Were pesticides to blame for the death of Knut, the polar bear?

Many thousands of people mourn the sudden death of Knut, the polar bear. He was the darling at a German zoo. Why did Knut die? Initial autopsy results showed that Knut, the polar bear, suffered from a brain disease. A former animal keeper at a zoo reported the death of gorilla babies dying from pesticide use. The keeper herself fell ill and nearly died. Were pesticides the cause of death of the polar bear, Knut? Recent scientific research has shown that pesticides cause different brain diseases. What caused Knut’s brain disease will require further investigation. It is possible, because pesticides are used regularly in zoos to keep the zoo animals free of vermin.

All mourn the loss of Knut, the polar bear

In the media, on Twitter and Facebook, the death of Knut, the polar bear , remains the main topic for days now. The sweet polar bear was raised by a nurse with a bottle in the German zoo after his mother abandoned him. The little polar bear in no time, won the hearts of all the visitors. Now the sadness is great, and the cause of Knut’s brain disease is still under investigation. Zoo visitors witnessed the polar bear turning itself around several times and falling into the pond. Over 500 people observed the death of this polar bear and reported that he had an epileptic-like seizure before he sank into the water in his polar bear enclosure. Knut’s keeper also died suddenly at the age of 44 from a heart attack in 2008.

Dream job, but health went downhill

The young woman worked in one of the biggest zoos in Germany. She loved her job as a veterinary nurse above everything. She was responsible for the gorillas. With the bottle, she helped gorilla babies grow when needed. Most of all, she never wanted to go home after work because she loved her job so much. During her training, her health was deteriorating. The reason for her health decline was first discovered years later. Several radiological studies including SPECT, CT, and MRT scans of her brain showed severe brain damage and atrophy. Pesticides were the reason the keeper’s health went downhill.

Gorilla babies dead due to the use of pesticides

During training, the young keeper had to deal with pesticides during the spraying of the gorilla’s sleeping quarters. The pesticide nerve agents, pyrethroids and organophosphates were used. The young woman had to spray the sleeping caves. As she kneeled in front of the caves, she couldn’t avoid breathing in the poison. “The gorilla babies died, and now I know it was because they were exposed to the pesticides,” she told me several years ago when we met at a special clinic. Her immune and nervous system were severely damaged, and she had problems with her muscles and her heart was weakening. Her hair was falling out and she had the typical nerve agent seizures. She stated, “I initiated a workers’ compensation lawsuit and won.” There was no question that the health of the animal keeper was destroyed by pesticides.

Knut died from pesticide exposure?

We do not know exactly which brain disease Knut, the public’s favorite animal in the Berlin Zoo, suffered from, but further studies will hopefully determine the nature and cause of his brain disease. Pesticides may well be on the short list, because they are regularly used in zoos to keep the zoo animals free of fleas and other parasites. Certain herbicides, which are often used on pavements and along roadsides in zoos in order to be kept free of weeds, are quite capable of causing life-threatening seizures.

Author: Silvia K. Müller, CSN – Chemical Sensitivity Network, March 21, 2011

Translation: Thanks to Christi Howarth.

Related articles:

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• Pesticide Exposure linked to sucidial Thoughts
• Common Household Pesticides linked to Childhood Cancer Cases in Washington Area

International Appeal from Wuerzburg

The European Academy for Environmental Medicine (EUROPAEM) invited many renowned national and international scientists and health care professionals to a medical conference held in Wuerzburg, Germany from April 23 to April 25, 2010. These professionals were from the fields of environmental medicine, toxicology, immunology, neurology and genetics and other health fields as well as physicians and dentist. Also in attendance were representatives of patient initiatives. The theme of this international medical conference was Science Meets Practice. It dealt specifically with the issues of Neuro- Endocrine- Immunology and their importance in environmental medicine.

