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Study Outlines Why Antidepressant Drugs Could Be Completely Useless & Harmful

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Antidepressants are supposed to work by fixing a chemical imbalance, specifically, a lack of serotonin in the brain. Indeed, their supposed effectiveness is the primary evidence for the chemical imbalance theory. But analyses of the published data and the unpublished data that were hidden by drug companies reveals that most (if not all) of the benefits are due to the placebo effect. Some antidepressants increase serotonin levels, some decrease it, and some have no effect at all on serotonin. Nevertheless, they all show the same therapeutic benefit. Even the small statistical difference between antidepressants and placebos may be an enhanced placebo effect, due to the fact that most patients and doctors in clinical trials successfully break blind. The serotonin theory is as close as any theory in the history of science to having been proved wrong. Instead of curing depression, popular antidepressants may induce a biological vulnerability making people more likely to become depressed in the future.

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Irving Kirsch offered the above information in a publication obtained from the US National Library of Medicine. He is the Associate Director of the Program in Placebo Studies and a Lecturer in Medicine at Harvard Medical School. He is also Professor Emeritus of Psychology at the Universities of Hull and Plymouth in the United Kingdom, and a few others in the United States.  Needless to say, he’s done a lot of research, and his revelations above should be read by anybody taking, or considering taking, antidepressant drugs.

The Effectiveness of Anti-Depressant Drugs Compared To Placebo

In a 2002 study conducted by Kirsch and his team of researchers, published in The American Psychological Association’s Prevention & Treatment, it was discovered that 80 percent of the effect of antidepressants, as measured in clinical trials, could be attributed to the placebo effect. The difference between the response of the drugs and the response of the placebo was less than two points on average on a clinical scale that goes from fifty to sixty points. This is a very small difference, and is, according Kirsch, clinically meaningless:

I assumed that antidepressants were effective. As a psychotherapist, I sometimes referred my severely depressed clients for prescriptions of antidepressant drugs. Sometimes the condition of my clients improved when they began taking antidepressants; sometimes it did not. When it did, I assumed it was the effect of the drug that was making them better. Given my long standing interest in the placebo effect, I should have known better, but back then I did not.

Analyzing the data we had found, we were not surprised to find a substantial placebo effect on depression. What surprised us was how small the drug effect was. Seventy-five percent of the improvement in the drug group also occurred when people were give dummy pills with no active ingredient in them.  (source)

The response from critics was harsh, who emphasized that antidepressants have been evaluated in many trials and their effectiveness well documented.

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“Unpublished Data That That Were Hidden By Drug Companies”

The idea that scientific literature has firmly established the benefits of antidepressants has lost all credibility, thanks in large part to Kirsch and his team. They used the Freedom of Information Act to request that the Food and Drug  Administration (FDA) send data that pharmaceutical companies had sent to it for the process of obtaining approval for multiple antidepressants, which accounted for the bulk of antidepressant prescriptions at the time.  As a result, the researchers were able to obtain data on both published and unpublished trials:

 This turned out to be very important. Almost half of the clinical trials sponsored by the drug companies have not been published (Melander, Ahlqvist-Rastad, Meijer, & Beermann, 2003Turner, Matthews, Linardatos, Tell, & Rosenthal, 2008). The results of the unpublished trials were known only to the drug companies and the FDA, and most of them failed to find a significant benefit of drug over placebo. . . .  [T]he data in the FDA files were the basis upon which the medications were approved. In that sense they have a privileged status. If there is anything wrong with those trials, the medications should not have been approved in the first place. (source)

All in all, the data sent to the researchers by the FDA showed that only 43% of the trials showed a statistically significant  benefit of drug over placebo. The remaining 57% were failed or negative trials.

Many other studies have also demonstrated just how ineffective antidepressants are, as well as how often that fact is obscured by pharmaceutical companies. What’s worse, studies have since determined that anti-depressants can cause real harm to those who take them, and this information is often withheld, too. For example, a study published in The British Medical Journal by researchers at the Nordic Cochrane Center in Copenhagen revealed that pharmaceutical companies were not disclosing all information regarding the results of their drug trials. Researchers looked at documents from 70 different double-blind, placebo-controlled trials of selective serotonin reuptake inhibitors (SSRI) and serotonin and norepinephrine reuptake inhibitors (SNRI) and found that the full extent of serious harm in clinical study reports went unreported. These are the reports sent to major health authorities like the U.S. Food and Drug Administration.

