Dr. Weyrich's Naturopathic Functional Medicine Notebook is a collection of information on topics of interest to Dr. Weyrich that may be of interest to the world wide audience. Due to limitations of time, not all information that Dr. Weyrich knows or would like to further research is published here. Dr. Weyrich welcomes financial contributions to support specific research topics, as well as copies of non-free access journal articles for him to review on a topic. Constructive criticism is also welcome.


Overview of Alzheimer's Disease

Alzheimer's disease and senile dementia are growing problems worldwide. The cause of these disorders is not clear at this time, and many different disease mechanisms have been proposed. It is probable that different individuals are susceptible to one or more of these different disease mechanisms, which suggests that multiple different treatments may be necessary to cover all aspects of the disease process for a given individual.

While there is no "magic bullet" for treating this disease, there are a number of approaches to slowing the progress and in some cases gaining partial regression of symptoms. Most notably, integrative/holistic practitioners [Bredesen2014] have demonstrated remarkable success in reversing cognitive decline using a number of synergistic treatment protocols. Apparently, the more different treatments that are applied simultaneously, the better the results.

Dr. Weyrich suggests that ALL of the treatments described below be considered on a personalized basis, and those most appropriate for individual circumstances be implemented for each patient.

Complimentary and alternative treatments for Alzheimer's disease and other dementias that are considered below include:

  • Low Dose Naltrexone
  • Neuro-Gen High Performance Neuromodulation (HPN)
  • Conventional Neuro-feedback
  • Neurotransmitter Balancing

Etiology of Alzheimer's Disease

The cause of Alzheimer's disease is unknown. Theories that have been advanced include the following. More than one mechanism may occur:

  • It is observed that the development of amyloid (Aβ) plaque deposits in the brain from amyloid precursor protein (APP) is associated with neuronal atrophy in the brain, and with the onset and progression of the disease. However, a cause-effect relationship has not been established, nor has the possibility that the Aβ plaques are a marker of disease rather than a cause of disease, or even a protective response to another disease process has not been ruled out. Depending on protein folding, the APP may either support neurite extension or else promote neurite retraction, synaptic inhibition, and apoptosis. This process has been likened to prion pathogenesis in degenerative brain diseases such as Kuru and Mad Cow Disease [Bredesen2013]. The balance between neurite extension and neurite retraction mediated by the various APP derivatives may be disrupted, leading to loss of brain tissue in the same way that disruption of the balance between osteoblasts and osteoclasts can lead to osteoporosis and loss of bone density [Bredesen2013]. There is much yet to be learned regarding these regulatory mechanisms, but to date, all attempts to slow the progression of neurodegeneration by inhibiting APP metabolism have failed (ineffective or even counterproductive). This suggests the importance of APP in normal physiologic functioning of the brain, and perhaps also suggests that Aβ plaque formation is a disease MARKER, not a disease cause (i.e. do not shoot the messenger!).
  • It is observed that the development of neurofibrillary tangles (NFT) consisting of hyperphosphorylated tau peptides inside neuronal axons is associated with neuronal atrophy in the brain, and with the onset and progression of the disease. However, a cause-effect relationship has not been established, nor has the possibility that the NFT are a marker of disease rather than a cause of disease has not been ruled out. Although pharmaceutical companies have invested heavily (and without so far without success) in drugs to slow neurodegeneration by inhibiting Amyloid (Aβ) plaque formation, relatively little research has been devoted to preventing NFT formation.
  • Suppression of mitochondrial energy production [DeLaMonte2000], perhaps due to mitochondrial dysfunction secondary to hypothyroidism, free-radical damage, heavy metal toxicity, or lack of certain nutrients and metabolic intermediates such as CoQ-10.
  • Formation of pentosidine links due to toxic arabinose metabolites originating in yeast dysbiosis.
  • Autoimmune reaction.
  • Aluminum or heavy metal toxicity.
  • Inflammatory process mediated by TNF-alpha or by homocysteine [Rogers2008, pg 9] [Bredesen2013] [Akiyama2000].
  • Inflammatory process mediated by estrogen receptors: [Risbridger2007] has pointed out the inflammatory effect of stimulating estrogen-receptor-alpha (ER-A) on microglia, and the anti-inflammatory effect on microglia of stimulating estrogen-receptor-beta (ER-B). Both estriol and the naturally occurring substance genistein have been shown to selectively stimulate ER-B.
  • Low vitamin D status [Bredesen2013]. It is important to directly measure the active form of vitamin D, calcitriol and supplement calcitriol levels in patients with renal disease, since the kidneys may be unable to convert the more commonly measured dietary cholecalciferol (Vitamin D-3) into calcitriol.
  • Inability of neurons to obtain energy from glucose, possibly due to a form of insulin resistance (Type-2 Diabetes of the brain).
  • Decreased blood flow to the parts of the brain that are affected by Alzheimer's disease.
  • Imbalance in neurotransmitters, especially disruption of serotonin biochemical pathways.
  • Copper toxicity has been linked with Alzheimer's Disease.
  • Imbalance or deficiency of sex hormones: The brain has receptors for estrogens, androgens, and progesterone [Henderson2004]; specific linkage to various sex hormones are listed below.
  • Estrogen deficiency: Early oophorectomy (ovarian removal) [Bredesen2013] or other cause of estrogen deficiency. [ORWJr: However the ovaries also produce testosterone, so the link to estrogen is unclear].
  • DHEA deficiency. However, one research group that found a significant inverse association between free testosterone and risk of Alzheimer's, found no such correlation with DHEA-S [Moffat2000].
  • Testosterone deficiency: Low testosterone levels in men and women are associated increased incidence of Alzheimer's, and surprisingly, higher levels of estradiol are also associated with increased incidence of Alzheimer's [Paoletti2004]. In a longitudinal study of men, Alzheimer's was inversely associated with free testosterone index (FTI). A 26% decrease in risk of Alzheimer's for each 10-nmol/nmol FTI increase was found! The authors report that "FTI was associated with better scores on visual and verbal memory, visuospatial functioning, and visuomotor scanning and a reduced rate of longitudinal decline in visual memory. However, total testosterone and sex hormone binding globulin showed no significant association [Moffat2002], [Moffat2004]. One of the mechanisms of action of free testosterone on the brain has been shown to be increase regional cerebral blood flow as measured by PET in the hippocampus and other regions critical for memory and attention [Moffat2007]. Dr. Weyrich notes that neurofeedback may also improve brain function by modulating regional cerebral blood flow.
  • Metabolic syndrome [Bredesen2013].
  • Head trauma [Bredesen2013].
  • Genetic mutation of the ApoE4 gene increases risk for Alzheimer's Disease [Bredesen2013]. Estrogen use has been shown to half the rate cognitive decline among ApoE4-negative women but not ApoE4-positive women [Yaffe2000] While the genetic mutation is a non-modifiable risk factor, it may be theoretically possible to modulate the aberrant behavior of the mutant gene.
  • Vitamin B12 deficiency [Pacholok2011].
  • Elevated levels of the pituitary gonadotropin luteinizing hormone (LH) levels are higher in individuals who succumb to Alzheimer's. LH can modulate cognitive behavior, and has relatively high receptor levels in the hippocampus, which is associated with Alzheimer's Disease. There is some evidence that this may be due to LH modulating amyloid-? protein precursor processing, whereby amyloid-? plaque deposition may be inversely associated with LH levels [Webber2007], [Casadesus2006]. In these studies, gonadotropin-releasing hormone analogue, leuprolide acetate, was used to decrease effective LH levels in a mouse model. Dr. Weyrich notes that bio-identical progesterone administration may have the same effect on LH via normal negative-feedback regulation, and elevated LH may simply be a marker of low progesterone levels in the same way that TSH is a marker of low thyroid hormone levels.

Diagnosis of Alzheimer's Disease

Dr. Weyrich recommends the following lab-work as part of the workup of a patient with dementia. Unless otherwise noted, the labs are standard labs that can be obtained (in the Phoenix AZ area) at lowest cost (for cash pay patients) from Go to Theranos Theranos. Note that the cash-pay option is important, since many insurance companies (especially Medicare and ObamaCare) will not cover many of the tests for what they consider to be a "hopeless" diagnosis of Alzheimer's Disease. Other labs that may offer reduced cash pay options include Go to AnyLabTestNow AnyLabTestNow and Go to LabXpress LabXpress. As a last resort, consider the major labs that cater to the insurance companies, Go to LabCorp LabCorp and Go to SonoraQuest SonoraQuest. Beware that if you ask to have your labs submitted to insurance, and insurance does not pay for a particular lab, that you may be billed an outrageous price by the lab. It may be better to pay the cash price up-front, and then file for reimbursement. When paying cash you MAY be able to get the lab to meet the Theranos price (which is clearly posted on their web site for all to see, in contrast to the "secret" price structure of the major labs).

