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Improving Cognition with the Bredesen Protocol

Clinical insights from Metagenics Institute LIVE event

 

Host: Deanna Minich, PhD

Guest: Amylee Amos, MS, RDN

In this discussion, Amylee Amos, MS, RDN and Deanna Minich, PhD examine how nutrition and lifestyle factors can be leveraged in an individualized way in primary intervention for different subtypes of Alzheimer’s disease. Amylee brings a unique set of nutrition knowledge, having trained under neurologist Dale Bredesen, MD, a pioneer in the area of individualized treatment for cognitive decline who believes we have entered an era of treatable Alzheimer’s disease. Having been personally affected and shaped by a family history of Alzheimer’s disease, Amos chose to specialize in the area of nutrition and cognitive decline to help these unique patients.

Amylee explains that the interventions in the Bredesen protocol are personalized—a multi-targeted approach designed to identify and address the root causes of the cognitive decline for the individual. While mainstream medicine discussions focus on Alzheimer’s disease as it relates to the neurotoxin amyloid-beta and its plaque accumulation in the brain, Amos mentions that the latest research suggests that these amyloid-beta protein fragments are in fact, a protective antimicrobial response, so the Bredesen protocol aims to target factors farther upstream.

Amos describes six different subtypes of cognitive decline and their associated profiles: Type 1 inflammatory subtype (anti-inflammatory approach); type 2 atrophic subtype (trophic support, e.g., sex hormones, thyroid, etc.); type 1.5 glycotoxic subtype, a mixture of inflammatory and atrophic subtypes (anti-inflammatory and deal with glucose control and insulin resistance); type 3 toxic (address toxic exposures from heavy metals, mold, etc.); type 4 vascular, and type 5 traumatic (brain injury). Many patients are a combination of these subtypes. Further, the apolipoprotein E ε4 (ApoEε4) genetic variant (i.e., the number of alleles the patient has: 0, 1, or 2) informs risk for cognitive decline.

Amylee explains that her nutritional interventions for cognitive decline often start with improving gut health, which influences neurogenesis. Significant benefit can be gained by simply having the patient add color into their diet, as that facilitates a more plant-based approach that includes a variety of fruits and vegetables. Other diet modifications include emphasizing mono- and polyunsaturated fats and limiting refined carbohydrates, added sugars, and red meats. Amos mentions the utility of a mildly ketogenic diet for ApoEε4 carriers within a plant-based approach, where meats are used “as a condiment, instead of the star of the plate.” On a personalized basis, Amos utilized time-restricted feeding or intermittent fasting for certain individuals, particularly for extending an overnight fast.

While food is the foundation that primes the body and brain, additional nutrients and bioactives are incorporated based on the patient’s labs and symptomology. For example, Amos leverages medium-chain triglyceride (MCT) oil for a transient period to assist the patient in achieving mild ketosis. She also emphasizes the importance of aerobic exercise and resistance training, including exercises that target mobility and balance. Re-testing labs during follow-up, in combination with tracking changes in symptoms, allows for the practitioner to re-assess and pivot their individualized clinical recommendations.

Dr. Minich and Amylee discuss the Bredesen et al. 2018 publication from the Journal of Alzheimer’s and Parkinsonism, which reports on 100 patients with varying degrees of cognitive decline (different subtypes represented) who experienced symptom improvement or reversal while following the Bredesen protocol. Amos emphasized that the intervention was individualized, and the improvements were, too—underscoring the importance of a personalized clinical approach.

In a discussion on accountability and adherence to the Bredesen protocol, Amylee shares insights on a predictive factor for success in her patients with cognitive decline—a strong support system. Amos explains that patients who have “people in their corner” tend to do better, since the interventions can be challenging, particularly in individuals with memory loss. To that end, she has found that a group education approach in her practice, which includes the patients’ support system, is helpful for patient compliance to the regimen.

Lastly, Amylee explains that not all indicators of improvement are quantifiable through objective means, like labs. She encourages practitioners to also pay attention to the subjective facet of thriving, which the patient may communicate, and/or family and friends may share, “their person is coming back.”

This Metagenics Institute LIVE broadcast took place live May 13, 2019 on the Metagenics Institute Facebook page.

Resources

Bredesen DE et al. Reversal of cognitive decline: 100 patients. J Alzheimers Dis Parkinsonism. 2018;8(5):6.

Theendakara V et al. Transcriptional effects of ApoE4: relevance to Alzheimer’s disease. Mol Neurobiol. 2018;55(6):5243-5254.

Bredesen DE et al. Ayurvedic profiling of Alzheimer’s disease. Altern Ther Health Med. 2017;23(3):46-50.

Bredesen DE et al. Reversal of cognitive decline in Alzheimer’s disease. Aging (Albany NY). 2016;8(6):1250-1258.

Bredesen DE. Reversal of cognitive decline: a novel therapeutic program. Aging (Albany NY). 2014;6(9):707-717.

Bredesen DE et al. Next generation therapeutics for Alzheimer’s disease. EMBO Mol Med. 2013;5(6):795-798.

 

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