Ban on 'Endosulfan' aimed at destroying India's exports
12/22/2010
22.12.2010 (UNI) The insecticide industry was up in arms against banning of Endosulfan, an input used in agriculture production, saying the European Union (EU) lobby wanted its elimination to destroy 70 per cent of the world exports of the product from India.
The industry was of the view that arguments put forward by an international committee for imposing the ban was not based on scientific evidence, but by the brute display of voting power by the members.
The manufacturers, who came under one umbrella, dared the committee to bring forth scientific data, justifying its proposed ban.
They said that they would be willing to swallow the bullet if it was proved on the basis of emperical evidence that it causes dreaded diseases like cancer.
At a joint press conference, representatives of Pesticides Manufacturers and Formulators Association of India (PMFAI), Endosulfan Manufacturers and Formulators Association (EMFA) and International Stewardship Centre (ISC), argued that the EU has alternate products which it can bring into use as an insecticide, but India will be at complete loss if the ban is effected.
Talking to reporters, ISC chairman R Hariharan said on the basis of submissions made by EU, the Chemical Review Committee of Persistent Organic Pollutant had recommended Endosulfan for listing as a (POP) which is based on voting, rather than on scientific data.
Several countries, including India and China have strongly opposed the decision which has been taken by voting, and favoured decision making by consensus.
Though the Stockholm Convention is yet to take a final decision on the recommendation on Endosulfan in April 2011, Mr Hariharan said a number of countries announced a ban or a phase out of the product over a 3 to 5 year period.
'Based on these recommendations, over 60 countries have joined the EU call for a ban on Endosulfan,' the chairman said.
The 60 countries include 27 EU member states and 21 countries in Africa.
Strangely none of the independent regulatory actions in many of these countries have been based on incidences of adverse human health in any of these countries, he said.
He said the EU manufacturers, which hold nearly 60 per cent of world's exports of chemicals, intends to maintain its control over chemicals which are the second largest traded merchandise in the world, next only to fuels.
India's share in the global Endosulfan market is over 70 per cent, Mr Hariharan said.
The European manufacturers, whose exports share of Endosulfan is declining, have decided to stop selling the product by the end of this year.
Speaking on the occasion, PMFAI president Pradip Dave said thousands of farmers using Endosulfan have not had any issues relating to human health.
Currently, the Indian market of Endosulfan is about 12 million litres annually valued at Rs 270 crore.
In India, there are three manufacturers of Endosulfan, including Hindustan Insecticides Ltd.
At present, the overall Indian agrochemical market stands at Rs 5,200 crore and Endosulfan Rs 300 crore. UNI
Thursday, December 23, 2010
Tuesday, December 14, 2010
U.S.-backed pesticide spraying in Guatemala draws fire.
U.S.-backed pesticide spraying in Guatemala draws fire
By MATTHEW CREELMAN, SHNS contributing correspondent
international
GUATEMALA CITY - For most of three decades, the U.S. has financed massive aerial spraying of pesticides over a large part of Guatemala in an attempt to eradicate the Mediterranean fruit fly, but common precautions to limit exposure to the toxic chemicals are not being followed.
In the 1980s and 1990s, malathion was sprayed from aircraft over thousands of acres of Guatemala's forests and farmlands. More recently the U.S.-financed program has been spraying Spinosad GF 120 Naturalyte Fruit Fly Bait, produced by Dow Agrosciences.
According to Guatemalan government data, the U.S.-backed program has applied more than 6 million liters of GF-120 since 2002, equivalent to more than 5,000 tons of this pesticide-bait.
Dow scientists say that Spinosad is highly toxic to beneficial insects and aquatic species, and that precautions should be taken to avoid daytime spraying and avoid bodies of water.
However, in Guatemala, spraying occurs during the day and over water. In contrast, in California, which is also waging an ongoing battle with medflies, the use of Spinosad sprays to control the pests is carefully regulated, and residents and farm workers are warned prior to spraying to keep out of sprayed zones for at least four hours.
This is not the case in Guatemala.
The U.S. has spent $266 million on the fruit-fly eradication program since 1976. The original purpose of the program was to create a barrier that would keep the Medfly from "migrating" to California fruit farms about 2,200 miles away.
But the characterization of the medfly as a destructive "illegal alien" is challenged by Dr. James Carey, an entomologist with the University of California, Berkeley, who has concluded from DNA tests that the medfly is a permanent resident of California, detected in 167 municipalities --one third of the state -- since 1975.
Carey is recognized as a pre-eminent expert on the medfly, who served
on the California Department of Food and Agriculture´s Medfly
Scientific Advisory Panel from 1987 to 1994.
Campesinos, beekeepers, environmentalists, coffee growers and others who work the land and study it have opposed the program for years.
Israel Gramajo, the mayor of San Antonio, Suchitepequez, in southern Guatemala, is currently leading an effort to remove a Mosca Del Mediterraneo (or MOSCAMED) quarantine post from his town and prohibit aerial spraying. The medfly larvae develop in fruit such as coffee berries, oranges and mangos. The quarantine posts are set up on highways to keep potentially contaminated fruit from entering into
regions considered free of the medfly. Ironically, the quarantine in San Antonio has been designed to keep contaminated fruit from entering a region already infested by the fruit fly.
Guatemala is the only Central American country using massive aerial spraying of pesticides to control the medfly. According to medfly program protocol, the plane sprays up to seven times each area treated, for a total of 500 droplets per 10 square feet.
According to a 2009 medfly report by a Mexican scientist working with
the MOSCAMED Program, 1,650 square miles were infested with the Medfly
in Guatemala, and another 5,600 square miles were subject to
"suppression".
Guatemalans complain of damages to their crops, along with allergic reactions and conjunctivitis. MOSCAMED authorities deny the charges and say they provide important support to beekeepers, along with baking classes and medical campaigns in towns where the program is active.
When scientific studies in the 1980s and 1990s began raising concern regarding the potential environmental and human risks from massive aerial spraying of malathion, the MOSCAMED program sought out alternative pesticides, and began using GF-120. In 2002 the Guatemalan government requested an environmental impact study, to assure that the spraying is benign.
But that study, approved by the Guatemalan Ministry of Environment and Natural Resources in 2005, heavily relied on data from Dow Agrosciences and the U.S. and Guatemala agencies involved in the MOSCAMED program.
And the consultant who directed the study, Ricardo Santa Cruz Rubi, only months earlier had been vice minister of agriculture, responsible for approving aerial aspersions by the MOSCAMED program in Guatemala. Once the study was completed he was rehired by the ministry.
The study's conclusion was highly favorable regarding the use of Spinosad to control the fruit fly, even though the consultants reported that "there is a lack of information regarding the situation under field conditions and we recognize the limitations in our analysis due to this circumstance."
Over the years aerial spraying has covered a broad swath of Guatemala ´s coffee-growing regions, in an attempt to create a barrier from the southwest to the northeast of the country. In recent years the program has focused on spraying in five departments in western Guatemala. The spraying is followed by the aerial release of sterile male Mediterranean fruit flies to mate with females, thus interrupting the fruit flies´ reproduction cycle.
Just as medfly outbreaks continue to recur in California, outbreaks were recorded as recently as September in southern Mexico and in northern regions of Guatemala´s Peten department, or state, both of which have been declared by MOSCAMED as "medfly free areas".
Spinosad is described in MOSCAMED documents as "environmentally friendly." A repellent in GF-120 is designed to keep beneficial insects from consuming the pesticide. However, scientists have warned against daytime applications and spraying over bodies of water, since active bees and aquatic species are unable to avoid contact with the substance.
In the 1980s, more than 264,000 gallons of malathion had been sprayed from aircraft covering an area of more than 4,000 square miles.
Beekeepers reported major losses in hive populations and honey production. "There were mounds of dead bees on the ground in front of the hives," said Julio Juarez, a beekeeper and environmental activist from San Antonio, Suchitepequez.
With Spinosad, there are no longer mounds of dead bees in front of the hives, possibly because of its sub-lethal impacts, which according to Canadian biologist Lora Morandin, undermine foraging ability and causes disorientation. Morandin reported these concerns in a 2005 study, "Lethal and Sublethal effects of Spinosad on Bumblebees."
But in spite of the Dow scientists' warnings regarding Spinosad´s toxicity to bees, the Guatemalan environmental study did not discuss alternatives to daytime aerial spraying as a means of controlling the fruit fly.
Nor did the evaluators address the issue of possible contamination when poisoned fruit flies become food for birds and other animals in a country home to numerous endangered species of birds and insects.
Instead, the mass spraying was advocated largely because of cost issues. It is far less expensive to massively spray a region than it is to apply site specific measures. And in Guatemala the MOSCAMED budget is a windfall for the resource-starved ministry of agriculture.
(Matthew Creelman is a free-lance journalist and political analyst who has reported from Guatemala since 1984. E-mail Creelman at Matthew_creelman(at)hotmail.com)
http://www.scrippsnews.com/node/57906
By MATTHEW CREELMAN, SHNS contributing correspondent
international
GUATEMALA CITY - For most of three decades, the U.S. has financed massive aerial spraying of pesticides over a large part of Guatemala in an attempt to eradicate the Mediterranean fruit fly, but common precautions to limit exposure to the toxic chemicals are not being followed.
In the 1980s and 1990s, malathion was sprayed from aircraft over thousands of acres of Guatemala's forests and farmlands. More recently the U.S.-financed program has been spraying Spinosad GF 120 Naturalyte Fruit Fly Bait, produced by Dow Agrosciences.
According to Guatemalan government data, the U.S.-backed program has applied more than 6 million liters of GF-120 since 2002, equivalent to more than 5,000 tons of this pesticide-bait.
Dow scientists say that Spinosad is highly toxic to beneficial insects and aquatic species, and that precautions should be taken to avoid daytime spraying and avoid bodies of water.
However, in Guatemala, spraying occurs during the day and over water. In contrast, in California, which is also waging an ongoing battle with medflies, the use of Spinosad sprays to control the pests is carefully regulated, and residents and farm workers are warned prior to spraying to keep out of sprayed zones for at least four hours.
This is not the case in Guatemala.
The U.S. has spent $266 million on the fruit-fly eradication program since 1976. The original purpose of the program was to create a barrier that would keep the Medfly from "migrating" to California fruit farms about 2,200 miles away.
But the characterization of the medfly as a destructive "illegal alien" is challenged by Dr. James Carey, an entomologist with the University of California, Berkeley, who has concluded from DNA tests that the medfly is a permanent resident of California, detected in 167 municipalities --one third of the state -- since 1975.
Carey is recognized as a pre-eminent expert on the medfly, who served
on the California Department of Food and Agriculture´s Medfly
Scientific Advisory Panel from 1987 to 1994.
Campesinos, beekeepers, environmentalists, coffee growers and others who work the land and study it have opposed the program for years.
Israel Gramajo, the mayor of San Antonio, Suchitepequez, in southern Guatemala, is currently leading an effort to remove a Mosca Del Mediterraneo (or MOSCAMED) quarantine post from his town and prohibit aerial spraying. The medfly larvae develop in fruit such as coffee berries, oranges and mangos. The quarantine posts are set up on highways to keep potentially contaminated fruit from entering into
regions considered free of the medfly. Ironically, the quarantine in San Antonio has been designed to keep contaminated fruit from entering a region already infested by the fruit fly.
Guatemala is the only Central American country using massive aerial spraying of pesticides to control the medfly. According to medfly program protocol, the plane sprays up to seven times each area treated, for a total of 500 droplets per 10 square feet.
According to a 2009 medfly report by a Mexican scientist working with
the MOSCAMED Program, 1,650 square miles were infested with the Medfly
in Guatemala, and another 5,600 square miles were subject to
"suppression".
Guatemalans complain of damages to their crops, along with allergic reactions and conjunctivitis. MOSCAMED authorities deny the charges and say they provide important support to beekeepers, along with baking classes and medical campaigns in towns where the program is active.
When scientific studies in the 1980s and 1990s began raising concern regarding the potential environmental and human risks from massive aerial spraying of malathion, the MOSCAMED program sought out alternative pesticides, and began using GF-120. In 2002 the Guatemalan government requested an environmental impact study, to assure that the spraying is benign.
But that study, approved by the Guatemalan Ministry of Environment and Natural Resources in 2005, heavily relied on data from Dow Agrosciences and the U.S. and Guatemala agencies involved in the MOSCAMED program.
And the consultant who directed the study, Ricardo Santa Cruz Rubi, only months earlier had been vice minister of agriculture, responsible for approving aerial aspersions by the MOSCAMED program in Guatemala. Once the study was completed he was rehired by the ministry.
The study's conclusion was highly favorable regarding the use of Spinosad to control the fruit fly, even though the consultants reported that "there is a lack of information regarding the situation under field conditions and we recognize the limitations in our analysis due to this circumstance."
Over the years aerial spraying has covered a broad swath of Guatemala ´s coffee-growing regions, in an attempt to create a barrier from the southwest to the northeast of the country. In recent years the program has focused on spraying in five departments in western Guatemala. The spraying is followed by the aerial release of sterile male Mediterranean fruit flies to mate with females, thus interrupting the fruit flies´ reproduction cycle.
Just as medfly outbreaks continue to recur in California, outbreaks were recorded as recently as September in southern Mexico and in northern regions of Guatemala´s Peten department, or state, both of which have been declared by MOSCAMED as "medfly free areas".
Spinosad is described in MOSCAMED documents as "environmentally friendly." A repellent in GF-120 is designed to keep beneficial insects from consuming the pesticide. However, scientists have warned against daytime applications and spraying over bodies of water, since active bees and aquatic species are unable to avoid contact with the substance.
In the 1980s, more than 264,000 gallons of malathion had been sprayed from aircraft covering an area of more than 4,000 square miles.
Beekeepers reported major losses in hive populations and honey production. "There were mounds of dead bees on the ground in front of the hives," said Julio Juarez, a beekeeper and environmental activist from San Antonio, Suchitepequez.
With Spinosad, there are no longer mounds of dead bees in front of the hives, possibly because of its sub-lethal impacts, which according to Canadian biologist Lora Morandin, undermine foraging ability and causes disorientation. Morandin reported these concerns in a 2005 study, "Lethal and Sublethal effects of Spinosad on Bumblebees."
But in spite of the Dow scientists' warnings regarding Spinosad´s toxicity to bees, the Guatemalan environmental study did not discuss alternatives to daytime aerial spraying as a means of controlling the fruit fly.
Nor did the evaluators address the issue of possible contamination when poisoned fruit flies become food for birds and other animals in a country home to numerous endangered species of birds and insects.
Instead, the mass spraying was advocated largely because of cost issues. It is far less expensive to massively spray a region than it is to apply site specific measures. And in Guatemala the MOSCAMED budget is a windfall for the resource-starved ministry of agriculture.
(Matthew Creelman is a free-lance journalist and political analyst who has reported from Guatemala since 1984. E-mail Creelman at Matthew_creelman(at)hotmail.com)
http://www.scrippsnews.com/node/57906
WHAT TO DO IF YOU HAVE USED ASPARTAME.
WHAT TO DO IF YOU HAVE USED ASPARTAME
By Neurosurgeon Russell Blaylock, M.D.(c) 2003
Web Site: http://www.russellblaylockmd.com
The most important starting point of any detoxification program is to stop exposure to the toxin or toxins. This means avoiding even small amounts, since once sensitized to the toxin even minute amounts can produce full-blown toxicity. This is especially so with accumulative toxins, such as aspartame. It has been shown conclusively that the metabolic products of methanol breakdown, formaldehyde in particular, accumulates on the DNA and cellular proteins. Once you have cleansed your diet of the toxin, removal of the toxin and its metabolic products from your system will begin. Central to this process is the body's detoxification system, which exist in all cells of the body, with the bulk of detoxification taking place in the liver. The detoxification system is divided into two components called phase I and phase II, which work in tandem. Toxins pass through phase I and then pass to phase II where they are further detoxified and made water-soluble for eventual disposal. It is now known that you can significantly enhance the body's ability to detoxify these substances through the judicious use of specific supplements. Of the two systems phase II is most important and most often impaired.
The following is a list of nutrients that enhance detoxification:
Indole-3 carbinol-100 mg twice a day. This natural substance enhances phase II. It is extracted from cruciferous vegetables such as broccoli, Brussel's sprouts and cauliflower. It can be purchased as an extract.
Taurine 500 mg a day- This is a sulfur-containing amino acid that is used by the liver for sulfonation reactions. It is to be taken between meals.
Milk Thistle (silymarin) 175 mg. Take two twice a day. This extract has been shown to substantially enhance liver detoxification and is also a very powerful antioxidant for all cells.
Curcumin- 500 mg three times a day with olive oil. This is an extract taken from turmeric. It is an extremely powerful antioxidant, enhances both phases I and II detoxification, is a radioprotectant, enhances bile flow, inhibits cancer growth, and is a very powerful anti-inflammatory. Also enhances DNA repair enzymes.
Panthethine 250 mg Take one capsule 3X a day- This vitamin is the enzyme form of pantothenic acid. It plays a vital role in enhancing the aldehyde dehydrogenase enzyme. (For formaldehyde detoxification)
Thiamine- 100 mg. Take three a day. (Vitamin B1) This vitamin plays a major role in protecting nerves as well as the brain. It is commonly depleted with pesticide exposure.
Pyrodoxyl-5 phosphate 50 mg- Take one a day. This is the functional form of vitamin B6. People exposed to chemical toxins frequently have low levels of this vitamin. When vitamin B6 is deficient, taurine is also low. It plays a major role in protecting against glutamate and aspartate toxicity.
In addition to detoxification, other nutrients play a more direct role in protecting cells and in promoting their recovery from toxicity. These include:
Magnesium- 750 to 1000 mg a day. (Magnesium citrate/malate) Magnesium plays a major role in cell protection, especially against excitotoxicty. In addition it protects against strokes and heart attacks.
Selenium- 200 ug a day. This mineral also plays a role in protecting cells from toxins, especially mercury. It plays a major role in protecting against free radicals.
N-acetyl L-cysteine (NAC)- 750 mg a day. This is a substance that in cells is converted to glutathione. Glutathione is your cell's major protection against free radicals produced by toxins such as aspartame.. In addition, NAC removes mercury. NAC also enhances detoxification.
Multi-"B" vitamins- This should be a multivitamins that contains 25 to 50 mgs of each of the B vitamins. The multivitamin should not contain iron. Take one a day.
Vitamin E (as mixed tocopherols) 400 IU twice a day. A powerful antioxidant, prevents heart attacks an stokes and the gamma-tocopherol is a powerful anti-inflammatory.
Vitamin C (as magnesium ascorbate) 2000 mg twice to three times a day. Plays a major role in cell protection against oxygen stress, protects the nervous system and enhances tissue repair.
CoQ10 100 mg twice a day. This is a major energy molecule and protects the brain against excitotoxicity.
DHA 200 mg a day. This is a component of omega-3-fatty acids. It plays a vital role in membrane repair and repair of synapses.
In addition to avoiding aspartame you must avoid other toxins as well. This includes MSG, pesticides, herbicides, bug sprays, fluoride, mercury, cadmium, aluminum and the many other toxins found commonly in the environment. Many of these toxins act synergistically, that is, when combined they have toxic effects that exceed their additive effects.
In addition, you need regular, moderate exercise (never aerobic), avoid soy products, cheese, and vegetable oils. Do not smoke or use drugs. All of these things increase free radical damage and prevent tissue repair. You should eat a diet high in vegetables and with some fruits, no sugar (or honey), moderate complex carbohydrates and pure water free of contaminants, including fluoride. Do not use fluoride toothpaste, mouthwashes or receive fluoride treatments. If you follow these principles you will notice quick recovery from your toxic encounter. More serious toxic encounters may take several months for recovery.
Please refer to my web site at http://www.russellblaylockmd.com for more information on my books. Russell Blaylock, M.D. (Health & Nutrition Secrets To Save Your Life, Excitotoxins: The Taste That Kills, etc.)
Aspartame sites:
http://www.dorway.com
http://www.wnho.net
http://www.holisticmed.com/aspartame
By Neurosurgeon Russell Blaylock, M.D.(c) 2003
Web Site: http://www.russellblaylockmd.com
The most important starting point of any detoxification program is to stop exposure to the toxin or toxins. This means avoiding even small amounts, since once sensitized to the toxin even minute amounts can produce full-blown toxicity. This is especially so with accumulative toxins, such as aspartame. It has been shown conclusively that the metabolic products of methanol breakdown, formaldehyde in particular, accumulates on the DNA and cellular proteins. Once you have cleansed your diet of the toxin, removal of the toxin and its metabolic products from your system will begin. Central to this process is the body's detoxification system, which exist in all cells of the body, with the bulk of detoxification taking place in the liver. The detoxification system is divided into two components called phase I and phase II, which work in tandem. Toxins pass through phase I and then pass to phase II where they are further detoxified and made water-soluble for eventual disposal. It is now known that you can significantly enhance the body's ability to detoxify these substances through the judicious use of specific supplements. Of the two systems phase II is most important and most often impaired.
