April 4, 2008

Help Save America’s Last Wild Forests

Filed under: Forest Protection - Waldschutz — omeganews @ 8:40 pm

One-third of America’s national forests are protected from road-building and other industrial development by the Roadless Area Conservation Rule — but now the administration is working state-by-state to open these treasured places to logging, mining and other development. As it gets ready to head out the door, the Bush government seems intent on handing the keys to our national forests over to the timber and mining industries. Without your help, their future is at risk.

Currently at stake:

* Alaska’s Tongass National Forest, where the administration has proposed to increase logging in the world’s largest remaining temperate rainforest;

* Idaho’s Greater Yellowstone Ecosystem, where the administration has announced plans to open the largest swath of wild forest in the Lower 48 to logging and mining;

* Colorado’s Rocky Mountains, where the administration plans to open to development a majestic landscape with trout streams, rock-ribbed trails, and diverse wildlife that make it a world-class destination for outdoor recreation.

The Roadless Area Conservation Rule currently protects these special places despite ongoing efforts by the Bush administration to undo it — stymied only because Americans stood tall and took action. Our national forests should be our gift to future generations, not a giveaway to corporate special interests.

The Forest Service needs to hear from you by next Monday, April 7th. Please send your comments in today!

Click here to take action

Administration Opens Millions of Acres of Wild Forests to Development

In a triumph of special interests over public interest, the Roadless Area Conservation Rule, one of the most significant and popular conservation measures in U.S. history, was repealed by the Bush administration in May 2005. Issued in January 2001 following the most extensive public rulemaking in history, this landmark conservation initiative protected 58.5 million acres of wild roadless areas in our national forests from most commercial logging and road building. With more than one-half of America’s national forests already open to logging, mining, and drilling, the rule was intended to preserve the last third of undeveloped forests as a home for wildlife, a haven for recreation, and a heritage for future generations.

The Roadless Area Conservation Rule was enacted following more than two decades of broad debate and three years of official review and public participation. It provided a national policy for national lands that was hailed for refocusing resources on maintaining roads while protecting wildlife habitat, clean air, and water quality.

The Administration’s New Policy

The new roadless policy issued in 2005 left millions of acres of our last wild forests at risk from logging, mining, drilling, and other harmful activities. It replaces environmental protection with a voluntary process that allows governors to petition for protection of roadless areas in their states — or for more logging, mining, or drilling. In the end the policy does not ensure any type of federal protection for our heritage public lands.

One justification of the administration’s repeal of the 2001 rule was that its fate was tied up in the courts. Defenders of the 2001 rule point out, however, that the administration has refused to defend it in court cases brought by the timber industry and its allies, breaking its promise to do so.

Most conservationists were not surprised by the administration’s action. The repeal was consistent with a set of policy positions that favored resource-extracting interests through generous giveaways to corporations. The most egregious example, prior to repeal of the Roadless Rule in its entirety, was when the administration exempted the nation’s largest national forest, Alaska’s Tongass, from the Roadless Rule.

As a result of the new rule, millions of acres of public forest are now at risk of being opened to development. These include:

* Alaska’s Tongass National Forest, where the administration has proposed to increase logging in the world’s largest remaining temperate rainforest;

* Idaho’s Greater Yellowstone Ecosystem, where the administration has announced plans to open the largest swath of wild forest in the Lower 48 states to logging and mining;

* Colorado’s Rocky Mountains, where the administration plans to open to development a majestic landscape with trout streams, rock-ribbed trails and diverse wildlife that make it a premier destination for outdoor recreation.


Chief Arvol Looking Horse calls for prayer ceremony in Yellowstone National Park April 15, 2008

Filed under: Buffalo Field Campaign (BFC) — omeganews @ 8:19 pm
P.O. BOX 957


Chief Arvol Looking Horse, 19th Generation Keeper of the White Buffalo Calf Pipe calls for prayer ceremony in Yellowstone National Park April 15, 2008

Press Contacts:
Rosalie Little Thunder, Seventh Generation Fund’s Tatanka Oyate Project, 605-719-3012 (work),
Darrell Geist, Buffalo Field Campaign, 406-531-9284,
Stephany Seay, Buffalo Field Campaign, 406-646-0070,
(RAPID CITY, SD & WEST YELLOWSTONE, MT) – Seventh Generation Fund’s Tatanka Oyate Project and Buffalo Field Campaign are honored to share this announcement of a Releasing of the Buffalo Spirits Ceremony to be held in Yellowstone National Park on Tuesday, April 15, beginning at 12:00 noon (MST). The ceremony is open to all, and all are welcome. Following the ceremony, a community meal will be served at the Gardiner Community Center on 206 Main Street. A flyer for distribution and posting is available at

The ceremony will be led by Chief Arvol Looking Horse, 19th Generation Keeper of the White Buffalo Calf Pipe, who last performed the Spirit Releasing ceremony in 1997 when 1,084 wild buffalo were slaughtered that winter.
According to the U.S. National Park Service, so far this winter Yellowstone National Park and the Montana Department of Livestock have trapped and slaughtered 1,187 wild buffalo migrating from the Yellowstone plateau to winter range in the Gardiner Basin and upper Madison Valley. Hundreds more buffalo remain in a trap operated by Yellowstone National Park inside the Park at Stephens Creek. 80 bison calves have been separated from their family groups and placed in a quarantine research project at Corwin Springs, Montana.An excerpt from Arvol Looking Horse’s full press statement attached in PDF follows:“Let it be known that Yellowstone territory; the habitat of the last wild Buffalo Nation – is sacred ground, it has been a SACRED SITE for the First Nation’s people, and for all humanity who hold deep respect for all Creation. The Buffalo Nation has confirmed this fact; by where they have ended up, continuing to survive in their natural migration, struggling to live in a peaceful manner. Our ancestors also gave us this message by fasting in this area long ago, as they recognized this place of sacredness. This understanding is how we maintain the balance upon Un-ci Ma-ka (Grandmother Earth), to protect these places, especially for the survival of our future generations to come.

“These Buffalo that lost their lives in Yellowstone did not die by Natural Law, nor were their spirits honored with ceremony. This is why we must go there to perform a ceremony of honor for those that lost their lives by the misunderstanding of human-kind and pray to Wakan Tankan (Great Spirit) for pity of how gifts were unappreciated. We must pray with all those who grieve and be grateful for them.

“I humbly ask for all People to make prayers on April 15th, at high noon; for a healing of humanity – for the decisions that are being made with no regard for the sacredness of life, for the massacred Buffalo’s spiritual journey and to protect what is left – in understanding of what our journey in this life represents in being responsible! We must pray for the healing of the human Spirit, to understand the connection to all living beings on Un-ci Ma-ka.”

Chief Arvol Looking Horse, 19th Generation Keeper of the White Buffalo Calf Pipe
Releasing of the Buffalo Spirits Ceremony Tuesday, April 15, 12:00 noon (MST)

GATHERING – Releasing of the Buffalo Spirits Ceremony. RECORDINGS – Protocols will be announced on what photos, video and all recordings of the ceremony, if any is permitted. WHEN – Tuesday, April 15, 2008 and begin 12:00 noon (MST). WHERE – Stephens Creek Road and Old Yellowstone Trail, west of the Yellowstone River, 2 1/2 miles north of Gardiner, Montana. DIRECTIONS – From the Arches landmark, located near the Gardiner, Montana Fee Entrance to Yellowstone National Park, head north past the football field/local school along the Old Yellowstone Trail County Road for 2 1/2 miles to Stephens Creek Road, that leads to the bison trap. Please note that Yellowstone National Park has a closure in effect from near the Fee Entrance to Stephens Creek west of the Old Yellowstone Trail. Please do not park off-road or block traffic. For people who are car pooling, there is extra parking at the Arches landmark along the gated fence.

