Alzheimer's Dementia Archives

My medical practice is located between the Sun Cities, the beautiful retirement communities on the North West side of the Phoenix Valley. Over the years my practice has grown with a predominantly large number of patients over 55 years old. It is a wonderfully diverse group of very dynamic and intelligent people. Yet, something that has bothered me for many years is the significant risk these patients have for dementia. One of the most disturbing parts of my job, over the 22 years of my practice, is to see these vibrant patients’ progress down the road to Alzheimer’s dementia.

To date, there have been over 400 failed clinical drug trials for the treatment of Alzheimer’s Dementia and only a few drugs that showed any mild success at slowing the progression of the dementia. The current medical literature estimates that 30% of these patients will die of Alzheimer’s type dementia. This statistic has played out in my practice until I started applying the principles of correct diet and lifestyle modification.

Four Stages of Dementia

There are four stages or phases of dementia that start 20 years before a person ever reaches the diagnosis of dementia. That is important, because this disease can be stopped in it’s tracks:

Phase 1 – asymptomatic – abnormal CSF and abnormal PET scans.
Phase 2 – Subjective cognitive changes (may last 10 years), symptoms without abnormal cognitive testing.
Phase 3 – MCI – (Mild cognitive impairment) – abnormal cognitive testing, normal activities of daily living (ADLs), 5-10% convert to dementia each year
Phase 4 – Final phase of Alzheimer’s disease, ADL’s affected, diagnosis made 20 years after initial biochemical changes.

I’ve been closely following Dr. Dale Bredesen and his protocols in treating and preventing dementia. To my delight, the following protocols have been very effective at delaying, preventing and actually reversing dementia in my patients.

So, to help you, I’ve written out my protocol (adapted from Dr. Bredesen’s protocol) for dementia treatment and prevention below.

Fat Burning

First, burning fat is crucial. The brain can use two fuels, glucose and fat, but it works better on fat. Alzheimer’s is associated with a decrease in glucose utilization. A three-pronged approach to begin burning fat includes:

Eating a low carbohydrate diet or carnivorous diet high in healthy fats
Fasting overnight for at least 12 hours
Exercising regularly, ideally for 30 minutes, 5 times weekly

Addressing Insulin Sensitivity

I cannot emphasize this enough. Controlling blood sugar and insulin excess is foundational. Abnormal insulin production dramatically effects the thyroid and all of the sex hormones. Restoring function of the pancreas through diet and the use of Berberine 500 mg twice daily. If you are diabetic, tight control of blood sugar and using appropriate medications that do not stimulate over production of insulin is essential.

Insulin resistance must be improved (lowering fasting insulin to < 5 ng/dL) and restoring the normal insulin sensitivity is key. This can take up to two years to improve with the correct diet. Insulin at the correct levels is a key growth factor for neurons.

Insulin sensitivity can be restored by the following:

The Ketogenic or Carnivorous diet.
Optimizing essential nutrients, such as Zinc 30-50mg daily
Exercising regularly
Reducing stress
Treating sleep apnea if present (see your doctor about this)
Taking a supplement such as berberine, cinnamon, alpha-lipoic acid, or chromium picolinate, if needed (Dr. Nally’s Ketoliving Multivitamin contains the alpha-lipoic acid needed and the additional trophic factors discussed below)

Health Support

Third, it is important to optimize all nutrient, hormone, and trophic (growth factor) support. This support means we can create resilience, optimize our immune systems, support our mitochondria, and begin to rebuild our brains’ synaptic networks.

Low levels of trophic factors (growth factors) such as vitamin B1 (thiamine), vitamin B12, vitamin D, testosterone, estrogen, and nerve growth factor are all associated with cognitive decline.

Other necessary nutrients for optimal cognitive function include vitamin C, vitamin E, vitamin K2, omega-3 fats, choline, and other neurotransmitter precursors, key metals such as zinc, magnesium, copper, and selenium.

Optimum hormone levels are critical for making and maintaining synapses. Optimal nutrition and lifestyle will lead to optimal hormone production for many of us. Ketones from the diet or used exogenously have been powerfully helpful.

However, other patients will need to support optimal brain function by achieving the healthiest levels of thyroid, pregnenolone, estradiol, progesterone, testosterone, DHEA, and cortisol. These are checked through your doctor and are levels that I monitor every 3-6 months with my patients.

Reducing Inflammation

Fourth, we want to optimize the way the body uses inflammation. It’s important to allow the body to increase inflammation when it’s actually necessary, but also to resolve inflammation when it’s no longer needed.