The following is a list of nutrients that enhance detoxification:
Indole-3 carbinol-100 mg twice a day. This natural substance enhances phase II. It is extracted from cruciferous vegetables such as broccoli, Brussel's sprouts and cauliflower. It can be purchased as an extract.
Taurine 500 mg a day- This is a sulfur-containing amino acid that is used by the liver for sulfonation reactions. It is to be taken between meals.
Milk Thistle (silymarin) 175 mg. Take two twice a day. This extract has been shown to substantially enhance liver detoxification and is also a very powerful antioxidant for all cells.
Curcumin- 500 mg three times a day with olive oil. This is an extract taken from turmeric. It is an extremely powerful antioxidant, enhances both phases I and II detoxification, is a radioprotectant, enhances bile flow, inhibits cancer growth, and is a very powerful anti-inflammatory. Also enhances DNA repair enzymes.
Panthethine 250 mg Take one capsule 3X a day- This vitamin is the enzyme form of pantothenic acid. It plays a vital role in enhancing the aldehyde dehydrogenase enzyme. (For formaldehyde detoxification)
Thiamine- 100 mg. Take three a day. (Vitamin B1) This vitamin plays a major role in protecting nerves as well as the brain. It is commonly depleted with pesticide exposure.
Pyrodoxyl-5 phosphate 50 mg- Take one a day. This is the functional form of vitamin B6. People exposed to chemical toxins frequently have low levels of this vitamin. When vitamin B6 is deficient, taurine is also low. It plays a major role in protecting against glutamate and aspartate toxicity.
In addition to detoxification, other nutrients play a more direct role in protecting cells and in promoting their recovery from toxicity. These include:
Magnesium- 750 to 1000 mg a day. (Magnesium citrate/malate) Magnesium plays a major role in cell protection, especially against excitotoxicty. In addition it protects against strokes and heart attacks.
Selenium- 200 ug a day. This mineral also plays a role in protecting cells from toxins, especially mercury. It plays a major role in protecting against free radicals.
N-acetyl L-cysteine (NAC)- 750 mg a day. This is a substance that in cells is converted to glutathione. Glutathione is your cell's major protection against free radicals produced by toxins such as aspartame.. In addition, NAC removes mercury. NAC also enhances detoxification.
Multi-"B" vitamins- This should be a multivitamins that contains 25 to 50 mgs of each of the B vitamins. The multivitamin should not contain iron. Take one a day.
Vitamin E (as mixed tocopherols) 400 IU twice a day. A powerful antioxidant, prevents heart attacks an stokes and the gamma-tocopherol is a powerful anti-inflammatory.
Vitamin C (as magnesium ascorbate) 2000 mg twice to three times a day. Plays a major role in cell protection against oxygen stress, protects the nervous system and enhances tissue repair.
CoQ10 100 mg twice a day. This is a major energy molecule and protects the brain against excitotoxicity.
DHA 200 mg a day. This is a component of omega-3-fatty acids. It plays a vital role in membrane repair and repair of synapses.
In addition to avoiding aspartame you must avoid other toxins as well. This includes MSG, pesticides, herbicides, bug sprays, fluoride, mercury, cadmium, aluminum and the many other toxins found commonly in the environment. Many of these toxins act synergistically, that is, when combined they have toxic effects that exceed their additive effects.
In addition, you need regular, moderate exercise (never aerobic), avoid soy products, cheese, and vegetable oils. Do not smoke or use drugs. All of these things increase free radical damage and prevent tissue repair. You should eat a diet high in vegetables and with some fruits, no sugar (or honey), moderate complex carbohydrates and pure water free of contaminants, including fluoride. Do not use fluoride toothpaste, mouthwashes or receive fluoride treatments. If you follow these principles you will notice quick recovery from your toxic encounter. More serious toxic encounters may take several months for recovery.
Please refer to my web site at http://www.russellblaylockmd.com for more information on my books. Russell Blaylock, M.D. (Health & Nutrition Secrets To Save Your Life, Excitotoxins: The Taste That Kills, etc.)
Aspartame sites:
http://www.dorway.com
http://www.wnho.net
http://www.holisticmed.com/aspartame
Cacao - An ancient medicine validated by modern science.
Cacao - An ancient medicine validated by modern science.
http://www.naturalnews.com/030603_cacao_medicine.html
by Carolanne Wright, citizen journalist
(NaturalNews) Legendary cacao has a long history of medicinal use throughout Mesoamerica and South America. Today, science confirms chocolate has many favorable qualities that support health and psychological well-being. This magical bean offers great benefits when the cacao is high-quality, raw and organic.
The native people of the Americas extolled the merits of cacao with oral histories, pottery, stonework, and colored documents that chronicled its use in rituals as well as in everyday life. The Mayan and Mexica religions believed cacao had divine origins. According to Mayan legend, after humans were created by the goddess Xmucane, the God Sovereign Plumed Serpent gave cacao to the Maya.
When Europeans began exploring the New World, Columbus and his crew were the first to encounter cacao when they seized a canoe at Guanaja that was filled with strange 'almonds'. Eventually it was discovered the 'almonds' were actually cacao beans used as a source of currency in Mesoamerica.
Chocolate is not only a food, but also a medicine. Preparations are well documented by the explorers who came in contact with cacao during their travels. Cacao medicinal properties were noted to alleviate fever, anemia, poor appetite, metal fatigue and poor breast milk production, as well as tuberculosis, gout, kidney stones and low virility. This delicious bean was famous for healing the nervous system and improving digestion and elimination.
Jump to the modern day and numerous studies celebrate the many virtues of chocolate. Research confirms that chocolate helps to relieve emotional stress. Stress hormones and stress-related biochemical agents were reduced when volunteers, who rated themselves as highly stressed, consumed 1.4 ounces of dark chocolate per day for a period of two weeks.
Another study found that cacao flavanols (CF) improve cognitive function. In a randomized, double-blind trial, 30 healthy adults consumed either 520 mg or 994 mg of a CF infused beverage. Both groups showed significant improvement in mental acuity, while a reduction in 'mental fatigue' was only found with the lower consumption of 520 mg. The researchers suspect the results may be related to the effects of CF on blood flow.
Cacao mass also contains potassium, phosphorus, copper, iron, zinc, and magnesium which contribute to cardiovascular health. Chocolate has the ability to trigger the release of dopamine and the endorphin phenylethylamine, both of which soothe the symptoms of premenstrual syndrome and depression. Due to its high valeric acid content, cacao has stress relieving properties despite the presence of the stimulants theobromine and caffeine.
Yet not all chocolate is created equal. Organic, raw cacao reigns supreme with maximum nutrient content compared to other forms. Since raw chocolate is processed at low temperatures, it retains much more of its famed nutritional value than if it were roasted. As seen in David Wolfe's, "Naked Chocolate: The Astounding Truth About the World's Greatest Food", raw chocolate has many high-quality nutrients such as manganese, vitamin C, and omega 6 fatty acids. Raw cacao also contains powerful antioxidants along with a significant amount of chromium, which balances blood sugar levels. Additional benefits are found in neurotransmitter modulating agents that act as natural antidepressants. "They allow our neurotransmitters like serotonin to remain in our bloodstream longer that usual. This makes us younger," explains Wolfe. He believes that raw cacao is an excellent way to enhance health while calming the heart, amplifying sensuality and enriching one's love life.
Live your bliss and savor the wisdom of the ancients. Invigorate modern vitality with the many extraordinary traits of raw cacao.
Sources for this article:
Teresa L. Dillinger, Patricia Barriga, Sylvia Escarcega, Martha Jimenez, Diana Salazar Lowe, Louis E. Grivetti, "Food of the Gods: Cure for Humanity? A Cultural History of the Medicinal and Ritual Use of Chocolate", The Journal of Nutrition. Retrived on November 28, 2010, from http://jn.nutrition.org/content/130/8/2057S.full.pdf
Francois-Pierre J. Martin, Serge Ressi, Emma Per-Trepat, Beate Kamlage, Sebastiano Collino, Edgar Leibold, Jurgen Kastler, Dietrich Rein, Laurent B. Fay, Sunil Kochhar, "Metabolic Effects of Dark Chocolate Consumption on Energy, Gut Microbiota, and Stress-Related Metabolism in Free-Living Subjects", Journal of Proteome Research, October 7, 2009, 8 (12), pp 5568-5579
Andrew B Scholey, Stephen J French, Penelope J Morris, David O Kennedy, Athea L Milne, Crystal F Haskell, "Consumption of coca flavanols results in acute improvements in mood and cognitive performance during sustained mental effort". Journal of Psychopharmacology, October 2010, 24 (10) pp 1505-1514
Pamela Moyers Scott, MPAS, PA-C, "Is chocolate really good for me?" JAAPA, January 2007, 20 (1) pp 55-56
Marisa Belger, "The raw, tasty truth about natural chocolate. Skip the average bar and reach for nutrient-packed cacao treats instead". Today GreenDAY, August 2009. Retrieved on November 30, 2010, from http://today.msnbc.msn.com/id/32271092/ns/today-green/
Kevin Gianni, "Nutritional Authority David Wolfe Discusses Metabolism and Chocolate", Natural News, August 22, 2008. Retrieved November 30, 2010, from
http://www.naturalnews.com/023939_food_chocolate_cacao.html
http://www.naturalnews.com/030603_cacao_medicine.html
by Carolanne Wright, citizen journalist
(NaturalNews) Legendary cacao has a long history of medicinal use throughout Mesoamerica and South America. Today, science confirms chocolate has many favorable qualities that support health and psychological well-being. This magical bean offers great benefits when the cacao is high-quality, raw and organic.
The native people of the Americas extolled the merits of cacao with oral histories, pottery, stonework, and colored documents that chronicled its use in rituals as well as in everyday life. The Mayan and Mexica religions believed cacao had divine origins. According to Mayan legend, after humans were created by the goddess Xmucane, the God Sovereign Plumed Serpent gave cacao to the Maya.
When Europeans began exploring the New World, Columbus and his crew were the first to encounter cacao when they seized a canoe at Guanaja that was filled with strange 'almonds'. Eventually it was discovered the 'almonds' were actually cacao beans used as a source of currency in Mesoamerica.
Chocolate is not only a food, but also a medicine. Preparations are well documented by the explorers who came in contact with cacao during their travels. Cacao medicinal properties were noted to alleviate fever, anemia, poor appetite, metal fatigue and poor breast milk production, as well as tuberculosis, gout, kidney stones and low virility. This delicious bean was famous for healing the nervous system and improving digestion and elimination.
Jump to the modern day and numerous studies celebrate the many virtues of chocolate. Research confirms that chocolate helps to relieve emotional stress. Stress hormones and stress-related biochemical agents were reduced when volunteers, who rated themselves as highly stressed, consumed 1.4 ounces of dark chocolate per day for a period of two weeks.
Another study found that cacao flavanols (CF) improve cognitive function. In a randomized, double-blind trial, 30 healthy adults consumed either 520 mg or 994 mg of a CF infused beverage. Both groups showed significant improvement in mental acuity, while a reduction in 'mental fatigue' was only found with the lower consumption of 520 mg. The researchers suspect the results may be related to the effects of CF on blood flow.
Cacao mass also contains potassium, phosphorus, copper, iron, zinc, and magnesium which contribute to cardiovascular health. Chocolate has the ability to trigger the release of dopamine and the endorphin phenylethylamine, both of which soothe the symptoms of premenstrual syndrome and depression. Due to its high valeric acid content, cacao has stress relieving properties despite the presence of the stimulants theobromine and caffeine.
Yet not all chocolate is created equal. Organic, raw cacao reigns supreme with maximum nutrient content compared to other forms. Since raw chocolate is processed at low temperatures, it retains much more of its famed nutritional value than if it were roasted. As seen in David Wolfe's, "Naked Chocolate: The Astounding Truth About the World's Greatest Food", raw chocolate has many high-quality nutrients such as manganese, vitamin C, and omega 6 fatty acids. Raw cacao also contains powerful antioxidants along with a significant amount of chromium, which balances blood sugar levels. Additional benefits are found in neurotransmitter modulating agents that act as natural antidepressants. "They allow our neurotransmitters like serotonin to remain in our bloodstream longer that usual. This makes us younger," explains Wolfe. He believes that raw cacao is an excellent way to enhance health while calming the heart, amplifying sensuality and enriching one's love life.
Live your bliss and savor the wisdom of the ancients. Invigorate modern vitality with the many extraordinary traits of raw cacao.
Sources for this article:
Teresa L. Dillinger, Patricia Barriga, Sylvia Escarcega, Martha Jimenez, Diana Salazar Lowe, Louis E. Grivetti, "Food of the Gods: Cure for Humanity? A Cultural History of the Medicinal and Ritual Use of Chocolate", The Journal of Nutrition. Retrived on November 28, 2010, from http://jn.nutrition.org/content/130/8/2057S.full.pdf
Francois-Pierre J. Martin, Serge Ressi, Emma Per-Trepat, Beate Kamlage, Sebastiano Collino, Edgar Leibold, Jurgen Kastler, Dietrich Rein, Laurent B. Fay, Sunil Kochhar, "Metabolic Effects of Dark Chocolate Consumption on Energy, Gut Microbiota, and Stress-Related Metabolism in Free-Living Subjects", Journal of Proteome Research, October 7, 2009, 8 (12), pp 5568-5579
Andrew B Scholey, Stephen J French, Penelope J Morris, David O Kennedy, Athea L Milne, Crystal F Haskell, "Consumption of coca flavanols results in acute improvements in mood and cognitive performance during sustained mental effort". Journal of Psychopharmacology, October 2010, 24 (10) pp 1505-1514
Pamela Moyers Scott, MPAS, PA-C, "Is chocolate really good for me?" JAAPA, January 2007, 20 (1) pp 55-56
Marisa Belger, "The raw, tasty truth about natural chocolate. Skip the average bar and reach for nutrient-packed cacao treats instead". Today GreenDAY, August 2009. Retrieved on November 30, 2010, from http://today.msnbc.msn.com/id/32271092/ns/today-green/
Kevin Gianni, "Nutritional Authority David Wolfe Discusses Metabolism and Chocolate", Natural News, August 22, 2008. Retrieved November 30, 2010, from
http://www.naturalnews.com/023939_food_chocolate_cacao.html
Monday, December 13, 2010
Supertoxic rat poisons threaten owls, other wildlife.
Supertoxic rat poisons threaten owls, other wildlife
http://www.environmentalhealthnews.org/ehs/news/rodenticides-kill-wildlife/document_view
Story by Robert McClure
Photos by Paul Joseph Brown
Environmental Health News
December 12, 2010
Part 1 of 2
VANCOUVER, British Columbia – With the spooky glow of his headlamp illuminating an antenna in his hand, Paul Levesque stalks one of Canada’s last remaining barn owls.
“Are you getting anything?” research team leader Sofi Hindmarch asks over a walkie-talkie.
“I got it!” Levesque responds. Then a few seconds later, dejected, he radios back: “No. I lost the signal.”
Working in darkness, with the quarter-moon obscured by clouds, these two scientists are trying to figure out what an elusive, radio-collared owl is eating along this country road just beyond the suburbs that ring Vancouver. Their mission is to determine whether the decline of Canada’s barn owl is tied, in part, to super-toxic rat poisons.
Scientists know that at least some owls are dying under gruesome circumstances, bleeding to death from stomach hemorrhages in an agonizing and days-long decline. The culprit: An extra-potent class of rat poisons that has flooded the market in recent decades, designed to more effectively kill rats, a food source for the owls.
An extra-potent class of rat poisons has flooded the market in recent decades, designed to more effectively kill rats, a food source for the owls. Six of 164 dead barn owls, barred owls and great horned owls in a 2009 western Canada study had rodenticide levels high enough to kill them outright, causing the fatal stomach hemorrhages. Pesticide readings in 15 percent to 30 percent of the others appeared toxic and seemed likely to handicap owls in a variety of ways, scientists say.
The study is the latest evidence amassed by researchers that poses an unsettling question: Are we willing to poison owls and a variety of other wild animals in order to fight rats?
“We’re finding this stuff all over the place,” said John Elliott, an Environment Canada scientist who co-authored the owl study published last year. “There’s a lot more rodenticide in the food chain than we would have ever thought. We’re surprised that there’s that much of the stuff kicking around.”
Studies in Canada, the United States and Europe show that this newer generation of rat poisons is killing a variety of wild animals, including mountain lions, bobcats, coyotes, foxes, skunks, deer, squirrels, possums and raccoons, along with bald eagles, golden eagles, owls, hawks and vultures.
Hundreds of wildlife poisoning deaths have been documented. In the United States, and the pesticides have been found in hundreds of animals, according to a 2006 memo by U.S. Environmental Protection Agency biologist Bill Erickson. Two years earlier, he documented more than 300 incidents of wild animals suspected of being killed by the chemicals.
“Clearly, more information is urgently needed on the potential impacts such exposure may be having on populations” of raptors and other wild animals, Erickson wrote.
Erickson’s memo was part of a years-long process at EPA that resulted in 2008 in new rules to better control the rat poisons. In June of 2011 those rules go into effect, although they did not go as far as desired by some wildlife advocates, including the U.S. Fish and Wildlife Service.
The chemicals in question are known as anti-coagulants because they prevent an animal’s blood from clotting or coagulating. The first of these, synthesized in the 1940s, is known as warfarin – the same chemical sold in miniscule concentrations to people as Coumadin, a prescription blood thinner.
This barn owl study is the latest evidence amassed by researchers that poses an unsettling question: Are we willing to poison owls and a variety of other wild animals in order to fight rats? The new strain of rat poisons came along in the 1970s. The reason: Warfarin and its cousins required the rats to return to feed on the pesticide over the course of several days. With the newer versions, only a single dose is needed, although it might take five days or more to do the job. Brand names include Havoc, Talon, Contrac, Maki, Ratimus and d-CON Mouse Pruf II.
Some animals are ingesting the pesticides by eating poisoned rats as the rats stagger about, dazed but not yet dead. This goes on for days before the rats succumb, in the meantime making them easy targets for owls and other predators.
But there’s a mysterious wrinkle in this picture. How are plant eaters like deer and sheep ingesting rat poison? Grain eaters like squirrels? What about hawks that subsist almost exclusively on songbirds – songbirds that probably aren’t eating rats?
Scientists wonder: Just how far into the food web have these poisons penetrated?
Canada’s vanishing barn owls
On a balmy but cloudy night, Hindmarch is trying to capture a barn owl, one of three owl species that ingested the rat poisons in the 2009 study. The hunt this night is in a gritty industrial outpost in Vancouver, where rats scamper boldly between the defunct lumber yard where they live and the bustling grain terminal where they sneak their dinner.
Between the wail of trains on tracks perhaps 30 yards away, Hindmarch and Levesque fiddle with their owl traps, preparing for their 9-5 shift – 9 p.m. until 5 a.m., that is.
“Can you grab one of the girls?” Hindmarch asks Levesque, referring to the mice that they hope will lure an owl to their traps.
The scientists have to carefully put the mice inside cages that will protect the mice when an owl swoops down, attracted by the rodents noisily munching on the crackers that Hindmarch is unwrapping. Hindmarch, of Simon Fraser University, doesn’t want the mice to be hurt.
How are plant eaters like deer and sheep ingesting rat poison? Grain eaters like squirrels? Hawks that subsist almost exclusively on songbirds that probably aren’t eating rats? Scientists wonder: Just how far into the food web have these poisons penetrated?
“It’s working time,” Hindmarch says as she grabs the first mouse in its transport cage and scoots it through the open door of a small cage that’s part of the owl trap. “You’ll get crackers soon.”
Levesque, a freelance contract scientist, puts the cage down in tall grass beside a nearby drainage ditch. He slips in some crackers and steals back to wait inside his truck. Under the tall grass, the noisy snacking attracts barn owls, which are then caught in the trap.
Hindmarch’s objective is twofold: to collect the owl’s blood so it can be tested for rat poisons; and to fit the owls with radio transmitters so she can track them and figure out where they are feeding. She wants to know whether urban owls are eating more poisoned rats than their country cousins.
“This our first time trying to get this guy,” Hindmarch says as she surveys the decrepit lumber yard. “I’d love to get this owl because it’s so urbanized that it’d be neat to see where he’s going and even if he has a nest or has a mate. We have no idea at this point.”