Greatly concerned, participants noted the increasing prevalence of chronic multisystem illnesses such as multiple chemical sensitivity (MCS), chronic fatigue syndrome (CSF), fibromyalgia (FMS) as well as cardiovascular diseases, metabolic syndrome, neurodegenerative diseases, auto immune diseases, and cancer.

At the conference it was impressively demonstrated that these chronic diseases are based on similar pathological mechanisms. Common mechanisms are chronic inflammatory processes influenced by environmental factors including chemical pollutants, biological infectious agents, and electromagnetic field (EMF) triggers.

Chronic diseases mean long-term patients and such patients require consecutive higher medical costs. This often leads to social exclusion of the affected people. Facing the appalling reports of Europe´s growing financial constraints, especially in public health, a further increase of chronic illnesses will accelerate the ongoing collapse of the National Health Service and medical insurance companies in Europe. Remedy is only possible with a change of priorities from today´s unilaterally symptomatic oriented medicine to causally oriented medicine focusing on cost-effective primary prevention.

Conference participants addressed an urgent appeal to the European environment and health ministers, to the European Commission, the European parliamentarians, national governments and to the directors of social and private insurance companies. They urge them to take these findings and developments into serious consideration, stressing and weighting financial investments primarily in prevention, precaution and best early detection and diagnosis of these chronic and environmentally related illnesses.

All over Europe this requires the full awareness of these research findings of the practicing physicians of environmental medicine and their integration into university research and teaching. The European governments are asked to finally implement the already ratified decisions of the Fourth Ministerial Conference on Environment and Health Ministers held in Budapest in 2004.

This appeal was unanimously adopted by the congress.

Wuerzburg April 25, 2010

For the board of EUROPAEM,

Jean Huss, Vice-Chairman

Dr. Kurt Mueller, Chairman

Dr. Peter Ohnsorge, Managing Chairman

Dr. Hans-Peter Donate, Press, Responsible

• German Version – International Appeal from Wuerzburg
• Japanese Version – International Appeal from Wuerzburg / Thanks to Takeshi for translation.

Yale scientists show how bisphenol A induces epigenetic changes in pregnant mice that cause hormonal imbalance in the later life of female progeny

Here’s more evidence that “safe” plastics are not as safe as once presumed: New research published online in The FASEB Journal suggests that exposure to Bisphenol A (BPA) during pregnancy leads to epigenetic changes that may cause permanent reproduction problems for female offspring. BPA, a common component of plastics used to contain food, is a type of estrogen that is ubiquitous in the environment.

“Exposure to BPA may be harmful during pregnancy; this exposure may permanently affect the fetus,” said Hugh S. Taylor, Ph.D., co-author of the study from Yale University School of Medicine in New Haven, Connecticut. “We need to better identify the effects of environmental contaminants on not just crude measures such as birth defects, but also their effect in causing more subtle developmental errors.”

Taylor and colleagues made this discovery by exposing fetal mice to BPA during pregnancy and examining gene expression and DNA in the uteruses of female fetuses. Results showed that BPA exposure permanently affected the uterus by decreasing regulation of gene expression. These epigenetic changes caused the mice to over-respond to estrogen throughout adulthood, long after the BPA exposure. This suggests that early exposure to BPA genetically “programmed” the uterus to be hyper-responsive to estrogen. Extreme estrogen sensitivity can lead to fertility problems, advanced puberty, altered mammary development and reproductive function, as well as a variety of hormone-related cancers. BPA has been widely used in plastics and other materials. Examples include use in water bottles, baby bottles, epoxy resins used to coat food cans, and dental sealants.

“The BPA baby bottle scare may be only the tip of the iceberg.” said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. “Remember how diethylstilbestrol (DES) caused birth defects and cancers in young women whose mothers were given such hormones during pregnancy. We’d better watch out for BPA, which seems to carry similar epigenetic risks across the generations. ”

Author: FASEB* – Federation of American Societies for Experimental Biology, Why BPA leached from ‘safe’ plastics may damage health of female offspring, 25-Feb-2010.