RECORDINGS – Actual ceremony is not to be filmed, recorded or photographed. Media/journalists should register with media coordinator for protocols.
LODGING – Accommodations in Gardiner, Montana and the surrounding area can be found online:
TRAVEL ADVISORY – DUE TO CLOSED ROADS IN YELLOWSTONE NATIONAL PARK, it is advised that you take the route from Interstate 90 through Livingston, Montana to Highway 89 south to Gardiner, Montana.
COMMUNITY MEAL FOLLOWING CEREMONY – Bear Creek Council is co-hosting a community meal in the historic Eagles Hall Gardiner Community Center on 206 Main Street following the ceremony. The purpose of our community meal is to share our gratitude with everyone who traveled near and far to participate in ceremony honoring America’s wild buffalo. We thank the Gardiner Community Center for sharing their space, and extend an invitation welcoming all to share in a meal together.
Media & Outreach
Buffalo Field Campaign
P.O. Box 957
West Yellowstone, MT 59758

BFC is the only group working in the field every day in defense of the last wild buffalo in the U.S.

Psychiatry – with a Vengeance

Filed under: Health - Gesundheit — omeganews @ 8:08 pm
Researching for a presentation on psychiatry I came across the following information.
Zyprexa, an anti-psychotic drug widely used to treat schizophrenia, produced by Eli Lilly, has become the best-selling drug although it is far more expensive that earlier anti-psychotics. Although first trials led to a high number of suicides the FDA approved the drug.
Other known side effects are weight gain leading to obesity, diabetes, metabolic syndrome, glaucoma and other often life-threatening diseases.Obviously Eli Lilly has good sales promoters with influence on the Irish Health Service Executive. Zyprexa is the third most prescribed drug for those who have a the Medical Card but for those who have to pay for medication themselves it is ranged 71 (2006 statistic)And then by coincidence someone from an autism yahoo group sent a scientific review article by Jonathan Campbell about natural treatment of schizophrenia with linseed oil. I’m copying and pasting it below.

It’s really time that someone writes the criminal history of psychiatry. I can suggest a title: “Psychiatry – with a Vengeance”.

You ask yourself why the psychiatric profession is allowed to kill people, to cause brain damage, make patients invalid although there is evidence that dietary changes can bring about complete recovery.I’ve seen that World-News has a link to the CCHR’s video Psychiatry – an Industry of Death. The Citizens Commission for Human Rights will stage an exhibition with the same title in Cork in June.Dorothee

“At much the same time Lilly began studies on Zyprexa in children. There are parallel problems to Pfizer’s studies. The studies in adults with Zyprexa that Lilly submitted to the FDA demonstrate, as far as I can establish, a higher death rate on Zyprexa than on any other anti-psychotic ever recorded. In addition to this Lilly have suppressed data on suicidal acts on Zyprexa from these trials. The data are not available in the scientific literature, nor from FOI requests to the FDA, nor from enquiries to the company. Despite this Lilly are engaged in trials with this agent in children. These trials will underpin vigorous company promotion for this drug in a wide swathe of children with hyperactivity, neurosis, bipolar and psychotic disorders – they won’t enable clinicians to use the drug if needed.”

Testing Psychotropic Drugs in Children

April 30, 2002

David Healy, MD
University of Wales College of Medicine
April 30th 2002.

UPDATE 1-Lilly settles Zyprexa case with Alaska for $15 mln

NEW YORK, March 26 (Reuters) – Eli Lilly and Co (LLY.N: Quote, Profile, Research) on Wednesday said it agreed to pay $15 million to settle a lawsuit by the state of Alaska accusing it of concealing possible side effects from Zyprexa, its widely used schizophrenia medicine.

The settlement includes no admission of wrongdoing, and will ensure that Alaska is treated as well as any other state that resolves similar claims, according to a joint statement from Lilly and Alaska Attorney General Talis Colberg.

Alaska had accused Indianapolis-based Lilly in a March 2006 lawsuit of failing to properly warn the state and healthcare providers that using Zyprexa could result in weight gain, high blood sugar and diabetes. A trial had begun on March 3 in the Superior Court in Anchorage.

Zyprexa is Lilly’s largest product by far, with sales of $4.76 billion in 2007, including $2.24 billion in the United States. Lilly said Zyprexa has been prescribed for more than 23 million people since the U.S. Food and Drug Administration approved it in 1996.

In a statement, Lilly general counsel Robert Armitage said the company had a “strong defense”, but that settling was in the best interests of all parties.

Colberg called the settlement a “good result” for Alaska.

On March 11 Connecticut also sued Lilly over Zyprexa, accusing it of concealing side effects and promoting it for unapproved uses, including the treatment of children.

Lilly said Zyprexa was not approved for people under 18.
Last month, the FDA rejected a long-acting injectable form of Zyprexa, saying it needed to better understand the excessive sedation seen in 1 percent of patients during clinical trials.

Lilly shares closed Tuesday at $50.17 on the New York Stock Exchange. (Reporting by Jonathan Stempel, editing by Will Waterman)

In Search of the Holy Grail:Natural Treatment of SchizophreniaIntroduction

Schizophrenia is a profoundly debilitating mental disorder. Victims often suffer from hallucinations, delusions of grandeur and/or paranoia, and disorganized thought and speech patterns. It knows no class, ethnic, or racial boundaries. Brilliant young scholars have had their lives destroyed. People from every walk of life have been reduced to living in padlocked wards for their self-protection. Even in the mildest of cases, the hallucinations and delusions interfere with cognitive abilities.

Most psychological and neurological researchers believe that the root cause of schizophrenia is a set of genetically caused malfunctions in neurotransmitter chemistry, and that people with schizophrenia are therefore just unfortunate victims of bad genes. The focus of treatment protocols has been the development of psychopharmacology – the synthetic creation of medicines that manipulate such factors as neurotransmitter production, storage, release, and reception.

People with schizophrenia are treated today primarily with powerful tranquilizers, mood stabilizers, and anti-psychotic drugs that tinker with neurotransmission. All of the drugs have serious side effects on brain functioning and body metabolism, some of them potentially deadly. Most of them require even more drugs to compensate for their side effects. Some of them are psychologically or physically addictive.

The usual explanation given for the affliction and its treatment lacks completeness. Most medical and psychological literature contains no analysis of the underlying neurobiology that caused the problem. The research that has revealed the cause came from a different source: people studying the chemistry of the membrane surrounding the nerve cells in our brain (neurons). About twenty-five years ago, a few researchers in the US and Canada hypothesized that the root cause of schizophrenia was a metabolic disturbance in cell membrane chemistry. Their research has expanded into a framework in which the many different causative factors in psychoses, as well as the action of the best anti-psychotic drugs, can be explained. This framework also provides the basis for research into and clinical trials of safe, natural, effective remedies that have no side effects.

This research has opened the possibility of finding a root cause and possible effective natural treatment for schizophrenia.

What is Schizophrenia?

Schizophrenia is the word that we use to describe a number of conditions in which the victim loses contact with reality. These are commonly defined as psychoses. “The hallmark of the schizophrenia is thus a more or less sharp break with the world in which most less disturbed people live, a world that is rooted in a basic consensus about what is true and real in our shared experience” (Carson, 2002, p. 396).

It is a profoundly debilitating affliction, affecting about 1 percent of the U.S. population in any given year. It accounts for 40 percent of admissions to mental hospitals and 50 percent of mental health bed occupancy. It is not a new affliction; in ancient writings people who likely had schizophrenia are described as being possessed by demons and evil spirits. During the Middle Ages “exorcism became a treatment of choice” in Europe (Carson, 2002, p. 15).

The classic symptoms are disruption of thought, perception, and behavior on every level. Thoughts become disorganized and appear to be totally random, and are often overwhelmed by delusions, or false beliefs, such as the notion that one owns a franchise to sell copies of the Bill of Rights and could potentially become wealthy by selling copies of it. Verbal communication is incoherent and disorganized. Sentences appear to be put together from unconnected phrases. “The guy across the street has the sky blue” would be a typical example. Perceptions are distorted and, according to reports by people with the affliction, overwhelming; it is as if the selectivity of the brain has been shut off.

Emotional responses and affect appear inappropriate or bizarre. Many people with schizophrenia experience hallucinations – false perceptions – such as voices and images that only they can hear and see. Some experience extreme paranoia, seeing the world and the people around them as evil and a personal threat to them. They often have a confused sense of self, often completely delusional, thinking that they are God, Jesus Christ, or someone tied intimately to universal powers.

Volition – that is, the coordination of thought leading to action – is impaired; some people with schizophrenia cannot even take care of their personal hygiene. Patients may retreat into an inner world, and become unable to interact with the outside world at all. Finally, many people with schizophrenia “look crazy.” There are disturbances in motor function and muscle control that appear to be bound up with the emotional aspects of the affliction, such as peculiar or bizarre facial expressions. These symptoms and signs are separated by psychologists into “positive symptoms” – such as hallucinations, delusions, bizarre behavior, and disorganized thought – and “negative symptoms,” which include withdrawal, absence of emotion, and loss of speech (Carson 2002).

