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Is Tylenol Damaging Your Child’s Brain?

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This article was written by William Parker,  an Associate Professor at Duke University, where he has worked in the Department of Surgery since 1993. It was printed here with the permission of Greenmedinfo.com. You can sign up for their newsletter here.

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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/behavioural 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.”

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Awareness

22 Out Of 25 Popular Burger Chains Just Failed Their Antibiotic Use Report

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In Brief

  • The Facts:

    A recent study was done examining how well top fast food chains actually implemented their antibiotic use policies in their beef. 22 of 25 failed including McDonald's, Sonic, Burger King and In-N-Out.

  • Reflect On:

    Do you still eat fast food? If so, why do you find yourself doing so? What healthier choices can be made instead? If we want to see a healthier world, population and animal kingdom, we have to choose what we support more wisely.

The modern-day food industry seems to pay no attention to health. Thankfully, global consciousness is shifting in several ways including how we live as humans, view our health, our economy, education, politics, and the environment. You could say that humanity is going through one MASSIVE change.

Today, billions of animals in the United States alone are raised, tortured, and slaughtered for human consumption. This reckless production and consumption, in turn, has created enormous environmental and health problems that continue to accelerate. That being said, awareness on this issue (food) in particular, has come along way. We are seeing changes in the food guide, a shift towards plant-based diets, and more corporations catering to new choices people are making around food and health. This is a good thing!

One common trend helping to create change is the continues ‘bad press’ unhealthy players in the food industry are getting.

The latest news to come out regarding food quality within fast food comes from a report recently released by six major consumer and environmental groups. They graded America’s 25 largest burger chains and their use of antibiotics in their beef supply.

22 popular fast food restaurants completely failed, including giants like McDonald’s, Burger King, Sonic and In-N-Out.  The evaluation looked at each chain’s antibiotic use policies and whether these policies were truly implemented in their product. They also examined how transparent the chains were with their antibiotic use.

The Problem With Antibiotic Use

Antibiotics given to farm animals can lead to antibiotic-resistant bacteria, among other things. This is actually one of the top threats to global public health, which is exemplified by the fact that each year, more than 2 million Americans alone suffer from these infections.

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In September 1999, Albrecht and Schutte published “Homeopathy Versus Antibiotics in Metaphylaxis of Infectious Diseases: A Clinical Study in Pig Fattening and Its Significance to Consumers” in Alternative Therapies. The study compared outcomes for four randomly assigned groups of pigs that were given placebo, homeopathic treatment, a standard blend of antibiotics and other conventional drugs in a routine low prophylactic dose, or conventional drugs in a high therapeutic dose.

There were 1440 pigs involved in the study, which took place at an intensive livestock farm in Germany. The primary outcome measured was the incidence of respiratory disease, a common problem for pigs on such farms.

The results were astounding.

Homeopathic treatment was far superior to prophylactic doses of antibiotics in preventing respiratory disease. The prophylactic antibiotic treatment made it only 11 percent less likely (than placebo) that the pigs would become sick. But homeopathic remedies made it 40 percent less likely. When the antibiotics were raised to therapeutic levels, meaning a level that is only given when people or an animal was sick, it became 70 percent less likely that the pigs would become diseased.

The significance of this is that homeopathic treatment on animals would already be better than routine antibiotic treatment. When an animal is actually sick, the farmer would then have the choice to increase homeopathic or use a legitimately high-level dose of antibiotics. This, significantly less cost and significantly fewer antibiotics in meat.

The List

The Takeaway

Simple, avoid fast food. There are many out there who seem to believe that people will always consume this food, but we fail to recognize that it’s not just our choice. The “food” these corporations offer is highly addictive to people, and that’s done on purpose.

If we can connect with caring about our health, quality of life and well-being of animals and the planet, these are places you must steer away from. In general, eating meat does not support the health and wellbeing of us nor animals, but this is a choice we each make.

Recommended Articles

A Native American Perspective On Veganism

Plant-Based Protein VS. Protein From Meat: Which One Is Better For You? 

