We are highly risk exposed to the world’s most widely used pesticide, glyphosate. We as a regulatory entity, an industry and a technology, fail to track glyphosate’s modalities, vectors and its actual EPA Part 180 Maximum Tolerance Limit compliance inside our food supply. This is called malfeasance in the business world, and bonus sive malum inside ethical skepticism. Otherwise known as criminal ignorance and pseudoscience.
Certainly yes, I am a skeptic. One of the first rules of ethical skepticism, after the tenets concerning conducting your own investigation and holding open an ‘allow-for’ disposition regarding multiple strong explanatory approaches, is to be skeptical of your own thoughts, and indeed, work. So yes, I am skeptical of the data I have produced below. But as an ethical skeptic I also have a problem in that I have never seen this data published, despite the critical importance of this issue inside social discourse on the rapid decline in American health and skyrocketing rates of auto-immune, allergy and microbiome related disorders since 1995. So I went and pulled the official sources and did the analysis myself. As a note, this is the reality I face in 90% of the instances regarding tough social issues inside which we find so many social skeptic ‘experts’ and so little actual data/research.
I would also not be maintaining integrity inside my own philosophical base, were I to not raise the warning flag of concern about what I see inside my data regarding glyphosate regulation and monitoring practices and risk vector pathways within the American food supply chain (see my chart below).
Raising a warning flag of plurality is an ethical skeptical action. It does not stand as a claim to final proof, neither is it an accusation of conspiracy, nor is it tantamount to credulousness/bias – nor any other of the red herring and strawman objection protocols employed by fake skeptics. It is simply a call for research, under the context of risk based necessity.
Now set aside the fact that the very foods in vector exposure V below are the very same ones which make me break out, gain weight, get painful intestinal disorders and become very sick. Set all that aside for whatever reason you choose: apophenia, placebo (just mistaking that I get sick), a priori confirmation bias, etc. I assure you that these are not contributors to my observation base in the least. But some of you use these things as methodical cynicism defense mechanisms, so I recognize that and allow for it. Be that as it may, yes let’s set this personal observation aside – and simply address the risk vector pathways incumbent inside the current practices involving application, regulation, tracking, and most importantly – weighted risk exposure, regarding glyphosate employment inside the United States food supply.
Set aside as well, the fact that the top two contribution vectors, Aspirated/Whole Grains and Corn Sweeteners, are the top two soaring allergy/sensitivity growth food commodities since 1995. Don’t let correlation move you to causality, we wouldn’t want that at all. Better to just ignore it instead. ‘Cuz that is being skeptical after all.
Below I have assembled a chart which is drawn from the following three resources on pesticide use, EPA Part 180 MTL tolerances and corresponding food consumption rates by commodity in the United States. I extracted the data on glyphosate and glyphosate bearing foods – and compared that to the rates of US consumption in pounds per capita, in the chart below. This took a good 8 hours of data assimilation and sorting in order to derive a picture which is not available to the American Public.
US Environmental Protection Agency Office of Pesticide Programs Index to Pesticide Chemical Names, Part 180 Tolerance Information, and Food and Feed Commodities (by Commodity) December 12, 2012¹
United States Department of Agriculture: Profiling Food Consumption in America, Chapter 2²
Food and Drug Administration: Pesticide Residues and Industrial Chemicals 2004 – 2005 sorted by Pesticide/Chemical³
Several alarms were raised inside this analysis. Not conclusions mind you – as I am always skeptical of my own work – rather, flags. Flags which not only indicate practice exposures inside the regulation, administration and monitoring of glyphosate in the US, but as well correlate highly with specific foods which are showing to produce health problems in the United States since glyphosate’s introduction to the food supply chain in starting in 1995. So without further ado, let’s outline these exposure pathways which emerge from the analysis in the chart below.
Vectors and Modalities for Glyphosate Entry and Risk Exposure in American Diets ¹ ² ³
I. Actual Pesticide Contents Are Not Measured nor MTL Tracked for Any Food
First, the most widely employed pesticide inside the American food supply is neither tracked for actual level compliance to EPA Part 180 MTL’s for ANY food at all, nor in many cases is even specified for Maximum Tolerance Limits on several critical foods which employ large scale use of glyphosate.¹ ³
II. Cheese, Butter & Dairy Contents are Highly Exposed and Neither Regulated nor MTL Tracked
Both the content of glyphosate inside these critical caloric contributors, as well as the fodder and feed contribution (100 – 400 ppm) to such foods is neither monitored for actual EPA Part 180 MTL compliance nor even specified for a Maximum Tolerance Limit.¹ ³
III. Dried Beans Contents are Highly Exposed and Neither Regulated nor MTL Tracked
Both the content of glyphosate inside these critical caloric contributors is neither monitored for actual EPA Part 180 MTL compliance nor even specified for a Maximum Tolerance Limit.¹ ³
IV. Animal Fats are Highly Exposed and Neither Regulated nor MTL Tracked
Both the content of glyphosate inside these critical caloric contributors, as well as the fodder and feed contribution (100 – 400 ppm) to such foods is neither monitored for actual EPA Part 180 MTL compliance nor even specified for a Maximum Tolerance Limit.¹ ³
V. High Risk/Content Exposed/Desiccated Foods Are Not MTL Tracked
The content of glyphosate inside these critical caloric contributors is not monitored for compliance to EPA Part 180 MTL’s at all.³
Set aside the increase in use (potentially attributable to desiccation practices – which has been recently claimed and disputed by several resources). No monitoring has been conducted to observe the prevalence, nor ppm impact of modalities and practices of any kind, including use of the Monsanto desiccation instruction. This is a risk exposure and a warning flag. You cannot make the claim that there is no problem, and attack people who bring up the issue, even if you are Snopes, if you have not conducted any actual research.†
VI. Feed and Forage Content Contribution is Neither Regulated nor Tracked
Both the content measures for glyphosate inside these critical caloric contributors to our meat supply (feed contribution 100 – 400 ppm) are neither monitored for actual EPA Part 180 MTL compliance nor are they even specified for a Maximum Tolerance Limit by modality contribution to our food.¹ ³
The bio-accumulation, given glyphosate’s persistence in soft tissue, is not modality measured and EPA Part 180 MTL tracked for bio-accumulation sensitive food derivatives such as Cheese, Cream, Butter, Milk, Dairy, Shortening and Animal Fat derivative products.
The Compiled Data From the Three Resources
List is complied from resource 1, matched to commodity measures from resource 2 (consumption lbs per capita indexed against MTL ppm ratios). Then sorted, highest to lowest in terms of contribution to overall amount in weight of glyphosate consumed (theoretical) in the per capita diet. !!! indicators show where risk exposure exists but is not Part 180 defined. Yellow commodity highlights indicate non-animal derived foods, while beige highlights indicate animal derived foods. Green highlights indicate animal feed and fodder commodities. Direct unknown risks rank first, quantified MTL risks second by theoretical per capita quantity of glyphosate exposure (lbs), while indirect (feed and fodder) risk ranks last in priority flagging. Resource 3 shows that none of these food commodity types are tracked for actual parts per million Part 180 MTL compliance and impact on the American diet.¹ ² ³ And here is why we need to be concerned about this:
Glyphosate, a synthetic amino acid and analogue of glycine, is the most widely used biocide on the planet. Its presence in food for human consumption and animal feed is ubiquitous. Epidemiological studies have revealed a strong correlation between the increasing incidence in the United States of a large number of chronic diseases and the increased use of glyphosate herbicide on corn, soy and wheat crops. Glyphosate, acting as a glycine analogue, may be mistakenly incorporated into peptides during protein synthesis. A deep search of the research literature has revealed a number of protein classes that depend on conserved glycine residues for proper function. Glycine, the smallest amino acid, has unique properties that support flexibility and the ability to anchor to the plasma membrane or the cytoskeleton. Glyphosate substitution for conserved glycines can easily explain a link with diabetes, obesity, asthma, chronic obstructive pulmonary disease (COPD), pulmonary edema, adrenal insufficiency, hypothyroidism, Alzheimer’s disease, amyotrophic lateral sclerosis (ALS), Parkinson’s disease, prion diseases, lupus, mitochondrial disease, non- Hodgkin’s lymphoma, neural tube defects, infertility, hypertension, glaucoma, osteoporosis, fatty liver disease and kidney failure. The correlation data together with the direct biological evidence make a compelling case for glyphosate action as a glycine analogue to account for much of glyphosate’s toxicity. Glufosinate, an analogue of glutamate, likely exhibits an analogous toxicity mechanism. There is an urgent need to find an effective and economical way to grow crops without the use of glyphosate and glufosinate as herbicides.
