Just Label It – We Have A Right To Know And Here’s Why

These agricultural pesticides have also been linked to autism, cancer and Alzheimer’s disease, you can read more about that here.

This is just one out of many reasons as to why we should just label Genetically Modified Organisms(GMOs), and why everybody has a right to know what they are eating. Everybody should be given the freedom of choice, regardless of whether they believe GMOs are harmful or not.

why everybody has a right to know what they are eating. Everybody should be given the freedom of choice, regardless of whether they believe GMOs are harmful or not.

Why We Have A Right To Know

“Any politician or scientist who tells you these products are safe is either very stupid or lying. The hazards of these foods are uncertain. In view of our enormous ignorance, the premature application of biotechnology is downright dangerous. By slipping it into our food without our knowledge, without any indication that there are genetically modified organisms in our food, we are now unwittingly part of a massive experiment.” – David Suzuki, CC,OBC,PH.D LLD, Geneticist

There’s a reason that several countries around the world have completely banned GMOs and the pesticides that go with them (or have severe restrictions). One of the biggest reasons are the detrimental effects they can and are having on human health.

For example, Sri Lanka recently banned glyphosate from their country because of its possible link to a fatal kidney disease. (6) You can read more about that here.

In Argentina, deaths from cancerous tumours have as much as doubled in areas where GM crops are grown and agro-chemicals are used. (7)

Several studies have also shed light on glyphosate’s potential to be an endocrine disruptor. Endocrine disruptors are chemicals that can interfere with the hormone system in mammals. These disruptors can cause developmental disorders, birth defects and cancer tumours. (8)(10)

Another popular study, supported by hundreds of scientists from all over the world was the Seralini study. It provided good evidence linking GMOs to cancer, liver/kidney damage as well as severe hormonal disruption. It was published and went through a rigorous peer-review process in the Journal of Food and Chemical Toxicology. The study was then retracted after Richard E. Goodman a former Monsanto researcher become the associate editor for biotechnology at the journal, which sparked outrage among many scientists who supported the study. (source)

Again, over a hundred  scientists condemned the retraction of the  study and a new study was conducted addressing the criticisms of the old ones . It was then republished  again in multiple journals. (9) You can read more about that study here.

What also has people scratching their heads when it comes to GMOs is the secrecy and political corruption that seems to follow. For example, Wikileaks cables reveal that the State Department was lobbying all over the world for Monsanto, and other major biotech corporations. They reveal that American diplomats requested funding to send lobbyists for the biotech industry to meet with politicians and agricultural officials in “target countries.” These included countries in Africa, Latin America and some European countries. This is significant because the documents also indicated that the United States government planned to “retaliate and cause pain” on countries refusing GMOs. You can read more about that, and access those documents here.

The list as to why GMOs should not be approved as completely safe for human consumption is very long and could probably fill up thousands of pages with information from science, to corruption and environmental degradation and more. Despite this fact, most of North America is still struggling to put a label on these foods.

Despite the setbacks, a tremendous amount of progress is being made. A large amount of awareness has now hit mainstream media as a large collective across the planet now openly opposes GMOs. They’ve been banned in various places and two counties in Oregon have even been successful with their ban efforts.

The GMO topic is a great example of a topic growing, being questioned and examined outside of the mainstream media. It’s a topic that became so big in the “underground” news world (for lack of a better term) that the mainstream media had no choice but to pick it up.

As we continue to push forward I have no doubt that GMOs will eventually become extinct, and that a large majority of us will be able to see through the false justifications that have been used to bring them into our world. They are not needed, and we shouldn’t be made to believe that they are.

For more CE articles on GMOs please click HERE.

The information presented in this article is when it comes to GMOs/Pesticides and human health is just a fraction of available information in the public domain. I hope this encourages you to further your research if interested.

(1) http://www.ncbi.nlm.nih.gov/pubmed/23267077

(2) http://www.ncbi.nlm.nih.gov/pubmed/22504123

(3)http://www.mdpi.com/1099-4300/15/4/1416

(4)http://www.scientificamerican.com/article/parkinsons-disease-and-pesticides-whats-the-connection/

(5)http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3955666/

(6) https://www.documentcloud.org/documents/1084784-jayasumana-glyphosate-study.html

(7) http://gmwatch.org/index.php/news/archive/2014/15506-cancer-deaths-double-where-gm-crops-and-agro-chemicals-used

