The Candida Expert

Posts tagged ‘Yeast’

Antibiotic Use In Infants Is Associated With Being Overweight

Antibiotics. Antibiotics. Antibiotics. Research continues to reveal the toll that these drugs take on human health. Antibiotics (meaning, “Against Life”) have been associated with many diseases in adults and children – obesity, asthma, inflammatory bowel disease, malnutrition, diabetes, neurodegeneration, and many others. Two new studies, just published in the International Journal of Obesity and Nature Journal, cite once again the link between antibiotic use and weight gain in children. Antibiotics are given to farm animals to increase their weight. This type of use alone can be considered to be practical scientific evidence that…http://candidaplan.com/blog/425/antibiotic-use-in-infants-is-associated-with-being-overweight/

 

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Gut Microbes Benefit Pregnancy

More and more science points out how critical and essential the intestinal flora (microbiome) is for health in the body. We are “Super-organisms.” The current point of view is that we consist of host cells (human cells) and support cells (bacteria, parasites, viruses, yeasts, fungi, etc.). Over thousands of years, we have co-evolved into a cohesive and co-dependent unit, where the presence and health of all the parts (human and non-human alike) constitutes the health of the whole. This recent research article demonstrates how the intestinal flora, or gut microbiota, play a regulatory role in creating a healthy pregnancy.

The composition of microbes in the gut –http://candidaplan.com/blog/?p=336

 

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Hydrochloric Acid and Health

Hydrcochloric acid (HCL) is produced in the stomach to aid in activating digestion of foods and protection of the intestinal flora. Excess stomach acid (HCL) has traditionally been treated as a result of low HCL levels that creates cycles of over- and under-production. With the advent of direct-to-consumer marketing by pharmaceutical companies, the public was entrained to believe that this was purely an excess HCL problem that needed to be suppressed with antacids, leaving behind the science, physiology, and wisdom of the body.

Continue reading at –  http://candidaplan.com/blog/699/hydrochloric-acid-and-health/

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Candida and Diabetes

Common symptoms associated with candida infections include hypoglycemia and insulin resistance. These often occur together in many people. Hypoglycemia is low blood sugar and insulin resistance is high blood sugar. Left alone long enough in the body, they can develop into diabetes. So what’s the connection with candida?

To discover this, we need to know more about how candida functions in the body. Candida has an amazing ability to adapt to the various environments found in the body’s many organs and tissues. When sugar is absent, it switches to burning fat as it’s main fuel source. So much for all of the candida diets that heavily restrict sugar. More about that in another post. Candida can thrive on sugar however and uses whatever is at hand, as well as creating conditions that serve it’s ability to continue to grow and spread.

The main mechanism by which candida causes tissue destruction in the human body is via a group of protease enzymes called Secteted Aspartyl Proteases (SAPs). Protease enzymes are responsible for breaking down protein and protein structures. SAPs are also considered to be candida’s main mechanism of virulence or pathogenicity – how it spreads in the body and causes damage.
Researchers at UCSD discovered that protease enzymes can lead to diabetes, hypertension, and immune system suppression (3 common symptoms of candida infections). They create diabetes by destroying the receptors on cells that insulin binds to. Insulin is a hormone produced by the pancreas gland. It works like a key in that it attaches to a receptor site on cells, which then opens gates in the cell wall that allow sugar to enter the cell and be used as a fuel. Without insulin or the receptors, sugar stays in the blood stream and continues to build up, leading to problems in regulating blood sugar.

Through SAPs, candida can destroy the protein-based receptors on the cell walls, leading to higher levels of sugar circulating in the body. These same SAP enzymes can destroy attachment sites on white blood cells that enable the ability of white blood cells to leave the blood stream and enter tissues where an infection is taking place. The mechanism of how they create hypertension is still not clear.

http://www.jacobsschool.ucsd.edu/news/news_releases/release.sfe?id=744.

