The Candida Expert

Archive for the ‘World’ Category

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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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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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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The Adventures of a Preterm Daddy: Part III

As the second day of our stay at Cedars rolled around, my wife’s symptoms had slowly subsided. Our substitute OB doctor, Dr. M, made another appearance early on and brought along another colleague, Dr. X, whom he introduced as a specialist in ultrasounds and neonatal care. Yet another ultrasound later, our specialist had determined that the cervix had once again shortened overnight. At this stage, Dr. M recommended a round of steroids. Steroids are typically given during pregnancy to help a babies lungs develop at an accelerated pace when there is a risk of a premature birth. A baby’s lungs aren’t designed to begin the work of breathing until 36-40 weeks, depending on the new math versus the old math approach to what is considered a full term baby. Steroids can speed up the maturation of the lungs and give a preterm baby a better chance of survival with fewer complications. When I asked about the effect of steroids suppressing the immune system, Dr. M denied it, while Dr. X stated that it was true. We had observed that Dr. M was so quick to deny that medications ever had any side-effects, that he was now denying the opinion of his proclaimed specialist and colleague. They went back and forth briefly with Dr. X citing several studies and winning out. When I asked which steroid would be used, Dr M mentioned that it would be dexamethasone or betamethasone. When I asked about studies where dexamethasone had been implicated in brain damage and developmental delays, Dr. M once again stated that it never happens, while Dr. X stated that it was a possibility. Dr. X pointed out however that previous studies had been done with multiple doses of dexamethasone and he would only advocate one dose, which he believed to be much safer. After listening to the facts and the fiction, we decided to hold off on the steroids until our regular doctors were back and I could do a little more research. A note to Dr. M: Don’t challenge your proclaimed expert. Either way, you lose. You either demonstrate that they’re not an expert, or you demonstrate your ignorance by challenging and losing to the person that you’ve just introduced as an expert. Both results don’t instill any confidence in your patients.

By Tuesday, both of my wife’s doctors were back in town and made their appearances at Cedars. Her sonogram doctor, Dr. S, appeared and told us that he expected to be sending us home after the ultrasound. He mentioned that it was better not to stay at the hospital because they tend to look for things to treat. This resonated with the words of a nurse whom I had spoken to earlier that day. She had been at the hospital for its 33 years of existence and stated that she avoids doctors at all costs and would rather do anything than end up at the hospital. Such words coming from a nurse seemed to speak of the mismanagement that she had seen over the years. The message that I took away from both conversations was, “time to go home.” Unfortunately, the ultrasound didn’t bring us the good news that would signal a rapid retreat. Instead, the cervix length had shortened instead of stabilizing. What had been 3.5cm on Friday was now 1.6cm. This meant that it was time for the steroids, as we didn’t want to run the risk of preterm babies with the added burden of more lung complications. We opted for the betamethasone which has been demonstrated to be safer. Dr. S told us to rest and hold tight and he’d be back for a follow-up ultrasound on Sunday and hopefully send us home.

The rest of the week was very much like the beginning of any roller-coaster ride, where you go through a few minor ups and downs until you reach that gradual climb that leads to a final jaw-dropping descent. My wife’s cramping and bleeding episodes would come and go, and for the most part seemed to be on their way out. It was starting to feel more like a car trip through a hilly countryside than a roller-coaster ride at Six Flags. We ventured out a little bit more in our take-out habits and discovered Jerry’s Deli around the corner from Cedars.

By Saturday, we were looking forward to Dr. S’s return on Sunday and an ultrasound result that gave us our return ticket home. The baby’s heart monitors strapped to my wife’s belly gave us the reassuring sounds of two hearts peacefully enjoying their time in the womb. As Saturday night rolled around, the winds changed and we found ourselves once again riding the ups and downs of cramping and spotting. Although I managed a couple of hours of sleep, half hoping that these symptoms would fade away as the others before them had, my wife was unable to sleep. The cramping intensified and mild muscle relaxants and pain killers were having no effect. By morning, with the symptoms increasing, we anxiously awaited Dr. S’s return. He was called in earlier than planned and the ultrasound revealed that the cervix was now .5cm, and my wife was dilated 3.5cm. Now 3.5cm is not very large for a full term baby, but for a 25 week old baby, it was an open barn door. Dr. S made the call and preparations were under way for a C-Section delivery. The tension became magnified as a flurry of nurses went into action. Within 45 minutes, we found ourselves in the operating room.

