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Antibiotics Cause Candida

This article from the Departments of Microbiology and Immunology and Medicine at Albert Einstein College of Medicine is one of the best articles that I’ve read in a while as it addresses the idea and concept of pathogenicity very well. At the same time, I consider it to be an indictment on the poor state of medicine as it is currently practiced. Conversely, it vindicates the centuries old approach to healing as practiced by holistic doctors around the world – http://www.biomedcentral.com/1741-7007/10/6

Pathogen vs. Non-pathogen –

“…this takes us to an ongoing debate that dates back to the late 19th century when the [Pasteur] germ theory of disease was established. …even then it was obvious that neat classifications were problematic, for it was known that a microbe could be attenuated in the laboratory, but virulence could be restored by passage in a host, suggesting that the same microbe could exist in pathogenic and non-pathogenic states.”

Pasteur’s famous confession on is deathbed that he was wrong about his germ theory was in reference to this as he finally realized that the interaction between the host and the microbe was the determining factor for infection, not the microbe itself. Pasteur’s theory was openly opposed by scientists at the time, as they better understood the host-microbe interaction, however Pasteur held a government position allowing him to craft “official” policy (similar to what’s happening at the FDA today). The pharmaceutical industry has found it to be more profitable to market Pasteur’s germ theory, instead of his later understanding and now current science’s opinion, that the host-microbe interaction is the most important consideration.

“…properties conferring pathogenicity depend as much on the host as they do on the microorganism…it was developments in the 20th century that clearly obliterated the hope of ever drawing a clear and unequivocal line of distinction between pathogens and non-pathogens. Beginning in the 1950s the introduction of broad spectrum antimicrobial agents, immunosuppressive therapies, newer types of surgery, including organ transplantation and joint replacement, implantable devices and indwelling catheters, each of which alters host-microbe interactions, turned out to create conditions in which the host became vulnerable to microbes that were previously considered non-pathogenic. As a result, it became apparent that many microbes previously considered non-pathogenic, or rarely pathogenic, such as Staphylococcus epidermis and Candida albicans, could cause serious disease.”

I would correct the 3rd line to “Beginning in the late 1940s” as that was when antibiotics were introduced and there was a significant jump in fungal Candida albicans cases. The early 1950s saw an even more significant jump in candida albicans cases, along with a strong push in research around candida infections and resulting conditions, as antibiotic use continued to escalate. Of those therapies listed above, it was antibiotic use that created the most significant change. Here we start to see why the medical profession isn’t readily willing to look at systemic fungal Candida as a result of antibiotic use. The widespread use of antibiotics creates an even greater problem by altering the host’s ability to resist infections that are created by their use. Antibiotics empower the pathogen and weaken the host. Some antibiotics have been implicated as a direct trigger for then conversion of the normal yeast form of Candida to it’s pathogenic fungal form. Most research shows that it alters the host terrain, creating the conditions necessary to cause the yeast-fungal conversion.

“Antibiotics make people more vulnerable to microbe-mediated damage because they alter the microbiota, or the normal microbial flora, and the balanced relationships between the microbes that reside in the mucosal niches in the body and the host structures that support these communities. Surgery can have the same effect by removing or altering normal mucosal and cutaneous barriers to infection. So the effects of antibiotics and surgery enhance the pathogenicity of microbes that do not ordinarily cause damage or disease in normal microbial communities, or intact mucosal and cutaneous surfaces, by making the host more susceptible to damage or invasion.”

Is there any more that needs to be said? Thank you Albert Einstein College! You do your namesake great credit. I would like to say more, however. Antibiotic use is not only associated with these immediate effects, but they can permanently alter the make-up of the intestinal flora, and are being implicated in more serious diseases and conditions such as life-threatening colitis, diabetes, cancers, obesity, and a host of as yet other unknown diseases – http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0060280

“many microbes that cause disease are already present in the individual and the individual is thus already ‘infected’. This is exemplified by microbes such as staphylococci and Candida spp., which are actually present in most individuals, but only cause disease in some. This also applies to many other microbes, including those to which an individual is immune, either through prior infection or through vaccination, as immune individuals are recognized as being resistant to the capacity of a microbe to cause disease.”