“Correlation does not prove causality.” You have heard the one-liner uttered by clueless social skeptics probably one thousand times or more. But real science rarely if ever starts with ‘proof.’ More often than not, neither does a process of science end in proof. Correlation was never crafted as an analytical means to proof. However this one-liner statement is most often employed as a means of implying proof of an antithetical idea. To refuse to conduct the scientific research behind such fingerprint signal conditions, especially when involving a risk exposure linkage, can demonstrate just plain ole malicious ignorance. It is not even stupid.
When a social skeptic makes the statement “Correlation does not prove causality,” they are making a correct statement. It is much akin to pointing out that a pretty girl smiling at you does not mean she wants to spend the week in Paris with you. It is a truism, most often employed to squelch an idea which is threatening to the statement maker. As if the statement maker were the boyfriend of the girl who smiled at you. Of course a person smiling at you does not mean they want to spend a week in Paris with you. Of course correlation does not prove causality. Nearly every single person bearing any semblance of rational mind understands this. But what the one who has uttered this statement does not grasp, while feeling all smart and skeptickey in its mention, is that they have in essence revealed a key insight into their own lack of scientific literacy. Specifically, when a person makes this statement, three particular forms of error most often arise. In particular, they do not comprehend, across an entire life of employing such a statement, that
1. Proof Gaming/Non Rectum Agitur Fallacy: Correlation is used as one element in a petition for ‘plurality’ and research inside the scientific method, and is NOT tantamount to a claim to proof by anyone – contrary to the false version of method foisted by scientific pretenders.
To attempt to shoot down an observation, by citing that it by itself does not rise tantamount to proof, is a form of Proof Gaming. It is a trick of trying to force the possible last step of the scientific method, and through strawman fallacy regarding a disliked observer, pretend that it is the first step in the scientific method. It is a logical fallacy, and a method of pseudoscience. Science establishes plurality first, seeks to develop a testable hypothesis, and then hopes, …only hopes, to get close to proof at a later time.
Your citing examples of correlation which fail the Risk Exposure Test, does not mean that my contention is proved weak.
… and yes, science does use correlation comparatives in order to establish plurality of argument, and consilience which can lead to consensus (in absence of abject proof). The correlation-causality statement, while mathematically true, is philosophically and scientifically illiterate.¹²³
2. Ignoratio Elenchi Fallacy (ingens vanitatum): What is being strawman framed as simply a claim to ‘correlation’ by scientific pretenders, is often a whole consilience (or fingerprint) of mutually reinforcing statistical inference well beyond the defined context of simple correlation.
Often when data shows a correlation, it also demonstrates other factors which may be elicited to demonstrate a relationship between two previously unrelated contributing variables or data measures. There are a number of other factors which science employs through the disciplines of modeling theory, probability and statistics which can be drawn from a data relationship. In addition these inferences can be used to mutually support one another, and exponentially increase the confidence of contentions around the data set in question.²³
3. Methodical Cynicism: Correlation is used as a tool to examine an allowance for and magnitude of variable dependency. In many cases where a fingerprint signal is being examined, the dependency risk has ALREADY BEEN ESTABLISHED or is ALLOWED-FOR by diligent reductive science. To step in the way of method and game protocols and persuasion in order to block study, is malevolent pseudoscience.
If the two variables pass the risk-exposure test, then we are already past correlation and into measuring that level of dependency, not evaluating its existence. If scientific studies have already shown that a chemical has impacts on the human or animal kidney/livers/pancreas, to call an examination of maladies relating to those organs as they relate to trends in use of that chemical a ‘correlation’ is an indication of scientific illiteracy on the part of the accuser. Once a risk relationship is established, as in the case of colon disorders as a risk of glyphosate intake, accusations of ‘correlation does not prove causality’ constitute a non-sequitur Wittgenstein Error inside the scientific method. Plurality has been established and a solid case for research has been laid down. To block such research is obdurate scientific fraud.²³
4. Correlation does not prove causality… however, even weaker in strength of inference is an implicit refutation by claim of coincidence.
Most often, when one poses the ‘correlation does not prove causality’ apothegm, they are attempting to enforce an implicit counter-claim to coincidence in the observed data. While this is the null, it is also most often not an actual hypothesis – nor can such a claim be made without evidence. Most often the evidence in support of a correlation being merely coincidence, is in fact weaker than the evidence in support of causality. A position of epoche is warranted – not denial, in such circumstances.
Calling or downgrading the sum total of these inferences through the equivocal use of the term ‘correlation,’ not only is demonstrative of one’s mathematical and scientific illiteracy, but also demonstrates a penchant for the squelching of data through definition in a fraudulent manner. It is an effort on the part of a dishonest agent to prevent the plurality step of the scientific method.
None of this has anything whatsoever to do with ‘proof.’
A Fingerprint Signal is Not a ‘Correlation’
An example of this type of scientific illiteracy can be found here (Note: a former article entitled Correlation Is Not Causation in Earth’s Dipole Contribution to Climate by Steven Novella, which was dropped by Discover Magazine). There is a well established covariance, coincidence, periodicity and tail sympathy; a long tight history of dynamic with respect to how climate relates to the strength of Earth’s magnetic dipole moment. This is a fingerprint signal. Steven Novella incorrectly calls this ‘correlation.’ A whole host of Earth’s climate phenomena move in concert with the strength of our magnetic field. This does not disprove anthropogenic contribution to current global warming. But to whip out a one liner and shoot at a well established facet of geoscience, all so as to protect standing ideas from facing the peer review of further research is not skepticism, it is pseudoscience. The matter merits investigation. This hyperepistemology one-liner does not even rise to the level of being stupid.
Measuring of An Established Risk Relationship is Not a ‘Correlation’
An example of this type of scientific illiteracy can be found inside pharmaceutical company pitches about how the increase in opioid addiction and abuse was not connected with their promotional and lobbying efforts. Correlation did not prove causality. Much of today’s opiate epidemic stems from two decades of promotional activity undertaken by pharmaceutical companies. According to New Yorker Magazine, companies such as Endo Pharmaceuticals, Purdue Pharma and Johnson & Johnson centered their marketing campaigns on opioids as general use pain treatment medications. Highly regarded medical journals featured promotions directed towards physicians involved in pain management. Educational courses on the benefits of opioid-based treatments were offered. Pharmaceutical companies made widespread use of lobbyist groups in their efforts to disassociate opiate industry practices from recent alarming statistics (sound familiar? See an example where Scientific American is used for such propaganda here). One such group received $2.5 million from pharmaceutical companies to promote opioid justification and discourage legislators from passing regulations against unconstrained opioid employment in medical practices. (See New Yorker Magazine: Who is Responsible for the Pain Pill Epidemic?) The key here is, that once a risk relationship is established, such as between glyphosate and cancer, one cannot make the claim that correlation does not prove causality in the face of two validated sympathetic risk-dependency signals. It is too late, plurality has been established and the science needs to be done. To block such science is criminal fraud.