Dr. Nally emphasizes minimizing inflammation without a purpose, which is often referred to as “chronic inflammation.” Amyloids often associated with Alzheimer’s disease are part of our body’s inflammatory response.

Leaky gut is the most common cause of chronic inflammation. This can be caused by:

Stress
Alcohol
Excessive sugar intake
Processed foods
Aspirin and related anti-inflammatories
Soft drinks with the crappy sweeteners
Excessive use of Proton Pump Inhibitors (PPIs) (used to treat reflux or heartburn)
Other damaging agents

We need to know the status of our gut health.

Chronic inflammation with or without a leaky gut may also be caused by periodontitis, gingivitis from suboptimal dentition, or an infection of a root canal in your mouth.

In fact, chronic periodontitis, an inflammatory condition of the gums, may be a direct link to Alzheimer’s disease.

Other causes include chronic sinus infections, or ongoing infection with pathogens such as Borrelia, or metabolic syndrome (insulin resistance, high blood pressure, high triglycerides, and inflammation, often accompanied by obesity).

There are also cases of chronic inflammation due to ongoing exposure to air pollution or mold toxins. Determining the root cause of inflammation is just the first step.

Next, the inflammatory agent or cause should be removed. Once that’s resolved, preventing further inflammation is essential. Several excellent anti-inflammatory alternatives to drugs (NSAIDs) include curcumin, fish oil or krill oil (omega-3 fats), ginger, and cinnamon.

Treating Pathogens

Fifth, we must treat chronic pathogens. Chronic undiagnosed infection can be a contributing factor in cognitive decline. It needs to be identified and targeted. We all live with more than a thousand different species of microbes.

Even the brain may harbor bacteria, viruses, spiral bacteria, fungi, or parasites. Our brain’s protective response to these pathogens causes the very changes we call Alzheimer’s disease. The goal here is to reach and maintain a balance of these microbes.

Addressing Toxin Exposure

Sixth, we emphasize the need to identify and remove toxins. Metals such as mercury, organics like toluene and benzene, and biotoxins like mold toxins (mycotoxins) can lead directly or indirectly to cognitive decline.

Optimizing Sleep

Dr Nally’s Protocol necessitates ruling out sleep disorders and optimize sleep. The amount of oxygen saturation in our blood as we sleep can plummet, which affects our brain’s optimum functioning. Oxygen saturation can be a significant contributor to cognitive decline.

Thankfully, it’s also easily addressed. A dental device APAP or CPAP device can improve oxygen intake through the night. On the other hand, simply reducing inflammation or weight can improve many people’s oxygen saturation and cognition.

That’s why it’s necessary to have a personalized program implemented by a qualified practitioner based on individual lab and other testing results.

Identifying and targeting the various contributing factors, even down to genetics, with a plan for removal, resilience, and rebuilding can tip the scale in preventing and even reversing Alzheimer’s disease. Early identification and treatment show the greatest promise.

This protocol is based on 40 years of research and the Amyloid Hypothesis, which has found that beta-amyloid accumulates and finds its way into synaptic clefts. This protein interferes with synaptic communication.

The amyloid then collects, forming plaques that activate enzymes. This leads to the formation of neurofibrillary tangles (NFTs) inside the neuron. NFT formation activates immune cells called microglia surrounding plaques, promoting microglial activation and local inflammatory response and contributing to neurotoxicity.

The Six Alzheimer’s Subtypes Identified by Dr. Bredesen

Type 1 Alzheimer’s disease is inflammatory, or hot
- Ongoing or chronic inflammation puts you at greater risk for developing Alzheimer’s
Type 2 Alzheimer’s disease is atrophic, or cold
- Sub-optimal levels of nutrients, hormones, trophic factors (cell growth factors like NCF, nerve growth factor) increases your risk for Alzheimer’s disease.
Type 1.5 Alzheimer’s disease is glycotoxic, or sweet
- High blood sugar or high fasting insulin levels increase your risk for Alzheimer’s disease. It is termed Type 1.5 because it has features of both Type 1 and Type 2. High cholesterol may also come into play.
Type 3 Alzheimer’s disease is toxic, or vile
- Exposure to toxins such as mercury, toluene, or mycotoxins (made by certain types of mold) leads to an increased risk for Alzheimer’s disease. Although we all experience this exposure to a greater or lesser degree, the key is to minimize it by identifying and removing or minimizing exposures.
Type 4 Alzheimer’s disease is vascular, or pale
- If you have cardiovascular disease, you are at an increased risk of Alzheimer’s disease. Vascular leakiness is one of the earliest changes identified in Alzheimer’s disease.
Type 5 Alzheimer’s disease is traumatic, or dazed
- A history of head trauma — from accidents, falls, or repeated sports-related head injuries — increases your risk for Alzheimer’s disease.

