Reversing Alzheimer’s and Preventing Cognitive Decline: Seven Steps You Can Take Today

Alzheimer’s disease is a devastating condition for both patients and their families. Unfortunately, Alzheimer’s disease (AD) is also on the rise globally. Effective treatment of AD has been of growing concern within the medical community because its prevalence continues to spread. The fact of the matter is that Alzheimer’s treatment demands a different approach.

While our treatments of many other chronic diseases ( heart disease, diabetes, cancer) have improved over the years, effective Alzheimer’s treatments continue to remain incomplete and disappointing.

Alzheimer’s disease not only impacts patients’ health, but it is physically, emotionally, and financially taxing on their families as well. It is estimated that AD will directly impact over 15% of the US population, meaning its indirect effect on families and caretakers is widespread and includes hundreds of millions of people.

Unfortunately, as a society, we have come to view cognitive decline, a precursor to Alzheimer’s disease, as an accepted sign of aging.

However, this is a myth that needs to be immediately dispelled. The types of cognitive decline associated with AD are NOT normal signs of aging.

Still, there is good news when it comes to Alzheimer’s disease. New methods have shown promise in completely stopping and even reversing cognitive decline in patients.

Let’s look more deeply into these methods and uncover ways you can help yourself or your loved ones who are suffering from this devastating disease.

Today, there is more hope than ever before for those touched by Alzheimer’s.

Alzheimer’s Reaches Epidemic Proportions

According to the World Alzheimer Report 2016, approximately 47 million people globally live with dementia, and estimates for 2050 are projected to be more than 131 million. In fact, Alzheimer’s disease (AD) is now considered the third leading cause of death in the United States, just behind cardiovascular disease and cancer.

Women are at the heart of this epidemic. About 65% of all those who develop AD are women, and 60% of all caretakers of those affected by AD are women. Women are now more likely to develop AD than breast cancer. Many believe this is because women live longer than men, but this reasoning still does not explain or justify why this condition is on the rise. Of significance is that only 5% of Alzheimer’s cases are familial, i.e., having a genetic basis that causes early onset Alzheimer’s. The rest are caused by lifestyle factors that are influenced by many variables over which patients have a significant degree of choice and control.

Nonetheless, the question remains: Why is Alzheimer’s worsening, and what can be changed in how we approach the treatment of such a deadly and heartbreaking disease?

Other treatments of chronic illnesses such as cardiovascular disease, HIV, and cancer have improved because of the combination therapies that have been applied, and yet a majority of AD treatment has been focused primarily on monotherapeutic drug treatments. It is a startling fact that neurodegenerative diseases have not benefitted as other diseases have from advances in modern medicine. Only through tackling a disease like Alzheimer’s with multiple therapies can we find a successful approach to reducing the growing global impact it is having on our society.

Research has found that AD involves extensive networks of molecular interactions, which means the disease demands a network-based, multi-system treatment approach. The key issue in understanding Alzheimer’s is that it is not a single disease; the different biochemical imbalances involved require different treatments. There is no single drug that will cure Alzheimer’s, and nor will there ever be one. Present Alzheimer’s drug treatments make only slight differences to symptoms but do little to address disease progression.

At the forefront of this functional medicine approach to AD is Dr. Dale Bredesen and his team from the Buck Institute for Research on Aging. Through careful examination of the pathogenesis of Alzheimer’s, Dr. Bredesen and his team have found promising results. They have developed a multiple modality approach to achieving what they call metabolic enhancement for neurodegeneration (MEND), now referred to as Reversal of Cognitive Decline or ReCODE.

Through the approach Dr. Bredesen has developed, patients have been able to dramatically improve cognitive function, achieve reversal of symptoms, and in some cases, return to work. The ReCODE program includes lifestyle interventions, therapeutic diets, and targeted nutrients.

Before we dive into Dr. Bredesen’s program, it is important that we understand the pathogenesis of AD and its six subtypes. Let’s take a closer look at this disease, how it presents itself, how it develops, and what can be done to prevent it.

The Development of Alzheimer’s

The reason a multifaceted approach is needed for the treatment of Alzheimer’s is because its cause is not due to any single factor. Many metabolic processes are at play. In fact, there are six different subtypes of AD, distinguished by the different metabolic abnormalities that underlie the root causes of each form of this condition.