Health is a state of constant vigilance and maintenance. When you consider that most everyone already carries a heavy body burden of tens of thousands of chemicals and heavy metals from the environment, foods, and water from past exposures, and is constantly faced with even more, it becomes clearer how maintaining health has become an challenge.

“…when a host is immune, pathogenicity is not expressed. What is important to recognize is that pathogenicity and virulence are microbial properties that can only be expressed in a susceptible host.”

Health is a state of constant vigilance and maintenance. Worth repeating.

“…pathogenicity is an outcome of host-microbe interaction and is thus inextricably linked to characteristics of the host as well as those of the microbe. Rather than distinguishing commensals from pathogens/non-pathogens, the immune system of healthy hosts actually depends on these microbes. Commensals (also called the microbiota) are acquired by infection soon after birth, after which they establish residence in mucosal niches where they replicate, and there is increasing evidence that the microbiota play a crucial role in the development of the immune system and that the immune response to the bacteria in mucosal niches helps maintain barriers to invasion on surfaces exposed to potentially harmful microorganisms. The commensal bacteria themselves do no harm, provided that the immune system and mucosal barriers remain normal and intact. The immune system provides a large variety of tools – cells and molecules – that recognize, react to and control microbial growth and invasion, often in a manner that does not result in host damage or disease, and when this happens, there is no readout. In this instance, the immune system might be thought to have distinguished a pathogen from a non-pathogen, but in fact, it simply controls microbial growth and/or invasion in a manner that does not translate into microbial pathogenicity.”

The intestinal tract is an ecosystem composed of bacteria and other micro-organisms. As a whole, it doesn’t matter if some are pathogenic and some are commensal/friendly. They all exist in a harmonious state, as long as the host is healthy. Antibiotics disrupt this harmony.

“An interesting paradox occurs in the case of two bacteria that produce toxins generally regarded as factors increasing the virulence of the microbe: staphylococci that produce a so-called leukocidin, and pneumococci that produce a toxin called pneumolysin. Because these toxins also activate the innate immune response, bacteria that do not produce them can sometimes be more pathogenic than bacteria that do. Thus, when the immune response to a microbe is insufficient, microbial factors can cause damage, and when microbial factors fail to stimulate the immune system, the microbe can disseminate and cause disease.”

The standard medical approach is to see everything as bad and the body doesn’t know what its doing, regardless of what science continues to reveal. It’s not a black and white picture, it’s everything taken as a whole. These type of paradoxes in the human body are present everywhere. As I constantly point out to people when I lecture, we know about 1% of what goes on in the human body.

“At the other end of the spectrum, when the immune response to a microbe is too exuberant, it can be the immune response itself that is responsible for the pathology. When damage occurs in this setting, it is most commonly due to detrimental inflammation and can occur whether the microbe is controlled or contained or not.”

Crohn’s, IBS, IBD, and Colitis are good examples of this. Some authors have stated that most autoimmune diseases originate with imbalances in the intestinal tract.

“There is no difference between an opportunistic pathogen and any other kind of pathogen. Both are microbes and both have the potential to cause damage/disease in a host. The definition that is often used for opportunistic pathogens is that these microbes cause disease in people with impaired immunity but not in normal individuals. However, this definition is purely operational: the same microbe – consider Candida albicans and Staphylococcus epidermidis – can cause disease in one individual but live harmlessly in others, which means that the same microbe would be called an opportunist in one individual and a commensal in another. Indeed, the identification of certain microbes as a cause of disease in certain hosts can unmask or be a sentinel for an underlying immunodeficiency.”

Another way to look at this is, “if you have an infection, it’s diagnostic of a deficient or altered immune response.” One of the most consistent effects of antibiotic use is suppression of the immune system. It doesn’t make sense to suppress the immune system further, when it is already struggling. The reason that most doctors use it and most people continue to turn to its use is that it suppresses the normal immune response that causes the common symptoms of fevers, aches, and pains. It is the suppression of the normal inflammatory response that makes people “feel” better, but at the same time alters the natural healing process of the body. This process is necessary to promote ongoing immune function and improvement of health in the body. Pharmaceutical companies through advertising have raised a generation of doctors and consumers believing that we shouldn’t have to deal with that. We need to quit interfering with the body’s normal healing process by using drugs.