Her work is a follow up to the study analyzing owls found dead in British Columbia and the Yukon Territory, which showed that nearly three-quarters of the birds had rodenticides in their livers. The Canadian findings follow earlier studies in Europe, New Zealand, New York and elsewhere that documented the poisons spreading to wild animals.
The barn owls in and around Vancouver are among the last remaining barn owls in Canada. Two weeks ago, they were declared a “threatened” species. A smaller population, classified as “endangered,” lives in eastern Canada.
Although plenty remain alive in the United States, Hindmarch and her colleagues are eager to find out what role rat poisons may be having in the Canadian owls’ decline. The findings will have implications in the United States too.
Taken together, the research suggests that these improved rat-killers are imposing a toxic load on the environment that no one bargained for. It seems clear that some rats are being eaten by owls and other wild animals after they have ingested extraordinarily high doses of poison, researchers say.
“The rats are really little toxic packages running around before they die,” said Michael Fry, a wildlife toxicologist and pesticides expert with the American Bird Conservancy. “If the rat is carrying 10 or 15 times a lethal dose, the animal that consumes it is at a much higher risk of consuming a lethal dose.”
The research suggests that improved rat-killers are imposing a toxic load on the environment that no one bargained for.
In some cases, the dose isn’t lethal, but “maybe it’s affecting their flying ability and they’re getting hit more by cars,” said Kirstin Webster, a colleague of Hindmarch’s at Simon Fraser University in Vancouver, citing a fairly common way for owls to die.
Owls that aren’t killed outright by the poisons also can easily bleed to death because their blood fails to clot. Wild animals get hurt on a regular basis, scientists say; what otherwise would have been just a painful cut could spell death.
Webster’s work to find a way to test birds’ blood for exposure to rat poisons involved dosing quail and owls with a second-generation rodenticide called brodificoum. The quail given high doses bled not only internally, but also through their eyes, she said.
Once an owl or other animal eats a poisoned rat, the pesticides stay around in the predator’s system for a very long time. It takes six months or longer for just half the dose to be eliminated from some animals’ bodies.
Imagine you’re a barn owl like the one Hindmarch is trying to catch by the grain depot.
“If you’re just getting one dose on top of another, you get this constant exposure,” said Nancy Golden, a U.S. Fish and Wildlife Service toxicologist. “It’s one thing to have enough to kill you outright.
Once an owl or other animal eats a poisoned rat, the pesticides stay around in the predator’s system for a very long time. “But what about the ones that are just carrying this body burden? What effect does that have on their fitness? That’s what worries me.”
These “sublethal” effects are difficult to gauge, but research suggests they are real. For example, a study at McGill University in Montreal allowed a sparrow to perch on a pesticide-laden surface. The bird absorbed pesticide through its feet. Then researchers put the sparrow into a big cage along with three undosed sparrows and a kestrel, a small type of falcon that eats sparrows.
Although the scientists could not see any differences in the behavior of the pesticide-dosed sparrows, the kestrel apparently could. In 12 of the 15 instances in which the kestrel preyed on one of the sparrows, it picked the one that had absorbed the pesticide. (That study did not involve rat poisons but it shows that animals not visibly affected may be extremely vulnerable, Environment Canada’s Elliott said.)
The toll of six owls killed outright by rat poisons in the Canadian study almost certainly underestimates the actual rate at which owls are dying from rat poison, Elliott said. Animals that feel sick are likely to secret themselves away to protect themselves against predators.
The birds’ bodies are routinely scavenged by other wild animals, further spreading the poison into the food chain. The chemicals have the “potential to cause additional mortality that may not be sustainable in populations already experiencing critical limitations,” biologists from the United Kingdom’s University of Leicester reported in 2005.
California’s threatened San Joaquin kit fox is an example. Scientists collected carcasses of the big-eared, long-legged fox that died from various causes in Bakersfield and in an area 30 miles out in the country. Nearly all the dead foxes from Bakersfield had residues of the long-lived second-generation rodenticides, while none from the outlying desert did.
Chemicals in rat poison may cause additional mortality that may not be sustainable in populations already experiencing critical limitations, said biologists from the United Kingdom’s University of Leicester.
How are these rat poisons getting into plant eaters low on the food chain? There is no sure answer for now. Scientists wonder, though, if carcasses of poisoned animals are being scavenged by creatures low on the food chain. Or perhaps insects are crawling inside the bait stations. But there could be other ways, too. Elliott, the Environment Canada researcher, notes that scientists have seen voles and birds hopping inside the holes on the side of bait stations that approximate the size of the openings to their burrows or homes inside trees.
And as for deer? The seven that tested positive for rat poison in New York “apparently were exposed due to misuse and careless bait application,” Erickson of the EPA reported. Elliott noted that big blue blocks of the poisoned bait are sometimes thrown out into the wild – blue blocks that look a whole lot like the salt licks that deer are known to frequent.
Cracking down on rat poisons
Pushed by environmentalists who successfully sued in federal court, the EPA in 2008 issued rules for these rat poisons that largely take them out of the consumer market.
Pesticide manufacturers say EPA’s action was overkill, but should eliminate any doubts about the products’ safety for wildlife.
“There was not strong evidence to compel (EPA) to put into place the (new rules). However, they did so,” said Karen Reardon, director of communications at Responsible Industry for a Sound Environment, which represents pesticide manufacturers. “We have now even further added protections for secondary wildlife exposure.”
Pushed by environmentalists who successfully sued in federal court, the EPA in 2008 issued rules for these rat poisons that largely take them out of the consumer market.
Dale Kemery, an EPA spokesman, said the agency does not track the amount of pesticides manufactured or applied. But New York state does tote up the applications. New York State Department of Conservation records requested by the Natural Resources Defense Council for use in a lawsuit to limit the rodenticides’ use showed more than 20 tons a year were applied in eight New York City Zip codes in 2002. The pesticide manufacturer Syngenta International in 2004 revealed that some 10 million pounds of first- and second-generation rat poisons were sold annually in California. And in British Columbia, scientists obtained records showing large increases in their use during the 1990s.
The western Canadian study documented a 100 percent increase in sales of one of the rat poisons, brodifacoum, and a 24 percent increase in another, bromadiolone, in British Columbia between 1991 and 2003.
Canada in 2006 changed the rodenticides’ labels to require that they be used in dog- and child-proof bait stations that allow only rats access to the poison, or that the bait be limited to where kids and animals don’t have access.
Then, in 2009, six months before release of the study of the owl poisonings, Health Canada issued stricter regulations. Their inspiration came from a contentious rule approved south of the border.
In the United States, the EPA knew by the early 1980s that the pesticides that emerged the decade before were affecting non-targeted wildlife. But it was 1999 before the agency’s scientists launched a comprehensive risk analysis of the pesticides’ effects on wildlife.
George W. Bush was president by the time an EPA document outlining the environmental risks of the rat poisons was ready to go out for public comment. EPA sent a draft of the document to the pesticide industry in September 2001 for what was supposed to be a 30-day technical review. The stated purpose was to allow industry officials to make technical corrections.
Instead, the agency held a series of closed-door meetings with industry officials, environmentalists charged. “There has been excessive undue influence from industry on the entire process,” said the group Beyond Pesticides. “There has been little to no opportunity for any other stakeholder to provide input or even attend any of these meetings with EPA.”
Reardon of the pesticide industry group said it’s clear the pesticide industry didn’t get special treatment from EPA because the industry opposed what the agency ended up requiring. “EPA has added additional safeguards on top of what was already required. One must conclude that EPA’s actions satisfied what they believed was additional risk,” she said.
In January of 2003, the agency released preliminary results for public comment. This came more than three years after the risk analysis began. It took EPA five more years, until May of 2008, to complete a regulatory review.
And then, a quarter-century after the poisoning of wildlife became well known, the agency decreed that rules to protect wildlife would go into effect more than three years later, in June 2011.
Under the new rules, use of the second-generation rat poisons by consumers will be curtailed. The sale of loose rat baits will be banned in “big box” stores like Home Depot as well as other retail outlets. However, consumers can purchase up to one pound of bait in bait “stations” that are designed to keep out kids and dogs.
Professional exterminators as well as employees of farms, warehouses and other commercial installations may continue to use the more-toxic rat poisons, and loose baits. However, they are required to use above-ground bait stations if the bait is left outdoors or in any place accessible to children, pets or wildlife.
The rules represent a significant check on unsafe use of the products by consumers, said Rick Keigwin, director of EPA’s Pesticide Re-evaluation Division “We wanted people who are professionals in the field, who have the training, to use these products in the appropriate way,” he said.
The U.S. Fish and Wildlife Service and others pushed for EPA to disallow all outdoor uses of the rodenticides, with narrow exceptions.
EPA didn’t go that far, said Laura Parsons, an EPA biologist specializing in pesticides, because of pushback from some businesses. For example, she said, “restaurants and food-service facilities felt very strongly that they needed some kind of perimeter control.” The EPA’s position was backed by the U.S. Department of Housing and Urban Development and the federal Centers for Disease Control and Prevention.
Professional pesticide applicators support the new “common-sense” rules, said Bob Rosenberg, vice president of the National Pest Management Association, and opposed efforts to ban outdoor use of the more-toxic products.
The U.S. EPA knew by the early 1980s that the pesticides that emerged the decade before were affecting non-targeted wildlife. But it was 1999 before the agency’s scientists launched a comprehensive risk analysis of the pesticides’ effects on wildlife.
“Rodents are serious problem for all the reasons you know about – public health reasons,” Rosenberg said. “It’s a lot better to get them outside rather than inside the structure. You want to get them before they get to the food.”
Meanwhile, the multinational Reckitt Benckiser, which markets d-CON rat baits, is challenging the EPA’s new rules in court in an effort to prevent them from going into effect.
The least-toxic answer, said Golden, the Fish and Wildlife Service toxicologist, is a system known as “integrated pest management.” It emphasizes use of non-toxic pest-control methods, which in the case of rats translates to trapping the rats inside the house and finding ways to keep any more from getting in.
Golden predicted that poisoning of wild animals will continue.
“I wouldn’t use anticoagulants in my back yard,” said Golden. “These things are pervasive and are turning up in places we did not expect. . . . They’re certainly not contained where we think they are.”
----------------------------------------
EHN commissioned this story from InvestigateWest, a non-profit journalism studio based in Seattle and focused on the environment, public health and social justice in western North America. http://invw.org/
Photographer Paul Joseph Brown is at www.Ecosystemphoto.com.
http://www.environmentalhealthnews.org/ehs/news/rodenticides-kill-wildlife/document_view
Story by Robert McClure
Photos by Paul Joseph Brown
Environmental Health News
December 12, 2010
Part 1 of 2
VANCOUVER, British Columbia – With the spooky glow of his headlamp illuminating an antenna in his hand, Paul Levesque stalks one of Canada’s last remaining barn owls.
“Are you getting anything?” research team leader Sofi Hindmarch asks over a walkie-talkie.
“I got it!” Levesque responds. Then a few seconds later, dejected, he radios back: “No. I lost the signal.”
Working in darkness, with the quarter-moon obscured by clouds, these two scientists are trying to figure out what an elusive, radio-collared owl is eating along this country road just beyond the suburbs that ring Vancouver. Their mission is to determine whether the decline of Canada’s barn owl is tied, in part, to super-toxic rat poisons.
Scientists know that at least some owls are dying under gruesome circumstances, bleeding to death from stomach hemorrhages in an agonizing and days-long decline. The culprit: An extra-potent class of rat poisons that has flooded the market in recent decades, designed to more effectively kill rats, a food source for the owls.
An extra-potent class of rat poisons has flooded the market in recent decades, designed to more effectively kill rats, a food source for the owls. Six of 164 dead barn owls, barred owls and great horned owls in a 2009 western Canada study had rodenticide levels high enough to kill them outright, causing the fatal stomach hemorrhages. Pesticide readings in 15 percent to 30 percent of the others appeared toxic and seemed likely to handicap owls in a variety of ways, scientists say.
The study is the latest evidence amassed by researchers that poses an unsettling question: Are we willing to poison owls and a variety of other wild animals in order to fight rats?
“We’re finding this stuff all over the place,” said John Elliott, an Environment Canada scientist who co-authored the owl study published last year. “There’s a lot more rodenticide in the food chain than we would have ever thought. We’re surprised that there’s that much of the stuff kicking around.”
Studies in Canada, the United States and Europe show that this newer generation of rat poisons is killing a variety of wild animals, including mountain lions, bobcats, coyotes, foxes, skunks, deer, squirrels, possums and raccoons, along with bald eagles, golden eagles, owls, hawks and vultures.
Hundreds of wildlife poisoning deaths have been documented. In the United States, and the pesticides have been found in hundreds of animals, according to a 2006 memo by U.S. Environmental Protection Agency biologist Bill Erickson. Two years earlier, he documented more than 300 incidents of wild animals suspected of being killed by the chemicals.
“Clearly, more information is urgently needed on the potential impacts such exposure may be having on populations” of raptors and other wild animals, Erickson wrote.
Erickson’s memo was part of a years-long process at EPA that resulted in 2008 in new rules to better control the rat poisons. In June of 2011 those rules go into effect, although they did not go as far as desired by some wildlife advocates, including the U.S. Fish and Wildlife Service.
The chemicals in question are known as anti-coagulants because they prevent an animal’s blood from clotting or coagulating. The first of these, synthesized in the 1940s, is known as warfarin – the same chemical sold in miniscule concentrations to people as Coumadin, a prescription blood thinner.
This barn owl study is the latest evidence amassed by researchers that poses an unsettling question: Are we willing to poison owls and a variety of other wild animals in order to fight rats? The new strain of rat poisons came along in the 1970s. The reason: Warfarin and its cousins required the rats to return to feed on the pesticide over the course of several days. With the newer versions, only a single dose is needed, although it might take five days or more to do the job. Brand names include Havoc, Talon, Contrac, Maki, Ratimus and d-CON Mouse Pruf II.
Some animals are ingesting the pesticides by eating poisoned rats as the rats stagger about, dazed but not yet dead. This goes on for days before the rats succumb, in the meantime making them easy targets for owls and other predators.
But there’s a mysterious wrinkle in this picture. How are plant eaters like deer and sheep ingesting rat poison? Grain eaters like squirrels? What about hawks that subsist almost exclusively on songbirds – songbirds that probably aren’t eating rats?
Scientists wonder: Just how far into the food web have these poisons penetrated?
Canada’s vanishing barn owls
On a balmy but cloudy night, Hindmarch is trying to capture a barn owl, one of three owl species that ingested the rat poisons in the 2009 study. The hunt this night is in a gritty industrial outpost in Vancouver, where rats scamper boldly between the defunct lumber yard where they live and the bustling grain terminal where they sneak their dinner.
Between the wail of trains on tracks perhaps 30 yards away, Hindmarch and Levesque fiddle with their owl traps, preparing for their 9-5 shift – 9 p.m. until 5 a.m., that is.
“Can you grab one of the girls?” Hindmarch asks Levesque, referring to the mice that they hope will lure an owl to their traps.
The scientists have to carefully put the mice inside cages that will protect the mice when an owl swoops down, attracted by the rodents noisily munching on the crackers that Hindmarch is unwrapping. Hindmarch, of Simon Fraser University, doesn’t want the mice to be hurt.
How are plant eaters like deer and sheep ingesting rat poison? Grain eaters like squirrels? Hawks that subsist almost exclusively on songbirds that probably aren’t eating rats? Scientists wonder: Just how far into the food web have these poisons penetrated?
“It’s working time,” Hindmarch says as she grabs the first mouse in its transport cage and scoots it through the open door of a small cage that’s part of the owl trap. “You’ll get crackers soon.”
Levesque, a freelance contract scientist, puts the cage down in tall grass beside a nearby drainage ditch. He slips in some crackers and steals back to wait inside his truck. Under the tall grass, the noisy snacking attracts barn owls, which are then caught in the trap.
Hindmarch’s objective is twofold: to collect the owl’s blood so it can be tested for rat poisons; and to fit the owls with radio transmitters so she can track them and figure out where they are feeding. She wants to know whether urban owls are eating more poisoned rats than their country cousins.
“This our first time trying to get this guy,” Hindmarch says as she surveys the decrepit lumber yard. “I’d love to get this owl because it’s so urbanized that it’d be neat to see where he’s going and even if he has a nest or has a mate. We have no idea at this point.”
Her work is a follow up to the study analyzing owls found dead in British Columbia and the Yukon Territory, which showed that nearly three-quarters of the birds had rodenticides in their livers. The Canadian findings follow earlier studies in Europe, New Zealand, New York and elsewhere that documented the poisons spreading to wild animals.
The barn owls in and around Vancouver are among the last remaining barn owls in Canada. Two weeks ago, they were declared a “threatened” species. A smaller population, classified as “endangered,” lives in eastern Canada.
Although plenty remain alive in the United States, Hindmarch and her colleagues are eager to find out what role rat poisons may be having in the Canadian owls’ decline. The findings will have implications in the United States too.
Taken together, the research suggests that these improved rat-killers are imposing a toxic load on the environment that no one bargained for. It seems clear that some rats are being eaten by owls and other wild animals after they have ingested extraordinarily high doses of poison, researchers say.
“The rats are really little toxic packages running around before they die,” said Michael Fry, a wildlife toxicologist and pesticides expert with the American Bird Conservancy. “If the rat is carrying 10 or 15 times a lethal dose, the animal that consumes it is at a much higher risk of consuming a lethal dose.”
The research suggests that improved rat-killers are imposing a toxic load on the environment that no one bargained for.
In some cases, the dose isn’t lethal, but “maybe it’s affecting their flying ability and they’re getting hit more by cars,” said Kirstin Webster, a colleague of Hindmarch’s at Simon Fraser University in Vancouver, citing a fairly common way for owls to die.
Owls that aren’t killed outright by the poisons also can easily bleed to death because their blood fails to clot. Wild animals get hurt on a regular basis, scientists say; what otherwise would have been just a painful cut could spell death.
Webster’s work to find a way to test birds’ blood for exposure to rat poisons involved dosing quail and owls with a second-generation rodenticide called brodificoum. The quail given high doses bled not only internally, but also through their eyes, she said.
Once an owl or other animal eats a poisoned rat, the pesticides stay around in the predator’s system for a very long time. It takes six months or longer for just half the dose to be eliminated from some animals’ bodies.
Imagine you’re a barn owl like the one Hindmarch is trying to catch by the grain depot.
“If you’re just getting one dose on top of another, you get this constant exposure,” said Nancy Golden, a U.S. Fish and Wildlife Service toxicologist. “It’s one thing to have enough to kill you outright.
Once an owl or other animal eats a poisoned rat, the pesticides stay around in the predator’s system for a very long time. “But what about the ones that are just carrying this body burden? What effect does that have on their fitness? That’s what worries me.”
These “sublethal” effects are difficult to gauge, but research suggests they are real. For example, a study at McGill University in Montreal allowed a sparrow to perch on a pesticide-laden surface. The bird absorbed pesticide through its feet. Then researchers put the sparrow into a big cage along with three undosed sparrows and a kestrel, a small type of falcon that eats sparrows.
Although the scientists could not see any differences in the behavior of the pesticide-dosed sparrows, the kestrel apparently could. In 12 of the 15 instances in which the kestrel preyed on one of the sparrows, it picked the one that had absorbed the pesticide. (That study did not involve rat poisons but it shows that animals not visibly affected may be extremely vulnerable, Environment Canada’s Elliott said.)
The toll of six owls killed outright by rat poisons in the Canadian study almost certainly underestimates the actual rate at which owls are dying from rat poison, Elliott said. Animals that feel sick are likely to secret themselves away to protect themselves against predators.
The birds’ bodies are routinely scavenged by other wild animals, further spreading the poison into the food chain. The chemicals have the “potential to cause additional mortality that may not be sustainable in populations already experiencing critical limitations,” biologists from the United Kingdom’s University of Leicester reported in 2005.
California’s threatened San Joaquin kit fox is an example. Scientists collected carcasses of the big-eared, long-legged fox that died from various causes in Bakersfield and in an area 30 miles out in the country. Nearly all the dead foxes from Bakersfield had residues of the long-lived second-generation rodenticides, while none from the outlying desert did.
Chemicals in rat poison may cause additional mortality that may not be sustainable in populations already experiencing critical limitations, said biologists from the United Kingdom’s University of Leicester.
How are these rat poisons getting into plant eaters low on the food chain? There is no sure answer for now. Scientists wonder, though, if carcasses of poisoned animals are being scavenged by creatures low on the food chain. Or perhaps insects are crawling inside the bait stations. But there could be other ways, too. Elliott, the Environment Canada researcher, notes that scientists have seen voles and birds hopping inside the holes on the side of bait stations that approximate the size of the openings to their burrows or homes inside trees.