Perhaps We Need a New Name Besides Correlation for Such Robust Data Fit
Both of these examples above elicit instances where fake skeptic scientific illiteracy served to mis-inform, mis-lead or cause harm to the American Public. Correlation, in contrast, is simply a measure of the ‘fit’ of a linear trend inside the relationship between a two factor data set. It asks two questions (the third is simply a mathematical variation of the second):
Can a linear inference be derived from cross indexing both data sets?, and
How ‘close to linearity’ do these cross references of data come?
How ‘close to curvinlinearity’ do these cross references of data come?
The answer to question number 2 is called an r-factor or correlation coefficient. Commonly, question number 3 is answered by means of a coefficient of determination and is expressed as an r² factor (r squared).³ Both are a measure of a paired-data set fit to linearity. That is all. In many instances pundits will use correlation to exhibit a preestablished relationship, such as the well known relationship between hours spent studying and academic grades. They are not establishing proof with a graph, rather simply showing a relationship which has already been well documented through several other previous means. However, in no way shape or form does that mean that persons who apply correlation as a basis of a theoretical construct are therefore then contending a case for proof. This is a relational form of the post hoc ergo propter hoc fallacy. This is a logical flaw, served up by the dilettante mind which confuses the former case, an exhibit, and conflates it with the later use, the instance of a petition for research.
/philosophy : logic : evidence : fallacy/ : when employing the ‘correlation does not prove causality’ quip to terminally dismiss an observed correlation, when the observation is being used to underpin a construct or argument possessing consilience, is seeking plurality, constitutes direct fingerprint evidence and/or is not being touted as final conclusive proof in and of itself.
THIS is Correlation (Pearson’s PPMCC) It does not prove causality (duh…)¹²
This is a Fingerprint Signal and is Not Simply a Correlation³∋
There are a number of other methods of determining the potential relationship between two sets of data, many of which appear to the trained eye in the above graph. Each of the below relational features individually, and increasingly as they confirm one another, establish a case for plurality of explanation. The above graph is not “proving” that glyphosate aggravates diabetes rates. However, when this graph is taken against the exact same shape and relationship graphs for multiple myloma, non-Hodgkin’s Lymphoma, bladder cancer, thyroid disease, pancreatic cancer, irritable bowel syndrome, inflammatory bowel syndrome, lupus, fibromyalgia, renal function diminishment, Alzheimer’s, Crohn’s Disease, wheat/corn/canola/soy sensitivity, SIBO, dysbyosis, esophageal cancer, stomach cancer, rosacea, gall bladder cancer, ulcerative colitis, rheumatoid arthritis, liver impairment and stress/fatty liver disease, … and for the first time in our history a RISE in the death rates of of middle aged Americans…
… and the fact that in the last 20 years our top ten disease prescription bases have changed 100%… ALL relating to the above conditions and ALL auto-immune and gut microbiome in origin. All this despite a decline in lethargy, smoking and alcohol consumption on average. All of this in populations younger than an aging trend can account for.
Then plurality has been argued. Fingerprint signal data has been well established. This is an example of consilience inside an established risk exposure relationship. To argue against plurality through the clueless statement “Correlation does not prove causality” is borderline criminal. It is scientifically illiterate, a shallow pretense which is substantiated by false rationality (social conformance) and a key shortfall in real intelligence.
Contextual Wittgenstein Error Example – Incorrect Rhetoric Depiction of Correlation
The cartoon to the left is a hypoepistemology which misses the entire substance of what constitutes fingerprint correlation. A fingerprint signal is derived when the bullet-pointed conditions exist – None of which exist in the cartoon invalid comparison to the left – this is a tampering with definition, enacted by a person who has no idea what correlation in this context, even means. A Wittgenstein Error. In other words: scientifically illiterate propaganda. Conditions which exist in a proper correlation, or more, condition:
A constrained pre-domain and relevant range which differ in stark significance
An ability to fit both data sets to curvinlinear or linear fit, with projection through golden section, regression or a series of other models
A preexisting contributor risk exposure between one set of unconstrained variables and a dependent variable
A consistent time displacement between independent and dependent variables
A covariance in the dynamic nature of data set fluctuations
A coincident period of commencement and timeframe of covariance
A jointly shared arrival distribution profile
Sympathetic long term convex or concave trends
A risk exposure (see below) – the cartoon to the left fails the risk exposure test.
Rhetoric: An answer, looking for a question, targeting a victim
Fingerprint Elements: When One or More of These Risk Factor Conditions is Observed, A Compelling Case Should be Researched¹²³
Corresponding Data – not only can one series be fitted with a high linear coefficient, another independent series can also be fitted with a similar and higher coefficient which increases in coherence throughout a time series both before and during its domain of measure, and bears similar slope, period and magnitude. In this instance as well, a preexisting risk exposure has been established. This does not prove causality, however is a strong case for plurality especially if a question of risk is raised. To ignore this condition, is a circumstance where ignorance ranges into fraud.
Covariant Data – not only can one series be fitted with a high coefficient, another independent series can also be observed with a similar fit which increases in coherence as a time series both before and during its domain of measure, and bears similar period and magnitude. Adding additional confidence to this measure is the dx/dy covariance, Browning Covariance, or distance covariance, etc. measure which can be established between the two data series; that is, the change in x(1)…x(n) versus y(1)…y(n). In this instance as well, a preexisting risk exposure has been established. This does not prove causality, however is a very strong case for plurality especially if a question of risk is raised. To ignore this condition, is a circumstance where socially pushed skepticism ranges into fraud.
Co-incidence Data – two discrete measures coincide as a time series both before and during its domain of measure, and bear similar period and magnitude. Adding additional confidence to this measure magnitude consistency which can be established between the two data series; that is, the discrete change in x(1)…x(n) versus y(1)…y(n). In this instance as well, a preexisting risk exposure has been established. This does not prove causality, however is a moderately strong case for plurality especially if a question of risk is raised. To ignore this condition, is a circumstance where arrogant skepticism ranges into fraud.
Jointly Distributed Data – two independent data sets exhibit the same or common arrival distribution functions. Adding additional confidence to this measure magnitude consistency which can be established between the two data series; that is, the discrete change in x(1)…x(n) versus y(1)…y(n). In this instance as well, a preexisting risk exposure has been established. This does not prove causality, however is a moderately strong case for plurality especially if a question of risk is raised. To ignore this condition, is a circumstance where arrogant skepticism ranges into fraud.
Probability Function Match – two independent data sets exhibit a resulting probability density function of similar name/type/shape. Adding additional confidence to this measure magnitude consistency which can be established between the two data series; that is, the discrete change in x(1)…x(n) versus y(1)…y(n). In this instance as well, a preexisting risk exposure has been established. This does not prove causality, however is a moderately strong case for plurality especially if a question of risk is raised. To ignore this condition is not wise.
Marginal or Tail Condition Match – the tail or extreme regions of the data exhibit coincidence and covariance. Adding additional confidence to this measure magnitude consistency which can be established between the two data series when applied in the extreme or outlier condition; that is, the discrete change of these remote data in x(1)…x(n) versus y(1)…y(n). In this instance as well, a preexisting risk exposure has been established. This does not prove causality, however is a moderately strong case for plurality especially if a question of risk is raised. To ignore this condition, is a circumstance where even moderate skepticism ranges into fraud activity.
