Alzheimer’s Disease: The Chiropractic Role
INTEGRATIVE CARE
Dr. Jeffrey Tucker
My dad recently passed away peacefully in his sleep at the age of 93. As a young man in the Army, he was on day two of the invasion at Normandy Beach. He made it through to the end of the war and helped liberate a concentration camp. He left the Army with a Purple Heart, but really with a heart that understood the value of life and living it every day. He was an avid handball and racquetball player, and at about age 65, he fell in love with playing tennis, which he continued to play until he was over 90 years old. He enjoyed going to work and running his business, which he was passionate about. When people asked Dad when he was going to retire, he answered by saying, “I’m not ready yet.” He worked until he was 92, when we finally had to take him away from his business because he had Alzheimer’s disease. He had a slowly developing case of Alzheimer’s disease, which seemed to rapidly progress the last six months of his life. Dad was an incredible father and guide. We had dinner together every Monday night for the past 35 years. His major message through demonstration to me was, “Love your family, love your friends, take care of and be fair to your customers, and don’t dwell on the bad stuff.” My mom has Parkinson’s disease (another neurodegenerative disease) and just celebrated her ninetieth birthday. I wrote this article to share the following message: we have to take care now, so we can take care later in life.
Alzheimer’s disease (AD) may be the number one problem in health care today. It has huge financial ramifications and the problem could bankrupt Medicare. Both of my parents have required 24/7 caregiver help. Both wished to remain at home, which required a team of six full-time caregivers—three for each of them. It is estimated that approximately 45 million currently living Americans (baby boomers) will develop AD, and that’s about 15% of the population.
One of the leading researchers in AD is Dr. Dale Bredesen who is an expert in the mechanisms of neurodegenerative diseases such as Alzheimer’s. Dr. Bredesen has demonstrated that cognitive decline can be reversed with a multifactorial approach. The standard has been to hide our early symptoms, so people don’t go in for help until very late because they feel there is nothing that can be done about it. We need to change the dialogue about this because if inaugurated early enough, patients can experience dramatic recovery of functionality. A comprehensive program for reversing symptoms of dementia and AD will include lifestyle modification, improved oxygen consumption, stress reduction, supplements, proper nutrition, hydration, elimination/detoxifi-
cation, movement/exercise, rest/sleep, adequate temperature, bioidentical hormones, sexual release, touch, security and belonging, and more.
The genetic risk factor for AD is called ApoE status. If you do not have the ApoE4 allele, then your chance of getting this illness in your lifetime is about 9%. If you have one of two alleles, the risk goes up to about 30%. If you have two copies of ApoE4, the risk becomes about 90%. There aie about seven million Americans that have two copies. Genetics like the ApoE4 aie not inevitable and can be reversed.
AD presents as the erosion of memory. Dr. Bredesen describes four broad phases of AD:
1. Presymptomatic phase (PSP) is when you can already see abnormalities on a PET scan, but the person is asymptomatic.
2. Subjective cognitive impairment (SCI) is when the person knows there is something wrong. Often a spouse will notice something wrong, but the person is still testing within normal limits. SCI can continue for a decade and frequently does.
3. Mild cognitive impairment (MCI) is when you know there is a problem. Tests will show it as well, but you can still do your activities of daily living (ADL) and care for yourself.
4. Full-blown AD in which you begin to lose activities of daily living.
Our message has to be, “Why wait? Because the earlier the intervention, the better the outcome.” Current health prevention recommendations (such as getting a colonoscopy at age 50, régulai' Pap tests, etc.) include identifying our ApoE status genetics, and at age 45, people should get a cognitive assessment to find out where they stand. The longer you wait, the more difficult it is to completely reverse the problem.
