Why Is Exercise an Important Part of the Bredesen Protocol™?

Exercise is largely the modern day substitute for work/survival associated with intense physical activity.  This activity was not only essential for survival providing access to food and other essential resources but also has been important in optimizing physiologic functioning essential to survival.

Physical activity activates the expression of “neurotrophic factors” in the brain.  Most noted of this family of signaling factors is brain derived neurotrophic factor, or BDNF.  Neurotrophic is defined by the two words it is derived from.  Neuro refers to nervous system cells including brain neurons. Trophic refers to growth and function stimulation.  Neurotrophism is an ongoing process needed to maintain brain cell health and function.

A recent study randomized 95 adults to an exercise training group, a cognitive training group, a combined exercise and cognitive training group and a control group who did not participate in either training.  Exercise training produced significant memory improvements as did the cognitive training compared to the controls.  The combined exercise and cognitive training group improved memory function to an even greater extent than either the exercise alone or cognitive training alone groups.

The images to the left show differences in brain activity on functional MRIs in subjects regularly exercising versus those who are sedentary.  Exercise induces stimulus to the brain to increase activity and synaptic formation, the formation of connections that allow neurons to communicate with each other.  These increased connections translate to higher levels of function such as memory processing.

The effect of exercise correlated with increased BDNF levels.  The researchers concluded that both cognitive training and exercise training improve memory function.  Combining the two has an even greater effect which appears to be the result of stimulating the neurotrophic factor BDNF.

The study relates to important points in the Bredesen Protocol™ for Alzheimer’s.  The protocol derived its success from the fact that it combines multiple treatments that have synergistic effects on brain restoration.  This is in sharp contrast to the typical drug treatments that focus on one mechanism resulting in no significant effect on the disease outcome.  The disease is multifactorial in origin, and treatment needs to be approached similarly.

The second point relevant to the Bredesen Protocol™ is that the disease has to be approached from two different areas.  The first is to find and treat the factors that drive the disease.  These are diverse and are addressed in the extensive testing that precedes treatment.  Once the factors that are responsible for injuring the brain are corrected, brain volume and function must be rebuilt using a broad program of neurofeedback, cognitive training, exercise and sleep restoration.

There is a tendency to question if daily exercise is essential.  Our ancestors of long ago were thought to be physically active in pursuit of food and other survival essentials for 12 or more hours daily.  While modern humans are more than 99% genetically identical to these ancestors and therefore share their same activity dependent physiology, our physical activity levels have diminished to only a fraction of our predecessors.  This has not been without serious health impacts including on brain health.

Attention to lifelong exercise is ideal.  However, if that has not been the case, properly managing exercise once brain dysfunction and disease have developed can help in restoring function.

Heisz et al.  The Effects of Physical Exercise and Cognitive Training on Memory and Neurotrophic Factors .  Journal of Cognitive Neuroscience, 2017:29;1895-1907.

If We Had This Drug, I Would Be on It

One of the largest studies on the reduction of chronic disease risk and mortality was recently published in The Lancet.  The study looked at the use of a particular treatment and the reduction of cardiovascular disease risk, stroke risk, as well as the risks of cardiovascular, non-cardiovascular and overall mortality.  The study was very comprehensive involving 135,335 individuals aged 35 to 70 years without cardiovascular disease from 613 communities in 18 low-income, middle-income, and high-income countries in seven geographical regions: North America and Europe, South America, The Middle East, South Asia, China, Southeast Asia, and Africa.

The results shown to the left were fairly striking with the treatment reducing the risks uniformly for all of the followed measures.  The vertical black line is the risk in the non-treatment group.  That is arbitrarily called “1” in a comparative study.

The graphic shows the risk reductions circled in red compared to those not taking the treatment regularly.  The red line shows the risk reduction to 0.7 which means a 30% reduction.  For cardiovascular events (CV disease) the reductions were all about 20%.  The mortality reductions were more dramatic, all being more than 30%.

The conclusion is that this treatment resulted in broad reductions in disease rates and deaths for the leading cause in developed and less developed countries.  The results occurred regardless of age, income status or country of residence.

Participation in this treatment would not take much persuasion if this drug existed, was widely available and relatively inexpensive.  While it meets all of those criteria, it has been and continues to be a hard sell to the population at large.  This is because the “drug” used in the study was actually “more than 3 servings per day of fruits, vegetables and legumes”. 