“…there are only microbes and hosts and the outcomes of their interactions, which include commensalism, colonization, latency and disease. Hence, attempts to classify microbes as pathogens, non-pathogens, opportunists, commensals and so forth are misguided because they attribute a property to the microbe that is instead a function of the host, the microbe, and their interaction.”

The entire approach of antibiotic use is severely questioned with the above statement. Antibiotics destroy the balance of the host leaving us susceptible to any number of pathogens, along with newly created antibiotic-resistant superbugs. Antibiotic resistance is now classified as the 3rd leading threat to human health by the World Health Organization (WHO). Antibiotics are connected to life-threatening colitis, diabetes, obesity, and cancers. Antibiotics are part of the problem.

“Pathogenicity and virulence are emergent properties, meaning that they cannot be predicted directly from the properties of the microorganism. The environment, an individual host or population of hosts and/or an individual microbe or population of microbes can change independently, or as a function of complex interactions, including those between environment and host, host and microbe, microbe and environment, and all three. Thus, microbial pathogenicity is intrinsically unpredictable. Host and microbial characteristics are subject to predictable and unpredictable changes prompted by known, unknown, and random environmental, immunological, and other factors. Thus, as it is an outcome of host-microbe interaction whereby each entity is subject to independent and dependent changes at any point in time, pathogenicity is an emergent property.”

This paragraph brings into question the use of vaccines as effective therapies, as well as all antimicrobial drugs. I think that it also points out the reversibility of conditions and diseases by improving host-microbe interactions, not destroying them.

“…however, neither the complexity nor the variability or randomness that occurs in nature occurs or can be recapitulated in models systems. Thus, while predictions on how given (known) variables might affect the potential for a (new) microbe to be pathogenic in a given (known) population might be possible, such predictions are only possible in the context of available knowledge and paradigms. This being the case, prediction of the emergence of new microbes with the potential for pathogenicity will always be subject to severe limitations.”

This paragraph, along with the preceding one, are important because it explains why infectious agents like the H5N1 Bird flu have never materialized into the epidemic that pharmaceutical companies would have us believe in order to get us to use their vaccines. In general, it implicates all vaccines. This paragraph also points out how limited current science is, even though we’re always being lead to believe that the “authorities” are knowledgeable beyond any doubt and we should do whatever they say or recommend. Obviously not. Just say, “No!”

Excerpts from:
Q&A: What is a pathogen? A question that begs the point
Liise-anne Pirofski and Arturo Casadevall
Departments of Microbiology and Immunology and Medicine (Division of Infectious Diseases) of the Albert Einstein College of Medicine and Montefiore Medical Center, 1300 Morris Park Ave, Bronx, NY 10461, USA
BMC Biology 2012, 10:6

 

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Candida Linked To Arthritis, Multiple Sclerosis, Psoriasis, and Other Autoimmune Conditions

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/

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Can You Eat Too Many Healthy Fruits and Veggies?

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!

Does Candida Know When To Attack

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.

More on Bacillus subtilis

Here’s a list of antibiotics that Bacillus subtilis is used with. It’s effects are against aerobic and non-aerobic bacteria. There is no differentiating between good and bad bacteria, as some people are lead to believe. That differentiation is something put out by the pharmaceuitical companies and MDs. The warrior model of destroying this and that as used in medicine, is antiquated and has been so many decades. The “holistic” approach used by many people is just a variation on the medical warriot model, whereby medications are substituted with something else to bring about destruction. The approach to destroying anything in the body, fails to consider that in doing so, we are destroying ourselves in the process. It’s okay if you want to support those groups, it’s just that the information is misleading.

All bacteria in a balanced system benefit the system. Create the balance and you also create the safeguards against anything that shouldn’t be there. Destroy that balance and you’ll see health start to slip away as the ecosystem starts to collapse into chaos.

As you’ll see below, Bacillus subtilis has been associated with food poisoning, disease conditions, and has been tested for biological applications as a biolgical agent.

Bacillus subtilis is the basis for many antibiotics due to its strong antibacterial function. This antibacterial function will create imbalance within the body by destroying bacteria. It also has a strong antifungal effect and is the basis for antifungal medications, but these, as we know, create other imbalances.

You’ll see below this list of B. subtilis-based antibiotics some more information on B. subtilis. It’s not a risk-free choice. Whatever your decision, make it an informed choice.