Doctor Explains How Humans Have A “Strict” Vegan Physiology

Vegan Activist James Aspey Beautifully Shows How To Consciously Inform People

9 Things That Happen When You Stop Eating Meat

Internal Medicine Physician Shares What Happens To Your Body When You Stop Eating Meat

Animals – Why Do We Love One But Eat The Other? 

The Heart Disease Rates of Meat-Eaters Versus Vegetarians & Vegans

Were Those Who Roamed The Earth Before US Nearly All Vegetarian?

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The demand for Collective Evolution's content is bigger than ever, except ad agencies and social media keep cutting our revenues. This is making it hard for us to continue.

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Awareness

Epigenetic Memories Are Passed Down 14 Successive Generations, Game-Changing Research Reveals

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In Brief

  • The Facts:

    It's amazing how much information can be passed on to our offspring. Scientist have discovered that our DNA has memories, and these can also be passed down. We are talking about thoughts, feelings, emotions and perceptions.

  • Reflect On:

    Biological changes are shaped by our environment, as well as our thoughts, feelings, emotions and reaction to that environment. Our DNA can be changed with belief, the placebo is a great example. Thoughts feelings and emotions are huge in biology.

This article was written by the Greenmedinfo research group, from Greenmedinfo.com. Posted here with permission.

Until recently, it was believed that our genes dictate our destiny. That we are slated for the diseases that will ultimately beset us based upon the pre-wired indecipherable code written in stone in our genetic material. The burgeoning field of epigenetics, however, is overturning these tenets, and ushering in a school of thought where nurture, not nature, is seen to be the predominant influence when it comes to genetic expression and our freedom from or affliction by chronic disease.

Epigenetics: The Demise of Biological Determinism

Epigenetics, or the study of the physiological mechanisms that silence or activate genes, encompasses processes which alter gene function without changing the sequence of nucleotide base pairs in our DNA. Translated literally to mean “in addition to changes in genetic sequence,” epigenetics includes processes such as methylation, acetylation, phosphorylation, sumolyation, and ubiquitylation which can be transmitted to daughter cells upon cell division (1). Methylation, for example, is the attachment of simple methyl group tags to DNA molecules, which can repress transcription of a gene when it occurs in the region of a gene promoter. This simple methyl group, or a carbon bound to three hydrogen molecules, effectively turns the gene off.

Post-translational modifications of histone proteins is another epigenetic process. Histones help to package and condense the DNA double helix into the cell nucleus in a complex called chromatin, which can be modified by enzymes, acetyl groups, and forms of RNA called small interfering RNAs and microRNAs (1). These chemical modifications of chromatin influence its three-dimensional structure, which in turn governs its accessibility for DNA transcription and dictates whether genes are expressed or not.

We inherit one allele, or variant, of each gene from our mother and the other from our father. If the result of epigenetic processes is imprinting, a phenomenon where one of the two alleles of a gene pair is turned off, this can generate a deleterious health outcome if the expressed allele is defective or increases our susceptibility to infections or toxicants (1). Studies link cancers of nearly all types, neurobehavioral and cognitive dysfunction, respiratory illnessesautoimmune disorders, reproductive anomalies, and cardiovascular disease to epigenetic mechanisms (1). For example, the cardiac antiarrhythmic drug procainamide and the antihypertensive agent hydralazine can cause lupus in some people by causing aberrant patterns of DNA methylation and disrupting signalling pathways (1).

Genes Load the Gun, Environment Pulls the Trigger

Pharmaceuticals, however, are not the only agents that can induce epigenetic disturbances. Whether you were born via vaginal birth or Cesarean section, breastfed or bottle-fed, raised with a pet in the house, or infected with certain childhood illnesses all influence your epigenetic expression. Whether you are sedentary, pray, smoke, mediate, do yoga, have an extensive network of social support or are alienated from your community—all of your lifestyle choices play into your risk for disease operating through mechanisms of epigenetics.