To give some perspective on these results, the results of similar clinical trials using statin drugs on total cardiovascular mortality have found risk reductions varying between 0 and 12%.  Seems like one could do twice as much just by eating enough fruits and vegetables daily.

The irony of all of this is that virtually every guideline out there supports this “therapy”, yet the minority of the population follow this in practice.  The breakdown seems to occur for many reasons.  Medical practice has become largely “this drug for that problem” with insufficient time spent or emphasis on implementing this very effective prevention.  This is driven by time restraints in patient care, patients preferring a pill over lifestyle change, and intense pharmaceutical advertising biasing opinions.

The bottom line is that you can’t fight data and in this case, it is convincing.  We are in the era of chronic lifestyle related disease and the biggest piece of lifestyle appears to be diet.

Chronic Inflammation as a Risk Factor for Alzheimer’s Disease

Acute or short-term inflammation is a protective response that occurs in injury or infection to help the body defend itself and begin repair.  It is one of the tools the immune system uses to attack whatever is injuring us.  It is, however, a nonselective response taking a toll on us as well. While this is OK when fighting a virus for a week, it causes important damage to the body if continued over very long periods of time.

Chronic inflammation is involved in virtually all chronic degenerative disease.  It has long been established as an important mechanism of degenerative brain disease, especially Alzheimer’s disease.  Over 5400 studies discussing both “Alzheimer’s” and “Inflammation” appear in a search of PubMed, the search engine of the National Library of Medicine.

While the data linking chronic inflammation to Alzheimer’s disease has been growing, one of the strongest links has recently been found.  The study examined the presence of midlife inflammatory markers and the presence of one of the important diagnostic indicators of Alzheimer’s disease, loss of volume or physical size in key brain areas involved in memory processing and storage.

The study population involved 1633 subjects with a mean age of 53 years. Two- thirds were women reflecting the female predominance seen in the disease. Five inflammatory markers were used to create an "inflammatory composite score". Volumetric MRI scans which accurately digitize the volume of each brain area were used to compare brain volume losses.

The images show the loss of volume in the key memory areas typical of Alzheimer’s disease.  The gray areas are areas of brain cells, while the black is cerebrospinal fluid that fills empty areas. The image on the left shows the loss of volume in the hippocampus (pink area in green circle) and temporal lobe (red circle), key areas in memory function.  It also shows increased volume of CSF fluid in the ventricles (black area in the white circle) which results from gray matter/brain cell loss.

Follow-up testing was done 24 years later. The results of the study were striking.  For every 1 standard deviation higher inflammatory composite score at midlife, there was a 110 mm³ loss in hippocampal volume, and 532 mm³ loss in the total region where Alzheimer’s affects the brain. There was also a 1788 mm³ increase in the ventricle volume representing cell loss at the center of the brain.

In addition to the brain volume changes correlating to level of midlife inflammation the researchers also correlated changes in episodic memory which is the memory of events including when, where, what and other details.  Episodic memory decline paralleled with brain volume loss connecting loss of memory function with brain volume loss driven by chronic inflammation.

There were also trends for the correlations being stronger in whites and in those of younger age at the beginning of the study.  The latter suggests that the longer inflammation has to work on the brain, the more damage it will do by the typical age of onset of Alzheimer’s disease.

A major emphasis of the Bredesen or ReCode Protocol for the treatment of Alzheimer’s is measuring inflammatory markers and using intense treatment efforts to reduce them.  Of course, the best time to address inflammation would be in prevention but as Dr. Bredesen has shown, it is an important piece of reversing early stages of the disease itself if coordinated with all other contributing disease mechanisms.

Walker et al.  Midlife systemic inflammatory markers are associated with late-life brain volume: The ARIC study.   Neurology, 2017 ePub

New Research Findings on Alzheimer’s Disease

Omega-3 fatty acids

Neurons or brain cells contain high amounts of omega-3 fatty acids particularly DHA.  This fatty acid plays several important roles in brain health including controlling inflammation (a known driver of neurodegeneration), influencing brain blood flow, helping lower brain deposition of the toxic protein β-amyloid and maintaining brain volume.

How Much Omega-3 FAs are Enough?

There is broad agreement that the omega-3 FAs in our diet have declined progressively.  Our ancient hunter/gather ancestors were estimated to consume 12-15 grams each day, while the current intake is 0.5-1.0 grams.  As the importance of these FAs to brain health are appreciated, a question becomes how much is adequate supplementation to restore brain health?  Two studies have addressed this question recently.