B. subtilis
does produce an extracellular toxin known as subtilisin. Although subtilisin has very low toxigenic properties (Gill, 1982), this proteinaceous compound is capable of causing allergic reactions in individuals who are repeatedly exposed to it (Edberg, 1991). Sensitization of workers to subtilisin may be a problem in fermentation facilities where exposure to high concentration of this compound may occur. Exposure limits to subtilisin are regulated by Occupational Safety and Health Administration (OSHA) (29 CFR 1900, et seq.)Biotechnology Program Under Toxic Substances Control Act (TSCA)

Bacillus subtilis Final Risk Assessment

III. HAZARD ASSESSMENT

A. Human Health Hazards

1. Colonization

B. subtilis is widely distributed throughout the environment, particularly in soil, air, and decomposing plant residue. It has shown a capacity to grow over a wide range of temperatures including that of the human body (Claus and Berkeley, 1986). However, B. subtilis does not appear to have any specialized attachment mechanisms typically found in organisms capable of colonizing humans (Edberg, 1991). Given its ubiquity in nature and the environmental conditions under which it is capable of surviving, B. subtilis could be expected to temporarily inhabit the skin and gastrointestinal tract of humans, but it is doubtful that this organism would colonize other sites in the human body (Edberg, 1991).

2. Gene Transfer

The transfer of gene sequences between strains of B. subtilis has been demonstrated when the strains were grown together in soil (Graham and Istock, 1979). In addition, Klier et al. (1983) demonstrated the ability of B. subtilis and B. thuringiensis to exchange high frequency transfer plasmids. Other studies have shown that B. subtilis has the ability to express and secrete toxins or components of the toxins that were acquired from other microorganisms through such transfers of genetic material. B. subtilis expressed subunits of toxins from Bordatella pertussis (Saris et al., 1990a, 1990b), as well as subunits of diphtheria toxin (Hemila et al., 1989) and pneumolysin A pneumococcal toxin (Taira et al., 1989). Although B. subtilis does not appear to possess indigenous virulence factor genes, it is theoretically possible that it may acquire such genes from other bacteria, particularly from closely related bacteria within the genus.

3. Toxin Production

A review of the literature by Edberg (1991) failed to reveal the production of toxins by B. subtilis. Although it has been associated with outbreaks of food poisoning (Gilbert et al., 1981 and Kramer et al., 1982 as cited by Logan, 1988), the exact nature of its involvement has not been established. B. subtilis, like other closely related species in the genus, B. licheniformis, B. pumulis, and B. megaterium, have been shown to be capable of producing lecithinase, an enzyme which disrupts membranes of mammalian cells. However, there has not been any correlation between lecithinase production and human disease in B. subtilis.

4. Measure of the Degree of Virulence

B. subtilis appears to have a low degree of virulence to humans. It does not produce significant quantities of extracellular enzymes or possess other virulence factors that would predispose it to cause infection (Edberg, 1991). There are a number of reports where B. subtilis has been isolated from human infections. Earlier literature contains references to infections caused by B. subtilis. However, as previously stated,the term B. subtilis was synonymous for any aerobic sporeforming bacilli, and quite possibly, many of these infections were associated with B. cereus. In a recent British review article, Logan (1988) cites more recent cases of B. subtilis infections in which identification of the bacterium appeared reliable. Infections include a case of endocarditis in a drug abuse patient; fatal pneumonia and bacteremia in three leukemic patients; septicemia in a patient with breast cancer; and infection of a necrotic axillary tumor in another breast cancer patient. Isolation of B. subtilis was also made from surgical wound-drainage sites, from a subphrenic abscess from a breast prosthesis, and from two ventriculo-atrial shunt infections (as cited by Logan, 1988).

Reviews of Bacillus infections from several major hospitals suggest that B. subtilis is an organism with low virulence. Idhe and Armstrong (1973) reported that Bacillus infections were encountered only twelve times over a 6-1/2 year period. Species identification of these Bacillus infections was not made. In another hospital study over a 6-yr. period, only two of the 24 cases of bacteremia caused by Bacillus (of a total of 1,038 cases) were due to B. subtilis (as cited by Edberg, 1991). Many of these patients were immunocompromised or had long term indwelling foreign bodies such as a Hickman catheter.

B. subtilis has also been implicated in several cases of food poisoning (Gilbert et al., 1981 and Kramer et al., 1982 as cited by Logan, 1988).

