Friday, October 2, 2015

A Good Soldier

Ed Gehrman

April 18, 2000
A Good Soldier
Questions about VA Disability and Multiple Sclerosis

He fell suddenly, not a hundred feet from my moving car. It was a solid, bone breaking tumble and I was surprised when he got to his feet, brushed himself off and resumed walking hesitantly toward a car parked next to the curb from which he'd just fallen. I drove slowly alongside, then braked and asked if he were all right. He smiled when he saw me; I recognized him as one of my daughter's friends, Sam. I had known him for over ten years. We'd met just after his return from an enlistment with Army Rangers. It had come as a shock to all of us when we learned he had Multiple Sclerosis. He'd gone to a doctor because of numbness in his leg and blurred vision and after extended testing, was diagnosed with the disease.
Over the years I'd hear bits and pieces of Sam's progress from my daughter. After I witnessed his fall, I asked her for an update and she told me that he'd had some problems walking and that he was using a cane most of the time. I asked her what he was doing for money and she said that he was getting paid by the Army, full disability and all medical benefits. I was dumbfounded and told her that she must be wrong and would she check as soon as possible. She did and confirmed that he was indeed receiving full benefits and that MS was considered a service connected disability.
I found this so hard to believe that I contacted Sam myself and he agreed to an interview. He confirmed that he was on disability. He said that the VA will grant disability status if the condition becomes apparent to a degree of ten percent or more within seven years from the date of a veteran's separation from the service. Sam didn't realize he was eligible for these benefits until a friend, an ex-serviceman, told him, three years after his initial diagnosis. The VA confirmed Sam's disability and service connection.
I'm glad that Sam's needs are being met by the VA. He was a good soldier. But it's difficult, if not impossible to understand the VA's reasoning and justification for granting disability status and a service connection for MS. There is no know cause for MS. If the cause is unknown, how can a connection be made between a person's stay in the service and MS? It doesn't make sense. A service-connected disability can be granted for any condition which is incurred or aggravated by a veteran's military service. The big questions are: What is it in the service environment that causes folks to become susceptible to MS and how did the VA make a connection between this environmental factor, service in the armed forces, and Multiple Sclerosis?
Multiple Sclerosis is an unpredictable disease of the central nervous system. Myelin, which facilitates the high speed transmission of electrochemical impulses between the brain and the spinal cord, becomes scarred and hardened into what are known as plaques. These multiple plaques damage the myelin and cause the neurological transmissions to be slowed or blocked completely which leads to diminished and, sometimes, lost functioning. The symptoms, severity and duration of MS varies from person to person. Most patients experience muscle weakness and loss of muscular control, fatigue, vision problems and cognitive impairments such as poor memory and concentration. Other symptoms include pain, tremor, vertigo, bladder and bowel dysfunction, depression and euphoria.
There are 350,000 Americans who have MS and about two hundred new cases are diagnosed each week. Most folks experience their first symptoms between the age of twenty and forty, rarely before fifteen and seldom after sixty. Caucasians are more than twice as likely to contract MS than other races; MS is five times more prevalent in temperate climates than in tropical. There does seem to be a genetic relationship or connection between those who are susceptible to MS. In the population at large, a person has a one-tenth of one percent chance of contracting MS but if one person in a family has MS then the other family members have a three percent chance of getting it also.
The cause for MS is not known. Some think it's an auto immune disease that launches an attack on its own tissues. While this is certainly a clear possibility, nothing conclusive has ever been established. One plausible theory is that the causative agent could be a unique microorganism such as a mycoplasma. These poorly understood organisms are able to alter protein, and then sensitize the host against itself. For example it was found that mycoplasmas can cause the formation of the rheumatoid factor. A similar mechanism could apply to Lupus and many other auto immune disorders. Another interesting factor is that females, who are infected four times more frequently with mycoplasmas than males, are twice as likely to contract MS.
But this is all only speculation because the truth is we simply don't know what causes MS. Then how did the VA decide that MS was connected to a person's stay in the Armed Forces? I wrote the Department Of Defense, through Barbara Boxer's office, and they refused to answer any questions. I also contacted the Veterans Administration. They did confirm that MS was a service connected disability and answered some of my inquiries. They seemed puzzled that I was skeptical of the MS disability designation and informed me that "congressional legislation would be required to change these provisions of the law".
There are currently about eleven thousand veterans who have been granted a service connected disability for MS. The only condition is that the disease be confirmed within seven years of a veteran's separation from service. As any one familiar with the labyrinthian process of obtaining a service related disability can attest, it isn't easy getting money from the VA. The problems surrounding "Gulf War Illness" is a certain reminder of this fact
The VA and the Department Of Defense must possess information that they're not sharing with the rest of us and certainly not with the new enlistees. I know the Sergeant isn't telling new recruits that they should look out for MS, as they do with AIDS or syphilis. If there is a chance that MS might be contracted or complicated by their time in military service, then why aren't enlistees told this? Would this complicate the recruitment process? Probably, but I have the sneaking suspicion that it would complicate something far more important to the modern Armed Forces: vaccinations. This is the one factor, aside from the traditional haircut, that all service folks have in common. If, as some believe, the causative agent is a mycoplasma, vaccinations could conceivably be the mode of transmission.
What bothers me most is that I'm sure the VA and the DOD have research that justifies granting this disability to thousands of veterans. If they have information that connects MS to military service, then we should all know what that information is. Multiple Sclerosis is a serious and growing disorder that afflicts millions of persons. To purposefully withhold information that would better our understanding of this disease is unjustified.