An individual usually develops Alzheimer’s disease after the age of 65. Symptoms begin showing as general memory loss and eventually progress to further impact daily life. The 10 warning signs and symptoms of Alzheimer’s disease versus normal signs of aging are listed below.

Alzheimer’s disease Symptoms Signs of Normal Aging
Memory loss that disrupts daily life, especially forgetting newly learned information Forgetting newly learned information such as appointments or names but being able to recall them later
Having difficulty solving everyday problems such as paying billsMaking occasional errors but none that are significant or out of the ordinary
Struggling to complete familiar tasks such as driving home or to workNeeding help setting up new equipment or electronics
Losing track of dates, seasons, or timeTemporarily forgetting the day but having the ability to recall it later
Difficulty judging distance, spatial relationships, and contrastWorsening vision caused by cataracts
Trouble recalling words for things, following conversations, and speakingOccasionally having difficulty finding the preferred word while not forgetting names of items
Misplacing items and not being able to retrace stepsBeing able to remember steps to find misplaced items
Poor judgement or decision-making; inability to multitask Occasionally making poor decisions, but  rarely with major negative consequences
Social withdrawalPreferring to socialize a bit less
Changes in personality and moodBecoming irritated when things are not done a particular and preferred way.

Click here for an Alzheimer’s Questionnaire.

Signs and symptoms of AD are not normal signs of aging. If you or someone you love is experiencing any of these symptoms, it is important to make an appointment with your functional medicine doctor as soon as possible because AD worsens over time.

AD is a progressive disease and although there is no cure, Dr. Bredesen’s protocol has been able to slow and reverse cognitive decline. Remember, the earlier AD is caught, the easier it is to successfully treat the condition.

Once a person has noticeable symptoms, they are in the later stages of cognitive decline. AD has an initial “silent phase,” where brain degeneration is occurring but these changes are not detectable using objective tests. Patients may, however, notice slight memory and cognitive changes. See the image below.

Alzheimer’s disease (and dementia) does not begin suddenly.

Before AD develops, there is a noticeable slow decline in mental health. It has been estimated that the pathophysiology of the disease exists for approximately 20 years before any diagnosis is made. This means that many individuals have the beginnings of the disease without actually realizing it.

Preclinical begins with a subtle loss of neurons and a subjective sense of the brain’s mental processes not being as sharp as they once were.

Mild Cognitive Impairment is said to be present when a noticeable decline in mental functioning is noticed by others, and objective cognitive testing (performed simply by doing a mini-mental exam, computerized cognitive testing such as the CNS Vital Signs test, or a more sophisticated workup by a neuro-psychologist) is decreased. Activities of daily living have not yet been affected.

Dementia is said to occur when cognitive decline is sufficient to interfere with daily life. Objective testing such as PET scans and Neuroquant MRIs will show distinct patterns of brain changes such as cortical and hippocampal atrophy, reduced glucose uptake, and amyloid-beta-production.

Temporal Progression of Cognitive Impairment

What exactly is Alzheimer’s disease?

Simply put, Alzheimer’s has been observed to occur when the genes associated with the disease cause brain cells to become suicidal. The question that Dr. Bredesen asked was, “What are the fundamental processes and mechanisms that drive these genes to turn on and cause brain cells to die?”

Based on numerous studies, we now know that AD results from an imbalance in the destruction of neurons and synapses and the building up and maintenance of synapses and neurons. It has been observed that a molecule known as amyloid-beta accumulates in higher than normal concentrations in the brain, which causes the synapses, along with the neurons essential for memory, to die.

Where does amyloid-beta come from? It is derived from the amyloid precursor protein (APP), of which amyloid-beta is but a small portion. The APP, once produced by neurons, is cut by molecular scissors called proteases, which can cut at any of the three spots along the APP or at one distinct site. If the APP is cut at three particular sites, the four peptides produced from this action underlie the process of the synaptic loss and neuronal death that characterize AD. If, however, the APP is cut at just a single site, the two peptides that result cause just the opposite to occur; synaptic connections are maintained and neuron growth is nourished. These two peptides are referred to as the anti-Alzheimer’s peptides. See image below.

