Overview

Alzheimer's disease and senile dementia are growing problems worldwide. The cause of these disorders is unclear, and many different disease mechanisms have been proposed.

Different individuals are probably susceptible to one or more of these various disease mechanisms, suggesting multiple different treatments may be necessary to cover all aspects of the disease process for a given individual.

While no "magic bullet" exists for treating this disease, many approaches can slow its progress, and in some cases give regression of symptoms. Most notably, integrative/holistic practitioners [Bredesen2014  🕮 ] have demonstrated remarkable success in reversing cognitive decline using several synergistic treatment protocols that are applied simultaneously.

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

Please see conventional, complementary, and alternative medical treatments for important background information regarding the different types of medical treatments discussed on this page. Naturopathic, Complementary, and Alternative treatments that may be considered include:


Etiology

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 [need citation]. However, a cause-effect relationship has not been established. Nor has it been ruled out that the Aβ plaques are a marker of disease rather than a cause of disease, or even a protective response to another disease process [need citation]. Depending on protein folding, the APP may either support neurite extension or 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  🕮 ]. Much is yet to be learned regarding these regulatory mechanisms. However, to date, all attempts to slow the progression of neurodegeneration by inhibiting APP metabolism have failed (ineffective or counter-productive). This failure 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 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-alpha) on microglia and the anti-inflammatory effect on microglia of stimulating estrogen-receptor-beta (ER-beta). Both estriol and the naturally occurring substance genistein have been shown to selectively stimulate ER-beta [need citation].
  • Low vitamin D status [Bredesen2013  🕮 ]. Because the kidneys in patients with renal disease may not convert the more commonly measured dietary cholecalciferol (vitamin D3) into the active form of vitamin D (calcitriol), it is essential to directly measure and to supplement calcitriol in these patients.
  • The inability of neurons to obtain energy from glucose, which is 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. [Dr. Weyrich notes that the ovaries also produce testosterone, so the link to estrogen is unclear].
  • DHEA deficiency. However, one research group found a significant inverse association between free testosterone and the risk of Alzheimer's, but found no such correlation with DHEA-S [Moffat2000  🕮 ].
  • Testosterone deficiency: Low testosterone levels in men and women are associated with increased incidence of Alzheimer's, and surprisingly, higher levels of estradiol are also associated with increased incidence of Alzheimer's [Paoletti2004  🕮 ]. This longitudinal study of men showed that Alzheimer's was inversely associated with free testosterone index (FTI) and revealed a 26% decrease in the risk of Alzheimer's for each 10nmol/nmol FTI increase. 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 is by increasing 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 the risk for Alzheimer's Disease [Bredesen2013  🕮 ]. [Yaffe2000  🕮 ] reports that estrogen use halves the rate of cognitive decline among ApoE4-negative women but not ApoE4-positive women. While this genetic polymorphism is a non-modifiable risk factor, it may be theoretically possible to epigenetically 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; it has relatively high receptor levels in the hippocampus, a part of the brain that is associated with Alzheimer's Disease. There is 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, the 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 be a marker of low progesterone levels in the same way that TSH is a marker of low thyroid hormone levels.

Diagnosis

Dr. Weyrich recommends the following lab tests as part of the workup of a patient with dementia. Unless otherwise noted, the labs are standard tests that can be obtained from several different labs in the Phoenix, Arizona, area.

Note that the cash-pay option is critical because many insurance companies (primarily government-affiliated plans such as Medicare, Medicaid (AHCCCS in Arizona), and Obamacare) will not cover many of the tests for what they consider to be a "hopeless" diagnosis of Alzheimer's Disease. Another lab that may offer reduced cash pay options is Go to AnyLabTestNowAnyLabTestNow As a last resort, consider the major labs that cater to the insurance companies, such as Go to LabcorpLabcorp and Go to Sonora QuestSonora Quest. Beware that if you ask to have your labs submitted to insurance and insurance does not pay for a particular test, then 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.

  • Methylmalonic Acid (Sonora Quest test number 7073)
  • ApoE4 (Alzheimer's Risk) (LabCorp test number 504040)
  • Calcitriol (in patients with renal disease) (LabCorp test number 081091; Sonora Quest test number 904253).
  • Ceruloplasmin (LabCorp test number 001560; Sonora Quest test number 2083)
  • Zinc, Plasma/Serum (LabCorp test number 001800; Sonora Quest test number 14154)
  • Complete Blood Count (BC) with differential, reflex to manual.
  • Comprehensive Metabolic Panel (CMP), AM fasting
  • Lipids
  • Homocysteine
  • High Sensitivity C Reactive Protein (hs-CRP)
  • Erythrocyte Sedimentation Rate (Sed Rate)
  • Hemoglobin A1c (HbA1C)
  • Vitamin D (cholecalciferol)
  • Thyroid Stimulating Hormone (TSH), ideally 8 AM before thyroid meds
  • Free T3, ideally 8 AM 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)

Treatment

Naturopathic, Complementary, and Alternative Treatments

Nutritional Medicine

B Vitamin Deficiency

Unless your doctor says that supplementation is contraindicated, Dr. Weyrich recommends that ALL patients, especially 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 Coenzymated B" (take one daily). Talk to your doctor to determine what is best for you.