Spiroplasma and Transmissible Spongiform Encephalopathies

Ed Gehrman
 June, 1998
Transmissible Spongiform Encephalopathy (TSE) is identified by the plaques of mutated amyloid protein that form within the brain tissue and destroy synapses and neurotransmitter functions and take on a characteristic sponge or Swiss cheese appearance. CJD, Scrapie and Kuru are all members of this degenerative disease family, afflictions known about for over two hundred years but not studied intently until the early sixties when they were found to be transmissible.
Dr. Carleton Gajdusek was a young researcher looking for unusual diseases when he visited the Fore Peoples of Papau, New Guinea during the late 1950s. The Papuans of those years were suffering from a population density that put a strain on very limited resources. They practiced female infanticide and cannibalism and were in a constant state of warfare with their neighbors over land and pigs. Severe limitations on normal heterosexual relations were imposed; the men spent most of their time at the men's clubhouse where they prepared for war and engaged in homosexual relations with the young boys. This homosexual activity was all part of an elaborate bonding thought needed to ensure macho warriors and dependable compatriots. The warfare was brutal, often hand-to-hand; capture meant being tortured and killed. Solidarity was essential and achieved through the sharing of semen. The females of the group were disrespected and often abused because they were thought to steal the men's strength and resolve in battle as well as their vital semen. The malnourishment of females and young children was part of this intense process; they supplemented their diet by eating anything that "crawled or crept". Midwives ate placentas of the new born and women dug up the partly decomposed bodies of relatives and ate and shared with young children the flesh, brains and the accumulations of maggots and mites. This was not a religious ceremony but an attempt to fend off malnutrition. (1)
Gajdusek observed that some of the Fore women and a few children died from symptoms indicating a neurological disorder: dementia, frenzied behavior, blindness and eventual agonizing death. He studied the tribal dynamics and soon hypothesized that the condition, known as Kuru, came from their habit of eating the brains of dead relatives; he brought some diseased brain tissue back to the USA. Gajdusek soon discovered that when he made a broth from the Kuru tissue and injected this mixture into lab animals, they too exhibited the Kuru symptoms. He then processed Kuru diseased lab animals' brains and injected the mixture into other lab animals. They also died the same excruciating deaths. This meant that the condition could be transmitted from organism to organism and was therefore transmissible, hence Transmissible Spongiform Encephalopathy (TSE).
Gajdusek and his colleagues at the National Institute of Health were never able to isolate or positivly identify the agent that causes the TSE even though they've been trying since the early sixties. Scrapie and CJD were also studied and found to be transmissible. All this was well known underground medical information; many doctors refused to autopsy CJD victims. For years the NIH conjectured that the infective culprit was a "slow virus". Nothing seemed to distroy the agent; not heat, cold, or any of the normal chemical disinfectants. Nor could they find a trace of its chemical or molecular identity. Furthermore, the virus didn't cause inflamation so antibodies failed to leave a calling card. Some completely new agent was essential.
Another tenacious TSE researcher is Dr. Frank O. Bastian, MD, a professor of pathology and director of neuropathology at the University of South Alabama, Mobile. He has published numerous research articles relating to the etiology of Creutzfeldt-Jakob Disease and also edited a book entitled Creutzfeldt-Jakob Disease and Other Transmissible Spongiform Encephalopathies.(2)
In 1976, Bastian examined a brain biopsy from a patient with CJD using electron microscopy. He saw a spiral structure foreign to the tissue. It had features of the newly reported spiroplasmas (spiroplasmas were only discovered in 1976). In 1981, a team in New York reported finding a fibril protein in scrapie-infected brain tissue. This scrapie-associated fibril (SAF) protein was 4 nm in diameter and 200 nm long. In 1983, the team looked at various tissues of CJD and Kuru and demonstrated scrapie-associated fibrils consistently in these diseases but not in control tissues. These SAF were identical morphologically to the internal fibrils of spiroplasmas.
Moreover, antibodies to SAF react with internal fibrillar proteins from Spiroplasma and digested brain material from people with CJD, suggesting that these proteins essentially are the same. This similarity solidified in Bastian's mind the link between spiroplasmas and CJD.
Dr. Bastian has postulated that Spiroplasma bacteria causes CJD and other TSE. His twenty years of research indicates a role for Spiroplasma. The evidence includes the following: spiroplasma-like inclusions were seen in brain biopsies from patients with CJD (Arch Pathol Lab Med. 1979;103:665-669); spiroplasma internal fibril proteins are identical morphologically to those seen in TSE's; the spiroplasma proteins show immunological cross reactivity with the TSE proteins (J Clin Biol. 1987;25:2430-2431); and spiroplasma, when inoculated into rodents, produces a similar neuropathology (Amer J Pathol. 1984;114:496-514). Spiroplasmas are present in the hemolymph of almost all insects; there probably are several million strains. They can also cause diseases in plants but are usually associated with a vector. For example, a leaf hopper carries a spiroplasma that infects orange trees Spiroplasmas are similar to mycoplasmas. They do not have a cell wall (cell wall deficient) and have among the smallest genomes of any living organism. Mycoplasma are the smallest and perhaps the oldest life form. These bacteria, one cause of "walking pneumonia", are thought by many to be rather fragile, but nothing could be further from the truth. They tolerate extreme fluctuations in temperature, lay dormant in the soil for generations and survive the harshest elements; only drano-like chemicals kill them effectively outside the body. Under normal circumstances our immune system efficiently deals with this complicated, membrane enclosed piece of DNA. A common phenomenon among the mycoplasmas is that the organisms bind host proteins that often are of identical molecular weight to their surface proteins and, therefore, are looked at by the immune system as being the same as the host. The spiralin protein on the surface of spiroplasmas shows a migration pattern on gel electrophoresis with a molecular weight of 27,000 Da to 30,000 Da, similar to that of the prion protein. This biochemical similarity is compatible with spiroplasma etiology.
Bastian was able to show that spiroplasmas were neurotropic. When inoculated peripherally into suckling rats, they will eventually localize to the brain tissues. The organisms will produce a persistent infection and produce a spongy change in the brain tissue of these animals. The neuropathologic changes are similar to those seen in CJD. Spiroplasmas are also within the size range of the agent that transmits CJD and other transmissible Spongiform encephalopathies. Spiroplasmas will pass through a 50 nm-pore filter. The transmissible agent's size has been determined to be 42 nm.
The obvious way to look for an agent directly is by electron microscopy, but this method may not be appropriate for spiroplasmas. Spiroplasmas are similar to mycoplasmas, and it is a well-known phenomenon that mycoplasmas are able to blend with cell membranes. What happens, possibly, is that spiroplasmas essentially fuse with host-cell organelle membranes, thereby blending with the background, so you would not see it unless you had a marker to label it. Developing such a marker has been difficult because spiroplasmas are very fastidious (difficult to cultivate)organisms. .
Bastian also inoculated suckling rats with spiroplasmas, and examined their brain tissues by electron microscopy early in the infection process; he documented the organisms in the tissues. They appeared as membrane-bound forms, except for the one instance where he observed the spiral form. Later in infection, when he knew that the tissues were infectious by broth culture, he couldn't find any evidence of spiroplasmas by looking at the tissues extensively with electron microscopy. Bastian insists that the infection-related protein that most researchers refer to as a "prion" is produced by the host in response to the infection and is not the causative agent. Prions are thought to be self-replicating proteins. Some researchers believe prions are the cause of CJD and related illnesses because they have found prions in brain tissue from people with CJD and sheep with scrapie but not in normal brain tissue. Bastian states that a shortcoming in the prion theory is that CJD and scrapie can be transmitted without prions.
Brain material from which the prion has been removed with antibodies can still infect animals. Moreover, the prion has been found in unrelated disease processes, such as Kawsaski syndrome and inclusion body myositis. Prion researchers have jumped to conclusions and have not considered any other possibility. It is quite possible that spiroplasmas may be inducing the formation of the prion protein to protect itself from the immune system. The immune system is very important in the pathogenesis of CJD. The agent replicates in the spleen and lymph nodes and occasionally causes an immunologic reaction. Auto-antibodies are characteristically seen in the late stages of experimental and naturally occurring disease. The gene for the host protein is located on the chromosome in the region of the major histocompatibility complex (MHC) in the mouse. "Occasionally, you see elevation of immuno globulins; there are morphological alterations of the leukocytes; there is leukopenia," Bastian explains, "and auto antibodies are characteristically seen in the late stages of both experimental and naturally occurring infection. There is partial MHC restriction in both human and animal disease."
"The immune reaction seen in these Spongiform diseases can be explained by super antigen activity, Bastian says. He notes that, normally, an antigen is presented to the cell surface in the MHC and interacts with the T-cell receptor—the antigen lying in a groove in the T-cell-MHC sets in motion the standard reaction. A super antigen, on the other hand, binds outside the groove of the T-cell and interacts with the MHC. This results in some immunoglobulin production, but only transiently. The major effect is clonal deletion of T cells, resulting in a state of immune tolerance. Autoantibodies can also form. In Spongiform diseases, PrP presumably acts as a super antigen. It is noteworthy that inclusion body myositis, a condition in which prions are seen, is an established super antigen disease."
Dr. Bastian also notes that investigators have reported transmitting a TSE to mice from hay mites gathered from farms in Iceland where scrapie is endemic (Lancet. 1996;347:1114). He is virtually certain that these hay mites contain spiroplasma, noting that the investigators have not so far found PrP in the mites.
If hay mites can cause TSE, why couldn't the same be true for the maggots and mites on the Fore corpses? (3) Could Gajdusek have overlooked the main factor connecting Kuru to the Fore women and children? Was the initial cause of Kuru the ingesting of large quantities of maggots and mites by protein famished women and children? We know that the maggots and mites contain spiroplasma. By eating the brains of the Papuans that died from Kuru, the disease (Spiroplasma) was retransmitted to those remaining, in a deadly cycle. Transmissible Spongiform Encephalopathies will continue to be misunderstood unless we begin to study and understand these simple connections.

(1) This information comes from several sources. It is well known to anthropologists that these conditions existed among the Fore peoples and many other New Guinea tribes like the Sambia. I know it's hard to believe in these modern times but we must if we are to understand the world in which we live. My main source is Our Kind by Marvin Harris; Harper & Row; 1989. He took much of his information from Shirley Lindenbaum, Kuru Sorcery: Disease and Danger in the New Guinea Highlands; 1979; Mayfield  back to text
(2) JAMA August 14, 1996 DC Capital Conference spring 1996 A dissenting view on the cause of Mad Cow Disease Bastian regards the prion theory as a red herring. The cause of Transmissible Spongiform Encephalopathies (TSEs), he says, is a conventional microorganism -- a mollicute or, more specifically, a spiroplasma. "The infection-related protein is produced by the host in response to the infection,".  back to text
[Infectious Disease News Homepage] (June 1996) Spiroplasma may cause Creutzfeldt-Jakob Disease - An interview with a leading expert in infectious diseases, Frank O. Bastian, MD. In 1992, Bastian arranged an international symposium on bovine Spongiform Encephalopathy.
I used information, quotes, and descriptions from the above article and interview to weave together Dr Bastian's ideas, knowledge and words, with my own research. I edited and rearranged both words and sequence for coherence sake. I did the best I could to convey this important message.
I've had three phone conversations with Dr Bastian. He was cooperative and helpful at first and sent me much useful information which I have included. But he cut a scheduled interview short when I began to suggest that biowarfare research might help to spread the TSE agent, inadvertently. I called one more time and he refused to talk. He has refused to answer a long letter I wrote. I thought it both rude and arrogant, but even with that nonsense, I still believe Bastian's elegant hypothesis is far more rational than any I've studied.
(3) Common arthropods occuring on dead bodies: The Acari, or mites as they also are called, are small organisms, usually less than a mm in lenght. Mites occur under the dead body in the soil, during the later stages of decay. Many mites are transported to the body via other insects, such as flies or beetles. Other mites are soil dwelling forms which can be predators, fungus feeders or detritus feeders. Most species will be found in soil samples from seepage area under the body. Sarchophagidae Among the Sarcophagids we find the large flesh-flies with red eyes and a grey-checkered abdomen. These flies does not deposit eggs, but larvae on the corpse. They are, together with the Calliphorids, among the first insects to arrive at the corpse. The larvae are predators on blowfly larvae, as well as carrion feeders. Many Sarcophagids are feeding on snails and earthworms.