And as for deer? The seven that tested positive for rat poison in New York “apparently were exposed due to misuse and careless bait application,” Erickson of the EPA reported. Elliott noted that big blue blocks of the poisoned bait are sometimes thrown out into the wild – blue blocks that look a whole lot like the salt licks that deer are known to frequent.
Cracking down on rat poisons
Pushed by environmentalists who successfully sued in federal court, the EPA in 2008 issued rules for these rat poisons that largely take them out of the consumer market.
Pesticide manufacturers say EPA’s action was overkill, but should eliminate any doubts about the products’ safety for wildlife.
“There was not strong evidence to compel (EPA) to put into place the (new rules). However, they did so,” said Karen Reardon, director of communications at Responsible Industry for a Sound Environment, which represents pesticide manufacturers. “We have now even further added protections for secondary wildlife exposure.”
Pushed by environmentalists who successfully sued in federal court, the EPA in 2008 issued rules for these rat poisons that largely take them out of the consumer market.
Dale Kemery, an EPA spokesman, said the agency does not track the amount of pesticides manufactured or applied. But New York state does tote up the applications. New York State Department of Conservation records requested by the Natural Resources Defense Council for use in a lawsuit to limit the rodenticides’ use showed more than 20 tons a year were applied in eight New York City Zip codes in 2002. The pesticide manufacturer Syngenta International in 2004 revealed that some 10 million pounds of first- and second-generation rat poisons were sold annually in California. And in British Columbia, scientists obtained records showing large increases in their use during the 1990s.
The western Canadian study documented a 100 percent increase in sales of one of the rat poisons, brodifacoum, and a 24 percent increase in another, bromadiolone, in British Columbia between 1991 and 2003.
Canada in 2006 changed the rodenticides’ labels to require that they be used in dog- and child-proof bait stations that allow only rats access to the poison, or that the bait be limited to where kids and animals don’t have access.
Then, in 2009, six months before release of the study of the owl poisonings, Health Canada issued stricter regulations. Their inspiration came from a contentious rule approved south of the border.
In the United States, the EPA knew by the early 1980s that the pesticides that emerged the decade before were affecting non-targeted wildlife. But it was 1999 before the agency’s scientists launched a comprehensive risk analysis of the pesticides’ effects on wildlife.
George W. Bush was president by the time an EPA document outlining the environmental risks of the rat poisons was ready to go out for public comment. EPA sent a draft of the document to the pesticide industry in September 2001 for what was supposed to be a 30-day technical review. The stated purpose was to allow industry officials to make technical corrections.
Instead, the agency held a series of closed-door meetings with industry officials, environmentalists charged. “There has been excessive undue influence from industry on the entire process,” said the group Beyond Pesticides. “There has been little to no opportunity for any other stakeholder to provide input or even attend any of these meetings with EPA.”
Reardon of the pesticide industry group said it’s clear the pesticide industry didn’t get special treatment from EPA because the industry opposed what the agency ended up requiring. “EPA has added additional safeguards on top of what was already required. One must conclude that EPA’s actions satisfied what they believed was additional risk,” she said.
In January of 2003, the agency released preliminary results for public comment. This came more than three years after the risk analysis began. It took EPA five more years, until May of 2008, to complete a regulatory review.
And then, a quarter-century after the poisoning of wildlife became well known, the agency decreed that rules to protect wildlife would go into effect more than three years later, in June 2011.
Under the new rules, use of the second-generation rat poisons by consumers will be curtailed. The sale of loose rat baits will be banned in “big box” stores like Home Depot as well as other retail outlets. However, consumers can purchase up to one pound of bait in bait “stations” that are designed to keep out kids and dogs.
Professional exterminators as well as employees of farms, warehouses and other commercial installations may continue to use the more-toxic rat poisons, and loose baits. However, they are required to use above-ground bait stations if the bait is left outdoors or in any place accessible to children, pets or wildlife.
The rules represent a significant check on unsafe use of the products by consumers, said Rick Keigwin, director of EPA’s Pesticide Re-evaluation Division “We wanted people who are professionals in the field, who have the training, to use these products in the appropriate way,” he said.
The U.S. Fish and Wildlife Service and others pushed for EPA to disallow all outdoor uses of the rodenticides, with narrow exceptions.
EPA didn’t go that far, said Laura Parsons, an EPA biologist specializing in pesticides, because of pushback from some businesses. For example, she said, “restaurants and food-service facilities felt very strongly that they needed some kind of perimeter control.” The EPA’s position was backed by the U.S. Department of Housing and Urban Development and the federal Centers for Disease Control and Prevention.
Professional pesticide applicators support the new “common-sense” rules, said Bob Rosenberg, vice president of the National Pest Management Association, and opposed efforts to ban outdoor use of the more-toxic products.
The U.S. EPA knew by the early 1980s that the pesticides that emerged the decade before were affecting non-targeted wildlife. But it was 1999 before the agency’s scientists launched a comprehensive risk analysis of the pesticides’ effects on wildlife.
“Rodents are serious problem for all the reasons you know about – public health reasons,” Rosenberg said. “It’s a lot better to get them outside rather than inside the structure. You want to get them before they get to the food.”
Meanwhile, the multinational Reckitt Benckiser, which markets d-CON rat baits, is challenging the EPA’s new rules in court in an effort to prevent them from going into effect.
The least-toxic answer, said Golden, the Fish and Wildlife Service toxicologist, is a system known as “integrated pest management.” It emphasizes use of non-toxic pest-control methods, which in the case of rats translates to trapping the rats inside the house and finding ways to keep any more from getting in.
Golden predicted that poisoning of wild animals will continue.
“I wouldn’t use anticoagulants in my back yard,” said Golden. “These things are pervasive and are turning up in places we did not expect. . . . They’re certainly not contained where we think they are.”
----------------------------------------
EHN commissioned this story from InvestigateWest, a non-profit journalism studio based in Seattle and focused on the environment, public health and social justice in western North America. http://invw.org/
Photographer Paul Joseph Brown is at www.Ecosystemphoto.com.
Friday, December 10, 2010
Indian officials push Dow to pay $1.1bn to Bhopal victims.
Indian officials push Dow to pay $1.1bn to Bhopal victims
On Dec. 6, three days after the anniversary of the 1984 Bhopal pesticide plant explosion, India’s Attorney General asked the country’s supreme court to force Dow Chemical to pay $1.1 billion in compensation to victims, reports the Wall Street Journal. The move follows on persistent advocacy and recent trials in India and around the world to hold Dow accountable for the liabilities of Union Carbide, acquired by Dow in 2001. The tragedy is now estimated to have caused 20,000 deaths and some 500,000 injuries.
Dow maintains that the two companies are separate, and that it has no responsibility for the toxic legacy of Bhopal. U.S. State Dept. spokesperson P. J. Crowley has stated that Bhopal is a closed case. In response, the International Campaign for Justice in Bhopal has been calling on President Obama to intervene “to publicly recognize the ongoing nature of this disaster, and to demand that Dow Chemical [and] Union Carbide Corporation ... respect the jurisdiction of Indian courts and allow the law to take its course.” Satanath Sarangi, head of Sambhavna Clinic serving Bhopal survivors, declared: "The US government had taken stern action against British Petroleum in the oil spill case in which only 11 people were killed but they never acknowledged the worst industrial disaster caused by an American company."
Since 1998, December 3 has been marked by Pesticide Action Network groups around the world as a “Day of No Pesticide Use,” in honor of the Bhopal victims. This year, PAN Asia Pacific decided to extend the campaign as “No Pesticides Use Week,” culminating on December 10, World Human Rights Day, highlighting “the continuing inability of the concerned governments in bringing the perpetrators of the crime to justice”. PAN groups in the Philippines and eight other countries are participating, united in focusing specifically on the impact on women of highly hazardous pesticides, and promoting sustainable and organic agriculture in place of pesticide use.
http://www.panna.org/blog/indian-officials-push-dow-pay-11bn-bhopal-victims
On Dec. 6, three days after the anniversary of the 1984 Bhopal pesticide plant explosion, India’s Attorney General asked the country’s supreme court to force Dow Chemical to pay $1.1 billion in compensation to victims, reports the Wall Street Journal. The move follows on persistent advocacy and recent trials in India and around the world to hold Dow accountable for the liabilities of Union Carbide, acquired by Dow in 2001. The tragedy is now estimated to have caused 20,000 deaths and some 500,000 injuries.
Dow maintains that the two companies are separate, and that it has no responsibility for the toxic legacy of Bhopal. U.S. State Dept. spokesperson P. J. Crowley has stated that Bhopal is a closed case. In response, the International Campaign for Justice in Bhopal has been calling on President Obama to intervene “to publicly recognize the ongoing nature of this disaster, and to demand that Dow Chemical [and] Union Carbide Corporation ... respect the jurisdiction of Indian courts and allow the law to take its course.” Satanath Sarangi, head of Sambhavna Clinic serving Bhopal survivors, declared: "The US government had taken stern action against British Petroleum in the oil spill case in which only 11 people were killed but they never acknowledged the worst industrial disaster caused by an American company."
Since 1998, December 3 has been marked by Pesticide Action Network groups around the world as a “Day of No Pesticide Use,” in honor of the Bhopal victims. This year, PAN Asia Pacific decided to extend the campaign as “No Pesticides Use Week,” culminating on December 10, World Human Rights Day, highlighting “the continuing inability of the concerned governments in bringing the perpetrators of the crime to justice”. PAN groups in the Philippines and eight other countries are participating, united in focusing specifically on the impact on women of highly hazardous pesticides, and promoting sustainable and organic agriculture in place of pesticide use.
http://www.panna.org/blog/indian-officials-push-dow-pay-11bn-bhopal-victims
Thursday, December 9, 2010
Revealed: What the GM Lobby Doesn’t Want You to Know.
Revealed: What the GM Lobby Doesn’t Want You to Know.
Research linking a controversial herbicide with birth defects highlighted the potential health dangers posed by GM crop-spraying in Argentina - and led to violence and intimidation for those behind the study.
By Claire Robinson
In August 2010, community activists and residents gathered in La Leonesa, an agricultural town in Argentina, to hear a talk by Professor Andres Carrasco, lead embryologist at the University of Buenos Aires Medical School and the Argentinean national research council.
Carrasco was due to speak about his research, which found that glyphosate, an agrochemical used on genetically modified soy and rice in Argentina, causes birth defects in animal embryos at levels far below those frequently used in agricultural spraying. A delegation of public officials and residents from the nearby community of Resistencia also came to La Leonesa to hear the talk.
But the talk never took place. As the delegation headed for the school where it was to be held, it was attacked by a violent mob of approximately 100 people. Three people were seriously injured. Carrasco and a colleague shut themselves in a car and were surrounded by people beating the vehicle for two hours. Witnesses believe that a local rice producer and officials had organised the attack to protect agribusiness interests. As the police seemed reluctant to intervene, Amnesty International subsequently called for an independent investigation.
A Political Hot Potato
Carrasco's research was never destined to gather dust on a library shelf. It has become a political hot potato: scientific confirmation of a human rights tragedy that is unfolding on a massive scale in Argentina. Over the past decade, doctors and residents have reported escalating rates of birth defects, as well as infertility, stillbirths, miscarriages and cancers in areas where glyphosate is sprayed on genetically modified (GM) soy. Because GM soy is engineered to tolerate glyphosate, the herbicide can be sprayed liberally, killing weeds but allowing the crop to survive. Spraying is often carried out from the air, causing problems of drift.
Carrasco and his team discovered that Roundup and its active ingredient glyphosate caused malformations in frog and chicken embryos that were similar to human birth defects found in GM soy-producing areas. In particular, the researchers found malformations of the head and cyclopia (where a single eye is present in the centre of the forehead). Carrasco said people should be worried by these findings as humans share with the experimental animals the same mechanisms of development. The researchers also pointed out that women living in soy-producing areas of South America have high rates of repeated miscarriage - often the result of a malformed foetus.
After Carrasco announced his findings ahead of publication - the study was later published in the journal Chemical Research in Toxicology - a group of environmental lawyers petitioned the supreme court of Argentina to implement a national ban on the use of glyphosate. But such is Argentina's dependence on GM soy that Guillermo Cal, executive director of the crop-protection trade association CASAFE, said a ban would mean 'we couldn't do agriculture in Argentina'. Much of Argentina's GM soy is imported into Europe as livestock feed.
Unprecedented Ruling
No national ban on glyphosate has yet been implemented, but in a revolutionary ruling in March 2010, a regional court in Santa Fe province banned the spraying of glyphosate and other agrochemicals near populated areas. While the ruling is limited to the area around San Jorge, other courts are expected to follow suit.
Just a month after the court ruling, another bombshell dropped in Argentina's GM soy republic. The provincial government of Chaco province issued a report on health statistics from La Leonesa, the town where Carrasco was due to give his talk. The report said that from 2000 to 2009 the childhood cancer rate tripled in La Leonesa and the rate of birth defects increased nearly fourfold over the entire province. The report said that these staggering increases in disease coincided with the expansion of GM soy and rice crops in the region and the corresponding rise in agrochemical use.
Argentina is a unique experiment in the GM soy-farming model. In the 1990s the country rebuilt its collapsed economy around growing GM soy for export, becoming the world's largest exporter of soybean meal and oil. In 2009 the crop covered 19 million hectares - more than half the country's cultivated land area - which were sprayed with more than 200 million litres of glyphosate.
The Argentine government has come to depend on tariffs of more than 30 per cent levied on soy exports and is protective of the industry. Critics of the soy model have complained of harassment and persecution. Carrasco said after he went public with his findings, four people from CASAFE were sent to try to search his laboratory, and he was 'seriously told-off' by Argentina's science and technology minister.
Serious Health Impacts
Carrasco's study was not the first to show that glyphosate is not as safe as is made out. A report released in September 2010 and co-authored by nine international scientists, including Carrasco, called "GM Soy: Sustainable? Responsible?" gathered a series of studies showing links between exposure to glyphosate and premature births, miscarriages, cancer and damage to DNA and reproductive organ cells. The roster more than justifies Carrasco's verdict: 'I suspect the toxicity classification of glyphosate is too low ... in some cases this can be a powerful poison.'
Resistance against the GM soy with glyphosate model is growing. On 9 November, forest engineer and activist Claudio Lowy began a hunger strike in the doorway of the Ombudsman's office in Buenos Aires. In Argentina, the Ombudsman is called la Defensoria del Pueblo de la Nación - the Defender of the Nation's People.
In Lowy's view, the Ombudsman wasn't living up to his romantic title. Almost a year earlier, Lowy had signed a 2,700-strong petition to the Ombudsman requesting him to ask the government to change the way it classifies the toxicity of agrochemicals. When Lowy arrived on the Ombudsman's doorstep, the new GM soy-planting season was beginning, once again putting 12 million people in the path of the spray planes - and the petitioners still hadn't received a reply.
Long-term Effects
Three days later, Lowy called off his hunger strike when the Ombudsman put in a formal request to the ministry of agriculture to reassess the toxicity of agrochemicals according to their entire range of health effects. The Ombudsman asked the ministry to consider sublethal and chronic effects involving low doses over long periods, as happens with people exposed to spraying of fields, rather than just short-term (acute) and lethal effects, as is the case now.
The Ombudsman also advised that the toxicity of agrochemicals should be assessed based on independent scientific studies, not data provided by agribusiness companies. The Ombudsman's request will be sent to the ministry with a dossier of scientific research on the ill-health effects of agrochemicals, reports on sprayed residents and submissions from civil society organisations, scientists and health professionals.
Real science takes longer and costs more than rubber-stamping a company's data on its own chemicals. Often, the time and money needed to carry out proper studies becomes an excuse for inaction on the part of regulators. But that escape route has been closed off by the Ombudsman's final recommendation - that any chemicals that have not yet been evaluated for chronic and sublethal effects should be placed in the highest category of toxicity until they are proven safer. That would mean that they could not be sprayed near schools and residential neighbourhoods. Glyphosate is expected to be among them.
If the Ombudsman's recommendations are written into law, they will set an important precedent for science-based regulation of agrochemicals worldwide. Will it happen? A reply from an activist sounded familiar. Variations on it have been voiced by several Argentine people caught up in the fight against agrochemical poisoning - from the anonymous authors of the Chaco report to Carrasco himself: 'We don't know. There are powerful interests at stake.' - Third World Network Features.
-ends-
About the writer: Claire Robinson is an editor at GMWatch
The above article is reproduced from the Ecologist, 24th November, 2010.
Research linking a controversial herbicide with birth defects highlighted the potential health dangers posed by GM crop-spraying in Argentina - and led to violence and intimidation for those behind the study.
By Claire Robinson
In August 2010, community activists and residents gathered in La Leonesa, an agricultural town in Argentina, to hear a talk by Professor Andres Carrasco, lead embryologist at the University of Buenos Aires Medical School and the Argentinean national research council.
Carrasco was due to speak about his research, which found that glyphosate, an agrochemical used on genetically modified soy and rice in Argentina, causes birth defects in animal embryos at levels far below those frequently used in agricultural spraying. A delegation of public officials and residents from the nearby community of Resistencia also came to La Leonesa to hear the talk.
But the talk never took place. As the delegation headed for the school where it was to be held, it was attacked by a violent mob of approximately 100 people. Three people were seriously injured. Carrasco and a colleague shut themselves in a car and were surrounded by people beating the vehicle for two hours. Witnesses believe that a local rice producer and officials had organised the attack to protect agribusiness interests. As the police seemed reluctant to intervene, Amnesty International subsequently called for an independent investigation.
A Political Hot Potato
Carrasco's research was never destined to gather dust on a library shelf. It has become a political hot potato: scientific confirmation of a human rights tragedy that is unfolding on a massive scale in Argentina. Over the past decade, doctors and residents have reported escalating rates of birth defects, as well as infertility, stillbirths, miscarriages and cancers in areas where glyphosate is sprayed on genetically modified (GM) soy. Because GM soy is engineered to tolerate glyphosate, the herbicide can be sprayed liberally, killing weeds but allowing the crop to survive. Spraying is often carried out from the air, causing problems of drift.
Carrasco and his team discovered that Roundup and its active ingredient glyphosate caused malformations in frog and chicken embryos that were similar to human birth defects found in GM soy-producing areas. In particular, the researchers found malformations of the head and cyclopia (where a single eye is present in the centre of the forehead). Carrasco said people should be worried by these findings as humans share with the experimental animals the same mechanisms of development. The researchers also pointed out that women living in soy-producing areas of South America have high rates of repeated miscarriage - often the result of a malformed foetus.
After Carrasco announced his findings ahead of publication - the study was later published in the journal Chemical Research in Toxicology - a group of environmental lawyers petitioned the supreme court of Argentina to implement a national ban on the use of glyphosate. But such is Argentina's dependence on GM soy that Guillermo Cal, executive director of the crop-protection trade association CASAFE, said a ban would mean 'we couldn't do agriculture in Argentina'. Much of Argentina's GM soy is imported into Europe as livestock feed.
Unprecedented Ruling
No national ban on glyphosate has yet been implemented, but in a revolutionary ruling in March 2010, a regional court in Santa Fe province banned the spraying of glyphosate and other agrochemicals near populated areas. While the ruling is limited to the area around San Jorge, other courts are expected to follow suit.
Just a month after the court ruling, another bombshell dropped in Argentina's GM soy republic. The provincial government of Chaco province issued a report on health statistics from La Leonesa, the town where Carrasco was due to give his talk. The report said that from 2000 to 2009 the childhood cancer rate tripled in La Leonesa and the rate of birth defects increased nearly fourfold over the entire province. The report said that these staggering increases in disease coincided with the expansion of GM soy and rice crops in the region and the corresponding rise in agrochemical use.
Argentina is a unique experiment in the GM soy-farming model. In the 1990s the country rebuilt its collapsed economy around growing GM soy for export, becoming the world's largest exporter of soybean meal and oil. In 2009 the crop covered 19 million hectares - more than half the country's cultivated land area - which were sprayed with more than 200 million litres of glyphosate.
The Argentine government has come to depend on tariffs of more than 30 per cent levied on soy exports and is protective of the industry. Critics of the soy model have complained of harassment and persecution. Carrasco said after he went public with his findings, four people from CASAFE were sent to try to search his laboratory, and he was 'seriously told-off' by Argentina's science and technology minister.
Serious Health Impacts
Carrasco's study was not the first to show that glyphosate is not as safe as is made out. A report released in September 2010 and co-authored by nine international scientists, including Carrasco, called "GM Soy: Sustainable? Responsible?" gathered a series of studies showing links between exposure to glyphosate and premature births, miscarriages, cancer and damage to DNA and reproductive organ cells. The roster more than justifies Carrasco's verdict: 'I suspect the toxicity classification of glyphosate is too low ... in some cases this can be a powerful poison.'