  • Methylmalonic Acid (SonoraQuest test number 7073)
  • ApoE4 (Alzheimer's Risk) (LabCorp test number 504040)
  • Calcitriol (in patients with renal disease) (LabCorp test number 081091; SonoraQuest test number 904253).
  • Ceruloplasmin (LabCorp test number 001560; SonoraQuest test number 2083)
  • Zinc, Plasma/Serum (LabCorp test number 001800; SonoraQuest test number 14154)
  • Complete Blood Count with differential, reflex to manual.
  • Comprehensive Metabolic Panel (CMP), AM fasting
  • Lipids
  • Homocysteine
  • High Sensitivity C Reactive Protein (hsCRP)
  • Erythrocyte Sedimentation Rate (Sed Rate)
  • Hemoglobin A1c (HbA1C)
  • Vitamin D (cholecalciferol)
  • Thyroid Stimulating Hormone (TSH), ideally 8 AM before thyroid meds
  • Free T3, ideally 8AM before thyroid meds
  • Insulin, fasting (same time as CMP)
  • Cortisol, fasting AM (same time as CMP)
  • IGF-1, fasting (same time as CMP)
  • FSH
  • LH
  • Cortisol, PM (as late as possible)
  • Borrelia Antibody (Lyme disease)
  • RPR with reflex confirmation (tertiary neurosyphilis)
  • Erythrocyte or whole blood Zn, Cu, Mg (LabCorp test numbers 070032, 081041, 080283; Specialty labs such as Go to Doctor's Data Doctor's Data, Go to Genova Genova, and Go to Great Plains Great Plains)

Treatment of Alzheimer's Disease

Please see conventional, complimentary and alternative medical treatments for important background information regarding the different types of medical treatments discussed below.

Naturopathic, Complimentary and Alternative Treatments

B Vitamin Deficiency

Unless your doctor says that supplementation is contraindicated, Dr. Weyrich recommends that ALL patients, especially including patients with Alzheimer's or dementia, take a supplement containing the B vitamins (see below) in their methylated forms, and avoid all vitamins that have the synthetic (folate, folic acid) forms. The product that Dr. Weyrich personally uses is "Country Life Co-enzymated B" (take one daily). Talk to your doctor to determine what is best for you.

It is well known that a number of different B vitamins are important for healthy brain and nerve function. Some of these will be highlighted below. There are a number of tests for adequate vitamin B status, but insurance coverage may be a problem for some of the better, but more expensive tests. It is generally more cost-effective to simply take an appropriate vitamin B supplement than it is to test for deficiency. B vitamins are water soluble, and generally excess intake is simply excreted in the urine, leading to low risk of overdose toxicity. The most notable side effects of excess B-vitamin supplementation is that the patient's urine turns bright yellow. This is harmless. In addition, vitamin B-3 may cause flushing ("hot flashes"), which can be mitigated by careful adjustment of dosage and other strategies.

Vitamin B-12

This is one of the interventions used by [Bredesen2014]. This vitamin is particularly important for nervous system health, and has been shown to protect against Alzheimer's Disease [Hooshmand2010] and cognitive decline [Tangney2009]. Unfortunately the patient's ability to absorb this vitamin tends to decline with age. This situation is further exacerbated by patients taking prescription or over-the-counter antacid preparations such as H2-blockers and Proton Pump Inhibitors. Since vitamin B-12 is only found in animal products, vegans are particularly at risk for vitamin B-12 deficiencies [Pacholok2011].

Note that excessive supplementation with folic acid (Vitamin B-9) can create a relative deficiency of vitamin B-12, and thereby accelerate cognitive decline [Tangney2009].

In some cases, proper consideration of diet and food sensitivities can eliminate the need to take B-12 depleting drugs.

In order to assure adequate B-12 status, sublingual administration of the methyl form of B-12 is recommended. In some cases, vitamin B-12 injections may be indicated. A commonly used vitamin therapy used by naturopathic medical doctors is called the "Myer's Cocktail"; some allopathic doctors also prescribe what they call a "banana bag" IV injection, which is similar but lower in dose.