Update to Mad Cows and Mad Scientists

by Ed Gehrman

Update —Mad Cows — Mad Scientists

Open letter to Sheldon Rampton & John Stauber

January 13, 1998

Re: Mad Cow U.S.A.: Could the Nightmare Happen Here?
A book about the ramifications of BSE/TSE
Released November, 1997
Dear Sheldon and John:
About a month ago a friend contacted me; he had received a galley advance of Mad Cows USA and wanted to know if I would review it. After editing many of my recent articles on the subject, he was sated on Mad Cows. I told him to send it on and I'd write a review for my next column in the Sonoma County Free Press.
Having heard some rumors about this particular book, I had planned to purchase it anyway so a free copy was a bonus. I was not disappointed, and more than a bit surprised! Mad Cow USA is a fascinating read. I couldn't put it down and continued late into the night. Then the next morning as I tried to finish the last couple of chapters before leaving for work, my name suddenly jumped from the page: Internet essayist Ed Gehrman. I was shocked, dumbfounded and I must admit, a little pleased since you aptly summarized my point of view, although your interpretation of my position is wrong-headed and perplexing.
You characterize my contentions as "imaginative" because you say I offer no evidence for stating that 200,000 citizens succumb each year to misdiagnosed TSE caused diseases. But it is common knowledge for anyone who bothers to look closely at the published evidence; there are many cases of misdiagnosed TSE. Michael Greger has done excellent research on the subject. I used the figure 200,000 because of a study done at Yale by Elias E. & Laura Manuelidis: "In our own neuropathological material, in 46 cases diagnosed clinically as AD(Alzheimer's), 6 cases were proven to be CJD at autopsy --13%."
I calculated using thirteen percent of deaths from dementia and Alzheimers each year. I soon realized that this figure was unreasonable and that I had miscalculated the number of deaths, mainly because there is so little information about how many folks do in fact die from Alzheimer's each year.
Perhaps I should have shown sources and all but I did footnote most of my writing on TSE. This was one of my first drafts, sent to Tom Pringle for peer review and then published on his web site. Although it did appear in the Sonoma County Free Press, I have since rewritten it many times as new information came into circulation and critics challenged my stance.
I also no longer believe that prions play much of a role in spreading this disease. Prions are a "red herring" and are secondary to the agent itself which seems to be able to manipulate protein or cause its production. After completing the article you quote, I came across the work of Dr. Frank Bastian. His research convinced me that spiroplasma are the infectious agent in all TSE disease. I have since done everything I could to help folks see the wisdom in his sound and well thought-out theory.
Dr. Bastian, director of Pathology, University of Alabama, Mobile, is a known authority on CJD, having edited the only scholarly book on the subject. He first saw the spiroplasma in 1976 during the autopsy of a brain from a CJD cadaver, and since then has been slowly and meticulously gathering information and data. We can not afford to ignore his arguments much longer.
I still believe that the national labs that enact our bio-warfare bidding are responsible for putting Kuru into cows. They have been experimenting with Kuru and other TSE diseases since the early 60's. How else did it get there? Gajdusek as well as others have affirmed that BSE is Kuru, not Scrapie, though I believe both are caused by the minuscule spiroplasma, only different strains of the same.
The nature of TSE is misunderstood by many. The mixture of genetic factors and infectivity throws researchers off. Those interested in solving this puzzle would best begin by reading Dr. Bastian's material. There definitely is a genetic component to these ailments. Some folks can't contract the disease, while others are susceptible, about fifty-fifty. That is clear. What isn't clear is the level of exposure to TSE infection. It's lucky that the genetic barrier is probably wide and deep, otherwise we would all be demented or dead.
Dan Marsh was too conservative in his estimates of 100,000 downers in US herds; this number is far too small. We have no idea how many downers there actually are in the present population of US cattle because accurate records are not kept. There could be a million or more. We just don't know! Think of the implications of this paragraph from Beyond Beef by Jeremy Rifkin: "The cattle are transported for hours or the end of their journey the intact animals are deposited in a holding pen... Downers, however, must wait hours to be unloaded. Although downed animals are frequently in severe pain,they are rarely euthanized or anesthetized,as that would translate into a lost carcass and additional expenses. Often spread-eagled on the floor of trailers, unable to stand or walk, these hapless animals are chained by their broken legs and dragged from the truck onto the loading ramp to wait their turn for slaughter."
Indisputably, this is a common event. Mink-fed downer cattle have died from a TSE disease. Until we know more about downers than we do, I think it's probable that any downer is a TSE carrier. Remember it only takes a teaspoon of infected material to begin the disease process.
Putting all that aside, I must congratulate you on this excellent and fact-filled book. You've certainly proved your case. If we let the meat industry set the rules on how we raise and process our food, there will be "no limit to what we will swallow, and the nightmare of mad cow disease, or something just as bad, or worse, not only can happen here, but most certainly will."
Everyone interested in our "Mad Cow" dilemma should read Mad Cow USA.
Ed Gehrman
January, 1998

