Article written by Written by Sayer Ji, founder of Greenmedinfo.com, a reviewer at the International Journal of Human Nutrition and Functional Medicine, Co-founder and CEO of Systome Biomed, Vice Chairman of the Board of the National Health Federation, Steering Committee Member of the Global Non-GMO Foundation.
Without much more than a whisper from the mainstream media, Monsanto’s newest Frankenfood has received full EPA approval and will be arriving on dinner plates by the end of the decade. The implications of this are harrowing, to say the least.
While you may not have made up your mind on the dangers of GMOs, you likely feel entitled to know when you’re consuming a food that is the product of laboratory research. For this reason, I am reporting on Monsanto’s latest food technology, unfortunately, already in the pipeline. And quite silently so. I write this with a certain degree of solemnity, if not also a tinge of regret, because, for three years, I have heard rumblings of Monsanto’s next project – RNA interference technology. It was actually the late Heidi Stevenson, my friend, colleague, and founder of the platform Gaia Health, who first alerted me to the dangers of RNA interference-based tinkering with our food supply when she reported on the near disastrous approval of GMO wheat using RNA interference technology in Australia. Thankfully a few brave scientists and informed public stood up and, together, averted the disaster. But since then, both the dangers and the breakneck speed of development of this technology have gone largely ignored, even among activists deep in the non-GMO movement. In order to truly appreciate the gravity of the situation, and why the EPA’s approval of RNAi corn intended for human consumption, is so concerning, it will first require a little background information on the fascinating topic of non-coding small RNAs, and their formidable relevance to our health.
How Non-Coding, Small RNAs Link Together The Entire Biosphere
One of the most important discoveries of our time is that all plants, including those we use for food and animal feed, contain a wide range of RNA molecules capable of inhibiting gene expression or translation. These non-coding RNA molecules neutralize targeted messenger RNA molecules (mRNAs), which prevents their translation into a protein, i.e. they “silence genes.”
Compelling research has surfaced suggesting that not only do these genome-regulating small RNA molecules exist in our foods, but that they are capable of surviving digestion, and being absorbed into our bodies fully intact where they alter, suppress or silence genes, post-transcriptionally. Moreover, some of these small RNAs — primarily microRNAs (miRNAs) and small interfering RNAs (siRNAs) — are believed to be cross-kingdom mediators of genetic information, making it possible for RNAs in one species impacting many others through both their active and passive exposure to them.
Food therefore is essentially an epigenetic modifier of gene expression, making it a form of information, and not only a source of bodily building blocks and caloric energy, as conventionally understood. As such, any significant changes to food or feed staples within our food chain could have powerful impacts on the physiological fate of those consuming them, essentially rewriting the functionality of our genomic hardware via software like changes in RNA profiles. The entire biosphere, therefore, is held together in a web-like fashion through these molecular RNA messengers, lending a plausible mechanism to the biotic aspect of Lovelock and Margulis’ Gaia theory of Earth as a self-regulating, meta-organism. You can learn more by reading my article Genetic Dark Matter, Return of the Goddess, and the Post-Science Era.
Monsanto and Co Capitalizing on RNA interference Technology
While this discovery will have profound implications for the field of nutrition and medicine, it has also created enormous interest among biotech and agricultural firms, namely, Monsanto and Dow, looking to capitalize on the design of proprietary products using interference (RNAi) technology. In mid June, last month Monsanto received EPA approval for a type of corn genetically altered to produce an RNA-based pesticidal agent (aka, a plant-incorporated protectant (PIP)) which lethally targets a metabolic pathway within the corn rootworm, known within the industry as the “billion dollar bug.” Branded as Smartstax PRO, the newly minted GMO plant produces a small, double-stranded RNA known as DvSnf7 dsRNA which disrupts a critical gene within the rootworm, causing its death. This was added on top of four other “stacked” GMO traits, such as the ability to produce two other pesticidal proteins (Cry1A.105 and Cry2Ab2), as well as survive exposure to both glyphosate (aka Monsanto’s Roundup 2) and Glufosinate (aka Dow’s Libertylink), highly toxic herbicides. Roundup, for instance, has demonstrated carcinogenicity in the parts per trillion range. Yet, the EPA considers it perfectly safe for consumers to ingest many orders of magnitude higher concentrations than that, proving its function as a cheerleader and not a regulator of the industry that controls our food supply.
The Atlantic, one of the only mainstream news outlets to report on the topic, pointed out how surprisingly low key the approval process was:
“The EPA’s decision attracted little attention from the press or even from environmental groups that reliably come out against new genetically modified crops.”
Bill Freese, The Center for Food Safety’s science policy analyst, told the Atlantic he was caught off guard by EPA’s decision to only allow 15 days of public comment, and the fact that it did not post its decision to the Federal Register, as it customary, especially considering how unprecedented the use of a RNAi insecticide in a plant intended for human consumption is. Monsanto anticipates the new corn will be on the market by the end of the decade.