As previously mentioned, B. subtilis produces a number of enzymes, including subtilisin, for use in laundry detergent products. There have been a number of cases of allergic or hypersensitivity reactions, including dermatitis and respiratory distress after the use of these laundry products (Norris et al., 1981).

5. Conclusions

B. subtilis is not a human pathogen, nor is it toxigenic like some other members of the genus. The virulence characteristics of the microorganism are low. According to Edberg (1991) either the number of microorganisms challenging the individual must be very high or the immune status of the individual very low in order for infection with B. subtilis to occur.

B. Environmental Hazards

3. Hazards to Other Microorganisms

B. subtilis has been shown to produce a wide variety of antibacterial and antifungal compounds (Katz and Demain, 1977; Korzybski et al., 1978). It produces novel antibiotics such as difficidin and oxydifficidin that have activity against a wide spectrum of aerobic and anaerobic bacteria (Zimmerman et al., 1987) as well as more common antibiotics such as bacitracin, bacillin, and bacillomycin B (Parry et al., 1983). The use of B. subtilis as a biocontrol agent of fungal plant pathogens is being investigated because of the effects of antifungal compounds on Monilinia fructicola (McKeen et al., 1986), Aspergillus flavus and A. parasiticus (Kimura and Hirano, 1988), and Rhizoctonia (Loeffler et al., 1986).

Although B. subtilis produces a variety of antibiotic compounds in culture media, the importance of antibiotic production in the environment is unknown (Alexander, 1977).

B. subtilisis not a frank human pathogen, but has on several occasions been isolated from human infections. Infections attributed to B. subtilis include bacteremia, endocarditis, pneumonia, and septicemia. However, these infections were found in patients in compromised immune states. There must be immunosuppression of the host followed by inoculation in high numbers before infection with B. subtilis canoccur. There also have been several reported cases of food poisoning attributed to large numbers of B. subtilis contaminated food. B. subtilis does not produce significant quantities of extracellular enzymes or other factors that would predispose it to cause infection. Unlike several other species in the genus, B. subtilis is not consider toxigenic. B. subtilis does produce the extracellular enzyme subtilisin that has been reported to cause allergic or hypersensitivity reactions in individuals repeatedly exposed to it.

In conclusion, the use of B. subtilis in fermentation facilities for the production of enzymes or specialty chemicals has low risk. Although not completely innocuous, the industrial use of B. subtilis presents low risk of adverse effects to human health or the environment.

Candida and Inflammation in the Athlete

There’s a certain sense of loss in realizing that the best of each us is being eroded away, or lies wasting away, as hidden potential within the cells of our bodies. The gradual erosion of potential is often found in cases where there is an underlying imbalance in the body that creates chronic inflammation and the inability to absorb nutrients for normal function and repair. When chronic inflammation and nutritional imbalances are combined, degeneration of tissues advances at a far faster rate than it normally would. I have found this to repeatedly be the case in people who have been exposed to antibiotics and as a result suffer from the system-wide imbalances that are created from their usage.

In many people, this may look like a normal aging process. In the athlete, it usually is associated with excessive wear and tear on joints and failure of the muscles and the body to respond and perform as they once did. Athletic careers and pursuits can end prematurely, and the hopes and dreams of what could have been, remain forever as hopes and dreams.

Under these types of constant inflammatory conditions, the serious athlete or weekend warrior who pushes the limits of his body’s ability in pursuit of personal records and goals, will end up driving the inflammatory machinery that will eventually rob them of their potential for excellence. Exercise produces pro-inflammatory immune system responses and oxidative stress that play a role in repair and remodeling of muscle tissues. Intense exercise carries this response further, and over the long-run can produce immune system suppression and autoimmune-type responses. The following excerpt from Journal of the International Society of Sports Nutrition helps to explain a little more on this topic:

“DOMS (Delayed Onset Muscle Soreness) typically occurs after unaccustomed or high-intensity exercise, most commonly anaerobic. Soreness is usually noted at 24 hours post-exercise and can last as long as 5 to 7 days post-exercise. Although several models of DOMS have been suggested, researchers generally agree that muscle damage initiates a cascade of events leading to DOMS. The muscle damage and oxidative stress response following anaerobic exercise have been deemed necessary to promote skeletal muscle remodeling to gain benefit from the exercise, but enhanced recovery may be advantageous for more rapidly promoting an anabolic environment.