Mad Cows and Mad Scientists

by Ed Gehrman

January, 1998

Mad Cows & Mad Scientists

"Michelle Bowen, 29, died a slow painful death which ended in a coma three weeks after giving birth to her son via emergency caesarean section. Stephen Churchill, a student, started feeling depressed and dizzy last year, then sank into a living nightmare of terrifying hallucinations; he was dead in 12 months at age 19. Peter Hall, 20, showed the first signs of depression around Christmas, 1994; within twelve months he couldn't walk, talk, or do anything for himself. They all died of Creutzfeldt-Jakob disease, a relentlessly progressive and invariably fatal dementia which usually attacks people in their sixties. Cases such as these involving people under age 30 were until recently exceedingly rare.An uproar ensued when a leading British neuropathologist Bernard Tomlinson announced he refused to feed his children hamburgers out of fear that they might contract this disease from infected beef. On Wednesday, March 20, 1996, Sir Tomlinson's fears were validated. The British government announced that "exposure to a cattle disease called Bovine Spongiform Encephalopathy was the most likely explanation of these deaths and seven other recently diagnosed cases of Creutzfeldt-Jakob Disease among British young people." Michael Greger 1
By year's end British citizens will have consumed the meat of 750,000 mad cows. That's the number of diseased critters that will slip through the jerry-rigged system meant to contain Mad Cow Disease - about ten pounds per person in the form of roasts, sausages, meat pies and other assorted beef scraps. Since the first indication in 1985 that something was amok in the beef and dairy industry, government officials and government scientists world wide have done their best to confuse and downplay the grim ramifications of this emerging disease. How serious is Mad Cow Disease? Many people may already be infected with this gruesome malady, and even though it should be front page news you'll never read what I'm about to tell you in your local newspaper.
Mad Cow Disease made headlines on March 22, 1996: "Deaths cause British panic over 'Mad Cow Disease'." 2
Newspapers across the USA announced a drastic slump in British beef prices and the plausible connection between a rare human brain disease called Creutzfeldt-Jakob Disease (C-JD) and a disease that afflicts cows known as Bovine Spongiform Encephalopathy (BSE). American consumers were assured that "mad cow disease had never been detected in cattle in the U.S.". Government scientists worldwide made bold pronouncements concerning the safety of their nations' and the world's beef supply but they didn't have a clue about how terrible this situation could become. The absence of proof of risk doesn't mean there is no risk; the risk factors were dreadfully under-estimated.
BSE was first diagnosed in British cows in April of 1985. Government scientists claimed that there was no danger in eating British beef. After thousands of cattle began dying of BSE in 1988, the government finally ordered measures to curtail dangerous practices, such as feeding cows other ground-up cows to improve milk productivity, and using offal (waste parts) to make hot dogs and kidney pies. But all this came too late; some humans had already contracted the deadly mad cow disease.
The tenuous connection between Mad Cow Disease and the eating of English beef has been strengthened through research recently published by a group of London scientists. They examined the patterns of protein taken from the brains of cows that died from Mad Cow Disease and compared them with patterns of protein taken from brains of humans who died from vC-JD (British Mad Human Disease, a variant form of C-JD but it struck younger folks and it took them longer to die ) and found these proteins to be almost identical. John Colling"All lines of evidence converge on this conclusion...I think we should take it (vCJD) very seriously. We cannot predict how many future cases there may be".3
Folks contemplating kicking their beef-eating habits might appreciate knowing a bit of the setting and history of this ongoing scientific tragedy. The diverse threads of information coming from the media and official sources have become as tangled and misshapen as any twisted protein strand found in a demented brain.
While the wide variety of brain diseases in the world have their own distinctive symptoms and markers, mis-diagnosis occurs in as many as twenty percent of disorders like Alzheimers and Creutzfeldt-Jakob Disease . The only sure diagnosis is through the examination of the brain after death and then comparing tissue samples with identified samples of known disease. Transmissible Spongiform Encephalopathy (TSE) is identified by the characteristic sponge or Swiss cheese appearance of the brain tissue and by the plaques of mutated protein that form in the brain tissue and destroy synapses and neurotransmitter functions.
Mad Cow Disease, Creutzfeldt-Jakob Disease, Scrapie and Kuru are all Transmissible Spongiform Encephalopathies; none had been studied intently until early in the1960's when they were found to be transmissible. The most common form of domestic animal TSE is Scrapie, a neurological disease of older sheep and goats that has been around for over two hundred years. Afflicted animals become irritable, lose vision, rub themselves raw (hence Scrapie), and die.
Creutzfeldt-Jakob Disease (C-JD) and Kuru are the human TSE diseases. They afflict about one in one million people each year and are characterized by bizarre behavior, dementia, memory loss, stiffening of the muscles and difficulty walking; they are always fatal.
Kuru was first studied by Dr. Carleton Gajdusek when he visited the Fore Peoples of Papua, New Guinea during the late 1950's. The Fore were suffering from a population density that put a strain on limited resources. They practiced female infanticide and cannibalism and were in a constant state of warfare with their neighbors over land and pigs. Heterosexual relations were severely limited; the men spent most of their time preparing for war and engaging in homosexual relations with the young boys of the tribe, all part of an elaborate bonding needed to ensure macho warriors and dependable compatriots; solidarity was achieved through the sharing of semen.
The females were often abused and were thought to steal the men's strength and resolve in battle as well as their vital semen. Malnourishment of females and young children was normal so they supplemented their diet by eating anything that "crawled or crept". Midwives ate placentas of the new born and women dug up the partly decomposed bodies of relatives and ate and shared with young children the putrid flesh, brains and the accumulations of maggots, not as a religious ceremony but an attempt to fend off malnutrition.
Gajdusek observed that some of the Fore women and a few children died from symptoms indicating a neurological disorder: dementia, frenzied behavior, shuddering, loss of balance and eventual agonizing death. He studied the tribal dynamics and hypothesized that Kuru, which means "shaking disease" in Fore dialect, came from their habit of ceremoniously eating the brains of dead relatives.
He brought some diseased brain tissue back to the USA and soon discovered that when pureed Kuru tissue was injected into lab animals, they too developed the Kuru symptoms. When the diseased lab animals' brains were injected into other lab animals, they died the same excruciating deaths. This meant that the condition could be transmitted from organism to organism and was therefore transmissible, hence Transmissible Spongiform Encephalopathy (TSE). Scrapie and C-JD were also studied and later proven to be transmissible. Dr. Gajdusek received the Nobel Prize in 1976 for this research.
While much is known about TSE, Gajdusek and his colleagues at the National Institute of Health were never able to isolate or identify an infectious agent in TSE. There were no tests to identify TSE in living tissue and only two ways to determine infectivity. A dead brain can be examined for sponge-like holes and plaques; or a broth of suspect brain tissue can be injected into a susceptible lab animal, which will become mad in 300 to 600 days if the mixture was infective.
At first, scientists working on TSE research suspected that the infective agent was a "slow virus". To determine the nature of this "slow virus", tissue containing TSE was injected into countless lab animals. Just one ongoing experiment could kill thousands including cows, mice, hamsters and monkeys. They were searching for a possible bio-warfare agent.
In 1969 World Health Organization reported their progress: "from painstaking work with visna and Scrapie, degenerative diseases of the central nervous system, and Kuru, a degenerative disease of the central nervous system of man... distinguished by the languishing character of the infection process they initiate. The incubation period in the host may be months or years, and the disease itself may progress laggardly towards an irreversible deterioration of the victim. Cells infected with 'slow' viruses are in general neither impaired nor stimulated to proliferate. Their functions are impaired but the nature of the dysfunction has not yet been clarified...The resistance of the Scrapie agent to heat, ether, formalin, and other enzymatic and chemical agents, as well as its very small particle size, poses the question whether it is a conventional virus, an incomplete virus, or some other agent. . . "
The Department of Defense also began trying to develop "a new infective microorganism which could differ in certain important aspects from any known disease-causing organism." In 1970 the Army awarded a ten million dollar grant toward the goal of developing a "super germ" that would inhibit or destroy the immune system.4
Political and economic interests have limited the debate on contentious issues exploring the genesis of the BSE agent by denying or misrepresenting the views of contrary scientists. At stake are the intensive farming methods that have become so common during the last three decades. Increased profits come from packing as many animals as possible into as small a space as possible, exploiting them to the maximum.
Their diet is the most unnatural aspect of the process. Cost effectiveness demands that every shred of every animal be used. A third to a half is saved for human consumption; most of the leftovers are rendered into high protein food for other animals. There1s not much time for grazing or scratching in the world of pens and cages and this foodstuff supplies much of the necessary protein needed for eggs, marbled beef and rich butter fat. We will soon understand the ramifications of forcing animals that we eat to become cannibals.
Foresight should have warned us that this was not healthy. But in the modern world we've created, where science and technology have conjured up a seemingly bounteous existence, we have come to rely on scientists for truth. We're all in danger of ingesting a TSE contaminated meal at any time yet our government and its scientists continue protecting moneyed and powerful interests over those of the consumer. As Michael Greger, a BSE researcher and scholar, writes: ". . .I think this crisis shows to what length governments will go to prevent financial harm to powerful lobbies in general, and in doing so risk immeasurable harm to those they claim to represent".
The Veterinary Committee of the European Union was told in 1990 to "take a cold attitude towards BSE so as not to provoke unfavorable reactions from the market. . .no more talk of BSE. . .we are going to ask the United Kingdom,through official channels, to stop publishing the research results. . .this BSE affair must be minimized through disinformation. Better to say the press has a tendency to exaggerate." 5
When Oprah declared she wouldn't eat another burger after learning on her show that cows eat cows, the Texas Agricultural Commissioner stated: "We're not going to sit back and let trash TV trash a vital industry . . ." He wanted to bring a lawsuit against one of the guests on the show under the state law that bans insulting perishable foods.
The USDA is doing everything in its power to suppress any notion that BSE exists in the USA. The wholesale price of beef has been plummeting for the last two years; consumers are frightened of beef for other valid reasons but the realization that it causes premature madness could result in a panic. Disregarding the vast accumulation of evidence, our current clumsy and ineffective research program is not objectively examining whether there is a form of mad cow disease in our food supply. The meat and dairy lobby controls the current government research and they have decided that a search is "not appropriate at this time".
Nor will they even consider banning the unnatural cannibalistic eating patterns they've imposed on former grass eaters; this habit is now intensifying with the introduction of bovine growth hormone. All it takes is a single teaspoon of infective mad cow meat or bone meal to begin the disease process but all feed manufactures still use meat and bone meal in high protein food. The FDA proposed the banning of at least the brains from the rendered feed mix but this was opposed by the American Meat Institute: "no good is accomplished by prejudicing segments of society against the meat industry".
With a hundred million cattle, the USA has the highest per capita beef consumption in the world. What is not generally known and which the US Department of Agriculture denies is that we have a form of Transmissible Spongiform Encephalopathy in our herds. It is known as "Downer Cow Syndrome" and causes over 300,000 cattle deaths every year. When these cows are put under stress they stagger around, bellowing, and then fall down and are unable to get back up. If these "downers" are kept alive long enough (some are literally dragged to the market), they can be ground up and fed to you, and the bones, lips, head,etc. boiled into a gelatin which soon may become the marshmallow topping and the ice cream for your favorite sundae. 6
If unsafe for human consumption, the sorry creature is melted down and used as pet food and animal feed. Did you even know that the diet of dairy cows consists of other ground up animals - not just cows but sheep, goats, chickens, and whatever other dead meat they can scrape off the slaughterhouse floor? When cows fed this diet, including the downers, are no longer productive, they are then ground into hamburgers, 2.6 billion lbs. yearly. Does this seem safe?
The "slow virus" was never found. That theory has recently been supplanted by the prion (pree-on) hypothesis. Prions (Proteinaceous Infectious Particles) were named by Dr. Stanley Prusiner before he even discovered them because "Prion is a terrific word. It1s snappy. . .It isn't easy to come up with a good word in biology. One hell of a lot of bad words people introduce get thrown away."7
Prusiner's research and public relations campaign has convinced many scientists that prions and prions alone are the infectious agents that cause Transmissible Spongiform Encephalopathy. These mutant or rogue proteins are found in most autopsies of Transmissible Spongiform Encephalopathy brain tissue and form the plaques that cause neural disruption. The prions seem to transform the healthy protein into harmful plaques and tangles. How this occurs is not quite clear. To accept Prusiner's theory is to accept changes in the basic concepts of biology.
He and his supporters have garnered millions of dollars in research grants and are said to be doing brilliant work. He wins award after award, but reasonable doubt still exists. How do prions replicate without DNA or RNA? How can he account for the various strains of TSE? Where is the one to one relationship between prions and TSE infection that he promised? One critic commented that "some parts of the prion hypothesis are getting into medieval thought processes".8
Frank O. Bastian, director of neuropathology at the University of South Alabama, is also skeptical of the prion theory. "The prion was bull-dozed in the press and scientific community. The prion is a red herring."9 He maintains that the TSE infective agent is a spiroplasma. "Spiroplasmas are similar to mycoplasmas in that they do not have a cell wall and have among the smallest genomes of any living organisms. Spiroplasmas, which were only discovered in 1976, are present in the hemolymph of almost all insects. There are probably several million strains of spiroplasmas."
Dr. Bastian has been scrutinizing and writing about spiroplasmas since 1976 when he first observed the minute organisms in the brain tissue of a C-JD cadaver. "I saw a spiral structure foreign to the tissue. It had features of the newly reported spiroplasmas".
As the editor of the only reference book on C-JD, he considers himself an authority on the subject, but his opinion is seldom asked on the BSE crisis, nor are his views given much credence. "A shortcoming in the prion theory is that C-JD and Scrapie can be transmitted without prions. Brain material from which the prion has been removed with antibodies can still infect animals." He insists that the prion is nothing more than reconfigured protein, created by the host as a defense against the machinations of the invading spiroplasma.
The spiroplasmas replicate in the spleen and the lymph nodes; then they migrate toward the brain. They1re able to bind protein in a way that confuses the immune system into believing they they1re part of the host. "Spiroplasmas are similar to mycoplasmas, (small bacteria-like organisms) and it is a well known phenomenon that mycoplasmas are able to blend with cell membranes. What happens, possibly, is that spiroplasmas essentially fuse with host. . .blending with the background, so you would not see it unless you had a marker to label it. Developing such a marker has been difficult because spiroplasmas are difficult to cultivate. No more than half of the known strains are culturable."10
There's a simple elegance to this direct and understandable hypotheses, but the prion theory has become accepted by scientists; spiroplasmas are seldom if ever mentioned as the possible cause of these diseases even though Bastian indicates that it would be a relatively simple task to prove his suppositions. "Definitive evidence of this link would be to demonstrate that spiroplasma DNA occurs in the brain tissue of people with C-JD and related illnesses, but not in brain tissue from controls. This could be done by using polymerase chain reaction assays to detect nucleotide sequences in genes unique to spiroplasmas and common to all types of spiroplasmas. I have 15 types of spiroplasmas in my laboratory and am in the process of looking for nucleotide sequences common to all of them." This research is the only hope we have for developing a test that can determine how serious Mad Cow Disease has become and where it has spread. Resistance to Bastian1s ideas means resistance to such a test. Is the National Institute of Health afraid of what we might find? In March of this year, just as the furor over mad cow disease began to peak, Dr. Gujdusek was arrested at gun point in his driveway by six FBI agents. He was charged with two counts of child abuse and two counts of having oral sex with a juvenile. He was released on $350,000 bond and placed on administrative leave by the National Institute of Health. The journals he kept on the sexual practices of the New Guinea males had been given to the US Senate. Why or by whom is not clear. The Senate asked the FBI to investigate. Gujdusek brought 56 Papaun children to the US for education. One of these kids has admitted that he had sex with Gujdusek.11
These journals have been around for 30 years. Why the big uproar just now? Gajdusek knows more about these diseases that anyone but has been effectively silenced since his arrest. It would be helpful to question him.
I believe he made two serious mistakes in his work with Kuru. The first was his misunderstanding of the way that Kuru was transmitted. His assumption that Papuans were circulating the disease among themselves through ceremonial cannibalism was only partially correct. Another vital factor must have been their habit of consuming vast amounts of maggots and mites attached to the decayed flesh. Hundreds of common arthropods reside on dead bodies, the most common being a wide variety of maggots and mites. Researchers have transmitted Scrapie to mice by inoculating them with material from hay mites gathered from Scrapie infected farms. Bastian found this information "very exciting data." He insists that spiroplasmas are found in all arthropods. If this is true then our bodies must have built a strong barrier between us and them or we'd all be goners by now. Until lately, these diseases were very rare, one in a million.
This brings me to Gajdusek's second mistake. He thoughtlessly brought Kuru brain tissue to US labs and began injecting it into countless numbers of lab animals. Usually the more hosts a pathogen passes through, the more virulent it becomes. Apparently the new and more communicable form of Kuru has escaped the confines of our national labs and is now in the food supply. Did some of the infected cows or other lab animals or their infected offspring end up in high protein supplements?
The involvement of National Institute of Health in spreading this sickness from a frenzied tribe in New Guinea to British cows and then back into British citizens must be examined. They would like you to believe that Scrapie infected sheep, ground up and fed to cows, caused the outbreak. They argue that the process used to extract protein from all the leftover meat scraps was modified in 1980. This allowed the disease to spread because the new methods didn't kill the infective agent in Scrapie.
This is plausible since the new process doesn't destroy the infective agent, but Mad Cow Disease isn't Scrapie, it's Kuru, a completely different strain of Transmissible Spongiform Encephalopathy . Gujdusek has admitted this much but no one seems to understand or care about the implications of such admissions.
How did Kuru get into cows if it wasn't put there by thousands of bio-warfare experiments carried out by the National Institute of Health? Mad Cow Disease is another startlingly clear reminder of what can happen when we allow scientists to secretly muck around with biologically hazardous substances.
  1. Michael Greger "The Public Health Implications of Mad Cow Disease"
  2. The Sacramento Bee, March 22, 1996
  3. The Times:Britain: Oct. 24,1996 by Nigel Hawkes
  4. Leonard G.Horowitz, "Emerging Viruses:AIDS and Ebola—Nature, Accident or Genocide", ppg. 15-19
  5. Fabienne Maleysson, Que Choisir, September 1994, pg. 308
  6. Michael Greger, "The Public Health Implications of Mad Cow Disease"
  7. Gary Tauber, "The Name of the Game Is Fame", Discover, December, 1986
  8. Rosie Mestel, "Putting Prions to the Test", Science, July 12, 1996
  9. Dr. Frank Bastian, personal correspondence, September 4, 1996
  10. Infectious Disease News, June, 1996
  11. Claire W. Gilbert, Ph.D., "Dr. Gujdusek and Mad Cows"
References found on the World Wide Web:
  • Prusiner S.B, "The Prion Diseases" Scientific American Jan 1995
  • Richard Lacy, "How Now Mad Cow", 1995
  • Dr. Shaun Heaphy, "Prion Diseases"1996
  • Michael Greger, "Mad Cow Disease-Much More Serious Than AIDS"
  • James Wood, "Some Facts To Help Inform About BSE/CJD"
  • Larry Mark, "Bovine Spongiform Encephalopathy" USDA
  • Michael Greger,"The Public Health Implications of Mad Cow Disease"
  • John Collinge M.D. "New Diagonstic Tests for Prion Diseases", New England Journal of Medicine Editoral, September 1996
  • Karen Kreeger, "Researchers Homing in on Mechanisms of Encephalopathic Diseases", The Scientist, June 10, 1996