One would imagine that such revolutionary technology would require short and long-term (decades) of safety testing before licensure. Instead, as is often the case with big-ticket market agendas, the product is being rushed to market. There are already significant biases in place within the EPA and USDA in regard to nucleic acids – assumptions that exempt them from cautionary considerations. RNA is considered Generally Accepted As Safe (GRAS), but this is because it is defined and perceived only as a physical substance rather than as the powerful signaling/informational molecule it is. The EPA’s approval of RNAi food crops ignores the fact that it takes a multi-generational timescale to understand the influence of epigenetic modifiers on the genome of a species, much less the human species, whose timescale is orders of magnitude beyond animal models used to establish much of the risk/benefit data used in pre-approval evaluations. RNAi interference technology promises specificity — one RNAi molecule change equals one gene suppressed — but ignores the virtually infinite possibility of unintended, adverse effects in what are incomprehensibly complex biological systems. Indeed, researchers have warned that RNAi can not only profoundly affect gene expression, but that the changes it induces can permanently alter a species through inherited traits 1:
“Once a silencing effect is initiated, the effect may be inherited. The biochemistry of this process varies depending on the organism and remains an area of active research with many unknown aspects. Nevertheless, it is known for example that human cells can maintain the modifications necessary for TGS, creating actual or potential epigenetic inheritance within tissues and organisms (Hawkins et al., 2009). In some cases the dsRNA pathways induce RNA-dependent DNA methylation and chromatin changes (TGS) that persist through reproduction or cell division, and in other cases the cytoplasmic pathways remain active in descendents (Cogoni and Macino, 2000).”
GM Technology and Unintended Consequences
Indeed, critics of RNA interference technology make the point that RNAi technology aims to target the production of a specific protein by identifying the sequence in question. But two or more genes can have sequence homologies. This means, as applies to the use of RNA interference in medicine, a gene that is targeted to turn off a “disease-causing gene” could have a number of off-target effects, one of which w
Criticisms of RNAi in the agricultural sector are long-standing among the highly informed. For instance, Jonathan Latham, Ph.D. and Allison Wilson, Ph.D., wrote a seminal paper on the topic over a decade ago titled “Off-target effects of plant transgenic RNAi: three mechanisms lead to distinct toxicological and environmental hazards,” wherein 3 of the primary safety concerns are addressed: 1) Off target effects leading to non-specific down-regulation of plant RNAs 2) Off target effects affecting non-target invertebrates feeding on plant material 3) potential effects on mammals. In mammals, long (>30 bp) perfectly duplexed RNAs (such as are typically produced by plant RNAi transgenes) are Pathogen Associated Molecular Patterns (PAMPS) and are consequently highly potent triggers of innate anti-viral defences. The effects of long dsRNAs on mammalian cellular functions are typically profound and extend to complete inhibition of protein translation and cell death. Nevertheless, the implications of such molecules in the mammalian diet have hardly been tested.
That’s quite a serious list of concerns. As you can see, concern #3 includes the possibility that these dsRNAs may lead to protein translation and cell death. Clearly if the EPA has declared Monsanto and Dow’s new RNAi corn safe for human consumption, they would need to prove this a non-issue.
Monsanto Falling On Their Own ‘Peer-Reviewed’ Sword
Surprisingly, Monsanto itself has produced one of the most damning papers on the topic yet. Several years ago I stumbled upon a study funded by Monsanto that raised a number of red flags for me. Titled, “Endogenous small RNAs in grain: Semi-quantification and sequence homology to human and animal genes,” researchers employed by Monsanto in their St. Louis, MO, laboratory analyzed the presence of endogenous small RNAs in common food and feed staples — soybeans, corn, rice — discovering that hundreds of these plant RNAs had a perfect 100% complementary match to human genes as well as other mammals.
Why is this significant? Endogenous small RNAs, such as small interfering RNAs (siRNAs) and microRNAs (miRNAs), are effector molecules of RNA interference (RNAi), which is a gene suppression mechanism found in plants, mammals, and other eukaryotes. The implication, therefore, of Monsanto’s finding is that plant RNAs — were they capable of surviving digestion and accumulating in target tissues to physiologically relevant concentrations — are capable of epigenetically silencing hundreds of genes within the human body. Below you will find a list of the RNA/gene matches between rice and the human genome:
Despite the abundance of perfect 100% complementarity matches listed above, Monsanto’s conclusion was a conveniently pollyannish dismissal of the safety implications of these findings, stating that:
“The abundance of endogenous small RNA molecules in grain from safely consumed food and feed crops such as soybean, corn, and rice and the homology of a number of these dietary small RNAs to human and animal genomes and transcriptomes establishes a history of safe consumption for dietary small RNAs.”
While this may be true for traditionally used plants, it does not follow that genetically modified organisms would necessarily be safe because non-GMO versions are. [The pseudo-scientific conceptual ploy of “substantial equivalency“ behind traditional and GMO cultivars has been the basis for the approval of GMOs since their inception.] Monsanto’s conclusion relates to the fact that it has invested a great amount of resources into developing proprietary RNAi-based organisms which help it to maintain and further expand its monopolizing control on the global food supply.