Sympathetic Long Term Shared Concave or Convex – long term trends match each other, but more importantly each is a departure from the previous history and occurred simultaneously, offset by a time displacement, are both convex or concave and co-vary across the risk period. Adding additional confidence to this measure magnitude consistency which can be established between the two data series; that is, the discrete change in x(1)…x(n) versus y(1)…y(n). In this instance as well, a preexisting risk exposure has been established. This does not prove causality, however is a compellingly strong case for plurality especially if a question of risk is raised. To ignore this condition, is a circumstance where even moderate skepticism ranges into fraud activity.
Discrete Measures Covariance – the mode, median or mean of discrete measures is shared in common and/or in coincidence, and also vary sympathetically over time. Adding additional confidence to this measure magnitude consistency which can be established between the two data series; that is, the discrete change in mode and mean over time. In this instance as well, a preexisting risk exposure has been established. This does not prove causality, however is a moderate case for plurality especially if a question of risk is raised. To ignore this condition is not wise.
Risk Exposure Chain/Test – two variables, if technical case were established that one indeed influenced the other, would indeed be able to influence one another. (In other words, if your kid WAS eating rat poison every Tuesday, he WOULD be sick on every Wednesday – but your kid eating rat poison would not make the city mayor sick on Wednesday). If this condition exists, along with one or more of the above conditions, a case for plurality has been achieved. To ignore this condition, is a circumstance where even moderate skepticism ranges into fraud activity.
These elements, when taken in concert by honest researchers, are called fingerprint data. When fake skeptics see an accelerating curve which matches another accelerating curve – completely (and purposely) missing the circumstance wherein any or ALL of these factors are more likely in play – to say “correlation” is what is being seen, demonstrates their scientific illiteracy. It is up to the ethical skeptic to raise their hand and say “Hold on, I am not ready to dismiss that data relationship so easily. Perhaps we should conduct studies which investigate this risk linkage and its surrounding statistics.”
To refuse to conduct the scientific research behind such conditions, especially if it involves something we are exposed to three times a day for life, constitutes just plain active ignorance and maliciousness. It is not even stupid.
epoché vanguards gnosis
¹ Madsen, Richard W., ” Statistical Concepts with Applications to Business and Economics,” Prentice-Hall, 1980; pp 604 – 610.
² Gorini, Catherine A., “Master Math Probability,” Course Technology, 2012; pp. 175-196, 252-274.
³ Levine, David M.; Stephan, David F., “Statistics and Analytics,” Pearson Education, 2015; pp. 137-275.
∋ Graphic employed for example purposes only. Courtesy of work of Dr. Stephanie Seneff, sulfates, glyphosates and gmo food; MIT, september 19, 2013.
The Largest Single Health Damaging Event in American History
and where were our ‘skeptics’ for the last 24 years while this occurred? Chasing ghosts, Bigfoot and UFO hunters…
It has always been more than simply interesting that our 1995-genesis epidemics of gluten sensitivity and IBS just mysteriously happened to coincide with our introduction of glyphosate into 95+% of the wheat, corn, soy and canola food supply. But if that were the only two flash-skyrocketing maladies the American public has suffered since 1995 then my curiosity might not have been piqued. And let’s be clear, Americans are the heaviest consumers of glyphosate, and are for the most part, the ones suffering most from these new top 10 prescribed-for epidemic maladies. Parsimony under an ethical governance of science, would dictate plurality due to observation, relationship and risk, under the scientific method. However, it has taken the sickening of our entire nation to alert us to this horrendous act.
Why? Because of corrupt oligarch influence and fake skepticism, plain and simple. The act of blocking or not skeptically researching the impact of glyphosate on our collective intestinal health since 1995 – is unconscionable pseudoscience. This should be pursued by a class action lawsuit – god knows that my family has suffered enough from this malfeasance and incompetence. Your claims that we are anti-science be damned. On the contrary, science is stepping back in and taking control back from this case study in corruption.
There are six compelling reasons why the science performed to date on Glyphosate is woefully insufficient, and re-disposition by the EPA, through complete science performed by neutral third parties regarding Glyphosate and its enabling GMO seed monopoly, should be once again evaluated. The scientific method does not dictate that preliminary conclusions, once published, can never again be examined just because SSkeptics declare otherwise. In fact, Ethical Skepticism demands that we re-examine the role of this harmful technology in American diets and in overall human and ecological health.
/ N-(phosphonomethyl) glycine / : Herbicide, assigned EPA Human Toxicity Category III and WHO Toxicity Group 2A ‘probably carcinogenic to humans.’ Toxicity enabled to varying levels in different species, by acting as a water soluble analog of the protein glycine, which deleteriously interferes with the synthesis of the aromatic amino acids phenylalanine, tyrosine and tryptophan; effectively killing bacteria and plants which depend upon the EPSP Synthase pathway. A dependency based technology utilized by Monsanto to establish a strategically planned seed sourcing monopoly. This an outcome of Glyphosate’s complimentary relationship with patented GMO seed modifications, enforced for use throughout a compliant ABCD Seed Cartel,‡ regarding Glyphosate tolerance.
Glyphosate Use Originally Approved/Mandated Under Outdated and Incomplete Science. Which now shows alarming real world test data, to wit:
We conclude that: (1) GBHs are the most heavily applied herbicide in the world and usage continues to rise; (2) Worldwide, GBHs often contaminate drinking water sources, precipitation, and air, especially in agricultural regions; (3) The half-life of glyphosate in water and soil is longer than previously recognized; (4) Glyphosate and its metabolites are widely present in the global soybean supply; (5) Human exposures to GBHs are rising; (6) Glyphosate is now authoritatively classified as a probable human carcinogen; (7) Regulatory estimates of tolerable daily intakes for glyphosate in the United States and European Union are based on outdated science.
Genetically engineered crops, glyphosate and the deterioration of health in the United States of America
Journal of Organic Systems, 9(2), 2014; ISSN 1177-4258
A huge increase in the incidence and prevalence of chronic diseases has been reported in the United States (US) over the last 20 years. Similar increases have been seen globally. The herbicide glyphosate was introduced in 1974 and its use is accelerating with the advent of herbicide-tolerant genetically engineered (GE) crops. Evidence is mounting that glyphosate interferes with many metabolic processes in plants and animals and glyphosate residues have been detected in both. Glyphosate disrupts the endocrine system and the balance of gut bacteria, it damages DNA and is a driver of mutations that lead to cancer. In the present study, US government databases were searched for GE crop data, glyphosate application data and disease epidemiological data. Correlation analyses were then performed on a total of 22 diseases in these time-series data sets.
The Pearson correlation coefficients are highly significant (< 10-4) between the percentage of GE corn and soy planted in the US and hypertension (R = 0.961), stroke (R = 0.983), diabetes prevalence (R =0.983), diabetes incidence (R = 0.955), obesity (R= 0.962), lipoprotein metabolism disorder (R =0.955), Alzheimer’s (R = 0.937), Parkinson’s (R = 0.952), multiple sclerosis (R = 0.876), hepatitis C (R= 0.946), end stage renal disease (R = 0.958), acute kidney failure (R = 0.967), cancers of the thyroid (R = 0.938), liver (R = 0.911), bladder (R = 0.945), pancreas (R = 0.841), kidney (R = 0.940) and myeloid leukaemia (R = 0.889). The significance and strength of the correlations show that the effects of glyphosate and GE crops on human health should be further investigated.
Shehata AA1, Schrödl W, Aldin AA, Hafez HM, Krüger M.; Curr Microbiol. 2013 Apr;66(4):350-8. doi: 10.1007/s00284-012-0277-2. Epub 2012 Dec 9.