(8)http://www.ncbi.nlm.nih.gov/pubmed/23756170

(9) http://www.enveurope.com/content/26/1/14

(10) http://www.ncbi.nlm.nih.gov/pubmed/12148884

Parkinson's disease reverted at a experimental stage

Mexican scientists demonstrated experimentally, with adult rats, that mobility can be restored in patients with Parkinson's disease, the major degenerative disease of the motor system worldwide. The experiments have not yet been transferred to humans, but are a scientific, measurable and repeatable basis to fight against this disease

The Mexican study, led by Jorge Aceves Ruiz, an expert in physiology and emeritus researcher at the Center for Research and Advanced Studies (CINVESTAV), uses stem cells to generate dopaminergic nerve cells and reactivate the production of dopamine in the brain of rats with symptoms of shaking palsy or Parkinson's disease.

Aceves Ruiz's group has over 35 years of experience in research on brain physiology, but particularly in a region near the base in which the basal ganglia are located. In that area, there are accumulations of nerve cells that make and release neurotransmitters such as dopamine. The treatment they have designed and tested in the laboratory uses stem cells that develop into dopamine producers.

"Our treatment has allowed us to recover these motor impairments, which is associated with the recovery of neurons and dendritic spines of striatal neurons, which is the first thing that gets damaged in Parkinson's disease," explained Aceves Ruiz, who belongs to the permanent Seminar in Science and Technology of Mexico in the medical center "XXI Century" in Mexico City.

"We found that apparently the treatment by neurogenesis allows these newly formed neurons to be able to innervate, meaning that from stem cells present in the tissue itself, cell differentiation towards dopaminergic phenotype is induced".

After, at least four processes occur before regaining motor behavior: new dopaminergic cells send their terminals to the striatum, functionally reinnervate neurons, induce recovery of dendritic spines and recover the functionality of the cortical input, said the physiologist graduated from the National Autonomous University of Mexico (UNAM).

Stimulating dopamine

Until 35 years ago virtually nothing was known about the part of the brain called the basal ganglia, which are clusters of nerve cells at the base of the brain in which different molecules that help transmit messages between neurons are produced.

Following a period of study at the University of Cambridge, Aceves Ruiz met his Argentine colleague Claudio Cuello, with whom he began conducting experiments to see if they could produce dopamine by electrical stimuli. With trepidation he initiated a research path that has generated over 73 pioneering papers in pharmaceutical neurology.

"Now we know that, for example, basal ganglia are organized primarily in two ways: one that facilitates movement and one that inhibits it, under the action of dopamine," says Aceves.

"We know how the neurotransmitter works, and this has enabled us to design experiments that allow us to recover motor activity, we also determined through experiments that dopamine can promote or inhibit the movement under normal conditions; the problem is knowing when it promotes and when it stops, and to perform the process it uses different receptors".

Experiments with adult rats to give back control of movement continues, but also Mexican research has opened other fields of study on the action of dopamine and the consequences of its absence, for example, its effects on motor hyperactivity syndrome.

"We are the only group that knows, through our experimental work, what does the D4 receptor do, whcih activation causes decreased motor activity, because it would be acting in this special kernel that controls attention and partly motor activity " explained Aceves Ruiz.

 Explore further: An important study for Parkinson's disease: Researchers uncover mechanism regulating dopamine levels in the brain

http://health.einnews.com/article/240626537/6hM6H26DOfVB57oo

Italy's Newron soars on EU green light for Parkinson's drug

Dec 19 (Reuters) - Share's in Italian drugmaker NewronPharmaceuticals soared to a six-year high on Friday as European regulators gave a green light to its experimental Parkinson's disease drug Xadago.

The medicine, also known as safinamide, is the first new drug in 10 years to receive a positive opinion from the European Medicines Agency for the treatment of Parkinson's, marking a landmark for the small Milan-based firm.

"2015 will see the company join an elite group of Europeanbiotechnology companies that have managed to develop and get a drug launched on to the market," said Samir Devani of Rx Securities.

Newron is partnering with privately-held drugmaker Zambon to market the drug, which analysts expect to compete with Azilect from Teva Pharmaceutical Industries and Lundbeck .

Swiss-listed shares in Newron were 13 percent higher at 26.30 francs by 1345 GMT, after hitting a high of 30.40.

(Reporting by Ben Hirschler; editing by David Clarke)

http://health.einnews.com/article/240633432/XVf_d8qXkcpZ2GCR

How does prostate cancer form? Parkinson's Link?