Tamang Sharma, a PhD student at Cochrane and Lead Author of the study, noted that they “found that a lot of the appendices were often only available upon request to the authorities, and the authorities had never requested them,” revealing that she was “actually kind of scared about how bad the actual situation would be if [they] had the complete data.”

Joanna Moncrieff, a psychiatrist and researcher at University College London, elaborates:

[This study] confirms that the full degree of harm of antidepressants is not reported. They are not reported in the published literature, we know that – and it appears that they are not properly reported in clinical study reports that go to the regulators and from the basis of decisions about licensing.

This is precisely why, as I have mentioned many times in previous articles, Dr. Richard Horton, the current Editor-In-Chief of one of the most reputable peer-reviewed medical journals in the world, boldly described most published scientific literature as untrue. (source)

Marcia Angell, a physician who spent two decades as the Editor-In-Chief of The New England Journal of Medicine, puts it equally as bluntly:

It is simply no longer possible to believe much o the clinical research that is published, or to rely on the judgement of trusted physicians or authoritative medical guidelines. I take no pleasure in this conclusion, which I reached slowly and reluctantly over my two decades as an editor of The New England Journal of Medicine. (source)

Unfortunately, it’s not just antidepressants. A few years ago, Lucia Tomljenovic, a PhD in biochemistry and a senior postdoctoral fellow in UBC’s Faculty of Medicine, uncovered documents that reveal vaccine manufacturers, pharmaceutical companies, and health authorities have known about multiple dangers associated with vaccines but chose to withhold them from the public. The documents were obtained from the UK Department of Health (DH) and the Joint Committee on Vaccination and Immunization (JCVI), who advise the Secretaries of State for Health in the UK about diseases preventable through immunizations. The JCVI made “continuous efforts to withhold critical data on severe adverse reactions and contraindications to vaccinations to both parents and health practitioners in order to reach overall vaccination rates.” (source)

Now, vaccines are a completely different topic, but the point to be made here is that pharmaceutical companies withhold critical data from physicians, researchers, and the general public. They are motivated by profit, and when pitted against consumer safety, profit always wins.

“The Serotonin Theory is as Close as Any Theory in the History of Science to Having Been Proved Wrong.”

I have written about this many times before, and it’s only fitting that I do so now as well. Is the chemical imbalance theory of depression really true, or is it just a tool used to push more drugs onto the market? After all, antidepressant drugs are the most commonly prescribed drugs in North America. Pharmaceutical companies are bringing in billions of dollars every single year from the sale of antidepressant drugs alone, and they also spend billions of dollars marketing and advertising their products.

Joseph Coyle, a neuroscientist from Harvard Medical School, sums it up best, writing that “chemical imbalance is sort of last-century thinking. It’s much more complicated than that.” And it’s true; depression is much more complicated than that, at least compared to the commonly accepted belief that depression results from a chemical imbalance in the brain. This idea was posed in the late 1950s and has since taken hold in everyone’s minds. It’s the general idea that a deficiency of select neurotransmitters exists (chemical messengers) at critical points, like synapses. One of these neurotransmitters, for example, is serotonin; others include norepinephrine and dopamine.

As Scientific American reports, “much of the general public seems to have accepted the chemical imbalance hypothesis uncritically,” and that “it is very likely that depression stems from influences other than neurotransmitter abnormalities.” (source)

Harvard Medical School put out a press release a few years ago stating that it’s “often said that depression results from a chemical imbalance, but that figure of speech doesn’t capture how complex the disease is.”  (source)

Of course, there are brain events and biochemical reactions occurring when someone feels depressed, as there are all the time, but no research has ever established that a particular brain state causes, or even correlates with, depression. . . . In all cases studies yield inconsistent results, and none have been shown to be specific to depression, let alone causal. 

The fact that more than 50 years of intense research efforts have failed to identify depression in the brain may indicate that we simply lack the right technology, or it may suggest we have been barking up the wrong tree!

Dr. Joanna Moncrieff,  British Psychiatrist, Author (source)

The most commonly cited evidence to support the chemical imbalance theory is simply that some drugs have been shown to increase and decrease mood in human and animal models, and yes — many antidepressants increase the amounts of serotonin and other neurotransmitters at synapses, but what we fail to realize today is, just because mood can be artificially manipulated with drugs, does not mean the chemical imbalance theory is true. Just because these antidepressants do increase and decrease certain chemical levels in the brain does not prove the chemical imbalance theory of depression.

