What the new research shows
The Bredesen Protocol for the prevention and
treatment of Alzheimer’s disease derives its success from its core
concept. That concept is that the
disease is driven by the coalescence of multiple metabolic imbalances that are
driven by lifestyle factors such as diet, exercise, sleep, stress and
others.
A growing body of research has been showing that these
factors such as chronic low omega-3 fatty acid intake or low blood vitamin B12
levels impair brain health and cognitive function. However, preventing or correcting these
factors individually has been shown to impart only small preventative/protective effects which help but are not enough to make large
impacts on the disease. The core concept
of the Bredesen Protocol assumes that finding all of the collective factors
that are involved and correcting all of them simultaneously will yield much
broader results.
To date about 40 factors have been identified and are
investigated in the protocol. Any given
individual may have 21 factors that are imbalanced, and a specific treatment
program will target that pattern. The
next individual may have 30 different factors that are imbalanced and their
specific treatment program will be targeted to those. It is this comprehensiveness and individually
specific design of each treatment program that has resulted in the excellent
treatment outcomes. The whole really has
proven greater than simply the sum of the parts.
I thought it would be good to look at some the latest
research examining some of these factors that relate to the risk of developing
the disease.
The Inflammatory US Diet and Dementia/Alzheimer’s Disease
Chronic
inflammation is a potent risk factor for the developments and progression of
Alzheimer’s disease. Lifestyle factors
that contribute to chronic inflammation are therefore therapeutic targets in
treatment. One of those lifestyle
factors that has been shown to contribute to chronic inflammation is diet.
A new study
looked at the relationship between dietary patterns known to be associated with
chronic inflammation and the risk of developing pre-Alzheimer’s (MCI) or
dementia. Compared to those chronically
eating the anti-inflammatory Mediterreanean dietary pattern, those consuming
the standard American diet which is considered pro-inflammatory had a 27%
increased risk. The results led the
researchers to conclude: “Diets with the highest pro-inflammatory potential
were associated with higher risk of MCI or dementia.”
Diet is
perhaps the single lifestyle factor most associated with broad chronic disease
risks.
Hayden et al. The association between an inflammatory diet
and global cognitive function and incident dementia in older women: The Women's
Health Initiative Memory Study.
Alzheimers & Dementia, ePub 2017.
The Importance of Cognitive Reserves
In a previous
post I discussed the impact of cognitive reserve of
the risk of Alzheimer’s disease. Simply
put, the more exercise and development the brain has had during life the more
resistant it is to developing the disease with age. This study looked at risk associated with low
cognitive development and reserves.
During a 44
year follow-up each standard deviation of decreased cognitive ability was
associated with increased risk of dementia of 33%. In this type of analysis they take the
average cognitive ability across a large group and compare those with moderate
(1 standard deviation) and substantial (2 standard deviations) lower from this
average.
The key
point here is that the brain needs exercise throughout life and the greater the
“strength” it has, the more resistant it is to developing Alzheimer’s. Although not looked at in this study, other
study has shown that cognitive exercise even in later life has preventative and
therapeutic benefit.
Osler et al. Cognitive ability in young adulthood and risk
of dementia in a cohort of Danish men, brothers, and twins. Alzheimers & Dementia, ePub 2017.
The Impact of Low Vitamin D Levels on Cognitive Decline
One of the
important variables in the Bredesen Protocol which is measured and closely
managed is the blood vitamin D levels. A
new study looked at this variable in older subjects to see if it correlated
with the rate of cognitive decline and the risk of transitioning to Alzheimer’s
or some other form of dementia.
Compared to
individuals with normal vitamin D levels participants with vitamin D deficiency
exhibited a faster cognitive decline over the study period. A total of 177
dementia cases, including 124 cases of Alzheimer’s disease occurred. Those with vitamin D deficiency had a nearly
three-fold increased risk of Alzheimer’s disease.
The normal
lab range for blood vitamin D is 32-100 mg/dL.
Research has found that the ideal level for the prevention of chronic
disease is 50 mg/dL. This suggests that
many individuals assuming that their levels are adequate are actually at
greater risk.
Feart et al. Associations of lower vitamin D concentrations
with cognitive decline and long-term risk of dementia and Alzheimer's disease
in older adults. Alzheimers &
Dementia, ePub 2017.