Vitamin B-9

This vitamin is also important for nervous system health, and works hand-in-hand with vitamin B-12. Unfortunately, many commercial vitamins, supplements, and "enriched" food products are made with a synthetic form of the vitamin called "folic acid" or "folate". In many individuals, the body is able to convert this inactive synthetic folic acid into the active form "5-methyltetrahydrofolate" (5-MTHF). However, a substantial number of people have a genetic deficiency that does not allow their body to convert the synthetic folic acid into 5-MTHF. For these people, taking folate may be harmful (block necessary enzymes), so taking the more natural 5-MTHF is necessary. Again, it is possible to test for Vitamin B-9 deficiency or the genetic defect, but it is generally more cost-effective to simply take an appropriate 5-MTHF supplement than it is to test for deficiency or genetic polymorphism.

Vitamin B-6

This vitamin is also important for nervous system health. Again, the vitamin is available in both synthetic and methylated forms that are sometimes more effective.

Vitamin B-5 (Pantothenic Acid)

This vitamin is required for synthesis of the neurotransmitter Acetyl Choline. Deficiency of this neurotransmitter has been associated with Alzheimer's Disease. It is also necessary for the synthesis of the energy metabolism intermediate acetyl-CoA.

Vitamins B-2 and B-3

These two vitamins (B-2 and B-3) are also known as riboflavin and niacin. Both are important cofactors for energy metabolism. Since the brain has high metabolic rate, these two vitamins are essential to support proper brain function.

Vitamin D

This is one of the interventions used by [Bredesen2014]. Serum Vitamin D (25OHD) concentrations have been shown to be 1.4 standard deviation units lower in Alzheimer's Disease cases compared to cognitively healthy controls [Annweiler2013]. If renal disease prevents conversion of 25OHD into the bioactive form Calcitriol (1,25OHD), preformed Calcitriol must be supplemented.

Low Dose Naltrexone (LDN)

A number of researchers have noted that low dose naltrexone (LDN) has a beneficial effect on reducing neuroinflammation. Preliminary studies are mixed; some show some benefit from higher doses of naltrexone over a prolonged period (over a month) [Knopman1986].

[LDN] reports that all patients with autoimmune processes who were treated by the late Dr. Bihari [Bihari2003] using LDN "have experienced a halt in progression of their illness. In many patients there was a marked remission in signs and symptoms of the disease." Dr. Bihari suggests a 50% to 70% overall response rate [Bihari2003].

According to [LDN], "given the repeated demonstration of LDN's efficacy in halting progression in all cases of MS, and the possibility of its having a therapeutic effect in PD, it now may be timely to consider LDN in treating the full spectrum of neurodegenerative diseases whose etiology is unknown - all of which may well have a significant underpinning of immunodeficiency/autoimmunity causing the neurological syndromes. Alzheimer's disease ... [is a ] prominent possibilit[y] that spring[s] to mind."

In fact, [Dudley_conditions] does report that Alzheimer's disease is responsive to LDN.

Dr. Weyrich is following this research carefully and recommends a therapeutic trial of the compounded prescription form of Low Dose Naltrexone for Alzheimer's and other dementia patients.

Dr. Weyrich has been trained in the use of Low Dose Naltrexone (LDN). However, Dr. Weyrich has not treated any cases of Alzheimer's Disease or other Dementias with LDN.

Please see What is Low Dose Naltrexone? for more information.

Neuro-Gen High Performance Neuromodulation (HPN)

HPN has been reported to be useful for treating the symptoms of Alzheimer's disease [Snook], [Willis]. Dr. Weyrich has been trained in the use of Neuro-Gen High Performance Neuromodulation system by it's inventor, Corey Snook. However, Dr. Weyrich has not treated any cases of Alzheimer's disease with this technique.

Please see What is Neuro-Gen High Performance Neuromodulation? for more information.

Conventional Neuro-feedback

Neuro-feedback may be useful for treating or preventing Alzheimer's disease. Some researchers, however have reported that neuro-feedback as a mono-therapy does not appear to be effective in treating Alzheimer's Disease. (But one of the main points of this article is that combinations of monotherapies may be synergistic, and therefore more effective than any single therapy). Dr. Weyrich has been certified in Neuro-feedback since 2008, and more recently completed an additional residency training program at ADD Clinic of Scottsdale, AZ. While at the ADD clinic, he treated several cases of age-related mental decline.

Please see What is Neurofeedback? for more information.