We simply can’t currently determine if a human being has a chemical imbalance (to whatever extent) or say what neurotransmitters are involved, which is why the chemical imbalance theory of depression remains a theory. It’s not like chemical levels in the brain can accurately be measured or ‘looked at,’ either.

Yet much of the general public still accepts the chemical imbalance theory. Indeed, a survey conducted in 2007 of 262 undergraduates at Cleveland State University found that more than 80 percent of the participants found it “likely” that chemical imbalances cause depression.

“At best, drug-induced affective disturbances can only be considered models for natural disorders, while it remains to be demonstrated that the behavioral changes produced by these drugs have any relation to naturally occurring biochemical abnormalities which might be associated with the illness.” (source)

Keep in mind, as Harvard Medical School points out, there are probably many chemicals involved, working both inside and outside of our nerve cells: “There are millions, even billions, of chemical reactions that make up the dynamic system that is responsible for your mood, perceptions, and how you experience life.”

“The cause of mental disorders such as depression remains unknown. However, the idea that neurotransmitter imbalances cause depression is vigorously promoted by pharmaceutical companies and the psychiatric profession at large.” (source)

Again, theories like the low serotonin one came into existence because scientists were able to observe the effects of drugs on the brain. It was a hypothesis that attempted to explain how drugs could be fixing something, yet whether or not depressed people actually had lower serotonin levels actually remains to be proven. You can read more about the science here.

“The serotonin theory is simply not a scientific statement. It’s a botched theory – a hypothesis that was proven incorrect.” – Dr. Joseph Mercola (source)

Not only is there no solid scientific proof to back up the chemical imbalance theory, many depressed people are not even helped by taking antidepressants like SSRIs. For example, a review done by the University of California in 2009 found that one third of people treated with antidepressants do not improve, and a significant portion of these people remain depressed. As Scientific American observes, “if antidepressants correct a chemical imbalance that underlies depression, all or most depressed people should get better after taking them.”

Depression has one focus, brain chemistry, even though it is a multifaceted issue involving many concerns and many chemicals. Focusing on this one chemical imbalance theory, and then dishing out drugs that actually alter brain chemistry, is shortsighted and dangerous.

“In spite of the enormous amount of money and time that has been spent on the quest to confirm the chemical imbalance theory, direct proof has never materialized.”  (source)

The irony of this situation is hopefully not lost on everyone. The only imbalances we know for sure to exist in the brains of ‘mentally ill’ people are the ones inflicted on them by psychiatric drugs. We are making a false claim that they have biochemical imbalances and then actually giving them biochemical imbalances based on that claim.

For some natural ways to combat depression. You can read THIS article. 

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Awareness

Tylenol Damages The Brains of Children, Research Reveals

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In Brief

  • 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?

Original Article Link

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.

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(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.\

Read their related article on Tylenol: 

Tylenol Kills Emotions As Well As Pain, Study Reveals

Sign Up For The Greenmedinfo Newsletter HERE.


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.

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Awareness

Vaccine Mandates Results Don’t Safeguard Children’s Rights or Health: How Did We Get Here?

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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:

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  • 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.


Sign up for free news and updates from Robert F. Kennedy, Jr. and the Children’s Health Defense. CHD is planning many strategies, including legal, in an effort to defend the health of our children and obtain justice for those already injured. Your support is essential to CHD’s successful mission.


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Awareness

How X-Ray Mammography Is Accelerating The Epidemic of Cancer

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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.[1]

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.

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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.[2]

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.[3]

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.

Additional Reading

Is X-ray Mammography Findings Cancer or Benign Lesions?

The Dark Side of Breast Cancer Awareness Month

Does Chemo & Radiation Actually Make Cancer More Malignant?


*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.


[1] Enhanced biological effectiveness of low energy X-rays and implications for the UK breast screening programme. Br J Radiol. 2006 Mar ;79(939):195-200. PMID: 16498030

[2] Screening for breast cancer with mammography. Cochrane Database Syst Rev. 2009(4):CD001877. Epub 2009 Oct 7. PMID: 19821284

[3] Possible net harms of breast cancer screening: updated modelling of Forrest report. BMJ. 2011 ;343:d7627. Epub 2011 Dec 8. PMID: 22155336


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.

If you want to learn more from Greenmedinfo, sign up for their newsletter here

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