February 2015

Lipstick on a Pig: Stelara’s Unethical Ads

Published on February 26, 2015

4385 views

This 2014 commercial for Stelara is deplorable:

This commericial a disgusting example of everything that is wrong about pharmaceutical advertisements. It appeals to viewers’ vanity and insecurity – which we all possess – in order to sell a dangerous drug. The drug advertised, Stelara (a Johnson & Johnson product), causes cancer. The FDA warning label for Stelara notes that it can cause cutaneous squamous cell carcinoma, prostate, melanoma and breast and cancers, each of which can lead to death. It suppresses the immune system and leaves those who take it susceptible to dangerous infections, which can also lead to death.

Apparently it needs to be said, because there isn’t uproar and disgust in the general public over this wretched ad (and others like it for immunosuppressive drugs)–it is WRONG to utilize the same slimy sales techniques used to sell cosmetics in order to sell dangerous drugs that can severely hurt people and lead to their death. It is wrong to prey on people’s vanity and insecurity in order to sell them something that can hurt or even kill them. It is wrong to promote the frivolous and inappropriate use of a dangerous drug.

A drug like Stelara, that suppresses the immune system and can cause cancer, should not be used lightly and it is not even remotely appropriate to use it in order to have clearer skin. Just listen to the ad, “In a medical study, seven out of ten Stelara patients saw at least 75% clearer skin at twelve weeks.” Look at the model living a glamorous lifestyle, being adored, and flaunting her perfect skin, hair and body. This ad isn’t about helping people with plaque psoriasis, it’s about vanity and aspiration. It’s about selling a product and greed. It is not appropriate, and it even crosses the line of being wrong, to use manipulation and vanity to sell pharmaceuticals–especially pharmaceuticals that can cause cancer and death.

As is the case with all pharmaceutical ads, the risks associated with using Stelara are downplayed. At the end of the ad, after the marketers have thoroughly convinced the viewers (at least on a subconscious level) that if only they took Stelara they would look like the glamorous model in the commercial, a list of the most severe adverse effects is given. These risks include lowering one’s ability to fight infections, increasing one’s risk of cancer, headaches, seizures, vision problems, serious allergic reactions, and it is also stated that patients should, “tell your doctor if you, or anybody in your house needs or has recently received a vaccine.”

Do other people find that warning about not being around people who have recently been vaccinated to be concerning? It certainly piqued my interest when I first heard it. It made me wonder, “What is THAT about??” It made me wonder WHY people who are on Stelara shouldn’t be around those who have recently been vaccinated.

The written warning label for Stelara goes into a little more detail. It states, “People who take STELARA® should not receive live vaccines. Tell your doctor if anyone in your house needs a vaccine. The viruses used in some types of vaccines can spread to people with a weakened immune system, and can cause serious problems. You should not receive the BCG vaccine during the one year before taking STELARA® or one year after you stop taking STELARA®.”

Live vaccines include MMR (measles, mumps and rubella combined), chickenpox, nasally administrated flu, and rotavirus vaccines.

Additionally, recent studies have revealed that the whooping cough / pertussis vaccine can be spread from those who are vaccinated to those who are not vaccinated. A story published in the New York Times noted that, “’When you’re newly vaccinated (with the whooping cough / pertussis vaccine) you are an asymptomatic carrier, which is good for you, but not for the population,’ said Tod J. Merkel, the lead author of the study, who is a researcher in the Office of Vaccines Research and Review in the Food and Drug Administration.”

There is nothing okay about a vaccine spreading the disease that it is supposed to protect against. It is entirely indefensible. If a vaccine spreads disease it should be removed from the market. Try again, pharma companies that make live and whooping cough / pertussis vaccines. Not all vaccines spread the diseases that they are trying to prevent, so there must be some techniques and technologies that can keep that from occurring. Make it so, because endangering those who have suppressed immune systems is not acceptable.

Immune system suppressing drugs like Stelara, Humira, Enbrel, Remicade and others, are used by millions of people every day (it is estimated that 20% of the American population has an autoimmune disease, the diseases that these cancer-causing drugs are supposed to make more manageable). Everyone on an immunosuppressive therapy has a weakened immune system and is susceptible to catching a disease from someone who has recently received a live vaccine (or the pertussis/whooping cough vaccine). However, the people taking immune-suppressive drugs like Stelara aren’t the only ones who have compromised immune systems. Pregnant woman have compromised immune systems, so do people who are HIV positive or have AIDS, people going through chemotherapy, and many others.

The combination of live, virus containing, vaccines, along with a large portion of the population taking immunosuppressive drugs, may make the spread of diseases throughout the US population more common in the future. Unvaccinated people will be blamed, but perhaps more of the blame should sit with the pharmaceutical companies that are making billions off of suppressing people’s immune systems ($6.1 billion in immunosuppressive drugs like Stelara were sold in 2012 alone) and selling live virus vaccines.

Projections of diseases being spread through a population that is immune-suppressed are conjecture. It is not conjecture, however, that dangerous drugs are being sold via immoral marketing techniques. If it were demanded that there be truth in advertising, Tony’s story would be the advertisement one would see for Stelara:

Though Tony’s story is tragic, at least it is real. Pharmaceutical advertisements are not real. We all know, on some level, that pharmaceutical advertisements are not real. Perhaps it’s time we get angry about these types of commercials. Anger may even lead to change. At the very least, it’s time to get educated about the real risks associated with heavily marketed medications. The risks are real. The ads are not.

About the Author: Lisa Bloomquist was “Floxed” on her 32nd birthday by Cipro, a fluoroquinolone antibiotic. After 2 years of battling the mysterious health ailments that come with an adverse reaction to a fluoroquinolone, she has fought her way back to health. She is now fighting for recognition of the harm that these drugs can cause and hoping to help those who are suffering from them through their fluoroquinolone induced illness to find recovery. Her web site, Floxie Hope, highlights stories of hope and recovery. Mito Madness, also started by Lisa, focuses on the absurdity of ignoring the role of mitochondria in forming disease models.