Our initial hopes for an intimate home water birth had now been officially replaced by a 20-person production in a hospital operating room complete with surgeons, nurses, anesthesiologists, and assorted neonatal assistants. Sitting next to my wife’s head, I watched the entire surgery via an overhead mirror above and behind us on the ceiling. It was only two weeks earlier that I had been watching the same surgical procedure on the Discovery channel, unaware of what was to come. On Sunday, May 3rd, my wife delivered a baby boy, Ethan Kai at 1 pound, 10 ounces and a baby girl, Ana Sophia at 1 pound, 9 ounces. With these twin miracles, our ticket was punched for admission to the Cedar-Sinai’s Neonatal Intensive Care Unit, hereafter know as the NICU.

The Adventures of a Preterm Daddy: Part II

There’s an old spiritual saying that goes something like, “God will never give you more than you can handle,” to which Mother Teresa was quoted responding, “I just wish that he didn’t trust me so much.” These statements will soon become a core part of our life during this pregnancy.  

As the last week of April approached, all of our plans for a long pregnancy seemed to be in place. I left town for a neurology seminar and my wife attended a birthday party for another set of twins while I was gone. An April heat wave left her feeling faint, dehydrated, and thirsty at the party. After cooling off a bit she left the party early and went home to rest and relax. By the time that I returned home that Sunday night she was experiencing some cramping which gradually increased over the next 2 days. We made a quick trip to her OB doctor to check things out. Yet another ultrasound (http://www.huffingtonpost.com/dr-jeffrey-mccombs/the-adventures-of-a-prete_b_215874.html) revealed the possibility of a slight detachment of the placental sac that keeps the babies safe and nourished in the womb during pregnancy. She recommended rest and no exercise and informed us that she’d be out of town that coming weekend but there would be another doctor covering for her while she’s gone, if needed. She also recommended going to the Sonogram Doctor for a more detailed ultrasound if things didn’t improve, and noted that he would also be out of town with another doctor covering for him. That weekend also happened to be the weekend that our midwife was going to be out of town. Somewhere in the back of my mind, I remember an old marine saying about rats leaving a sinking ship, so as the last weekend of April approached, we had the setting for a perfect storm. 

Friday morning came with more cramping and spotting. We quickly made our way to the sonogram doctor’s office where we were greeted by an admittedly neurotic doctor. As can be expected, neurotic doctors and worried expectant mothers don’t make a good combination. Another more detailed ultrasound revealed the same results of a possible slight placenta detachment. The sonogram also indicated that the length of the cervix was long. The length of the cervix is one of the deciding factors as to when the delivery process will commence. A long cervix indicates that there is a ways to go before it’s time to deliver, and in our case this was a very good sign. Fetal heart monitors showed that the twins were doing fine, seemingly oblivious to the events shaping the world around them. We were given a reprieve and sent home with instructions for complete bed rest and if the symptoms didn’t stop, we were to go to the hospital. 

That Friday night, the symptoms continued to worsen and by Saturday morning we had called the substitute OB doctor (Dr. M) and we were on our way to Cedars-Sinai Medical Center in Los Angeles. Cedars-Sinai was founded at its current location in 1976. With some 10,000 employees and over 75,000+ patients being served each year, Cedars ranks as one of the top hospitals in the country. Its proximity to Beverly Hills is underscored by the names of celebrities found adorning the many rooms, centers, and buildings, as well as the streets surrounding the hospital. We were quickly ushered to one of the Labor-Delivery rooms on the 3rd floor, where yet two more ultrasounds and some IV fluids later, my wife was stabilized. The ultrasounds revealed that the cervix had shortened overnight, so we were wheeled down the hall and admitted to the Maternal-Fetal Care Unit. The nurses and doctors told us that our stay there would last until the cervix had stabilized and the other symptoms had diminished or disappeared. As a side note, one of the nurses mentioned that the previous occupant of the room had been there 7 weeks under similar circumstances, but had gone home stabilized and pregnant. We kept our hopes high and our fingers crossed, as I became familiar with the art of shallow breathing 