In Defense of Anarchy

by Ed Gehrman

January, 1998

In Defense of Anarchy
For ten million years during the Pliocene our ancestors scampered after crabs and small shrimps or climbed seaside cliffs in search of birds eggs. We hunted immature sea mammals, foraged for shellfish, and repelled leopards with pebbles while standing chest-deep in water. Over these eons we lost most of our body hair, inherited a nose job, elongated and repositioned our genital organs, developed a subcutaneous layer of fat, and discovered how to make simple tools and throw a mean fast stone.
When the weather changed during the Pleistocene, we retreated to the woodlands and forests with our upright stance, hairless bodies, and stone tool kits. Life was intense; being alive in the morning to stretch and scratch and alive at night curled up with brothers, sisters, fathers, mothers in familial embrace was a major accomplishment. Organized into small bands of between 25 to 30 members, cooperation and reciprocity were our only social safety nets. Anarchy reigned; it was organization without coercion. There were no chiefs, leaders, priests. We all knew what had to be done to stay alive, and if we were skilled and lucky, we might make it to 50. Status came from attaining old age and having functional skills that contributed to the success of the small community. Change came slowly; thousands of generations passed with only minor alteration, a continuum incomprehensible today. We were all brothers and sisters then.
These are our roots: egalitarian, functional, and self-regulated. They served us well for millions of years. We populated the earth, walking together, heads up, eyes alert, a song in our hearts.
About ten thousand years ago, this scene slowly began to change. With the introduction of agriculture and with the domestication of animals, Eden was left behind; we can never return. The new knowledge demanded by this new technology began to alienate us from hunter-gathering and our egalitarian roots. Except for a few small and scattered exceptions, we have now evolved into civilized tool-makers extraordinary, but still singing. If the songs we sing are any indication of our true feelings, we are also creatures of love, frustrated love, unable to get much satisfaction.
Two behaviors have separated humans from other primates and have led to our dominance: our ability to share and cooperate and our escape from the hierarchical arrangements that molded other primate societies. We substituted symbolic status and reciprocity for hierarchical chain-of-command and physical dominance. These new behaviors gave us a competitive edge over other primate rivals.
Reciprocity is the key to cooperation. It relies on balance, on a mutuality of goals: you make me happy and secure and I'll do the same for you, brother; you treat me as I treat you, sister. Since the advent of the "state", in Mesopotamia (3500 B.C.), the concept of reciprocity has been devalued as a functional skill. Its slow disappearance from our repertoire of behaviors has disrupted our ability to relate to one another in ways we find mutually satisfying. Those who can ignore these emotional and reciprocal needs and keep their nose to the grindstone attain success, while those that are unable to repress these ancient yearnings find life's path difficult to negotiate. Possessiveness and competition have replaced the shared regard we once valued.
Mystical religions, psychosomatic illnesses, and holocausts are symptoms of the general frustration resulting from this exchange. We can never return to stone age hunter-gathering, but our evolutionary roots will not be ignored. Doing so has resulted in sexual repression, fascism and inequality. We all still long for the lost reciprocal love forged by millions of years of selection and learned behavior. These longings are subconscious. Consciously, the "normal" person remains in a state of denial.
There is a popular tendency to attribute aggressiveness and bellicose behavior to the intrinsic psychology of humans and our primate forbearers. We believe that we are inherently cantankerous and could never concur on anything without some "authority" laying down the law. There is no clear evidence for these assumptions, but promoting these attitudes helps justify the dog-eat-dog, social Darwinism that dominates our current belief systems and our present social organization, "the state".
Originally the hierarchical "state" was an attempt by humans to expand and stabilize the subsistence base, necessitated by the environmental catastrophe of too many people and not enough food. It is a recent development, established for no more than 6,000 years. The "state" evolved from "ranked" society, itself the direct descendant of egalitarian bands. The "state" can be seen as a distortion of egalitarian and "rank" societies which are fundamental modes of social organization. The success of egalitarian societies is their ability to allow equal access to both the basic necessities of life and individual status. The "state" systems limit not only access to positions of prestige but to the basic resources needed to sustain life as well. This results in the stratification we see all around us in our "civilized" world.
The political dilemma that has confronted humans since " state civilization" is as follows: Can a society be designed that allows equal access to all basic resources and to all positions of status? Can egalitarian reciprocity, sharing, and cooperation be reintroduced as the basis for social organization? This is the stuff of revolutions. Utopian dreamers, romantic poets, hippies, early Christians, Marxists and Social Democrats all shared essentially this same perplexity.
The nature of "rank" society provides some insight into this thought-provoking quandary. "Ranking" evolved in situations of abundance and modified egalitarianism when an agricultural base and domestication practices were adopted. There remained no limit on the access a person had to the basic resources on which life depended. The main difference between the two systems is that in "rank society" the positions of prestige are partially limited.
"Rank" was earned through some form of personal endeavor or through contributions made to the over-all well being of the community. Individuals did not attain high rank without being deserving of the honor. There seems to be a natural tendency for some humans to contribute more than others. Those who do so are usually rewarded in some fashion by those who benefit. The vestiges of this behavior are still evident today.
In "rank" societies, increased individual status did not mean an increase in personal power. The symbols of rank had no economic value nor could they be traded for commodities. They were only indications of, and rewards for, individual accomplishments. Rank bestowed no rights of coercion. Highly ranked individuals were listened to because, in most cases, these were wise folks, and listening to them was generally beneficial.
Rank societies can be complex. The oldest known farming village is Catal Huyuk on the banks of the Carsamba river in modern Turkey. Established 9000 years ago, it was prosperous, sophisticated and well-organized, with impressive craftsmanship and an extensive trade network. While rank played a part in this culture, communal burials indicate that the basic egalitarian nature of society was intact.
As slash and burn agriculture and "rank" societies expanded, world populations soon increased dramatically; though for several thousand years humans were able to make do. Eventually, soil depletion, overpopulation and other environmental factors led to shortages in basic necessities. Once there were more people than food, the ensuing competition disrupted previous reciprocal arrangements. Stratification, slavery and the "state" soon became the new paradigm and has been so ever since.
The contemporary expression of egalitarianism is anarchy. Anarchism postulates that humans are essentially benign creatures, but are corrupted by authority and coercion. We are social animals, fulfilled through voluntarily helping one another and our community. Organized religion, education, politics, and economic life distort our natural egalitarian tendencies. The prevailing institutions of private property and the "state" advance our exploitation.
Anarchy means merely the absence of any form of political authority, but in a modern context, anarchy always implies confusion, political disorder, lack of control, and terrorism. The mere mention of anarchy sends chills down the spines of property owners and other law-abiding citizens. The common belief is that the anarchist life, based on egalitarian principles, is a fantasy, and that humans are basically a violent and disorganized bunch of rascals, who could never survive without "some" centralized control.
Anarchists disagree with this image. They believe in the basic goodness of humankind. They insist that social change must be spontaneous and human based, expressing functional, human attributes. While there's nothing precluding organization or even leaders in this arrangement, leadership carries no authority in our modern sense of this word. Expertise is the only criterion, and when this expertise is no longer needed, the role of leadership is turned over to others with other types of needed expertise. Coercion is counterproductive to these goals. All humans are rooted in this wisdom. We see it clearly operating in smooth functioning volunteer organizations.
The hunter-gathering way of life and its concomitant egalitarian philosophy evolved through a time of relative abundance. Equal access to life's necessities allowed for mellow interactions and serene dispositions. Recreating this environment is the subconscious drive underlying most social revolution. We are bound to rediscover that reciprocal agreements create an atmosphere of equality and social cohesion. It's under these circumstances that individuals contribute their best skills to the common good. Perfecting this behavior will eventually lead to general abundance and egalitarian living, and our antisocial, competitive, warlike culture, a symptom of frustrated possibility, will become a historical curiosity from a sorrowful era.