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Pregnancy Hypertension

by Chandler Marrs, PhD

Published on February 24, 2015

3270 views

Every now and again I have the great pleasure of stumbling upon a brilliant piece of research; research that shakes the very core of medical science. Sadly, this is not one of those times. No, with the research I write about here, I cannot help but wonder why? Why was this study conducted? Why was it funded? Why was it published in such a prominent journal? And perhaps most importantly, why are there 15, well-credentialed, and likely, very highly accomplished individuals, lending their names to such a weak piece of research? Did they not read the study?

Just last month, published in the esteemed The New England Journal of Medicine, whose impact factor (54) far exceeds most journals in the space by a factor of 10, published a purportedly seminal piece on pregnancy hypertension: Less-Tight versus Tight Control of Hypertension in Pregnancy. The study was a huge, presumably well-funded (through a grant from the Canadian government), multi-center, international, randomized controlled trial set to investigate the important topic how best to treat pregnancy hypertension.

Pregnancy Hypertension

Hypertension during pregnancy is a growing problem that brings with it substantial risk to maternal and fetal health. How to treat pregnancy hypertension is of critical importance but not a single anti-hypertensive medication on the market currently has been tested for safety on pregnant women. Few data exist to evaluate the risks of taking such medications on short-term maternal or fetal health and no data exist to identify long term consequences. Not even the most basic of studies, those that evaluate drug pharmacokinetics and delineate appropriate dosing have been conducted for pregnancy (or any other complex hormonal environment).

Drug disposition and metabolism are altered significantly by pregnancy when hormone concentrations, plasma volume, enzymes, binding proteins, liver and kidney function change radically. These changes impact drug dosing and safety. Without proper consideration for these variables during pregnancy, the potential for overdosing and mis-dosing is significant, increasing the possibility of evoking serious maternal and/or fetal ill-effects. Setting aside the question of whether medications should be given at all during pregnancy (I don’t think they should be), I think we can all agree that when medications are necessary, safety and efficacy data must exist prior to administration.

It is from this perspective, that I approached the current study; a long overdue investigation about the safety and efficacy of anti-hypertensive drugs during pregnancy. Boy was I disappointed. In fact, the authors state: “We did not collect information on common adverse effects of anti-hypertensive medications…” In fairness, however, other important outcome data were collected, but the design of the study was so arbitrary that any potential insight these outcomes might have contributed, was lost.

Study Details

The current study asked whether controlling maternal blood pressure strictly within a pre-defined range of parameters provided better or worse maternal or fetal outcomes compared to a more flexible approach with a broader range of accepted blood pressure metrics. For the tight control group, the goal was to maintain diastolic blood pressure at or below 85 mm Hg. For the less tight group, diastolic pressure was to be maintained at or below 100 mm Hg. The study accepted medicated and non-medicated hypertensive women (n = 987, 56-58% were medicated from each group prior to entering the study), who were anywhere from 14 weeks of pregnancy through 33 weeks pregnancy (mean = ~23 weeks).

Once participants were enrolled into the study, decisions regarding whether to medicate (if not previously medicated), which medication to use, and at what dosages, were left to the providing obstetrician’s discretion. The study excluded women who, at the time of admission into the study, showed signs of pre-eclampsia, demonstrated high systolic blood pressure (>160 mm Hg), had pre-gestational diabetes, renal disease or were utilizing ACE inhibitors (angiotensin-enzyme-converting enzyme inhibitors). If these conditions developed subsequently, patients remained in the study.

The primary outcome variables included: pregnancy loss (miscarriage, ectopic pregnancy, elective termination, perinatal death), high level of neonatal care for greater than 48 hours, gestational age and weight at delivery and a range of neonatal complications. Secondary outcome variables, measured at a much more rigorous statistical significance level (p>.001) compared to the primary variables (p>.05) included: serious maternal complications (uncontrolled hypertension, transient ischemic attack or stroke, pulmonary edema, renal failure and transfusion), placental abruption, severe hypertension (>160 mm Hg systolic or >110 mm Hg diastolic blood pressure), pre-eclampsia or abnormal labs indicative of incipient pre-eclampsia.

Results

The reported results of this study were as follows:

There were no between group differences in either maternal or fetal complications.
Women in the less tightly controlled group had higher blood pressure.

So for all of the money and time spent, we learned that anti-hypertensives do, in fact, reduce blood pressure, and that how intensely one uses these medications has no statistical bearing on this particular set of outcomes. This is not to say that there were not negative outcomes. There were plenty in both groups of participants; from severe maternal hypertension, pulmonary embolism and pre-eclampsia, to serious neonatal complications and fetal death. There were simply no statistically identifiable differences in the rates of these complicatiosn between the two groups. In other words, both groups had similar rates of negative outcomes.

Flaws in Study Design

Why weren’t there any statistically relevant differences between the two groups? The answer to this question involves study design and herein we have a number of problems. First, the participant pool was largely hypertensive and medicated before entry into the study, providing no real control group from which the assess differences between blood pressure and outcomes in unmedicated versus medicated women. Elevated blood pressure is a significant risk factor for a number of maternal complications but so too are medications. What is the risk/benefit calculus that determines when the inherent risks of medications during pregnancy are outweighed by the risks of maternal blood pressure? In other words, when should we medicate to control hypertension? Delineating between the dangers of the blood pressure versus those of the medication would have been more telling. Admittedly, such a study would present ethical considerations and quite possibly could have only been done retrospectively. Nevertheless, without these types of data, it is impossible to discern either the safety or efficacy of any therapeutic intervention; effectively nullifying the results from the onset.

A second methodological problem is the failure to address statistically pre-existing health conditions and environmental variables that confound results. That is, we don’t know what portion of the overall negative outcomes might be attributable to pre-existing or even extraneous maternal health issues versus medication use or blood pressure control. For example, a good percentage of the women in both groups were not only medicated prior to entry into the study but were significantly overweight pre-pregnancy, smoked and/or had additional health considerations. These variables would independently impact maternal and fetal outcomes, but also, could additively or synergistically influence blood pressure and other maternal risk factors. Although the mean data for both groups were presented, no analyses that might provide a richer understanding of the relationship between blood pressure and perinatal outcomes was given.

Perhaps the most problematic aspect of this study was the failure to analyze data regarding the types and dosages of medications relative to the negative outcomes. Though the researchers collected medication data and reported some of those data in the supplementary appendices (number of women per group who took a particular type of medication absent dosages was reported), there were no analyses presented. This made it impossible to identify whether certain medications were more dangerous than others and would account for the observed negative outcomes in either group. Neither did this report tell us about the dose-response relationship relative to effective blood pressure management versus adverse reactions – a very basic calculation – nor did they tell us about the role of medication interactions in the observed negative outcomes.