Additionally, one of their primary justifications for concluding the safety of endogenous plant RNAs on human health was that: “…there does not appear to be any evidence in the scientific literature suggesting that intact RNA is absorbed following ingestion.” This bold claim has been disproven. The Monsanto paper was written in 2008, 3 years before the groundbreaking discovery of Zhang et al published in the Cell Research, entitled,”Exogenous plant MIR168a specifically targets mammalian LDLRAP1: evidence of cross-kingdom regulation by microRNA,” wherein it was demonstrated that human subjects fed rice containing the microRNA MIR168a have measurable amounts of it present in their blood and tissue, and that it binds to the lipoprotein receptor adapter protein in the liver. More succinctly:
“These findings demonstrate that exogenous plant miRNAs in food can regulate the expression of target genes in mammals.”
Since then, a hotly contested debate has ensued, which is understandable, given the increasingly politicized and financially-motivated nature of scientific debate and findings.
Here’s Monsanto’s conclusion about the safety of RNAi-based food technology:
“Based on this evidence it can be concluded that RNAi-mediated regulation of gene expression in biotechnology-derived crops is as safe for food and feed use as conventional crops that harness RNAi-based gene regulation as one of several ways to achieve new plant traits. The safety of future crops generated through applications of RNAi should thus be evaluated for safety using the existing comparative safety assessment paradigm, which has been developed for biotechnology-derived Crops.”
First of all, the “evidence” they are referring to is based on an axiomatic absurdity: equating the absence of evidence with evidence of absence. In other words, you can’t prove this negative: “that a hazard does not exist” because positivistic proof of anything requires that you demonstrating something, not nothing.
Let’s also not overlook the conflict of interest statement at the end of their paper: “All authors are employees of the Monsanto Company. The Monsanto Company is an agricultural company that produces,” which speaks to Monsanto’s long history of funding science that denies safety risks of their products, such as the Roundup-Cancer link, which now even the California EPA accepts as fact.
The Heart of the Problem
In a seminal paper published in 2016 in Trends in Microbiology, entitled, “How Our Other Genome Controls Our Epi-Genome,” it is proposed that the very RNAs biotech/agrochemical companies like Monsanto and Dow are tinkering with in our food should be reconsidered as part of the definition of our species versus the conventional view that it is just something informationally inert that we eat and exists “out there.” Using a revised version of Da Vinci’s Vitruvian man, as pictured below, they propose that there are 4 inseparable parts of our species: 1) human cells 2) human microbiota and other bacteria 3) Fungi and Viruses 4) Food.
As you can see, because of the interconnectivity and “social networking” functionalities of RNAs packaged in microvesicles called exosomes, all four parts of this new definition of man become united in an indivisible whole. Because these RNAs packed in edible exosomesepigenetically active, the food we eat “literally talks to our mRNA and DNA,” as I have explained in greater detail here: “Amazing Food Science Discovery: Edible Plants ‘Talk’ To Animal Cells, Promote Healing.”
As we have seen in Monsanto’s own paper on the topic, foods contain hundreds of small RNAs whose 100% complementarity match with human genes imply they can directly impact, and even silence those genes. This silencing is not necessarily “bad,” but it is clear that we are tinkering with a design that we are only just beginning to understand, much less know how to ascertain the risks of and properly regulate. But, considering that Monsanto’s research reveals how intricately connected the human and the food genomes are are — and furthermore, that post-2008 research has surfaced showing Monsanto was wrong and plant RNAs from food do have direct impacts on human genome/epigenome expression — it is highly irresponsible for them to continue to claim that food manipulation technologies will not have unintended, adverse effects in principle. Sadly, with the EPAs approval of four new RNAi forms of corn already completed, and likely many more on the way, we may be stuck with secondary and much slower forms of recourse: post-marketing, epidemiological surveillance of exposed populations, where patterns of disease can take decades if not generations to surface — and then with so many confounding factors at play, not with any certainty.
That said, I believe education and the awareness it generates is our best bet at countermanding the widespread acceptance of this highly experimental and obviously dangerous form of genetic engineering. As has been the case recently with glyphosate being classified as a carcinogen by the California EPA, and a growing mainstream movement to fight the forced feeding of non-labeled GMO laden products (March Against Monsanto), the tides are turning. Please help us spread this information far and wide.
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1 Heinemann JA, Agapito-Tenfen SZ, Carman JA. A comparative evaluation of the regulation of GM crops or products containing dsRNA and suggested improvements to risk assessments. Environ Int. 2013 May;55:43-55. doi: 10.1016/j.envint.2013.02.010. Epub 2013 Mar 20. PubMed PMID: 23523853.
Tylenol Damages The Brains of Children, Research Reveals
- The Facts:
Tylenol has a wide range of toxic side effects you should be aware of, especially if you are pregnant or use it with your children. Article written by William Parker, Ph.D for Greenmedinfo.com, published here with permission.
- Reflect On:
Why do we keep taking Tylenol and other over-the-counter drugs when it's unquestionable that they do more harm than good? Why don't we ever look into healthy ways to alleviate our symptoms?
