Alzheimer’s and other dementias are common disorders in the elderly, usually involving symptoms of memory loss, confusion, personality changes, or physical issues including loss of balance or impaired movement.
Misdiagnosis of symptoms is very common in the elderly, and a number of medical issues must be ruled out. Many of these symptoms can be caused by treatable conditions including infections, prescription and over the counter drugs, nutritional deficiencies and hormone imbalances. If left untreated, these conditions may result in permanent brain damage.
Alzheimer’s is a type of dementia. Dementias share many common symptoms. People with mild symptoms of Alzheimer’s and other dementias often seem healthy, but they may be having trouble making sense of the world around them. It often takes time for an observer to realize that something is wrong because the initial symptoms of dementia are often confused with changes that take place in normal aging. Typical Alzheimer’s and other dementia symptoms may include:
- Recent memory loss. Everyone forgets things for awhile, but remembers them later. Dementia patients often forget things, and never remember them. They might ask the same question repeatedly, each time forgetting that you already answered it. They don’t remember they already asked the question.
- Difficulty performing familiar tasks. Dementia patients might cook a meal but forget to serve it. They might even forget cooking it.
- Problems with language. Dementia patients may forget simple words or use the wrong words, making it hard to understand what they want, causing an outburst of anger directed at the person they’re talking to.
- Time and place disorientation. Dementia patients may get lost on their own street, forgetting how they got to a certain place and how to get back home.
- Poor judgment. Anyone might get distracted and forget to watch a child closely for a short time. Dementia patients might forget about the child and just leave the house for the day.
- Problems with abstract thinking. Anyone might have trouble balancing a checkbook from time to time; dementia patients can forget what numbers are and how to use them.
- Misplacing things. Dementia patients may put things in the wrong places — an iron in the freezer or a wristwatch in the sugar bowl. Then they can’t find them later.
- Changes in mood. Everyone is moody occasionally, but dementia patients may have fast mood swings, going from calm to tears to anger in just minutes.
- Personality changes. Dementia patients may have drastic changes in personality, often becoming irritable, suspicious or fearful.
- Loss of initiative. Dementia patients may become passive, not wanting to go places or see other people.
At CHS we follow the guidelines of The American Academy of Neurology (AAN) in diagnosing and treating Alzheimer’s and other dementias. They specify what tests are necessary to diagnose Alzheimer’s and other dementias, and what steps must be taken in assessing cognitive impairment.
Unsure what to order? Please call us, we can help! Call a CHS healthcare Professional at 714-886-9026 for guidance.
Natural Treatment Approaches
There are no cures for dementia, either in Western or Eastern medicine. The dementing process involves damage and destruction of neurons (nerves) in the brain. Once these neurons are destroyed the functions, knowledge and memories stored within their connections are also destroyed.
According to Western Naturopathic thought, dementias are increasingly being accepted by scientists to be disorders of inflammation, leading to neuronal damage. Western naturopaths consider this inflammation to be a result of nutritional deficiencies of key vitamins, minerals and amino acids, invading pathogens and foreign proteins, and neuron-damaging ions and environmental chemicals penetrating the blood-brain barrier. All treatment approaches for dementia are aimed at preventing, slowing or stopping further neuron damage through management of these factors.
Drug-free approaches have been well studied and have been proven to help with dementia symptoms. Most current dementia drugs are based on molecules first extracted from plants, including Aricept. Specific herbal and nutritional therapies have substantial evidence of effectiveness, although have not yet been approved by the FDA for these uses.
Traditional Chinese Medicine sees many symptoms of Alzheimer’s disease and most forms of dementia, such as loss of memory and irritability, to be associated with the Kidneys or the Heart. The Spleen is also considered important, as qi and blood decrease over time. As kidney and Spleen function declines, dampness and phlegm will be produced. Lack of movement may cause qi and blood stagnation. According to TCM theory, phlegm can produce symptoms such as disordered thinking; drooling; nausea; profuse sputum; somnolence; a stuck sensation in the throat (plum pit qi); a coated tongue; and a slippery pulse. Modern Chinese Formulas take into account the most recent phytonutrient research and share many ingredients with Western formulas.
Dr. Reinhardt is a Board Certified Medical Psychologist with extensive experience in diagnosing and treating dementia. Call us at (714) 886-9026 to book an appointment for an in-person discreet consultation, telehealth consultation, or for a referral in your area.
Statements contained herein have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat and cure or prevent disease. Information provided by CHS is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. Any information given is only intended as a sharing of knowledge and information from scientific world literature. You are encouraged to make your own health care decisions based upon your own research of the subject and in partnership with a qualified health care professional.
