Nutritional Support for Dementia and Alzheimer's

By Chris Kresser
Published on June 7, 2018

Alzheimer’s disease and other dementias are truly heartbreaking for patients and their families. Drug trials target amyloid-beta plaques in a bottom-level approach that has yet to be successful. In contrast, Functional Medicine offers a top-level approach that addresses the many underlying causes of dementia. Read on to learn about the lesser-known causes of Alzheimer’s disease, what nutrients support brain function, and what a Functional Medicine approach to dementia looks like.

More than 30 million Americans suffer from some type of dementia. Alzheimer’s disease (AD) in particular affects more than five million Americans, and its associated healthcare costs surpass $200 billion each year (1). Considering genetics and other risk factors, up to 45 million currently living Americans may develop AD within their lifetimes (2).

The hallmarks of AD are extracellular amyloid-beta plaques, intracellular neurofibrillary tangles, and activated glial cells in the brain. The conventional approach views amyloid-beta plaques as the enemy: the plaques build up, destroy synapses between nerve cells, and promote neuronal cell death, eventually leading to cognitive impairment. But conventional medicine fails to address what is causing and contributing to plaque build-up.

Nutritional deficiencies are associated with and sometimes can predict severity of Alzheimer’s disease and cognitive decline in the elderly. Learn which dietary patterns support dementia and brain health.

Alzheimer’s Is a Multifactor Pathological Condition

Dr. Dale Bredesen, a renowned AD researcher, challenges the mainstream view. I have interviewed him on my podcast and written about his work in this article. He argues that AD is a multifactor pathological condition. Amyloid-beta is not the main problem, but rather the brain’s response to one (or more than one) insult (3). By removing the insults and optimizing health, he has reversed AD in many cases. Through years of work, he has identified several types of AD, each with unique causes (4, 5):

- Type 1 (“inflammatory”) is due to an antimicrobial response to pathogens or other inflammatory causes.

- Type 2 (“atrophic”) is associated with reductions in factors that support brain health, like estradiol, progesterone, testosterone, insulin, and vitamin D.

- Type 1.5 (“glycotoxic”) is a composite of types 1 and 2. Inflammation from high blood glucose levels combines with a trophic loss of insulin sensitivity.

- Type 3 (“toxic” or “cortical”) is associated with exposure to toxins such as heavy metals, insecticides/pesticides, antimicrobials, and commercial/industrial toxins.

- Type 4 (“vascular”) is associated with reduced vascular support.

- Type 5 (“traumatic”) is associated with previous head trauma.

Monotherapy Isn’t the Answer

The quest for a miracle AD pharmaceutical has been expensive and fruitless. Most AD drug trials have targeted amyloid-beta itself or BACE1, the protease that catalyzes the rate-limited step in synthesizing amyloid-beta from amyloid precursor protein (APP). By treating a symptom and failing to address the underlying problem(s), more than 99 percent of monotherapy trials to halt or reverse AD have been unsuccessful (6).

In contrast, a Functional Medicine approach to AD identifies the underlying insults—inflammation, oxidative stress, nutrient deficiencies, atrophy, toxins, pathogens, or some combination—and treats them on an individualized basis. Using this method, Dr. Bredesen has seen dramatic improvements in AD. One patient’s hippocampal volume increased from the 17th percentile to the 75th percentile after 10 months of treatment (2). In several cases, his patients have been able to return to work following treatment (7). This article will focus on the nutritional strategies for managing cognitive decline, and in particular, AD.