Date:

December 18, 2014

Source:

Thomas Jefferson University

Summary:

The cause of prostate cancer may be linked to Parkinson’s disease through a common enzyme family called sirtuins. Finding an enzyme that regulates this process could provide excellent new prevention approaches for this common malignancy, researchers say. Sirtuin enzymes have been implicated in neurodegeneration, obesity, heart disease, and cancer.

Prostate cancer affects more than 23,000 men this year in the USA however the individual genes that initiate prostate cancer formation are poorly understood. Finding an enzyme that regulates this process could provide excellent new prevention approaches for this common malignancy. Sirtuin enzymes have been implicated in neurodegeneration, obesity, heart disease, and cancer. Research published online Thursday (Dec 18th) in The American Journal of Pathology show the loss of one of sirtuin (SIRT1) drives the formation of early prostate cancer (prostatic intraepithelial neoplasia) in mouse models of the disease.

      

"Using genetic deletion we found that SIRT1 normally restrains prostatic intraepithelial neoplasia in animals. Therefore too little SIRT1 may be involved in the cellular processes that starts human prostate cancer," said Dr. Richard Pestell, M.D., Ph.D., MBA, executive Vice President of Thomas Jefferson University and Director of the Sidney Kimmel Cancer Center. "As we had shown that gene therapy based re expression of SIRT1 can block human prostate cancer tumor growth, and SIRT1 is an enzyme which can be targeted, this may be an important new target for prostate cancer prevention."

The researchers led by Dr. Pestell, created a mouse model that lacked SIRT1 and noticed that these mice were more likely to develop an early form of prostate cancer called prostatic intraepithelial neoplasia (PIN).

Other researchers had shown that SIRT1 can defend the cell against damage from free radicals. Pestell's group took the work further by showing that in this prostate cancer model, free radicals built up in cells lacking SIRT1. They showed that normally, SIRT1 proteins help activate a mitochondrial protein called SOD2, in turn activating those proteins to keep free-radical levels in check. When SIRT1 level are diminished, SOD2 is no longer effective at removing free radicals, allowing a dangerous build up in the cells, and leading to PIN.

"The next step," says first author Gabriele DiSante, Ph.D., a postdoctoral fellow in the department of Cell Biology at Jefferson, "is to determine if this is also important in the development of human prostate cancer."

This work was supported in part by awards from the National Institutes of Health R01CA70896, R01CA75503 and R01CA86072. Work conducted at the Sidney Kimmel Cancer Center was supported by the NIH Cancer Center Core grant P30CA56036. This project was partially supported by the China Scholarship Council. This project is funded in part by the Pennsylvania Department of Health grant. The Department specifically disclaims responsibility for any analyses, interpretations or conclusions.

Story Source:

The above story is based on materials provided by Thomas Jefferson University. Note: Materials may be edited for content and length.

Journal Reference:

1  Gabriele Di Sante, Timothy G. Pestell, Mathew C. Casimiro, Sara Bisetto, Michael J. Powell, Michael P. Lisanti, Carlos Cordon-Cardo, Mireia Castillo-Martin, Dennis M. Bonal, Valentina Debattisti, Ke Chen, Liping Wang, Xiaohong He, Michael W. McBurney, Richard G. Pestell. Loss of Sirt1 Promotes Prostatic Intraepithelial Neoplasia, Reduces Mitophagy, and Delays Park2 Translocation to Mitochondria. The American Journal of Pathology, 2015; 185 (1): 266 DOI: 10.1016/j.ajpath.2014.09.014

Cite This Page:

•   MLA
APA
Chicago

Thomas Jefferson University. "How does prostate cancer form? Parkinson's Link?." ScienceDaily. ScienceDaily, 18 December 2014. <www.sciencedaily.com/releases/2014/12/141218080827.htm>.

Evidence That Natural Toxin is Responsible for Triggering Parkinson’s

Researchers have found evidence that a toxin produced by the brain is responsible for the series of cellular events that lead to Parkinson’s disease. The study found that the brain toxin DOPAL plays a key role in killing the dopamine neurons which trigger the illness.In earlier research, investigators found that DOPAL seemed to be responsible for killing healthy dopamine cells, which in turn causes Parkinson disease to develop. Now, research in an animal model gives them further reason to suspect the chemical as the culprit.Parkinson’s disease is a debilitating neurodegenerative movement disorder, affecting 2 percent of individuals older than age 65 and 4 to 5 percent older than 85 years. The disorder is due to a loss of dopamine neurons and is characterized by bradykinesia and tremors while at rest.