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In fact, the Centers for Disease Control (CDC) states that genetics account for only 10% of disease, with the remaining 90% owing to environmental variables (2). An article published in the Public Library of Science One (PLoS One) entitled “Genetic factors are not the major causes of chronic diseases” echoes these claims, citing that chronic disease is only 16.4% genetic, and 84.6% environmental (3). These concepts make sense in light of research on the exposome, the cumulative measure of all the environmental insults an individual incurs during their life course that determines susceptibility to disease (4)

In delineating the totality of exposures to which an individual is subjected over their lifetime, the exposome can be subdivided into three overlapping and intertwined domains. One segment of the exposome called the internal environment is comprised of processes innate to the body which impinge on the cellular milieu. This encompasses hormones and other cellular messengers, oxidative stress, inflammation, lipid peroxidation, bodily morphology, the gut microbiotaaging and biochemical stress (5).

Another portion of the exposome, the specific external environment, consists of exposures including pathogens, radiation, chemical contaminants and pollutants, and medical interventions, as well as dietary, lifestyle, and occupational elements (5). At an even broader sociocultural and ecological level is the segment of the exposome called the general external environment, which may circumscribe factors such as psychological stress, socioeconomic status, geopolitical variables, educational attainment, urban or rural residence, and climate (5).

Transgenerational Inheritance of Epigenetic Change: Endocrine Disruptors Trigger Infertility in Future Generations

Scientists formerly speculated that epigenetic changes disappear with each new generation during gametogenesis, the formation of sperm and ovum, and after fertilization. However, this theory was first challenged by research published in the journal Science which demonstrated that transient exposure of pregnant rats to the insecticide methoxychlor, an estrogenic compound, or the fungicide vinclozolin, an antiandrogenic compound, resulted in increased incidence of male infertility and decreased sperm production and viability in 90% of the males of four subsequent generations that were tracked (1).

Most notably, these reproductive effects were associated with derangements in DNA methylation patterns in the germ line, suggesting that epigenetic changes are passed on to future generations. The authors concluded, “The ability of an environmental factor (for example, endocrine disruptor) to reprogram the germ line and to promote a transgenerational disease state has significant implications for evolutionary biology and disease etiology” (6, p. 1466). This may suggest that the endocrine-disrupting, fragrance-laden personal care products and commercial cleaning supplies to which we are all exposed may trigger fertility problems in multiple future generations.

Transgenerational Inheritance of Traumatic Episodes: Parental Experience Shapes Traits of Offspring

In addition, traumatic experiences may be transmitted to future generations via epigenetics as a way to inform progeny about salient information needed for their survival (7). In one study, researchers wafted the cherry-like chemical acetophenone into the chambers of mice while administering electric shocks, conditioning the mice to fear the scent (7). This reaction was passed onto two successive generations, which shuddered significantly more in the presence of acetophenone despite never having encountered it compared to descendants of mice that had not received this conditioning (7).

The study suggests that certain characteristics of the parental sensory environment experienced before conception can remodel the sensory nervous system and neuroanatomy in subsequently conceived generations (7). Alterations in brain structures that process olfactory stimuli were observed, as well as enhanced representation of the receptor that perceives the odor compared to control mice and their progeny (7). These changes were conveyed by epigenetic mechanisms, as illustrated by evidence that the acetophenone-sensing genes in fearful mice were hypomethylated, which may have enhanced expression of odorant-receptor genes during development leading to acetophenone sensitivity (7).

The Human Experience of Famine and Tragedy Spans Generations

The mouse study, which illustrates how germ cells (egg and sperm) exhibit dynamic plasticity and adaptability in response to environmental signals, is mirrored by human studies. For instance, exposures to certain stressors such as starvation during the gestational period are associated with poor health outcomes for offspring. Women who undergo famine before conception of her offspring have been demonstrated to give birth to children with lower self-reported mental health and quality of life, for example (8).