In my own experience working with people with schizophrenia, I have found that it is an incredibly frustrating affliction to deal with. For, unlike the panic and mood disorders and those caused by trauma, people with schizophrenia appear to be suffering from an organic and permanent brain disorder, rather than a situational or emotionally based illness. Traditional therapy can be useful, but it must be intensive. Given the nature of the medical and human service support systems in place today, this is not usually a viable option. While some cases of schizophrenia have cycles of illness and remission, most cases do not and remissions are rare.

It is almost impossible for people with untreated schizophrenia to function in society or even to take care of themselves physically. The anti-psychotic drugs, even the best ones such as Clozapine, are only partially successful in resolving the disorder, and the side effects are absolutely dreadful. In the case of Clozapine, they are potentially life-threatening, as will be explained below. Many patients are on multiple drugs, each with their own side effects and interactions. These drugs sometimes allow people to pursue their lives, but although the symptoms are more manageable, they are most often still there, along with horrible drug side effects. Thus the pursuit of meaningful career goals is often thwarted.

From modern MRI scanning we now know that some people with schizophrenia have larger than average brain ventricles – the “holes in your head” that contain the cerebral spinal fluid, which is the primary mechanism for nutrient and waste transport in the brain. In addition, there may be enlarged “sulci” – the fissures on the surface of the brain. This ventricle and sulci enlargement is generally thought to be a sign of brain atrophy or degeneration (Carson 2002).

Finding a Cause

There have been a number of possible explanations of the cause of schizophrenia. These range from genetic models to those that attribute the disease to social environment.

Diathesis-stress model

One of the more useful concepts in psychology is the “diathesis-stress model” of mental disorders, which hypothesizes that many psychological disorders are brought about by genetic or early childhood factors (diathesis) followed by stresses later in life (Carson, 2002, p. 37). Following this line of reasoning, researchers of origins of schizophrenia have been looking long and hard for evidence of genetic predisposition for the affliction, but have been only partially successful. There are strong correlations, especially if both parents have schizophrenia. But without knowledge of the actual biological cause, this research quickly reaches a dead-end: “Thus, evidence of a shared family trait, while persuasive, remains incomplete because of the difficulty of figuring out where genetic influences end and environmental influences begin” (Carson, 2002, p. 412).

Neurodevelopmental explanations

As modern medical study of schizophrenia and the possible causes of the physical abnormalities progressed, several researchers began looking into the possibility that it was a neurodevelopmental affliction, that is, that it progressed over time, perhaps even starting before birth. In several studies, researchers found a correlation between schizophrenia and maternal influenza in the second trimester of pregnancy. It was discovered that more people with schizophrenia were born during winter months than during warmer seasons, suggesting another possible connection to maternal illness.

In another quite startling study, the early home movies of people who later developed schizophrenia were compared by trained observers with those of healthy people. (This was a “blind” study: the observers were not informed of the children’s outcomes). The children who later developed schizophrenia showed less emotionality in their expressions, had poorer motor skills, and also had a higher rate of peculiar movements. Thus there were signs that these children’s brains had been profoundly compromised in some way during gestation or very early infancy. (Carson 2002).

Blaming the victim and circular reasoning

For psychologists and psychiatrists it appears that the root cause of schizophrenia remains a mystery. Some psychology textbooks refer to its cause as “elusive” (Hockenbury, 2003, p. 612), or “unclear” (Carson, 2002, p. 411), or, quoting Winston Churchill, “a riddle wrapped in a mystery inside an enigma” (Coon, 2004, p. 610). Unfortunately, these textbooks (and researchers) do not leave it at that. Their proposed causative factors, besides the genetic factors discussed above, include poverty, problematic families and upbringing. These shed little light on the affliction while further stigmatizing its victims. In addition, it should be noted that having a disturbed individual in a household itself causes family problems. This seems to be a confusion of cause and effect.

Some research into the brain chemistry of people with schizophrenia have found that one of the neurotransmitter chemicals, called dopamine, appears to be overactive. This symptom has been turned into one of the proposed possible “causes,” now referred to the “dopamine hypothesis” (Hockenbury, 2004, p. 610). This is a classic scientific mistake referred to as circular reasoning, in this case turning a symptom into a cause. A good analogy might be blaming a train wreck on two moving trains being in the same place at the same time, rather than a failing brake, broken rail, burnt-out semaphore lamp, or human error.

Outside the U.S., however, an unusual group of researchers in cell membrane chemistry were hot on the trail to a real answer to this mystery.

The Cell Membrane (Phospholipid) Hypothesis

About twenty-eight years ago, a few researchers in brain cell membrane chemistry began to report new findings on the root causes of schizophrenia. In 1977, David Horrobin, who at that time was at the Clinical Research Institute and the University in Montreal, wrote what appears to have been the first short peer-reviewed paper on the connection between schizophrenia and the cell membrane, published in the British Medical Journal The Lancet. He hypothesized a root cause of schizophrenia having to do with defects in cell membrane chemistry, specifically a deficiency in chemicals called prostaglandins that are manufactured from essential fatty acids (Horrobin 1977, p 936).

Four years later Donald Rudin from the Eastern Pennsylvania Psychiatric Institute wrote a major journal article in Biological Psychiatry, in which he expanded upon this idea. He hypothesized that the major neuroses and psychoses were an “Omega-3 Essential Fatty Acid Deficiency Syndrome,” a profound metabolic disturbance involving the creation of prostaglandins, that caused these mental illnesses as well as a physical skin disorder: pellagra (Rudin, 1981, p. 837). Rudin gave testimony of fairly dramatic results merely using flaxseed oil (“linseed oil”) for twelve patients with serious mental disorders.

By the early 1990s, a network of researchers working on the cell membrane hypothesis had formed, and in 1996 these researchers were able to present their work in a peer-reviewed journal devoted to human lipid chemistry (Prostaglandins, Leukotrienes, and Essential Fatty Acids) that had been established by Horrobin. Since then, their work has begun to appear in prominent psychological journals (such as Schizophrenia Research and Archives of General Psychiatry), and the interest in lipid research has increased dramatically. But it has not yet entered the mainstream of psychiatric treatment.

An explanation of the phospholipid hypothesis

Every cell in living tissue is surrounded by a permeable membrane to enable nutrients to enter the cell and to enable waste products to leave. In the brain, a part of this cell membrane, sometimes referred to as the neural membrane, makes up the connection point, called the synapse, between neurons (Klein, 2000). The membrane is composed of a collection of phospholipids (complex molecules containing phosphorus and essential fatty acids) as well as special proteins, receptors, and a number of other structures that allow nutrients, hormones, and neurotransmitters to enter the cell and waste products to leave (Marieb, 2004, p. 49). Our bodies need a collection of fats, called essential fatty acids, in order to build and maintain this cell membrane, as well as to properly create the packets of neurotransmitters that are sent from one neuron to another in the brain (Haag, 2003).

Essential fatty acids (EFAs) are called “essential” because they cannot be created by the body. The most important of these are alpha linoleic acid (ALA), linoleic acid (LA), arachadonic acid (AA), docosahexanoic acid (DHA), and eicosapentanoic acid (EPA). We must consume them in order to stay healthy. The human body is capable of creating the latter three fatty acids (AA, DHA, and EPA), from the former two, but this transformation mechanism is weak in infants and in old age. Furthermore, the ratio of ALA to LA is important in maintaining a proper balance of EFAs in the cell membranes. The primary source of LA in Western diets is cooking oils such as corn and safflower oil. ALA comes from cereals such as flaxseed. The primary direct source of AA is meat, and the direct source of DHA and EPA is fish. For infants, the source of all EFAs is mother’s milk.

Three essential fatty acids – EPA, DHA and AA – are the most important for healthy neural membranes. These membranes serve as a reservoirs of these fatty acids, and exchange two of them – DHA and AA – on a regular basis for neurotransmission and other cell functions. To enable this pattern of fatty acid exchange, the body produces certain chemicals called phospholipases, which remove fatty acids from the membrane, and enzymes that attach them again. As the fatty acids are used up, they must be replaced from the foods we eat (Horrobin 1998).