What Value is This?

From the standpoint of a practicing physician, a researcher or a patient, what use is a study on medication safety and efficacy during pregnancy, if there are no analytics delineating dose-response relationships by medication(s) and risk factor? Is one medication safer than the others? Does a particular medication work better or worse for a specific group of women? Are there anti-hypertensive medications that are more or less effective during pregnancy at managing blood pressure? Or even more basically, are the dosages we currently use correct? With such a large study group, we could have learned which medications could be used safely during pregnancy, at what dosages, and with which groups of women. It is likely that some women should absolutely not be given medications due to confounding health conditions.

To answer any of these questions would have been highly useful and added significantly to the body of scientific research on pregnancy hypertension. In its current form, however, this study adds little, if anything, to our understanding of the pregnancy hypertension, the use of medications to control hypertension during pregnancy or their potential negative side effects. All this study tells us is that blood pressure medications tend to lower blood pressure and evoke complications in some women. Well, of course they do. That is not novel. We knew that already.

There are so many missed opportunities here. Not parsing the medication, dosage data was an egregious omission; one that makes me wonder why it was funded and why it was published in such an esteemed journal. And with 15 authors attributed to this study, why did no one on the masthead push to expand the analytics beyond what was presented? Pregnancy hypertension can be deadly and there is a striking lack of research in this area. Why are we not asking the big questions?

Potential Link between Oral Contraceptives and Autism

by Kim Elizabeth Strifert, MA

Published on February 24, 2015

8260 views

It is estimated that 1 in 68 children are diagnosed with ASD in the United States. Increasing awareness and the rapidly growing number of cases of Autism Spectrum Disorder (ASD) have caused national alarm, compelling scientists to search for clues about the causes and contributing factors of ASDs. Many explanations for the rise in prevalence of ASD have been offered and yet, causal factors for ASD are still inadequately understood. Scientists agree that ASD is a complicated disorder thought to be due to interactions between genes and the environment, but as yet, there is no known cause that explains the increase in prevalence of autism and autism spectrum disorders.

Oral contraception use is one possible risk factor for the increase in prevalence that has been profoundly overlooked in the biomedical and epidemiologic literature. Interestingly, as the prevalence of ASD has risen over the last fifty years, so has the prevalence of the usage of oral contraceptives. Usage of oral contraceptives in the United States has increased from 1 million women in 1962 to almost 11 million women today. Because oral contraceptives were created to mimic natural human hormones and disrupt endogenous endocrine function to inhibit pregnancy, there is good reason for concern that the synthetic hormonal components may be causing the harmful neurodevelopmental effects that lead to the increase in ASDs.

Oral Contraceptives are Endocrine Disruptors

One of the compounds found in oral contraceptives is the synthetic estrogen called Ethinylestradiol (EE2). EE2 is a known endocrine disrupting compound (EDC) capable of causing harm to the endocrine system and to progeny. Studies show that EDCs have the potential to do harm by adversely affecting the sensitive hormonal pathways that regulate reproductive function in a variety of species including humans. The National Institute for Environmental Health Sciences (NIEHS) reports that EDCs may disturb the endocrine system and produce adverse developmental, reproductive, neurological, and immune effects in humans and wildlife. The NIEHS indicates that research also shows that the highest risk of endocrine disruption occurs during prenatal and early postnatal development. Humans might be exposed to EDCs through foods, beverages, pesticides, and cosmetics, but the case with EE2 is particularly striking because EE2 exposure in female humans occurs at a pharmacologically effective dose, administered every day, for extended periods of time.

Hormones and their signaling pathways are essential to normal functioning of all tissues and organs in invertebrate and vertebrate species. Normal communication of the endocrine system can be disrupted by exogenous substances like EDCs, which have the same attributes as endogenous hormones. EDCs possess the ability to be active at low concentrations and like endogenous hormones, they are able to bind to receptors at very low concentrations. Therefore, endocrine disruption can occur from low-dose exogenous hormone exposure or from hormonally active substances that interfere with receptors for other hormonally assisted processes. In addition, some EDCs are able to interact with multiple hormone receptors concurrently. They can work simultaneously to create additive or synergistic effects not observed with the individual compounds. EDCs can act on a number of physiological processes in a tissue specific manner. And, as with endogenous hormones, it is often not feasible to extrapolate low-dose effects from the high-dose effects of EDCs. Thus the mimicry of estradiol (E2) and the information that such compounds can cause harmful effects on reproduction and the endocrine system provide mechanistic evidence that EE2 found in oral contraceptives may adversely affect the oocyte or developing embryo.

Disrupting Hormones Chronically: Is This Safe?

Exposure timing is of interest and importance. When does exposure to the endocrine disruptor EE2 in oral contraceptives disrupt the endocrine system? Oral contraceptives were designed to disrupt the endocrine system throughout the month to keep a woman from becoming pregnant. During this disruption, what happens to follicles or the oocytes? As they are repeatedly exposed to the compound EE2, does this modify or change either or both of them? It is conceivable that with contraceptive EE2 exposure alteration in follicles or oocytes occurs, since data from animal models suggest that hormonal compounds do cause changes in follicular, embryonic, and fetal development. Does repeated exposure to the synthetic hormone EE2 cause harmful changes to human follicles and/or oocytes as well? If so, in this case, the adverse effects of disruption would happen even before fertilization occurs.

Becoming Pregnant while on Oral Contraceptives: Potential Dangers

Oral contraceptives are reported to be 99.9% effective if used properly. Less than 1 out of 100 women will get pregnant each year if they always take the pill each day as directed. Moreover, about 9 out of 100 women will get pregnant each year if they don’t always take the pill each day as directed. That means that out of the 11 million U.S. women using oral contraceptives, up to 100,000 may get pregnant while continuing to take EE2 after oocyte fertilization. Those embryos would then be directly exposed to pharmacologic doses of EE2. It is conceivable that exposure to EE2 could adversely affect the developing embryo. And, the time-frame for oral contraceptive wash-out is not clear even after discontinued use of the pills. Even if there is full drug wash-out, persisting toxicological, genetic, and epigenetic effects are possible. Harmful EE2 exposure could then occur after fertilization and during early development of the embryo.