Lost Frogs

by Ed Gehrman

October, 1997

Lost Frogs

I recently read a short news clip from the London Times that piqued my interest. It was entitled: "Frog Hunters Told to Hang Up Their Jam Jar", and was a call from England's Wildlife Trust, a conservation organization, to stop the collection of "frog spawn" by schoolchildren. "Given the apparent serious decline in frog populations, schoolchildren collecting frog spawn must now be listed as another pressure and predator." Frog numbers were declining in 140 countries; this indicated that something was "seriously amiss" with the environment and could mean danger to humans. Then in an ominous tone, "Amphibians are the most perfect indicators of any pollution that we have got. If frogs go, it is the end of the world."
Frogs and toads have survived on this planet for over two hundred million years and have done so by being sensitive to the environment. They spend their youth in water and as adults live and feed on land, returning to the water for safety and breeding. Their skin is readily absorbent, and their frog spawn is exposed to all water born pollutants. Could pesticides be the culprit in the diminishing stock of these beneficial animals? I decided to investigate this possible connection since my own research into pesticides had indicated its link to the decline of other beneficial animals.
The New Country School, located in Minnesota, is a year around charter school that uses student centered projects as a basis for the curriculum. During a nature studies field trip last August to a wildlife game refuge, students noticed frogs with what seemed to be "developmental problems. . . fully 50% of the frogs caught that day had deformities of their hind legs. Many had one leg which was underdeveloped and webbed together, preventing normal function. One frog captured that day had only one hind leg, while another had two feet on one leg and a bony protrusion from the spine."
Thus began an intensive investigation of the frogs, which is still ongoing in conjunction with scientists from the Minnesota Pollution Control Agency. The exact cause of the deformities found in these frogs may never be known, although circumstantial evidence certainly points in pesticide's direction. Their discoveries soon reached the national news media; the school received a national environmental award. It was portrayed in the media as a cute story about children serving science, but to me it indicated something much more disturbing. It took wide-eyed school children to notice important indicators of danger that we should all be recognizing. This incident in Minnesota is only one of many.
The Journal of Conservation Biology published a study which documents the the decline of toads and frogs in Yosemite. The authors, an ecologist and a zoologist, studied seven native species and found that all but one had declined when compared with a 1915 survey. This was surprising since they never expected these results in the middle of a wilderness, but folks who work in Yosemite have suspected as much. One field biologist reported that twenty years ago he used to have to tiptoe around the yellow-legged frogs, but now he walks without worry. Is such a drastic plunge in numbers within one generation a portent of our frogless future?
The once numerous Southern California red-legged frog is now reduced to a small population around Riverside while the arroyo toad is no longer found in three fourths of its previous territory. The curator of herpetology at the Los Angles Museum of Natural History stated:"There is a series of declines among the amphibians that cannot be explained by the usual means. These are not just declines but appear to be absolute losses. They are not just dropping down, they are in a catastrophe."
As indicators of environmental damage, the significance of these frog studies can not be overlooked, particularly for the red flags they provide about pesticide-related destruction. Part of the reason that pesticides have not been viewed with proper skepticism is because, until recently, they have been examined only individually, and not in their most toxic form, which is in combination. A study appearing last month in "Science" magazine stated that researchers from Tulane University are beginning to see the deadly possibilities of pesticide mixing. Their findings indicate that pesticides in combination boost their toxicity by over a thousand fold, and that these increases lead to birth defects, cancer, and reproductive problems in humans, domestic animals, and wildlife.
Many studies abroad indicate similar findings. The Canadian Wildlife Service has been gathering data about the affects of pesticides on Amphibians from research labs across the country. Their results are not encouraging for frogs or humans. Studies at Trent University in Ontario focused on common pesticides such as Roundup in low concentrations typical of runoff after a normal application to a field or roadside. While not immediately lethal, there were long term effects such as paralysis and inability of frogs to move away from a prod. Green frog tadpoles were never able to survive more than minimal exposure, thus decreasing the population over time.
Another study in southern Quebec measuring the overall health of frogs living in agricultural habitats subjected to pesticides found outbreaks of disease and hind limb deformities. But the worst news was that while some pesticide exposed frogs showed no apparent physiological problems, a study of their eggs indicated a substantial increase in abnormalities.
Pesticides used in apple orchards were studied in Ontario and again the results were disheartening. Orchards using pesticides and the non sprayed reference sites showed significant differences in their frog populations. The sprayed areas contained considerably smaller adult males, fewer young frogs, and stunted tadpole growth; embryos and larvae suffered significantly higher mortality rates.
Mudpuppies along the St. Lawrence and Ottawa river systems were examined in relation to their exposure to pesticides. Pesticide residues were found in the ovarian tissues of Mudpuppies from contaminated waters and X-ray analysis revealed a high incidence of limb deformities. Again they found a more numerous aging population, indicating that something serious was affecting the development of young frogs. These researchers speculated that the cause was toxic stress to the environment.
One of the common herbicides in these studies is Simazine. Simazine is used regularly, in every state, to kill weeds; millions of pounds are poured on fields, roadsides and lawns every year. Our soil has been saturated with this stuff even though Simazine is highly toxic if inhaled, moderately toxic if ingested, and slightly toxic via dermal exposure. The triazine herbicides such as Simazine disturb animal metabolism. Symptoms include difficulty in walking, tremor, convulsions, paralysis, cyanosis, slowed respiration, gut pain, diarrhea and impaired adrenal function. Sheep and cattle are especially susceptible to poisoning by Simazine. Symptoms exhibited by poisoned sheep include lower food intake, higher water intake, tremors, and weakness, especially in the hindquarters.
It's clear that not just frogs and toads are negatively influenced by the presence of pesticides in their environment; the common symptom of hindquarter abnormalities and fetal deformities is certainly no coincidence. If, as biologists have indicated, amphibians are perfect indicators of environmental health, their demise may foreshadow the consequences of our pesticide habits that Rachel Carson warned us about thirty years ago: "where the effects on humans are already known, they are found to be destructive. Beyond these known effects is the even more frightening prospect of damage that cannot be detected for years, and of possible genetic effects that cannot be known for generations, by which time the havoc we have wrought cannot be undone."