While it would be ideal to measure these FAs in brain cells directly, this is not possible.  Typically, the levels in red blood cells are measured and thought to closely reflect brain cell levels.  The first study compared SPECT scans which show brain perfusion or blood delivery to different brain areas compared to the red blood cell levels of omega-3 FAs.(1)  Higher red blood cell omega-3 levels correlated with higher profusion of several brain areas involved in cognitive processing. 

The study went a step further also correlating the omega-3 levels in red blood cells to neuropsychological testing.  Higher red blood cell levels of omega-3 FAs correlated with better scores on measures of depressive tendencies.  This is important as depressive tendencies both are a risk factors for Alzheimer’s, and they are also caused by the disease itself.

Another recent study also compared red blood cell omega-3 FA content in subjects with minor cognitive impairment (MCI) or Pre-Alzheimer’s disease to similar aged cognitively normal individuals.(3)  The MCI group had lower levels of total omega-3 FAS and particularly of DHA.  The researchers concluded that the lower omega-3 FA levels might be predictive of the development of MCI or Pre-Alzheimer’s given this relationship.

While multiple studies have found that higher levels of omega-3 FAs correlate with improved brain function and cognition, perhaps the most striking finding has been that omega-3 FA levels directly correlate with the loss of brain volume associated with Alzheimer’s disease.  Many of the pathological changes in the brain that are associated with Alzheimer’s disease such as the build-up of the toxic protein β-amyloid show up many years before cognitive function declines resulting in the symptoms such as memory loss.  The one finding that is the exception to this is brain volume.  Symptoms typically correlate with the loss of brain volume as seen on MRI examination.

Two studies have looked at omega-3 FA levels in older adults compared to brain volume loss.(2, 4)  In a study of 1100 postmenopausal women it was found that for each 1 standard deviation higher of red blood cell omega-3 FA levels, the key brain memory area called the hippocampus was 50 mm³ greater. Women in the lowest 20% of omega-3 levels had hippocampal volumes 159 mm³ smaller than those in the highest 20% of the group.

So, how much omega-3 FA intake is enough?  This is best determined by a simple test measuring red blood cell levels.   The data indicates that the omega-3 FAs should account for >10% of the total red blood cell fatty acid levels.  Because of variations of absorption of fatty acids in the digestive tract and transport into cell membranes, different persons will require different supplemental amounts.

The process should begin with a red blood cell omega-3 test.  A targeted level of supplementation is started, and the test is redone in about 4 months.  Supplementation levels are then adjusted from there to obtain and maintain the >10% level.

An important fact not to get lost here is that the best time to give attention to omega-3 FA levels is prior to the development of the disease as it appears to be preventative.  However, even when symptoms have developed optimizing levels of these important fatty acids is an essential part of treatment.

1)     Amen et al.  QUANTITATIVE ERYTHROCYTES OMEGA-3 EPA AND DHA LEVELS ARE RELATED TO HIGHER REGIONAL CEREBRAL BLOOD FLOW ON BRAIN SPECT.  Journal of Alzheimer’s Disease, 2017.

2)     Tan et al.  RED BLOOD CELL OMEGA-3 FATTY ACID LEVELS AND MARKERS OF ACCELERATED BRAIN AGING.

3)     Yuan et al.  THE ERYTHROCYTE FATTY ACID PROFILE AND COGNITIVE FUNCTION IN OLD CHINESE ADULTS.  Nutrients, 2016;8:385.

4)     Pottala et al.  HIGHER RBC EPA AND DHA CORRESPONDS WITH LARGER TOTAL BRAIN AND HIPPOCAMPAL VOLUMES: WHIMS-MRI STUDY.  Neurology, 2014;82:435-442.

Having a “Cognoscopy”

Most of us know what a colonoscopy or an endoscopy is but are probably unfamiliar with what a “cognoscopy” is.  Just as a colonoscopy looks at the colon as a preventative procedure against more advanced colon cancer, cognoscopy refers to a battery of tests that look at the status of and the factors that may cause cognitive decline.  The term was coined by Dale Bredesen, MD, the developer of the only treatment protocol to have shown success with cognitive decline.  While most appreciate having a colonoscopy by age 50, few appreciate the importance of cognoscopy.

The value of cognoscopy is that it looks at broad groups of risk factors that have been associated with the risk of cognitive decline and Alzheimer’s.  The importance of this lies in two areas.  The first is that while colon cancer causes just over 50,000 deaths in the U.S. each year, Alzheimer’s causes 500,000 in just the 75 year-old or older population, or ten times more than colon cancer across all age groups.  Alzheimer’s is now the 3^rd leading cause of death in seniors.  While all other of the top ten causes of death have declined over the past 14 years, Alzheimer’s deaths have risen dramatically.