A number of non-peer-reviewed articles have been written and published on the web claiming that there is literally nothing to fear from acetaminophen during pregnancy. There are two types of articles that fall into this category. First, reputable watchdog organizations have weighed in on the issue, declaring acetaminophen use during pregnancy and during childhood to be proven safe. In particular, the National Health Service of the UK and the Center for Accountability in Science have both strongly criticized the Spanish study from 2016 showing a link between acetaminophen use during pregnancy and ADHD/autism.
The second type of article is generally written by a science writer working for an organization that runs a website. Often quoting one to three experts who claim that is perfectly safe and that pregnant women and families should not be concerned, many of these articles are published by reputable sources that are generally trustworthy. Typically, an expert is being asked to comment on one particular publication showing a link between acetaminophen use (usually during pregnancy) and some sort of neuropsychiatric problem (autism, lowered IQ, hyperactivity, and/or social/behavioral problems, depending on the study). There are several important things to consider when evaluating these articles:
1. There are a number of University Professors who have studied the use of acetaminophen on the developing brain and who are keenly aware of the potential dangers. A partial list of these individuals is provided below.
2. Being an expert in acetaminophen neurotoxicity during development means that considerable time has been invested in studying the issue. Any true expert in this issue will be aware of basic facts regarding acetaminophen neurotoxicity. These facts include the following:
(a) Studies in animal models (both in mice and in rats) demonstrate that acetaminophen use during a sensitive period of brain development causes long-term alterations in the brain and is manifested as problems with social function.
(b) Margaret McCarthy, Chair of Pharmacology at the University of Maryland, has worked out the probable mechanism by which acetaminophen-induced brain damage occurs. Her research team has found that the male brain is considerably more sensitive to acetaminophen than the female brain, possibly accounting for the gender bias in autism.
(c) There are (as of January 2017) a total of 8 published studies evaluating the long terms effects on children of acetaminophen use during pregnancy or during childhood. Two of these (one in 2014, one in 2016) were published in JAMA Pediatrics, one of the most highly respected pediatric journals. All studies point toward acetaminophen use being associated with long-term problems with neurological function. Each study design has included some attempt to control for indication. In all studies, acetaminophen use rather than indication has been identified as the key factor associated with cognitive problems. A formal meta-analysis is not currently possible because of the varied outcome measures and study designs, but all 8 studies point in the same direction: Acetaminophen is neurotoxic to the developing brain. The studies are not “cherry picked”, selecting only those which find an effect. All studies point toward a neurotoxic effect of acetaminophen in the developing brain.
(d) Acetaminophen substantially alters brain chemistry and temporarily impairs awareness of social issues in adult humans.
(e) Testing of acetaminophen safety in children did not include any evaluation of brain function, and no long-term studies were ever conducted. The primary manufacturer of acetaminophen in the US acknowledges that the drug has never been shown to be safe for brain development when used during pregnancy or in childhood. All safety tests were performed with the assumption that any side effects would be acute in nature (e.g., bleeding or acute organ damage). This assumption was based on observations made with acetaminophen in adults and with aspirin in children. It was not based on any experience with acetaminophen use in children.
3. Having prescribed tens of thousands of doses of acetaminophen does not make anyone an expert on the neurotoxicity of acetaminophen, any more than eating thousands of pounds of chips makes somebody an expert in the effects of an inflammatory diet. Credentials and certifications that allow physicians to prescribe acetaminophen do not make them experts, and elevated positions in the medical community do not qualify anybody as an expert on the effects of acetaminophen. If somebody does not know those basic facts listed above, then they are not an expert on the neurotoxicity of acetaminophen. Usually, the experts will have published one or more peer-reviewed manuscripts on the topic. Those are the people to ask when an expert is needed.
4. It is tempting to point accusing fingers at physicians who say that acetaminophen is safe when they literally have no grasp whatsoever of the relevant scientific literature. However, this would be a mistake. I have tracked down a few of these individuals who were quoted in a very public format, and one individual, in particular, didn’t even remember having made a comment on the topic. The most likely explanation is that a reporter asked them if acetaminophen was safe, and their response based on their training (not on the knowledge of the literature) was that it is safe. After all, if they didn’t think it was safe, they would not be administering it dozens of times per day. So, if a reporter asks a physician if something is safe, and they provide their knowledge based on what they have been taught and how they practice, then it is hard to blame them. The reporter didn’t ask them to spend days or even weeks reviewing the literature in detail, but rather assumed that any physician administering something dozens of times per day would know the literature. (This is a false assumption. No physician has the time to study all current literature on every drug they administer.) So, in a nutshell, a tragic propagation of incorrect information is occurring despite the best of intentions of all parties involved.
5. Unless an organization such as the National Health Service has the time to review a topic thoroughly, they should remain silent on an issue. It took a team of us two years to put together our summary of the evidence, both direct and circumstantial, regarding the potential neurotoxicity of acetaminophen during development. It took the NHS only days to publish their recent criticism of the 2016 Spanish study. Offering questionable criticisms of a single paper without reviewing the literature to see how that publication fits into the big picture is a disservice to the public being served.
6. Reading the published quotes from many “experts” who exonerate acetaminophen, it is apparent that the logic falls into one of two categories.