Stress Reduction

This is one of the interventions used by [Bredesen2014]. Stress increases inflammation and reduces the repair mechanisms of the body. Stress reduction can reduce corticotropin-releasing factor (CRF) production in the hypothalamus, adrenocorticotropic hormone (ACTH) production in the pituitary, and excessive cortisol production by the adrenal glands. There are many methods of stress reduction, ranging from prayer, meditation, yoga, breathing exercises to biofeedback. Dr. Weyrich is trained in the application of "Heart Rate Variability" biofeedback training for stress reduction.

Lower Homocysteine Levels

This is one of the interventions used by [Bredesen2014]. Considerable evidence suggests that controlling the inflammatory marker "homocysteine" (which is easily measured by an inexpensive blood test, and can be controlled with targeted nutritional supplements) is important not only for reducing risk of Alzheimer's Disease [Hooshmand2010], but also for cardiovascular health. In fact, elevated homocysteine levels are considered as important a predictor of future cardiovascular events as elevated cholesterol. Unlike cholesterol, there are no patented drugs that lower homocysteine, but over the counter supplements that are "Generally Regarded as Safe" (GRAS) are effective without the toxic side effects of statin drugs.

Note that the common diuretic hydrochlorothiazide (HCTZ) increases homocysteine levels [Westphal2003].

Dr. Weyrich highly recommends that all patients be tested for elevated homocysteine levels, which Dr. Weyrich can treat using nutritional methods.

Note that homocysteine is also elevated when there is renal failure [Allen1993].

Lower Methylmalonic Acid Levels

Elevated methylmalonic acid levels, which is a marker for vitamin B-12 deficiency, have been correlated with faster rates of cognitive decline [Tangney2009]. The serum level of methylmalonic acid should be monitored and vitamin B-12 supplementation considered if methylmalonic acid is elevated.

Note that methylmalonic acid is elevated when there is renal failure [Allen1993].

Treat Renal Failure

Since both methylmalonic acid [Allen1993] and homocysteine [Hooshmand2010] are elevated when there is renal failure, and elevated levels of each are associated with cognitive decline [Tangney2009], renal disease should be addressed. While conventional medicine has little to offer other than dialysis, there are certain herbs that have been reported which benefit kidney function, and should be considered.

Get off Statin Drugs

There is some evidence linking statin drug use with transient memory loss (see the book "Lipitor: Thief of Memory" by NASA flight surgeon and former astronaut Duane Graveline [Graveline2006]). In fact, cholesterol is necessary for proper brain function, as well as making a number of hormones. Statins also suppress the body's production of the cofactor CoQ-10, which is necessary for mitochondrial energy production.

A cause-effect relationship between cholesterol and cardiovascular disease has not been proven (association does not prove causation). Nor has the possibility been ruled out that the cholesterol plaques are a marker of another disease process (such as inflammation) rather than a cause of disease per se, or even a protective response to another disease process (such as inflammation). The Naturopathic Medical principle "Find and treat the cause" (e.g. inflammation) is applicable here.

Since homocysteine and cholesterol are both independent risk factors for cardiovascular disease, it may make more sense to target reducing homocysteine using vitamin therapy instead of reducing cholesterol levels with statin drugs.

While you should never discontinue medications without discussing the matter with your prescribing doctor, there are some important questions to ask:

  1. Given my current age and life expectancy, is there any actual evidence that continuing statin drug therapy will allow me to live longer (reduce all-cause mortality)?
  2. Given my current age and life expectancy, is there any actual evidence that continuing statin drug therapy will slow the progression of my dementia?

It is highly unlikely that the prescriber will be able to cite an actual clinical trial that answers either of these questions in the affirmative. However, there is "expert opinion" that will say yes; but keep in mind that in the past "expert opinion" has recommended replacing butter with trans-fat containing margarine. This is now known to be very bad advice.

Note that the above advice is different than the current standard of care endorsed by conventional medicine - you must decide whom to trust.

Optimize Thyroid Function

This is one of the interventions used by [Bredesen2014]. Treat hypothyroidism if present. Test free T3 and free T4 (and maybe reverse T3), and not just TSH. There are anecdotal reports that geriatric patients treated for hypothyroidism had much lower incidence of Alzheimer's than age-matched peers [Starr2005, pg 57].

Optimize Mitochondrial Energy Production

In addition to optimizing thyroid function (see above), vitamins B-2 (riboflavin), B-3 (niacin), and B-5 (pantothenic acid) are components of the cofactors FAD, NAD, and CoA that are essential for mitochondrial energy production. Co-Q10, PQQ, D-Ribose, and carnitine are also necessary for mitochondrial energy production.

