Alzheimer disease (AD) and dementia from other causes is a leading cause of disability
and death. In individuals over 71 years of age, the prevalence of dementia
in the U.S. is estimated to be nearly 14%, with 10% attributed to Alzheimer disease
and 4% to other causes such as vascular disease. The prevalence of dementia increases
from 5% of those ages 71 to 79 to 37% of those over 90.5 According to the
Alzheimer Association, 5.4 million Americans are living with the disease today, and
that number could rise as high as 16 million by 2050.

People with the apolipoprotein E4 (ApoE4) gene (and a few other rare genes) are at
high risk of Alzheimer disease. About 25% of Americans have a single copy of the
ApoE4 gene and a lifetime Alzheimer risk of 30%. The 2% to 3% with two copies
have a lifetime risk of between 50% and 90%. This can be compared to a risk of 9%
to 10% for most people who are without any copies of the ApoE4 gene. The greatly
increased risk of Alzheimer disease with either one, or worse yet with two copies of
the ApoE4 gene, suggests that genetic testing should be considered, especially if a
family member has Alzheimer and, even more urgently, if it occurs at a young age.

Although considered the sixth leading cause of death, many death certificates will
list other diseases such as urinary tract infection, pneumonia, or generalized organ
failure as the cause of death when AD has caused the deterioration of basic bodily
functions or other health problems that led to the terminal illness. One recent
study estimates that the number of deaths caused or contributed to by AD is six
times higher than previously thought, and therefore, AD is possibly the third leading
cause or contributing cause of death with as many as 503,000 U.S. deaths in 2010.

Nearly 20% of Medicare dollars are spent on people with Alzheimer disease and
other dementias. The Alzheimer Association projects that in 2050, treatment may
require as much as one of every three Medicare dollars. Total payments for health
care, long-term care, and hospice for patients with dementia were estimated to be
$236 billion in 2016 with the potential to grow to more than $1 trillion in 2050.

The brain pathology of Alzheimer disease is characterized by extracellular plaque
deposits of the protein fragment beta-amyloid and intracellular twisted strands or
tangles of the protein tau, inflammation, brain nerve cell damage, and nerve cell
death. A theory, espoused by Dale Bredesen and others, is that the damaging beta-
amyloid deposition is a response of the brain attempting to protect itself from
three metabolic and toxic threats:
• Inflammation, from infection, diet (e.g., trans-fats), or other causes
• Decline and shortage of supportive nutrients, hormones, and other brain
supporting chemicals
• Toxic substances such as metals or biotoxins, produced by microbes such as
Bredesen considers AD to be the result of a lack of brain nourishing factors and a
surfeit of toxic factors, many of which relate to modern lifestyles that lead to brain
damage. His recommended approach to prevention and treatment of Alzheimer
disease is to identify which of the many contributors to the three classes of threats
to brain health are afflicting an individual, to minimize or better yet remove the
threats, and to increase brain supporting factors.

My UCSF colleague Edward Blonz, has advanced a theory that the genesis of AD is
a lack of adequate brain cell nourishment with energy resources. He considers that
an age-related decline in the ability of glucose to cross the blood-brain barrier creates
metabolic stress that shifts the normal, benign processing of amyloid-protein
precursors toward pathways associated with the production of the amyloid-plaques
and the tau-containing neurofibrillary tangles that are characteristic of the disease.
The implication of this hypothesis is to focus research on developing various methods
to maintain adequate brain energy resources. For example, ensuring the health
of the vascular system through maintaining physical fitness may improve the ability
of glucose to cross the blood-brain barrier, and a high fiber diet may make it easier
for other nutrients to cross the blood-brain barrier.

This blog presents opinions and ideas and is intended to provide helpful general information. I am not engaged in rendering advice or services to the individual reader. The ideas, procedures and suggestions in that are presented are not in any way a substitute for the advice and care of the reader’s own physician or other medical professional based on the reader’s own individual conditions, symptoms or concerns. If the reader needs personal medical, health, dietary, exercise or other assistance or advice the reader should consult a physician and/or other qualified health professionals. The author specifically disclaims all responsibility for any injury, damage or loss that the reader may incur as a direct or indirect consequence of following any directions or suggestions given in this blog or participating in any programs described in this blog or in the book, The Building Blocks of Health––How to Optimize Your Health with a Lifestyle Checklist (available in print or downloaded at Amazon, Apple, Barnes and Noble and elsewhere). Copyright 2021 by J. Joseph Speidel.