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* FASEB comprises 23 societies with more than 90,000 members, making it the largest coalition of biomedical research associations in the United States

Male reproductive disorders that are of interest from an environmental point of view include sexual dysfunction, infertility, cryptorchidism, hypospadias and testicular cancer.

Several reports suggest declining sperm counts and increase of these reproductive disorders in some areas during some time periods past 50 years. Except for testicular cancer this evidence is circumstantial and needs cautious interpretation. However, the male germ line is one of the most sensitive tissues to the damaging effects of ionizing radiation, radiant heat and a number of known toxicants.

So far occupational hazards are the best documented risk factors for impaired male reproductive function and include physical exposures (radiant heat, ionizing radiation, high frequency electromagnetic radiation), chemical exposures (some solvents as carbon disulfide and ethylene glycol ethers, some pesticides as dibromochloropropane, ethylendibromide and DDT/DDE, some heavy metals as inorganic lead and mercury) and work processes such as metal welding. Improved working conditions in affluent countries have dramatically decreased known hazardous workplace exposures, but millions of workers in less affluent countries are at risk from reproductive toxicants. New data show that environmental low-level exposure to biopersistent pollutants in the diet may pose a risk to people in all parts of the world.

For other noxicants the evidence is only suggestive and further evaluation is needed before conclusions can be drawn. Whether compounds as phthalates, bisphenol A and boron that are present in a large number of industrial and consumer products entails a risk remains to be established. The same applies to psychosocial stressors and use of mobile phones.

Finally, there are data indicating a particular vulnerability of the fetal testis to toxicants – for instance maternal tobacco smoking. Time has come where male reproductive toxicity should be addressed form entirely new angles including exposures very early in life.

Literatur:
Bonde JP., Male reproductive organs are at risk from environmental hazards, Department of Occupational and Environmental Medicine, Bispebjerg University Hospital, Copenhagen, Denmark, Asian J Androl. 2009 Dec 7.

Press release of the German Professional Association of Environmental Medicine (Deutscher Berufsverband der Umweltmediziner – DBU)

from 26. October 2009

Swine flu vaccine is unsuitable for patients with environmental diseases and other chronic multi-system illnesses.  Pandemrix® poses substantial health risk with respect to mass immunization programs due to the lack of proof of safety.  Because of the producer’s release from liability by the German Federal Government (BRD), the risk of adverse reactions and/or permanent damage due to the vaccine rests with the patient.

The German Professional Association of Environmental Medicine (DBU) has, in spite of press releases from the BRD, the Paul-Ehrlich-Institute, as well as the vaccine producer’s assurances of safety, serious concerns relating to Pandemrix® (GlaxoSmithKline), the only vaccine which has been approved for mass vaccination by the BRD.

The DBU discusses at this point neither the medical use of immunization in general nor the necessity of such measures in the, up until now, mild course of the swine flu pandemic.

Our criticism is directed only against the pandemic vaccine Pandemrix®.

• There exists considerable doubt as to the effectiveness of the vaccine: during the licensing phase, the vaccine tested had a 40% higher portion of virus antigen (5. 25µg) than the vaccine (3.75µg) now being delivered. An unequivocal consensus has not been reached as to whether the vaccination should be given once or twice a season !!!

• There exists considerable doubt concerning the safety of the adjuvanted active amplifier since it is being used for the first time. The vaccine contains 27.4mg AS03, an emulsion of polysorbate, squalene and tocopherol. Sufficient studies are lacking, because in the test phase, only the development of antibody titers was determined as a surrogate criterion, and not any potential adverse reactions.

• The producer as well as government agencies have concealed the fact that squalene, if used subcutaneously or intramuscularly is an inflammatory immune activation immunogen, unlike when ingested. (Squalene is, among other things, for example, naturally contained in olive oil.)