As discussed below, several different B vitamins are essential for healthy brain and nerve function. There are tests for adequate vitamin B status, but insurance coverage may be a problem for some of the better, but more expensive, tests. A clinical trial of an appropriate vitamin B supplement is generally more cost-effective than testing for deficiency. B vitamins are water-soluble, and generally, excess intake is excreted in the urine, leading to low risk of overdose toxicity. Excess B-vitamin supplementation's most notable side effect is that the patient's urine turns bright yellow, which is harmless. In addition, vitamin B3 may cause flushing ("hot flashes"), which can be mitigated by careful dosage adjustment and other strategies.

Vitamin B12

Vitamin B12 is one of the interventions used by [Bredesen2014  🕮 ]. This vitamin is essential for nervous system health and protects against Alzheimer's Disease [Hooshmand2010  🕮 ] and cognitive decline [Tangney2009  🕮 ]. Unfortunately, the patient's ability to absorb vitamin B12 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. Vegans are particularly at risk for vitamin B12 deficiencies since vitamin B12 is only found in animal products, [Pacholok2011].

In addition, excessive supplementation with folic acid (Vitamin B9) can create a relative deficiency of vitamin B12 and thereby accelerate cognitive decline [Tangney2009  🕮 ].

In some cases, proper consideration of diet and food sensitivities can eliminate the need to take B12-depleting drugs.

In order to assure adequate B12 status, sublingual administration of the methyl form of B12 is recommended. In some cases, vitamin B12 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 B9

Vitamin B9 is essential for nervous system health and works synergistically with vitamin B12. Unfortunately, many commercial vitamins, supplements, and "enriched" food products are made with a synthetic form of the vitamin called "folic acid." In many individuals, the body can convert this inactive synthetic folic acid into the active form "5-methyltetrahydrofolate" (5-MTHF). However, some people have a genetic deficiency preventing synthetic folic acid from being converted into 5-MTHF. For these people, taking folate may be harmful (blocking necessary enzymes), so taking the more natural 5-MTHF is necessary. Again, it is possible to test for Vitamin B9 deficiency or the genetic defect; however, clinical trial of an appropriate 5-MTHF supplement is generally more cost-effective than testing for deficiency or genetic polymorphisms.

Vitamin B6

Vitamin B6 is also essential for nervous system health. Again, vitamin B6 is available in both synthetic and methylated forms; the methylated form is sometimes more effective.

Vitamin B5 (Pantothenic Acid)

Vitamin B5 is required for the 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 B2 and B3

Vitamins B2 and B3 are also known as riboflavin and niacin. Both are essential cofactors for energy metabolism. Since the brain has a high metabolic rate, these two vitamins are essential for proper brain function.

Vitamin D

This is one of the interventions used by [Bredesen2014  🕮 ]. Serum Vitamin D (also known as calcifediol, 25OHD, or 25(OH)D) concentrations have been shown to be 1.4 standard deviation units lower in Alzheimer's disease cases compared to cognitively healthy controls [Annweiler2013  🕮 ] [Evatt2008  🕮 ]. If renal disease prevents the conversion of 25OHD into the bioactive form calcitriol (1,25(OH)D), the patient must be supplemented with preformed calcitriol.

Ketogenic Diet

Several authors have discussed the benefits of the ketogenic diet for treating a variety of neurological conditions: [Achanta2017  🕮 ] [Augustin2018  🕮 ] [Hertz2015  🕮 ] [Maalouf2009  🕮 ] [Newport2023] [Watson2015] For general information on the ketogenic diet, please see: Ketogenic Diet

Adopt a Low-glycemic Diet

A low-glycemic diet is one of the interventions used by [Bredesen2014  🕮 ]. This diet is suggested because Alzheimer's disease is sometimes called "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, 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 Go to AxonaAxona (caprylidene) or integrating MCT oil or coconut oil into the daily diet. Dr. Weyrich can prescribe the medical food Axona.

Adopt a Low-grain Diet

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

Adopt a Low-Inflammatory Diet

A low-inflammatory diet 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; fat is actually a vital 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.

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 differs from conventional medicine's the current standard of care - you must decide whom to trust.