Studies similarly highlight that, “Maternal famine exposure around the time of conception has been related to prevalence of major affective disorders, antisocial personality disorders, schizophrenia, decreased intracranial volume, and congenital abnormalities of the central nervous system” (8). Gestational exposure to the Dutch Famine of the mid-twentieth century is also associated with lower perceived health (9), as well as enhanced incidence of cardiovascular disease, hypertension, and obesity in offspring (8). Maternal undernourishment during pregnancy leads to neonatal adiposity, which is a predictor of future obesity (10), in the grandchildren (11).

The impact of epigenetics is also exemplified by research on the intergenerational effects of trauma, which illuminates that descendants of people who survived the Holocaust exhibit abnormal stresshormone profiles, and low cortisol production in particular (12). Because of their impaired cortisol response and altered stress reactivity, children of Holocaust survivors are often at enhanced risk for post-traumatic stress disorder (PTSD), anxiety, and depression (13).

Intrauterine exposure to maternal stress in the form of intimate partner violence during pregnancy can also lead to changes in the methylation status of the glucocorticoid receptor (GR) of their adolescent offspring (14). These studies suggest that an individual’s experience of trauma can predispose their descendants to mental illness, behavioral problems, and psychological abnormalities due to “transgenerational epigenetic programming of genes operating in the hypothalamic-pituitary-adrenal axis,” a complex set of interactions among endocrine glands which determine stress response and resilience (14).

Body Cells Pass Genetic Information Directly Into Sperm Cells

Not only that, but studies are illuminating that genetic information can be transferred through the germ line cells of a species in real time. These paradigm-shifting findings overturn conventional logic which postulates that genetic change occurs over the protracted time scale of hundreds of thousands or even millions of years. In a relatively recent study, exosomes were found to be the medium through which information was transferred from somatic cells to gametes.

This experiment entailed xenotransplantation, a process where living cells from one species are grafted into a recipient of another species. Specifically, human melanoma tumor cells genetically engineered to express genes for a fluorescent tracer enzyme called EGFP-encoding plasmid were transplanted into mice. The experimenters found that information-containing molecules containing the EGFP tracer were released into the animals’ blood (15). Exosomes, or “specialized membranous nano-sized vesicles derived from endocytic compartments that are released by many cell types” were found among the EGFP trackable molecules (16, p. 447).

Exosomes, which are synthesized by all plant and animal cells, contain distinct protein repertoires and are created when inward budding occurs from the membrane of multivesicular bodies (MVBs), a type of organelle that serves as a membrane-bound sorting compartment within eukaryotic cells (16). Exosomes contain microRNA (miRNA) and small RNA, types of non-coding RNA involved in regulating gene expression (16). In this study, exosomes delivered RNAs to mature sperm cells (spermatozoa) and remained stored there (15).

The researchers highlight that this kind of RNA can behave as a “transgenerational determinant of inheritable epigenetic variations and that spermatozoal RNA can carry and deliver information that cause phenotypic variations in the progeny” (15). In other words, the RNA carried to sperm cells by exosomes can preside over gene expression in a way that changes the observable traits and disease risk of the offspring as well as its morphology, development, and physiology.

This study was the first to elucidate RNA-mediated transfer of information from somatic to germ cells, which fundamentally overturns what is known as the Weisman barrier, a principle which states that the movement of hereditary information from genes to body cells is unidirectional, and that the information transmitted by egg and sperm to future generations remains independent of somatic cells and parental experience (15).

Further, this may bear implications for cancer risk, as exosomes contain vast amounts of genetic information which can be source of lateral gene transfer (17) and are abundantly liberated from tumor cells (18). This can be reconciled with the fact that exosome-resembling vesicles have been observed in various mammals (15), including humans, in close proximity to sperm in anatomical structures such as the epididymis as well as in seminal fluid (19). These exosomes may thereafter be propagated to future generations with fertilization and augment cancer risk in the offspring (20).