Resistance against the GM soy with glyphosate model is growing. On 9 November, forest engineer and activist Claudio Lowy began a hunger strike in the doorway of the Ombudsman's office in Buenos Aires. In Argentina, the Ombudsman is called la Defensoria del Pueblo de la Nación - the Defender of the Nation's People.
In Lowy's view, the Ombudsman wasn't living up to his romantic title. Almost a year earlier, Lowy had signed a 2,700-strong petition to the Ombudsman requesting him to ask the government to change the way it classifies the toxicity of agrochemicals. When Lowy arrived on the Ombudsman's doorstep, the new GM soy-planting season was beginning, once again putting 12 million people in the path of the spray planes - and the petitioners still hadn't received a reply.
Long-term Effects
Three days later, Lowy called off his hunger strike when the Ombudsman put in a formal request to the ministry of agriculture to reassess the toxicity of agrochemicals according to their entire range of health effects. The Ombudsman asked the ministry to consider sublethal and chronic effects involving low doses over long periods, as happens with people exposed to spraying of fields, rather than just short-term (acute) and lethal effects, as is the case now.
The Ombudsman also advised that the toxicity of agrochemicals should be assessed based on independent scientific studies, not data provided by agribusiness companies. The Ombudsman's request will be sent to the ministry with a dossier of scientific research on the ill-health effects of agrochemicals, reports on sprayed residents and submissions from civil society organisations, scientists and health professionals.
Real science takes longer and costs more than rubber-stamping a company's data on its own chemicals. Often, the time and money needed to carry out proper studies becomes an excuse for inaction on the part of regulators. But that escape route has been closed off by the Ombudsman's final recommendation - that any chemicals that have not yet been evaluated for chronic and sublethal effects should be placed in the highest category of toxicity until they are proven safer. That would mean that they could not be sprayed near schools and residential neighbourhoods. Glyphosate is expected to be among them.
If the Ombudsman's recommendations are written into law, they will set an important precedent for science-based regulation of agrochemicals worldwide. Will it happen? A reply from an activist sounded familiar. Variations on it have been voiced by several Argentine people caught up in the fight against agrochemical poisoning - from the anonymous authors of the Chaco report to Carrasco himself: 'We don't know. There are powerful interests at stake.' - Third World Network Features.
-ends-
About the writer: Claire Robinson is an editor at GMWatch
The above article is reproduced from the Ecologist, 24th November, 2010.
Two children killed by insecticide in Kuwait
Two children killed by insecticide in Kuwait
By Staff - Published Monday, December 06, 2010
Two Kuwaiti children died of asphyxia after inhaling poisonous insecticide that spread into their house from a neighbouring food store sprayed by a local company, the Kuwait Alanba newspaper reported on Monday.
The father of the unidentified two, told court his children died after that company illegally used poisonous pesticides and insecticides to spray a new food store set up next to their house in Kuwait City, the paper said.
The paper did not specify the age of the two boys but said the court ordered the company to pay KD100,000 (Dh1.2 million) in damages to the victims’ family.
“This sentence should constitute a deterrent to any company that does not care for human lives and underestimate risks besetting such acts,” the paper quoted lawyer Nawaf Sari as saying.
By Staff - Published Monday, December 06, 2010
Two Kuwaiti children died of asphyxia after inhaling poisonous insecticide that spread into their house from a neighbouring food store sprayed by a local company, the Kuwait Alanba newspaper reported on Monday.
The father of the unidentified two, told court his children died after that company illegally used poisonous pesticides and insecticides to spray a new food store set up next to their house in Kuwait City, the paper said.
The paper did not specify the age of the two boys but said the court ordered the company to pay KD100,000 (Dh1.2 million) in damages to the victims’ family.
“This sentence should constitute a deterrent to any company that does not care for human lives and underestimate risks besetting such acts,” the paper quoted lawyer Nawaf Sari as saying.
NEW EVIDENCE: Bee-Killing Pesticide Never Should Have Been Registered
NEW EVIDENCE: Bee-Killing Pesticide Never Should Have Been Registered
Environmental working groups across the United States are demanding
that the Environmental Protection Agency pull pesticides containing
synthetic nicotine off the market due to proof of a bogus test run by
the pesticide manufacturer. Stating: “Our nation cannot afford, and
the environment cannot tolerate another growing season of
clothianindin use,” a group of beekeepers and activists sent a letter
to EPA Director Lisa Jackson.
Probably most significantly, Penn State scientist James Frazier joined
the beekeeping community in calling for a ban on this pesticide —
which SafeLawns has been implicating in bee decline for the past four
years. The professor of entomology at Penn State’s College of
Agricultural Sciences said, “Among the neonicotinoids, clothianidin is
among those most toxic for honey bees; and this combined with its
systemic movement in plants has produced a troubling mix of scientific
results pointing to its potential risk for honey bees through current
agricultural practices. Our own research indicates that systemic
pesticides occur in pollen and nectar in much greater quantities than
has been previously thought, and that interactions among pesticides
occurs often and should be of wide concern.” Dr. Frazier said that the
most prudent course of action would be to take the pesticide off the
market while the flawed study is being redone.
Please forward this press release to all elected officials to your
states and local districts and let them know that you demand that
these products be taken off the shelves.
HERE IS THE RELEASE
Contacts:
Heather Pilatic, Pesticide Action Network
cell: 415.694.8596
Jay Feldman, Beyond Pesticides
202.543.5450, ext 15
Beekeepers Ask EPA to Remove Pesticide Linked to Colony Collapse
Disorder,
Citing Leaked Agency Memo
Pesticide Already Illegal in Germany, Italy & France Based on
Scientific Findings
SAN FRANCISCO and WASHINGTON, D.C – Beekeepers and environmentalists
today called on EPA to remove a pesticide linked to Colony Collapse
Disorder (CCD), citing a leaked EPA memo that discloses a critically
flawed scientific support study. The November 2nd memo identifies a
core study underpinning the registration of the insecticide
clothianidin as unsound after EPA quietly re-evaluated the pesticide
just as it was getting ready to allow a further expansion of its use.
Clothianidin (product name “Poncho”) has been widely used as a seed
treatment on many of the country’s major crops for eight growing
seasons under a “conditional registration” granted while EPA waited
for Bayer Crop Science, the pesticide’s maker, to conduct a field
study assessing the insecticide’s threat to bee colony health.
Bayer’s field study was the contingency on which clothianidin’s
conditional registration was granted in 2003. As such, the groups are
calling for an immediate stop-use order on the pesticide while the
science is redone, and redesigned in partnership with practicing
beekeepers. They claim that the initial field study guidelines, which
the Bayer study failed to satisfy, were insufficiently rigorous to
test whether or not clothianidin contributes to CCD in a real-world
scenario: the field test evaluated the wrong crop, over an
insufficient time period and with inadequate controls.
According to beekeeper Jeff Anderson, who has testified before EPA on
the topic, “The Bayer study is fatally flawed. It was an open field
study with control and test plots of about 2 acres each. Bees
typically forage at least 2 miles out from the hive, so it is likely
they didn’t ingest much of the treated crops. And corn, not canola, is
the major pollen-producing crop that bees rely on for winter
nutrition. This is a critical point because we see hive losses mainly
after over-wintering, so there is something going on in these winter
cycles. It’s as if they designed the study to avoid seeing
clothianidin’s effects on hive health.”
Clothianidin is of the neonicotinoid family of systemic pesticides,
which are taken up by a plant’s vascular system and expressed through
pollen, nectar and gutation droplets from which bees then forage and
drink. Scientists are concerned about the mix and cumulative effects
of the multiple pesticides bees are exposed to in these ways.
Neonicotinoids are of particular concern because they have cumulative,
sublethal effects on insect pollinators that correspond to CCD
symptoms – namely, neurobehavioral and immune system disruptions.
According to James Frazier, PhD., professor of entomology at Penn
State’s College of Agricultural Sciences, “Among the neonicotinoids,
clothianidin is among those most toxic for honey bees; and this
combined with its systemic movement in plants has produced a troubling
mix of scientific results pointing to its potential risk for honey
bees through current agricultural practices. Our own research
indicates that systemic pesticides occur in pollen and nectar in much
greater quantities than has been previously thought, and that
interactions among pesticides occurs often and should be of wide
concern.”
Dr. Frazier said that the most prudent course of action would be to
take the pesticide off the market while the flawed study is being
redone.
Clothianidin has been on the market since 2003. With a soil half-life
of up to 19 years in heavy soils, and over a year in the lightest of
soils, commercial beekeepers are concerned that even an immediate stop-
use of clothianidin won’t save their livelihoods or hives in time.
“We are losing more than a third of our colonies each winter; but
beekeepers are a stubborn, industrious bunch. We split hives, rebound
as much as we can each summer, and then just take it on the chin – eat
our losses. So even these big loss numbers understate the problem,”
says 50-year beekeeper, David Hackenberg. “What folks need to
understand is that the beekeeping industry, which is responsible for a
third of the food we all eat, is at a critical threshold for economic
reasons and reasons to do with bee population dynamics. Our bees are
living for 30 days instead of 42, nursing bees are having to forage
because there aren’t enough foragers and at a certain point a colony
just doesn’t have the critical mass to keep going. The bees are at
that point, and we are at that point. We are losing our livelihoods at
a time when there just isn’t other work. Another winter of ‘more
studies are needed’ so Bayer can keep their blockbuster products on
the market and EPA can avoid a difficult decision, is unacceptable.”
Citing the imminent economic and environmental hazards posed by the
continued use of clothianidin, the National Honey Bee Advisory Board,
Beekeeping Federation, Beyond Pesticides, Pesticide Action Network,
North America and Center for Biological Diversity are asking EPA
administrator Lisa Jackson to exercise the Agency’s emergency powers
to take the pesticide off the market.
“The environment has become the experiment and all of us – not just
bees and beekeepers – have become the experimental subjects,” said Tom
Theobald, a 35-year beekeeper. “In an apparent rush to get products to
the market, chemicals have been routinely granted “conditional”
registrations. Of 94 pesticide active ingredients released since 1997,
70% have been given conditional registrations, with unanswered
questions of unknown magnitude. In the case of clothianidin those
questions were huge. The EPA’s basic charge is “the prevention of
unreasonable risk to man and the environment” and these practices
hardly satisfy that obligation. We must do better, there is too much
at stake.”
Environmental working groups across the United States are demanding
that the Environmental Protection Agency pull pesticides containing
synthetic nicotine off the market due to proof of a bogus test run by
the pesticide manufacturer. Stating: “Our nation cannot afford, and
the environment cannot tolerate another growing season of
clothianindin use,” a group of beekeepers and activists sent a letter
to EPA Director Lisa Jackson.
Probably most significantly, Penn State scientist James Frazier joined
the beekeeping community in calling for a ban on this pesticide —
which SafeLawns has been implicating in bee decline for the past four
years. The professor of entomology at Penn State’s College of
Agricultural Sciences said, “Among the neonicotinoids, clothianidin is
among those most toxic for honey bees; and this combined with its
systemic movement in plants has produced a troubling mix of scientific
results pointing to its potential risk for honey bees through current
agricultural practices. Our own research indicates that systemic
pesticides occur in pollen and nectar in much greater quantities than
has been previously thought, and that interactions among pesticides
occurs often and should be of wide concern.” Dr. Frazier said that the
most prudent course of action would be to take the pesticide off the
market while the flawed study is being redone.
Please forward this press release to all elected officials to your
states and local districts and let them know that you demand that
these products be taken off the shelves.
HERE IS THE RELEASE
Contacts:
Heather Pilatic, Pesticide Action Network
cell: 415.694.8596
Jay Feldman, Beyond Pesticides
202.543.5450, ext 15
Beekeepers Ask EPA to Remove Pesticide Linked to Colony Collapse
Disorder,
Citing Leaked Agency Memo
Pesticide Already Illegal in Germany, Italy & France Based on
Scientific Findings
SAN FRANCISCO and WASHINGTON, D.C – Beekeepers and environmentalists
today called on EPA to remove a pesticide linked to Colony Collapse
Disorder (CCD), citing a leaked EPA memo that discloses a critically
flawed scientific support study. The November 2nd memo identifies a
core study underpinning the registration of the insecticide
clothianidin as unsound after EPA quietly re-evaluated the pesticide
just as it was getting ready to allow a further expansion of its use.
Clothianidin (product name “Poncho”) has been widely used as a seed
treatment on many of the country’s major crops for eight growing
seasons under a “conditional registration” granted while EPA waited
for Bayer Crop Science, the pesticide’s maker, to conduct a field
study assessing the insecticide’s threat to bee colony health.
Bayer’s field study was the contingency on which clothianidin’s
conditional registration was granted in 2003. As such, the groups are
calling for an immediate stop-use order on the pesticide while the
science is redone, and redesigned in partnership with practicing
beekeepers. They claim that the initial field study guidelines, which
the Bayer study failed to satisfy, were insufficiently rigorous to
test whether or not clothianidin contributes to CCD in a real-world
scenario: the field test evaluated the wrong crop, over an
insufficient time period and with inadequate controls.
According to beekeeper Jeff Anderson, who has testified before EPA on
the topic, “The Bayer study is fatally flawed. It was an open field
study with control and test plots of about 2 acres each. Bees
typically forage at least 2 miles out from the hive, so it is likely
they didn’t ingest much of the treated crops. And corn, not canola, is
the major pollen-producing crop that bees rely on for winter
nutrition. This is a critical point because we see hive losses mainly
after over-wintering, so there is something going on in these winter
cycles. It’s as if they designed the study to avoid seeing
clothianidin’s effects on hive health.”
Clothianidin is of the neonicotinoid family of systemic pesticides,
which are taken up by a plant’s vascular system and expressed through
pollen, nectar and gutation droplets from which bees then forage and
drink. Scientists are concerned about the mix and cumulative effects
of the multiple pesticides bees are exposed to in these ways.
Neonicotinoids are of particular concern because they have cumulative,
sublethal effects on insect pollinators that correspond to CCD
symptoms – namely, neurobehavioral and immune system disruptions.
According to James Frazier, PhD., professor of entomology at Penn
State’s College of Agricultural Sciences, “Among the neonicotinoids,
clothianidin is among those most toxic for honey bees; and this
combined with its systemic movement in plants has produced a troubling
mix of scientific results pointing to its potential risk for honey
bees through current agricultural practices. Our own research
indicates that systemic pesticides occur in pollen and nectar in much
greater quantities than has been previously thought, and that
interactions among pesticides occurs often and should be of wide
concern.”
Dr. Frazier said that the most prudent course of action would be to
take the pesticide off the market while the flawed study is being
redone.
Clothianidin has been on the market since 2003. With a soil half-life
of up to 19 years in heavy soils, and over a year in the lightest of
soils, commercial beekeepers are concerned that even an immediate stop-
use of clothianidin won’t save their livelihoods or hives in time.
“We are losing more than a third of our colonies each winter; but
beekeepers are a stubborn, industrious bunch. We split hives, rebound
as much as we can each summer, and then just take it on the chin – eat
our losses. So even these big loss numbers understate the problem,”
says 50-year beekeeper, David Hackenberg. “What folks need to
understand is that the beekeeping industry, which is responsible for a
third of the food we all eat, is at a critical threshold for economic
reasons and reasons to do with bee population dynamics. Our bees are
living for 30 days instead of 42, nursing bees are having to forage
because there aren’t enough foragers and at a certain point a colony
just doesn’t have the critical mass to keep going. The bees are at
that point, and we are at that point. We are losing our livelihoods at
a time when there just isn’t other work. Another winter of ‘more
studies are needed’ so Bayer can keep their blockbuster products on
the market and EPA can avoid a difficult decision, is unacceptable.”
Citing the imminent economic and environmental hazards posed by the
continued use of clothianidin, the National Honey Bee Advisory Board,
Beekeeping Federation, Beyond Pesticides, Pesticide Action Network,
North America and Center for Biological Diversity are asking EPA
administrator Lisa Jackson to exercise the Agency’s emergency powers
to take the pesticide off the market.
“The environment has become the experiment and all of us – not just
bees and beekeepers – have become the experimental subjects,” said Tom
Theobald, a 35-year beekeeper. “In an apparent rush to get products to
the market, chemicals have been routinely granted “conditional”
registrations. Of 94 pesticide active ingredients released since 1997,
70% have been given conditional registrations, with unanswered
questions of unknown magnitude. In the case of clothianidin those
questions were huge. The EPA’s basic charge is “the prevention of
unreasonable risk to man and the environment” and these practices
hardly satisfy that obligation. We must do better, there is too much
at stake.”
‘Produce improves by 80% through organic farming.'
‘Produce improves by 80% through organic farming’
The promise of organis farming is not only limited to safe and healthy lifestyle, it also doubles produce by 80 percent per hectare, Humayan Ministry pastor Jerry Dionson said.
Dionson said that traditional farming gain is only pegged at P25,000 per hectare every crop cycle while organic farming can reach P45,000.
In traditional farming, farmers use chemically-based pesticides and fertilizers to help improve the soil and prevent infestation. This factor usually eats up most of the budgeting of the farmers, Dionson said.
On the other hand, in organic farming, the same inputs are used but the material is all organic like using trichogramma to prevent army worm influx, he added. The farmers will also have to discover it for themselves that in a span of five years, organic production will double its number because of the proper land use that provides nutrients to the plantation, Dionson added.
Farmers do not need to change their farming techniques but the inputs they use to cultivate their plantation, which must be free from chemicals, Dionson also said. He said that this is the ministry’s way of keeping the island safe and the consuming public healthy.
Humayan Ministry also offers pastoral care, camp site, and farming community.
Meanwhile, the 5th Organic Negros festival ended Saturday with 64 exhibitors from various organic producers and retailers.
Organik Na! Negros Organic Producers and Retailers Association president Ramon Uy, Sr. said that the continuous programs of going organic will help the farmers become better at the craft.
Uy said the festival also provides new ventures for farmers to increase their production. Farmers must be proud of their work, for without them, the entire country will starve, he added.
Coffee grower Angel Vic Labrador, meanwhile, said he hopes for the approval of the Organic Act of 2010 because the province is already on the right track of organic living. The approval of the act means that Negros Occidental will be the first beneficiary and implementer, he added.
Meanwhile, Biyahe Negros head Maricar Dabao also promised to include in their tours the leading organic farms of the province. Davao said that it is not only the scenic places that bring tourists in the province, but also the organic farms.
Dabao said that there is a great potential for the province to boost its tourism industry because of its strong drive to go organic.
She also said that the festival is one way to educate and involve the youth in living organic and choosing a healthier lifestyle.*LTG
The promise of organis farming is not only limited to safe and healthy lifestyle, it also doubles produce by 80 percent per hectare, Humayan Ministry pastor Jerry Dionson said.
Dionson said that traditional farming gain is only pegged at P25,000 per hectare every crop cycle while organic farming can reach P45,000.
In traditional farming, farmers use chemically-based pesticides and fertilizers to help improve the soil and prevent infestation. This factor usually eats up most of the budgeting of the farmers, Dionson said.
On the other hand, in organic farming, the same inputs are used but the material is all organic like using trichogramma to prevent army worm influx, he added. The farmers will also have to discover it for themselves that in a span of five years, organic production will double its number because of the proper land use that provides nutrients to the plantation, Dionson added.
Farmers do not need to change their farming techniques but the inputs they use to cultivate their plantation, which must be free from chemicals, Dionson also said. He said that this is the ministry’s way of keeping the island safe and the consuming public healthy.
Humayan Ministry also offers pastoral care, camp site, and farming community.
Meanwhile, the 5th Organic Negros festival ended Saturday with 64 exhibitors from various organic producers and retailers.
Organik Na! Negros Organic Producers and Retailers Association president Ramon Uy, Sr. said that the continuous programs of going organic will help the farmers become better at the craft.
Uy said the festival also provides new ventures for farmers to increase their production. Farmers must be proud of their work, for without them, the entire country will starve, he added.
Coffee grower Angel Vic Labrador, meanwhile, said he hopes for the approval of the Organic Act of 2010 because the province is already on the right track of organic living. The approval of the act means that Negros Occidental will be the first beneficiary and implementer, he added.
Meanwhile, Biyahe Negros head Maricar Dabao also promised to include in their tours the leading organic farms of the province. Davao said that it is not only the scenic places that bring tourists in the province, but also the organic farms.
Dabao said that there is a great potential for the province to boost its tourism industry because of its strong drive to go organic.
She also said that the festival is one way to educate and involve the youth in living organic and choosing a healthier lifestyle.*LTG
Wednesday, December 8, 2010
ANTI-INFLAMMATORY DRUG RESEARCH
ANTI-INFLAMMATORY DRUG RESEARCH – A Pointer To The Better Role Of Phytochemicals From Fruits And Berries
(A Short Note)
Beldeu Singh
Billions of dollars have been spent on research and production of anti-inflammatory drugs but they are all toxic. These drugs were developed with the intention to find chemicals that will suppress the Cox-2 enzymes that are associated with the inflammatory process and promote inflammations.