A Toxic Nightmare

by Ed Gehrman

A Toxic Nightmare:
The Dunsmuir Metam Sodium Spill Revisited 

July, 1997
This toxic nightmare began Sunday, July 14th. 1991 at 9:50 P.M. when a 97-car Southern Pacific train lurched while rounding the Cantara loop in the upper Sacramento River gorge. Seven tankers suddenly derailed and plunged from the river trestle. One landed in the middle of the Sacramento River in about two feet of water. The conductor first checked to see if the tanker's contents were listed as hazardous. Finding no reason for concern, he and the engineer went to survey the damage but were put off by the poisonous smell. They radioed headquarters that they were "getting the hell out of there!" Uncoupling the engine, they hurried on to Mt. Shasta, the next town up the line. The tanker, left lying on its side, slowly leaked nineteen thousand gallons of the pesticide, metam sodium, into one of the more well known, pristine wild trout streams in California. It wasn't until early the next morning that the full extent of this tragedy started to materialize.
"Because we did not initially believe we had a hazardous material involved in the derailment, we did not react to this as we would have if someone had called and said we have a chlorine tank leaking, for example." (R.J. Webb, investigator for the state Public Utilities Commission).
Nine hours after the accident it became clear that metam sodium was indeed having a toxic effect on the river and the entire ecosystem. "At daybreak the smell was so noxious near Dunsmuir that it was difficult to breathe. A pea-green foam was running down the Sacramento River, and dead trout were everywhere, upside down, many on the bottom of pools, some floating. Under the rocks, the insect larvae were dead. Residents seemed confused but there was no doubt what was happening: A river was being murdered." (Tom Stienstra, San Francisco Examiner).
Early Monday morning some volunteer fireman realized the imminent danger and went from house to house warning folks around Dunsmuir and asking others to help spread information about what was happening. But for some these warnings came too late. Many residents living along the river had already become ill with symptoms that included headaches, shortness of breath, chest pains, rashes, dizziness, and vomiting. They filled local emergency rooms and doctors' offices. And the constant smell of sulfur hung in the air, a grim reminder of the trail of death in the river below.
Moving slowly, the plume had passed beyond Dunsmuir and reached Castle Crags State Park by Tuesday morning. Acrid vapors remained in the air, and local authorities continued to warn everyone away from the river. Officials just monitored the spill since there seemed to be no way to dam the poison or skim it off the surface. Metam sodium is water-soluble and it had mixed thoroughly with the river. "Once the material was in the water, under the circumstances that we had here, there was very little we could do to remove it."(Peter Bontadelli, director of Fish and Game).
Wednesday evening the green ooze had reached Lakehead and began to enter Lake Shasta. Its progress slowed to about one mile an hour as it started to sink when the colder river water mixed with the warmer lake. Interstate 5 was directly above the spill at that point and travelers were being warned by the Highway Patrol to "Roll up [their] windows, don't breathe, to drive like hell and don't stop" (Ron McCloud, Dunsmuir businessman).
By Friday evening most of the spill had entered the lake and formed a plume 18 feet thick, one hundred yards wide and three quarters of a mile long, lying 18 to 36 feet below the surface. An elaborate plan was devised: "Using an experimental aeration method, chemical spill specialists from the Southern Pacific railroad set up a ring of barges bearing heavy equipment that pumped air into the lake, sucked tainted water out and sprayed it into the air." (Sacramento Bee). This tentative system was somewhat successful in breaking up and dispersing the poison before it did any noticeable damage to Shasta's fish population or human vacationers.
By the first week in August things were pretty much back to normal. Southern Pacific had dismantled the barges and recreation vehicles and boats were allowed to return to the lakefront. Testing of the lake waters found toxic substances in only one out of 78 samples. There was hardly a trace in in the river, either. If it weren't for the 200,000 dead fish, three-hundred ill residents, and millions of dollars in damage and lost tourist business, one might not even know that California's largest inland water disaster had even happened.
Of the ten thousand disinfectants and pesticides registered for use in California, only 2,000 have been given the designation "hazardous" by the EPA, and metam sodium wasn't one of those. One would think that a product that kills all life forms should be considered extremely dangerous and therefore, hazardous; but as the post disaster discussion continued, what constituted hazardous became murkier and murkier. A week after the spill, a San Francisco Examinereditor called for the Dept. of Transportation to "look again at its definition of 'hazardous'. We suggest as a basic guideline: 'If a substance can wipe out an ecosystem, its a hazard' ".
Barbara Boxer used the House Government Operations subcommittee to investigate just how an accident of this magnitude could occur. The more she looked at the methods of risk assessment used by the EPA and the Dept. of Transportation, the more confused the whole issue became. The Coast Guard considered metam sodium extremely hazardous because it becomes poisonous when mixed with water, but the Dept. of Transportation didn't consider it a problem.
"When Boxer asked whether Don Clay (EPA official) might want to add the pesticide, metam sodium, to its list of hazardous chemicals if it killed people as well as fish, Clay replied: "The number of fish killed or the number of people killed is not the criterion we use". Boxer stared in disbelief, then said: "This is an outrage. I'm stunned". (Press Democrat).
The most startling bit of information to come out of these hearings was the under- reported testimony of Linda Fisher, EPA assistant administrator of pesticides and toxic substances. She admitted that the EPA had studies dating from 1987 that linked metam sodium with birth defects in lab animals. But the EPA hadn't bothered to read these reports since EPA policy required reviewers to "read only manufacturers summaries of studies on chemicals with potential adverse affects. Even if read, birth defects were not enough to warrant the hazardous chemical designation." (Press Democrat)
This one moment of candor conveys the enormity of our pesticide dilemma.

The Ignorant & The Unwarned

by Ed Gehrman

May 1997

The Ignorant — The Unwarned
Biological Warfare for You and Your Family
and all the Rest of the Folks in Your Neighborhood