(a) Everybody is doing it, so it must be OK.
(b) This single study is not perfect, so no change in practice should be made.
Neither of these criticisms is logically sound, of course. These two criticisms are often combined and were, in fact, part of the critical comments directed toward the first paper showing that acetaminophen probably has substantial neurotoxicity during development (published in 2008 by Steve Shultz). Further, the evaluation of study weaknesses is usually skewed and not entirely valid. Since the idea that acetaminophen is safe is being embraced, then any merit in the paper is often undermined to make the case. This is certainly true of the published (peer reviewed) criticisms of the 2008 Shultz paper.
7. Many on-line sources support the view that acetaminophen can be very dangerous to the developing brain. Probably the most reliable source, the FDA, is remaining silent on the topic until something more definitive is done. The FDA knows that this is extremely urgent, but unfortunately, our FDA is not linked well (in a practical manner) with our NIH, and thus they can’t dictate research priorities.
8. Here is a list (not comprehensive) of experts regarding the neurotoxicity of acetaminophen during brain development.
a) First, I’ll thank the wonderful team of individuals who helped put together our comprehensive review on this topic. Shu Lin, a professor with me in Duke’s Surgery Department, is a very dear and long-time friend of mine who has supported me through countless projects over the past 22 years. Staci Bilbo, director for research on Autism at Harvard, is a friend and collaborator who has helped me understand what causes inflammation and the role of inflammation in brain dysfunction. Chi Dang Hornik, a pediatric pharmacist at Duke, contributed greatly to our understanding of the frequency of acetaminophen administration and the available formulations of the drug. Many thanks to Martha Herbert. As a Harvard professor and clinician, she has a great appreciation for the clinical data obtained from patients with autism. Cindy Nevison, a professor at the University of Colorado at Boulder, rounds out our team, providing critical information about the epidemiology of autism. (Thanks also to our interns (Rasika Rao and Lauren Gentry) and research analyst (Zoie Holzknecht) who were a tremendous help in compiling information and preparing that information for publication.)
b) Margaret McCarthy, chair of Pharmacology at the University of Maryland, it the most knowledgeable person I know regarding the biochemistry of the human brain and how that is affected by acetaminophen and other drugs in that class.
c) Chittaranjan Andrade, Chair of Psychopharmacology at the National Institute of Mental Health and Neurosciences, Bangalore, India, has written a peer reviewed paper on the topic of acetaminophen induced brain damage. He nicely summarized a number of studies looking at the connection between acetaminophen and neurological damage. His final conclusion is that the drug is probably more associated with ADHD than autism, but the conclusion was limited to exposure during pregnancy and his work was conducted before some critical studies were published in 2016.
d) Henrik Viberg is a professor in the Department of Organismal Biology at Uppsala University in Sweden. He has studied how exposure of mice to acetaminophen during development can cause long term brain damage.
e) In 2015, a group of scientists working with Laurence de Fays at the Federal Agency for Medicines and Health Products in Brussels acknowledged the clinical studies and the studies in animal models which indicated that acetaminophen could be dangerous to the developing fetus, but concluded that paracetamol is “still to be considered safe in pregnancy”. At the same time, they state that “additional carefully designed studies are necessary to confirm or disprove the association (between acetaminophen and brain damage to children)”, and that “care should be taken to avoid raising poorly founded concerns among pregnant females”. We very strongly agree with the conclusion that more studies are needed, but very strongly disagree with the conclusion that women should be kept in the dark about the matter. It is important to point out that several more studies have come out since Laurence de Fays’ report. One of those is a 2016 manuscript in JAMA Pediatrics(see the next expert), a highly reputable peer reviewed journal, which addresses the concerns raised by de Fays, so it is possible that de Fays’ group may now have a different opinion.
f) A team of scientists and doctors working with Evie Stergiakouli at the University of Bristol analyzed data from a prospective birth cohort, and concluded that “children exposed to acetaminophen prenatally are at increased risk of multiple behavioral difficulties”. They found considerable evidence indicating that the association was not due to the confounding factors that concerned de Fays’ group (previous expert).
g) Jordi Julvez at the Centre for Research in Environmental Epidemiology in Barcelona, Spain worked with a team of a dozen clinicians and scientists to publish their 2016 study linking acetaminophen with autism and ADHD.
h) Amany A. Abdin, a professor in the Department of Pharmacology, Tanta University, Egypt, wrote a review of the acetaminophen/autism connection and published it in the journal Biochemistry and Pharmacology: Open Access. Her conclusion in 2013 was that the drug is not safe and that the acetaminophen/autism connection should receive attention.
i) The original paper that identified a connection between neuropsychiatric disorders and acetaminophen was published by Steve Shultz while at the University of California at San Diego. Coauthors on the paper included Hillary Klonoff-Cohen, currently an Endowed Professor and Director of the MPH program at the University of Illinois.
j) Four scientists, including research scientist Ragnhild Eek Brandlistuen and professors Hedvig Nordeng and Eivind Ystrom in the Department of Pharmacy at the University of Oslo, coauthored a study showing a connection between adverse neurodevelopment and acetaminophen use during pregnancy.
k) Jorn Olsen, Professor and Chair of the Department of Epidemiology at UCLA, published one of the more recent papers (2016) showing a connection between autism and acetaminophen use during pregnancy.
l) Five professors (John M. D. Thompson, Karen E. Waldie, Clare R. Wall, Rinky Murphy, and Edwin A. Mitchell) from four different departments at The University of Auckland published their findings in PLOSone in 2014 which “strengthen the contention that acetaminophen exposure in pregnancy increases the risk of ADHD-like behaviours. Our study also supports earlier claims that findings are specific to acetaminophen.”