Alternative processing of, and signaling by, APP

Thus, the APP appears to act as a molecular switch that mediates plasticity-related processes. In summary, in order to reduce your risk of AD, you have to maintain all the necessary lifestyle practices and therapies that induce the two brain-affirming, anti-AD peptides and reduce all the factors that induce the production of the four pro-AD-inducing peptides. How exactly to achieve this, forms the basis of Dr. Bredesen’s ReCODE program.

AD is similar to other chronic illnesses in that there is an age-associated imbalance between the building up of cells that mediate neural plasticity and the destruction of cells. In AD, this occurs at the level of neuronal synapses, called synaptoblastic (building up of synapses), as opposed to synaptoclastic (destruction of synapses) activity. These intricate processes happen over time, in reinforcing cycles.

Six Subtypes of Alzheimer’s disease

Understanding the different Alzheimer’s subtypes is also critical for creating the best treatment plan for each patient.

There are numerous metabolic processes involved in contributing to AD, with six different subtypes that have been identified by Dr. Bredesen. These six subtypes are based on three papers by Dr. Bredesen: The first paper, in 2014, describes the initial contributions to his protocol (first called MEND), the second paper in 2016 outlines 10 case studies, and the third paper, also in 2016, describes neurodegeneration due to biotoxin exposure.

These subtypes are not widely used in diagnostic workups and clinical protocols at this time, but understanding the differences is essential to creating a comprehensive treatment plan. The six subtypes of Alzheimer’s disease are as follows:

Subtype 1 (inflammatory or “hot”) Alzheimer’s: Patients with this form of AD have predominantly inflammatory symptoms. These proinflammatory factors include cytokines, chemokines, acute-phase reactants, and other inflammation-causing mediators.

Patients with subtype 1 AD also have increased levels of c-reactive protein, high interleukin-6, and a low albumin-to-globulin ratio. The microglia and activated astroglia (brain structures) are also inflamed.

There is also an antagonism between the sirtuinT1 enzyme (anti-inflammatory) and NFkB (the nuclear factor k-light-chain enhancer of activated B cells [proinflammatory]); when NFkB inflammation is activated and SirT1 is suppressed, it can alter gene transcription and turn on gamma-secretase and beta-secretase. Gamma-secretase cleaves to the APP and contributes to synaptoclastic destructive processes within the brain.

The inflammation in subtype 1 primarily involves the innate immune system, and usually (but not always), there is systemic inflammation. Onset of this subtype typically occurs in an individual’s 70s or later.

Subtype 1.5 (glycotoxic or “sweet”) Alzheimer’s: This subtype is the in-between of subtypes 1 and 2 because it involves both inflammatory perpetrators and atrophic processes. Glucose regulation is impaired, resulting in insulin resistance and inflammation due to hyperglycemia (increased blood glucose). This glucose dysfunction also disrupts hormone-signaling and trophic factors (molecules that allow neurons to maintain and create neighboring connections).

Subtype 2 (atrophic, non-inflammatory, or “cold”) Alzheimer’s: Patients with subtype 2 AD have atrophic symptoms, meaning there is degeneration and dysfunction of neurological functions due to the insufficiency of certain nutritional and metabolic factors. Even though this underlying cause is different from inflammation, it still results in the same disease.

Similar to subtype 1, subtype 2 causes the APP to create amyloid plaques. Subtype 2 AD is associated with declining trophic factors, such as nerve growth, brain-derived neurotrophic factors (BDNF), testosterone, estradiol, vitamin D, thyroid hormone function, and insulin levels.

All of these declining trophic factors cause your brain to stop synaptogenesis (creation of new synapses), which is why learning new things becomes more difficult and worsens over time.

Subtype 3 (toxic or “vile”) Alzheimer’s: Subtype 3 is caused by toxin exposures, most commonly inhaled toxins (such as mold mycotoxins), and is sometimes called inhalational Alzheimer’s disease (IAD). One 2014 study showed fungal proteins in the brains of Alzheimer’s patients, and another study in 2015 showed fungal infections in the brains of Alzheimer’s patients. Fungal DNA and proteins were detected in the brain tissue from AD patients, but not in controls. Fungal particles could also be detected in the neurons of the same AD patients. Herpes simplex type 1 (HSV-1) and chlamydia pneumoniae have also been associated with amyloid protein production in AD.