If this exchange mechanism is not functioning properly, or there is a dietary deficiency in these essential fatty acids, and the neural membrane is weakened, the neuron and neurotransmission will be weakened as well. If, for some reason, the membrane of every neuron (or nerve cell) in the brain began to deteriorate as a result of depletion of its essential fatty acid building blocks, one could well imagine that neuron function throughout the brain would deteriorate as well.

If this happened, neurotransmission would likely become random, irregular, distorted, and asynchronous. Thought patterns and images from the past, images and sounds from TV and movies, and images from dreams might suddenly arise and present themselves as current thought. Coordination of thought patterns and their presentation as speech would become impossible. Eventually, there would be neuron death and anatomical changes that would be visible by means of various diagnostic procedures. These are precisely the diagnoses of schizophrenia (Carson, 2002).

Recent findings

The network of cell membrane researchers, discussed above, correlated anomalies among people with schizophrenia and possible explanations relating to phospholipid breakdown (Horrobin, 1998; Yao, 1996; Mahadik, 1996; Hudson, 1996; Bates, 1996):

People with schizophrenia have a surplus of Phospholipase A2 (PLA2) circulating in their bloodstream. This chemical splits essential fatty acids from the cell membrane.
There are reduced levels of DHA and AA in the red blood cell membranes of people with schizophrenia.
People with schizophrenia often show a reduced maximum response to light. This response is dependent on the availability of DHA in the retina.
People with schizophrenia often have increased pain tolerance, indicating a defect in the neural membrane.
People with schizophrenia appear to have a defect in the mechanism that binds essential fatty acids to the neural membrane.
Two genetic abnormalities relating to the excessive production of Phospholipase A2 have been found in people with schizophrenia.
The kinds of brain abnormalities found in people with schizophrenia are consistent with a defective response to high fever caused by severe colds or influenza during gestation. Some people with schizophrenia were exposed to hyperthermia (fever) and viral infection (primarily influenza) during gestation and/or hypoxia (lack of oxygen) at birth.
The increased ventricular size in brains of some people with schizophrenia, which is indicative of loss of brain matter, is consistent with brain atrophy, or neuron death, caused by EFA depletion and/or oxidative stress.
The behavioral and neuromotor function abnormalities in childhood that are predictors of schizophrenia and are consistent with the brain dysfunction that would be caused by EFA depletion.
Schizophrenia is highly correlated with poor health, it increases with stress and old age, and it is more common among men than women. These correlations are consistent with EFA deficiency. David Horrobin wrote in 1998: “The rate of synthesis and of incorporation of these EFAs into phospholipids is reduced by viral infections, male sex, stress and old age…”(Horrobin, 1998)In summary, schizophrenia can result from one or more genetic metabolic abnormalities and/or events during gestation and childbirth that are then accentuated by poor nutrition, in particular a deficiency in certain essential fatty acids in the diet common in the United States.Schizophrenia and oxidative stress

There is now also strong evidence that depletion or failure of the body’s antioxidant system is correlated with schizophrenia. This comes from several lines of research. First, studies have found that people with schizophrenia have measurable amounts of pentane – the hydrocarbon molecule most identified with gasoline – in their breath. This chemical is produced by oxidative damage of the omega-6 fatty acids (Peet 1996). Second, there is evidence that there is depletion of the body’s primary antioxidant enzyme, glutathione, which is correlated with increased size of the brain ventricles – a sign of brain tissue destruction – common in schizophrenia (Buckman, 1987, reported by Peet, 1996).

Schizophrenia, influenza and heat stress

There is some evidence that there is a correlation between maternal influenza during gestation and the development of schizophrenia in the affected offspring (Carson, 2002). Bates et al. (1996) have hypothesized that the genetic defect in lipid metabolism correlated with schizophrenia, and the resultant compromised phospholipid membrane system in the developing fetus, set the stage for an abnormal heat shock response. Such an abnormal response, which leads to a deficiency of protective heat shock proteins, would lead to the anatomical abnormalities commonly found in the brains of people with schizophrenia.

Evidence for the Hypothesis

A hypothesis such as this, which appears to be very different from the current view of the origins of schizophrenia and its pharmacological treatment, demands clinical evidence.

Clinical studies of people with schizophrenia and trials using various EFAs to treat schizophrenia, both as a sole agent and as an adjunct to pharmacological treatments, have been moderately to extremely successful in reducing or eliminating the positive and negative symptoms of schizophrenia. In one case, a man with long-term stable schizophrenia experienced complete remission of all positive and negative symptoms by simple administration of EPA. The most recent research has revealed that supplemental EPA inhibits excess PLA2, identified as the central cause of lipoprotein breakdown and resultant schizophrenia (Puri 1998).

Additionally, the most effective psychopharmacological treatment for schizophrenia, Clozapine, is a “prostaglandin E analog.” More simply stated, this drug, whose anti-psychotic properties have never been adequately explained using classical neurotransmission theories, inhibits the action of Phospholipidase A2 and thereby increases the availability of AA and DHA to the neural membrane (Horrobin 1996). This may not be totally coincidental; Clozapine was developed by the pharmaceutical company Novartis shortly after publication of David Horrobin’s first paper in 1977, in which he suggested that schizophrenia was a prostaglandin E deficiency disease.

The clinical studies

Since Horrobin’s first publication of the phospholipid hypothesis, there have been several small but significant clinical studies of natural treatment protocols. Some of these were analytical studies, which sought to obtain information about a set of patients with schizophrenia. Others were clinical tests of various amounts and mixtures of essential fatty acids added to the diet. These clinical tests demonstrated the effect of EFAs in reducing or eliminating the characteristics of schizophrenia in the research subjects.

An analytical study done by Peet et al. (1996) was designed primarily to confirm the phospholipid hypothesis. Twenty-three drug-treated schizophrenic patients were measured for essential fatty acid content in their red blood cell membranes. Depletions were evident for linoleic acid (LA), arachidonic acid (AA), eicosapentanoic acid (EPA) and docosahexanoic acid (DHA), with the most significant depletion reported for AA and DHA.

The first clinical trial was done even before the mechanism of EFA destruction was known. In this study, Donald Rudin administered daily doses of flaxseed oil (then called linseed oil), in increasing amounts, to five patients with schizophrenia, three patients with major depression, and four patients with agoraphobia (Rudin, 1981). Three of the five people with schizophrenia reported improvement that was fairly dramatic. These were people with “remitting schizophrenia,” that is, those people for whom schizophrenic symptoms cycled from mild symptoms or none at all to severe symptoms. They reported (and were observed to have) very long, sustained periods of remission.

Four other studies used specific amounts of eicopentaenoic acid (EPA). One by Mellor et al. (1996) involved giving twenty chronic hospitalized schizophrenic patients a daily dose of ten grams of a supplement called MaxEPA. After six weeks their mean schizophrenic symptom rating (called PANSS) had decreased from 78.9 to 65.6, which is a significant drop. The amount of omega-3 fatty acids in the patients’ blood correlated directly with the improvement of their symptoms. Even more significantly, a measure of tardive dyskenesia, a dreadful side effect of many anti-psychotic drugs, had dropped from 20.2 to 12.3.

A randomized, double-blind, placebo-controlled study by Emsley et al. (2002) used a fixed amount of EPA to confirm its efficacy. Forty patients with schizophrenia with ages varying from eighteen to fifty-five took part in this twelve-week study. They were assessed for symptoms using PANSS at the beginning of the study and at three, six, nine, and twelve weeks, and assigned to receive three grams of EPA per day or a placebo, in addition to their usual anti-psychotic medications. The patients taking EPA showed a significant reduction of negative and positive symptoms of schizophrenia, as well as symptoms of tardive dyskenesia.

Peet and Horrobin (2002) conducted a study to determine the most effective amount of EPA to use for schizophrenia. They studied 115 patients, all taking various anti-psychotic medications. Patients were given placebo or one, two, or four grams of EPA per day in addition to their regular medications. There were significant improvements reported for patients taking two grams per day, and a positive relationship found between these improvements and the concentration of arachadonic acid in their blood. The researchers hypothesized that larger doses of EPA overload the cellular membranes and compete with AA and DHA, which are needed for neurotransmission.

