The age old view of seeing modern medicine as being scientifically up-to-date is rapidly fading away. More and more people are falling outside of medicine’s ability to care for them and seeking help elsewhere. Nowhere is this more evident than with systemic fungal candida. Medical doctors don’t acknowledge its existence, except in severely immunosuppressed patients as those with AIDS, some cancers, and patients taking drugs to suppress the immune system.
Science has published over 62,000 studies about candida since the introduction of antibiotics in the mid-1940s, with scientists weighing in on its effects in all types of individuals, including those with healthy immune systems. Obviously, there is a huge gap between science and medicine when it comes to candida.
While medical doctors continue to insist that candida only affects the immunosuppressed, scientists and researchers state otherwise, and extend the list of those affected to include: diabetics, premature infants, surgical patients (4)(5)(6); hospitalized patients, especially in Intensive Care Units, or having major injuries, burn victims (5); nutritional deficiencies, dentures, salivary abnormalities (7); as well as aging (7)(8)(9)(10); stress (2); Alcoholism, cirrhosis, tuberculosis, intravenous drug abuse, and granulocytopenia (6).
Researchers continuously broaden the scope of those being affected. Valdimarsson et al. state that there are no common immunological denominators (1). Senet states that the pathogenic behavior of Candida may appear following even a slight modification of the host (2). Berg et al. on behalf of Biocodex Pharmaceuticals states that Candida spreads in immunocompetent individuals (3).
Medical doctors state that candida only causes problems in immunosuppressed individuals, yet there are over 100 symptoms, conditions, and diseases that can be caused by or modulated by candida. The common factor in all of these is not immunosuppression, but inflammation. Candida causes an increase in Matrix Metalloproteases (MMPs) and a decrease in inhibitors of MMPs that can lead to Lupus, Scleroderma, Glaucoma, Cirrhosis, Fibrosis, Tumors, Dementia, Aortic Aneurysms, Arthritis, Psoriasis, Multiple Sclerosis, Rheumatism, Crohn’s, and autoimmune conditions and syndromes (11)(12)(13).
Given that fungal candida is associated with so many symptoms, conditions, and diseases, one would think that a medical doctor would be aware of well-documented, evidence-based, scientifically-backed research that demonstrates time and time again a common causative agent. Once this cause was known, it would serve the best interests of the patient to be aware of and avoid when possible, the use of any predisposing factors that would create such a cause. If for some reason this was unavoidable, then the doctor should provide the patient with this information and then instruct them on how to compensate and remedy any imbalances caused by it. This however, as far as candida is concerned, does not happen in medicine today. If it did, medical doctors would be acutely aware that antibiotics cause systemic fungal conditions whenever they are used, and that this can then then lead to other conditions and diseases. Upon giving antibiotics, they would recommend that the patient follow protocols that can help to correct and remedy the effects of antibiotics in the body.
The widespread use of antibiotics, which induce neutropenia, an abnormally low number of neutrophils (white blood cells), and immune system suppression is commonly attributed by science to be the most consistent cause of systemic Candida (14)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(7)(2)(26)(27)(28)(29)(3)(30)(32)(33). Corticosteroids suppress immune system function and can lead to fungal candida (34)(21)(3). Intestinal homeostasis is critical for human health (15)(4)(2)(27)(3)(31). This is just a sampling of what’s documented, but medicine acknowledges none of it in the practice of medicine.
The science of candida and how it affects the body goes far beyond what is written here. The ability of antibiotics to create systemic fungal candida is documented in thousands of studies dating back to the introduction of antibiotics in the 1940s. This gap between science and the practice of modern medicine is a major cause of sickness and illness today. In truth, it cannot be referred to as a gap, for it is a wide chasm that millions of people fall into while under modern medical care. As modern medicine continues its decline, patients will search for the truths that lead them back to a state of health and a life of vitality.
Start living a healthier life today. Dr. McCombs Candida Plan.
1. Immunological phenomena associated with chronic mucocutaneous candidiasis have recently been intensively studied by many workers (reviewed by Kirkpatrick, Rich & Bennett, 1971). The results have shown that there is no common immunological denominator in this disease. The most common finding, however, is defective cellular immunity, which may or may not be accompanied by failure of in vitro lymphocyte transformation.
Immunological Feautures in a Case of Chronic Granulomatous Candidiasis and its Treatment with Transfer Factor
H. VALDIMARSSON, C. B. S. WOOD, J. R. HOBBS AND P. J. L. HOLT
2. Clinical studies show that any modification of the host immune status can facilitate the proliferation of endogenous Candida which, according to the importance of the immune deficiency, can provoke diseases ranging from benign localized mucocutaneous candidosis to sometimes lethal systemic invasions. The pathogenic behavior of Candida cells is mainly due to a very high phenotypic biodiversity. Following even very slight environmental modifications, it may change its behavior through the appearance of new or amplified such as tube formation, adherence, protease secretion, etc. Together with the impairment of host defenses, these new invasive properties lead to the so-called opportunistic pathogenicity of Candida cells. From a host point of view, after the integrity of surface teguments, the mucosal protection is ensured by the Th1 “cellular” immune response which, through pro-inflammatory cytokine production, boosts the efficacy of the phagocytes (Polymorphonuclear cells and macrophages). Neutrophils are of particular importance as deep seated Candida proliferation is mostly associated with neutropenia. Whatever the pathogenic process, it is mostly due to modifications provoked by increasing medical awareness which makes patients more susceptible to illness. A better knowledge of the precise mechanisms involved and would lead to improved strategies for prevention.