Many patients with subtype 3 AD have markers of chronic inflammatory response syndrome (CIRS) but do not fit the official criteria for a CIRS diagnosis. Dr. Bredesen says that those with IAD will have lab results similar to those of CIRS patients, but their symptoms are mostly Alzheimer’s-like dementia.

Typically, patients with this form of AD have high levels of the complement component C4a and the transforming growth factor beta-1 (TGF-b1), both of which are specific inflammatory cytokines, as well as high levels of matrix metallopeptidase 9 (MMP9), an enzyme involved in the cell membrane penetration of inflammation. Patients also have decreased levels of the melanocyte-stimulating hormone (MSH), the vascular endothelial growth factor (VEGF), and the antidiuretic hormone (ADH). Usually, there are other abnormalities present such as high levels of cortisol and low levels of the adrenocorticotropic hormone (ACTH) and the antidiuretic hormone (ADH).

Symptoms of subtype 3 AD are similar to those of the other subtypes in that they include memory loss and difficulty with word recall; however, patients may also report having a metallic taste in their mouth and an increased sensitivity to smell. These patients rarely have the respiratory complaints, chronic fatigue, muscle pain, or other symptoms usually associated with CIRS.

Subtype 4 (vascular) Alzheimer’s: Alzheimer’s development in subtype 4 patients is a protective response to vascular insufficiency and results in a triggered amyloid response.

Subtype 5 (traumatic) Alzheimer’s: This subtype is characterized by head trauma, and these patients typically have significant personality changes. Not all head trauma patients will develop AD. One major study showed an 2.3 times increased risk of developing AD in older adults with a history of moderate traumatic brain injury than seniors with no history of head injury. Those with a history of severe traumatic brain injury had a 4.5 times greater risk of developing AD. Traumatic brain injury changes brain chemistry by inducing beta-amyloid and tau proteins, the hallmark proteins linked to AD. Traumatic brain injury may be more likely to cause dementia in individuals who have either one or two of the APOE-e4 genes. There are no studies linking mild brain injury or concussion to the development of AD.

Genetics and Alzheimer’s Disease

It is important to note subtypes 1, 1.5, and 2 are all associated with the ApoE4 gene mutation. Although 95% of all Alzheimer’s cases are not caused by genetics, genetic testing is essential to determine if there is a propensity for these forms of Alzheimer’s. In fact, what is called familial Alzheimer’s is very rare, appears to be clustered in families, and presents earlier in life. That said, two-thirds of AD patients carry one or two copies of the ApoE4 gene.

Individuals who are ApoE4-positive with one copy of the gene (approximately 75 million Americans) have a 30% lifetime risk of developing AD. Those with two copies of the gene (approximately 7 million Americans) face a 50% lifetime risk of developing AD.

Interestingly, scientists have found that while the ApoE4 gene increases the risk of subtypes 1 and 2, it decreases a person’s risk for developing subtype 3. This is believed to be due to the protective nature of ApoE4, which can fight off the microbes that cause subtype 3 AD. Ultimately, ApoE4 is thought to be an advantage in your youth but can contribute to chronic illnesses as you age.

You can be tested for ApoE4 with your functional medicine doctor. This is a good idea because if you have the ApoE4 gene mutation, there are certain measures you can take to decrease the chances of developing Alzheimer’s. The website is an excellent resource for individuals with one or two copies of this gene.

One fascinating behavior a person with the ApoE4 gene can implement in order to favorably influence the outcome is 12-hour fasting. The ApoE4 gene helps you survive famine, and so it makes sense that intermittent fasting can help those with the gene avoid Alzheimer’s. The ApoE4 allows your body to use fat more efficiently and go longer without eating. This means if you find out through testing you have this gene, fasting can be used as a tool to have your body switch to burning ketones for energy over glucose, which is believed to aid in preventing AD.

Even if you do have the APoE4 gene, you can still prevent Alzheimer’s disease from developing, but you have to be proactive, educate yourself, and implement as many of the lifestyle factors as you possibly can. Let’s look at how to do that.

What Do All Forms of Alzheimer’s Disease Have in Common?

