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

 

CATCH UP on more recent posts at our new blog – Candida Plan Blog

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

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 3^rd, 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 3^rd 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,…