Exercise elicits mechanical and hormonal reactions from the body. The resulting muscle damage from these reactions elicits inflammatory and oxidative responses that may exacerbate muscle injury and prolong the time to regeneration. The hormonal contributor to muscle damage during exercise is derived through basic neuroendocrine responses to exercise demands. High intensity exercise triggers the activation of the hypothalamic-pituitary-adrenal (HPA) axis leading to the release of cortisol and other catabolic hormones. These hormones function to meet increased energy needs by recruiting substrates for gluconeogenesis via the breakdown of lipids and proteins. Through their catabolic nature, these hormones also indirectly lead to muscle cell damage.

Inflammation following anaerobic exercise functions to clear debris in preparation for muscle regeneration. The magnitude of the increase in inflammatory cytokines (such as IL-6) varies proportionately to the intensity and duration of the exercise. However, a prolonged inflammatory response can increase muscle damage and delay recovery by exacerbating oxidative stress and increasing production of reactive oxygen species (ROS). The increased ROS production seen with high intensity training can lead to oxidative stress such as lipid peroxidation (1).”

While intense exercise is usually associated with greater degrees of DOMS, inflammation, immune system suppression, and oxidative stress, mild-to-moderate exercise is typically associated with boosting the immune system and supporting greater health in the body. If however, there is an underlying state of chronic inflammation due to an infectious agent, then even mild-to-moderate exercise may result in many of the symptoms commonly found with intense exercise, as fuel is added to an already burning fire. Over a period of months and years, this can lead to shortened productivity and limited excellence in today’s athletes. In one sense, it is the equivalent of driving with the brakes on.

The most frequent infectious agent that fits this model is Candida albicans. C. albicans commonly exists as a yeast organism in the human body and is considered a normal part of healthy tissue flora. Due primarily to the effect of antibiotics, this yeast organism transforms into a pathogenic, problematic fungal form that has been associated with a multitude of conditions and diseases in the body.

Since the introduction of antibiotics in the late 1940s following WWII, there has been a remarkable increase in the research of candida-related conditions and diseases (2) with over 24,000 research articles being published since 1949. On average, that is enough for one research article per day in the last 51 years, with enough left over to fill another 6 years of daily research publications. With a one-to-one association between antibiotic use and the development of systemic fungal infections, implications exist for society as whole being afflicted with a post-antibiotic syndrome of fungal candida and immune system dysregulation.

In systemic fungal candida infections, ongoing pro-inflammatory reactions from both systemic and localized immune system responses combine with the virulence mechanisms of fungal candida to create a constant state of oxidative stress, pro-inflammatory hormonal imbalances, chronic tissue inflammation, and tissue degeneration. This type of smoldering, nonresolving inflammation becomes a constant component of the microenvironment within and is implicated in many diseases and conditions.

Joint restriction, pain, swelling and inflammation, weight gain, fatigue, blood sugar imbalances, nutrient deficiencies, slower post-exercise recovery periods and other symptoms are commonly associated with this underlying condition in today’s athletes and others.

In response to patients who had these problems, I developed a well laid out plan to counteract this post-antibiotic syndrome and subsequent systemic imbalances. Athletes who have followed the McCombs Plan have seen a decrease in the degree and amount of inflammation experienced during exercise, as well as pre- and post-exercise inflammatory responses with faster recovery times. Many of the conditions associated with fungal candida that impact human performance have been diminished and resolved. Marathon runners and Tri-atheletes found themselves competing without “hitting the wall.” Wrestlers, weight lifters and others found that their joint pains and restrictions decreased and disappeared. Increased energy and vitality that is sustained throughout the day has been a common response.

If we are to achieve the best that we can be, we must rid ourselves of these types of physiological limitations, or settle for less and be happy with what could have been.

