gut microbiota (the collective name for the bacteria that live in the digestive/intestinal tract) can protect many people from developing certain diseases including cancer and various bowel related syndromes. The idea that probiotics, the “good” bacteria, promotes a healthy gut microbiota and supports our cognitive system by regulating inflammation is a widely held scientific belief.
In December 2019, a team of university researchers published the results of their study (1) on how folate (folic acid is one form of folate) and vitamin B12 deficiencies worsened memory function and disturbed the gut microbiota in amyloid-β infused (Alzheimer’s induced) rats.
The learning points of this research were:
Folate and vitamin B12 deficiencies are associated with metabolic diseases that may impair memory function.
Folate and vitamin B12 deficiencies and a high-fat diet exacerbated memory impairment. (The laboratory rats could not or had difficulty remembering how to get out of a water maze).
Folate and vitamin B12 may differently alter mild cognitive impairment, glucose metabolism, and inflammation by modulating the gut microbiome in rats with Alzheimer’s disease (AD)-like dementia.
The key to this research was that there was an alteration in the way the gut works and this led to a problem in the brain. Specifically the development of Alzheimer’s disease.
The “Lost-Link” to preventing Alzheimer’s disease?
A December 2019 study in the Journal of Alzheimer’s disease (2) suggested that gut inflammation and the regulation of brain-gut-microbiome axis may be a “lost link” in understanding and treating Alzheimer’s disease. The researchers noted:
“Despite extensive research into Alzheimer’s disease pathogenesis and therapeutic targets, there remains no breakthroughs in its management. In recent years, there has been a spark of interest in the connection between the brain and gastrointestinal tract, referred to as the brain-gut axis, and its potential implications for both metabolic and neurologic disease. Moreover, the gastrointestinal flora, referred to as the microbiome, appears to exert significant influence over the brain-gut axis.
With the need for expanded horizons in understanding and treating Alzheimer’s disease, many have turned to the brain-gut-microbiome axis for answers. . . we conclude with a brief description of documented clinical support for brain-gut-microbiome axis alteration in Alzheimer’s disease, including potential microbiome-based therapeutics for Alzheimer’s disease. Collectively, these findings suggest that the brain-gut-microbiome axis may be a “lost link” in understanding and treating Alzheimer’s disease and call for future work.”
The key findings of this research is, if you treat the gut, and you create harmony and balance in the gut, you may be treating Alzheimer’s disease.
A March 2019 study in the journal Molecular neurobiology (3) takes this one step further.
Alzheimer’s disease may begin in the gut
“One of the most important scientific discoveries of recent years was the disclosure that the intestinal microflora takes part in bidirectional communication between the gut and the brain. Scientists suggest that human gut microflora may even act as the “second brain” and be responsible for neurodegenerative disorders like Alzheimer’s disease.
Brain destructive mechanisms, that can lead to dementia and Alzheimer’s disease, start with the intestinal microbiome dysbiosis, development of local and systemic inflammation, and dysregulation of the gut-brain axis. . . It is strongly postulated that Alzheimer’s disease may begin in the gut, and is closely related to the imbalance of gut microbiota. This is promising area for therapeutic intervention. Modulation of gut microbiota through personalized diet or beneficial microbiota intervention, alter microbial partners and their products including amyloid protein, will probably become a new treatment for Alzheimer’s disease.”
Exploring your options
At the Magaziner Center for Wellness, we approach disease and imbalance by first determining all contributing factors and creating an individualized, patient-centered treatment plan. The latest research has shown that there are a host of factors that can cause and contribute to Alzheimer’s- from environmental toxins to nutrition to heavy metal toxicity and more. Every person has a unique biochemistry which reacts to pollutants and toxins differently, and requires an individualized course of treatment. While the disease may look similar from person to person, we are not treating the disease. We are healing the individual.
In order to determine the unique contributing factors of each individual, we utilize extremely thorough blood and urine tests, as well as a complete examination of every aspect of the body, from mitochondrial function to heavy metal toxicity and more. We then create a personalized care plan based on these findings,which may include treatments such as chelation therapy, hyperbaric oxygen therapy, antioxidant nutritional supplements, intravenous vitamins, diet and nutrition.
If you would like to explore more information, please contact our office so we can start a conversation with you.
1 Park S, Kang S, Kim DS. Folate and vitamin B-12 deficiencies additively impaired memory function and disturbed the gut microbiota in amyloid-β infused rats. International Journal for Vitamin and Nutrition Research. 2019 Dec 16.1: Sun M, Ma K, Wen J, Wang G, Zhang C, Li Q, Bao X, Wang H.
2 Brain-Gut-Microbiome Axis and the Potential Role of Microbiota in Alzheimer’s Disease. J Alzheimers Dis. 2019 Dec 26. doi: 10.3233/JAD-190872. [Epub ahead of print] PubMed PMID: 31884474.
3 Sochocka M, Donskow-Łysoniewska K, Diniz BS, Kurpas D, Brzozowska E, Leszek J. The Gut Microbiome Alterations and Inflammation-Driven Pathogenesis of Alzheimer’s Disease-a Critical Review. Mol Neurobiol. 2019 Mar;56(3):1841-1851. doi: 10.1007/s12035-018-1188-4. Epub 2018 Jun 23. PMID: 29936690; PMCID: PMC6394610.