In 2011, it was found that the brain has a plasticity system similar to bone balance (clastic and blastic activity) or imbalance (i.e., osteoporosis). Dr. Bredesen found evidence that Alzheimer’s disease stems from an imbalance in nerve-cell signaling. In the normal brain, synaptic-blastic activity (laying down of connections in the brain that ai e memory making), versus synaptic-clastic activity signals support memory breaking, allowing irrelevant information to be forgotten. With Alzheimer’s disease, the balance of these opposing signals is disturbed, nerve connections aie suppressed, and memories aie lost. Many factors feed into this balance, such as estradiol, progesterone, estradiol to progesterone ratio, vitamin D levels, stress and cortisol levels, and dozens of other factors that all feed into this balance at a molecular species level.
Dr. Bredesen uses increases in MRI hippocampal volume (where neurons aie continuously generated and subsequently incorporated into existing, local circuitry) and nem o testing to show that the treatment for AD is not a placebo effect. He suggests that we have the ability to slow down the loss and reverse the process of neuroplasticity breakdown. Increased hippocampal volume can be improved with exercise and other lifestyle activities. An increased hippocampus may be related to increased survival of stem cells, increased dendritic arborization, and increased glial support. They don’t know, but they can see the increase in the hippocampal volume.
As the metabolism goes, so goes cognition. Hormones appeal'
to be one key and aie generally categorized as metabolic, such as thyroid, anabolic (testosterone, estrogen, growth hormone, DHEA, and insulin), and catabolic (cortisol, glucagon, and adrenaline). There could be more than a hunch ed variables to look at to access people’s health. For example, if a patient has a fasting insulin level of 30, we aie not going to make them better until we get it below five; other tests include optimization of homocysteine, B12, CRP, insulin, vitamin D, and other vitamins. Tests that check for pernicious anemia and stroke aie not enough to optimize the brain. For example, homocysteine is considered normal up to 12, and anything over six is associated with an increased atrophy of tlie brain over time. You don’t want to walk around with a 12; you want a five or six if y ou want to be good to your brain. Same thing with vitamin D and other vitamins. We want to look at what is optimal for your brain function. If you aie eating too much sugar, you may have increased hs-CRP, which can lead to the degenerative process. Treatment includes reducing your hs-CRP. If you have a constant “inflamed” state, you have to work on reducing it. Insulin resistance has a high correlation with AD. The neural exosomes of people with AD display insulin-resistant signaling. This is type 3 diabetes, or diabetes of the brain. A faulty sugar metabolism can lead to a “brownout” of the brain due to improper energy metabolism.
Alzheimer’s has been thought of as a disease of toxicity, caused by the accumulation of sticky plaques called amyloids in the brain. You make amyloids as a protective response not a destructive cause; it causes downsizing of the brain. The brain makes amyloids as a protective response to three metabolic and toxic perturbations:
1. Inflammation or infection. If you have Porphyromonas gingivalis from oral microbes in your brain, you will make amyloids to kill it; it turns out amyloids aie a good antimicrobial. The same goes with herpes simplex virus, Candida, and spirochetes. Amyloids will respond as good antimicrobials.
2. If you have a sudden withdrawal of trophic support (sud-
denly cut off the nerve growth factors, estradiol, progesterone, pregnenolone, vitamin B12, vitamin D, or any of these sorts of things that support neuronal structure) you will make amyloids.
3. Amyloids are a very good binder of toxics. Metals such as extra mercury, copper, or iron can bind with an amyloid. Biotoxics are reason alone to make amyloids.
Resistance to insulin is a trophic factor that leads to a reduction in trophic support. The damage from sugar alone causes advanced glycation end products and you’ll produce autoreactive antibodies. This causes an inflamed state and we call this type 1.5 because it has features of both type 1 and type 2. We want to drive down your insulin resistance and create insulin sensitivity again. Other biomarkers Dr. Bredesen suggests we look at closely aie to make sure to drive your homocysteine to six or below; we want to make sure your B12 is over 500; and make sure you get seven to eight hours of sleep and use melatonin if you need to because it reduces amyloids. We also want to reduce stress because it increases cortisol. People with high cortisol levels for years will eventually experience adrenal exhaustion, and then the cortisol will become too low and you lose that support. Pregnenolone “steal” can be related to sex hormone support. Testosterone (T) is very important for synaptic support—low T causes increased risk for AD. Low D causes increased risk for AD. Low D receptors aie a risk for AD.