Optimize Sex and Adrenal Hormone Levels

This is one of the interventions used by [Bredesen2014]. Balance Cortisol, Estradiol, Testosterone, and their precursors DHEA and pregnenolone.

Estrogen use in Medicare-eligible women was associated with about a 50% slower rate of cognitive decline (1.5 point decline/6 years for estrogen users vs 2.7 point decline/6 years for non-users) among ApoE4-negative women; ApoE4-positive women did not display any benefit from estrogen use [Yaffe2000].

Testosterone use improves verbal learning and memory in healthy postmenopausal women [Davison2011]. Small-scale clinical trials of elderly men suggest that some cognitive deficits may be reversed, at least in part, by testosterone supplementation, although these researchers found no benefit for women [Hogervorst2005].

Treat the Gut

This is one of the interventions used by [Bredesen2014]. It has been said "all disease begins in the gut." While this may seem to be hyperbole, it is well known that problems such as dysbiosis can aggravate both autoimmune diseases that may attack the nervous system, promote systemic inflammation that negatively impacts neuroplasticity, and also produce neurotoxins that can adversely affect brain function. H. pylori, Food Allergy, Stool Analysis, Intestinal Permeability, and Organic Acid Testing may be appropriate; Treatments may include probiotics, prebiotics, natural and pharmaceutical antimicrobials, and healing nutrients. Dr. Weyrich highly recommends testing before planning an intervention in the digestive system.

Adopt a Low-glycemic Diet

This is one of the interventions used by [Bredesen2014]. This is important because Alzheimer's disease is sometimes referred to as "Diabetes of the Brain." The low-glycemic diet helps reduce insulin resistance.

Add Medium-chain Triglycerides to Diet

This is one of the interventions used by [Bredesen2014]. Medium-chain triglycerides are processed differently by the body, and tend to promote thermogenesis and provide the brain with ketone bodies to use as an alternate fuel in the case of "Diabetes of the Brain". Dr. Weyrich recommends a trial of the prescription-only medical food "Axona" or else integrating MCT oil or coconut oil into the daily diet. The medical food Axona can be prescribed by Dr. Weyrich.

Adopt a Low-grain Diet

This is one of the interventions used by [Bredesen2014]. This is important because many grains are high in carbohydrates, and may contain gluten, which may aggravate auto-immune conditions that may lead to neurodegeneration [Perlmutter2013].

Adopt a Low-Inflammatory Diet

This is one of the interventions used by [Bredesen2014]. See also "Get an Oil Change" below.

Get an Oil Change

A healthy diet contains an adequate supply of essential fatty acids, and minimizes the consumption of "bad" fats that cause inflammation. Contrary to popular belief, not all fat is bad, and in fact fat is an important building block of the brain. Saturated fats are NOT necessarily bad. However, modern agricultural practices can lead to many animal products containing "bad fats" that can cause inflammation. On the other hand, organic farming practices can produce very healthy animal fats.

You should replace the "bad fats" in your diet with "good fats" as follows:

Bad FatReplace with Good Fat
Margarine and trans fatsButter
Corn-fed beef productsGrass-fed beef products and pasture-fed chicken eggs
Omega-6 rich oils (corn, safflower, sunflower, canola, etc)Coconut, Palm, Olive oils, Omega-3 rich oils (Cod Liver)
Farm-raised fish (including Atlantic salmon)Wild-caught cold water fish (preferably smaller fish)

Note that the above advice is different than the current standard of care endorsed by conventional medicine - you must decide whom to trust.

Treat Insulin Resistance

This is one of the interventions used by [Bredesen2014]. Insulin resistance is characterized by normal fasting blood glucose levels but elevated fasting insulin levels; or mildly elevated HbA1C levels. There are many treatments for this condition, but most involve dietary modification. [Bredesen2014] recommends Fasting Insulin < 7; HbA1c < 5.5.

Intermittent Fasting

This is one of the interventions used by [Bredesen2014]. By fasting at least 12 hours each day (mostly at night), insulin levels may be lowered, ketogenesis and autophagy enhanced, and perhaps Aβ may be reduced.

Curcumin

This is one of the interventions used by [Bredesen2014]. Curcumin has been reported to attenuate cognitive deficits, neuroinflammation, and amyloid plaque deposition in Alzheimer's Disease rat [Frautschy2001] and mouse [Yang2005] [Garcia_Alloza2007] models. The later reference also reports partial regression of neuronal damage. The properties of Curcumin have been reviewed by [Aggarwal2007].