Investigators found that DOPAL, a breakdown product of dopamine, killed healthy dopamine cells in an animal model of Parkinson’s disease, giving them evidence to suspect that DOPAL is the culprit.

Dopamine, a vital chemical that allows for coordinated function of neurons controlling the body’s muscles and movements, is produced by nerve cells in the substantia nigra. When 80 percent of these cells die or become damaged, symptoms of Parkinson’s disease begin to appear, including tremors, slowness of movement, rigidity and stiffness, and difficulty with balance.

Lead researcher W. Michael Panneton says the research offers a big step forward in the understanding of Parkinson disease.

“In Parkinson disease, we knew that the death of dopamine cells is responsible for patients’ symptoms,” said Panneton. “But no one knew why the cells are dying.”

From a cellular perspective, doctors know some pieces of the puzzle. They know that Parkinson patients have a loss of dopamine neurons in a part of the brain called the substantia nigra, leading to severe dopamine loss in another part of the brain called the striatum, and the aggregation of a protein called alpha-synuclein.

Alpha-synuclein is found throughout the brain. In some people, the protein clumps together. Researchers found that it is DOPAL that causes alpha-synuclein protein in the brain to aggregate. This induces further increases of DOPAL leading to the death of the dopamine-producing cells, which in turn causes Parkinson’s symptoms to develop.

Currently, the main approach to Parkinson’s disease is to treat symptoms by replacing dopamine that’s lost when the cells die. This approach however does not prevent the loss of dopamine neurons causing Parkinson’s disease.

This new research opens up promising new research avenues to prevent dopamine neuron loss and the progression of Parkinson’s disease.

References:
1. W. Michael Panneton, et al. The Neurotoxicity of DOPAL: Behavioral and Stereological Evidence for Its Role in Parkinson Disease Pathogenesis. PLoS ONE, 2010; 5 (12): e15251 DOI: 10.1371/journal.pone.0015251

http://www.ahealthblog.com/evidence-that-natural-toxin-is-responsible-for-triggering-parkinsons.html

Team Develops ‘Cool’ New Method for Probing How Molecules Fold

The Scripps Research Institute’s Associate Professor Ashok Deniz (left) and Research Associate Priya Banerjee are among the authors of the new paper.LA JOLLA, CA—December 18, 2014—Collaborating scientists from The Scripps Research Institute (TSRI) and the University of California (UC) San Diego have developed a powerful new system for studying how proteins and other biological molecules form and lose their natural folded structures.

Using the new system, researchers can force a sample of molecules to unfold and refold by boosting and then dropping the temperature, so quickly that even some of the fastest molecular folding events can be tracked.

“One way of studying these structures has been to make them unfold or fold using heat, and to observe the kinetics and other properties of those unfolding and folding events,” said TSRI Associate Professor Ashok A. Deniz. “The new system allows us to do this in a way that overcomes some key limitations of previous methods.”

The invention can be applied to the study not only of normal biomolecules but also many abnormal, misfolding ones that have been implicated in human diseases.

The findings of Deniz’s laboratory and the laboratory of a close collaborator, biophysicist Alex Groisman at UC San Diego, are reported in Nature Communications this week.

Too Small, Too Fast

Studying how proteins, DNA and other biological molecules fold is one of the most challenging areas of biology, in particular because these tiny molecules—tinier than the wavelengths of visible light—can fold or unfold in intervals as short as a few millionths of a second (microseconds).

Researchers in this field have come up with some powerful innovations in the past decade or so, including the use of exotic quantum optical phenomena to track fast molecular motions. But techniques for perturbing folded molecules with sudden temperature changes have lagged. “The size of temperature jumps has been limited to about 15 degrees Celsius, and we’ve lacked a way to cool samples quickly back to room temperature,” said Deniz.

In the new study, the Deniz and Groisman laboratories teamed up to develop a device that overcomes both limitations. Their microfluidic device, like others that have been developed in this field, is a small block of silicone fabricated with tiny channels through which a biomolecule-containing solution can flow. In this case, the observation channel is less than a millionth of a meter deep, is lined with sapphire for conducting heat away quickly, and also contains a thin gold plating for effectively absorbing power of an infrared laser beam and converting it into heat.

The combination of the small heating volume and the energy-absorbing gold plating means that the laser can heat a sample of molecules very rapidly, with a temperature jump of more than 50 degrees Celsius in less than a microsecond. The heat-conducting sapphire substrate in turn allows the sample to cool down by several tens of degrees, again within about a microsecond, as soon as the laser is switched off.