There are 36 mechanisms that Dr. Bredesen has identified as contributing to Alzheimer’s, but mitochondrial dysfunction is at the core of all of these.

Your mitochondria are the powerhouses of your cells, creating the energy molecules (ATP) every cell of your body needs to function. Additionally, free radicals (damaging molecules produced as byproducts of normal metabolism but enhanced by toxic exposures, genetic detoxification, and nutritional deficiencies) tend to be created in your mitochondria. When you have a higher incidence of free radicals in your cells, your mitochondria suffer damage and cannot produce adequate amounts of ATP, resulting particularly in neuronal cell death.

Through his research, Dr. Bredesen found that the APP makes amyloid in response to your cells being under attack by free radicals and toxic substances. Your body’s trophic support may also be decreased. Together, both low trophic factors and increased amyloid levels contribute to cognitive decline.

The complexity behind the pathogenesis of Alzheimer’s disease is why a comprehensive, multivariable approach is necessary. With that in mind, Dr. Bredesen’s recommendations include addressing these 36 mechanisms:

  • Increasing mitochondrial function; mitochondria produce ATP, the necessary chemical responsible for the energy needed for nerve growth, health, and maintenance.
  • Increasing mitochondrial protection
  • Decreasing beta-amyloid production, the main component of amyloid plaques found in Alzheimer’s
  • Increasing beta-amyloid degradation
  • Decreasing beta-amyloid oligomerization, i.e., the creation of longer molecules of beta-amyloid
  • Increasing the brain-derived nerve factor (BDNF), a neuropeptide with growth effects on neurons
  • Increasing the nerve-growth factor (NGF), a neuropeptide involved in the growth and maintenance of neurons
  • Increasing the granulocyte-stimulating factor (G-CSF), a growth factor that has neuroprotective effects and that increases neuronal growth
  • Increasing the activity-dependent neuroprotective protein (ADNP), a protein essential to brain health and cognitive function
  • Decreasing p-tau; neurofibrillary tangles are aggregates of hyperphosphorylated tau proteins, which are primary markers of Alzheimer’s disease.
  • Decreasing homocysteine, a proinflammatory protein
  • Building synapses
  • Increasing beta-amyloid breakdown
  • Increasing the albumin/globulin (A/G) ratio, indicative of inflammatory AD
  • Decreasing inflammation
  • Inhibiting NF-kB, a protein complex that controls inflammatory cytokines
  • Increasing glutathione (GSH), a major antioxidant
  • Increasing antioxidants, which decrease neuroinflammation
  • Decreasing iron, a pro-inflammatory mineral
  • Increasing cerebral blood flow
  • Increasing acetylcholine, a neurotransmitter involved in memory
  • Increasing alpha-seven nicotinic acetylcholine receptors (α7), a critical link between neurodegeneration and AD
  • Increasing amyloid-beta transport
  • Increasing amyloid beta clearance
  • Decreasing the ApoE4 effect; this gene determines increased risk for AD, with the 4/4 gene having the highest risk
  • Increasing gamma-aminobutyric acid (GABA), a calming and neuroprotective neurotransmitter that downregulates glutamate, an excitatory neurotransmitter
  • Decreasing N-methyl-D-aspartate receptor activity (NMDA), a receptor that regulates the activity of glutamate, an important neurotransmitter in the brain involved in learning and memory
  • Optimizing hormones, especially estradiol, progesterone, testosterone, DHEA, and thyroid
  • Increasing vitamin D
  • Decreasing the pro-form of the neuron growth factor (pro-NGF), a protein expressed at higher levels in brains of AD patients
  • Decreasing caspase-6, the activity of which is associated with increased risk of AD
  • Decreasing the N-terminal fragment of the beta-amyloid precursor protein (N-APP)
  • Enhance detoxification
  • Increasing vascularization
  • Increase telomere length
  • Reduce toxic metals

Dr. Bredesen explains that these are like holes in a roof, which need to be individually addressed in order for a full recovery to be made.

It is important to realize that AD is a protective response to three major metabolic and toxic disturbances:

  1. Inflammation- be it infectious (viruses) or sterile (modified inflammatory proteins)
  2. The withdrawal of trophic support (e.g. nerve growth factor, estradiol, testosterone, vitamin D etc.)
  3. Exposure to toxins such as mercury, aluminum, mold mycotoxins.