The researchers concluded that sperm cells can act as the final repositories of somatic cell-derived information, which suggests that epigenetic insults to our body cells can be relayed to future generations. This notion is confirmatory of the evolutionary theory of “soft inheritance” proposed by French naturalist Jean-Baptiste Lamarck, whereby characteristics acquired over the life of an organism are transmitted to offspring, a concept which modern genetics previously rejected before the epigenetics arrived on the scene. In this way, the sperm are able to spontaneously assimilate exogenous DNA and RNA molecules, behaving both as vector of their native genome and of extrachromosomal foreign genetic material which is “then delivered to oocytes at fertilization with the ensuing generation of phenotypically modified animals” (15).

Epigenetic Changes Endure Longer Than Ever Predicted

In a recent study, nematode worms were manipulated to harbor a transgene for a fluorescent protein, which made the worms glow under ultraviolet light when the gene was activated (21). When the worms were incubated under the ambient temperature of 20° Celsius (68° Fahrenheit), negligible glowing was observed, indicating low activity of the transgene (21). However, transferring the worms to a warmer climate of 25°C (77° F) stimulated expression of the gene, as the worms glowed brightly (21).

In addition, this temperature-induced alteration in gene expression was found to persist for at least 14 generations, representing the preservation of epigenetic memories of environmental change across an unprecedented number of generations (21). In other words, the worms transmitted memories of past environmental conditions to their descendants, through the vehicle of epigenetic change, as a way to prepare their offspring for prevailing environmental conditions and ensure their survivability.

Future Directions: Where Do We Go From Here?

Taken cumulatively, the aforementioned research challenges traditional Mendelian laws of genetics, which postulate that genetic inheritance occurs exclusively through sexual reproduction and that traits are passed to offspring through the chromosomes contained in germ line cells, and never through somatic (bodily) cells. Effectively, this proves the existence of non-Mendelian transgenerational inheritance, where traits separate from chromosomal genes are transmitted to progeny, resulting in persistent phenotypes that endure across generations (22).

This research imparts new meaning to the principle of seven generation stewardship taught by Native Americans, which mandates that we consider the welfare of seven generations to come in each of our decisions. Not only should we embody this approach in practices of environmental sustainability, but we would be wise to consider how the conditions to which we subject our bodies—the pollution and toxicants which permeate the landscape and pervade our bodies, the nutrient-devoid soil that engenders micronutrient-poor food, the disruptions to our circadian rhythm due to the ubiquity of electronic devices, our divorce from nature and the demise of our tribal affiliations—may translate into ill health effects and diminished quality of life for a previously unfathomed number of subsequent generations.

Hazards of modern agriculture, the industrial revolution, and contemporary living are the “known or suspected drivers behind epigenetic processes…including heavy metals, pesticides, diesel exhaust, tobacco smoke, polycyclic aromatic hydrocarbons, hormones, radioactivity, viruses, bacteria, and basic nutrients” (1, p. A160). Serendipitously, however, many inputs such as exercise, mindfulness, and bioactive components in fruits and vegetables such as sulforaphane in cruciferous vegetables, resveratrol from red grapes, genistein from soy, diallyl sulphide from garlic, curcumin from turmeric, betaine from beets, and green tea catechin can favorably modify epigenetic phenomena “either by directly inhibiting enzymes that catalyze DNA methylation or histone modifications, or by altering the availability of substrates necessary for those enzymatic reactions” (23, p. 8).

This quintessentially underscores that the air we breathe, the food we eat, the thoughts we allow, the toxins to which we are exposed, and the experiences we undergo may persevere in our descendants and remain in our progeny long after we are gone. We must be cognizant of the effects of our actions, as they elicit a ripple effect through the proverbial sands of time.

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References

1. Weinhold, B. (2006). Epigenetics: The Science of Change. Environmental Health Perspectives, 114(3), A160-A167.

2. Centers for Disease Control and Prevention. (2014). Exposome and Exposomics. Retrieved from https://www.cdc.gov/niosh/topics/exposome/

3. Rappaport, S.M. (2016). Genetic factors are not the major causes of chronic diseases. PLoS One, 11(4), e0154387.

4. Vrijheid, M. (2014). The exposome: a new paradigm to study the impact of environment on health. Thorax, 69(9), 876-878. doi: 10.1136/thoraxjnl-2013-204949.

