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/
Archive for the ‘The Candida Expert’ Category
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
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/
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.
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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.
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.”
In this recent study, Candida albicans was shown to cause inflammatory and autoimmune reactions that lead to arthritis, psoriasis and other skin rashes, multiple sclerosis, and many other conditions and diseases – http://candidaplan.com/blog/620/candida-linked-to-arthritis-multiple-sclerosis-psoriasis-and-other-autoimmune-conditions/
When I developed the McCombs Plan about 20 years ago, I was fortunate enough NOT to be familiar with the anti-candida programs or books that were around. That meant that I could discover for myself what worked and what didn’t work for my patients. Three years later, I started getting questions from my patients about why this or why not that.
The Plan as it had been developed was very successful from the beginning and is still the original Plan as it is laid out today. One of the common questions that I received was why – http://candidaplan.com/blog/432/candida-fruit-and-dr-mccombs-candida-plan/
Is it possible to overeat healthy foods? I guess that would depend on the context. The point of the article below is that it is possible to consume too many calories and gain weight, regardless of whether the food is healthy or not. Contrary to this type of logic however, when doing Dr. McCombs Candida Plan – http://candidaplan.com/, we find that eating plenty actually helps to increase weight loss. This is due to the fact that detoxifying the body takes lots of energy and you need to fuel this process. Many people comment that they “haven’t eaten this much in years and they’re still losing weight,” which brings us back to context. Here’s the short article anyway – http://www.sciencedaily.com/releases/2012/07/120724144423.htm
It may make you scratch your head, but in fact it is possible to overeat healthy foods, according to Loyola University Health System registered dietitian Brooke Schantz.
“While fruits are nutritious, too much of even a healthy food can lead to weight gain,” Schantz said. “The key is to remember to control the portion sizes of the foods you consume.”
Schantz reported that overeating healthy foods is easy to do, but the same rules apply to healthy food as junk food. Weight fluctuates based on a basic concept — energy in versus energy out. If your total caloric intake is higher than the energy you burn off in a day, you will gain weight. If it is lower, you will lose weight.
“I have had many patients tell me that they don’t know why they are not losing weight,” Schantz said. “Then they report that they eat fruit all day long. They are almost always shocked when I advise them to watch the quantity of food they eat even if it is healthy.”
Schantz said that one exception applies. Nonstarchy vegetables are difficult to overeat unless they are accompanied by unnecessary calories from sauces, cheeses and butter. This is due to the high water and fiber content of these vegetables coupled with the stretching capacity of the stomach. The vegetables she suggested limiting are those that are high in starch, such as peas, corn and potatoes. Foods that are labeled as fat-free or low-fat are another area of concern.
“People tend to give themselves the freedom to overeat ‘healthy’ foods,” Schantz said. “While the label might say that a food or beverage is low-fat or fat-free, watch the quantity you consume and refrain from eating an excessive amount. Foods that carry these health claims may be high in sugar and calories.”
Context, context, context!
There is always a wealth of information coming forth that helps to provide greater clarity on how candida becomes problematic in the body. This recent study, as reported in Science Daily, provides some good information and some confusing information. I’ll add some editorial throughout the article – http://www.sciencedaily.com/releases/2012/07/120724153651.htm
The opportunistic fungal pathogen Candida albicans inconspicuously lives in our bodies until it senses that we are weak when it quickly adapts to go on the offensive. The fungus, known for causing yeast and other minor infections, also causes a sometimes-fatal infection known as candidemia in immunocompromised patients An in vivo study, published in mBio, demonstrates how C. albicanscan distinguish between a healthy and an unhealthy host and alter its physiology to attack. [There are several factors that cause the conversion of the normal yeast form of candida to its pathogenic, problematic fungal form - pH, temperature, antibiotics, bacterial cell wall components, etc., The phrase, "senses we are weak" isn't something that I have ever seen in scientific studies, but it may be another way to state immunsuppression. Even so, I have yet to see that listed as a trigger for yeast-to-fungal conversion. Immunosuppression can play a role in the spread of candida, but some studies indicate that it isn't a pre-requisite for this to happen. Candidemia is another term for fungal sepsis, or blood-borne fungal infection. Sepsis is one of the top 10 or 11 leading causes of death in the United States, depending on year of reference, and fungal candida causes over 50% of that].
