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candidiasis articles
Candidiasis-Alzheimer's Disease
By Marc J. Bielski, M.D.
Neurodegenerative diseases have one thing in common—various cells of the central nervous system stop working or die.
From “Unraveling Candidiasis”-Chapter 10: Psychological and Neurological Manifestations of Neurodegenerative Diseases.
“Although Alzheimer’s disease (AD), multiple sclerosis (MS), and Parkinson’s disease (PD) are discussed in this section, other notable expressions are amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD), multiple system atrophy (MSA), and prion diseases. There seems to be a genetic predisposition to develop some of these diseases. Other causes include medical conditions such as alcoholism, a tumor, and a stroke, as well as exposures to toxins (heavy metals, chemicals, plastics, etc.) and viruses.
Alzheimer’s Disease & Dementia
● It’s important to mention that dementia is a broad term, describing a range of symptoms that impair someone’s ability to perform their daily activities.
● Common symptoms include a decline in memory, changes in thinking, poor judgment and/or reasoning, decreased focus and attention, language changes, and behavior changes.
● These can occur from aging or result from the candidiasis-related psychological and neurological manifestations that are discussed in this chapter.
● In 2020, there were more than 55 million people living with dementia worldwide, and this number is expected to double every 20 years (78 million by 2032 and 139 million by 2050). In 2019, the global economic costs related to dementia were reported to be 1.3 trillion U.S. dollars. (And, given the numbers of increasingly sick people, these are underestimates of the global health crisis that is unfolding.)
There are many different types and causes of dementia, but Alzheimer’s disease (AD) is the most common; it is thought to contribute to 60 to 70 percent of cases. In 2022, according to the Alzheimer’s Association, AD was estimated to affect 6.5 million Americans, which is expected to double by 2060. The worldwide prevalence is about 33 to 38.5 million people.
Cause and Effect?
● Alzheimer’s disease is thought to be caused by a combination of age-related changes within the brain, involving genetic, environmental, and lifestyle factors.
● The risk factors for AD include age, alcohol consumption, aluminum ingestion, concussion, cerebral hypoperfusion, diabetes, homocysteine, hypercholesterolemia, hypertension, obesity, pesticides, pollution, physical inactivity, sleep disruption, and smoking. *Except for trauma, self-induced abuse, and toxin exposures, all of these are risk factors for developing candidiasis and its manifestations. (Holistic physicians are aware that other toxic metals can contribute and are more problematic than aluminum.)
There are four stages of AD:
- Preclinical, involving brain changes without disease signs;
- Mild early, cognitive problems;
- Moderate, middle; and
- Severe, late.
History Lesson
● In 1901, Alois Alzheimer, a German psychiatrist and neuropathologist, observed a 51-year-old female patient in a Frankfurt asylum who had strange behavioral symptoms, including a loss of her short-term memory.
● After the patient died on April 8, 1906, Dr. Alzheimer acquired her medical records and brain, which were taken to a laboratory in Munich.
● Using the newly developed Bielschowsky stain, he identified the amyloid plaques and neurofibrillary tangles that later became the brain anomalies indicative of AD.
● Since then, another noted feature is the loss of connections between neurons within the brain.
● The initial damage involves parts of the brain that participate in memory, including the entorhinal cortex and hippocampus.
● As AD progresses, it can adversely affect areas within the cerebral cortex that are involved with language, reasoning, and social behavior.
● With further insults, many other brain areas are damaged.
Modern Science
AD is a brain disorder involving mental deterioration that occurs in middle or old age because of degenerative insults that occur within the brain (and nervous system).
● Amyloid plaques are aggregates of misfolded proteins that arise in the spaces between nerve cells, whereas neurofibrillary tangles are abnormal accumulations of a “tau” protein that collects inside neurons.
● In a healthy brain, certain glial cells perform valuable functions; microglia are supposed to engulf and destroy waste and toxins, whereas astrocytes assist in clearing plaque and cellular debris.
● In AD, the microglia and astrocytes surround the neurons but fail to perform their debris-clearing functions. Even worse, they release inflammatory chemicals that further damage the neurons they are supposed to protect.
● The acetaldehyde hypothesis was previously mentioned in this chapter (10). In short, disease- causing yeast can manufacture acetaldehyde (and ethanol), which can be absorbed, circulate throughout the blood, and enter the brain. Since it is a toxic chemical, prolonged exposure or large amounts can promote injury by free radical reactions and peroxidation (chapter 7).