1. The effects of theaflavin-enriched black tea extract on muscle soreness, oxidative stress, inflammation, and endocrine responses to acute anaerobic interval training: a randomized, double-blind, crossover study

Shawn M Arent, Meghan Senso, Devon L Golem and Kenneth H McKeever

Journal of the International Society of Sports Nutrition 2010, 7:11doi:10.1186/1550-2783-7-11

http://www.jissn.com/content/7/1/11

2. SciTrends of Biomedical Sciences

http://rzhetskylab.cu-genome.org/cgi-bin/trendshow?MeSHID=1191

Antibiotics and Candida

I often get asked about antibiotics and systemic candida. Antibiotics are definitely the best way to create systemic fungal infections and lifelong intestinal flora imbalances in the body, as well as an unlimited number of other problems. Although the medical profession doesn’t even acknowledge this, scientists and researchers state this obvious fact over and over again.

 

Antibiotics kill good and bad bacteria. Killing these bacteria causes a massive hemorrhaging of the internal components of all bacteria. This is particularly problematic because our bodies respond to these internal components by producing acute and eventually chronic long-term inflammation that can affect all tissues and cells throughout the body. This massive inflammatory cascade can breakdown tissues and interfere with cellular function. One of these internal substances, Lipopolysaccaharide (LPS) is common in gram-negative bacteria and is a substance that most researchers use in laboratory testing due to the overwhelming reliable strong immune response that it causes.

 

Some of these intracellular bacterial components, like Peptidoglycans (PGN) also act directly on the cellular membrane of the yeast Candida Albicans causing it to transform into its pathogenic fungal form. This is in addition to antibiotics eliminating millions of beneficial bacteria that help to keep the Candida Albicans yeast within ratios that benefit the overall health of the intestinal tract and therefore the rest of the body.

 

Antibiotics can also suppress the immune system response. This primarily affects the macrophages which go around cleaning up pathogenic organisms that would otherwise harm us. By suppressing macrophages, antibiotics can reduce the pro-inflammatory cascade which macrophages play a big role in initiating. While this may seem beneficial, it actually aids in the spread of the pathogenic fungal form of C. Albicans. First, with antibiotic-induced suppression of the immune system, the fungal candida now can spread more rapidly without macrophages to inhibit it. Secondly, by suppressing the macrophages and the inflammatory response, the liver does not release positive acute-phase proteins which are necessary for preventing the spread of pathogenic organisms throughout the body. Three of these acute-phase proteins (Ferritin, Ceruloplasmin, & Haptoglobin) function by binding iron and making it unavailable to pathogenic fungal candida. Without these 3 proteins, fungal candida can now attach itself to our blood cells and feed on an unlimited source of iron in the form of hemoglobin to help it spread throughout the body. This also goes for other pathogenic microbes that will be spreading as a result of the effect of antibiotics in the body. 

 

By killing off the beneficial bacteria that inhabit and help to regulate the normal healthy intestinal flora, we lose the beneficial enzymes and acids that these organisms produce. This causes the pH of the intestinal tract to become more alkaline. An alkaline intestinal pH also promotes the conversion of C. Albicans into its pathogenic fungal form. When the intestinal pH is acidic, candida remains in its normal yeast form. 

 

The above examples are just some of the ways that antibiotics promote and maintain the ongoing growth and spread of fungal candida throughout the body.

 

Killing off the beneficial bacteria also leads to decreased absorption of nutrients that our cells and tissues need to function in a healthy state. Certain strains of acidophilus help to synthesize B vitamins. A deficiency of these alone would create innumerable problems within the body.

 

There are an estimated 100 trillion micro-organisms within the intestinal tract. For many years, researchers were able to identify some 300-500 species of micro-organisms that were responsible for making up the 100 trillion cells. Recent advances in the use of technology have now identified close to 6,000 species in the large intestine alone. Most of what these organisms do and how they interact is unknown. As long as there is a sufficient amount of beneficial bacteria to keep everything in balance, then we have a better chance at staying healthy. Research now tells us that some these species are permanently eliminated from the body by the use of antibiotics – http://www.sciencedaily.com/releases/2008/11/081118121941.htm.

 

Apart from the use of antibiotics being responsible for thousands of deaths and over 144,000 visits to emergency rooms each year in the U.S. alone, the incidence of antibiotic resistance continues to escalate worldwide to the point that we are rapidly approaching a new era where antibiotics won’t be useful for most people – http://www.sciencedaily.com/releases/2009/01/090128183925.htm.

As this continues to happen, we will see an increase in the use of natural methods that help restore balance without creating additional problems. This is the goal of the McCombs Plan for Health, Vitality, and Transformation – http://mccombsplan.com/.

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