The use of glyphosate modifies the environment which stresses the living microorganisms. The aim of the present study was to determine the real impact of glyphosate on potential pathogens and beneficial members of poultry microbiota in vitro. The presented results evidence that the highly pathogenic bacteria as Salmonella Entritidis, Salmonella Gallinarum, Salmonella Typhimurium, Clostridium perfringens and Clostridium botulinum are highly resistant to glyphosate. However, most of beneficial bacteria as Enterococcus faecalis, Enterococcus faecium, Bacillus badius, Bifidobacterium adolescentis and Lactobacillus spp. were found to be moderate to highly susceptible. Also Campylobacter spp. were found to be susceptible to glyphosate. A reduction of beneficial bacteria in the gastrointestinal tract microbiota by ingestion of glyphosate could disturb the normal gut bacterial community. Also, the toxicity of glyphosate to the most prevalent Enterococcus spp. could be a significant predisposing factor that is associated with the increase in C. botulinum-mediated diseases by suppressing the antagonistic effect of these bacteria on clostridia.
Glyphosate interferes with :
Intestinal Dendritic Cell EPSP Synthase, effectively killing those critical immune system messenger cells as part of glyphosate’s well established EPSPS microbicide effectiveness. This renders the gut/immune system unable to communicate microbial tolerance to the innate and adaptive immune systems; effectively triggering celiac disease-like symptoms in humans, including nausea, diarrhea, skin disorders, macrocytic anemia, b-vitamin depletion, depression, IBS, IBD, rosacea and several other longer term chronic illnesses.
Samsel A, Seneff S. Glyphosate, pathways to modern diseases II: Celiac sprue and gluten intolerance. Interdisciplinary Toxicology. 2013;6(4):159-184. doi:10.2478/intox-2013-0026.
Phenylalanine – Elevates the mood, ensures good function of the autonomous and central nervous system (breathing, sleeping, calmness), essential for memory and learning and regulates the appetite by causing excess hunger until this minor protein is fulfilled. Otherwise one short of phenylalanine will overeat in order to attain minor proteins needed.
Tyrosine – It is a building block for several important neurotransmitters, including epinephrine, norepinephrine, serotonin, and dopamine. Neurotransmitters help nerve cells communicate and influence mood. Tyrosine also helps produce melanin (the pigment responsible for hair and skin color) and helps in the function of organs responsible for making and regulating hormones, including the adrenal, thyroid, and pituitary glands.
Tryptophan – The body uses tryptophan to help in the uptake of niacin (Vitamin B3 – lower cholesterol and triglycerides (types of fat) in the blood) and serotonin. Serotonin is thought to produce healthy sleep and a stable mood.
Glycine – Essential for a healthy, normally functioning digestive system. It helps regulate the synthesis of the bile acid used to digest fats. Helps establish the mucosa barrier which blocks toxins from crossing the intestinal boundary – reduces the amount of auto-immune triggers in the blood.
Disruption of Kidney and Liver mRNA splicing and small nucleolar RNA – were mostly upregulated, suggesting disruption of normal spliceosome activity. Electron microscopic analysis of hepatocytes confirmed nucleolar structural disruption.
Disruption of Genes Controlling Chromatin Structure – Genes (especially histone-lysine N-methyltransferases) were mostly upregulated in Kidney and Liver measures.
Disruption of Genes Related to Respiratory Chain Complex I and the Tricarboxylic Acid Cycle – Pathway analysis suggests a modulation of the mTOR and phosphatidylinositol signalling pathways. Gene disturbances associated with the chronic administration of ultra-low dose Roundup reflect a liver and kidney lipotoxic condition and increased cellular growth that may be linked with regeneration in response to toxic effects causing damage to tissues.
Collectively – the interference with these proteins, DNA functions and elimination of vital gut flora causes in humans:
Loss of well being and up mood – creates anxiety
Endocrine function loss (Hypo-thyroid, Hypo-pituitary, Adrenal-Thyroid-Pituitary Axis)
Digestive screening loss and Auto-Immune flareups
Loss of protein synthesis in muscles
Loss of B vitamin uptake – especially in low-methylation genetic profile individuals
Higher triglycerides and cholesterol, liver stress
Chronic inflammatory diseases
Chronic digestive tract diseases
Liver pathology and morphology changes
Kidney pathology and morphology changes
Disruption of cell’s ability to break down and burn sugars (diabetes)
Where were the SSkeptics when this was all approved inside 3 years? Busy ranting about supplements, ghosts, UFO’s, the Loch Ness Monster, alternative medicine and ulcers being caused by coffee and stress.
1. The studies upon which EPA Approval was granted are based on preliminary and aged experimental observation.
EPA Initial Approval
1991 RED Facts: Glyphosate; EPA-738-F-93-011; U.S. Environmental Protection Agency, Office of Prevention, Pesticides, and Toxic Substances, Office of Pesticide Programs, U.S. Government Printing Office: Washington, DC, 1993.
2. The EPA Approval was granted on only one scant 1970 / 80’s study series, conducted on animals (rats, rabbits, beagles); wherein the objectivity is in question, of both the EPA and Monsanto in assessing the regulatory applicability of these early studies, as they were all completed only by Monsanto.
Approval Basis: All Monsanto Studies
Reregistration Eligibility Decision (RED) Glyphosate; EPA-738-F-93-011; U. S. Environmental Protection Agency, Office of Prevention, Pesticides, and Toxic Substances, Office of Pesticide Programs, U.S. Government Printing Office: Washington, DC, 1993. Referenced studies (Increase in autism study on right from Nevison, Environmental Health; 2014, 13:73 Page 4 of 16 : http://www.ehjournal.net/content/13/1/73).
1985 Reyna, M. Twelve month study of glyphosate administered by gelatin capsule to beagle dogs. Unpublished Report no. 830116, project no. ML-83-137, 1985, submitted to U.S. Environmental Protection Agency by Monsanto Company Environmental Health.
1983 Knezevich, A.; Hogan, G. A chronic feeding study of glyphosate (Roundup technical) in mice. Unpublished Report no. BDN-77420, project no. 77-2061, 1983, submitted to U.S. Environmental Protection Agency by Monsanto Company, prepared by BioDynamics, Inc.
1970 Birch, M. Toxicological investigation of CP 67573-3. Unpublished Report no. 4-70-90, 1970, submitted to U.S. Environmental Protection Agency by Monsanto Corporation, prepared by Younger Laboratories, Inc.
1988 Blaszcak, D., Primary dermal irritation study in rabbits for glyphosate technical (wetcake). Unpublished Report no. BD-88- 114, project number 4887, 1988, submitted to U.S. Environmental Protection Agency by Monsanto Corporation, prepared by BioDynamics, Inc.
1980 Rodwell, D. E.; Tasker, E. J.; Blair, A. M.; et al. Teratology study in rats. Unpublished report no. 401-054, unpublished study no. 999- 021, 1980, submitted to U.S. Environmental Protection Agency by Monsanto Company, prepared by International Research and Development Corporation.
1980 Rodwell, D. E.; Tasker, E. J.; Blair, A. M.; et al. Teratology study in rats. Unpublished report no. 401-056, 1980, submitted to U.S. Environmental Protection Agency by Monsanto Company, prepared by International Research and Development Corporation.
1988Monsanto Corporation. The metabolism of glyphosate in Sprague Dawley rats- Part I. Excretion and tissue distribution of glyphosate and its metabolites following intravenous and oral administration. Unpublished report no. MSL-7215, 1988, submitted to WHO by Monsanto Ltd, prepared by Monsanto Environmental Health Laboratory.
1988 Ridley, W.; Mirly, K. The metabolism of glyphosate in Sprague-Dawley rats. Part I. Excretion and tissue distribution of glyphosate and its metabolites following intravenous and oral administration. Unpublished report no. 86139 (MSL 7215), RD no. 877, 1988, submitted to U.S. Environmental Protection Agency by Monsanto Company.