• Autoimmune diseases can be provoked by squalene; already existing ones can be activated. Squalene has been connected with the emergence of Guillan-Barré Syndrome (GBS) and is now considered a trigger for Gulf War Syndrome (GWS). In animal studies squalene brought on rheumatoid arthritis.

• Squalene from food sources is mainly incorporated into membranes in the body. The production of squaline antibodies resulting from an immunization sets off chronic inflammation of the membranes, which explains diseases such as Gulf War Syndrome and also degenerative neurological diseases such as Multiple Sclerosis, Amyotrophic Lateral Sclerosis, Chronic Inflammatory Demyelinating Polyneuropathy and Guillan-Barré Syndrome.

• The delivery of vaccine in multiple dose ampules is obsolete. In single dose ampules the mercury used for preservation, as in thimerosal – which is included in Pandemrix – would be unnecessary.  Also, mercury has been proven to set off autoimmune diseases.

• Since the vaccine has not been tested on either young children or pregnant women (Ethics Commission objection), the call to give preference in the first phase of vaccination to precisely this particularly endangered segment of the population represents an improper and totally unjustifiable field test.

• The vaccine poses a higher risk than the swine flu itself for patients with environmental illness and for patients with compromised immune systems (e.g. AIDS).

• The vaccine producer GlaxoSmithKline (GSK), according to the contract with the BRD, is largely exempt from liability. In case of damage from the vaccination, the affected vaccinee would have to sue the government and therefore the country of Germany, usually a futile exercise.

• To avoid the trap of liability, the doctor giving the vaccination must meticulously inform the patient of all risks concerning the vaccination and the vaccine. It is recommended to give this information in the presence of an assistant and to have it be confirmed by the patient’s signature. The explanation should also include the liability features. Also the indication that other, lower risk vaccines are available in Europe and that due to a faulty decision by the German government, they are currently not available to the German population. This information should definitely be included in the explanation.

For general and environmental health considerations the DBU urgently advises against carrying out a vaccination with Pandemrix® !

Dr.med. Hans-Peter Donate

for the board of the German Professional Association of Environmental Medicine (DBU)

Translation: CSN – Chemical Sensitivity Network

Lead is a ubiquitous environmental toxin that is capable of causing numerous acute and chronic circulatory, neurological, hematological, gastrointestinal, reproductive and immunological pathologies.  

The mechanism of lead induced toxity is not fully understood. The prime targets to lead toxicity are the heme synthesis enzymes, thiol-containing antioxidants and enzymes (superoxide dismutase, catalase, glutathione peroxidase, glucose 6-phosphate dehydrogenase and antioxidant molecules like GSH). The low blood lead levels are sufficient to inhibit the activity of these enzymes and induce generation of reactive oxygen species and intensification oxidative stress.  

Oxidative stress plays important role in pathogenesis of lead-induced toxity and pathogenesis of coupled disease. The primary target of lead toxicity is the central nervous system. There are different cellular, intracellular and molecular mechanisms of lead neurotoxicity: such as induction of oxidative stress, intensification of apoptosis of neurocites, interfering with Ca(2+) dependent enzyme like nitric oxide synthase.  

Population studies have demonstrated a link between lead exposure and subsequent development of hypertension and cardiovascular disease. The vascular endothelium is now regarded as the main target organ for the toxic effect of lead. Lead affects the vasoactive function of endothelium through the increased production of reactive oxygen species, inactivation of endogenous nitric oxide and downregulation of soluble guanylate cyclase by reactive oxygen species, leading to a limiting nitric oxide availability, impairing nitric oxide signaling.  

This review summarizes recent findings of the mechanism of the lead-induced toxity and possibilities of its prevention. 

Reference:  Nemsadze K, Sanikidze T, Ratiani L, Gabunia L, Sharashenidze T., Mechanisms of lead-induced poisoning, Tbilisi State Medical University; National Center of child development, Georgian Med News. 2009 Jul-Aug;(172-173):92-6.