Cancer cells have high cell membrane potential, having lost electrons from molecules in the cell membrane to free radicals and oxidants like the peroxynitrite (ONOO-) or heavy metals and accordingly are highly inflamed, more than cells at lesions in psoriasis and arthritis.
In the New Straits Times, today at p26 the headline reads - "small daily doses of aspirin cuts many cancer risks" - it is about research on aspirin, a drug that can destroy the cementing material that binds and holds cells together and if this is destroyed in the tissue of the intestines, it can cause intestinal bleeding. Furthermore, aspirin intereferes with and blocks the blood coagulating factors which can be dangerous, especially in the older population and in accident victims.
This short newsreport says that researchers at Oxford say that low daily doses of aspirin cuts cancer the rate of cancer deaths and suggested (quite correctly) “that it does so by blocking the enzyme Cox-2 which promotes inflammation” as cancer cells have high CMB (ie they are highly inflamed) and if aspirin can suppress the inflammatory process it prevents the initiation of the formation of cancer cells. There are several epidemiological studies that clearly show that in populations that consume traditional diets and diets with relatively high fruit and vegetable intake tend to have lower incidence of cancers, which is primarily due to the role of natural antioxidants in preventing inflammations and organic minerals (iron, copper, mnaganese, zinc) that work as catalysts with the SOD-Catalase enzyme system to effecftively and efficienctly convert the superoxide into water and oxygen and thereby prevent excess hydrogen peroxide and oxygen free radical in the body and support optimal cell function that tends to decline with age and with lowering of blood antioxidant levels with consequent lower output of citric acid from the citric acid cycle and these appear to be factors in which micro-parasites and protozoa become active. In the active stage they consume more vitamin B12, competing with the host, causing vitamin B12 depletion or deficiencies and secrete more allergens that promote the inflammatory process.
Both aspirin and sulindac have been reported to display profound antiproliferative effects on tumor cell lines, alter the cell cycle distribution, and induce apoptosis (Shiff S J, Qiao L, Tsai L L, Rigas B. J Clin Invest. 1995;96:491–503: Ricchi P, Pignata S, Di Popolo A, Memoli A, Apicella A, Zarrilli R, Acquaviva A M. Int J Cancer. 1997;73:880–884: Sheng H, Shao J, Kirkland S C, Isakson P, Coffey R J, Morrow J, Beauchamp R D, DuBois R N. J Clin Invest. 1997;99:2254–2259).
However, what they did not also say is that like other anti-inflammatory drugs, aspirin also suppresses the Cox-1 enzyme which is very important for health. COX-1 is ubiquitously expressed and appears to be a housekeeping gene, whereas COX-2 expression is inducible by growth factors and oncogenes (Prescott S M, White R L. Cell. 1996;87:783–786) and fruits like strawberry is known to suppress Cox-2 (as effectively as drugs) without suppressing Cox-1. Suppression of Cox-1 can lead to serious health problems, including thinning of the stomach lining. Cayenne contains the potent chemical capsaicin, which acts on special nerves found in the stomach lining. In two rat studies, researchers reported that stimulation of these nerves by capsaicin might protect against the damage aspirin can cause to the stomach (Abdel Salam OME, Mószik G, Szolcsányi J. Studies on the effect of intragastric capsaicin on gastric ulcer and on the prostacyclin-induced cytoprotection in rats. Pharmacol Res 1995;32:209-15: Holzer P, Pabst MA, Lippe IT. Intragastric capsaicin protects against aspirin-induced lesion formation and bleeding in the rat gastric mucosa. Gastroenterology 1989;96:1425-33). The flavonoids found in the extract of licorice known as DGL (deglycyrrhizinated licorice) are helpful for avoiding the irritating actions aspirin has on the stomach and intestines. One study found that 350 mg of chewable DGL taken together with each dose of aspirin reduced gastrointestinal bleeding caused by the aspirin (Rees WDW, Rhodes J, Wright JE, et al. Effect of deglycyrrhizinated liquorice on gastric mucosal damage by aspirin. Scand J Gastroenterol 1979;14:605-7).
Some fifty cousins of aspirin exist, most of which appeared after World War II. Together they constitute a family known as non-steroidal anti-inflammatory drugs (NSAIDs). They can interfere with physiology including the formation of prostaglandins.
Many kinds of prostaglandin exist in the body to serve a plethora of physiological functions, some of which are irritable, others beneficial. Prostaglandins are among the chemicals secreted by the body’s immune system when it fights off bacteria and other invaders in injuries. Located around wounds , these chemicals cause pain and inflammation. Aspirin inhibits the production of prostaglandins (JR. Vane, 1971, Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs, Nature, New Biology: 231: 230-235). This happens because cyclooxygenase, a Cox enzyme which participates in the production of prostaglandins and thromboxanes, is irreversibly inhibited when aspirin acetylates it (Roth GJ and Majerus PW, The mechanism of the effect of aspirin on human platelets, I: acetylation of a particulate fraction protein, J Clin Invest., 1975;56:624–632: Lecomte M et al. Acetylation of human endoperoxide synthase-2 by aspirin, J Biol Chem,. 1994;269:13207–13215). Aspirin irresversibly binds cyclooxygenase (Cox-1 and Cox-2). Thereby blocking arachidonic acid from from porstaglandins (Carol D Morris, Principles of Orthopaedic Pharmacology, 7th ed, © 2008, Lippincott Williams & Wilkins).
Aspirin inhibits both Cox-1 and Cox-2 enzymes, aspirin more slectively inhibits COX-1 activity (found predominantly in platelets) than COX-2 activity (showed in tissues follwoing an inflammatory stimuli), its ability to prevent platelet aggregation is seen at relatively low doses, compared with it's anti-inflammatory effects, which require higher doses. Low-dose long-term aspirin irreversibly blocks formation of thromboxane A2 in platelets, producing an inhibitory affect on platelet aggregation, and this blood thinning property makes it useful for reducing the incidence of heart attacks (Aspirin, Pharpedia, 28th August 2005). So, how brilliant is their research?
Aspirin taken by patients while having a heart attack significantly reduces the chance of death. For people with various risk factors for heart diseases such as diabetes, obesity, or high blood pressure, aspirin lowers the probability of a first heart attack. For healthy people without cardiovascular risks, results on the effects of aspirin are inconclusive (G. Weissman, 1997, Aspirin, Scientific American, 264(1): 84-90 (1991). D. B. Jack. A hundred years of aspirin. The Lancet, 350: 437-439).
Salicylic acid, from the bark of the willow tree, is a monohydroxybenzoic acid, is a phenolic acid and a beta hydroxy acid. This colorless crystalline organic acid is widely used in organic synthesis and functions as a plant hormone. It is derived from the metabolism of salicin. It is a compound that is chemically similar to but not identical to the active component of aspirin (acetylsalicylic acid), it is probably best known for its use in anti-acne treatments and may have anti-protozoal properties. Salicylic acid is known for its ability to ease aches and pains and reduce fevers. These medicinal properties, particularly fever relief, have been known since ancient times and it was used as an anti-inflammatory drug (Philip A. Mackowiak, 2000, "Brief History of Antipyretic Therapy". Clinical Infectious Diseases, 31: 154–156). Salicylic acid (SA) is a phenolic phytohormone and is found in plants with roles in plant growth and development, photosynthesis, transpiration, ion uptake and transport. SA also induces specific changes in leaf anatomy and chloroplast structure. SA is involved in endogenous signaling, mediating in plant defense against pathogens (S. Hayat, A. Ahmad (2007). Salicylic acid - A Plant Hormone. Springer. ISBN 1402051832).
Sodium salicylate paradoxically inhibited prostaglandin synthesis when added to intact cells (Mitchell JA, et al. Selectivity of nonsteroidal anti-inflammatory drugs as inhibitors of constitutive and inducible cyclooxygenase. Proc Natl Acad Sci U S A. 1994;90:11693–11697). Furthermore, healthy subjects taking sodium salicylate excreted a significantly lower amount of prostaglandin metabolites in urine than those not taking sodium salicylate, and their levels of inhibition were comparable to those of patients taking aspirin and indomethacin (Hamberg M. Inhibition of prostaglandin synthesis in man. Biochem Biophys Res Commun. 1972;49:720–726). Aspirin also reduces human seminal prostaglandin levels (Collies JG, Flowers RJ. Effect of aspirin on human seminal prostaglandins. Lancet. 1971;i:852–853).
Aspirin, which suppresses cyclooxygenase, has the potential to interfere with implantation. Aspirin has potential risks. Aspirin inhibits platelet function and can contribute to maternal and fetal bleeding. Aspirin crosses the placenta. Although aspirin has not been associated with other congenital anomalies, it has been associated with an increased risk of vascular disruptions, particularly gastroschisis and possibly premature closure of the ductus arteriosus. Nonetheless, large trials demonstrate low-dose aspirin's relative safety (James et al, Aspirin and Reproductive Outcomes, Obstetrical & Gynecological Survey: January 2008 - Volume 63 - Issue 1 - pp 49-57).
Immunosuppressive and anti-inflammatory agents significantly inhibited T cell proliferation, especially in viral diseases such as influenza. Aspirin has an inhibitory effect because it is an effective suppressor of adhesion molecule expression and that is the molecular basis for the notion that part of the anti-atherogenic effect of aspirin may be due to the prevention of the adhesion of sensitized T cells to stressed cells and prevents cellular interaction between them for proper immune action (see: Amberger A et al, Suppressive effects of anti-inflammatory agents on human endothelial cell activation and induction of heat shock proteins, Mol Med. 1999 Feb;5(2):117-28) and there are a few other problems of aspirin.
Aspirin as well as other non-steroidal anti-inflammatory agents, can triple the rate of excretion of Vitamin C, B1 (thiamin), folic acid, and iron, in addition to decreasing the absorption of glucose, amino acids, folate, Vitamin K, thiamin, and potassium (Substances that destroy nutrients, www.innvista.com, december, 2005).
Aspirin consumption has been associated with increased loss of vitamin C in urine and has been linked to depletion of vitamin C (Coffey G, Wilson CWM. Ascorbic acid deficiency and aspirin-induced haematemesis, BMJ 1975;I:208). In a study of people hospitalized with heart disease, those who had been taking aspirin were nearly twice as likely as nonusers to have a low or marginally low blood level of vitamin B12 (Van Oijen MGH, Laheij RJF, Peters WHM, et al. Association of aspirin use with vitamin B12 deficiency (results of the BACH study), Am J Cardiol 2004;94:975-7). Intake of 3 grams of aspirin per day has been shown to decrease blood levels of zinc (Ambanelli U, Ferraccioli GF, Serventi G, Vaona GL. Changes in serum and urinary zinc induced by ASA and indomethacin, Scand J Rheumatol 1982;11:63-4).
Zinc plays a key role in the body's physiology as it is involved in the activities of many enzymes (Dréno B and Blouin E, Acne, pregnant women and zinc salts: a literature review, Ann Dermatol Venereol. 2008 Jan;135(1):27-33). Organic zinc is a very important nutrient for the immune system. Serum zinc was significantly lower in the chronic fatigue syndrome (CFS) patients than in the normal controls. This study shows that CFS is accompanied by a low serum zinc status and that the latter is related to signs of inflammation and defects in early T cell activation pathways. There was a trend toward a significant negative correlation between serum zinc and the severity of CFS (Maes M. et al, Lower serum zinc in Chronic Fatigue Syndrome (CFS): relationships to immune dysfunctions and relevance for the oxidative stress status in CFS, J Affect Disord. 2006 Feb;90(2-3):141-7). Zinc is also a cofactor for thymulin, a thymic hormone essential for T-cell maturation (Mocchegiani E, Santarelli L, Muzzioli M, Fabris N. Reversibility of the thymic involution and of age-related peripheral immune dysfunctions by zinc supplementation in old mice. Int J Immunopharmacol. 1995;17(9):703–718). Naturally Zinc deficiency is associated with the rapid progression of AIDs (Jones CY, Tang AM, Forrester JE, et al. Micronutrient levels and HIV disease status in HIV-infected patients on highly active antiretroviral therapy in the Nutrition for Healthy Living cohort. J Acquir Immune Defic Syndr. 2006;43(4):475–482).
Since zinc is an essential micronutrient for human metabolism that catalyzes more than 100 enzymes, facilitates protein folding, and helps regulate gene expression, “zinc deficiency is associated with impaired wound healing” (Institute of Medicine (U.S.). DRI: Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy Press; 2001).
Formulations made from strawberries and berries will also contain natural vitamins and natural antioxidants that support and promote healthy biochemistry and are more effective in the prevention of inflammations and can play a better role in health. There should be more research in this direction, naturally, for food is better medicine than drugs. I expect India to take the lead in such research including institutions like the Tuft University in the US with China showing a keen interest. Inflammations means pain and sickness but for those with good natural answers, it is a huge market.
Ample research indicates that age-related neuronal-behavioral decrements are the result of oxidative stress that may be ameliorated by antioxidants. Our previous study had shown that rats given dietary supplements of fruit and vegetable extracts with high antioxidant activity for 8 months beginning at 6 months of age retarded age-related declines in neuronal and cognitive function. The present study showed that such supplements (strawberry, spinach, or blueberry at 14.8, 9.1, or 18.6 gm of dried aqueous extract per kilogram of diet, respectively) fed for 8 weeks to 19-month-old Fischer 344 rats were also effective in reversing age-related deficits in several neuronal and behavioral parameters including: oxotremorine enhancement of K+-evoked release of dopamine from striatal slices, carbachol-stimulated GTPase activity, striatal Ca45 buffering in striatal synaptosomes, motor behavioral performance on the rod walking and accelerod tasks, and Morris water maze performance. These findings suggest that, in addition to their known beneficial effects on cancer and heart disease, phytochemicals present in antioxidant-rich foods may be beneficial in reversing the course of neuronal and behavioral aging (James A. et al, Reversals of Age-Related Declines in Neuronal Signal Transduction, Cognitive, and Motor Behavioral Deficits with Blueberry, Spinach, or Strawberry Dietary Supplementation, The Journal of Neuroscience, September 15, 1999, 19(18):8114-8121).
The inhibitory effects of strawberry extracts on the proliferation and transformation of human and mouse cancer cells were also evaluated. Strawberries had high activities of glutathione peroxidase, superoxide dismutase, guaiacol peroxidase, ascorbate peroxidase, and glutathione reductase. Strawberry extracts inhibited the proliferation of human lung epithelial cancer cell line A549 and decreased TPA-induced neoplastic transformation of JB6 P+ mouse epidermal cells. Pretreatment of JB6 P+ mouse epidermal cells with strawberry extract resulted in the inhibition of both UVB- and TPA-induced AP-1 and NF-κB transactivation. The ability of strawberries to block UVB- and TPA-induced AP-1 and NF-κB activation may be due to their antioxidant properties and their ability to reduce oxidative stress. The oxidative events that regulate AP-1 and NF-κB transactivation can be important molecular targets for cancer prevention. The strawberries may be highly effective as a chemopreventive agent that acts by targeting the down-regulation of AP-1 and NF-κB activities, blocking MAPK signaling, and suppressing cancer cell proliferation and transformation (Shiow Y. Wang et al, Inhibitory Effect on Activator Protein-1, Nuclear Factor-KappaB, and Cell Transformation by Extracts of Strawberries (Fragaria × ananassa Duch), J. Agric. Food Chem., 2005, 53 (10), pp 4187–4193).
Strawberry (Fragaria x ananassa Duch.) fruits contain phenolic compounds that have antioxidant, anticancer, antiatherosclerotic and anti-neurodegenerative properties (Navindra P. Seeram et al, Identification of phenolic compounds in strawberries by liquid chromatography electrospray ionization mass spectroscopy, Food Chemistry, Volume 97, Issue 1, July 2006, Pages 1-11).
The effects of elevated CO2 concentrations on the antioxidant capacity and flavonoid content in strawberry fruit (Fragaria x ananassa Duch.) were studied under field conditions. Increased CO2 (300 and 600 μmol mol-1 above ambient) concentrations resulted in increases in ascorbic acid (AsA), glutathione (GSH), and ratios of AsA to dehydroascorbic acid (DHAsA) and GSH to oxidized glutathione (GSSG), and a decrease in DHAsA in strawberry fruit. High anthocyanin and phenolic content were also found in fruit of CO2 treated plants. Growing strawberry plants under CO2 enrichment conditions significantly enhanced fruit p-coumaroylglucose, dihydroflavonol, quercetin 3-glucoside, quercetin 3-glucuronide, and kaempferol 3-glucoside contents, as well as cyanidin 3-glucoside, pelargonidin 3-glucoside, and pelargonidin 3-glucoside-succinate content. Fruit of strawberry plants grown in the CO2 enrichment conditions also had high oxygen radical absorbance activity against ROO•, O2•-, H2O2, OH•, and 1O2 radicals (Shiow Y. Wang, Elevated Carbon Dioxide Increases Contents of Antioxidant Compounds in Field-Grown Strawberries, J. Agric. Food Chem., 2003, 51 (15), pp 4315–4320).
Salicylic acid is responsible for the anti‐inflammatory action of aspirin, and may cause the reduced risk of colorectal cancer observed in those who take aspirin. Yet salicylic acid and other salicylates occur naturally in fruits and plants, while diets rich in these are believed to reduce the risk of colorectal cancer. Serum salicylic acid concentrations are greater in vegetarians than non‐vegetarians, and there is overlap between concentrations in vegetarians and those taking low‐dose aspirin. We propose that the cancer‐preventive action of aspirin is due to its principal metabolite, salicylic acid, and that dietary salicylates can have the same effect. It is also possible that natural salicylates contribute to the other recognized benefits of a healthy diet (JR Paterson and JR Lawrence, Salicylic acid: a link between aspirin, diet and the prevention of colorectal cancer, Oxford Journals, Medicine,QJM: An International Journal of Medicine, Volume94, Issue8, Pp. 445-448).
At least 46 % of global disease burden and 59 % of global mortality is due to chronic diseases associated with inflammations caused by various agents including allergens from protozoa, excess free radicals and advanced glycation products (AGEs) and advanced lipoxidation products (ALEs) (Baptista, J.A.B. and Carvalho, R.C.B, 2004, Indirect determination of Amadori compounds in milk-based products by HPLC/ELSD/UV as an index of protein detorioration, Food Research International, 37, 739-747), as glycation products are known to increase free radicals that rob electrons from molecules of cell membranes leading to the development of the inflammatory condition with loss of integrity of the cell membrane. All chronic diseases are in a way related, they develop all as a result of a prolonged and exaggerated inflammation (Bengmark S, 2004a, Acute and “chronic” phase response - A mother of disease. Clin. Nutr.23, 1256-1266).
Common to those suffering from chronic disease as well as critical illness is that they suffer an increased degree of inflammation (Stig Bengmark, Cucurmin As A Dietary Modulator Of Inflammation,Institute of Hepatology, University College, London Medical School, London, United Kingdom, 63-77).
Cancer is a group of more than 100 different diseases, which manifest itself in uncontrolled cellular reproduction, tissue invasion and distant metastases (Levi et al., 2001). Behind the development of these diseases are most often exposure to carcinogens, which produce genetic damage and irreversible mutations, if not repaired. During the last fifty years attempts have been made to find or produce substances that
could prevent these processes, so called chemopreventive agents. Cancers are generally less frequent in the developing world, which has been associated both with less exposure to environmental carcinogens and to a richer supply of natural chemopreventive agents (Stig Bengmark, Cucurmin As A Dietary Modulator Of Inflammation,Institute of Hepatology, University College, London Medical School, London, United Kingdom, 63-77).
Anthocyans are polyphenols ring-based flavonoids that are widespread in fruits and vegetables with red-blue color. Culture cells were used to investigate their chemopreventive effects. In mouse epidermal cells (JB6), a model for screening anticarcinogenic compounds, anthocyans inhibited cell transformation by targeting mitogen activated protein kinase (MAPK)-mediated activator protein-1 (AP-1) pathway. In mouse macrophage cells (RAW264), a model for identifying the anti-inflammation compounds, anthocyans suppressed LPS-evoked inflammation through targeting nuclear factor kappa B (NF-ΚB), AP-1 and CCAAT/enhancerbinding protein (C/EBPδ)-mediated cyclooxygenase-2 (COX-2) expression. In human leukemia cells (HL-60), a model for testing antitumoral compounds, anthocyans induced apoptosis of cancer cells through the reactive oxygen species (ROS)/c-Jun NH2-terminal kinase (JNK)-mediated mitochondrial dysfunction pathway. The data from this study provided the first molecular and cellular basis that anthocyans might have chemopreventive effects on several key steps involved in carcinogenesis (De-Xing Hou, Anthocyans and Chemoprevention: Evidence from Cellular Investigations, ACS Symposium Series, Vol. 993, Functional Food and Health, Chapter 26, pp 308–319).