● Within the brain, acetaldehyde is thought to block the connections between brain cells (synapses), which is consistent with the findings in AD. It also inhibits the synthesis of acetylcholine, decreasing the functioning of the autonomic nervous system. It may bind with or be incorporated into neurotransmitters, creating pseudo-neurotransmitters (false messengers) that readily disrupt the brain’s functioning.
● So, the presence of chronic candidiasis can certainly contribute to the brain degeneration that occurs in AD.
● In addition, disease-causing yeast (as well as Aspergillus fumigatus, Penicillium bilaii, and Gliocladium species) produce gliotoxin, which suppresses immunity and is toxic to different types of nervous system cells, including astrocytes, oligodendrocytes, and glial cells.
● Yes, there is strong evidence for a candidiasis-AD connection!
What about the vascular problems that are thought to contribute to AD? Is there an AD-cardiovascular connection? This can involve reduced blood flow within the brain, decreasing the amount of oxygen needed for proper functioning. More concerning, it may cause injury or damage to the blood-brain barrier (BBB), which is a vital immunological feature within the central nervous system.
The BBB is the interface between the blood vessels and interstitial fluid within the brain, and it is composed of four types of cells (endothelial cells, pericytes, astrocytes, and microglia).
● It usually protects the brain from harmful substances, while allowing glucose and other needed factors to enter the brain tissue.
● It also forms a structural-functional barrier that prevents various microorganisms circulating within the blood from entering the brain, including disease-causing yeast, molds, bacteria, parasites, and/or viruses.
In AD, a damaged BBB allows harmful substances to access the brain, while glucose is prevented from entering. This adds to the inflammation and vascular problems within the brain’s cells and tissue.
● In short, AD is a cause and consequence of vascular problems within the brain.
● Since there is a candidiasis-cardiovascular connection (chapter 7) and an AD-cardiovascular connection, this lends more support for a candidiasis-AD connection.
● Because chronic candidiasis is a persistent infection with allergic consequences, the constant inflammation and free radical damage can certainly contribute to the vascular disturbances that occur in AD.
● Moreover, the four types of cells comprising the BBB can directly and/or indirectly be adversely affected by the chronic presence of disease-causing yeast, including their infectious and allergic inflammation and toxins, so the pathology that occurs in AD is consistent with chronic candidiasis.
Yet, there are other possibilities…
Once the BBB is injured or damaged, one or more microorganisms may gain direct access to the brain tissue, causing various insults and harm. The following scientific studies may apply to all neurodegenerative diseases, but it is important to mention them here, with respect to AD…
● In 2018, B. Parady commented, “Various fungi and bacteria can colonize in the brain and produce physical alterations seen in Alzheimer’s disease (AD). Environmental and genetic factors affect the occurrence of fungal colonization, and how fungi can grow, enter the brain, and interact with the innate immune system. The essence of AD development is the defeat of the innate immune system, whether through vulnerable patient health status or treatment that suppresses inflammation by suppressing the innate immune system. External and mechanical factors that lead to inflammation are a door for pathogenic opportunity. Current research associates the presence of fungi in the etiology of AD and is shown in cerebral tissue at autopsy. From the time of the discovery of AD, much speculation exists for an infective cause. Identifying any AD disease organism is obscured by processes that can take place over years. Amyloid protein deposits are generally considered to be evidence of an intrinsic response to stress or imbalance, but instead amyloid may be evidence of the innate immune response which exists to destroy fungal colonization through structural interference and cytotoxicity. Fungi can remain ensconced for a long time in niches or inside cells, and it is the harboring of fungi that leads to repeated reinfection and slow wider colonization that eventually leads to a grave outcome. Although many fungi and bacteria are associated with AD affected tissues, discussion here focuses on Candida albicans as the archetype of human fungal pathology because of its wide proliferation as a commensal fungus, extensive published research, numerous fungal morphologies, and majority proliferation in AD tissues.”