 

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Azithromycin (Z-Pak, Z-MAX) and Levaquin Increase Cardiovascular Deaths

There never seems to be any good news coming out about antibiotics. This study compares usage to people who didn’t take antibiotics, clearly demonstrating that antibiotics kill people. The title states that they increase the risk of death, which minimizes the fact they are proven to cause more deaths – Worst Pills Best Pills Newsletter article August, 2012

Increased Risk of Cardiovascular Death With Azithromycin and Levofloxacin

A study just released in The New England Journal of Medicine (NEJM) has found that azithromycin (ZITHROMAX, ZMAX) and levofloxacin (LEVAQUIN), two widely used antibiotics, may increase the risk of cardiovascular death, especially sudden death from heart rhythm disturbances.

Based on an examination of the medical records of 3.5 million Tennessee Medicaid patients, those who took azithromycin (distributed commonly as the five-day “Z-PAK”) were almost three times more likely to die from cardiovascular causes, such as sudden cardiac death, during the five days of therapy than those who took no antibiotics. The patients who took azithromycin also were 2.5 times more likely to die from cardiovascular causes than those who took amoxicillin (AMOXIL), another antibiotic. This translated to 47 to 245 more cardiovascular deaths (the range of excess deaths depends on the patients’ cardiac risk factors) for every 1 million patients placed on the drug, relative to amoxicillin users.

Levofloxacin was associated with a 50 percent increased risk of cardiovascular death compared to the risk in those who took amoxicillin, although the results for levofloxacin were less clear than those for azithromycin.

Based on this research and previous studies, both azithromycin and levofloxacin are thought to cause a heart rhythm disturbance known as torsades de pointes, which can lead to sudden cardiac death, the most common cause of death in azithromycin users in the recent NEJM study.

Another article by researchers at Vanderbilt University appeared in the NEJM in 2004 showed an increase death rate with the use of erythromycin. Other research published by the Americam Medical Association (AMA) has shown a 50% increase risk of breast cancer in women who used antibiotics for any indication.

Tryptophan Reduces Intestinal Inflammation

It’s always nice to see good research that helps to clarify simple principles that demonstrate what effectively works and doesn’t work for our bodies. Researchers from Japan, Switzerlan, Germany, Austria, and the Netherlands have discovered the effectiveness of the natural amino acid, Tryptophan in controlling inflammation of the intestinal tract. Such inflammation is associated with malnutrition, diarrhea, Crohn’s, IBS, IBD, and Colitis – http://www.sciencedaily.com/releases/2012/07/120725132133.htm

More than one billion people in poor countries are starving, and malnutrition remains a major problem even in rich countries, making it a leading cause of death in the world. For over a hundred years, doctors have known that a lack of protein in the diet or low levels of amino acids, the building blocks of proteins, can lead to symptoms like diarrhoea, inflamed intestines and other immune system disorders, which weaken the body and can be fatal. However, the molecular mechanism which explains how malnutrition causes such severe symptoms has been largely unexplored.

Now a research group led by Josef Penninger, the director of the Institute of Molecular Biotechnology (IMBA) in Vienna, Austria, in cooperation with Philip Rosenstiel, University of Kiel, Germany, has found a molecular explanation for the increased susceptibility to intestinal inflammation in malnutrition.  The researchers were studying an enzyme which helps to control blood pressure, kidney failure in diabetes, heart failure and lung injury, called the Angiotensin Converting Enzyme 2, or ACE2.  This enzyme was identified as the key receptor for SARS virus infections, but the researchers also discovered an entirely new function.  ACE2 controls the way our intestines take in amino acids from our food, via amino acid transporters, and in particular the uptake of the essential amino acid tryptophan.

Too little tryptophan alters our natural immune system, which changes the types of bacteria which can live in our bowels and guts, leading to higher sensitivity and eventually diarrhoea and inflamed intestines.  Increasing the intake of tryptophan in their diet provided relief for mice suffering from intestinal inflammation. The mixture of bacteria returned to normal, the inflammation died down, and the mice also became less susceptible to new attacks.

“The research shows how the food we eat can directly change the good bacteria in our intestines to bad bacteria and so influence our health”, says Thomas Perlot, the first author of the study. “Our results might also explain nutritional effects that have been known for centuries and provide a molecular link between malnutrition and the bacteria living in our intestines. This discovery could be used in the future to treat patients with a simple regulated diet or by taking tryptophan as a food supplement.  And there is hardly any risk of side effects from artificially increasing an amino acid found in the normal diet.”