There is also the potential for some EDCs to produce effects that can cross generations, meaning that exposure may affect not only the development of the first offspring but also their offspring over generations. This means that effects of EDCs could increase over generations due to both transgenerational transmission of the modified epigenetic programming, and the continued exposure across generations possibly imparting disease sensitivity later in time. Thus, the ability of ancestral exposures to promote disease susceptibility greatly complicates the possible threat to the health of subsequent generations, through exposure to EDCs such as EE2.

Autism and Oral Contraceptives: Is there a Connection?

The need for human epidemiological investigation into the link between oral contraceptive use and ASD is motivated by the firmly grounded hypothesis that oral contraceptive use is a risk factor for ASD in offspring. In the realm of environmental risk factors this hypothesis is compelling due to several considerations. First, as a category of agents there are specific documented mechanisms through which oral contraceptives can affect the oocyte and/or developing embryo. Second, exposure concentration is directly administered and by definition pharmacologically effective. And, it may be of greater magnitude than other environmental exposures that largely occur through passive secondary mechanisms. The possibility exists that the effects of EE2 could intensify over generations due to transgenerational transmission of altered epigenetic programming and the continued exposure across generations possibly imparting sensitivity to developing ASDs. Lastly, the specific demographic at risk, women who are likely to have children, is the exact demographic that is taking oral contraceptives, specifically during child-bearing years (“first principles”).

If, as I have hypothesized, epidemiological investigation establishes a link between oral contraceptives and ASD, this information would be invaluable to women of child-bearing age evaluating birth control options. Considering the increased prevalence of ASD, the increasing usage of oral contraceptives and the striking lack of research in this area, this information has a sense of urgency for those women and their progeny.

To read more about possible connections between autism and oral contraceptives see: The link between oral contraceptive use and the increase in the prevalence of autism spectrum disorder.

About the Author: Kim Strifert has an MA and is currently a student of Public Health at the Graduate School, School of Public Health, University of Alabama at Birmingham. She was previously employed as a healthcare administrator at the Mayo Clinic and Baylor College of Medicine.

References

Armenti AE, Zama AM, Passantino L, Uzumcu M (2008) Developmental methoxychlor exposure affects multiple reproductive parameters and ovarian folliculogenesis and gene expression in adult rats. Toxicology and Applied Pharmacology 233: 286–296.

Csoka, A B, Szyf, M (2009) Epigenetic side-effects of common pharmaceuticals: A potential new field in medicine and pharmacology (Article). Medical Hypotheses. Vol. 73, Issue 5, 2009, 770-780.

Denslow ND, Bowman CJ, Ferguson RJ, Lee HS, Hemmer MJ, and Folmar LC (2001) Induction of gene expression in sheepshead minnow (Cyprinodon variegates) with 17β-estradiol, diethylstilbestrol, or ethinylestradiol: The use of mRNA fingerprints as an indicator of gene regulation. General Comparative Endocrinology 121:250-260.

Gandolfi F, Pocar P, Brevini TAL, Fischer B (2002) Impact of endocrine disrupters on ovarian function and embryonic development. Domestic Animal Endocrinology 23: 189–201.

Jobling, S, Coey S, Whitmore JG, et al. (2002) Wild intersex roach (Rutilus rutilus) have reduced fertility. Biology of Reproduction 67: 515-524.

Kasan P, Andrews J (1980) Oral contraception and congenital abnormalities. British Journal of Obstetrics and Gynaecology 87(7):545-51.

Kerdivel G, Habauzit D, Pakdel F (2013) Assessment and Molecular Actions of Endocrine-Disrupting Chemicals That Interfere with Estrogen Receptor Pathways. International Journal of Endocrinology 2013:501851.

Larkin, P, Folmar LC, Hemmer MJ, Poston AJ, Denslow ND (2003) Expression profiling of estrogenic compounds using a sheepshead cDNA macroarray. Environmental Health Perspectives 111:839-846

Leese HJ, Baumann CG, Brison DR, McEvoy TG, Sturmey RG (2008) Metabolism of the viable mammalian embryo: quietness revisited. Molecular Human Reproduction 14:667–672.

Leese HJ, Sturmey RG, Baumann CG, McEvoy TG (2007) Embryo viability and metabolism: obeying the quiet rules. Human Reproduction 22:3047–3050.

Martínez NA, Pereira SV, Bertolino FA, Schneider RJ, Messina GA, Raba J (2012) Electrochemical detection of a powerful estrogenic endocrine disruptor: ethinylestradiol in water samples through bioseparation procedure. Analytica Chimica Acta Apr 20;723:27-32.

Metcalfe CD, Metcalfe T L, Kiparissis Y, et al. (2001) Estrogenic potency of chemicals detected in sewage treatment plant effluents as determined by in vivo assays with Japanese medaka (Oryzias latipes). Environmental Toxicology and Chemistry 20:297-308.

National Institute of Environmental Health Sciences (2014) Accessible at: www.niehs.nih.gov/health/topics/agents/endocrine

Skinner M (2014) Endocrine disruptor induction of epigenetic transgenerational inheritance of disease. Molecular and Cellular Endocrinology Jul 31. pii: S0303-7207(14)00223-8.

The Collaborative on Health and the Environment’s Learning and Developmental Disabilities Initiative (2008) issued the “Scientific Consensus Statement on Environmental Agents Associated with Neurodevelopmental Disorders”. Accessible at: www.healthandenvironment.org/initiatives/learning. (accessed 10, December 2014)

Tilton SC, Foran CM, Benson WH (2004) Relationship between ethinylestradiol-mediated changes in endocrine function and reproductive impairment in Japanese medaka (Oryzias latipes). Environmental Toxicology and Chemistry 24:352-359.

Vaiserman A (2014) Early-life Exposure to Endocrine Disrupting Chemicals and Later-life Health Outcomes: An Epigenetic Bridge? Aging and Disease Jan 28;5(6):419-29.