Currently, we look at the brain and say, “You have Alzheimer ’s Disease.” AD is associated with accumulations of amyloid
plaques and/or phosphorylated tau tangles (two proteins involved in neuron structure and development), and type 2 diabetes being associated with resistance to insulin (the growth factor that controls glucose uptake by cells). Either means you have a protein called microtubule-associated protein tau (or tau, for short). Tau forms aggregates that may explain why the disease can affect specific circuits in file brain, rather than geographical regions. Tau’s neurofibrillary tangles ai e what we want to get rid of, but even more than that, we need to get rid of the inciters of amyloids.
In short, amyloid targeting strategies may have failed because there ai e two forms of Alzheimer ’s that might have different root causes. If this is the case, these two diseases aie being confused with each other because of the similarity of their symptoms and effects on the brain. In one (the early-onset genetic variety), problems with amyloid beta or its processing cause plaques that lead to neurological dysfunction. In the other, problems with tau cause defects in neurological function and form plaques of amyloid beta as a side effect. As time goes on, we will be closer to understanding the underlying causes of the two main forms of AD.
Promising suggestions and supplements for an individual therapeutic program can include:
Optimize diet: Is there a cognitive decline diet? Yes! The Mediterranean Diet and the Mind Diet aie recommendations. You want to be in a state of mild ketosis. Minimize simple CHO and
minimize inflammation using several low-glycemic, low-inflammatory, lowgrain, mostly plant-based diets. Increase consumption of vegetables and fruits; limit consumption offish to non-fanned, and limit meat to occasional grass-fed beef or organic chicken. Above all, help patients eliminate simple carbohydrates and processed foods horn the diet. Those with ApoE4, especially the double, should be on a low-carb diet and maintain a fat-based diet until you get insulin sensitization back (follow your LDL particle number and follow mild ketosis).
• Fasting: It is recommended to fast for a minimum of three hours between dinner and bedtime, and for a minimum of 12 hours between dinner and breakfast. Enhance ketogenesis with fasting and the diet. Some controversy remains, but the ideal food program should target insulin resistance and inflammation. To this end, ketogenic diets, plant-based nutrition, gluten avoidance, and intermittent fasting show promise.
High levels of mercury from fish can cause plaque; wild caught fish is best. Dr. Bredesen suggests we should know patients’ organic and inorganic mercury levels. Are you
^In short, amyloid targeting strategies may have failed because there are two forms of Alzheimer’s that might have different root causes. 5 5
gluten sensitive? Is there any evidence of gut leak or blood brain barrier leak? What is your response to gluten or gliadin?
•Probiotics: These help avoid inflammation and autoimmunity.
Coconut oil: This is a good idea and easily can be taken as 1 tsp of coconut oil twice a day.
Exercise: At least 30 to 60 minutes per day, four to six days a week. For those currently walking, encourage them to be more strenuous.
Optimize sleep: Strive for 8 hours per night; take melatonin 0.5 mg by mouth at bedtime.
Turmeric: Take 400 mg each day.
Methylcobalamin: Take 1 mg each day. Methyltetrahydrofolate: Take 0.8 mg each day. Pyridoxine-5-phosphate: Take 50 mg each day. Citicoline: Take 500 mg by mouth twice a day.
Vitamin C: Take 1 g each day.
Vitamin E: Take 400 IU per day. Vitamin E at 1,200 to 1,600 IU per day was utilized in a study for Parkinson’s disease, but it didn’t help out.
CoQlO: Take 200 mg per day.
Zinc picolinate: Take 50 mg per day.
• a-lipoic acid: Take 100 mg per day.