The authors investigated the association of early-life exposure to indoor air pollution with neuropsychological development in preschoolers and assessed whether this association differs by glutathione-S-transferase gene (GSTP1) polymorphisms. A prospective, population-based birth cohort was set up in Menorca, Spain, in 1997-1999 (n = 482).

Children were assessed for cognitive functioning (McCarthy Scales of Children’s Abilities) and attention-hyperactivity behaviors (Diagnostic and Statistical Manual of Mental Disorders, 4th Edition) at age 4 years.

During the first 3 months of life, information about gas appliances at home and indoor nitrogen dioxide concentration was collected at each participant’s home (n = 398, 83%). Genotyping was conducted for the GSTP1 coding variant Ile105Val. Use of gas appliances was inversely associated with cognitive outcomes (beta coefficient for general cognition = -5.10, 95% confidence interval (CI): -9.92, -0.28; odds ratio for inattention symptoms = 3.59, 95% CI: 1.14, 11.33), independent of social class and other confounders.

Nitrogen dioxide concentrations were associated with cognitive function (a decrease of 0.27 point per 1 ppb, 95% CI: -0.48, -0.07) and inattention symptoms (odds ratio = 1.06, 95% CI: 1.01, 1.12).

The deleterious effect of indoor pollution from gas appliances on neuropsychological outcomes was stronger in children with the GSTP1 Val-105 allele. Early-life exposure to air pollution from indoor gas appliances may be negatively associated with neuropsychological development through the first 4 years of life, particularly among genetically susceptible children.

Reference: Morales E, Julvez J, Torrent M, de Cid R, Guxens M, Bustamante M, Künzli N, Sunyer J., Association of early-life exposure to household gas appliances and indoor nitrogen dioxide with cognition and attention behavior in preschoolers, Center for Research in Environmental Epidemiology, Barcelona, Catalonia, Spain, Am J Epidemiol. 2009 Jun 1;169(11):1327-36.

PET scans critical for early, accurate diagnosis and treatment of dementia, say researchers at SNM’s 56th Annual Meeting  

TORONTO—A new study shows that the use of positron emission tomography (PET) scans may improve the accuracy of dementia diagnoses early in disease onset for more than one out of four patients. The results were presented at SNM’s 56th Annual Meeting.  

Early, accurate diagnosis of dementia is critical for providing the best available courses of treatment and therapies in the beginning stages of disease, when treatments can be most effective. PET scans enable physicians to identify the neurological conditions underlying each patient’s mental decline and choose appropriate courses of treatment.

 “Routine clinical assessments do not accurately identify the root causes of dementia in the early stages,” said Kirk A. Frey, a physician with the University of Michigan Hospitals’ Division of Nuclear Medicine and lead author of the study. “Our preliminary results clearly indicate that molecular imaging technologies, such as PET scans, can help diagnose a patient’s specific type of dementia. This is critical for providing the best possible care. Additionally, PET’s ability to pinpoint neurological underpinnings of different forms of dementia could lead to new, more targeted drugs and therapies.”

More than 5 million people each year are newly diagnosed with dementia, a disease that takes many forms and includes memory loss or other mental impairments that interfere with daily life. The most common type of dementia is Alzheimer’s disease. Other types include frontotemporal dementia, which affects the frontal and temporal lobes of the brain, and Lewy body dementia, which involves degeneration of dopamine nerves in addition to the temporal and parietal lobes. Although these types of dementia have different causes, patients can express similar symptoms in the early stages, making accurate diagnosis difficult. Providing appropriate treatments and therapies as early as possible can avoid unnecessary, and sometimes severe, side-effects and complications.  