World Health Organization (2012) State of the Science of Endocrine Disrupting Chemicals 2012 Summary for Decision-Makers. Available at: www.who.int/ceh/publications/endocrine/en/

Maternity Care: US Versus Malaysia

by Valerie Lynn McDonough

Published on February 23, 2015

4091 views

Undoubtedly, one of the happiest times of family life may also be one of the most stressful if a pregnant woman, in the United States, finds herself without health insurance, or with health insurance that doesn’t cover maternity care. Between, 1993-2007, the average cost of an uncomplicated cesarean section more than doubled; and the cost of an uncomplicated vaginal delivery tripled. “Looking at a sample of 9 states, researchers found that 17% to 41% of childbearing women lacked insurance before coming pregnant,” says Carol Sakala, director of programs at Childbirth Connection, a nonprofit organization that works on behalf of mothers and babies to improve the quality of maternity care in the U.S. “While 13% to 35% of the pregnant women qualified for Medicaid coverage, many either didn’t qualify or didn’t apply, finding private insurance or paying out of pocket,” Sakala says.

Let’s examine the costs, of what is considered essential care, associated with having a baby in the United States today. The average cost of prenatal care is roughly $2,000, which covers about fourteen doctors’ visits. High risk pregnancies normally incur more tests and monitoring, which significantly increases prenatal expenditures. Add an additional $0-$300 per test, should blood work, or any other test, be deemed necessary by an OBGYN. The cost of an ultrasound or sonogram costs $100 – $1,000, with an average number of 1-3 during a low-risk pregnancy. An amniocentesis test ranges between $1,100 and $2,000, depending on the facility. The average hospital charge for an uncomplicated cesarean section is $15,800; while an uncomplicated vaginal birth runs about $9,600. A hospital stay afterward can easily increase bills to anywhere from $10,000-25,000. The price range varies widely from area to area and will depend greatly on where a mother lives.

“It’s important to be aware that these numbers reflect the amount a hospital will charge for these services, rather than the actual cost,” says Anne Elixhauser, PhD, senior research scientist at the Agency for Healthcare Research and Quality. “The actual amount of what it costs the hospital to perform the service is about 30% of what’s charged.” Add up these costs and it’s no wonder the average family in the United States has only 1.5 children. The U.S. population growth rate has stagnated for years with a large percentage of its growth stemming from immigration.

Now let’s compare the cost of modern maternity care in the US, with a country that is considered to have a more a traditional culture, such as Malaysia, Southeast Asia; a country I’ve lived in for the last 12 years. In Malaysia, it’s common for maternity care, pre- and post-, not to be covered by insurance. However, maternity costs are very affordable for the typical Malaysian family. Actually, it can be downright cheap to have a baby in Malaysia depending where a family decides to deliver. It must be affordable because Malaysia is a developing economy that is categorized as second world by the World Trade Organization, with a middle income level economy. A typical family earns $15,100 annually; compared with a typical family in the US earning $48,000 per annum. The average number of children per family is 2.6; however this seems low to me. I know many families with at least three or more children.

Nowadays, most births take place in a hospital setting; there are no freestanding birthing clinics, and midwives only practice in hospitals. Malaysia has many public, or government sponsored hospitals. If a family decides to give birth at a public hospital most of the costs are covered by the government; and if you are a government employee, it’s even better, as all the maternity costs are free. At this time the Malaysian government employs one million civil servant with about half being women. Therefore the average government employee normally has more children than those employed by the private sector.

However, the costs for a non-government employee, who chooses to give birth in a government sponsored hospital, are very low. An uncomplicated vaginal birth is $160, a cesarean is $300, and twins are $250. If forceps or vacuum are used, or a breech birth is encountered, an additional $200 is added onto the bill. Daily ward charges range from $1 for a shared room, to $25 for a private room.

Due to the fact that most insurance policies don’t include maternity care, costs vary widely in Malaysia with most hospitals offering competitive “maternity care” packages. Then there is what is called specialist, and semi-private, hospitals that specialize in maternity care. The rates at these types of hospitals are mid-range, with pricing falling between that of public and private hospitals. If a women chooses to have a private OBGYN, at a private hospital, this family would certainly fall into a wealthy income level as the fees are much higher and not be affordable for a typical Malaysian family. For example the cost of each prenatal visit may range between, $30-$100. An uncomplicated vaginal birth is, $1,300–1,600, and an uncomplicated cesarean, $4,000; plus a three to five day hospital stay, costs on average $3,000. A hospital that I know offers the following Maternity Care packages, for a normal delivery with three days and two nights stay for $5,000; and for a cesarean $13,000. Again, this is the high end of the spectrum.

In traditional cultures, like Malaysia, it is considered every woman’s natural right to bear children if they are able to, which is why giving birth is affordable. It is expected that a woman will give birth in her lifetime, and if there is no medical reason not to, it is viewed as unusual if she doesn’t. Pregnant women are largely supported by the community they are part of, both in the work place and by their family at home. Pregnancy and child birth is an auspicious period, and both the mother and her baby are honored and celebrated in a variety of ceremonies. Birth is slowly becoming medicalized in Malaysia, but it is nowhere near to the degree it is in the US. I don’t think it ever will be like it is in the US, as the strong cultural beliefs and traditions that are firmly in place balance out the pace of the modernization of maternity care.

Photo by Stephen Andrews on Unsplash.

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Obesity and Childhood Vaccines: Is there a Connection?

by Viera Scheibner, PhD

Published on February 18, 2015

7460 views

The staggering increase in obesity affecting mainly people of the industrially developed world is an indisputable fact. Researchers have put forward a number of ideas of which overeating and/or eating too much sugar/carbohydrates and fats are the most popular. However, orthodox medical research points to some other factors and phenomena starting with a growing incidence of infantile and pediatric hyperinsulinemia.

Infantile hyperinsulinemia is sometimes considered a rare congenital disorder where excessive insulin secretion creates a state of hypoglycaemia – low blood sugar. Severe hypoglycemia in the newborn can lead to a myriad of health issues including severe neurological handicaps and seizures. The symptoms are recognized generally at around six months of age and are believed to develop in 1/50,000 births.
In regions where consanguinity are common the rate may be as high as 1-2/500. However, there are non-genetic, iatrogenic (medically induced) mechanisms of hyperinsulinemia that must be considered also.