Josef Penninger, the lead author, says “I have studied ACE2 for more than 10 years and was completely stunned by this novel link between ACE2 and amino acid balance in the gut. Biology continues to surprise me. Up to a billion people in the world are malnourished, especially the poor and disadvantaged. In Austria alone, around 80,000 people suffer from a chronic inflammatory bowel disease like ulcerative colitis or Crohn’s disease. I hope that our findings have opened a door to a better molecular understanding how malnutrition affects human health. Whether simple tryptophan diets can indeed cure the effects of malnutrition in humans now needs to be carefully tested in clinical trials.”

Common Questions About Candida

Here are three common questions that we get about Candida.

 

1) How Do I Know I Have Candida?

Dr. McCombs analysis of the research, dating back to 1949, shows that if you’ve ever done antibiotics, you’ll have systemic fungal candida. Most people however, won’t have any symptoms of fungal candida infections. Studies that have been done, show that candida albicans can persist undetected in the majority of individuals. For those of you have symptoms already, there’s really no short list of symptoms that would apply as fungal candida can affect every organ, tissue, and cell in the body, depending on several factors.

“Commensal organisms, such as Candida albicans, are able to persistently colonize the host without causing symptoms.”
Interactions of the fungal pathogen Candida albicans with the host
Steffen Rupp
Future microbiology. 01/05/2007; 2:141-51.
http://www.researchgate.net/publication/6176804

“The frequencies of the carriage of yeast pathogens and of serum precipitins to a variety of candida antigens among 254 patients generally tended to increase with the length of the patient’s stay in hospital. This trend was observed even though none of the patients investigated showed signs or symptoms of superficial or systemic candidosis.”
Distribution of pathogenic yeasts and humoral antibodies to candida among hospital inpatients.
J Clin Pathol 1980;33:750-756 doi:10.1136/jcp.33.8.750
http://jcp.bmj.com/content/33/8/750.abstract

“…based on the 15 to 25% rate of asymptomatic colonization in healthy adults or adolescents and especially the high asymptomatic vaginal fungal burden in adolescents.
An Intravaginal Live Candida Challenge in Humans Leads to New Hypotheses for the Immunopathogenesis of Vulvovaginal Candidiasis
Infection and Immunity, May 2004, p. 2939-2946, Vol. 72, No. 5
http://iai.asm.org/cgi/content/full/72/5/2939

 

2) What Causes Candida?

“Antibiotic treatment has also been shown to increase the rate of C. albicans isolation
in stool (15; M. Barza, M. Giuliano, and S. Gorbach, Program Abstr. 25th Intersci.”
“Factors identified that facilitate this dissemination include suppression of the intestinal bacterial flora…”
Factors Affecting Colonization and Dissemination of Candida albicans from the Gastrointestinal Tract of Mice
INFECTION AND IMMUNITY, JUlY 1987, p. 1558-1563
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC260558/pdf/iai00091-0028.pdf

“Candida albicans infections often occur during or shortly after antibacterial treatment.”
Influence of fluoroquinolones on phagocytosis and killing of Candida albicans by human polymorphonuclear neutrophils
Thomas Grúger; Caroline Mörler; Norbert Schnitzler; Kerstin Brandenburg; Sabine Nidermajer; Regine Horré; Josef Zúndorf
http://www.informaworld.com/smpp/content~db=all~content=a793116268?words=candida*%7Calbicans

“Risk factors for candidaemia include breakdown of mucosal barriers due to cytotoxic chemotherapy and surgical procedures, neutropenia, changes in the gut flora due to antibiotics, and invasive interventions that breach the skin, such as intravenous lines and drains (Wey et al, 1989).”
The immune response to fungal infections
Shmuel Shoham1 and Stuart M. Levitz
1Section of Infectious Diseases, Washington Hospital Center, Washington, DC, and 2Department of Medicine, Boston Medical Center and
Boston University School of Medicine, Boston, MA, USA
British Journal of Haematology, 129, 569–582
http://www.aspergillus.org.uk/secure/articles/pdfs/shoham05.pdf