Latest Science on Dementia
Metformin (glucophage) may prevent many cases of dementia
Brain insulin resistance in Alzheimer’s disease and related disorders: mechanisms and therapeutic approaches
There are no disease-modifying treatments for Alzheimer’s disease; current approaches target symptoms without addressing the underlying pathology, and their clinical benefit are limited in scope and duration. Drugs that reduce the aggregation or production of amyloid ß (Aß), the hallmark pathology of Alzheimer’s disease, have been extensively studied but yielded no treatment effect. These disappointing results highlight the need for a better understanding of Alzheimer’s disease and related disorders, including the mechanisms underlying the aggregation of Aß and tau and other contributory factors (eg, synaptic loss and neuroinflammation), thereby enabling identification of alternative therapeutic options.
One such area of research focuses on impaired brain metabolism and, in particular, the role of insulin. Evidence shows that insulin is crucial for brain health and that peripheral and brain insulin dysregulation might contribute to the development of Alzheimer’s disease and cerebrovascular pathology. This research suggests a novel area for therapeutic investigation in which increasing the availability of insulin in the CNS or increasing sensitivity to insulin could prevent or delay Alzheimer’s disease and related disorders.
An alternative strategy to the increasing insulin concentrations is instead to use interventions that make tissues more responsive to lower insulin concentrations. Several insulin sensitising compounds have been tested to restore CNS insulin sensitivity, although evidence of their effects in the human brain is scarce.
Metformin is possibly the most well studied class of drugs, and is widely used to treat type 2 diabetes. In mouse models of Alzheimer’s disease, metformin improved memory and decreased concentrations of Aß, hyperphosphorylated tau, and activated microglia. These benefits were accompanied by improved brain insulin signalling. In a randomised placebo-controlled trial, 80 participants without diabetes who had mild cognitive impairment received metformin or placebo daily for 12 months. Although promising results were obtained for memory assessed with the selective reminding test for the metformin group compared with the placebo group, no differences were observed for the ADAS-Cog12, CSF Aß42, and cerebral glucose metabolism, as measured by FDG PET. These results motivated a phase 2 trial for patients with mild cognitive impairment and Alzheimer’s disease that is currently underway.
Exercise is arguably the most powerful modulator of peripheral insulin resistance and has also become an active field of research in the prevention of Alzheimer’s disease and cognitive decline. A systematic review concluded that physical activity reduces the risk of Alzheimer’s disease. Many insulin resistance-related risk factors for Alzheimer’s disease, such as hypertension and metabolic disease, can be prevented or treated through exercise. Although exercise improved brain insulin sensitivity in rodent studies, resulting in enhanced mitochondrial function, reduced oxidative stress, and reduced tau hyperphosphorylation and aggregation in neurons, no human studies have yet examined the effects of exercise on brain insulin sensitivity.
The Lancet Neurology Published:July 27, 2020 https://doi.org/10.1016/S1474-4422(20)30231-3
Dr. Reinhardt: Metformin is used together with diet and exercise to improve blood sugar control in adults with type 2 diabetes. It is also an approved treatment for polycystic ovary syndrome. It is recommended as first line treatment for diabetes and pre-diabetes. Unlike nearly every other drug used to treat blood sugar issues, metformin will not worsen the condition over time.
Serious adverse reactions are lactic acidosis, hepatotoxicity and vitamin b12 deficiency. Lactic acidosis is a buildup of lactate (especially L-lactate) in the body, with formation of an excessively low pH in the bloodstream. This risk is low for metformin (less than 10 cases for 100,000 patient years).
Although gastrointestinal intolerance is frequent, metformin-induced hepatotoxicity is rare. Fewer than 10 cases have been reported. In all of those cases, metformin was associated with concomitant intake of other potentially hepatotoxic drugs. (Diabetes Care. 2012 Mar; 35(3): e21. 2012 Feb 10. doi: 10.2337/dc11-2306.) Still, it is not recommended in those with kidney disease with an eGFR under 30 (serious impairment).
Metformin will inhibit absorption of vitamin B12 in the gut, with studies indicating as much as 30% reduction. Those on metformin should use sublingual forms of B12 administration, or monthly injections, to bypass this issue. Those over age 60 are wise to supplement with sublingual B12: it is a primary component of red blood cells and production of SOD in the CNS. B12 deficiency is a known cause of dementia.
As with most drugs, metformin was first isolated from plants, primarily French lilac. After thousands of years use in traditional medicine, it’s synthesis was a major breakthrough in diabetes treatment.
Gum Disease Strongly Implicated in Alzheimer’s
Periodontal Disease and Incident Dementia: The Atherosclerosis Risk in Communities
To test the hypothesis that periodontal disease would be associated with increased risk for dementia and mild cognitive impairment 8,275 subjects (mean age 63) were assessed.