An emerging body of evidence suggests a connection between infantile hyperinsulinemia and the administered vaccines, the use of antibiotics and other medical and environmental factors. The timing of infant vaccines, in particular, corresponds closely to the recognition of infantile hyperinsulinemia. Could there be a connection between vaccines and/or antibiotic use and insulin dysregulation in infants and children? Moreover, would this also predispose children to obesity later in life?

Vaccine Induced Hyperinsulinemia?

With the pertussis portion of the DTP vaccine (diphtheria, tetanus and pertussis; and now DTaP [aP=acellular]) pertussis vaccine, there have been longstanding questions regarding safety. In 1978 Hannik and Cohen wrote, “There is a considerable concern about the reactions that sometimes occur in children following the injection of pertussis vaccine. Reactions have been observed and reported since 1933 (1) and range from the slightest minor reactions to status convulsivus resulting in permanent cerebral damage.”

Hannik and Cohen’s review cites a number of studies identifying adverse reactions to the pertussis portion of the vaccine and a relationship to insulin homeostasis, including: Parfentjev and Schleyer (1949), Szentivanyi et al. (1963) Tabachnik and Gulbekian (1968), Tabachnik and Gulbekian (1969). Respectively, these studies dealt with the influence of histamine on the blood sugar level of normal and pertussis vaccine sensitized animals (rats and mice), adrenergic changes due to pertussis [vaccine], insulin, glucose and free fatty acids and encephalopathy following pertussis vaccine prophylaxis. The pertussis vaccine proved to be the principal precipitating pathogen in all cases.

Hannik and Cohen (1978) wrote, “Infants injected with DTP-Polio vaccine with a pertussis component of 16 International Opacity Units per dose showed slight but significant elevation in concentration of plasma insulin and temperature.” They concluded that the phenomena (i.e. the elevation in concentration of plasma insulin and increased temperature) are not interrelated. They suggested that “infants who show serious reactions following pertussis vaccination suffer from a failure to maintain glucose homeostasis.” They also noted, “low blood sugar level and extremely low CFS-glucose concentration have been reported in children who developed convulsions 3 and 36 hours after receiving pertussis vaccine.”

A few years later, Katada and Ui (1981) wrote, “Islet-activating protein is a new protein isolated from the culture of Bordetella pertussis as one of the pertussis toxins. It interacts with islet cells slowly to give rise to striking reversal of alpha-adrenergic inhibition cAMP accumulation in, a consequent insulin release from the islet cells.” In other words, a protein toxin within the pertussis portion of the DTP/DTap vaccine was found to initiate insulin release, providing additional evidence connecting the vaccine to infant hyperinsulinemia.

Deranged Glucose Metabolism in Childhood

Interestingly, Zametkin et al. (1990) demonstrated that adults with hyperactivity of childhood onset suffer derangement of cerebral glucose metabolism affecting the prefrontal cortex and superior prefrontal cortex, the parts of the brain that control attention and motor activity. Could the pertussis protein toxin that activates insulin release identified by Katada and Ui (1981) be responsible for childhood derangement in sugar metabolism and not the consumption of sugar, as such, that is implicated? Even though the authors considered the cause of the altered glucose metabolism unknown, it is clear to me that impaired glucose homeostasis may be a result of childhood vaccination. The consequences of this impairment may then be related to many of the conditions plaguing modern society, including obesity. Indeed, the product insert for Tripedia Sanofi Pasteur DTaP vaccine lists autism (SIDS and other serious reactions) detected during post-marketing surveillance.

From Vaccines to Hyperinsulinemia to Obesity

Hughes (1997) demonstrated a significant increase in both the height and weight of the 5 to 11-year old English and Scottish children and called for an urgent need to realistic intervention to reduce obesity in this population.

Freedman et al. (1997) described secular increases in relative weight and adiposity among children over two decades, from 1973 to 1994 in a biracial community of Ward of Washington Parish, Louisiana, USA.

According to Medical Observer (2005; May 12), “Alarming levels of hyperinsulinism, fatty liver, dyslipidaemia and other complications are present in Australian primary school children with high body mass index (BMI)”.

According to Dunne et al. (2004), “hyperinsulinemia promotes hepatic and skeletal muscle glucogenesis, which decreases the amount of free glucose available in the blood stream and results in suppression of the formation of free fatty acids. Fatty acids do not cross the blood brain barrier and cannot be used by the brain as an energy substrate. The combination of hypoglycaemia, reduced fatty acids availability for cardiac and skeletal muscle metabolism and reduced ketones for cerebral metabolism result in adrenergic and neuroglycopenic symptoms with severe neurological dysfunction. Seizure activity will also manifest. Repeated episodes of severe prolonged hypoglycaemia can result in permanent neurological damage, including developmental delay, mental retardation, and/or focal CNS deficits.”

Although the research groups noted above identified hyperinsulinemia in the studied populations, none investigated the role of the administered vaccines, in the induction of hyperinsulinemia. Given the research highlighted previously, it seems plausible that protein toxins contained in the pertussis vaccine are capable of evoking hyperinsulinemia and by way of association may be responsible for the increasing rates of childhood obesity. To that end, Smith and Furman (1988) wrote, “Pertussis vaccine, pertussis toxin, and the alpha-adrenoreceptor blocking drug phentolamine augment glucose-induced insulin secretion. The present study was carried out to determine the relationship between the action and the ability of these agents to prevent the inhibitory action of adrenaline. Pertussis vaccine augmented glucose-induced secretion in rat islets ex vivo and prevented the inhibitory actions of adrenaline and clonidine.”

Antibiotics and Obesity

Another class of medications – antibiotics – might also be linked to the increase in childhood obesity. Antibiotics are widely prescribed for a great number of conditions. Most children suffer a series of ear infections and lower respiratory and urinary infections in the first year of life after vaccination, as documented by Craighead (1975) and may, as a rule, be given several rounds of antibiotics.

Antibiotics are used prolifically in the animal food industry to enhance the protein (flesh) production and weight in animals. These have the same effect on children as they have on young food animals: antibiotics make them fat and muscular.

Garly et al. (2006) unwittingly documented the fattening effect of antibiotics in children in a developing country. They wrote, “The group that received prophylactic antibiotics had less pneumonia and conjunctivitis and has a significantly higher weight gain in the months after inclusion.”