For evidence-based research on the dangers of acetaminophen, visit the GreenMedInfo.com Research Dashboard.\
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William Parker is an Associate Professor at Duke University, where he has worked in the Department of Surgery since 1993. William is currently investigating a number of issues associated with inflammation and Western society, including vitamin D deficiency, heart disease and alteration of the symbionts of the human body (“biota alteration”). He has been interested in “natural” immune function for some time, which has led him down a path that includes the first studies of immune function in wild rats and the discovery of the function of the human appendix.
Vaccine Mandates Results Don’t Safeguard Children’s Rights or Health: How Did We Get Here?
For decades, the U.S. government has made compulsory childhood vaccination one of the cornerstones of its public health policy. Outside the U.S., countries’ vaccination policies range from completely voluntary to “aggressive,” with some nations promoting vaccination but leaving the decision up to the individual, and others pushing a little harder by financially incentivizing vaccination. Some of the countries with mandatory vaccination have “modest” policies that focus on a single vaccine such as polio, and some—with broader mandates on the books—choose not to enforce them.
Regardless of the policy, no other country requires as many childhood vaccines as the U.S., but the legal edifice shoring up the compulsory childhood vaccine program is surprisingly flimsy. As New York University legal scholar Mary Holland explains in a 2010 working paper, this edifice relies primarily on two century-old Supreme Court decisions—from 1905 and 1922—and on the game-changing National Childhood Vaccine Injury Act (NCVIA) of 1986, which fundamentally altered the legal landscape for vaccination by exempting vaccine manufacturers and medical practitioners from liability for childhood vaccine injuries.
…current childhood mandates are not only radically different from what the earlier courts and legislators envisioned but are unreasonable and oppressive and have led to…perverse results that do not safeguard children’s rights and health.
The 1986 Act, in particular, resulted in an absence of legal protections for vaccinated children that is “striking compared to almost all other medical interventions.” Examining the legal trajectory of vaccine mandates since 1905, Holland argues that current childhood mandates are not only radically different from what the earlier courts and legislators envisioned but are “unreasonable and oppressive and have led to…perverse results” that do not safeguard children’s rights and health.
From mandates for emergencies to mandates for “prevention”
The Supreme Court’s 1905 Jacobson v. Massachusetts decision, as summarized by Holland, justified the imposition of one vaccine—smallpox—on adults “on an emergency basis” and under circumstances of “imminent danger.” At the same time, the Jacobson decision established medical exemptions, reasoning that it “would be cruel and inhuman in the last degree” to vaccinate someone who was medically unfit. Jacobson also contained “robust cautionary language,” calling attention to the potential for “arbitrary and oppressive” abuse of police power and warning against going “far beyond what was reasonably required for the safety of the public.” Jacobson urged courts to be “vigilant to examine and thwart unreasonable assertions of state power.”
Despite these words of warning, state-level courts did not wait long before broadening the judicial interpretation of Jacobson beyond the notion of imminent danger or necessity—although still within the context of just the smallpox vaccine:
- In 1916, Alabama and Kentucky courts affirmed states’ right to mandate vaccination for prevention of smallpox epidemics, stating that state Boards of Health “are not required to wait until an epidemic actually exists before taking action.” The Alabama court also broadened the rationale for mandates beyond adults to children.
- In 1922, the three-paragraph Zucht v. King Supreme Court decision sanctioned vaccine mandates as a condition for public school attendance. According to Holland, this decision further shifted Jacobson’s “paradigm…by upholding a mandate exclusively for children and not for the entire population.”
- Decisions in Mississippi and Texas in the early 1930s granted public health authorities the leeway to define public health emergencies in whatever manner they saw fit.
- A New Jersey court in the late 1940s interpreted Jacobson as justifying all vaccine mandates, “disregarding its language to reject unreasonable, arbitrary or oppressive state actions.”
- An Arkansas court in the early 1950s suggested that anyone questioning vaccine safety or efficacy should “lodge [their] objections with the Board of Health rather than the court.”
Occasionally, legal officials expressed their disapproval of vaccine mandates outside of emergencies, as with the North Dakota judge who, in 1919, pronounced childhood vaccination in the absence of a smallpox epidemic an act of “barbarism.” The same judge also wrote presciently about the self-interest of the medical profession and vaccine manufacturers—“the class that reap a golden harvest from vaccination and the diseases caused by it.” In comments that bear repeating today, the judge stated,
“Every person of common sense and observation must know that it is not the welfare of the children that causes the vaccinators to preach their doctrines and to incur the expense of lobbying for vaccination statutes. …And if anyone says to the contrary, he either does not know the facts, or he has no regard for the truth.”