There is also a dramatic case study of a thirty-one-year-old man with chronic, unremitting schizophrenia since his teen years, and who had taken only one dose of an anti-psychotic medication several years before this study (Puri et al., 1998, 2000). He was given two grams of EPA per day, and he experienced visible and sustained improvement, which was clinically evaluated as remission, of both his positive and negative symptoms of schizophrenia. Prior to this trial, it was also determined, by means of high-resolution 3D cerebral MRI scans, that his brain was undergoing cerebral atrophy. Follow-up scans revealed that this atrophy had been reversed.

The relative value of EPA versus DHA (docosahexaenoic acid) was demonstrated by a pair of studies (reported by Peet et al., 2001). In the first study, forty five schizophrenic patients were administered either EPA or DHA for three months, to determine the most efficacious EFA to use. In the second study, using placebo controls, EPA was used alone, without anti-psychotic drugs, except where the symptoms made it essential. Patients taking EPA had “significantly lower scores on the PANSS rating scale [used to measure the symptoms of schizophrenia] by the end of the study.”

All of this research indicates that schizophrenia is highly correlated with depletion of essential fatty acids. The clinical trials and the case study further demonstrate that supplementation with EFAs significantly reduces the symptoms of this disorder.


What is dramatic about the phospholipid hypothesis is that it explains, quite simply, all of the features, symptoms, progression, and epidemiological data known about schizophrenia. It takes into consideration and neatly explains the defective neurotransmission models that were previously proposed as “causative” but had unknown corresponding biological bases, as well as the neurodevelopmental stresses that are highly correlated with schizophrenia.

The phospholipid hypothesis holds out the promise of prevention of schizophrenia in the future, as well as safe, natural treatment of schizophrenia, and, by analogy, bipolar disorder and other mental disorders such obsessive-compulsive disorder (OCD), attention deficit disorder (ADD), and attention deficit hyperactivity disorder (ADHD), since aberrations or severe deficiency in EFAs could cause a wide range of abnormal, compromised neurotransmission. There is strong evidence, already published, that unipolar depression – the most common psychological disorder – responds to treatment with EFA supplementation (Stoll 2001).

For prevention, a simple blood test could be provided for expectant parents to test for low essential fatty acids in blood cells, the hallmark of elevated phospholipase PLA2 that these researchers found be the root cause of schizophrenia. Expectant mothers could be provided with sufficient ascorbate (vitamin C) to prevent oxidative stress and reduce the chances of causing the heat shock reaction mentioned earlier. Finally, newborns could be tested with the same red blood cell test, and provided with supplemental essential fatty acids to allow their brains to develop normally and avoid schizophrenia.

Current medical treatments for schizophrenia, as mentioned earlier in this paper, are deficient and dangerous. The most successful medication, called Clozapine, has terrible side effects and it is horrifically dangerous. It reportedly causes impotence, weight gain, and slowing of peristalsis, and often requires daily laxatives to prevent intestinal blockage. According to its official side-effect literature, Clozapine causes depletion of the essential mineral selenium, and compromises immunity. Any sudden increase in dosage, including a patient forgetting to take the drug for several days and then starting again, can cause seizures or coma. It can spontaneously cause sudden, rapid depletion of white blood cell count and resultant death. Patients taking Clozapine must have their white blood cell count monitored every two weeks before being allowed to continue taking the drug.

And even this drug is not completely effective. In my own experience, Clozapine is often used in concert with the standard anti-psychotic drugs, such as Haldol, and some of the newer, atypical ones, such as Risperdal. Additionally, people with schizophrenia often have co-occurring disorders such as depression, for which even more drugs are prescribed. Each of these carries its own side effects and extreme risks of drug interactions, such as serotonin syndrome, a potentially deadly interaction between SSRI anti-depressants and other drugs (Ener 2003, Karki 2003).

One of the side effects of the standard anti-psychotic medications, commonly called “neuroleptic” drugs, is so common and so serious that it has itself become a named affliction: tardive dyskinesia, or TD. It is “a persistent and often irreversible syndrome characterized by abnormal movements, including lingual and orofacial dyskinesia, grimacing, tics, choreic movements of the limbs or trunk, and athetosis and dystonia.” (Retrosin 1996).

TD is so common that the Massachusetts Department of Mental Health, for instance, requires that psychiatrists report whether TD has been noted at each patient visit. According to some statistics, its prevalence is “on the order of 10-15% in young populations, 12-25% in more chronic patients, and 25-40% in very chronic patients…TD is a social handicap that leads to social isolation and compromises dignity and quality of life. They are less likely to be accepted into rehabilitation programs, and they are less likely to be employable…” (Retrosin 1996).

Thus a natural treatment for schizophrenia, even one that could substantially reduce a patient’s dependence on anti-psychotic medications, is greatly needed. The clinical studies cited above indicate that use of supplemental essential fatty acids – particularly EPA supplementation – appears to alleviate the EFA imbalance and improve the symptoms of schizophrenia.

Retrosin’s finding regarding oxidative stress caused by anti-psychotic medications and the successful use of antioxidants to alleviate it indicates that an antioxidant supplementation regimen should be used as an adjunct to EFAs.

Current thinking vs. the phospholipid hypothesis

I believe that it is merely wishful thinking to imagine that the entire psychiatric establishment in the United States is going to readily accept the idea that a few capfuls of pharmaceutical-grade fish oil are going to take the place of the anti-psychotic medicines that are prescribed for schizophrenia today. The biochemistry involved in the phospholipid hypothesis is outside of the worldview of most doctors who treat patients with psychotic disorders; the last time they ever studied the nature of the cell membrane was in their Anatomy and Physiology in college. These doctors – as dedicated as they are to helping their clients – are stuck in the pharmaceutical paradigm. Their approach is defined by the search for the correct amounts of various drugs for each individual, and looking to the pharmaceutical industry for the next “miracle drug.” This paradigm is bolstered by mountains of industry-funded research reports, advertising, and sales representatives. There are few, if any, truly independent clinics or universities without any kind of pharmaceutical company connection.

Even if the psychiatric profession understood the science, the very structure of psychiatric care is focused around drug administration. Many major psychiatric hospitals now have Clozapine testing labs, where patients come every two weeks to have their blood monitored for white blood cell counts and Clozapine levels. Reductions of funding during the last thirty years has meant that patients spend only a few minutes with their psychiatrists every three months, just enough time for the psychiatrists to figure out whether the drugs are working to bring the worst symptoms under control.

Adverse outcomes: nutritional status and health

Schizophrenia is so debilitating, even when compensated by drugs, that many people who have it fall into poverty because it interferes with their cognitive and reasoning abilities and especially their social skills. Often homeless or on poverty’s edge, many turn to alcohol or drugs. Compounding the problem is that many people with schizophrenia follow a diet that is deficient in nutrients, high in saturated fats and sugars, and low in essentially fatty acids, a diet associated with worse long-term outcomes (Peet 2004). These findings make it clear that closer monitoring of dietary health would be needed if even people with schizophrenia were to begin long-term therapy with EFAs.


David Horrobin began an entirely new and innovative research direction in the study of schizophrenia – the malfunctioning of the cell membrane in neurons. In order to publish his own research and the work of an expanding network of research physicians intent on developing this new line of study, he apparently needed to establish a new peer-reviewed journal: Prostaglandins, Leukotrienes, and Essential Fatty Acids. Given the historical context, that virtually all psychological research was focused on the role of neurotransmitters in abnormal psychology and the creation of drugs to manipulate them, this is not surprising.

I believe that Horrobin and his colleagues have found the Holy Grail of psychology – an integrative root cause explanation for schizophrenia that takes into consideration all of the manifestations of this horrible syndrome that has wrecked so many people’s lives through the ages. The clinical and case studies have provided ample evidence. The phospholipid hypothesis provides insights into safe, natural treatment protocols that have been tested with some success. It identifies the specific genetic predisposition and the biological/environmental stressors that lead to the progression of the syndrome, thus providing some possible strategies for prevention and very early treatment.

But influencing the medical system so that the phospholipid hypothesis is accepted and acted upon is a daunting challenge. David Horrobin’s breathtaking and extensive article in Schizophrenia Research appeared in 1998, but there is little evidence that this knowledge is making its way into mainstream medicine yet. Psychology textbooks that I reviewed, some written as recently as 2004, have no mention of it at all, and quick scans using google and PubMed, the National Library of Medicine’s public access website, result mostly in pointers to the original work done by Horrobin and his colleagues.