Polyphenols have in recent few years received an increasing attention for their strong chemo-preventive ability. Curcumin and many other plantderived substances are increasingly regarded as shields against disease. Curcumin is the most explored of the so called curmenoids, a family of chemopreventive substances present in the spice turmeric. Although the substance has been known for some time, it is in the most recent years that the interest has exploded, much in parallel with increasing concern for severe side effects of synthetic COX-2 inhibitors (Stig Bengmark, Cucurmin As A Dietary Modulator Of Inflammation,Institute of Hepatology, University College, London Medical School, London, United Kingdom, 63-77).
Glucocorticoids like NSAID, inhibit prostaglandin synthesis, but at an earlier step in the pathway, prior to arachidonic acid synthesis. They also block cytokine secretion and T cell activation, and inhibit COX-2 activity. Since these agents bind to almost all cells in the body, they have profound effects on physiological systems. If used in long-term therapy they can cause profound immunosuppression, with an increased risk of cancer and infection, osteoporosis, gastrointestinal ulceration, hypertension and endocrine abnormalities (Pincus T and Callahan LF. 1993, What is the natural history of rheumatoid arthritis? Rheum. Dis. Clin. North Am. 19: 123–51). Aspirin and its relatives (more than 20 related drugs) inhibit the activity of both forms of the enzyme and since COX-1 is required for the production of protective prostaglandins in the digestive tract (Rodnan GP, Benedek TG. The early history of antirheumatic drugs. Arthritis Rheum. 1970; 13: 145–65) can cause problems in patients with inflammations.
Curcumin is a potent inhibitor of TGF-β and fibrogenesis (Srinisan, P. and Libbus, B., 2004, Mining Medline for implicit links between dietary substances and diseases. Bioinformatics 20, Suppl. 1, 1290-1296, and suggested to have positive effects in fibrotic diseases in kidneys, liver, intestine (Crohn’s Disease), body cavities (prevention of fibrous adhesions) (Chang, D.M., 2001, Curcumin: A heat shock response inducer and potential cytoprotector, Crit. Care Med. 29, 2231-2232) and on conditions with lung fibrosis, including cystic fibrosis. Significant antifungal properties against various fungal, especially phytopathogenic, organisms by curcumin are also reported (Kim et al, 2003, Fungal property of Curcuma longa rhizome-derived curcumin against phytopathogenic fungi in greenhouse. J. Agr. Food Chem.,51, 1578-1581). Curcumin has very good anti-parasitic properties. Curcumin is suggested to be especially effective in Th1-mediated immune diseases as it effectively inhibits Th1 cytokine profile in CD4+ T cells by interleukin-12 production (Kang et al., 1999, Curcumin inhibits Th1 cytokine profile in CD4+ T cells by suppressing interleukin-12 production in macrophages, Br. J. Pharmacol., 128, 380-384) which may partly explain its anti-parasitic action as the chemokines from protozoa mimic human molecular action and block their action against the protozoa. Together with high doses of L-ascorbic acid, they could possibly help to activate white blood cells or improve their role in the immune system unlike the anti-inflammatory drugs that exhibit an immunosuppresive role in the human body.
“Numerous other plants contain compounds that reduce inflammation and protects against disease. Among them are several thousands of plantderived chemo-preventive agents, polyphenols and many other, most often unexplored, substances, which seem to
have potential to reduce inflammation, speed of aging, prevent degenerative malfunctions of organs and development of chronic diseases. Among them isothiocyanates in cruciferous vegetables, anthocyanins and hydroxycinnamic acids in cherries, epigallocatechin-3-gallate (EGCG) in green tee, chlorogenic acid and caffeic acid in coffee beans and also in virgin tobacco leaves, capsaicin in hot chilli peppers, chalcones in apples, euginol in cloves, gallic acid in rhubarb, hisperitin in citrus fruits, naringenin in citrus fruits, kaempferol in white cabbage, myricetin in berries, rutin and quercetin in apples and onions, resveratrol and other procyanidin dimers in red wine and virgin peanuts, various curcumenoids, the main yellow pigments in turmeric curry foods, and daidzein and genistein from the soy bean. These compounds have all slightly different functions and seem to complement each other well” (Stig Bengmark, Cucurmin As A Dietary Modulator Of Inflammation,Institute of Hepatology, University College, London Medical School, London, United Kingdom, 63-77).
To use medicinal plants and their active components is becoming an increasingly attractive approach for the treatment of various inflammatory disorders among patients unresponsive or unwilling to take standard medicines (Stig Bengmark, Cucurmin As A Dietary Modulator Of Inflammation,Institute of Hepatology, University College, London Medical School, London, United Kingdom, 63-77).
(A Short Note)
Beldeu Singh
Billions of dollars have been spent on research and production of anti-inflammatory drugs but they are all toxic. These drugs were developed with the intention to find chemicals that will suppress the Cox-2 enzymes that are associated with the inflammatory process and promote inflammations.
Cancer cells have high cell membrane potential, having lost electrons from molecules in the cell membrane to free radicals and oxidants like the peroxynitrite (ONOO-) or heavy metals and accordingly are highly inflamed, more than cells at lesions in psoriasis and arthritis.
In the New Straits Times, today at p26 the headline reads - "small daily doses of aspirin cuts many cancer risks" - it is about research on aspirin, a drug that can destroy the cementing material that binds and holds cells together and if this is destroyed in the tissue of the intestines, it can cause intestinal bleeding. Furthermore, aspirin intereferes with and blocks the blood coagulating factors which can be dangerous, especially in the older population and in accident victims.
This short newsreport says that researchers at Oxford say that low daily doses of aspirin cuts cancer the rate of cancer deaths and suggested (quite correctly) “that it does so by blocking the enzyme Cox-2 which promotes inflammation” as cancer cells have high CMB (ie they are highly inflamed) and if aspirin can suppress the inflammatory process it prevents the initiation of the formation of cancer cells. There are several epidemiological studies that clearly show that in populations that consume traditional diets and diets with relatively high fruit and vegetable intake tend to have lower incidence of cancers, which is primarily due to the role of natural antioxidants in preventing inflammations and organic minerals (iron, copper, mnaganese, zinc) that work as catalysts with the SOD-Catalase enzyme system to effecftively and efficienctly convert the superoxide into water and oxygen and thereby prevent excess hydrogen peroxide and oxygen free radical in the body and support optimal cell function that tends to decline with age and with lowering of blood antioxidant levels with consequent lower output of citric acid from the citric acid cycle and these appear to be factors in which micro-parasites and protozoa become active. In the active stage they consume more vitamin B12, competing with the host, causing vitamin B12 depletion or deficiencies and secrete more allergens that promote the inflammatory process.
Both aspirin and sulindac have been reported to display profound antiproliferative effects on tumor cell lines, alter the cell cycle distribution, and induce apoptosis (Shiff S J, Qiao L, Tsai L L, Rigas B. J Clin Invest. 1995;96:491–503: Ricchi P, Pignata S, Di Popolo A, Memoli A, Apicella A, Zarrilli R, Acquaviva A M. Int J Cancer. 1997;73:880–884: Sheng H, Shao J, Kirkland S C, Isakson P, Coffey R J, Morrow J, Beauchamp R D, DuBois R N. J Clin Invest. 1997;99:2254–2259).
However, what they did not also say is that like other anti-inflammatory drugs, aspirin also suppresses the Cox-1 enzyme which is very important for health. COX-1 is ubiquitously expressed and appears to be a housekeeping gene, whereas COX-2 expression is inducible by growth factors and oncogenes (Prescott S M, White R L. Cell. 1996;87:783–786) and fruits like strawberry is known to suppress Cox-2 (as effectively as drugs) without suppressing Cox-1. Suppression of Cox-1 can lead to serious health problems, including thinning of the stomach lining. Cayenne contains the potent chemical capsaicin, which acts on special nerves found in the stomach lining. In two rat studies, researchers reported that stimulation of these nerves by capsaicin might protect against the damage aspirin can cause to the stomach (Abdel Salam OME, Mószik G, Szolcsányi J. Studies on the effect of intragastric capsaicin on gastric ulcer and on the prostacyclin-induced cytoprotection in rats. Pharmacol Res 1995;32:209-15: Holzer P, Pabst MA, Lippe IT. Intragastric capsaicin protects against aspirin-induced lesion formation and bleeding in the rat gastric mucosa. Gastroenterology 1989;96:1425-33). The flavonoids found in the extract of licorice known as DGL (deglycyrrhizinated licorice) are helpful for avoiding the irritating actions aspirin has on the stomach and intestines. One study found that 350 mg of chewable DGL taken together with each dose of aspirin reduced gastrointestinal bleeding caused by the aspirin (Rees WDW, Rhodes J, Wright JE, et al. Effect of deglycyrrhizinated liquorice on gastric mucosal damage by aspirin. Scand J Gastroenterol 1979;14:605-7).
Some fifty cousins of aspirin exist, most of which appeared after World War II. Together they constitute a family known as non-steroidal anti-inflammatory drugs (NSAIDs). They can interfere with physiology including the formation of prostaglandins.
Many kinds of prostaglandin exist in the body to serve a plethora of physiological functions, some of which are irritable, others beneficial. Prostaglandins are among the chemicals secreted by the body’s immune system when it fights off bacteria and other invaders in injuries. Located around wounds , these chemicals cause pain and inflammation. Aspirin inhibits the production of prostaglandins (JR. Vane, 1971, Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs, Nature, New Biology: 231: 230-235). This happens because cyclooxygenase, a Cox enzyme which participates in the production of prostaglandins and thromboxanes, is irreversibly inhibited when aspirin acetylates it (Roth GJ and Majerus PW, The mechanism of the effect of aspirin on human platelets, I: acetylation of a particulate fraction protein, J Clin Invest., 1975;56:624–632: Lecomte M et al. Acetylation of human endoperoxide synthase-2 by aspirin, J Biol Chem,. 1994;269:13207–13215). Aspirin irresversibly binds cyclooxygenase (Cox-1 and Cox-2). Thereby blocking arachidonic acid from from porstaglandins (Carol D Morris, Principles of Orthopaedic Pharmacology, 7th ed, © 2008, Lippincott Williams & Wilkins).
Aspirin inhibits both Cox-1 and Cox-2 enzymes, aspirin more slectively inhibits COX-1 activity (found predominantly in platelets) than COX-2 activity (showed in tissues follwoing an inflammatory stimuli), its ability to prevent platelet aggregation is seen at relatively low doses, compared with it's anti-inflammatory effects, which require higher doses. Low-dose long-term aspirin irreversibly blocks formation of thromboxane A2 in platelets, producing an inhibitory affect on platelet aggregation, and this blood thinning property makes it useful for reducing the incidence of heart attacks (Aspirin, Pharpedia, 28th August 2005). So, how brilliant is their research?
Aspirin taken by patients while having a heart attack significantly reduces the chance of death. For people with various risk factors for heart diseases such as diabetes, obesity, or high blood pressure, aspirin lowers the probability of a first heart attack. For healthy people without cardiovascular risks, results on the effects of aspirin are inconclusive (G. Weissman, 1997, Aspirin, Scientific American, 264(1): 84-90 (1991). D. B. Jack. A hundred years of aspirin. The Lancet, 350: 437-439).
Salicylic acid, from the bark of the willow tree, is a monohydroxybenzoic acid, is a phenolic acid and a beta hydroxy acid. This colorless crystalline organic acid is widely used in organic synthesis and functions as a plant hormone. It is derived from the metabolism of salicin. It is a compound that is chemically similar to but not identical to the active component of aspirin (acetylsalicylic acid), it is probably best known for its use in anti-acne treatments and may have anti-protozoal properties. Salicylic acid is known for its ability to ease aches and pains and reduce fevers. These medicinal properties, particularly fever relief, have been known since ancient times and it was used as an anti-inflammatory drug (Philip A. Mackowiak, 2000, "Brief History of Antipyretic Therapy". Clinical Infectious Diseases, 31: 154–156). Salicylic acid (SA) is a phenolic phytohormone and is found in plants with roles in plant growth and development, photosynthesis, transpiration, ion uptake and transport. SA also induces specific changes in leaf anatomy and chloroplast structure. SA is involved in endogenous signaling, mediating in plant defense against pathogens (S. Hayat, A. Ahmad (2007). Salicylic acid - A Plant Hormone. Springer. ISBN 1402051832).
Sodium salicylate paradoxically inhibited prostaglandin synthesis when added to intact cells (Mitchell JA, et al. Selectivity of nonsteroidal anti-inflammatory drugs as inhibitors of constitutive and inducible cyclooxygenase. Proc Natl Acad Sci U S A. 1994;90:11693–11697). Furthermore, healthy subjects taking sodium salicylate excreted a significantly lower amount of prostaglandin metabolites in urine than those not taking sodium salicylate, and their levels of inhibition were comparable to those of patients taking aspirin and indomethacin (Hamberg M. Inhibition of prostaglandin synthesis in man. Biochem Biophys Res Commun. 1972;49:720–726). Aspirin also reduces human seminal prostaglandin levels (Collies JG, Flowers RJ. Effect of aspirin on human seminal prostaglandins. Lancet. 1971;i:852–853).
Aspirin, which suppresses cyclooxygenase, has the potential to interfere with implantation. Aspirin has potential risks. Aspirin inhibits platelet function and can contribute to maternal and fetal bleeding. Aspirin crosses the placenta. Although aspirin has not been associated with other congenital anomalies, it has been associated with an increased risk of vascular disruptions, particularly gastroschisis and possibly premature closure of the ductus arteriosus. Nonetheless, large trials demonstrate low-dose aspirin's relative safety (James et al, Aspirin and Reproductive Outcomes, Obstetrical & Gynecological Survey: January 2008 - Volume 63 - Issue 1 - pp 49-57).
Immunosuppressive and anti-inflammatory agents significantly inhibited T cell proliferation, especially in viral diseases such as influenza. Aspirin has an inhibitory effect because it is an effective suppressor of adhesion molecule expression and that is the molecular basis for the notion that part of the anti-atherogenic effect of aspirin may be due to the prevention of the adhesion of sensitized T cells to stressed cells and prevents cellular interaction between them for proper immune action (see: Amberger A et al, Suppressive effects of anti-inflammatory agents on human endothelial cell activation and induction of heat shock proteins, Mol Med. 1999 Feb;5(2):117-28) and there are a few other problems of aspirin.
Aspirin as well as other non-steroidal anti-inflammatory agents, can triple the rate of excretion of Vitamin C, B1 (thiamin), folic acid, and iron, in addition to decreasing the absorption of glucose, amino acids, folate, Vitamin K, thiamin, and potassium (Substances that destroy nutrients, www.innvista.com, december, 2005).
Aspirin consumption has been associated with increased loss of vitamin C in urine and has been linked to depletion of vitamin C (Coffey G, Wilson CWM. Ascorbic acid deficiency and aspirin-induced haematemesis, BMJ 1975;I:208). In a study of people hospitalized with heart disease, those who had been taking aspirin were nearly twice as likely as nonusers to have a low or marginally low blood level of vitamin B12 (Van Oijen MGH, Laheij RJF, Peters WHM, et al. Association of aspirin use with vitamin B12 deficiency (results of the BACH study), Am J Cardiol 2004;94:975-7). Intake of 3 grams of aspirin per day has been shown to decrease blood levels of zinc (Ambanelli U, Ferraccioli GF, Serventi G, Vaona GL. Changes in serum and urinary zinc induced by ASA and indomethacin, Scand J Rheumatol 1982;11:63-4).
Zinc plays a key role in the body's physiology as it is involved in the activities of many enzymes (Dréno B and Blouin E, Acne, pregnant women and zinc salts: a literature review, Ann Dermatol Venereol. 2008 Jan;135(1):27-33). Organic zinc is a very important nutrient for the immune system. Serum zinc was significantly lower in the chronic fatigue syndrome (CFS) patients than in the normal controls. This study shows that CFS is accompanied by a low serum zinc status and that the latter is related to signs of inflammation and defects in early T cell activation pathways. There was a trend toward a significant negative correlation between serum zinc and the severity of CFS (Maes M. et al, Lower serum zinc in Chronic Fatigue Syndrome (CFS): relationships to immune dysfunctions and relevance for the oxidative stress status in CFS, J Affect Disord. 2006 Feb;90(2-3):141-7). Zinc is also a cofactor for thymulin, a thymic hormone essential for T-cell maturation (Mocchegiani E, Santarelli L, Muzzioli M, Fabris N. Reversibility of the thymic involution and of age-related peripheral immune dysfunctions by zinc supplementation in old mice. Int J Immunopharmacol. 1995;17(9):703–718). Naturally Zinc deficiency is associated with the rapid progression of AIDs (Jones CY, Tang AM, Forrester JE, et al. Micronutrient levels and HIV disease status in HIV-infected patients on highly active antiretroviral therapy in the Nutrition for Healthy Living cohort. J Acquir Immune Defic Syndr. 2006;43(4):475–482).
Since zinc is an essential micronutrient for human metabolism that catalyzes more than 100 enzymes, facilitates protein folding, and helps regulate gene expression, “zinc deficiency is associated with impaired wound healing” (Institute of Medicine (U.S.). DRI: Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy Press; 2001).
Formulations made from strawberries and berries will also contain natural vitamins and natural antioxidants that support and promote healthy biochemistry and are more effective in the prevention of inflammations and can play a better role in health. There should be more research in this direction, naturally, for food is better medicine than drugs. I expect India to take the lead in such research including institutions like the Tuft University in the US with China showing a keen interest. Inflammations means pain and sickness but for those with good natural answers, it is a huge market.
Ample research indicates that age-related neuronal-behavioral decrements are the result of oxidative stress that may be ameliorated by antioxidants. Our previous study had shown that rats given dietary supplements of fruit and vegetable extracts with high antioxidant activity for 8 months beginning at 6 months of age retarded age-related declines in neuronal and cognitive function. The present study showed that such supplements (strawberry, spinach, or blueberry at 14.8, 9.1, or 18.6 gm of dried aqueous extract per kilogram of diet, respectively) fed for 8 weeks to 19-month-old Fischer 344 rats were also effective in reversing age-related deficits in several neuronal and behavioral parameters including: oxotremorine enhancement of K+-evoked release of dopamine from striatal slices, carbachol-stimulated GTPase activity, striatal Ca45 buffering in striatal synaptosomes, motor behavioral performance on the rod walking and accelerod tasks, and Morris water maze performance. These findings suggest that, in addition to their known beneficial effects on cancer and heart disease, phytochemicals present in antioxidant-rich foods may be beneficial in reversing the course of neuronal and behavioral aging (James A. et al, Reversals of Age-Related Declines in Neuronal Signal Transduction, Cognitive, and Motor Behavioral Deficits with Blueberry, Spinach, or Strawberry Dietary Supplementation, The Journal of Neuroscience, September 15, 1999, 19(18):8114-8121).
The inhibitory effects of strawberry extracts on the proliferation and transformation of human and mouse cancer cells were also evaluated. Strawberries had high activities of glutathione peroxidase, superoxide dismutase, guaiacol peroxidase, ascorbate peroxidase, and glutathione reductase. Strawberry extracts inhibited the proliferation of human lung epithelial cancer cell line A549 and decreased TPA-induced neoplastic transformation of JB6 P+ mouse epidermal cells. Pretreatment of JB6 P+ mouse epidermal cells with strawberry extract resulted in the inhibition of both UVB- and TPA-induced AP-1 and NF-κB transactivation. The ability of strawberries to block UVB- and TPA-induced AP-1 and NF-κB activation may be due to their antioxidant properties and their ability to reduce oxidative stress. The oxidative events that regulate AP-1 and NF-κB transactivation can be important molecular targets for cancer prevention. The strawberries may be highly effective as a chemopreventive agent that acts by targeting the down-regulation of AP-1 and NF-κB activities, blocking MAPK signaling, and suppressing cancer cell proliferation and transformation (Shiow Y. Wang et al, Inhibitory Effect on Activator Protein-1, Nuclear Factor-KappaB, and Cell Transformation by Extracts of Strawberries (Fragaria × ananassa Duch), J. Agric. Food Chem., 2005, 53 (10), pp 4187–4193).
Strawberry (Fragaria x ananassa Duch.) fruits contain phenolic compounds that have antioxidant, anticancer, antiatherosclerotic and anti-neurodegenerative properties (Navindra P. Seeram et al, Identification of phenolic compounds in strawberries by liquid chromatography electrospray ionization mass spectroscopy, Food Chemistry, Volume 97, Issue 1, July 2006, Pages 1-11).