The new study identified 66 patients with mild dementia or mild cognitive impairment who were evaluated through standard neurological testing and anatomic brain imaging. Three clinical experts reviewed the results of these data to make diagnoses of either Alzheimer’s disease, frontotemporal dementia or dementia with Lewy bodies. Patients then underwent PET scans for amyloid deposits and for dopamine nerve integrity. Patients’ initial diagnoses changed more than 25 percent of the time after PET imaging. PET scans provided images of important signals for disease that other examinations missed, such as deposits of amyloid plaque, which are a common indicator of Alzheimer’s disease, and damage to dopamine nerves in Lewy body dementia.  

The study will track patients for two years to confirm the accuracy of their diagnoses. 

Reference:

Scientific Paper 251: K. Frey, J. Burke, B. Giodani, R. Koeppe, R. Albin, The University of Michigan, Ann Arbor, MI; “PET neurochemical vs. clinical phenotypes in mild-early dementia,” SNM’s 56th Annual Meeting, June 13-17, 2009.

SNM – Society of Nuclear Medicine, PET Scans May Improve Accuracy of Dementia Diagnosis, June 10, 2009

About SNM – Advancing Molecular Imaging and Therapy

SNM is an international scientific and medical organization dedicated to raising public awareness about what molecular imaging is and how it can help provide patients with the best health care possible. SNM members specialize in molecular imaging, a vital element of today’s medical practice that adds an additional dimension to diagnosis, changing the way common and devastating diseases are understood and treated.  

SNM’s more than 17,000 members set the standard for molecular imaging and nuclear medicine practice by creating guidelines, sharing information through journals and meetings and leading advocacy on key issues that affect molecular imaging and therapy research and practice. For more information, visit www.snm.org.

Paris, France – June 04, 2009 – The cause of Parkinson’s disease (PD), the second most frequent neurodegenerative disease after Alzheimer’s disease, is unknown, but in most cases it is believed to involve a combination of environmental risk factors and genetic susceptibility. Laboratory studies in rats have shown that injecting the insecticide rotenone leads to an animal model of PD and several epidemiological studies have shown an association between pesticides and PD, but most have not identified specific pesticides or studied the amount of exposure relating to the association.  

A new epidemiological study involving the exposure of French farm workers to pesticides found that professional exposure is associated with PD, especially for organochlorine insecticides. The study is published in Annals of Neurology, the official journal of the American Neurological Association.  

Led by Alexis Elbaz M.D., Ph.D., of Inserm, the national French institute for health research in Paris, and University Pierre et Marie Curie (UPMC, Paris 6), the study involved individuals affiliated with the French health insurance organization for agricultural workers who were frequently exposed to pesticides in the course of their work. Occupational health physicians constructed a detailed lifetime exposure history to pesticides by interviewing participants, visiting farms, and collecting a large amount of data on pesticide exposure. These included farm size, type of crops, animal breeding, which pesticides were used, time period of use, frequency and duration of exposure per year, and spraying method. 

The study found that PD patients had been exposed to pesticides through their work more frequently and for a greater number of years/hours than those without PD. Among the three main classes of pesticides (insecticides, herbicides, fungicides), researchers found the largest difference for insecticides: men who had used insecticides had a two-fold increase in the risk of PD. 

“Our findings support the hypothesis that environmental risk factors such as professional pesticide exposure may lead to neurodegeneration,” notes Dr. Elbaz.  

The study highlights the need to educate workers applying pesticides as to how these products should be used and the importance of promoting and encouraging the use of protective devices. In addition to the significance of the study for those with a high level of exposure to pesticides, it also raises the question about the role of lower-level environmental exposure through air, water and food, and additional studies are needed to address this question.  

Reference: Alexis Elbaz, Jacqueline Clavel, Paul J. Rathouz, PhD 6, Frédéric Moisan Jean-Philippe Galanaud, Bernard Delemotte, Annick Alpérovitch, Christophe Tzourio, Professional exposure to pesticides and Parkinson’s disease, Annals of Neurology, Press Release Wiley Blackwell, June 4, 2009