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.
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.