5. Wild, C.P. (2012). The exposome: from concept to utility. International Journal of Epidemiology, 41, 24–32. doi:10.1093/ije/dyr236

6. Anway, M.D. et al. (2005). Epigenetic transgenerational actions of endocrine disruptors and male fertility. Science, 308(5727), 1466-1469.

7. Dias, B.G., & Ressler, K.J. (2014). Parental olfactory experience influences behavior and neural structure in subsequent generations. Nature Neuroscience, 17(1), 89-98.

8. Stein, A.D. et al. (2009). Maternal exposure to the Dutch Famine before conception and during pregnancy: quality of life and depressive symptoms in adult offspring. Epidemiology, 20(6), doi:  10.1097/EDE.0b013e3181b5f227.

9. Roseboom, T.J. et al. (2003). Perceived health of adults after prenatal exposure to the Dutch famine. Paediatrics Perinatal Epidemiology, 17, 391–397.

10. Badon, S.E. et al. (2014). Gestational Weight Gain and Neonatal Adiposity in the Hyperglycemia and Adverse Pregnancy Outcome Study-North American Region. Obesity (Silver Spring), 22(7), 1731–1738.

11. Veenendaal, M.V. et al. (2013). Transgenerational effects of prenatal exposure to the 1944-45 Dutch famine. BJOG, 120(5), 548-53. doi: 10.1111/1471-0528.

12. Yehuda, R., & Bierer, L.M. (2008). Transgenerational transmission of cortisol and PTSD risk. Progress in Brain Research, 167, 121-135.

13. Aviad-Wilcheck, Y. et al. (2013). The effects of the survival characteristics of parent Holocaust survivors on offsprings’ anxiety and depression symptoms. The Israel Journal of Psychiatry and Related Sciences, 50(3), 210-216.

14. Radke, K.M. et al. (2011). Transgenerational impact of intimate partner violence on methylation in the promoter of the glucocorticoid receptor. Translational Psychiatry, 1, e21. doi: 10.1038/tp.2011.21.

15. Cossetti, C. et al. (2014). Soma-to-Germline Transmission of RNA in Mice Xenografted with Human Tumour Cells: Possible Transport by Exosomes. PLoS One, https://doi.org/10.1371/journal.pone.0101629.

16. Zomer, A. et al. (2010). Exosomes: Fit to deliver small RNA. Communicative and Integrative Biology, 3(5), 447–450.

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Brain Imaging Shows Autistic Brains Contain HIGH Amounts of Aluminum

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In Brief

  • The Facts:

    A study published early in 2018 identified very high amounts of aluminum lodged in the brains of multiple people with autism.

  • Reflect On:

    We know little about where the heavy metals used as adjuvants in vaccines end up in the body. We now know that injected aluminum doesn't exit the body like aluminum intake from other sources. When injected, it ends up in the brain.

A study published earlier in 2018 should have made headlines everywhere, as it discovered historically high amounts of aluminum in autistic brains. The study was conducted by some of the worlds leading scientists in the field.

Five people were used in the study, four males and one female, all between the ages of 14-50. Each of their brains contained unsafe and high amounts of aluminum compared to patients with other diseases where high brain aluminum content is common, like Alzheimer’s disease, for example.

Of course, this caused people to downplay the study, citing a low sample group, but that’s not entirely a valid argument given the reason why this study was conducted. As cited in the study above, recent studies on animals, published within the past few years, have supported a strong connection between aluminum, and aluminum adjuvants used in human vaccinations, and Autism Spectrum Disorder (ASD.)