Dr. Bredesen has identified a number of factors that induce the APP receptor to go in the right direction of trophic or building synapses and neuronal health. The APP responds to dozens of molecules that assist brain health and anti-Alzheimer’s protection. Our brains have 100 billion neurons, and each neuron has approximately 10,000 connections, called synapses. Synapses are critical for cognitive functioning, memory storage, decision-making, and neurotransmitter communication. One’s brain has nearly one quadrillion energy-demanding synapses to power and run efficiently with energy-producing raw materials. In short, the APP has to constantly assess if the incoming data is shifting the lever in the direction of neuronal building or in the direction of neuronal destruction.

The sum total of the way one lives one’s life minute-to-minute affects this highly complex algorithm shift in either one of two directions—towards brain protection and maintenance, or towards brain inflammation, destruction, and reduced neuronal death. It really does come down to choice. AD begins with the loss of function of the synapses, the loss of the synapses themselves, and eventually, the loss of brain cells themselves, leading to brain shrinkage that is visible on MRI scans.

When one is young, the ratio between neuronal growth and destruction is equally balanced between the two. As we age, the destructive (clastic) part of the process tends to dominate over the building (blastic) part of brain preservation. We must decide to do all we can do to downregulate any of the factors that induce inflammation and further clastic activity and upregulate anything we can that induces growth, blastic activity, and hence, neuronal plasticity.

The realization that multiple factors induce brain growth as well as brain destruction will explain why the single drug model of AD treatment has not borne any fruit. There is no single drug that can ever address the complexity of all the metabolic factors that contribute to brain health maintenance and optimization. Dr. Bredesen’s analogy is that of a roof with 36 holes in it. A roofer called in to fix only one hole where the rain is pouring in will never be able to stem the flood of water pouring in through the other 35 holes no matter how well he patches the one hole.

Robert M Cardiff, MD, Commissioner of the Food and Drugs Administration (FDA) concurs with this observation:

“Multimodal therapy approaches that combine interventions aimed at different aspects of disease are emerging as potential-and perhaps essential-ways to enhance clinical outcomes for patients with psychiatric and neurological disorders. Indeed, for most chronic diseases, multiple pathways are involved simultaneously, making it unlikely that a single treatment will prove sufficiently effective.”

From these insights it is important to realize that we do not get Alzheimer’s for no reason. There are many possible reasons and the doctors of the future will be trained to investigate and look for many if not most of these factors identified to date.

Dr. Bredesen’s ReCODE program aims to achieve the following:

  1. Optimize metabolic parameters to the maximum, not just simply normalize them.
  2. Address as many of the causative network components as necessary with the understanding that combination effects will be additive and cumulative and will create an effect that is more than the sum of the many single therapies.
  3. The more that patients are able to achieve in terms of their therapeutic input, the more likely it is that a certain threshold will be reached that will tip them over from a pathogenic process to a therapeutic benefit. This implies that a combination of therapies will be more than the sum of individual parts.
  4. A personalized approach is needed with a prioritization of therapeutic inputs, which needs to be computerized and analyzed according to the laboratory values affecting the plasticity networks.
  5. Repetitive application of therapeutics is necessary to optimize outcomes over time.
  6. The goal of therapy is to use a physiological approach with as much of an upstream causative approach that can possibly be implemented.

A Therapeutic System was developed by Dr. Bredesen

Therapeutic System (adapted from Bredesen, 2014 and cited by Ash, 2015)

The critical role of several factors in Alzheimer’s disease necessitates several therapeutic interventions. The required interventions seek to:

  • reduce inflammation
  • address autoimmunity
  • minimize insulin resistance
  • decrease amyloid-beta (Aβ)
  • reduce excess cortisol and the corticotropin-releasing factor (CRF).

In so doing:

  • the hypothalamic adrenal axis is supported
  • antioxidant function is optimized
  • blood glucose is balanced
  • acetylcholine synthesis is supported.