The cumulative incidence and incidence density of dementia during follow-up (average=18.4 Study years) were 19%, 11.8 cases per 1,000 person-years. Rates vs condition per 1000 person-years were:
Healthy gums 8.3
Mild peridontal disease 10.4
Severe periodontal disease 12.7
Severe tooth loss 15.1
Edentulous (lacking teeth) 16.9
Results showed that participants with worse periodontal status were more likely to have risk factors for vascular disease and dementia, such as smoking, hypertension, diabetes, and coronary heart disease.
Conclusions: Periodontal disease was modestly associated with incident MCI and dementia in a community-based cohort of black and white participants.
The association between periodontal disease and MCI or dementia “is rooted in the infection hypothesis, meaning adverse microbial exposures in the mucosal surfaces of the mouth, especially the subgingival space. One notion is that there could somehow be a direct infection of the brain with oral organisms, which posits that the oral organism could travel to the brain, colonize there, and cause damage that impairs cognition. Another possible mechanism is that chronic systemic inflammation in response to oral infections can eventually lead to vascular disease which, in turn, is a known risk factor for future dementia.”
Neurology July 29, 2020, DOI: https://doi.org/10.1212/WNL.0000000000010312
Dr. Reinhardt: Enough is known about the correlation of gum disease and dementia to suggest everyone take adequate precautions to reduce risk. This may include regular visits to the dental hygienist, brushing after meals (AFTER breakfast is often ignored!), flossing, and use of a Water Pik. The sugar substitute Xylitol may be particularly useful as a mouth rinse or when added to the Water Pik to reach under the gum line.
Xylitol is a naturally occurring sugar alcohol found in small amounts in fruit. Xylitol has negligible effects on blood sugar because it is metabolized independently of insulin. Absorbed more slowly than sugar, xylitol supplies 40% fewer calories than table sugar. Xylitol is used to prevent middle ear infections (otitis media) in young children, and as a sugar substitute for people with diabetes. Xylitol is added to some chewing gums and other oral care products to prevent tooth decay and dry mouth. It has been approved by the European Food Safety Authority (EFSA): “xylitol chewing gum reduces the risk of cavities in children.”
“Xylitol decreases the incidence of dental caries by increasing salivary flow and pH13 and reducing the number of cariogenic (MS) and periodontopathic (Helicobacter pylori) bacteria, plaque levels, xerostomia, gingival inflammation, and erosion of teeth.” (Clin Cosmet Investig Dentv.6; 2014PMC4232036)
Commercial xylitol rinses are up to 25% xylitol. Alternately, place about 1 teaspoon of xylitol in your mouth, with or without adding a small amount of water, and swish for 30 seconds or more. For use in a Water Pik, completely dissolve 1 teaspoon in 1 cup of warm water, add to the tank and irrigate!
Microglia in Alzheimer’s disease
Proliferation and activation of microglia in the brain, concentrated around amyloid plaques, is a prominent feature of Alzheimer’s disease (AD). The majority of risk genes for AD are highly expressed (and many are selectively expressed) by microglia in the brain. There is mounting evidence that microglia protect against the incidence of AD, as impaired microglial activities and altered microglial responses to ß-amyloid are associated with increased AD risk. On the other hand, there is also abundant evidence that activated microglia can be harmful to neurons. Microglia can mediate synapse loss by engulfment of synapses, likely via a complement-dependent mechanism; they can also exacerbate tau pathology and secrete inflammatory factors that can injure neurons directly or via activation of neurotoxic astrocytes. Gene expression profiles indicate multiple states of microglial activation in neurodegenerative disease settings, which might explain the disparate roles of microglia in the development and progression of AD pathology.
J Cell Biol. 2018 Feb 5; 217(2): 459–472.
Dr. Reinhardt: This is an interesting line of reasoning. It is more extensively explored in the following study:
Microglia in Neurological Diseases: A Road Map to Brain-Disease Dependent-Inflammatory Response
Microglia represent a specialized population of macrophages-like cells in the central nervous system (CNS) considered immune sentinels that are capable of orchestrating a potent inflammatory response. Microglia are also involved in synaptic organization, trophic neuronal support during development, phagocytosis of apoptotic cells in the developing brain, myelin turnover, control of neuronal excitability, phagocytic debris removal as well as brain protection and repair. Microglial response is pathology dependent and affects to immune, metabolic. In this review, we will shed light on microglial activation depending on the disease context and the influence of factors such as aging, environment or cell-to-cell interaction.
Compelling evidences shed light on the role of innate immune system and microglia response in the progression of neurodegenerative diseases, such as PD or AD. Microglial cells can develop different functional activation states, actively participating in brain homeostasis. However, an uncontrolled inflammatory response by microglial cells can lead to a detrimental outcome. Mainly, JAK/STATs and NFkB pathways govern microglial pro-inflammatory response and molecules such as TNF-a, IL-1ß and iNOS are the main outcome the downstream signaling of these pathways. This activation is linked to a deleterious role in neurodegenerative diseases, expanding the inflammatory response and increasing the neuronal damage.