There are many medical truths in recent history that have not entered into mainstream thinking simply because there is so much investment (money, facilities, resources, and personnel) in the current paradigms. More than ten years ago, for instance, two research scientists, Matthias Rath and Linus Pauling, identified the true root cause of cardiovascular disease (Pauling, 1991) They proposed a treatment – now clinically proven – that reverse this affliction without drugs, stents, or bypass surgery. Their work provides a simple nutritional regimen that would eradicate the affliction worldwide. It would also eradicate a $200 billion dollar per year industry along with the entire profession of cardiology. Needless to say it is still virtually unknown among health professionals.

Fortunately there are well-placed researchers and clinicians who understand and accept the phospholipid hypothesis and are making it part of their daily practice. For instance, Andrew Stoll, who is the director of the psychopharmacology clinic at McLean Hospital in Belmont, Massachusetts is using EFAs in his clinical research. He also wrote a popular book, The Omega-3 Connection, which has an entire chapter devoted to the Horrobin’s phospholipid hypothesis of schizophrenia. When he spoke at the recent Defeat Autism Now conference held in Quincy, Massachusetts, he showed a slide indicating that the interest in EFA research has increased dramatically just in the last two years.

David Horrobin unfortunately passed away last year, before his hypothesis and the treatment protocols he and his colleagues developed had the opportunity to become accepted theory and practice. Let us hope that their research has not been in vain.


Bates P, Hawkins A, Mahadik S, McGrath J. Heat stress lipids and schizophrenia. Prostaglandins, Leukotrienes and Essential Fatty Acids 1996; 55(1&2): 101-107

Carson RC, Butcher, JN, Mineka S. Fundamentals of Abnormal Psychology. Boston. Allyn and Bacon. 2002.

Coon D. Introduction to Psychology: Gateways to Mind and Behavior. Belmont, California. Wadsworth/Thomson Learning. 2004.

Emsley R, Myburgh C, Oosthuizen P, Van Rensburg S. Randomized, placebo-controlled study of ethyl-eicosapentaenoic acid as supplemental treatment in schizophrenia. American Journal of Psychiatry 2002; 159(9):1596-1597.

Ener RA, Meglathery SB, Van Decker WA, Gallagher RM. Serotonin syndrome and other serotonergic disorders. Pain Medicine 2003; 4(1):63-74

Gattaz WF, Brunner J. Phospholipase A2 and the hypofrontality hypothesis of schizophrenia. Prostaglandins, Leukotrienes and Essential Fatty Acids 1996; 55 (1&2):109-113.

Haag M. Essential fatty acids and the brain. The Canadian Journal of Psychiatry 2003 (April). From the website of the Canadian Psychiatric Association,

Hockenbury, D, Hockenbury S. Psychology. Third Edition. New York, N.Y. Worth Publishers. 2003.

Horrobin, DF. Schizophrenia as a prostaglandin deficiency disease. The Lancet 1977 (April 30): 936-937.

Horrobin DF. Schizophrenia as a membrane lipid disorder which is expressed throughout the body. Prostaglandins, Leukotrienes and Essential Fatty Acids 1996; 55(1&2):3-7.

Horrobin DF. The membrane phospholipid hypothesis as the biochemical basis for the neurodevelopmental concept of schizophrenia. Schizophrenia Research 1998; 30:193-208.

Hudson CJ, Lin A, Horrobin DF. Phospholipases: in search of a genetic base of schizophrenia. Prostaglandins, Leukotrienes and Essential Fatty Acids 1996; 55 (1&2):119-122.

Karki S, Masood G. Combination Risperidone and SSRI-Induced Serotonin Syndrome, Annals of Pharmacotherapy 2003; 37:388-391.

Klein SB. Biological Psychology. Upper Saddle River, NJ. Prentice-Hall. 2000.

Marieb EN. Human Anatomy & Physiology, Sixth Edition. San Francisco. Pearson Benjamin Cummings. 2004.

Mellor J, Laugharne J, Peet M. Omega-3 Fatty Acid Supplementation in Schizophrenic Patients. Human Psychopharmacology 1996; 11:39-46

Peet M. Essential fatty acids: theoretical aspects and treatment implications for schizophrenia and depression. Advances in Psychiatric Treatment 2002;8:223-229.

Peet M. Eicosapentaenoic acid in the treatment of schizophrenia and depression: rationale and preliminary double-blind clinical trial results. Prostaglandins, Leukotrienes and Essential Fatty Acids 2003;69(6):477-85.

Peet M. Nutrition and schizophrenia: beyond omega-3 fatty acids. Prostaglandins, Leukotrienes and Essential Fatty Acids 2004; 70(4):417-22.

Peet M, Brind J, Ramchand CN, Shah S, Vankar GK. Two double-blind placebo-controlled pilot studies of eicosapentaenoic acid in the treatment of schizophrenia. Schizophrenia Research 2001; 49(3):243-51.

Peet M, Horrobin, DF. A dose-ranging exploratory study of the effects of ethyl-eicosapentaenoate in patients with persistent schizophrenic symptoms. Journal of Psychiatric Research 2002; 36(1):7-18.

Peet M, Laugharne JDE, Mellor J, Ramchand CN. Essential fatty acid deficiency in erythrocyte membranes from chronic schizophrenic patients, and the clinical effects of dietary supplementation. Prostaglandins, Leukotrienes and Essential Fatty Acids 1996; 55 (1&2):71-75.

Puri B, Richardson A, Horrobin DF, et al. Eicosapentaenoic acid treatment in schizophrenia associated with symptom remission, normalization of blood fatty acids, reduced neuronal membrane phospholipid turnover and structural brain changes. International Journal of Clinical Practice 2000; 54:57-63.

Puri BK, Steiner R, Richardson A. Sustained remission of positive and negative symptoms of schizophrenia following treatment with eicosapentaenoic acid. Archive of General Psychiatry 1998; 55(2):188-189.

Retrosen J, Adler L, Lohr J, Edson R, Lavori P. Antioxidant treatment of tardive dyskinesia. Prostaglandins, Leukotrienes and Essential Fatty Acids 1996; 55(1&2):77-81.

Rudin DO. The major psychoses and neuroses as Omega-e essential fatty acid deficiency syndrome: substrate pellagra. Biological Psychiatry 1981; 16(9):837-850.

Stoll AL. The Omega-3 Connection. New York: Fireside, 2001.

Vaddadi K. Dyskinesias and their treatment with essential fatty acids: a review. Prostaglandins, Leukotrienes and Essential Fatty Acids 1996; 55 (1&2):89-94.

Williamson PC, Brauer M, Leonard S, Thompson T, Drost D. 31P magnetic resonance spectroscopy studies in schizophrenia. Prostaglandins, Leukotrienes and Essential Fatty Acids 1996; 55 (1&2):115-118.

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BioPro’s Fabricated Science Fiction

Filed under: Mobile Radio - Mobilfunk — omeganews @ 3:11 pm

BioPro’s Fabricated Science Fiction

George Carlo has just started to distribute a major message to entirely disassociate himself with BioPro, having encountered many comments over the last few years implying that he endorses their products. The following is his announcement in full

Click here for the full news story

Montana: Temperatures Rise, Rivers Fall, Fish Suffer

Filed under: USA — omeganews @ 7:30 am

Montana: Temperatures Rise, Rivers Fall, Fish SufferAs the climate in the West gets warmer and drier–even more quickly than in other parts of the country–the Montana fluvial Arctic grayling is shouldering much of the burden. Montana’s most imperiled fish, whose numbers have dropped to between five to 15 per mile, has fallen victim to the war for water as river diversions and agricultural dewatering have altered and drained its last remaining refuge: Montana’s Big Hole River. If the fish is to survive the dangerous water-temperature increases and critically low river levels caused by global warming, its habitat needs to be improved–and the fish must be protected.

After the government refused to protect the grayling under the Endangered Species Act last year, the Center for Biological Diversity filed suit.

Read more about it in the New York Times.