Most patients with Alzheimer’s disease have more than one type and present multiple risk factors.

Get Screened and Get Optimized

In our office we screen for dementia with regular labs looking at all the factors above, MRI scans and a yearly COGNITRAX mental status test. This is covered by insurance and by Medicare. In fact, they recommend it yearly with your annual wellness visit.

Second, we perform autonomic nervous system testing yearly that looks for metabolic causes of inflammation and stress.

The key markers that I have found essential to balance in this population are:

HS-CRP
HbA1c
HOMA-IR
TG:HDL ratio
small dense LDL particle
Fasting Insulin
Homocysteine
Vitamin D
MRI with grey matter volume measurements

This multi-factorial seven tiered approach has been tremendously effective the delaying and treating progressive dementia. If you have any risk for dementia, get in to your doctor and get your brain checked. Or, call my office and schedule a comprehensive dementia evaluation.

Alzheimer’s disease puzzle pieces now starting to fit

Alzheimer’s Disease is a progressively devastating, fatal disease that affects 5.2 million Americans and over 44 million people throughout the world. This disease is often more difficult on the families and caregivers, then on the patient’s themselves. With my office located near three of the country’s largest retirement communities, it is a disease that I see and treat every single day.

A paper published in the Journal of Alzheimer’s Disease this week, confirmed suspicions and patterns that I have been seeing for over 15 years. A significant number of my patients with Alzheimer’s dementia (AD) also have insulin resistance, impaired fasting glucose or diabetes mellitus – type II. I have long wondered if there was a tie to these diseases because of the patterns seen in my office. However, much of the research examining the association between type II diabetes and AD have come to differing conclusions about the cause. Some have concluded that insulin resistance is to blame and others have concluded that insulin deficiency may play a role. Other studies have found that a hormone called amylin secreted with insulin is to blame. And, other articles have found that both amylin and amyloid-beta protein form the plaques within the brain common to AD. Lastly, more recent data complied appears to point to the opposite conclusion – that amylin provides neruro-protective effects and may actually reduce the symptoms of AD. So, what are we to make of all of this? How is the doctor in the trenches to interpret and then advise those with or at risk for Alzheimer’s Disease?

The paper referenced above, by Dr. Schilling, takes all of this data into account and with careful attention to research methods and compiling immense amounts of data from all of these studies, it identifies the integration points with insulin and insulin-degrading enzyme (IDE) that have begun to disentangle the research. What it reveals is fascinating information.

First, under normal circumstances, we now know that insulin stimulates the expression of IDE, which subsequently breaks insulin down after it is used. IDE, however, also plays a roll in breaking down amyloid-beta protein and other amyloidogenic peptides. Alzheimer’s disease is caused by a build up of these amyloid based proteins forming plaques within the human brain.

Second, the body’s system for breaking down and removing these plaques can fail or become inefficient in four different ways. What has been confusion for many years to researchers is now much more clear with our clarified understanding of insulin resistance moving through five different stages (see my article on Diabetes Mellitus type II – really the fourth stage of insulin resistance).

What are these four possible points of breakdown?

In the fifth or last stage of insulin resistance (where insulin deficiency occurs due to pancreatic failure and lack of adequate insulin production) or in a type 1 diabetes patient who makes no insulin at all, inadequate IDE can result in accumulation of amyloid-beta in the brain. Poor IDE production may cause amylin and amyloid-beta plaques in the brain.
Diminished IDE production due to any other cause may lead to amylin and amyloid-beta plaque formation leading to AD
Excessive production of insulin, occurring in stages I-IV of insulin resistance, stimulates increased amylin production which competitively inhibit breakdown of amyloid-beta resulting in AD.
Production of more than the typical level of amyloidogenic peptide that outpaces the formation of IDE is the fourth mechanism occurring with insulin resistance and stimulates the formation of amyloid plaque in the brain consistent with AD.

Further study is essential to tease out what the nuts and bolts of the mechanism may be, but with our understanding of stages of insulin resistance, the puzzle pieces are falling into place. This conglomeration of data provides further confirmation that insulin resistance is likely the key player in the progression of Alzheimer’s Disease years before type II diabetes or type I insulin dependence are ever diagnosed in the individual.

What is the take home message today? Impaired fasting glucose, diabetes mellitus and Alzheimer’s disease are later expressions of the underlying problem: insulin resistance. This is where a low carbohydrate and/or ketogenic diet begins to play a huge role in both prevention and treatment of Alzheimer’s Disease.

More to come . . . In the mean time, pass the butter and the Keto//OS.