Studies have also shown that injected aluminum does not exit the body, and can be detected inside the brain even a year after injection. That being said, when we take aluminum in from sources such as food, the body does a great job of getting it out, but there is a threshold. It’s important to acknowledge that the aluminum found in the brain, could be due to the presence of aluminum adjuvants in vaccines. This latest study also identified the location of aluminum in these tissues, and where they end up. This particular study was done on humans, which builds upon, and still supports, the findings of the animal studies.

This is also important because the majority of studies that previously examined human exposure to aluminum have only used hair, blood and urine samples. The study also makes a clear statement regarding vaccines, stating that “Paediatric vaccines that include an aluminum adjuvant are an indirect measure of infant exposure to aluminum and their burgeoning use has been directly correlated with increasing prevalence of ASD.”

 Aluminum, in this case, was found in all four lobes of the brain.

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The aluminum content of brain tissues from donors with a diagnosis of ASD was extremely high (Table 1). While there was significant inter-tissue, inter-lobe and inter-subject variability the mean aluminium content for each lobe across all 5 individuals was towards the higher end of all previous (historical) measurements of brain aluminium content, including iatrogenic disorders such as dialysisencephalopathy[13][15][16][17][18][19]. All 4 male donors had significantly higher concentrations of brain aluminum than the single female donor. We recorded some of the highest values for brain aluminum content ever measured in healthy or diseased tissues in these male ASD donors

We Know, And Have Known, Aluminum Is Not Safe, Yet We Ignore It

When we talk about the ‘safe’ amount of aluminum here, there is no such thing. Aluminum is extremely toxic to any biological process, it’s not meant for us which is why it stayed deep within the Earth until we took it out. It has no place within us, and that’s simply due to the fact that it causes nothing but havoc. This makes it odd that we would put them in vaccinations despite the fact that for 100 years there has been no appropriate safety testing.

Aluminum is an experimentally demonstrated neurotoxin and the most commonly used vaccine adjuvant. Despite almost 90 years of widespread use of aluminum adjuvants, medical science’s understanding about their mechanisms of action is still remarkably poor. There is also a concerning scarcity of data on toxicology and pharmacokinetics of these compounds. In spite of this, the notion that aluminum in vaccines is safe appears to be widely accepted. Experimental research, however, clearly shows that aluminum adjuvants have a potential to induce serious immunological disorders in humans.

The quote above comes from a study published in 2011, it’s 2018 now and we’ve come along way in our understanding. We are starting to see even more research confirming the statement above.

Almost every study you read regarding previous studies on aluminum adjuvants within vaccines emphasized how the nature of its bioaccumulation is unknown, and a serious matter. We now know that it goes throughout the body, into distant organs eventually ends up in the brain.

Another fairly recent study from 2015 points out:

Evidence that aluminum-coated particles phagocytozed in the injected muscle and its draining lymph notes can disseminate within phagocytes throughout the body and slowly accumulate in the brain further suggests that alum safety should be evaluated in the long term.(source)

The pictures below come from the recent 2018 study and show ‘bright spots’ that indicate heavy metals in the brain.

 

The more recent study discussed in this article is adding to that evidence. Below you can watch one of the most recent interviews with Dr. Eric Exly, one of the world’s foremost leading authors on the subject, and one of the authors of this most recent study. He is a Biologist (University of Stirling) with a Ph.D. in the ecotoxicology of aluminum. You can read more about his background here.

Take Away

People need to understand that despite media bullying, it’s ok to question vaccine safety, and there is plenty of reason to. There are many concerns, and heavy metals are one of them. In fact, the persistence and abundant presence of heavy metals in our environment, foods and medications is a concern, one that has been the clear cause for a variety of health ailments, yet it’s one that’s hardly addressed by the medical industry.

You can detox from this with items such as Spirulina, and waters that contain a high Silica content. There are studies that show various methods of detoxing can be used to get this lodged aluminum, or some of it, out of your body, organs and brain. This is where educating yourself regarding the medicinal value of food and nutrition is a key Perhaps this can be a motivation to better your diet, especially if you have, are someone, or know someone with an ASD diagnosis.

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