1988 Howe, R.; Chott, R.; McClanahan, R. Metabolism of glyphosate in Sprague-Dawley rats. Part II: Identification, characterization, and quantitation of glyphosate and its metabolites after intravenous and oral administration. Unpublished report no. MSL-7206, RD No. 877, 1988, submitted to U.S. Environmental Protection Agency by Monsanto Company.
1978 Brightwell, B.; Malik, J. Solubility, volatility, absorption, and partition coefficients, leaching and aquatic metabolism of MON 0573 and MON 0101. Unpublished report no. MSL-0207, 1978, submitted to U.S. Environmental Protection Agency by Monsanto Company.
1990 McMullan, P.; Honeggar, J.; Logusch, E. Confined rotational crop study of glyphosate Part II. Quantitation, characterization and identification of glyphosate and its metabolites in rotational crops. Unpublished report no. MSL-981, 1990, submitted to U.S. Environmental Protection Agency by Monsanto Agricultural Labs.
1978 Fink, R.; Beavers, J. One-generation reproduction study in bobwhite quail: glyphosate technical. Unbpublished report no. 139- 141. 1978, submitted to U.S. Environmental Protection Agency by Monsanto Company, prepared by Wildlife International Ltd.
1982 McAllister, W.; McKee, M.; Schofield, M.; et al. Chronic toxicity of glyphosate (AB-82-036) to Daphnia magna under flow-through test conditions. Chronic toxicity final report ABC 28742. Unpublished report, 1982, submitted to U.S. Environmental Protection Agency by Monsanto Company, prepared by Analytical Bio-Chemistry Laboratories, Inc.
1974 Bentley, R., Acute toxicity of roundup (technical) to grass shrimp (Palaemonetas vulgaris) and fiddler crab (Uca pagilator). Unpublished report no. SF1536, 1974, submitted to U.S. Environmental Protection Agency by Monsanto Company, prepared by Bionomics, Inc.
1972 Frasier, W. D.; Jenkins, G. The acute contact and oral toxicities of CP67573 and MON2139 to worker honey bees. Unpublished report no. 4G1444, 1972, submitted to U.S. Environmental Protection Agency by Monsanto Company, prepared by Huntingdon Research.
In the instances of the third party labs which completed studies, subsequently routed through Monsanto to the EPA, a glance at LinkedIn and Moody’s shows that several of these companies were staffed by ex Monsanto and Syngenta employees, all in the St. Louis and Columbia, Missouri local area, or were small or one man or short lived businesses, operating around the period of the study. Nor did these firms continue their research after the EPA approval. A curious set of actions given that now human and higher order mammal and prodigious field data are available, which could improve their confidence interval risk profiles to an impeccable level of integrity. Yet they just ceased study altogether. This brings their third party objectivity, and their role as scientists, into essential question.
3. The sample sizes of observational data for all coincident maladies is much more easily accessible/collectible today. As well, Monsanto coordinated the release of studies, patents and EPA approvals as part of a liability risk mitigation strategy regarding these maladies, along with its connected seed sourcing monopoly business strategy
As you can see from the above graphic, the amount of human data available with which to truly assess the safety of Glyphosate, is on the order of 30,000 times as large as it was in the 1986 – 1991 timeframe in which the Approval studies were conducted. In addition, the littany of condemning, or alarm raising studies continues to proliferate AFTER the Approval in 1991 by the EPA. See the listing below.
What Monsanto has accomplished here is brilliant strategy. They planned the timed arrival of the Glyphosate Resistant Genome Abstracts onto the market commensurate with the expiration of their Glyphosate patents. This allowed their domain of Glyphosate to be liability umbrella covered by the former EPA guidance on the herbicide/toxicant/biocide, while the open domain market use of Glyphosate now will be administered under the newer understandings of toxicity which have been discovered since Approval by the EPA. In this way, Monsanto dodges the liability on the negative health effects of Glyphosate, endures the ramp up period for the growth of business from a gateway patent, and secures ultimate risk-free profitability through a complimentary and solely dependent technology: Glyphosate resistance through patented GM seed.
A brilliantly executed strategy.
Toxicology Studies Executed AFTER FDA Approval and Glyphosate Enabling GMO Maps were Abstracted by Monsanto
Please note that after the EPA approval in 1991, despite the prodigious amount of new contra indicative data since on HUMANS and higher order mammals, Monsanto ceased critical safety-oriented clinical studies of Glyphosate altogether. They left it to the rest of the world to perform lifecycle and safety-diligence science through a nascent sufficient level of observational and intelligence base of data. Knowing that these opponents would have a ‘King of the Hill’ battle against bureaucracy, collusion, corruption and false skeptics, Monsanto strategically planned to sit back and do nothing thereafter. Notice that not even one study since, has been completed by Monsanto or their shill third party labs which underpinned the 1991 EPA approval effort.
2015 Journal of Environmental Health, Environmental Health Aug 25 2015, 14:70 doi:10.1186/s12940-015-0056-1 – Transcriptome profile analysis reflects rat liver and kidney damage following chronic ultra-low dose Roundup exposure.
2000 Shaner, D. L. The impact of glyphosate-tolerant crops on the use of other herbicides and on resistance management. Pest Manag. Sci. 2000, 56, 320-326.
1991 Franz, J. E.; Mao, M. K.; Sikorski, J. A. Glyphosate: A Unique Global Herbicide; American Chemical Society: Washington, DC, 1997; pp 521-527, 604-605, 615.
1996 WHO. Data Sheets on Pesticides: Glyphosate; International Programme on Chemical Safety, World Health Organization, Food and Agriculture Organization: Geneva, Switzerland, 1996.
2006 Wu, J. Y.; Chang, S. S.; Tseng, C. P.; Deng, J. F.; Lee, C. C. Parenteral glyphosate-surfactant herbicide intoxication. Am. J. Emerg. Med. 2006, 24 (4), 504-506.
2000 Williams, G. M.; Kroes, R.; Munro, I. C. Safety evaluation and risk assessment of the herbicide Roundup and its active ingredient, glyphosate, for humans. Regul. Toxicol. Pharmacol. 2000, 31, 117-165.
2004 Bradberry, S. M.; Proudfoot, A. T.; Vale, J. A. Glyphosate poisoning. Toxicol. Rev. 2004, 23 (3), 159-167.
2000 Bates, N.; Campbell, A. Handbook of Poisoning in Dogs and Cats – Glyphosate; Campbell, A.; Chapman, M., Eds.; Blackwell Science Ltd: Oxford, England, 2000; pp 135-138.
1998 Monsanto Department of Medical and Health Sciences. Roundup and other gyphosate/tallowamine surfactant-containing herbicides: The clinical effects and their managment. Unpublished report, 1994, cited in Burgat, V.; Keck, G.; Guerre, P.; Bigorre, V.; Pineau, X. Glyphosate toxicosis in domestic animals: A survey from the data of the Centre National d’Informations Toxicologiques Veterinaires (CNITV). Vet. Hum.Toxicol. 1998, 40 (6), 363-367.
2004 Rattray, N. J. Glyphosate acid: 4-hour acute inhalation toxicity study in rats. Unpublished Report no. CTL/P/4882, study no. HR2884, 1996, submitted to WHO by Syngenta Crop Protection AG, Basel, Switzerland, prepared by Zeneca Agrochemicals, Central Toxicology Laboratory, Alderley Park, Maccelsfield, Cheshire, England. Pesticide Residues in Food – 2004: Toxicological evaluations; International Programme on Chemical Safety, World Health Organization: Geneva, Switzerland, 1996.