The legal sea change in 1986
Although vaccination mandates had become legally “well-entrenched” by the mid-1950s—regardless of emergency and “all but erasing” Jacobson’s cautionary language—Holland emphasizes that this legal framework arose in the context of a single vaccine for a contagious disease considered to be life-threatening. Even when the polio vaccine subsequently came on the scene, the nonprofit organization that helped develop and distribute the vaccine “opposed compulsion on principle.”
According to Holland, the creation of the Centers for Disease Control and Prevention’s (CDC’s) Advisory Committee on Immunization Practices (ACIP)—“a federal advisory body with little public participation and no direct accountability to voters”—laid the groundwork for far more coercive vaccine policies. In fact, ACIP has become, over time, the “driving force” behind vaccine mandates. Whereas Jacobson justified mandates under specific and rare circumstances, ACIP has created an “infrastructure” that pushes mandates for any vaccine-preventable illness.
…revenue-generating vaccine development and promotion have enjoyed priority over vaccine safety science and injury compensation since the Law’s (NCVIA) inception
By 1981, after ACIP helped ensure that multiple vaccines were obligatory for school attendance in all 50 states, the number of vaccine injuries began increasing. Against this backdrop, Congress enacted the NCVIA in 1986. Although some legislators may have been well-intentioned when they passed the Act, Holland makes it clear that it has been nothing short of a disaster. In essence, the Act located “vaccine promotion, safety and compensation under one [government] umbrella,” thereby creating “the risk of trade-offs among competing goals.” The rather predictable result is that “revenue-generating vaccine development and promotion have enjoyed priority over vaccine safety science and injury compensation since the Law’s inception.”
Holland identifies the paradox at the core of the 1986 Law. On the one hand, the legislation “for the first time publicly acknowledged that universal compulsory vaccination is likely to cause permanent injury and death to some infants and children”; on the other hand, it forces healthy children to give up ordinary legal protections, including informed consent, and takes away from injured children the right to sue manufacturers directly.
Meanwhile, ACIP has continued to promote a shift away from “necessity” as the rationale for vaccine mandates. A number of the vaccines that ACIP now calls for American children to get to attend school—70 doses of 16 vaccines by age 18—are for rarely fatal illnesses and for conditions “not contagious through ordinary social contact.” Holland’s conclusion is that:
“Necessity no longer determines the validity of state childhood vaccination mandates…. New vaccine mandates are guided by financial returns on low prevalence diseases, not protection of the entire population against imminent harm.”
“Ravenous corporate greed and mindless bureaucracy”
Some of the most troubling facts come at the end of Holland’s impressive legal review and concern the power of the pharmaceutical industry. She notes:
- The pharmaceutical industry has been the most profitable industry in the U.S. since the 1980s.
- In a single year in the early 2000s, “the combined profits of the ten largest drug companies in the Fortune 500 had higher net profits…than all the other 490 companies [in the Fortune 500] combined.”
- There are more full-time pharmaceutical industry lobbyists on Capitol Hill than there are legislators in both Houses of Congress.
- The leading manufacturers of childhood vaccines in the U.S. (Merck, Pfizer, GlaxoSmithKline and Sanofi Pasteur) have records of documented fraud and criminal/ethical misconduct.
Holland also tackles the extensive collusion between the pharmaceutical industry and government regulators, including a quote about “ravenous corporate greed and mindless bureaucracy” in a related article. Whereas “demonstrably predatory corporations selling compulsory products to a vulnerable population should lead to a high level of government scrutiny and skepticism,” Holland observes that “government appears to ally its interests with industry in the arena of vaccines.”
Coercion is backfiring
Fortunately, the public and even some health professionals are growing increasingly wise to this industry-government shell game. In one community, opposition to human papillomavirus (HPV) vaccine mandates recently put public health authorities on the defensive about the epidemic of autoimmunity in today’s youth, the “exorbitant” amount of neurotoxic aluminum in vaccines and the requirement to “get a vaccine for something that can’t be caught in a classroom.” A parent responding to the news article stated, “Why should I as a mother trust the Public Information Officer for the state Department of Health when he cannot even name the amount of aluminum in the vaccine?” Thus, it is up to the public—and ethical professionals—to engage in the “scrutiny and skepticism” that the U.S. government has unconscionably failed to exercise.
How X-Ray Mammography Is Accelerating The Epidemic of Cancer
Article written by Sayer Ji, Founder of Greenmedinfo LLC, posted here with permission.
While a growing body of research now suggests that x-ray mammography is causing more harm than good in the millions of women who subject themselves to breast screenings, annually, without knowledge of their true health risks, the primary focus has been on the harms associated with over-diagnosis and over-treatment, and not the radiobiological dangers of the procedure itself.