Stress is an often forgotten cause of temporary immunodeficiency. Neuroendocrine regulation and chronobiological effects may notably modulate the immune system and provide the opportunity of fungal proliferation.
As Wilson (1962) put it: “C. albicans is a better clinician and can discover abnormalities in persons much earlier in the course of the development of such abnormalities than we can with our chemical tests”.
The pathogenic behaviour of Candida may appear following even a slight modification of the host.
Risk factors and physiopathology of Candidiasis
3. We previously reported that the primary defense mechanisms inhibiting translocation from the GI tract are an ecologically balanced GI microflora (preventing intestinal microbial overgrowth or colonization by exogenous microorganisms, or both), the host immune defense system, and the physical barrier of an intact intestinal mucosa. Oral antibiotics are especially effective in disrupting the GI ecologic equilibrium, leading to intestinal overgrowth by certain normal flora bacteria and their subsequent translocation from the GI tract.
All mice were given streptomycin and penicillin ad libitum for 4 days (0-4) in drinking water to reduce their indigenous GI microflora.
Prednisolone immunosuppression increased the mean numbers of C albicans translocating to the MLN (mesenteric lymph node) from 775 to 9336 C albicans/g MLN.
Also, placing fresh C albicans in the drinking water each day was as effective a method of colonizing mice with the organism as was daily intragastric inoculation of C albicans.
Viable C albicans translocated across the GI mucosal barrier to the MLN in immunocompetent, antibiotic-decontaminated mice colonized with C albicans, but the translocating C albicans did not spread systemically from the MLN to other organs. S. boulardii treatment reduced the incidence of MLN positive for C albicans in these immunocompetent mice but did not reduce the mean numbers of C albicans per gram of MLN. The ileal and cecal populations of C albicans were not decreased whether S. boulardii was given prior to or following C albicans challenge.
Disruption of the intestinal microecology by oral antibiotics to cause intestinal microbial overgrowth and increased microbial translocation is clinically relevant since antibiotic therapy also predisposes humans to intestinal microbial overgrowth and infection by various bacteria and yeasts, such as C albicans.
Oral antibiotic therapy in humans often leads to colonization and over-growth of the GI tract by C. albicans (Stone HH, Geheber CE, Kolb LD, Kitchens WR. Alimentary tract colonization by Candida albicans. J Surg Res 1973;14:273-6.)
Inhibition of Candida albicans Translocation from the Gastrointestinal Tract of Mice by Oral Administration of Saccharomyces boulardii
R. Berg, P. Bernasconi, D. Fowler, and M. Gautreaux
Dept of Microbiology and Immunology, Lousiana State University Medical Center, Shreveport and BIOCODEX, Montrouge, France
The Journal of Infectious Diseases, Vol. 168, No. 5 (Nov., 1993), pp. 1314-1318
4. Candida albicans is a component of the normal flora of the alimentary tract and also is found on the mucocutaneous membranes of the healthy host. However, when immune defenses are compromised or the normal microflora balance is disrupted, Candida transforms itself into an opportunistic pathogenic killer. Candida is the leading cause of invasive fungal disease in premature infants, diabetics, and surgical patients, and of oropharyngeal disease in AIDS patients. As the induction of cell-mediated immunity to Candida is of critical importance in host defense, we sought to determine whether human dendritic cells (DC) could phagocytose and degrade Candida and subsequently present Candida antigens to T cells. Immature DC obtained by culture of human monocytes in the presence of granulocyte-macrophage colony-stimulating factor and interleukin-4 phagocytosed unopsonized Candida in a time-dependent manner, and phagocytosis was not enhanced by opsonization of Candida by the mannose-fucose receptor. Upon ingestion, DC killed Candida as efficiently as human M, and fungicidal activity was not enhanced by the presence of fresh serum. Although phagocytosis of Candida by DC stimulated the production of superoxide anion, inhibitors of the respiratory burst (or NO production) did not inhibit killing of Candida, even when phagocytosis was blocked by preincubation of DC with cytochalasin D. Further, although apparently only modest phagolysosomal fusion occurred upon DC phagocytosis of Candida, killing of Candida under anaerobic conditions was almost equivalent to killing under aerobic conditions. Finally, DC stimulated Candida-specific lymphocyte proliferation in a concentration-d