From: Endangered Earth, No. 403

No Idea Too Wacky to Keep Water Flowing in an Age of Global Warming, Except, Of Course, Stopping Global Warming

Filed under: Environmental Degradation - Umweltzerstoerung — omeganews @ 7:23 am

No Idea Too Wacky to Keep Water Flowing in an Age of Global Warming–Except, Of Course, Stopping Global WarmingIn a desperate attempt to address the Colorado River’s dwindling flow, a recent report proposed 12 ideas to keep the water flowing out of the river to industrial, agricultural, and urban uses–proposals including cloud seeding over the Rockies, removing salt from ocean water, and even building an undersea pipeline to transfer water to Southern California from the Columbia River. Perhaps the oddest idea of all was to ferry fresh water across the Pacific Ocean, most likely from Alaska, in the form of icebergs or massive water bladders.

The only notion apparently deemed too bizarre to consider was to actually stop global warming. Go figure.

Read more in the Las Vegas Review Journal.

From: Endangered Earth, No. 403

Suit Brewing Over Bush Refusal to Protect California Seabird from Global Warming

Filed under: USA — omeganews @ 7:16 am

Suit Brewing Over Bush Refusal to Protect California Seabird from Global WarmingThe U.S. Fish and Wildlife Service has missed the first deadline in the process for protecting the ashy storm-petrel, an imperiled California seabird, under the Endangered Species Act. The small, smoke-colored bird–long imperiled by threats from development to commercial fishing–now adds global warming to the list as rising temperatures alter its marine habitat and reduce its prey.

The Center for Biological Diversity filed a petition to protect the ashy storm-petrel last October, but since the government failed to respond as required by law, on March 31 we submitted a notice of intent to sue to move the protection process forward.

Read our press release.

There are 50 Simple Things You Can Do to Save the Earth

Filed under: Environmental Degradation - Umweltzerstoerung — omeganews @ 7:13 am

There are 50 Simple Things You Can Do to Save the Earth–and Uniting With the Center Is OneOn April 1, a brand-new edition of New York Times bestseller 50 Simple Things You Can Do to Save the Earth hit bookstores–and no fooling–it’s probably the best guide out there for helping you through your journey to save the environment, one simple action at a time. What’s one of the most important actions of all? Supporting the Endangered Species Act, of course. Check out page 104 for some background, statistics, and “steps for success”–including teaming up with the Center for Biological Diversity.

Visit the 50 Simple Things Web site to view a special page devoted to the Center.

From: Endangered Earth, No. 403

10 Million Baby Boomers Face Alzheimer’s Epidemic

Filed under: Mobile Radio - Mobilfunk — omeganews @ 6:59 am

—– Original Message —–

From: Art Kab
Sent: Tuesday, April 01, 2008 10:51 AM
Subject: 10 Million Baby Boomers Face Alzheimer’s Epidemic

I would like to preface the following article and comments posted on Dr. Mercola’s website (but originating with the Washington Post on March 18th, 2008) with a section on Alzheimer’s from B. Blake Levitt’s excellent book, Electromagnetic Fields, written 13 years ago in 1995. People can certainly make up their own minds what to believe, but I find this information extremely compelling, especially regarding the experiment done where chimpanzees who were subjected to repeated low-level nonthermal exposures of microwaves “produced clinical Alzheimer’s in [the] test animals.” I am extremely curious to know as to whether or not anymore research along these lines has been done. Or has the overreaching hand of the cell phone industry been able to halt such experiments?

Many people think that Alzheimer’s disease – a progressive, fatal, complete mental deterioration – is a a disorder of normal aging that afflicts an unlucky few. But there is nothing about Alzheimer’s that is normal to aging. Nor is it related to mild forgetfulness. It is a degeneration of the neurons in specific areas of the brain that results from some disturbance within nerve-cell networks utilizing the neurotransmitter acetylcholine.Just ten years ago, Alzheimer’s was considered an obscure and rare condition, but today it is the nation’s fourth leading cause of death. What happened? Is it simply that better diagnosis has turned up more statistically reliable numbers, which perhaps had been lumped together in years past with senile dementia? Or ware we dealing with another degenerative nerve disease increasing in incidence beyond a mere increase in the population? It looks like the latter is true – although increases increases in the population of those living beyond the age of eighty-five plays a significant role in the sheer numbers of cases today. And although there are only a handful of indicative studies and much speculation at this stage, there is a possibility that some EMF frequencies may play an important role, too.

Alzheimer’s is a specific organic disease that afflicts only some people. It is quite different from memory lapses that plague all of us as we age, in which long-term memory is crystal clear and short-term memory seems to all but evaporate. A typical memory lapse of old age would be a person’s remembering in vivid detail an event from youth as if it were yesterday but forgetting where his or her glasses were a minute ago. With Alzheimer’s, people forget that they ever wore glasses.

Alzheimer’s is a physical process in which the nerve cells of the brain take on the abnormal characteristics of “plaques” and “tangles.” In time brain tissue comes to resemble long strands of gray knotted rubber. The disease affects women twice as often as men. Women who have taken anti-inflammatory drugs for arthritis or have had estrogen-replacement therapy have been found in some studies to have a reduced risk of developing the disorder. These studies indicate that inflammation as well as hormonal changes may be important factors. (EMFs annd hormonal changes were discussed in Chapters 7 and 8.)

Research particular to acetylcholine was conducted in 1976 by a research group headed by J.J. Noval, at the Naval Air Development Center in Johnsville, Pennsylvania. Studies using rats exposed to very weak electric fields vibrated in the extremely-low-frequency ranges (the kind of EMF typical of any office or modern home) produces an increase in brain-stem acetycholine levels, indicating a subliminal stress response in test animals. (This also has implications for humans and low-level “contact currents” produced by touching any common machine, including small appliances. Far more work needs to explore this possibility.)

Genetics may also be involved. Several studies have found a genetic abnormality similar to those with Down’s syndrome also occurring in Alzheimer’s patients. And recent research has found that the presence of a protein molecule called apoliprotein E (ApoE4) was present in 64 percent of those studied with Alzheimer’s, whereas only 31 percent of those in the control group had E4. (However the presence or absence of E4 was found to have a clearer relationship to the age of the person at the onset of Alzheimer’s. Some of those without E4 did get the disease, but the onset was after age eight-four.)

Recent research by Daniel Alkon, at the National Institute of Neurological Disorders and Strokes, has turned up a fundamental difference between the skin cells of Alzheimer’s patients and healthy people. Alzheimer’s patients appear to have defective potassium ion channels, which funnel potassium out of the cells. It was found that Alzheimer’s patients had this cellular malfunction in the nerve cells leading from the nose to the brain. Learning and memory are associated with a number of changes in the flow of potassium ions through cellular channels. It is not known yet whether the defect originates within the brain, or even whether it precedes Alzheimer’s symptoms. All that remains to be seen.

Some important questions need to be asked, such as: Are different EMF frequencies responsible for opening and closing (or permanently shutting down) potassium channels in the same way that research indicates window effects for calcium ion channels at the cellular level? Could an EMF resonance factor be involved with potassium ions? Melatonin is also known to be suppressed in those with Alzheimer’s, and EMFs have been found to lower melatonin in some studies. is there any significance to the concentration of magnetite in the nasal area? What of the studies that have found EMFs to increase the permeability of the blood-brain barrier?

Recent work done jointly by Dr. Eugene Sobel, of the University of Southern California School of Medicine, and Dr. Joseph Bowman, of the National Institute for Occupational Safety and Health, found statistically significant increases in Alzheimer’s in some EMF-related occupations. The researchers combined the data from one American study and two Finnish studies and found that tailors, seamstresses, and dressmakers (who work with electric sewing machines) were overrepresented among the Alzheimer’s cases. Increases were also seen for carpenters and electrical engineers, among other EMF professions. A fourth study is in the offing, as well as additional research in Finland.

Dr. Sobel indicated that the use of certain high-EMF-emitting machines may eventually be linked with Alzheimer’s, but that a casual relationship between EMFs and specific people is premature. Kitchens, however, are high-EMF sources, and this may eventually account for the two-to-one ratio between women and men with Alzheimer’s.

There is also some indication that the microwave frequencies are particularly suspect. Dr. Sam Koslov, director of the Applied Physics Laboratory at John Hopkins University, found, in a study using microwave exposures on chimpanzees, that the repeated low-level nonthermal exposures to the eyes produced clinical Alzheimer’s in test animals. At autopsy, the classic plaques and tangles were found in brain tissue. (The researchers discovered this relationship by accident; they were testing for something else.)