In 2006, a paper published in the British Journal of Radiobiology, titled “Enhanced biological effectiveness of low energy X-rays and implications for the UK breast screening programme,” revealed the type of radiation used in x-ray-based breast screenings is much more carcinogenic than previously believed:
Recent radiobiological studies have provided compelling evidence that the low energy X-rays as used in mammography are approximately four times – butpossibly as much as six times – more effective in causing mutational damage than higher energy X-rays. Since current radiation risk estimates are based on the effects of high energy gamma radiation, this implies that the risks of radiation-induced breast cancers for mammography X-rays are underestimated by the same factor.
In other words, the radiation risk model used to determine whether the benefit of breast screenings in asymptomatic women outweighs their harm, underestimates the risk of mammography-induced breast and related cancers by between 4-600%.
The authors continued
Risk estimates for radiation-induced cancer – principally derived from the atomic bomb survivor study (ABSS) – are based on the effects of high energy gamma-rays and thus the implication is that the risks of radiation-induced breast cancer arising from mammography may be higher than that assumed based on standard risks estimates.
This is not the only study to demonstrate mammography X-rays are more carcinogenic than atomic bomb spectrum radiation. There is also an extensive amount of data on the downside of x-ray mammography.
Sadly, even if one uses the outdated radiation risk model (which underestimates the harm done),* the weight of the scientific evidence (as determined by the work of The Cochrane Collaboration) actually shows that breast screenings are in all likelihood not doing any net good in those who undergo them.
In a 2009 Cochrane Database Systematic Review,** also known as the Gøtzsche and Nielsen’s Cochrane Review, titled “Screening for breast cancer with mammography,” the authors revealed the tenuous statistical justifications for mass breast screenings:
Screening led to 30% overdiagnosis and overtreatment, or an absolute risk increase of 0.5%. This means that for every 2000 women invited for screening throughout 10 years, one will have her life prolonged and 10 healthy women, who would not have been diagnosed if there had not been screening, will be treated unnecessarily. Furthermore, more than 200 women will experience important psychological distress for many months because of false positive findings. It is thus not clear whether screening does more good than harm.
In this review, the basis for estimating unnecessary treatment was the 35% increased risk of surgery among women who underwent screenings. Many of the surgeries, in fact, were the result of women being diagnosed with ductal carcinoma in situ (DCIS), a “cancer” that would not exists as a clinically relevant entity were it not for the fact that it is detectable through x-ray mammography. DCIS, in the vast majority of cases, has no palpable lesion or symptoms, and some experts believe it should be completely reclassified as a non-cancerous condition.
A more recent study published in the British Medical Journal in 2011 titled, “Possible net harms of breast cancer screening: updated modeling of Forrest report,” not only confirmed the Gøtzsche and Nielsen’s Cochrane Review findings, but found the situation likely worse:
This analysis supports the claim that the introduction of breast cancer screening might have caused net harm for up to 10 years after the start of screening.
So, let’s assume that these reviews are correct, and at the very least, the screenings are not doing any good, and at worst, causing more harm than good. The salient question, however, is how much more harm than good? If we consider that, according to data from Journal of the National Cancer Institute (2011), a mammogram uses 4 mSv of radiation vs. the .02 mSv of your average chest x-ray (which is 200 times more radiation), and then, we factor in the 4-600% higher genotoxicity/carcinogenicity associated with the specific “low-energy” wavelengths used in mammography, it is highly possible that beyond the epidemic of over-diagnosis and over-treatment, mammograms are planting seeds of radiation-induced cancer within the breasts of millions of women.***
With the advent of non-ionizing radiation based diagnostic technologies, such as thermography, it has become vitally important that patients educate themselves about the alternatives to x-ray mammography that already exist. Until then, we must use our good sense – and research like this – to inform our decisions, and as far as the unintended adverse effects of radiation go, erring on the side of caution whenever possible.
*This discrepancy in radiation risk models/estimates follows from two fundamental problems: 1) the older risk model was based on higher-energy radiation emissions, such as are given off from atomic bomb blasts 2) it was a crude model, developed before the discovery of DNA and a full understanding of radiotoxicity/genotoxicity.
** Keep in mind that the Cochrane Database Review is at the top of the “food chain” of truth, in the highly touted “evidence-based model” of conventional medicine. Cochrane Database Reviews are produced by The Cochrane Collaboration, which is internationally recognized as the benchmark for high quality, evidence-based information concerning the effectiveness (or lack thereof) of common health care interventions. The organization, comprised of over 28,000 dedicated people from over 100 countries, prides itself on being an “independent” source of information, and historically has not been afraid to point out the corrupting influence of industry, which increasingly co-opts the biomedical research and publishing fields.
***The low-energy wavelengths cause double strand breaks within the DNA of susceptible cells, which the cell can not repair. Through time these mutations result in “neoplastic transformation”; radiation has the ability to induce a cancerous phenotype within formerly healthy cells that has cancer stem cell-like (CSC) properties.
Sayer Ji is founder of Greenmedinfo.com, a reviewer at the International Journal of Human Nutrition and Functional Medicine, Co-founder and CEO of Systome Biomed, Vice Chairman of the Board of the National Health Federation, Steering Committee Member of the Global Non-GMO Foundation.
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