“The composition of the microbiota is significantly affected by the use of antibiotics, which are often used extensively,…”
Host immune response to antibiotic perturbation of the microbiota
M Wlodarska and B B Finlay
http://www.nature.com/mi/journal/v3/n2/full/mi2009135a.html

“Mice were pretreated with antibacterial agents to alter their resident microflora, and then orally inoculated with C. glabrata and/or C. albicans. Elimination of detectable cecal bacteria facilitated colonization with both Candida species.”
Comparative abilities of Candida glabrata and Candida albicans to colonize and translocate from the intestinal tract of antibiotic-treated mice
Michelle J. Henry-Stanley; Robb M. Garni; Mary Alice Johnson; Catherine M. Bendel; Carol L. Wells
http://www.informaworld.com/smpp/content~db=all~content=a727729968?words=candida*|albicans*

“…antibiotic therapy has been reported to precede disseminated candidiasis in children.”
Interaction of Candida albicans with Human Leukocytes and Serum
ROBERT I. LEHRER AND MARTIN J. CLINE
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC315286/pdf/jbacter00585-0178.pdf

“Oral antibiotic therapy in humans often leads to colonization and over-growth of the GI tract by C. albicans”
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
http://www.jstor.org/stable/pdfplus/30113658?tokenId=KxZI8GrRjXWed9JhIfFv

“Antibiotic treatment decreased the total population levels of the indigenous bacterial flora, and predisposed mice to gastrointestinal overgrowth and subsequent dissemination by Candida albicans, C. parapsilosis, C. pseudotropicalis, C. tropicalis, and Torulopsis glabrata.”
Dissemination of yeasts after gastrointestinal inoculation in antibiotic-treated mice
1983, Vol. 21, No. 1 , Pages 27-33
http://informahealthcare.com/doi/abs/10.1080/00362178385380051

“Antibiotic treatment decreased the total population levels of the indigenous bacterial flora and predisposed hamsters to gastrointestinal overgrowth and subsequent systemic dissemination by C. albicans in 86% of the animals.”
Ecology of Candida albicans Gut Colonization: Inhibition of Candida Adhesion, Colonization, and Dissemination from the Gastrointestinal Tract by Bacterial Antagonism
INFECTION AND IMMUNITY, Sept. 1985, p. 654-663
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC261235/pdf/iai00114-0202.pdf

 

3) How Long Does It Take For Candida To Spread In The Body?

“Oral-intragastric inoculation of 5-6-day-old mice with yeast of a virulent strain of Candida albicans (CA30) resulted in systemic spread within 30 min after challenge. Histological examinations of the gastrointestinal (GI) tract have shown that the highest frequency of invasion of the mucosa by yeast cells occurred in the region of the jejunum 1-3 h after inoculation. Results of ultrastructural examinations of sites where the fungus invaded the bowel wall suggested that C. albicans yeast cells are capable of progressive extracellular digestion of the intestinal mucus barrier and microvillus layer, followed by intracellular invasion of columnar epithelial cells.”
Morphological aspects of gastrointestinal tract invasion by Candida albicans in the infant mouse.
J Med Vet Mycol. 1988 Jun;26(3):173-85.
http://www.ncbi.nlm.nih.gov/pubmed/3050009

“The pseudomycelium was found to invade animal epithelia at an average rate of 2 microns per hour, penetrating the entire epithelial thickness during 24-48 h. These data have been extrapolated to clinical pathology. On the basis of experimental data and by measuring the epithelial thickness in some human mucous membranes, the presumable periods of total epithelial penetration were calculated which may lead to vascular invasion and create the danger of dissemination. For different human mucous membranes these periods ranged from 22 to 59 h.”
Velocity of Candida albicans invasion into host tissues.
Mycoses ; 34:293-6.
http://www.ophsource.org/periodicals/ophtha/medline/record/MDLN.1803229

“Critical times in the development of infections in optimally challenged BALB/c mice were at 5-10 h (bloodstream fully cleared of fungi), 24 h (start of exponential fungal growth in kidneys) and 48 h (50% of blood cultures become positive.”
Temporal events in the intravenous challenge model for experimental Candida albicans infections in female mice.
Mycoses. 2005 May;48(3):151-61.
http://www.ncbi.nlm.nih.gov/pubmed/15842329

 

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