● In 2019, J. Block stated, “The development of Alzheimer’s Disease (AD) might reflect, in its acquired aspects, a cooperative pathogenesis whereby infectious enablers which do not necessarily cross the blood-brain barrier augment the invasive properties of a less virulent organism, thus enabling it to infect the brain. An example interaction is described which involves Chlamydia species, Human papillomavirus (HPV), microbiota, and yeast, where yeast is a pathogen of low virulence which crosses the blood-brain barrier. The cooperative pathogenesis begins at the mucosal epithelium. Infection by Chlamydia, HPV, or dysbiosis of commensal bacteria disrupts the integrity of the mucosal epithelium, thereby allowing colonizing yeast to penetrate the epithelial barrier and enter into the blood stream. Chlamydia and enabling commensals promote insulin resistance, which provides yeast with glucose and also sets the stage for accumulation of amyloid beta protein (ABP). Meanwhile, HPV-induced and hyperglycemia-induced immunological changes enable the spread of newly invasive yeast to the brain, where the release of inflammatory cytokines in response to yeast promotes production of ABP. Chlamydia also cross-reacts with Candida species, which may stimulate further brain inflammation in response to Candida and may augment production of ABP. The yeast’s less virulent origins, coupled with immune modulation by enablers, might explain why AD as a model of infectious encephalitis is always slow and insidious rather than occasionally febrile, accompanied by seizures, or marked by signs of meningeal inflammation.”
● In 2022, Z. X. Phuna et al. noted, “Candida spp., Malassezia spp., Cladosporium spp. and Alternaria spp. are among the most common fungi detected in the brain of patients with Alzheimer’s disease (AD)... In general, they enter the brain via systemic infection due to disrupted epithelial barrier from skin and gut colonization. Once it reaches the brain, Candida species has been postulated to induce fungal glial granulomas with amyloid precursor protein (APP) accumulated inside. Cleavage of APP can lead to the production of amyloid beta (Aβ). Malassezia species can lead to neuroinflammation via activating helper T-cell (Th) 1 and Th17 immune response. Besides that, the pathogenesis of Cladosporium species and Alternaria species 234 Multiple Sclerosis Unraveling Candidiasis in AD remains unknown, but it could be related to the neuroinflammation. . . . All these four fungi can be detected at the same time in the brain, which contribute to chronic neuroinflammation and neurodegeneration in the brain.”
● In 2022, A. Menden et al. were aware that “altered gut microbial composition has been widely acknowledged as a common feature of AD, which potentially contributes to progression or onset of AD.” They treated a strain of mice (APP/PS1), improving their gut microbiota (microbiome) composition, which reduced their neuroinflammation and memory deficits.
● In 2023, D. Cammann et al. reported, “A growing body of evidence suggests that dysbiosis of the human gut microbiota is associated with neurodegenerative diseases like Alzheimer’s disease (AD) via neuroinflammatory processes across the microbiota-gut-brain axis. The gut microbiota affects brain health through the secretion of toxins and short chain fatty acids, which modulates gut permeability and numerous immune functions. Observational studies indicate that AD patients have reduced microbiome diversity, which could contribute to the pathogenesis of the disease.” Their focus was on gut bacteria; they found “ten genera are significantly associated with AD.” They concluded, “Our results highlight that proinflammatory gut microbiota might promote AD development . . .” Their focus involved apolipoprotein E (APOE) because one variant (E4) seems to be a genetic risk factor for AD.
These researchers and others appreciate that there is a fungal contribution to AD, although other infectious invaders may participate, including harmful molds, bacteria, parasites, and/or viruses.
So, there is a Candidiasis-Alzheimer's Disease connection! Therefore, whether you want to prevent the development of neurodegenerative disease or minimize its effects within your body, please consider that a holistic-integrative medical approach to diagnose and treat your internal, infectious invaders is the best way to readjust your health and achieve long-term wellness. – And don’t ignore their allergic and inflammatory contributions because they must be addressed for a comprehensive cure.”
Marc J. Bielski M.D.
Recent Scientific Articles Confirming these Findings:
“Emerging research points to brain fungus as a potential trigger for Alzheimer’s disease”, Baylor College of Medicine; October 16, 2023
“World Health Organization releases the first-ever list of health-threatening fungi” October 25, 2022
https://www.who.int/news/item/25-10-2022-who-releases-first-ever-list-of-health-threatening-fungi
“Giant Study Pinpoints specific gut bacteria linked to Alzheimer’s”, April 6, 2023
https://www.sciencealert.com/giant-study-pinpoints-specific-gut-bacteria-linked-to-alzheimers