Front. Cell. Neurosci., 18 December 2018 | https://doi.org/10.3389/fncel.2018.00488
Dr. Reinhardt: This excellent, detailed review explores the numerous interactions involved and offers suggestions to actively counteract the progression of the pathology by regulation of microglial pro-inflammatory activation:
“Capsaicin has been used to block TNF-a or IL-1ß, reducing the neuronal degeneration induced by MPTP in PD models.” (Chung et al., 2017). “Similar to TNF-a or IL-1ß, capsaicin significantly suppressed the activation of MAPK related pathways.”
Web MD reports capsaicin is helpful for pain and inflammation associated with joint conditions like rheumatoid arthritis and osteoarthritis, fibromyalgia, muscle sprains and strains, migraines and other severe headaches, surgical pain, inflammation, redness, and pain from psoriasis, pain from nerve damage that’s due to shingles, postherpetic neuralgia, HIV, and peripheral diabetic neuropathy. Capsaicin is sold as a topical cream (about $8.00 for 4 ounces), and as capsules (as cayenne pepper) for about $0.06 per serving.
“Other inflammatory pathways, such as NLRP3 inflammasome or TLR4 pathways, became a therapeutic target due to its role in pro-inflammatory cytokines production in AD and PD (Fellner et al., 2013; Heneka et al., 2013; Burguillos et al., 2015). Recently, Slusarczyk et al. (2018), demonstrate the role of the antidepressant compound Tianeptine, in the inhibition of NLRP3 and TLR4 related pathways, reducing microglial activation. Similar to this compound, Resveratrol (a phenol compound) treatment also prevented the pro-inflammatory effect of fibrillar Aß on macrophages by inhibiting STATs and NFkB related pathways, affecting to TNF-a or IL-6 levels.”
“Resveratrol is a chemical found in red wine, red grape skins, purple grape juice, mulberries, and in smaller amounts in peanuts. Resveratrol is most commonly used for high cholesterol, cancer, heart disease, and many other conditions. Resveratrol might expand blood vessels and reduce the activity of cells important in blood clotting. Some research suggests that resveratrol has weak estrogen (a female hormone) effects. It may also decrease pain and swelling (inflammation).” (WebMD)
Tianeptine is a prescription drug sold in most of the world, although not the US. It enhances serotonin reuptake, essentially the opposite of normal “anti”depressants. It has been shown to be helpful with irritable bowel syndrome and asthma. It is the only agent known to both reduce free serotonin in plasma and enhance uptake in platelets. Tianeptine also has anticonvulsant and analgesic effects, is effective in treating pain due to fibromyalgia and has been shown to have efficacy with minimal side effects in the treatment of attention-deficit hyperactivity disorder.
”Another strategy followed to reduce the impact of AD progression is the use of non-steroidal anti-inflammatory drugs (NSAID). The use of NSAID, as a long run strategy to counteract AD progression, remains controversial due to not fully conclusive data. However, in a recent meta-analysis performed by Zhang et al. (2018) (the meta-analysis includes 121 studies: 16 cohort studies with 236,022 participants and published between 1995 and 2016), the authors conclude that the use of NSAIDs is significantly associated with a reduction in the risk of developing AD.”
Microbiome Research ‘Opening Doors’ to New Alzheimer’s Treatments
Studies that have examined a relationship between Alzheimer’s disease and gut microbiota have highlighted the potential of probiotics and prebiotics as a method of restoring the gut microbiota (Aging [Albany NY]. 2020 Mar 31; 12[6]:5539-50). Probiotics are popularly sold in health food aisles of grocery stores, and prebiotics are available in foods such as yogurts, tempeh, sauerkraut, and kimchi, as well as in drinks such as Kombucha tea. The effectiveness of probiotics and prebiotics also are being examined in randomized, controlled trials in patients with mild cognitive decline and mild Alzheimer’s disease, Dr. Grossberg said. One therapy, Sodium oligomannate, a marine algae–derived oral oligosaccharide, has shown effectiveness in remodeling gut microbiota and has been approved in China to treat patients with mild or moderate Alzheimer’s disease. Currently, no approved gut microbiota therapies are approved in the United States to treat Alzheimer’s disease; however, encouraging use of a prebiotic, a probiotic, or a Mediterranean diet is something clinicians might want to consider for their patients.
“The fact that we’re studying these things has really led to the notion that it may not be a bad idea for people to consume these healthy bacteria in later life, either as a way to prevent or delay, or to treat Alzheimer’s disease,” Dr. Grossberg said. “There’s really no downside.”
Neurology reviews July 29, 2020, https://www.mdedge.com/neurology/article/226225/alzheimers-cognition/microbiome-research-opening-doors-new-alzheimers?channel=39313