Interventions identified by Bredesen (2014) to achieve these aims include:

  • Diet optimization to minimize simple CHO, inflammation, and insulin resistance: Simple CHO, inflammation, and insulin resistance are minimized by providing patients with a choice of several low-glycemic, low-inflammatory, and low-grain diets.
  • Autophagy and ketogenesis enhancement: Autophagy and ketogenesis are enhanced by having the patient fast for 12 hours each night (including at least three hours before bedtime), thereby reducing insulin and Aβ levels.
  • Stress reduction: Stress is reduced by having the patient engage in personalized stress reduction activities (e.g., yoga, meditation, music, etc.) that target the stress axis, reduce cortisol, and equilibrate the CRF.
  • Sleep optimization: Sleep is optimized by having the patient follow a sleep regimen, including eight hours of sleep per night, the use of 0.5 mg melatonin and/or 500 mg of tryptophan if awakening, in addition to ruling out possible sleep apnea.
  • Exercise regimen: Patients are provided with an exercise regimen, including 30–60 minutes of physical exercise 4–6 days per week.
  • Brain training and stimulation: Patients are provided with BrainHQ or related brain-training software programs.
  • Homocysteine optimization: Homocysteine is optimized to <7 using methylcobalamin (Me-B12), methylfolate (MTHF), pyridoxal-5-phosphate (P5P), and, if necessary, trimethylglycine (TMG). Optimization of serum B12: Serum B12 is optimized to >500 using methylcobalamin (Me-B12).
  • Lowering c-reactive protein: Due to the critical role of inflammation in Alzheimer’s disease, c-reactive protein is lowered to <1 through the use of optimized hygiene and an anti-inflammatory diet that includes curcumin and fish oil (DHA/EPA).
  • Insulin optimization: Due to the role of inflammation in Alzheimer’s disease and the relationship it shares with type II diabetes, insulin levels are optimized to <7 (fasting) and hemoglobin A1c (HbA1c) to <5.5 through the use of an anti-inflammatory diet.
  • Hormone optimization: Hormones are optimized, including free T3, free T4, the thyroid-stimulating hormone (TSH), pregnenolone, progesterone, estradiol, testosterone, cortisol, and dehydroepiandrostenedione (DHEA).
  • Restoration and optimization of gastrointestinal health: Gastrointestinal health is restored, repaired, and optimized, including the use of prebiotics, probiotics, and avoidance of inflammation and autoimmunity.
  • Reduction of a-beta Levels: A-beta (Aβ) levels are reduced using curcumin and ashwagandha (an Ayurvedic adaptogenic herb).
  • Cognitive enhancement: Cognitive enhancement is achieved through the use of bacopa monniera (an Ayurvedic herb known for its cognitive enhancing properties) and magnesium threonate (MgT).
  • Optimization of vitamin D3: Vitamin D3 (25-OH-D3) levels are optimized to 50–100 ng/ml (US levels), using vitamins D3 and K2.
  • Nerve-growth factor optimization: The nerve-growth factor is increased using h. erinaceus or acetyl-l-carnitine.
  • Provision of synaptic structural components: Provide synaptic structural components using citicoline and docosahexaenoic acid (DHA).
  • Optimization of antioxidants: Optimize antioxidants using mixed tocopherols and tocotrienols, selenium (Se), blueberries, n-acetyl-cysteine (NAC), ascorbate, and a-lipoic acid.
  • Optimization of the zinc:copper (zn:cu) ratio: Optimize the zn:cu ratio based on values obtained.
  • Ensure nocturnal oxygenation: Ensure nocturnal oxygenation through treating or ruling out sleep apnea.
  • Optimize mitochondrial function: Optimize mitochondrial function through optimizing CoQ or ubiquinol, a-lipoic acid, pyrroloquinoline quinone (PQQ), n-acetylcysteine (NAC), N-acetyl-L-carnitine (ALCAR), selenium (Se), zinc (Zn), resveratrol, ascorbate, and thiamine.
  • Increase focus: Increase focus using pantothenic acid as required for acetylcholine synthesis.
  • Increase SirT1 function: Increase SirT1 function using resveratrol.
  • Exclude heavy metal toxicity: Evaluate mercury (Hg), lead (Pb), and cadmium (Cd) to confirm or exclude heavy metal toxicity; chelate if indicated to address the effects of heavy metals on the central nervous system.
  • Increase medium-chain triglyceride (MCT) oil effects: Use coconut oil or Axona.