Conclusion

Although not consistently considered a culprit in the widespread childhood obesity epidemic, iatrogenically impaired infant and childhood glucose homeostasis may be a contributing factor. Administration of DTP/DTaP and possibly other vaccines, alone or together with antibiotics could predispose children to chronic states of impaired insulin metabolism and glucose regulation irrespective of dietary considerations.

References

Kumaran et al. (2010). The clinical problem of hyperinsulinemic hypoglycemia and resultant infantile spasms. Pediatrics; 126(5): e1231-1236.

Hannik and Cohen. 1978. Changes in plasma insulin concentration and temperature of infants after pertussis vaccination. Third International Symposium on Pertussis. (Part 3): 297-299.

Parfentjev and Schleyer. 1949. Influence of histamine on the blood sugar level of normal and sensitized mice. Arch Biochem. 20: 341-346.

Szentivanyi et al. 1963. Adrenaline mediation of histamine and serotonin hyperglycemia in normal mice and the absence of adrenaline induced hyperglycemia in pertussis sensitized mice. J Infect Dis; 113: 86-98.

Tabachnik and Gulbekian. 1969. Adrenergic changes due to pertussis, insulin, glucose and free fatty acids. Eur J Pharmacol, 7(2): 186-195.

Toshiaki Katada and Michio Ui. 1981. Islet-activating protein. J Biol Chemistry; 16 (August 25): 8310-8317.

Zametkin et al. (1990). Cerebral glucose metabolism in adults with hyperactivity of childhood onset. NEJM; 323 (November 15): 1361-1366.

Hughes et al.(1997). Trends in growth in England and Scotland 1972-1994. Arch Dis Child; 76:182-189.

Freedman et al. 1997. Secular increases in relative weight and adiposity mong children over two decades, from 1972 to 1994, residing in Ward 4, Washington parish, Louisiana. Pediatrics; 99(3): 420-426.

Smith and Furman. 1988. Augmentation of glucose induced insulin secretion by pertussis vaccine, phentolamine and benextramine: involvement of mechanism additional to prevention of the inhibitory actions in rats. Acta Endocrinologica; 118:89-95.

Dunaif et al. 1989. Profound peripheral insulin resistance, independent of obesity in polycystic ovary syndrome. Diabetes; 38(9): 1165-1174l

Nestler et al.1990. A direct effect of hyperinsulimemia on serum, sex hormone-biuding globulin levels in obese women with the polycystic ovary syndrome.

Gambineri et al. 2002. Obesity and polycystic ovary syndrome. Journal of International Association for the study of obesity. 26(7): 883-896.

Scott et al. 1997. Characteristics of youth-onset of non-insulin dependent diabetes mellitus and insulin-dependent diabetes mellitus at diagnosis. Pediatrics; 100: 84-91.

Dunne et al. 2004. Hyperinsulinism in infancy. From basic science to clinical diseases. Physiology Rev; 84: 239-275.

Valdyula et al. 2006. Platelet and monocyte activation by hyperglycemia and hyperinsulinemia in healthy subjects. http://informahealthcare.com/doi/abs/10.1080/09537100600760814: 17(8): 577-585.

Burghen et al. 2013. Correlation of hyperandrogenism with hyperinsulinism in polycystic ovarian disease. J Clin Endocrinol and metabolism; 50 (issue 1). Published online July1, 2013,

Takizawa et al. (2001) Gender differences in the relationships among hyperleptinemia, hyperinsulinemia, and hypertension. Clinical and Experimental Hypertension; 23(4): 357-368.

Hussain et al. 2004. Infantile hyperinsulinemia associated with enteropathy, deafness and renal tubulopathy: clinical manifestations of a syndrome caused by a contigous gene deletion located on chromosome 11p. J Pediatr Endocrinol Metab; 17(12): 1613-1621.

Michaud et all; 2014. Acetaminophen-induced liver injury in obesity and non-alcoholic fatty liver disease. Liver Int; 34(7): e171-179. doi.1111

Weiss. 1975. Acetaminophen, a potential pediatric hazard. Pediatrics; 52 (6): 883.

Goulding 1973. Acetaminophen poisoning. Pediatrics; 52(6):883-885.

Craighead 1975. Report of a workshop: Disease accentuation after immunisation with inactivated microbial vaccines. J Infect Dis; 1312 (6): 749-754.

Garly et al. (2006). Prophylactic antibiotics to prevent pneumonia and other complication after measles, community based randomised double blind placebo controlled trial in Guinea-Bissau. BMJ, doi:10.1136/bmj.38989.AE published 23 October 2006.

Love Poems for Grown Up Valentines

by Nick Marco

Published on February 13, 2015

1948 views

From the Editor: For something a little different this Valentine’s Day, we are happy to introduce our readers to a long-time friend of Hormones Matter, Nick Marco. Nick was raised internationally and received his M.A. in 1971 from Johns Hopkins University, where he also served as university artist and scholar-in-residence. He mentors poets and book authors on the ‘Net; has poetry published there and in print. He has written magazine-journal-news articles, authored some 17 published books, winning two Hollywood options, two national awards for adult non-fiction. He lives in Las Vegas now where poet-peers once voted him Vegas’ best “classic” poet and his “Medicine Show” Vegas’ outstanding performance poem. From 2006-2008, Nick organized and co-hosted monthly street spoken word and music events at First Fridays. And he is married to the esteemed and much missed, Lana Hanson.

Let’s take a day to remember the beauty in our lives. Happy Valentine’s Day from Hormones Matter.

Thorns and Daisies
Nick Marco 2008

I bedded phantoms, dun-blossomed and thorned,
whose wraith-yens wracked my rest, fingernails pricked
and teeth gouged my real skin—yes, I’d been warned:
Illusions might meld plush perceptions, tricked
to lurk in silk-lined coffins smeared with red—
canned minor-key cellos puncture my ears,
digitized lies slice heart-aimed words that bled,
“luv” CDs drone to narcotize death-fears.
But now you’ve come, and near a ground-low fire
you chant high climax-cries I crave to clutch.
These petals from your tongue I never tire
to hold, nor do my veins bruise at their touch.
I nurse no scars while your lips heal my two:
Tonight, on daisies’ white I’ll sleep… with you.

Still-Dark, Half-Dreams…
Nick Marco, April 2013
For L.H.