“The ability of the fungus to sense the immune status of its host may be key to its ability to colonize harmlessly in some people but become a deadly pathogen in others,” said Jessica V. Pierce, BA, PhD student in the molecular microbiology program at the Sackler School of Graduate Biomedical Sciences at Tufts. [This is an interesting quote from an author in the study. It can be taken a couple of different ways. It might be interpreted that she is stating that it spreads throughout the body in its fungal form in the presence of an intact immune system, but doesn't create any imbalances. That would be ignoring a lot of other research that demonstrates how the fungal form of candida creates many imbalances within the body. It has been shown to spread through the body without the immune system being compromised. A second interpretation and the one that I believe she is stating is that as a fungus, it colonizes the digestive tract harmlessly or pathogenically depending on the host immune status. That would ignore the fact that candida colonizes the intestinal tract in its yeast form. It may not be much of a differentiation, but it can be misleading as the fungal form is problematic and the yeast form isn't.]
“Effective detection and treatment of disease in immunocompromised patients could potentially work by targeting the levels of a protein, Efg1p, that we found influenced the growth of Candida albicans inside the host,” she continued. [As stated before, there are several factors that cause the conversion of yeast-to-fungus. Efg1 has been identified previously as part of the internal mechanism that regulates the yeast-to-hyphal conversion and back again. It's not the only part and its presence may not be a good indicator of fungal infections, as it can exist in the yeast form also.]
The researchers knew from previous research that Efg1p influences the expression of genes that regulate how harmful a fungal cell can become. Surprisingly, the investigators found that lower Efg1p levels allow the fungal cells to grow to high levels inside a host. Higher levels of the protein result in less growth. [Would the high levels be associated with it's yeast form and the low levels with its fungal form. That can be a good reason for differentiating between yeast and fungus and not referring to both forms as though they were fungal.]
To examine how the immune status could affect the growth of C. albicans within a host, the researchers fed both healthy and immunocompromised mice equal amounts of two fungal strains containing two different levels of the Efg1p protein.
Fecal pellets from the mice were tested to determine which strain of fungi thrived. In a healthy host, the fungal cells with higher levels of the protein predominated.
In immunocompromised mice, the fungal cells with lower levels of the protein flourished. The researchers noted that lack of interactions with immune cells in the intestinal tract most likely caused the necessary environmental conditions favoring fungal cells that express lower levels of the protein, resulting in fungal overgrowth and setting the stage for systemic infection.
“By having a mixed population with some high Efg1p cells and some low Efg1p cells, the fungus can adjust its physiology to remain benign or become harmful when it colonizes hosts with varying immune statuses. These findings are important because they provide the first steps toward developing more effective methods for detecting and treating serious and stubborn infections caused by Candida albicans, such as candidemia,” said Carol A. Kumamoto, PhD, professor of molecular biology and microbiology at Tufts University School of Medicine and member of the molecular microbiology and genetics program faculties at the Sackler School of Graduate Biomedical Sciences.
The immune system and “good bacteria” within the body act to regulate the size of C. albicans fungal populations in healthy individuals. When the immune system is compromised, the fungus can spread throughout the body. Candidemia, i.e. blood-borne Candida, is the fourth most common blood infection among hospitalized patients in the United States and is found in immunocompromised patients such as babies, those with catheters, and the critically ill. [Here we see the authors state that it is the immune system and the “good bacteria” that help to regulate the candida populations. This would be a very strong statement against the use of antibiotics, as antibiotics destroy the “good bacteria” and suppress the immune system. With Sepsis being one of the top causes of death in the United States and over 50% of that being due to fungal candida, much of that can be prevented by not using antibiotics. That would eliminate sepsis as a leading cause of death and fungal candida as the 4th leading cause of hospital infections. Throughout this article I didn’t see any differentiation between the yeast and fungal forms of candida and I didn’t find it mentioned in the original abstract either. Many studies seem to be limited in the breadth of understanding of candida and the vast amount of past research. Through other studies, it has already been established that immunosuppression is not necessary for the spread of candida. For more research on this, view the Candida Facts Sheet article. Tests can only serve as indicators, not absolute measures of function in the body. Targeting something like Efg1 doesn’t seem to be a promising advancement in the understanding or treatment of candida. If the purpose is to create another target for antifungal medications, it must be remembered that all medications contain far more harmful effects than beneficial effects. One common effect of antifungal medications is immunosuppression.