Regarding the causes of Alzheimer’s, a range of possibilities exists, including subtle genetic alterations initiated by environmental EMFs. Or EMFs may be acting as co-factors in melatonin suppression and in changes to the blood-brain barrier, potassium ion channels, or acetylcholine levels in the brain stem, among other possibilities. With between 2 and 4 million people afflicted with Alzheimer’s in the United States alone, this will prove to be one of the most provocative research areas within the next few decades.

pp. 200-203

10 Million Baby Boomers Face Alzheimer’s Epidemic

10 Million Baby Boomers Face Alzheimer's EpidemicApproximately 10 million American baby boomers will develop Alzheimer’s disease in their lifetime. This will place enormous strains on the U.S. health-care system.At least 5.2 million Americans currently suffer from Alzheimer’s. By 2010, there will be 500,000 new cases each year, and nearly one million new cases annually by 2050.

The disease is now the seventh deadliest illness in the nation.

Dr. Mercola

Dr. Mercola’s Comments:

In last year’s Alzheimer’s Facts and Figures Report, the number of Americans stricken with the disease was 5.1 million. This year’s report brings us up to 5.2 million, including some 200,000 to 250,000 people under the age 65 who are inexplicably stricken with so-called “early-onset Alzheimer’s.”

By 2050, the report estimates that a full 10 million U.S. “baby boomers” will have come down with Alzheimer’s, which translates to 1 out of 8!

The strain this will place on the already faltering U.S. federal Medicare program boggles the mind, as most people with Alzheimer’s are eligible for Medicare. More than three times as much money is spent on people with Alzheimer’s and other dementias than the average Medicare recipient.

Currently, Medicare spends over $148 billion per year on Alzheimer’s patient care. A mere two years from now, that number is expected to reach $160 billion annually.

Alzheimer’s is just as much a threat to the future of American adults as the rampant rise in autism is to our children. Clearly something is wrong, but what? Because Alzheimer’s is not a normal part of aging, any more than autism is a “stage” that children commonly go through.

What is Alzheimer’s?

Alzheimer’s disease is a chronic form of dementia that results in severe memory loss and eventually death. The average lifespan of someone with Alzheimer’s is about eight years, although many can survive up to 20 years with proper care.

It’s not entirely clear what causes Alzheimer’s disease, but it (as well as autism) are related to thyroid hormone dysfunction, intracellular T3 (immune system cells) deficiency, and diabetes.

One type of Alzheimer’s, called frontotemporal dementia, is characterized by cellular damage in the front and side regions of your brain. Researchers still have no idea what causes it—only that excess production of a tiny protein fragment called beta-amyloid starts jamming the signals between your brain synapses, blocking information flow, leading to a cascade of damaging events that end in cell death.

Risk Factors for Alzheimer’s Disease

The risk factors for AD include genetic, environmental and dietary factors. Certain diseases also heighten your risk. People with diabetes, for example, have up to 65 percent higher risk of developing Alzheimer’s disease.

The primary genetic risk factor is the presence of the Apo lipoprotein E epsilon4 (APOE e4) allele, which is more common among Africans, Inuits, Amerindians, Northern Europeans than southern Europeans.

Primary dietary risk factors include trans-fatty acids that are found in so many processed foods (labeled as partially-hydrogenated vegetable oils). One prospective study also found that elevated homocysteine levels were associated with an increased risk for Alzheimer’s. Homocysteine levels are elevated when you are deficient in vitamin B6, folate, and vitamin B12.

Primary environmental factors include: smoking, obesity, and exposure to fluoride, aluminum and mercury.

How to Prevent Alzheimer’s

Fortunately, there are ways to reduce your chances of getting Alzheimer’s. These simple lifestyle changes can help keep your brain in optimal working order well past your 60’s.

  • Eat a nutritious diet with plenty of vegetables based on your nutritional type, and pay special attention to avoiding sugar
  • Eat plenty of high-quality omega-3 krill oil or fish oil. Avoid most fish (high in omega-3, but often contaminated with mercury)
  • Avoid and remove mercury from your body. Dental amalgam fillings are one of the major sources of mercury, however you should be healthy prior to having them removed. Once you have adjusted to following the diet described in my Total Health Program, you can follow the mercury detox protocol and then find a biological dentist to have your amalgams removed. Be careful as you could be jumping from the frying pan into the fire like I did if you see a conventional dentist to do the exchange. ONLY see a high quality biologically trained dentist or your health could get ruined.
  • Avoid aluminum, such as in antiperspirants, cookware, etc.
  • Exercise for three to five hours per week. According to one study, the odds of developing Alzheimer’s were nearly quadrupled in people who were less active during their leisure time, between the ages of 20 and 60, compared with their peers.
  • Avoid flu vaccinations as they contain both mercury and aluminum!
  • Wild blueberries, which have high anthocyanin and antioxidant content are known to guard against Alzheimer’s and other neurological diseases.
  • Challenge your mind daily. Mental stimulation, such as traveling, learning to play an instrument or doing crossword puzzles, is associated with a decreased risk of Alzheimer’s. Researchers suspect that mental challenge helps to build up your brain, making it less susceptible to the lesions associated with Alzheimer’s disease.

Art Kab
A ‘Good Student’ answers questions – but does not question answers.”
Medication ‘worsens Alzheimer’s’

Anti-psychotic drugs commonly given to Alzheimer’s patients often make their condition worse, a UK study suggests.

Neuroleptics provided no benefit for patients with mild behavioural problems, but were associated with a marked deterioration in verbal skills.

The research focused on 165 people with advanced Alzheimer’s who were living in nursing homes in four British cities.

Up to 60% of Alzheimer’s patients in nursing homes are given the drugs to control behaviour such as aggression.

The study appears in the journal Public Libary of Science Medicine.

Rita Clark’s husband was diagnosed with Alzheimer’s seven years ago.
Rita, from Cleveland, said: “My husband developed a range of side effects while receiving anti-psychotic drugs.
“Since the drugs have been withdrawn, the side effects have gone and he generally seems much better and more settled.
“I’m not saying it’s the same for everyone, but in my husband’s case, withdrawing the drugs has led to a clear improvement in his quality of life.”

The researchers, from Kings College London and the Universities of Oxford and Newcastle, found the drugs offered no long-term benefit for most patients with mild symptoms of disturbed behaviour.But just six months of treatment was enough for patients to show a marked deterioration in their verbal fluency.

Further preliminary analysis already under way on the data suggests the use of neuroleptics may also increase death rates.

The research focused on patients living in nursing homes in Oxfordshire, Newcastle, Edinburgh and London.

All patients had been taking neuroleptics for three months. They either continued on the same medication for a further 12 months, or took a dummy pill.

Lead researcher Professor Clive Ballard, said: “It is very clear that even over a six-month period of treatment, there is no benefit from neuroleptics in treating the behaviour in people with Alzheimer’s disease when the symptoms are mild.

“For people with more severe behavioural symptoms, balancing the potential benefits against adverse effects is more difficult.”

Rebecca Wood, of the Alzheimer’s Research Trust, said: “These results are deeply troubling and highlight the urgent need to develop better treatments.”

The trust says that neuroleptics should only continue to be prescribed long-term to dementia patients with severe behavioural problems, and then only as a last resort when non-drug methods have been tried and have failed.

Stroke risk

Neil Hunt, of the Alzheimer’s Society, said previous research had also shown that anti-psychotic drugs raised the risk of stroke and death for people with dementia.

“This widespread overprescription to people with dementia must stop,” he said.

“It is time we stop wasting money giving people drug treatments with no benefit and start investing in good quality dementia care.”

It is estimated that 700,000 people are affected by dementia in the UK, a figure that will double in the next 30 years.

A report into the use of anti-psychotics in care homes is due to be published by the All-Party Parliamentary Group on Dementia this month.

Jeremy Wright, group chairman, said: “‘We urgently need to ensure people with dementia are only prescribed drugs as a last resort, not as an easy option.

“We will set out simple changes that must be made to stop this abuse when we publish our findings at the end of April.”

The neuroleptics which came under analysis in the study were thioridazine (Melleril), chlorpromazine (Largactil), haloperidol (Serenace), trifluoperazine (Stelazine) and risperidone (Risperdal).

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