2004 Welch, S. Glyphosate. Clinical Veterinary Toxicology; Plumlee, K. H., Ed.; Mosby: St. Louis, 2004; pp 162-163.
1998 Burgat, V.; Keck, G.; Guerre, P.; Bigorre, V.; Pineau, X. Glyphosate toxicosis in domestic animals: A survey from the data of the Centre National d’Informations Toxicologiques Veterinaires (CNITV). Vet. Hum. Toxicol. 1998, 40 (6), 363-367.
1999 Acquavella, J. F.; Weber, J. A.; Cullen, M. R.; Cruz, O. A.; Martens, M. A.; Holden, L. R.; Riordan, S.; Thompson, M.; Farmer, D. Human ocular effects from self-reported exposures to Roundup herbicides. Hum. Exp. Toxicol. 1999, 18 (8), 479-486.
2009 Glyphosate. Human-Health Assessment Scoping Document in Support of Registration Review; U.S. Environmental Protection Agency, Office of Prevention, Pesticides, and Toxic Substances, Office of Pesticide Programs, U.S. Government Printing Office: Washington, DC, 2009.
2004 Acquavella, J. F.; Alexander, B. H.; Mandel, J. S.; Gustin, C.; Baker, B.; Chapman, P.; Bleeke, M. Glyphosate biomonitoring for farmers and their families: results from the Farm Family Exposure Study. Environ. Health Perspect. 2004, 112 (3), 321-326.
2007 Cavas, T.; Konen, S. Detection of cytogenic and DNA damage in peripheral erythrocytes of goldfish (Carassius auratus) exposed to a glyphosate formulation using the micronucleus test and the comet assay. Mutagenesis 2007, 22 (4), 263-268.
2004 FAO. Pesticide Residues in Food – Evaluations Part 2: Toxicological; International Programme on Chemical Safety, World Health Organization, Food and Agriculture Organization: Rome, Italy, 2004.
2005 De Roos, A. J.; Blair, A.; Rusiecki, J. A.; Hoppin, J. A.; Svec, M.; Dosemeci, M.; Sandler, D. P.; Alavanja, M. C. Cancer incidence among glyphosate-exposed pesticide applicators in the Agricultural Health Study. Environ. Health Perspect. 2005, 113 (1), 49-54.
2004 Moxon, M. E. Glophosate acid: multigeneration reproduction toxicity in rats. Unpublished report no. CTL/P/6332, study no. RR0784, 2000, submitted to WHO by Syngenta Crop Protection AG, Basel, Switzerland, prepared by Zeneca Agrochemicals, Central Toxicology Laboratory, Alderley Park, Macclesfield, Cheshire, England. Pesticide Residues in Food – Evaluations Part 2: Toxicological; International Programme on Chemical Safety, World Health Organization, Food and Agriculture Organization: Rome, Italy, 2004.
2003 Hori, Y.; Fujisawa, M.; Shimada, K.; Hirose, Y. Determination of the herbicide glyphosate and its metabolite in biological specimens by gas chromatography-mass spectrometry. A case of poisoning by roundup herbicide. J. Anal. Toxicol. 2003, 27 (3), 162-166.
2002 Aprea, C.; Colosio, C.; Mammone, T.; Minoia, C.; Maroni, M. Biological monitoring of pesticide exposure: a review of analytical methods. J. Chromatogr. B Analyt. Technol. Biomed. Life Sci. 2002, 769 (2), 191-219.
2008 Motojyuku, M.; Saito, T.; Akieda, K.; Otsuka, H.; Yamamoto, I.; Inokuchi, S. Determination of glyphosate, glyphosate metabolites, and glufosinate in human serum by gas chromatography-mass spectometry. J. Chromatogr. B 2008, 875, 509-514.
2004 Biagini, R. E.; Smith, J. P.; Sammons, D. L.; MacKenzie, B. A.; Striley, C. A.; Robertson, S. K.; Snawder, J. E. Development of a sensitivity enhanced multiplexed fluorescence covalent microbead immunosorbent assay (FCMIA) for the measurement of glyphosate, atrazine and metolachlor mercapturate in water and urine. Anal. Bioanal. Chem. 2004, 379 (3), 368-374.
2007 Curwin, B. D.; Hein, M. J.; Sanderson, W. T.; Striley, C.; Heederik, D.; Kromhout, H.; Reynolds, S. J.; Alavanja, M. C. Urinary pesticide concentrations among children, mothers and fathers living in farm and non-farm households in iowa. Ann. Occup. Hyg. 2007, 51 (1), 53-65.
2008 Tsui, M. T. 60. K.; Chu, L. M. Environmental fate and non-target impact of glyphosate-based herbicide (Roundup) in a subtropical wetland. Chemosphere 2008, 71, 439-446.
2005Curwin, B. D.; Hein, M. J.; Sanderson, W. T.; Nishioka, M. G.; Reynolds, S. J.; Ward, E. M.; Alavanja, M. C. Pesticide contamination inside farm and nonfarm homes. J. Occup. Environ. Hyg. 2005, 2 (7), 357-67.
2004 Howe, C. M.; Berrill, M.; Pauli, B. D.; Helbing, C. C.; Werry, K.; Veldhoen, N., Toxicity of glyphosate-based pesticides to four North American frog species. Environ. Toxicol. Chem. 2004, 23 (8), 1928-1938.
4. There exists a pronounced rise in diseases associated with the original toxicity issues evaluated in the EPA Approval; specifically pancreatic, endocrine and skin inflammation disorders
OCKHAM’S RAZOR PLURALITY HAS BEEN DRAMATICALLY SURPASSED: There Exists a Problem with Our Food – And No, Exercising More Will Not Fix This
Compare the chart at the right with the Glyphosate employment curve shown above; and remember that by 2008, Glyphosate tolerant crops constitute 85 – 90% of the food bio-availability in their respective use classes. I am not sure that we can wait to finally find out what it is we must to do to convince the oppressive Social Skepticism movement to step aside and allow real actual science to proceed. To continue to actively ignore this set of maladies, endocrine, inflammation and auto-immune in nature, is the height of malicious incompetence. And remember, one principal goal of the Social Skepticism cabal is the Cultivation of Ignorance, the false premise that you must bring final and conclusive proof at the beginning of the scientific method; along with the commensurate manipulation of the conscience of science to support oligarch cronies. This constituting just one technique inside the variety of ways to cultivate ignorance through manipulation of the scientific method. The graphic to the right is posted, courtesy of Farm Wars (http://farmwars.info/?p=11543) and demonstrates the dramatic growth in diabetes incident upon the US population underway. No, this is not simply because the population is aging. Our children are inheriting these diseases on a regular basis now. To presume that you know the impetus behind this alarming statistic, as a means to squelch study, not stimulate it – is pseudoscience. The advocate producing this comparative on the right, indexing the coincidence between GM Food technologies and the rate of increase in diabetes, is petitioning for research – not providing excuse to block research – so he or she is actually conducting work in accordance with the scientific method.
But the bad news is that diabetes apparently is a 2 year lag sensitive malady induced from environmental factors, apparently factors which appeared in the American diet around 1995. But cancer on the other hand is more of a 15 to 40 year lag statistic as we have seen from smoking data and its impacts on stomach, bladder, esophageal and lung cancer data. Accordingly we should see a curve building now, stemming from the 1995 introduction of the first broad scale glyphosate resistant crops in 1995. Indeed, when we examine pancreatic cancer, we see exactly what might be expected; in fact, a terrifying picture.