Over the course of the day, we were subjected to an ongoing parade of doctors, interns, and residents who were pushing for my wife to take the Rhogam vaccine. Rhogam is a human blood-derived vaccine that is typically given to Rh- mothers (my wife) who give birth to Rh+ babies. Since I’m Rh+, this was a possibility, but not necessarily likely. When Rh incompatibility occurs, the mother could become sensitized and in subsequent pregnancies, the baby could develop a serious blood disease. There are approximately 400,000 pregnancies in Rh- women every year. Of these, some 10,000 deaths in babies used to occur due to Rh incompatibility before the vaccine was developed. With the vaccine, these deaths have been averted by giving the vaccine to babies who are Rh incompatible within 72 hours after birth. This allows time for simple blood tests to be performed to determine if there is any incompatibility in the first place. When use of the vaccine is not necessary, it avoids other risks, such as blood-borne diseases, that are minimal but inherent in the vaccine. It has now become a practice in the US to give the vaccine at 28 weeks of pregnancy and then again at birth. The vaccine at 28 weeks is more of a prophylactic choice by physicians, which translates to preventative and usually unnecessary. Through some online research, I was able to find a non-invasive test to determine Rh compatibility that has been done for years on pregnant women in England, but not here in the US. After some email correspondence with the National Blood Bank of England, I was directed to a lab here in the US that has recently started doing this testing – www.lenetix.com. Lenetix Labs also has some other unique genetic tests that can avoid the use of routine invasive diagnostic tests like amniocentesis and CVS sampling that are frequently done during pregnancy and are known to cause miscarriages.  

With the parade over and some carry out food from my new favorite restaurant, Barefoot, to sustain us, we settled into our new Beverly Hills digs. Exhausted from the day’s events, my wife managed to get some sleep and I crawled into a hospital cot which folded up around me like a human taco. And as dreams of going home danced in our heads,…

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/.

Healthcare Abducted

Mainstream healthcare in America has been abducted by the pharmaceutical and insurance companies. As profits have moved to the center stage, patient care has become secondary.

 

We need to make healthcare more affordable for Americans once more. We can start by creating a law that drugs in the U.S. be sold at world market prices. This would eliminate the excessive profits that allow Pharmaceutical Giants to support the biggest lobby and drug marketing programs the world has seen. Drug sales in the U. S. accounts for almost half of the $643 billion world pharmaceutical market.

 

Year after year drug companies enjoy higher profits than any other industry in the United States. In 2002, the top 10 drug companies in the United States had a median profit margin of 17%, compared with only 3.1% for all the other industries on the Fortune 500 list. The pharmaceutical companies state that drug price increases are necessary to fund their Research & Development of new drugs. Why do Americans have to fund this R&D for the rest of the world, when the rest of the world pays significantly less for their drugs? As it is, we already play a major role in funding R&D through tax-payer funded and government research. If anything, we should be buying drugs discounted below the world market price average. The higher drug prices in the US also mean that we are paying for the marketing of these drugs to us. In some cases, Big Pharma spends twice as much on marketing, advertising, and administration as they do on R&D. This is yet another reason for us to be paying less, not more. The cost of marketing and research should not be a burden that is born by Americans, especially when those that bear this burden are the ones least able to afford it, the sick and elderly.

 

If the recent bailout of the banking industry has shown us anything, it is that compensation packages to executives tend to be outrageous. This is no less the case with Big Pharma where compensation packages reach into the tens of millions. This doesn’t make sense when senior citizens throughout America are forced to make the choice between paying the high cost of prescription drugs or buying food. As the economy faces a depression and unemployment climbs, the number of people who are in this predicament will also increase.

 

Another way to increase the quality of healthcare in America is to take back control of patient care away from insurance companies. Insurance companies do not heal or treat anyone, physicians and health practitioners do. Insurance companies have stepped into the role of determining what happens with patient care as opposed to the healthcare practitioner. Insurance companies sell a promise and then figure out every way that they can not to deliver on that promise. Patient care needs to be solely in the hands those who have been trained to address it.

 

Unless the next President and Congress make reforms that favor the interests of its citizens over that of the pharmaceutical and insurance industries, healthcare as we know it will continue on, business as usual. Some single payer plans call for lifestyle changes and patients assuming a greater degree of responsibility for their own health. These include the areas of diet, weight loss, cessation of smoking, and exercise. Although, I’m not convinced of the suitability of the single payer plans to fill our needs, they do show some merit.

 

The bottom line is that we as Americans need to take greater personal responsibility for our own health. The choice always has been and always will be ours. It is not up to others to make this right for ourselves, it is up to us.

 

Jack LaLane, an American icon, once said, “Exercise is King and Nutrition is Queen. Put them together and you have a kingdom.” Perhaps, the time has come for us to claim that kingdom.

 

 

 

 

 

 

 

 

 

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