The second concern that should heighten the importance of cognoscopy is that an innovative new protocol for prevention and treatment, the Bredesen protocol, is most effective early in the disease process.  By the time the disease is well established and diagnosed the success of treatment is diminished.  Beginning early is paramount and ideally the changes that may be identified by the cognoscopy should be managed before symptoms begin.

Our best defense against what many neuroscientists have called our greatest impending health crisis is to get ahead of the process.  “Cognoscopy” isolates the variables that drive the disease leading to a program of correction while there is still time.  It may be the most important test anyone could have after the age of 50 years.

More On apoE4 and Alzheimer's Disease Risk

In a previous post (apoE4and Genetic Mediated Risk of Alzheimer’s blog) we talked about apoE and the various forms such as apoE3 and apoE4 that are genetically determined.  ApoE is an apo protein that does several tasks such as carry cholesterol around the body.  The important task regarding Alzheimer’s Disease risk is that it is also used to remove beta amyloid (β amyloid), the abnormal protein that causes the brain degeneration in Alzheimer’s, from the brain.  The apoE4 variant does not work well in this capacity to remove this toxic protein from the brain.

An important concept is that the brain is always making some beta amyloid.  The amount it makes is dependent on the brain’s “environment”.  When the brain has low energy, is under toxic stress or has some other “environmental challenge,” it produces more beta amyloid which causes neurons to lose connections with other cells and eventually to kill some brain cells also.  This is referred to as “programed downsizing” during times of some sort of stressor.  When the brain’s environment improves, the β amyloid is removed and the brain begins to establish more connections, “programed learning”.

The diagram to the right shows a healthy brain environment.  The brain makes very little β amyloid in this state and what it makes it removes efficiently.  The large projection from the neuron is an axon used to connect to another neuron.  Along the axon there are many smaller connections called dendrites which connect the neuron to a large network of other cells.

A single neuron can establish up to about 200 connections with other neurons when in a healthy environment.  This complexity of how the human brain is “wired” is understood appreciating that there are 80 billion neurons with up to 200 connections each.  This collection of 80 billion x 200 potential connections allows all of the complex tasks the brain does including the formation and maintenance of memories.

When the brain environment is “stressed”, β amyloid (yellow structures) is produced causing this programed downsizing by removing dendrites and thus connections to other cells which results in loss of some functions.

Eventually with continued β amyloid build-up neurons themselves will become injured and die.  At this point, significant progression in the disease occurs. 

The identified factors that create the “stressed brain environment” include factors such as chronic inflammation, insulin resistance/diabetes, low hormone levels, chronic psychosocial stress and many others.  Some of the most important ones are reviewed in a previous post. (Lifestyle Factors and Alzheimer’s/Dementia Risk) 

Another factor in a stressed brain environment is the apoE4 variant.  One of the important jobs of apoE is it is 1 of the 3 important mechanisms the brain uses to remove β amyloid.  Basically, the build-up of β amyloid in the brain is the combined result of the stressors that cause excessive production and the efficiency of the removal.  ApoE4 is impaired in its ability to remove β amyloid so it importantly increases disease risk.

The other two mechanisms of removing β amyloid are through insulin action and by a white blood cell called a macrophage.  The ability of macrophages to remove β amyloid is dependent on the cell membrane content of omega-3 fatty acids making careful attention to their intake important.  Insulin resistance/diabetes hits both sides of the excessive production/removal balance.  It causes excessive β amyloid production and impairs the ability to remove it efficiently.

The important take away about apoE is two-fold. The first part is to know what one’s genetic type is which can be obtained easily by genetic testing.  The second part is to optimize lifestyle to carefully limit β amyloid production given the impaired ability the apoE4 genotype creates in removing it. 

Not everyone with apoE4 will develop the disease as they may have a protective lifestyle balance.  Many people without the apoE4 variant will still develop the disease as bad lifestyle/environment can overwhelm the balance of β amyloid production/removal.  Approximately 1 in 3 adults have either one or two copies of the apoE4 gene and therefore are at increased risk of Alzheimer’s.

While we do not control the genetic cards we are dealt, we do control the lifestyle environment we put our system in.

Lifestyle Factors and Alzheimer’s/Dementia Risk

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 10^th 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.

www.BanksNutrition.com