• DHA (docosahexaenoic acid) (Fish oil): Take 320 mg daily. When you aie making synapses, it’s important to have long chain omega-3 (22 carbons, not the shorter ones), and you need citicoline because they use both of those.
• EPA (eicosapentaenoic acid): Take 180 mg per day.
Resolvins aie important to include. Longchain omega-3 and citicolines aie important. Give the brain signals to make synapses—you need the appropriate building blocks.
• Ashwagandha: Take 500 mg per day. It has to be the “real deal” and the right amount. Ashwagandha increases the ability of your cells to bind and withdraw amyloids from your system. It is protective and contributes to the downsizing of AD.
• Bacopa monnieri: Take 250 mg per
day to improve cognitive function.
• Optimize Vitamin D (250H-D3):
We currently think that is about 60 to 70 ng/ml. Be sure to take it with K2. Take 2,000 to 5,000 IU of vitamin D3 per day
• Pregnenolone: It has a clear effect on the brain.
• Hormones: Attention must be given to hormones, especially testosterone and free testosterone, which can be neuroprotective. Check bioidentical hormone replacement for free T3 to reverse the T3 ratio. We must optimize free T4.
• Resveratrol: Part of the balance to APP signaling is related to the synaptoblastic/synapto-clastic activity, which relates directly to SirTl (sirturin) and NF-kappa B. Your cells have a critical balance between those two types of signaling. If you are more on the inflammatory side of NF-kappa B, or more on the longevity side of the metabolic side, the more noninflammatory side you are then on the more SirTl side. Those two are mutually antagonistic. Once you activate NF-kappa B, you decrease your SirT 1 ; ApoE4 binds to the promoter of the gene for SirTl and decreases the amount of SirTl you produce. The brain of someone with AD who is ApoE4 positive will demonstrate a reduced overall produc-
tion of SirTl. Resveratrol will reduce the autoinactivation (autoinhibition) of SirTl to give you a more active Tl, which leads toward the good side of cognition. Resveratrol is helpful with things related to NAD (neurodegenerative conditions).
• Curcumin: This herb binds tightly with the tau and amyloid. It helps as an anti-inflammatory and binds with amyloid removal. It has problems with absorption, so we need to take with fat.
• Acetyl-L-carnitine: Increases nerve growth factors (BDNF, NGF).
• Antioxidants: Dr. Bredesen thinks they have been overplayed.
I hope our profession, especially the Rehab Council, gets as excited about AD as our profession has about concussions. I also hope we further support studies that demonstrate adjustments that can help brain function. Mitochondria biogenesis and the regulation of energy metabolism and the compound nicotinamide adenine dinucleotide (NAD+) are hot topics in the brain field, and those of us using laser are familial' with this. There are many processes chiropractors can influence that aie affected during aging. Are you a chiropractor preparing to reverse cognitive decline?
References:
5. Bredesen DE. Reversal of cognitive decline: a novel therapeutic program. AGING. 2014 Sept;6(9):707-717.
6. Bredesen DE, John V. Next generation therapeutics for Alzheimer's disease. EMBO Mol Med. 2013;5:795-798.
7. Bredesen DE. Neurodegeneration in Alzheimer's disease: caspases and synaptic element interdependence. MolNeurodegener. 2009; 4:27.
8. Bredesen DE. Prionic loops, anti-prions, and dependence receptors in neurodegeneration. In: Legname GR, Detlev, ed. Prion Research of Stan Pmsiner and his Colleagues. 2013; (Gernamy: Dusseldorf University Press), pp. 1-24.
9. Bredesen DE, John V, Galvan V. Importance of the caspase cleavage site in amyloidbeta protein precursor. JAlzheimers Dis. 2010; 22:57-63.
10. Buck Institute for Research on Aging website.
of current the Jeffrey secre tary ACA Rehab Tucker treasurer Council. is the He practices in Los Angeles, California. His website is www. Dr Jeff rey Tucker, com.