Dr. Weyrich notes that benefits seen in animal models do not always translate to humans; and in particular pharmaceutical trials that directly target amyloid plaque formation in Alzheimer's Disease have not been successful, and may even be counter-productive. While Curcumin is reported to directly target plaque formation [Garcia_Alloza2007], it also has other immunomodulatory effects on inflammation, which may provide a benefit not found in the pharmaceutical agents targeting the plaque formation more directly.

Lower Highly-sensitive C-Reactive Protein

This is one of the interventions used by [Bredesen2014]. Highly-sensitive C-Reactive Protein (hsCRP) is a sensitive marker of inflammation. Since inflammation plays a significant role in neuroinflammation and consequent neurodegeneration, the root cause of elevated hsCRP should be identified and treated. Treatments aimed at directly reducing hsCRP are not likely to be useful, as they essentially "shoot the messenger" rather than addressing the problem that hsCRP serves as a marker for. Approaches to lowering hsCRP include (but are not limited to) Low-inflammatory and Oil-change diets (see above), curcumin, and optimize hygiene (especially dental).

Raise Albumin/Globulin Ratio

This is one of the interventions used by [Bredesen2014]. Low Albumin/Globulin (A/G) Ratio ia a marker of inflammation. Since inflammation plays a significant role in neuroinflammation and consequent neurodegeneration, the root cause of low A/G ratio should be identified and treated. Treatments aimed at directly increasing A/G ratio are not likely to be useful, as they essentially "shoot the messenger" rather than addressing the problem that low A/G serves as a marker for. Approaches to lowering the A/G ratio include (but are not limited to) Low-inflammatory and Oil-change diets (see above), curcumin, and optimizing hygiene (especially dental).

Optimize Sleep

This is one of the interventions used by [Bredesen2014]. Good sleep (8 hours of sound sleep) is necessary for minimizing inflammation and optimizing repair of all parts of the body, including the brain. Supplements such as melatonin or tryptophan may be helpful (ask your doctor about appropriate dosing). In addition to benefiting sleep, melatonin has been reported be protective in neurodegenerative diseases such as Alzheimer disease, Parkinson disease, Huntington's disease and Amyotrophic Lateral Sclerosis [Polimeni2014]. Many sleeping pills disrupt sleep architecture, and are therefore counter-productive.

Treat Sleep Apnea

This is one of the interventions used by [Bredesen2014]. An extension to the idea of optimizing sleep is the diagnosis and treatment of sleep apnea. Not only can sleep apnea disrupt sleep, but it can also lead to anoxia (loss of oxygen to the brain), which both can be damaging and also can inhibit repair. If you snore or stop breathing at night, ask your doctor for a referral for a sleep study.

Exercise

This is one of the interventions used by [Bredesen2014]. In an 18-month study, individuals at genetic risk for Alzheimer's Disease (who are positive for the apolipoprotein E-epsilon 4 (APOE-?4) allele) and who engaged in (self-reported) physical activity are protected from hippocampal atrophy, while those with similar genetic risk who did not engage in physical activity experienced a 3% decline in hippocampal volume over the same period [Smith2014].

Computerized Cognitive Training

This is one of the interventions used by [Bredesen2014]. Forty hours of computerized brain training was found to yield a statistically significant improvement in generalized measures of memory and attention over a control group. The magnitude of the effect sizes suggests that the results are clinically significant [Smith2009].

Neurotransmitter Balancing

Neuro Research [Hinz2015] reports that Alzheimer's disease and dementia can be benefited by balancing neurotransmitter levels in the body.

Dr. Weyrich has been trained in neurotransmitter balancing protocols, but has not treated Alzheimer's disease and dementia using this technique.

Please see What is Neurotransmitter Balancing? for more information.

Treat Heavy Metal Toxicity

While everybody does not have heavy metal toxicity, it is well known that environmental toxins such as lead and mercury can cause serious disruption of mental function. Consider for example the "Mad Hatter" syndrome, which was caused by the mercury compounds used to make felt hats. Here in Arizona, the "Dreamy Draw" area of Phoenix (near Northern and Arizona 51) was formerly a mercury mine, and was given its name because of the mental disruption observed in the miners.


ICD-10 Codes related to Alzheimer's Disease


References for Alzheimer's Disease