Exercise and Beta Amyloid Accumulation
The primary
toxic protein that causes the brain cell loss in Alzheimer’s disease is called
beta amyloid. While the brain is always
making some of this protein, it only becomes toxic when it builds up in higher
amounts in the brain tissue. There are
many factors that cause the brain to produce too much beta amyloid exceeding
the ability to remove it. Inflammation
is a key example. There are other
factors that affect beta amyloid removal such as low omega-3 fatty acid intake
which also increases the likelihood of build-up.
Exercise
seems to be another variable that influences the risk of beta amyloid
build-up. A new study examined the
presence of beta amyloid build-up with PET scans using a tracer that highlights
this protein. In those without positive PET
scans there were equal numbers of high and low-level exercisers. However, when they separated out those
subjects already showing some beta amyloid build-up, it was significantly
higher in those who had low exercise levels. This suggests that when there are
other factors driving beta amyloid build-up in the brain, higher levels of
regular exercise seems to prevent this from progressing.
This
observation is supported by other research that has found regular exercise to be
therapeutically helpful in preventing progression in pre-Alzheimer’s patients.
Brown et at al. Habitual exercise levels are associated with
cerebral amyloid load in presymptomatic autosomal dominant Alzheimer's disease. Alzheimers & Dementia, ePub 2017.
Mineral Deficiencies and Alzheimer’s
Risk
The body
uses two classes of antioxidants, endogenous (made within the body) and
exogenous (supplied from diet). The
endogenous antioxidants are also dietary dependent as they require dietary
factors such as minerals. Selenium is needed to produce the body’s major endogenous
antioxidants such as glutathione.
As oxidative
stress which is not effectively neutralized by antioxidants is a primary
mechanism that drives brain degeneration in Alzheimer’s and dementia, selenium
status is of concern. Most of human
selenium intake comes from plant based foods and those levels are determined by
the selenium content of the soil they are grown in.
Given the
above facts a study was set up to examine the relationship between selenium
levels in different geographic locations and Alzheimer’s risk. The risk of the disease in the 6 states with
the lowest selenium content was increased 53% compared to the 6 states with the
highest levels.
The
conclusion is simple. Inadequate supply
of dietary nutrients that are used in the inherent antioxidant systems is a
strong risk factor for Alzheimer’s disease.
Sun H. Associations of Spatial Disparities of
Alzheimer's Disease Mortality Rates and Soil Selenium, Sulfur Concentrations,
and Risk Factors in the United States.
J Alzheimers Dis. ePub 2017.
Too Few Good Fats or Too much Bad Fat Highly Associated with
Alzheimer’s Risk
apoE4
genotype causes decreased transport of needed long chain fatty acids such as
omega-3s that cell membranes need for growth of neurons to keep up with
establishing new synaptic connections. The
presence of the apoE4, which is the major genetic risk factor for
Alzheimer’s disease, may require higher daily intake of omega-3 fatty acids to
achieve adequate cell membrane levels that are associated with disease
protection.
The above
issue is why a cell omega-3 fatty acid test should be used to determine cell
membrane levels rather than simply using a certain dietary level particularly
in the 15% (1 in 6 adults) of the population with the apoE4 gene variant.
Intake of trans-FAs
(hydrogenated oils and fats in processed food) of 4.8g/day showed a 5-fold
higher relative risk to develop Alzheimer’s than subjects consuming
1.8g/day.
Grimm et al. Omega-3 fatty acids, lipids and apoE
lipidation in Alzheimer’s disease: a rationale for multi-nutrient dementia
prevention. Journal of Lipid
Research, ePub 2017.
Summary
The research
continues to expand on the risk of Alzheimer’s disease with modifiable
lifestyle factors such as diet and nutrient intake. While many factors are shown to have a
relationship to risk and their correction can be beneficial, no one factor
alone will generate a striking reduction.
However, when large groups of these factors are all examined and managed
together, the results can be striking as Dr. Bredesen has demonstrated.
The whole really has proven greater than simply the sum of the parts.
Banks Nutrition Center
We are proud
to be a certified Bredesen Protocol provider.
We are available to help anyone who is concerned about their risk of
developing the disease or those who have begun to notice cognitive difficulty.
The Bredesen
Protocol
Preventing
& Treating Alzheimer’s Disease
Dr. Scott Banks, D.C., M.S. - Clinical Nutritionist
Event Date: Saturday, June 10th 2017
Time: 11:00AM to 1:00PM
Banks Nutrition Center
Location: 200 Golden Oak Court, Suite 100
Reflections ll Building
Virginia Beach VA 23452
Office Phone Number: 757-456-5053
This is a free educational event to the public & seating
is limited.
If you would like to join us, please call our office to
reserve your seat.