Intermittent Fasting

Intermittent fasting 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
Curcumin, the active principle found in turmeric, is one of the interventions used by [Bredesen2014  🕮 ]. Curcumin attenuates cognitive deficits, neuroinflammation, and amyloid plaque deposition in Alzheimer's diseased rat [Frautschy2001  🕮 ] and mouse [Yang2005  🕮 ] [Garcia_Alloza2006  🕮 ] models. The latter 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_Alloza2006  🕮 ], it also has other immunomodulatory effects on inflammation, which may provide a benefit not found in the pharmaceutical agents targeting plaque formation more directly.

Low Dose Naltrexone (LDN)

Some 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 whom the late Dr. Bihari [Bihari2003] treated 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 [Parkinson's disease], 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 [possibility] 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 to use Low Dose Naltrexone (LDN). However, Dr. Weyrich has not treated any cases of Alzheimer's Disease or other forms of dementia with LDN.

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

Neuro-Gen High-Performance Neuromodulation (HPN)

HPN has been reported to help treat the symptoms of Alzheimer's disease [Snook], [Willis]. Dr. Weyrich has been trained to use the Neuro-Gen High-Performance Neuromodulation system by its 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.

Neurofeedback

Neurofeedback may help prevent and treat Alzheimer's disease. Some researchers, however, have reported that neurofeedback 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 neurofeedback 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.

Optimize Thyroid Function

This is one of the interventions used by [Bredesen2014  🕮 ]. Treat hypothyroidism if present. Test TSH, free T3, free T4, and maybe reverse T3. There are anecdotal reports that geriatric patients treated for hypothyroidism had a much lower incidence of Alzheimer's than age-matched peers [Starr2005, pg 57].

Mind-Body Approaches to Reduce Stress

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 has training in applying "Heart Rate Variability" biofeedback training for stress reduction.

Balance Metabolism

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 essential not only for reducing the risk of Alzheimer's Disease [Hooshmand2010  🕮 ] but also for cardiovascular health. Elevated homocysteine levels are considered as important a predictor of future cardiovascular events as elevated cholesterol. Unlike cholesterol, no pharmaceutical drugs lower homocysteine, but over-the-counter supplements that are Go to "Generally Regarded as Safe""Generally Regarded as Safe" (GRAS) by the FDA are effective without the toxic side effects of statin drugs.

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, marker for vitamin B12 deficiency, have been correlated with faster rates of cognitive decline [Tangney2009  🕮 ]. The serum level of methylmalonic acid should be monitored, and vitamin B12 supplementation should be considered if methylmalonic acid is elevated.

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

Optimize Mitochondrial Energy Production

In addition to optimizing thyroid function (see above), vitamins B2 (riboflavin), B3 (niacin), and B5 (pantothenic acid) are components of the cofactors FAD, NAD, and CoA that are essential for mitochondrial energy production. CoQ-10, PQQ, D-ribose, and carnitine are also necessary for mitochondrial energy production.

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.

Lower Highly sensitive C-Reactive Protein

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

Raise the Albumin/Globulin Ratio

This is one of the interventions used by [Bredesen2014  🕮 ]. Low Albumin/Globulin (A/G) Ratio is a marker of inflammation. Since inflammation plays a significant role in neuroinflammation and consequent neurodegeneration, the root cause of the low A/G ratio should be identified and treated. Treatments aimed at directly increasing the A/G ratio are not likely to be useful, as they essentially "shoot the messenger" rather than addressing the problem for which low A/G serves as a marker. 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).

Neurotransmitter Balancing

Neuro Research [Hinz2015] reports that Alzheimer's disease and dementia can benefit from 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 the Kidneys

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 besides dialysis, certain herbs have been reported to benefit kidney function and should be considered.

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 autoimmune diseases that may attack the nervous system, promote systemic inflammation that negatively impacts neuroplasticity, and 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.

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 the repair of all body parts, including the brain. Supplements such as melatonin or tryptophan may be helpful (ask your doctor about appropriate dosing). In addition to benefiting sleep, melatonin is protective in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease and Amyotrophic Lateral Sclerosis [Polimeni2014  🕮 ]. Many sleeping pills disrupt sleep architecture and are, therefore, counter-productive.

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

Environmental Medicine

Treat Heavy Metal Toxicity

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

Reconsider Pharmaceutical Drugs

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, and the production of important 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 critical 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 doubtful that the prescriber can cite an actual clinical trial that answers either of these questions in the affirmative. However, there is "expert opinion" that will say yes, but remember that in the past "expert opinion" has recommended replacing butter with trans-fat-containing margarine, which is now known to be terrible advice.

Note that the above advice differs from conventional medicine's current standard of care - you must decide whom to trust.

Physiotherapy

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 epsilon 4 (ApoE4) 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  🕮 ].

Exercise the Brain

Computerized Cognitive Training

This is one of the interventions used by [Bredesen2014  🕮 ]. Forty hours of computerized brain training yielded 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  🕮 ].


ICD-10


References