Novel Demonstrations

As a simple proof of the new device’s utility, the researchers used it to heat and cool a solution of a short DNA strand that naturally forms a hairpin-shaped loop. Hairpin DNA are dynamic structures that play key roles in cellular replication and other important biological processes.

The experiment, which included fluorescence techniques for detecting folded versus unfolded states of the DNA strand, revealed that the hairpin fold can form in just a few microseconds. “We could not have observed such a rapid folding with previous temperature-jump systems, which typically take thousands of microseconds to cool molecules,” said Priya R. Banerjee, a research associate in Deniz’s laboratory who was a first author of the report with Mark E. Polinkovsky of Groisman’s laboratory, and Yann Gambin, also a member of Deniz’s laboratory during the study. In addition, the scientists used the new setup to study a larger DNA hairpin, together confirming previously predicted behavior about the differential effect of sodium chloride—ordinary salt—on the folding and unfolding kinetics of different sized hairpins.

In a final demonstration of the novel capabilities of their new setup, the scientists were able to probe how the molecular system behaved as a low-pass filter, in some ways similar to ones in electronics or cellular circuits. The team used the ability to switch the heating laser on and off rapidly, combined with the rapid heating and cooling features of the new system, enabling new kinds of studies of molecular folding landscapes. Essentially, researchers can now subject a solution of molecules to a continuous series of heating and cooling cycles, altering the frequency and temperature range of this heating/cooling oscillation at will and observing how the molecules’ unfolding/refolding dynamics change.   

“We anticipate that this type of experiment will allow us to detect more complex or hidden features of biomolecule structural landscapes that haven’t been seen before,” said Deniz.

Deniz and his colleagues now plan to use their new system to study the folding dynamics of other molecules, including misfolding-prone proteins that can cause common human illnesses such as Alzheimer’s, Parkinson’s and Huntington’s disease.

In addition to Deniz, Groisman, Banerjee, Gambin and Polinkovsky, Michael J. Erickstad of UC San Diego was an author of the study, “Ultrafast Cooling Reveals Microsecond-Scale Biomolecular Dynamics” (doi: 10.1038/ncomm6737). For more information, see http://www.nature.com/ncomms/2014/141217/ncomms6737/full/ncomms6737.html

Support for the research was provided by the National Science Foundation (MCB 1121959 and PHY 0750049).

About The Scripps Research Institute

The Scripps Research Institute (TSRI) is one of the world's largest independent, not-for-profit organizations focusing on research in the biomedical sciences. TSRI is internationally recognized for its contributions to science and health, including its role in laying the foundation for new treatments for cancer, rheumatoid arthritis, hemophilia, and other diseases. An institution that evolved from the Scripps Metabolic Clinic founded by philanthropist Ellen Browning Scripps in 1924, the institute now employs about 3,000 people on its campuses in La Jolla, CA, and Jupiter, FL, where its renowned scientists—including two Nobel laureates—work toward their next discoveries. The institute's graduate program, which awards PhD degrees in biology and chemistry, ranks among the top ten of its kind in the nation. For more information, see www.scripps.edu.

The Hotel Dieu Shaver's rehabilitation centre for Parkinson's disease

The Hotel Dieu Shaver's rehabilitation centre for Parkinson's disease has 130 thousand reasons to smile

Posted on December 18, 2014 by 610 CKTB News

The Hotel Dieu Shaver's rehabilitation centre for Parkinson's disease has 130 thousand reasons to smile this morning.

St. Catharines MP Rick Dykstra was joined by the United Way of St. Catharines and District at a media conference Wednesday to give the Steve Ludzik Centre $50 thousand dollars of the more than $180 thousand raised from the annual Hockey Night in St. Catharines game.

The rest of the money raised through the game was directed to the United Way.

Ludzik, who suffers from Parkinson's, and former NHLer Rick Vaive presented the centre with another $85 thousand dollars raised during Ludzik' golf tournament and roast events that are held in conjunction with the annual hockey game.

The Steve Ludzik Centre is located at the Shaver facility by Brock University and is funded through private donations and provides a six week program that tries to improve the how Parkinson's patients move physically.

According to a Shaver press release, the centre “assists clients to identify goals related to improving depression and/or anxiety, strengthening their voice, improving bowel and bladder control and increase their knowledge of Parkinson’s disease.

http://www.610cktb.com/news/2014/12/18/the-hotel-dieu-shavers-rehabilitation-centre-for-parkinsons-disease-has-130-thousand-reasons-to-smile