Not only are we experiencing a pandemic rate of diabetes, but pancreatic cancer, once rare, has now skyrocketed to become the fourth leading cause of cancer death in the United States. The United States not only leads the world in rates of diabetes, but in rates and deaths of pancreatic cancer as well. We cannot continue to blame these observations on super sized meals, in absence of having really conducted any research. A counter claim cannot be tendered in a pluralistic argument, without evidence. According to the National Cancer Institute, in 2014, over 46,400 people will be diagnosed with pancreatic cancer – this is up 114% since the 2012 GLOBOCAN North American measured rate, which was already 18% higher than the rest of the planet on average. ¹ ³
US Pancreatic Cancer Case Incidence 2012 21,713 US Pancreatic Cancer Case Incidence 2014 46,400N American Avg Pancreatic Cancer Incidence 2.6%World Avg Pancreatic Cancer Incidence 2.2%
And no, arch cynic Steven Novella cannot blame these stats on ‘an increase in focus on and diagnosis of’ since 80+% of these victims die of this cancer and usually in about a little over a year on average. A study leader Dr. Peter Storz, a cancer biologist at the Mayo Clinic in Jacksonville, FL, who – with colleagues – describes their findings in the journal Cancer Discovery, says: ²
Our study shows a “direct link between Kras mutations and the inflammatory environment that drive the initiation of pancreatic cancer.”
It is clear from the post 1991 evidence and studies cited in section 3 above, that pancreatic inflammatory impacts were a principal observed element inside the observed set of effects of glyphosate on higher order mammals. The criminal stupidity displayed on the part of our arch SSkeptics, seeks to BLOCK, yes BLOCK the science which could prove matters such as the impact of this food additive, glyphosate, on our public health.
5. Glyphosate is not optional. You can’t wash Glyphosate off, and it is contained in 90% of the bio-available foods of each major US Consumer Food category.
One cannot avoid Glyphosate except through an enormous amount of diligent research and through a highly restrictive diet. The products do not inform their victims of the incumbent potential dangers documented since 1991. Rosacea, Obesity from Endocrine Collapse and the requisite Auto-Immune Disruption, are all a concern among Americans today. I was able to alleviate these symptoms by elimination of Glyphosate related foods. Elimination of corn, wheat, soy, canola dairy and alfalfa is not an accomplishment which the vast majority of Americans can achieve. The foods are not labelled such that they can, even if they wanted. Resource sites provided by the American Autoimmune Related Diseases Association, for persons truly interested In or suffering from Endocrine, Rheumatoid or Autoimmune Diseases:
Related original studies which cited that pancreatic, endocrine, skin and inflammation disorders were an issue
Arbuckle, T. E.; Lin, Z.; Mery, L. S. An exploratory analysis of the effect of pesticide exposure on the risk of spontaneous abortion in an Ontario farm population. Environ. Health Perspect. 2001, 109 (8), 851-7.
Maibach, H. I. Irritation, sensitization, photoirritation and photosensitization assays with a glyphosate herbicide. Contact Derm. 1986, 15, 152-156.
Talbot, A. R.; Shiaw, M. H.; Huang, J. S.; Yang, S. F.; Goo, T. S.; Wang, S. H.; Chen, C. L.; Sanford, T. R. Acute poisoning with a glyphosatesurfactant herbicide (‘Roundup’): A review of 93 cases. Hum. Exp. Toxicol. 1991, 10 (1), 1-8.
McConnel, R. A chronic feeding study of glyphosate (Roundup technical) in mice: pathology report on additional kidney sections. Unpublished project no. 77-2061A, 1985.
Stout, L.; Ruecker, F. Chronic study of glyphosate administered in feed to albino rats. Unpublished Report no. MSL-10495 R.D. 1014, 1990.
Lavy, T. L. Conifer seedling nursery worker exposure to glyphosate. Arch. Environ. Contam. Toxicol. 1992, 22, 6-13.
Jauhiainen, A.; Rasanen, K.; Sarantila, R.; Nuutinen, J.; Kangas, J. Occupational exposure of forest workers to glyphosate during brush saw spraying work. Am. Ind. Hyg. Assoc. J. 1991, 52 (2), 61-64.
Samsel A, Seneff S. Glyphosate, pathways to modern diseases II: Celiac sprue and gluten intolerance. Interdisciplinary Toxicology. 2013;6(4):159-184. doi:10.2478/intox-2013-0026.
6. The Public is asking that the science be completed/updated. They would like to be informed so they can make choices. This is their right.
Significant portions of the scientifically and medically minded, as well as the professional population of our country are standing up and raising concerns over what they are observing in their children. No, the rise in obesity, diabetes, thyroid disease and other maladies cannot be explained by calories and exercise. No, you cannot dissuade ethical questions by charades of ‘critical’ or ‘skeptical’ thinking.
“Nearly one quarter, 25 percent of all Americans ages 17-24 are too overweight to serve. Obesity is not only affecting those who can qualify for military service, it is also creating challenges for our active duty military,” Tomaszeski said.
– U.S. Navy Rear Admiral Steven Tomaszeski, CBS Baltimore, ‘Obesity Affects Number Of Those Eligible For Military Service;’ Nov 20, 2014.
Yes, there is a growing fire. The fire is the observed inflammation in our bodies, skyrocketing since 1995, along with the incumbent increase in Endocrine-Immune Disruption. Rome is burning. It is our national health, security and prosperity. All placed in danger while we fiddle with a
1.2% increase in the crop price (6 cents a bushel net on sale),
7.5% increase in yield and
savings of 2 cents a bushel on cost of production.†
As many others have expressed, let me offer up a resounding ‘yawn’ to this level of productivity and yield gain. Post harvest perishment rates, especially in famine stricken areas of the globe are well in excess of 40%. I work supporting nine of these nations, and trust me, yield is not the issue they face. Post harvest perishment is where the danger of famine resides, not in theoretical hectare ‘yields.’
I attended a symphony with an oncologist and her husband recently and the subject of autoimmune disease and diet came up. She was a cancer survivor herself at age 29! This is what she related to me:
“I could never say this on the record in my profession, but the incident of previously rare cancers no longer being that rare, along with a rise in the ‘old age’ associated cancers occurring in those my age, is dramatic. Whatever it is has occurred in the last 12 years because the stats are skyrocketing. It is obviously something environmental, but further, I think it is diet related.”
~ 29 Year Old Breast Cancer Survivor and Oncologist
The Michael Shermer’s of the world think that your suffering, your food sensitivities, your intestinal dysfunction, facial sores, cancers, anxiety, IBS, and endocrine maladies – ARE ALL A FICTIONAL COMEDY – they mock you in your suffering.
We cannot continue to sacrifice our bodies for this fairy tale of how famine works – along with Social Skeptic cluelessness and arrogance concerning the suffering of everyday people. This yield and productivity result is solely intended to be employed in predatory market dynamics, masquerading as a dilettante understanding of famine mercy. Parallel to much of American economics, we are using predatory pricing, efficiencies and sourcing cartels (seed sourcing in this case, emulating China) in order to put small and medium sized competitors out of business, to the benefit of social oligopolies. These tactics are NOT mechanisms of capital economies, rather socialist economies. The measurable rise of royalty and elite elicits indication as to what is occurring in our agri-foods industry. Socialism always bears a royalty class, hidden or visible.
Now it is up to activists like me, who were able to improve their health and reverse these diseases by eliminating specific foods (wheat, dairy, corn, canola oil, soy, cottonseed oil, alfalfa), who must petition scientists we work with and know, to start considering the idea that we must begin to conduct science on the safety and health impacts of the food we are consuming. Believe it or not, science that has been obstructed by the very organization who’s job it should have been to protect us in the first place.
Plurality has been established on this issue: Our food is in question – Glyphosate is in question – We must begin the actual third party, skeptical science.