The Candida Expert

Archive for the ‘Drugs’ Category

Hydrochloric Acid and Health

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

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

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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

H1N1 Vaccine: Licensed but Untested

Question: Dr. Jeff, What’s your opinion on getting the H1N1 vaccine?

Dr. Jeffrey McCombs: I don’t recommend the vaccine to anyone. The Swine Flu first appeared in 1976 and disappeared again until this year. At the time, there weren’t any of the mass marketing techniques used today by pharmaceutical companies. With viruses mutating thousands of times, you almost guaranteed that the vaccine wouldn’t cover what you’re exposed to. The majority of all mutations are weakened and non-infectious. Here’s another article put out by Dr. Tim O’Shea on the vaccine:

Licensed and Untested

This is exactly wherein lies the clear and present danger of the current swine flu vaccine program. This swine flu vaccine is actually being brought into existence for dissemination among the general public, starting with children. With 5 manufacturers having begun clinical trials only in August 2009, none scheduled for completion until next April, it is an astounding lesson in vaccine politics that the FDA approved the untested H1N1 vaccine on 15 Sep 09, just one month after the testing began!

Licensed and untested.

We see precisely the same sequence of events that led to the last swine flu fiasco in 1976 – 50 million were vaccinated with that untested vaccine. 21 deaths 565 paralyzed, withdrawn in 10 weeks. And never replaced. Never replaced – that’s the point. Why not? If the threat was so urgent that we had to start vaccinating before the vaccine was even tested, then where did that threat go? Why didn’t we just withdraw the toxic vaccine and then continue with researching and testing to develop one that worked?

With just a little research, independent of the popular media, a cognition begins to take shape in the mind of the discriminating reader, that there may be an ulterior agenda here, one that is not necessarily directed toward the overall well-being of children. If such a reader is a responsible parent, the next realization might be to change the default setting with respect to the decision to vaccinate. At present most parents default in favor of – when in doubt, vaccinate. Many today are changing that default setting: no more vaccines until it is proven to me beyond a doubt that – the vaccines have been tested and found to be 100% safe with no chance ofharming the child – that the child absolutely needs the vaccine for optimum immune development – there are no economic or political agendas involved in the vaccine being recommended.

It is becoming increasingly clear that natural selection will favor the lines of those parents who take these extra precautions to protect and safeguard the inner immunity of their children. Who else is going to come forward? The FDA, who does no testing of their own before making a decision, but relies entirely on the research submitted to them from the companies who stand to make billions in profits if the vaccine is approved? The vaccine manufacturers, who have been granted 100% immunity from liability for any deaths or injuries? The other regulatory agencies – NIH, CDC, HHS – whose political connections to the vaccine companies are a matter of public record? But that’s exactly what all the hurry, all the hyperbole, all the outright misdirection is about. They know that they don’t have time to come up with a fully tested vaccine – that would take a year. But by that time the imaginary disease will be gone, with no hope of raising it from the dead. The market is here and now. And everyone – the clinics, the manufacturers, the regulators, and the media – all want their share of the rewards.

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,…

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