The effects of elevated CO2 concentrations on the antioxidant capacity and flavonoid content in strawberry fruit (Fragaria x ananassa Duch.) were studied under field conditions. Increased CO2 (300 and 600 μmol mol-1 above ambient) concentrations resulted in increases in ascorbic acid (AsA), glutathione (GSH), and ratios of AsA to dehydroascorbic acid (DHAsA) and GSH to oxidized glutathione (GSSG), and a decrease in DHAsA in strawberry fruit. High anthocyanin and phenolic content were also found in fruit of CO2 treated plants. Growing strawberry plants under CO2 enrichment conditions significantly enhanced fruit p-coumaroylglucose, dihydroflavonol, quercetin 3-glucoside, quercetin 3-glucuronide, and kaempferol 3-glucoside contents, as well as cyanidin 3-glucoside, pelargonidin 3-glucoside, and pelargonidin 3-glucoside-succinate content. Fruit of strawberry plants grown in the CO2 enrichment conditions also had high oxygen radical absorbance activity against ROO•, O2•-, H2O2, OH•, and 1O2 radicals (Shiow Y. Wang, Elevated Carbon Dioxide Increases Contents of Antioxidant Compounds in Field-Grown Strawberries, J. Agric. Food Chem., 2003, 51 (15), pp 4315–4320).
Salicylic acid is responsible for the anti‐inflammatory action of aspirin, and may cause the reduced risk of colorectal cancer observed in those who take aspirin. Yet salicylic acid and other salicylates occur naturally in fruits and plants, while diets rich in these are believed to reduce the risk of colorectal cancer. Serum salicylic acid concentrations are greater in vegetarians than non‐vegetarians, and there is overlap between concentrations in vegetarians and those taking low‐dose aspirin. We propose that the cancer‐preventive action of aspirin is due to its principal metabolite, salicylic acid, and that dietary salicylates can have the same effect. It is also possible that natural salicylates contribute to the other recognized benefits of a healthy diet (JR Paterson and JR Lawrence, Salicylic acid: a link between aspirin, diet and the prevention of colorectal cancer, Oxford Journals, Medicine,QJM: An International Journal of Medicine, Volume94, Issue8, Pp. 445-448).
At least 46 % of global disease burden and 59 % of global mortality is due to chronic diseases associated with inflammations caused by various agents including allergens from protozoa, excess free radicals and advanced glycation products (AGEs) and advanced lipoxidation products (ALEs) (Baptista, J.A.B. and Carvalho, R.C.B, 2004, Indirect determination of Amadori compounds in milk-based products by HPLC/ELSD/UV as an index of protein detorioration, Food Research International, 37, 739-747), as glycation products are known to increase free radicals that rob electrons from molecules of cell membranes leading to the development of the inflammatory condition with loss of integrity of the cell membrane. All chronic diseases are in a way related, they develop all as a result of a prolonged and exaggerated inflammation (Bengmark S, 2004a, Acute and “chronic” phase response - A mother of disease. Clin. Nutr.23, 1256-1266).
Common to those suffering from chronic disease as well as critical illness is that they suffer an increased degree of inflammation (Stig Bengmark, Cucurmin As A Dietary Modulator Of Inflammation,Institute of Hepatology, University College, London Medical School, London, United Kingdom, 63-77).
Cancer is a group of more than 100 different diseases, which manifest itself in uncontrolled cellular reproduction, tissue invasion and distant metastases (Levi et al., 2001). Behind the development of these diseases are most often exposure to carcinogens, which produce genetic damage and irreversible mutations, if not repaired. During the last fifty years attempts have been made to find or produce substances that
could prevent these processes, so called chemopreventive agents. Cancers are generally less frequent in the developing world, which has been associated both with less exposure to environmental carcinogens and to a richer supply of natural chemopreventive agents (Stig Bengmark, Cucurmin As A Dietary Modulator Of Inflammation,Institute of Hepatology, University College, London Medical School, London, United Kingdom, 63-77).
Anthocyans are polyphenols ring-based flavonoids that are widespread in fruits and vegetables with red-blue color. Culture cells were used to investigate their chemopreventive effects. In mouse epidermal cells (JB6), a model for screening anticarcinogenic compounds, anthocyans inhibited cell transformation by targeting mitogen activated protein kinase (MAPK)-mediated activator protein-1 (AP-1) pathway. In mouse macrophage cells (RAW264), a model for identifying the anti-inflammation compounds, anthocyans suppressed LPS-evoked inflammation through targeting nuclear factor kappa B (NF-ΚB), AP-1 and CCAAT/enhancerbinding protein (C/EBPδ)-mediated cyclooxygenase-2 (COX-2) expression. In human leukemia cells (HL-60), a model for testing antitumoral compounds, anthocyans induced apoptosis of cancer cells through the reactive oxygen species (ROS)/c-Jun NH2-terminal kinase (JNK)-mediated mitochondrial dysfunction pathway. The data from this study provided the first molecular and cellular basis that anthocyans might have chemopreventive effects on several key steps involved in carcinogenesis (De-Xing Hou, Anthocyans and Chemoprevention: Evidence from Cellular Investigations, ACS Symposium Series, Vol. 993, Functional Food and Health, Chapter 26, pp 308–319).
Polyphenols have in recent few years received an increasing attention for their strong chemo-preventive ability. Curcumin and many other plantderived substances are increasingly regarded as shields against disease. Curcumin is the most explored of the so called curmenoids, a family of chemopreventive substances present in the spice turmeric. Although the substance has been known for some time, it is in the most recent years that the interest has exploded, much in parallel with increasing concern for severe side effects of synthetic COX-2 inhibitors (Stig Bengmark, Cucurmin As A Dietary Modulator Of Inflammation,Institute of Hepatology, University College, London Medical School, London, United Kingdom, 63-77).
Glucocorticoids like NSAID, inhibit prostaglandin synthesis, but at an earlier step in the pathway, prior to arachidonic acid synthesis. They also block cytokine secretion and T cell activation, and inhibit COX-2 activity. Since these agents bind to almost all cells in the body, they have profound effects on physiological systems. If used in long-term therapy they can cause profound immunosuppression, with an increased risk of cancer and infection, osteoporosis, gastrointestinal ulceration, hypertension and endocrine abnormalities (Pincus T and Callahan LF. 1993, What is the natural history of rheumatoid arthritis? Rheum. Dis. Clin. North Am. 19: 123–51). Aspirin and its relatives (more than 20 related drugs) inhibit the activity of both forms of the enzyme and since COX-1 is required for the production of protective prostaglandins in the digestive tract (Rodnan GP, Benedek TG. The early history of antirheumatic drugs. Arthritis Rheum. 1970; 13: 145–65) can cause problems in patients with inflammations.
Curcumin is a potent inhibitor of TGF-β and fibrogenesis (Srinisan, P. and Libbus, B., 2004, Mining Medline for implicit links between dietary substances and diseases. Bioinformatics 20, Suppl. 1, 1290-1296, and suggested to have positive effects in fibrotic diseases in kidneys, liver, intestine (Crohn’s Disease), body cavities (prevention of fibrous adhesions) (Chang, D.M., 2001, Curcumin: A heat shock response inducer and potential cytoprotector, Crit. Care Med. 29, 2231-2232) and on conditions with lung fibrosis, including cystic fibrosis. Significant antifungal properties against various fungal, especially phytopathogenic, organisms by curcumin are also reported (Kim et al, 2003, Fungal property of Curcuma longa rhizome-derived curcumin against phytopathogenic fungi in greenhouse. J. Agr. Food Chem.,51, 1578-1581). Curcumin has very good anti-parasitic properties. Curcumin is suggested to be especially effective in Th1-mediated immune diseases as it effectively inhibits Th1 cytokine profile in CD4+ T cells by interleukin-12 production (Kang et al., 1999, Curcumin inhibits Th1 cytokine profile in CD4+ T cells by suppressing interleukin-12 production in macrophages, Br. J. Pharmacol., 128, 380-384) which may partly explain its anti-parasitic action as the chemokines from protozoa mimic human molecular action and block their action against the protozoa. Together with high doses of L-ascorbic acid, they could possibly help to activate white blood cells or improve their role in the immune system unlike the anti-inflammatory drugs that exhibit an immunosuppresive role in the human body.
“Numerous other plants contain compounds that reduce inflammation and protects against disease. Among them are several thousands of plantderived chemo-preventive agents, polyphenols and many other, most often unexplored, substances, which seem to
have potential to reduce inflammation, speed of aging, prevent degenerative malfunctions of organs and development of chronic diseases. Among them isothiocyanates in cruciferous vegetables, anthocyanins and hydroxycinnamic acids in cherries, epigallocatechin-3-gallate (EGCG) in green tee, chlorogenic acid and caffeic acid in coffee beans and also in virgin tobacco leaves, capsaicin in hot chilli peppers, chalcones in apples, euginol in cloves, gallic acid in rhubarb, hisperitin in citrus fruits, naringenin in citrus fruits, kaempferol in white cabbage, myricetin in berries, rutin and quercetin in apples and onions, resveratrol and other procyanidin dimers in red wine and virgin peanuts, various curcumenoids, the main yellow pigments in turmeric curry foods, and daidzein and genistein from the soy bean. These compounds have all slightly different functions and seem to complement each other well” (Stig Bengmark, Cucurmin As A Dietary Modulator Of Inflammation,Institute of Hepatology, University College, London Medical School, London, United Kingdom, 63-77).
To use medicinal plants and their active components is becoming an increasingly attractive approach for the treatment of various inflammatory disorders among patients unresponsive or unwilling to take standard medicines (Stig Bengmark, Cucurmin As A Dietary Modulator Of Inflammation,Institute of Hepatology, University College, London Medical School, London, United Kingdom, 63-77).
Sunday, December 5, 2010
Subject: TSA radiation
Subject: TSA radiation
www.NaturalNews.com/files/TSA_Naked_Body_Scanners.pdf
cover letter from Dr. Sedat et al from U of Calif, S.F.
LETTER OF CONCERN
We are writing to call your attention to serious concerns about the potential health risks of the recently adopted whole body backscatter X-ray airport security scanners. This is an urgent situation as these X-ray scanners are rapidly being implemented as a primary screening step for all air travel passengers.
Our overriding concern is the extent to which the safety of this scanning device has been adequately demonstrated. This can only be determined by a meeting of an impartial panel of experts that would include medical physicists and radiation biologists at which all of the available relevant data is reviewed.
An important consideration is that a large fraction of the population will be subject to the new X-ray scanners and be at potential risk, as discussed below. This raises a number of ‘red flags’. Can we have an urgent second independent evaluation?
The Red Flags
The physics of these X-rays is very telling: the X-rays are Compton-Scattering off outer molecule bonding electrons and thus inelastic (likely breaking bonds).
Unlike other scanners, these new devices operate at relatively low beam energies (28keV). The majority of their energy is delivered to the skin and the underlying tissue. Thus, while the dose would be safe if it were distributed throughout the volume of the entire body, the dose to the skin may be dangerously high.
The X-ray dose from these devices has often been compared in the media to the cosmic ray exposure inherent to airplane travel or that of a chest X-ray. However, this comparison is very misleading: both the air travel cosmic ray exposure and chest X- rays have much higher X-ray energies and the health consequences are appropriately understood in terms of the whole body volume dose. In contrast, these new airport scanners are largely depositing their energy into the skin and immediately adjacent tissue, and since this is such a small fraction of body weight/vol, possibly by one to two orders of magnitude, the real dose to the skin is now high.
In addition, it appears that real independent safety data do not exist. A search, ultimately finding top FDA radiation physics staff, suggests that the relevant radiation quantity, the Flux [photons per unit area and time (because this is a scanning device)] has not been characterized. Instead an indirect test (Air Kerma) was made that emphasized the whole body exposure value, and thus it appears that the danger is low when compared to cosmic rays during airplane travel and a chest X-ray dose.
In summary, if the key data (flux-integrated photons per unit values) were available, it would be straightforward to accurately model the dose being deposited in the skin andadjacent tissues using available computer codes, which would resolve the potential concerns over radiation damage.
Our colleagues at UCSF, dermatologists and cancer experts, raise specific important concerns:
• A) The large population of older travelers, >65 years of age, is particularly at risk from the mutagenic effects of the X-rays based on the known biology of melanocyte aging.
• B) A fraction of the female population is especially sensitive to mutagenesis- provoking radiation leading to breast cancer. Notably, because these women, who have defects in DNA repair mechanisms, are particularly prone to cancer, X-ray mammograms are not performed on them. The dose to breast tissue beneath the skin represents a similar risk.
• C) Blood (white blood cells) perfusing the skin is also at risk.
• D) The population of immunocompromised individuals--HIV and cancer patients (see above) is likely to be at risk for cancer induction by the high skin dose.
• E) The risk of radiation emission to children and adolescents does not appear to have been fully evaluated.
• F) The policy towards pregnant women needs to be defined once the theoretical risks to the fetus are determined.
• G) Because of the proximity of the testicles to skin, this tissue is at risk for sperm mutagenesis.
• H) Have the effects of the radiation on the cornea and thymus been determined?
Moreover, there are a number of ‘red flags’ related to the hardware itself. Because this device can scan a human in a few seconds, the X-ray beam is very intense. Any glitch in power at any point in the hardware (or more importantly in software) that stops the device could cause an intense radiation dose to a single spot on the skin. Who will oversee problems with overall dose after repair or software problems? The TSA is already complaining about resolution limitations; who will keep the manufacturers and/or TSA from just raising the dose, an easy way to improve signal-to-noise and get higher resolution? Lastly, given the recent incident (on December 25th), how do we know whether the manufacturer or TSA, seeking higher resolution, will scan the groin area more slowly leading to a much higher total dose?
After review of the available data we have already obtained, we suggest that additional critical information be obtained, with the goal to minimize the potential health risks of total body scanning. One can study the relevant X-ray dose effects with modern molecular tools. Once a small team of appropriate experts is assembled, an experimental plan can be designed and implemented with the objective of obtaining information relevant to our concerns expressed above, with attention paid to completing the information gathering and formulating recommendations in a timely fashion.
We would like to put our current concerns into perspective. As longstanding UCSF scientists and physicians, we have witnessed critical errors in decisions that have seriously affected the health of thousands of people in the United States. These unfortunate errors were made because of the failure to recognize potential adverse outcomes of decisions made at the federal level. Crises create a sense of urgency that frequently leads to hasty decisions where unintended consequences are not recognized. Examples include the failure of the CDC to recognize the risk of blood transfusions in the early stages of the AIDS epidemic, approval of drugs and devices by the FDA without sufficient review, and improper standards set by the EPA, to name a few. Similarly, there has not been sufficient review of the intermediate and long-term effects of radiation exposure associated with airport scanners. There is good reason to believe that these scanners will increase the risk of cancer to children and other vulnerable populations. We are unanimous in believing that the potential health consequences need to be rigorously studied before these scanners are adopted. Modifications that reduce radiation exposure need to be explored as soon as possible.
In summary we urge you to empower an impartial panel of experts to reevaluate the potential health issues we have raised before there are irrevocable long-term consequences to the health of our country. These negative effects may on balance far outweigh the potential benefit of increased detection of terrorists.
www.NaturalNews.com/files/TSA_Naked_Body_Scanners.pdf
cover letter from Dr. Sedat et al from U of Calif, S.F.
LETTER OF CONCERN
We are writing to call your attention to serious concerns about the potential health risks of the recently adopted whole body backscatter X-ray airport security scanners. This is an urgent situation as these X-ray scanners are rapidly being implemented as a primary screening step for all air travel passengers.
Our overriding concern is the extent to which the safety of this scanning device has been adequately demonstrated. This can only be determined by a meeting of an impartial panel of experts that would include medical physicists and radiation biologists at which all of the available relevant data is reviewed.
An important consideration is that a large fraction of the population will be subject to the new X-ray scanners and be at potential risk, as discussed below. This raises a number of ‘red flags’. Can we have an urgent second independent evaluation?
The Red Flags
The physics of these X-rays is very telling: the X-rays are Compton-Scattering off outer molecule bonding electrons and thus inelastic (likely breaking bonds).
Unlike other scanners, these new devices operate at relatively low beam energies (28keV). The majority of their energy is delivered to the skin and the underlying tissue. Thus, while the dose would be safe if it were distributed throughout the volume of the entire body, the dose to the skin may be dangerously high.
The X-ray dose from these devices has often been compared in the media to the cosmic ray exposure inherent to airplane travel or that of a chest X-ray. However, this comparison is very misleading: both the air travel cosmic ray exposure and chest X- rays have much higher X-ray energies and the health consequences are appropriately understood in terms of the whole body volume dose. In contrast, these new airport scanners are largely depositing their energy into the skin and immediately adjacent tissue, and since this is such a small fraction of body weight/vol, possibly by one to two orders of magnitude, the real dose to the skin is now high.
In addition, it appears that real independent safety data do not exist. A search, ultimately finding top FDA radiation physics staff, suggests that the relevant radiation quantity, the Flux [photons per unit area and time (because this is a scanning device)] has not been characterized. Instead an indirect test (Air Kerma) was made that emphasized the whole body exposure value, and thus it appears that the danger is low when compared to cosmic rays during airplane travel and a chest X-ray dose.
In summary, if the key data (flux-integrated photons per unit values) were available, it would be straightforward to accurately model the dose being deposited in the skin andadjacent tissues using available computer codes, which would resolve the potential concerns over radiation damage.
Our colleagues at UCSF, dermatologists and cancer experts, raise specific important concerns:
• A) The large population of older travelers, >65 years of age, is particularly at risk from the mutagenic effects of the X-rays based on the known biology of melanocyte aging.
• B) A fraction of the female population is especially sensitive to mutagenesis- provoking radiation leading to breast cancer. Notably, because these women, who have defects in DNA repair mechanisms, are particularly prone to cancer, X-ray mammograms are not performed on them. The dose to breast tissue beneath the skin represents a similar risk.
• C) Blood (white blood cells) perfusing the skin is also at risk.
• D) The population of immunocompromised individuals--HIV and cancer patients (see above) is likely to be at risk for cancer induction by the high skin dose.
• E) The risk of radiation emission to children and adolescents does not appear to have been fully evaluated.
• F) The policy towards pregnant women needs to be defined once the theoretical risks to the fetus are determined.
• G) Because of the proximity of the testicles to skin, this tissue is at risk for sperm mutagenesis.
• H) Have the effects of the radiation on the cornea and thymus been determined?
Moreover, there are a number of ‘red flags’ related to the hardware itself. Because this device can scan a human in a few seconds, the X-ray beam is very intense. Any glitch in power at any point in the hardware (or more importantly in software) that stops the device could cause an intense radiation dose to a single spot on the skin. Who will oversee problems with overall dose after repair or software problems? The TSA is already complaining about resolution limitations; who will keep the manufacturers and/or TSA from just raising the dose, an easy way to improve signal-to-noise and get higher resolution? Lastly, given the recent incident (on December 25th), how do we know whether the manufacturer or TSA, seeking higher resolution, will scan the groin area more slowly leading to a much higher total dose?
After review of the available data we have already obtained, we suggest that additional critical information be obtained, with the goal to minimize the potential health risks of total body scanning. One can study the relevant X-ray dose effects with modern molecular tools. Once a small team of appropriate experts is assembled, an experimental plan can be designed and implemented with the objective of obtaining information relevant to our concerns expressed above, with attention paid to completing the information gathering and formulating recommendations in a timely fashion.
We would like to put our current concerns into perspective. As longstanding UCSF scientists and physicians, we have witnessed critical errors in decisions that have seriously affected the health of thousands of people in the United States. These unfortunate errors were made because of the failure to recognize potential adverse outcomes of decisions made at the federal level. Crises create a sense of urgency that frequently leads to hasty decisions where unintended consequences are not recognized. Examples include the failure of the CDC to recognize the risk of blood transfusions in the early stages of the AIDS epidemic, approval of drugs and devices by the FDA without sufficient review, and improper standards set by the EPA, to name a few. Similarly, there has not been sufficient review of the intermediate and long-term effects of radiation exposure associated with airport scanners. There is good reason to believe that these scanners will increase the risk of cancer to children and other vulnerable populations. We are unanimous in believing that the potential health consequences need to be rigorously studied before these scanners are adopted. Modifications that reduce radiation exposure need to be explored as soon as possible.
In summary we urge you to empower an impartial panel of experts to reevaluate the potential health issues we have raised before there are irrevocable long-term consequences to the health of our country. These negative effects may on balance far outweigh the potential benefit of increased detection of terrorists.
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