…we lie, one warm curve; my chest,
its night-sweat fading, damps
your back, this arm bras
your breasts, and first
light hardness hunts
your cheeks below;
my fingers sift your pillowy
hair through the tangled
tail of the dappled
cat who thrums
above our
waking…

Low Neonatal Vitamin D: A Risk Factor for Autism

by Susan Rex Ryan

Published on February 12, 2015

2339 views

An alarming number of children–in the United States and other industrialized countries—are being diagnosed with Autism Spectrum Disorder (ASD) or autism, a group of complex brain disorders. The medical community’s views about why the incidences of autism are escalating remain varied. Many believe genetics and environmental pollutants may serve as risk factors. Some believe vitamin D deficiency may be linked to the mounting cases of autism.

Vitamin D’s Importance to Brain Development

The link between brain development and vitamin D is far from new to me and other vitamin D experts. Autism may be caused–at least in part—by genetic impairment to a child’s developing brain. Vitamin D plays an essential role in brain development by influencing genetic expression.

Every cell in the brain includes vitamin D receptors (VDR) that control genes that influence brain development. In order to regulate gene expression, the VDR in the brain cells must be turned on by receiving activated vitamin D. Without sufficient vitamin D to activate its receptors, the brain cannot properly develop.

A Landmark Study

A groundbreaking study from Sweden has revealed that children who develop ASD have significantly lower vitamin D levels at birth than their non-ASD siblings.

The Swedish team, led by award-winning autism researcher Elisabeth Fernell, M.D., analyzed the circulating vitamin D levels (25-hydroxy (OH) vitamin D) of 58 Swedish-born sibling pairs, in which one sibling had ASD, the other did not. The children with ASD had significantly lower vitamin D levels at birth than their respective typically developing sibling. Of the paired siblings, the study included 28 pairs where the mother was of Swedish origin, 18 pairs who had African or Middle Eastern mothers, and 12 pairs with “miscellaneous” [1] maternal ethnicity.

The darker one’s skin, the more challenging it is to make vitamin D. Melanin, the pigmentation in our skin, absorbs ultraviolet B rays to synthesize vitamin D from sunlight. Not surprisingly, the researchers found an increased risk of ASD in offspring of dark-skinned moms as well as mothers who wear concealing clothing for cultural reasons.

In fact, many of the newborns with African and/or Middle East heritage had vitamin D levels that were barely traceable. Moreover, the researchers determined that their season of birth did not account for the differences. The research team opined that children born to dark-skinned mothers were exposed to “suboptimal” vitamin D levels during the year.

Finally, the authors of the Swedish study state, “Although low levels of vitamin D could have a genetic origin and as such be associated with ASD, our study is the first to rule out ASD-related lifestyle mechanisms as explanations for low 25(OH)D levels, since the samples were taken in the newborn period.” ASD-related lifestyle mechanisms include indoor living and dietary limitations.

Adequate Maternal Vitamin D May Prevent Autism

Newborns depend solely upon their mother’s nutrition for their cellular development including vitamin D levels. The founder of the Vitamin D Council, John Cannell, M.D., aptly stated that the brain levels of activated vitamin D in a baby “directly depend on the amount of vitamin D the mother makes in her skin or puts in her mouth.”

And, indeed, the findings of the Swedish study, recently published in the journal Molecular Autism, indicate that prenatal vitamin D deficiency may act as a risk factor for ASD in the child. The measurement of maternal vitamin D however was not included in this study. This omission in the study design also precluded a better understanding of the role genetic and environmental factors play in autism development.

Nonetheless, the researchers’ conclusion is implicit: vitamin D is essential to fetal development. These leading-edge results serve as a reminder to all women of reproductive age: ensure your vitamin D levels are adequate by getting a 25(OH)D test and taking a daily vitamin D3 supplement and/or getting optimal sun exposure.

It is also important to note that pregnant mothers typically rely on their prenatal vitamins, most of which only contain enough vitamin D to prevent rickets. Taking prenatal vitamins without supplementing with extra vitamin D3 provides expectant mothers a false sense of health for their babies, as well as a potential risk for their children to develop autism.

Footnote (1): Study participants in the designated “miscellaneous” group are of non-Scandinavian Europe, South America, and East Asia ethnic origins.

Note: For a further look at vitamin D’s role during pregnancy, lactation, and neonatal life, I offer my December 2014 article that includes vitamin D supplementation guidelines for pregnant and nursing mothers as well as babies.

About the Author: Susan Rex Ryan, author of the award-winning vitamin D book Defend Your Life, is dedicated to vitamin D awareness. Her extensive collection of health articles can be found on Hormones Matter as well as on her blog at smilinsuepubs.com. Follow Sue on FB “Susan Rex Ryan” and Twitter @vitD3sue.

Buy an Un-Subscription to Hormones Matter Today

by Chandler Marrs, PhD

Published on February 6, 2015

2197 views

Yes, that’s right we’re soliciting un-subscriptions to Hormones Matter. Why an un-subscription and not a subscription? Well, we’re an open access journal. We believe important health information should be open to all who need it. If we were to utilize a true subscription model, we’d have to block access to those who cannot afford it. We don’t want to do this and so we created the un-subscription model. This allows those who can afford an un-subscription to contribute and those who cannot, to still get all the great articles for free. In reality, just about everyone can afford the entry level un-subscriptions and most of us can afford much more.

If you like what we do and would like to see it continue, buy an un-subscription today. If you’re independently wealthy and would like to back Hormones Matter more fully, we’re amenable to that as well.

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Pregnancy Hypertension

Study Details

Results

Flaws in Study Design

What Value is This?

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Oral Contraceptives are Endocrine Disruptors

Disrupting Hormones Chronically: Is This Safe?

Becoming Pregnant while on Oral Contraceptives: Potential Dangers

Autism and Oral Contraceptives: Is there a Connection?

References

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Vaccine Induced Hyperinsulinemia?

Deranged Glucose Metabolism in Childhood

From Vaccines to Hyperinsulinemia to Obesity

Antibiotics and Obesity

Conclusion

References

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Vitamin D’s Importance to Brain Development

A Landmark Study

Adequate Maternal Vitamin D May Prevent Autism

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Subscribe to an Un-subscription Now

Is this a Donation?

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