According to Dr. Bredesen’s research and discussions, the effects of various targeted therapies may be additive, multiplicative, accumulative, and synergistic.

A functional medicine approach is the most effective way to implement these approaches.

7 Things You Can Do to Prevent Cognitive Decline Right Now

Here are some things you can do right now to work on your own personal cognitive health, using similar principles to those found in the Bredesen ReCODE Protocol.

1. You Must Get Quality Sleep

Getting seven to eight hours of quality sleep each night is critical to promoting cognitive function because during sleep is when your body removes metabolic waste from your body.

If you have sleep apnea, you must address it. Your brain is starved of oxygen when you have sleep apnea, and it directly impacts your cognitive abilities. Ask your doctor to refer you for a sleep study.

2. Implement Overnight Fasts

By putting your body in an overnight fast (12 hours at least), you induce ketogenesis (you also need a low-sugar and low-carb intake to promote this). When your body is in ketogenesis, your insulin levels are lowered. Additionally, amyloid-beta levels are reduced, which are a main contributor to the amyloid plaques found in Alzheimer’s patients. A low-sugar and low-carb diet makes overnight fasting surprisingly easy.

3. Reduce Carb and Sugar Intake

Diets with few carbs and little to no sugars are the best for reducing inflammation in the body, and they reduce your chances of developing insulin resistance. Additionally, low-sugar and low-carb diets have been linked to a decreased risk of developing Alzheimer’s disease.

4. Reduce Your Toxic Load

Reducing toxin exposure gives every bodily system a better chance at functioning properly, and your mitochondria and metabolic systems are no exception.

You can reduce your toxic load through having good air and water filters in your home. Additionally, avoid toxin-containing items such as:

  • Non-stick and aluminum pans
  • Harmful personal care products (you can check your items against the EWG Database)
  • Harsh cleaning products (opt for natural solutions)
  • Paints with volatile organic compounds (VOCs)
  • Metal dental fillings
  • Fish high in heavy metals
  • Plastics with BPA
  • Charred and fried meat (high-lipid peroxidation)

Remember, if your lab results are coming back similar to those of a CIRS patient, yet you are not having typical symptoms of CIRS, check for signs of Alzheimer’s and other indicators of toxin exposure due to building damage from mold and water (inflammagen exposures).

5. Add These Supplements

Dietary changes are at the heart of the Bredesen Protocol, and by adding certain supplements, you can protect your brain. Consider the following supplements because each has shown to promote healthy brain function.

  • Vitamin B12—methylcobalamin
  • Vitamin C – must be taken twice daily as it is water soluble and is excreted quickly
  • Vitamin E—mixed tocopherols
  • Turmeric—a lipophilic form is best
  • Vitamin D—measure your 25 OH Vitamin D levels to achieve the optimal dosage for you
  • DHA (found in fish and fish oil supplements)
  • Citicoline
  • Probiotics

6. Exercise Every Day

Having an exercise routine has been unequivocally linked to a reduction in cognitive decline. Studies have found that even a walk each day significantly slows the decline of Alzheimer patients.

I encourage you to get up and move at least once a day. Even a quick 15-minute high-intensity interval workout has been shown to be as effective as an hour-long workout.

7. Reduce Stress

Stress causes high levels of cortisol and CRF, which are both linked to Alzheimer’s. Add stress-reducing habits to your day. These can include quick meditations, yoga, listening to calming music, or taking walks.

Reversing Cognitive Decline Is Within Reach

We are living in an exciting time when it comes to Alzheimer’s treatments. Through a comprehensive approach to this illness, we may be able to slow down and even reverse most cases of Alzheimer’s.

While the Bredesen Protocol works to reverse cognitive decline, we can take the same science and apply it to our lives today to prevent Alzheimer’s from developing in the first place. We can even take these concepts one step further and optimize brain health to improve function overall.

Share this article with someone you know who would benefit from hearing about this monumental approach to a devastating disease. The future of Alzheimer’s treatment is bright.

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The End of Alzheimer’s. Dale Bredesen  Avery – An Imprint of Penguin Random House 375 Hudson Street New York, New York 10014, 2017