May, 1997
Both chemical and biological agents lend themselves to covert use in sabotage...As one pursues the possibilities of such covert uses, one discovers that the scenarios resemble that in which the components of a nuclear weapon are smuggled into New York and assembled in the basement of the Empire State Building. . . once that possibility is recognized to exist, about all one can do is worry about it. . .indeed, insofar as lethal chemical and biological weapons are concerned, all arguments for possessing them finally come down to the basic assertion that if the Soviets or some other potential aggressor possession them, then we must have them too. In essence, then, the real military effectiveness of lethal CWB, in terms of inflicting causalities, will accrue to the force that initiates use against an unwarned enemy.
The Chemical Weapons Convention, banning the production, stockpiling or use of chemical weapons went into affect on April 29, 1997. Eighty-seven countries, including the USA, have begun dismantling their Chemical weapons stockpiles. 1(see end notes) Maybe I should feel safer, but I don't; neither should you. My anxiety comes from knowing that chemicals were never a serious threat in the first place. Its not gas that we need fear but biologicals—bacteria, minute organisms created in small labs, cheaply, using uncomplicated and well known processes, the poor man's atom bomb.
A few days before the chemical warfare ban was to take effect, a mysterious package arrived at the Washington D.C office of B'nai B'rith, located a short distance from the White House. The package contained a broken petri dish. Fearing the worst, several blocks were cordoned off by authorities and one hundred workers were quarantined for nine hours until the contents of the dish were analyzed. This particular incident turned out to be a cruel hoax but the reality of the event was not lost on the participants.
The officials on the scene were hit with the realization that it is only a matter of time before a "germ bomb" explodes in our midst. We are not prepared. In drills conducted last year in major cities, firefighters moved into contaminated areas without any protective gear and health workers were overwhelmed and unable to give adequate care. The U.S. Office of Technology Assessment theorized that a crop dusting plane, spewing anthrax spores over Washington D.C. could kill three million people. A medical "war game" conducted by the National Institute of Health to simulate the spread of airborne Ebola concluded that there were no agencies, national or international, that could prevent this type of epidemic disease threat from spreading from a small initial location to every continent in the world within two months. 2
In spite of all efforts to portray bio-warfare microbiologists as careful, meticulous scientists, there is a surprising amount of serendipitous, chancy behavior. Take this account of the discovery of the Ebola (Marburg) virus by Dr. Frederick A. Murphy who was then the director of the National Center for Infectious Diseases at the CDC in Atlanta. "The specimen had come back from Zaire to the CDC in Atlanta in less than optimal condition, with the tubes in the box broken. Anyone else would have taken a look and put the whole box in the autoclave, but Dr. Patricia Webb, wearing gloves, gown and mask, squeezed a few drops of fluid out of the cotton surrounding the broken tubes. That was the material the virus was isolated from. It was placed in tissue culture (monkey kidney cells) for a couple of days then I got a drop of the tissue culture fluid and prepared a specimen for the electron microscope. When I saw what I was sure was Marburg, I shut the electron microscope down and went back to the room in which I had prepared the specimen. This was in the days when hoods were a lot more primitive. I 'chloroxed the hell' out of the place where I had done the preparation and carried my discard pan with gown and gloves etc. to the autoclave and ran it." 3
Nowadays, many diseases can be produced on an industrial scale using readily available resources. Trained technicians are easily able to culture large quantities of bacteria using methods formulated in U.S. bio-warfare labs; over a hundred Department of Defense funded laboratories are operating on campuses or in industrial parks across our nation. Our collective ignorance about participating in bio-warfare research is alarming and our seeming innocence, hypocritical. There are serious consequences in allowing our defense establishment and the scientific community to become involved in this grisly business. Shoddy scientific techniques, risky protocols, and the repressive secrecy that prevents peer review and free exchange of opinion are some of the perilous drawbacks.4
Almost all bio-warfare experiments are classified but those few that have become public should be enough to convince us that scientists doing this research need a new moral compass. Sixty-five years ago, four hundred black sharecroppers in Macon County, Alabama were chosen to participate in a bio-warfare experiment sponsored by the scientific community. The main factor these men shared in common, aside from being poor and illiterate, was syphilis. They were tested yearly during the years 1932 to 1972 by the public health service and were never told of their illness, only that they were being treated for "bad blood". The purpose of the study was to follow the long term effects of syphilis on the human body. Having no idea they were carrying around a deadly bacteria, the men tried to conduct their lives in a normal fashion.
Even in the 1940's when a penicillin cure became available, the men were still denied treatment. The impact of four hundred syphilitic men socializing in a relatively closed rural community can never be measured. When the experiment was terminated in 1972, fifty surviving wives and twenty surviving children were still infected with syphilis. Articles appeared in respected scientific journals during the forty years of the study reporting the progress of these untreated men. A belated apology from the government and ten million dollars to the six thousand survivors seems little recompense for the suffering and torment these folks endured. This experiment also spread syphilis far and wide throughout the US. Biologics cannot be contained.
There is a tendency in the scientific community to first ignore and then ridicule information or opinions that are contrary to prevailing beliefs; but a few balky doctors and health care workers have voiced their concern, often to a deaf public and media. Dr. Alan Cantwell M.D. represents this minority when he states: "Does the government secretly experiment with people? Of course, it does. This is not a paranoid fantasy. There is circumstantial evidence that shows AIDS is a man-made disease with a genetically engineered virus that came out of a cancer virus Bio-warfare laboratory. It is a commonly believed, particularly in the Black community, that AIDS is a secret government genocide plot to eliminate 'undesirables.' The major media never mention books written on the subject of AIDS as man-made, nor will they quote physicians, like myself and others, who publicly promote this idea. Without discussion, the media simply dismiss the idea as paranoid, or as right or left-wing, or as tied to extremist or terrorist or Militia groups." 5
To make matters worse, acute scientific mistakes are glossed over or covered up. Henrietta Lack died in 1965 of uterine cancer. She gained dubious immortality through her cancer cells for they were the first cells to be grown in perpetuity in tissue cultures. Before HELA (Henrietta Lack) cells, only one or two divisions were possible. The HELA cells were sent world wide. It's not well known but even during the peak of the "cold war", Soviet and U.S scientists were collaborating on bio-warfare and cancer virus research. In 1972 the Russians sent us six cell lines they thought contained cells with cancer causing viruses. As it turned out, these cell lines were all contaminated with HELA cells that contained monkey viruses. Dr. Walter Nelson Reese had the responsibility of keeping the cell lines in the U.S. cataloged. After the incident with the Russians, he decided to examine all cell lines. He discovered, much to his amazement, that over a third of them were HELA contaminated, probably when culture lids were opened and aerosolized particles would float around the lab and sometimes drop into another cell line. The aggressive HELA cells, often carrying viruses from other species, would soon take over a culture. Instead of rewarding these findings, Dr. Reese's program was defunded and he now runs an art studio. 6
Doctors Garth and Nancy Nicolson are prime examples of what can happen when one questions authority. They have been hounded from prestigious jobs and threatened, both physically and professionally; their labs have been vandalized, irreplaceable specimens destroyed, correspondence intercepted and phones tapped. Why? Because they had the audacity to suggest, and evidence to indicate that many sick gulf war vets are suffering from exposure to a bio-warfare, weaponized organism, a mycoplasma named incognitus.
Mycoplasma are the smallest and perhaps the oldest life forms. These cell wall deficient bacteria, the cause of "walking pneumonia", have been implicated in a variety of other &"emerging" diseases. Lyme disease is a mycoplasma spirochete dispersed by ticks and thought to originate at the Plum Island bio-warfare center. It escaped to the island's huge bird refuge and then across to New England, where it is still a major cause of illness. From there, the mainland states were contaminated via the migratory bird routes. A form of mycoplasma, a spiroplasma, is also implicated in Mad Cow Disease but is being ignored by most BSE researchers. Multiple Sclerosis, Chronic Fatigue Syndrome, and Alzheimers are also being investigated as possibly caused by mycoplasmic type bacteria. Mycoplasma are thought by many to be rather fragile, but nothing could be further from the truth. They tolerate extreme fluctuations in temperature, lay dormant in the soil for generations and survive the harshest elements; only drano-like chemicals kill them effectively outside the body. Under normal circumstances our immune system efficiently deals with mycoplasmas and other life-threatening bacteria; we evolved from this complicated, membrane enclosed piece of DNA and up until now have developed defenses that keep these critters in check. The new strains seem different. Difficult to spot in tissue, they do not react to normal bacterial tests. There has been no sure way to test for these organisms in living tissue since they are often not a problem until the immune system is exposed to stress. The symptoms are flu-like but to the extreme: headaches, sore joints, rashes, chest pain, heart problems, and neurological disorders. Dementia is common in advanced stages of these gruesome afflictions. 7
The Nicolsons' test is able to identify the presence of mycoplasma in living tissue. The normal way to determine infection is to inject a lab animal with tissue or cultured material and wait for the lab animal to develop the target disease. The Nicolson's claim that a method they have invented named Gene Sequencing seems to do a much better and more accurate job. Labor intensive, thus expensive, Gene Sequencing has been peer reviewed and found to be credible and dependable. Government scientists and the Defense Department refuse to even consider the validity of this approach because if the Nicolson's are correct, and the mycoplasmic infections sickening the Gulf War vets are found to have originated in government funded bio-warfare labs, these programs will be exposed as the dangerous and shortsighted escapades they have become.
The USA supplies much of the know how and advanced technology used in this deadly endeavor. Microbiologists from every country study at our universities and learn all the necessary techniques needed to establish successful germ labs. Scientists from the USA were working with Iraq's microbiologists on bio-warfare just weeks before the Gulf War, and Iraq was importing highly toxic bacteria and viruses from companies in the USA. By 1990 they were manufacturing large quantities of botulism toxin and anthrax bacteria.
The Army command knew of the possibility that our forces could be exposed to toxic agents while stationed in Iraq; the compulsory inoculations, with multiple vaccines, indicates foreknowledge. But the Command didn't notify the troops about what was about to happen; they were participating in a huge experiment without their informed consent. They still have not been informed and most of the information surrounding the inoculations has been classified, the contents of the vaccines have still to be positively identified. One of the doctors who complained and refused to cooperate because she felt using force was a violation of the Geneva Protocols was court marshaled and given eighteen months in federal prison. 8 "The nation's historical record on bio-warfare is replete with subterfuge, reckless experimentation, and rogue actions and is punctuated by violations of both domestic policy and international and national norms. . . the modern record is no more reassuring. . .If modern biology is to be a tool for human benefit, not the seed of our destruction, then all its facets, including military applications, must be opened to new levels of public understanding and to careful public scrutiny." 9
The perfect bio-warfare agent would be similar to that used to kill and control the rabbits in Australia: the virus Myxoma . It is ninety percent fatal for rabbits, but is harmless to almost everything else. The ideal agent would also be suitable for mass production, and contagious through the air, with a short incubation period, but still able to survive in the environment. Medical defense should be difficult, and counter measures available so that friendly forces could be inoculated, but like the rabbits, the enemy wouldn't have access to a vaccine. Most of all, the pestilence needs to produce terror and demoralization in its victims.
The average person has the impression that the USA has long since stopped hazardous biological experimentation and has destroyed its stockpiles of biological weapons. In 1975 Richard Nixon signed the Geneva Protocol which among other things states: "Each State party to this Convention undertakes never in any circumstances to develop, produce, stockpile or otherwise acquire or retain: 1) Microbial or other biological agents, or toxins whatever their origin or method of production, of types and in quantities that have no justification for prophylactic, protective or other peaceful purposes; 2) Weapons, equipment or means of delivery designed to use such agents or toxins for hostile purposes or in armed conflict."
This straight forward language makes the overall impression quite clear. Our country should not be mucking around with biological weapons. We have ignored this law since its signing. The main way we circumvent our legal obligations is to maintain that we have defensive reasons for all the research, but there is absolutely no difference between offensive research and defensive public health research. Our signing of the law was a sham and a sop to those scientists who foresaw the predicament we were getting ourselves into, but were mostly ignored. They were put off by statements like this: "Those who regard themselves as guardians of the public safety must count not only the speculative hazards of these marginal situations, but also the costs to the public health of impeding their (biological weapons) investigation."
These protocols may now be meaningless in an age of new technologies; advances in DNA and cloning could produce a deadly new agent almost overnight, with relative ease. Recombinant DNA is a process known to most biologists and is easily accomplished in well equipped labs. Bacteria contain plasmids which are tiny pieces of DNA. This DNA is much smaller than, and independent of, the DNA contained in the chromosomes. The plasmids are removed from the bacteria and then sliced apart using enzymes. A virus gene that has already been removed from the virus is fitted into the gap in the plasmid. Then this altered plasmid is inserted into a bacteria, where it can perform any number of tasks. As a bio-warfare bacteria the new DNA could manufacture toxins that would poison the body or cause disruptions in vital organs, like the brain. If mycoplasmas were the bacteria used in the transfer, they would be almost impossible to detect. Mycoplasmas have the ability to blend with the cell wall of the host and then move deeply into the nucleus of the cell where they stay hidden, waiting to emerge when the immune system weakens.
Mycoplasmas play only a small part in this tragic production. Any virus or bacteria that could cause a disease has or will be, or is now being studied and considered as a possible warfare agent. All means of transmission have been deliberated and researched and the stage is set for an emerging crisis. We could stop this before it's too late. We only need to lift the cloak of secrecy that hides the Frankensteinian nightmares we've created in our sequestered laboratories. When we see clearly what is happening in these government funded labs, we'll shut them down. 10
If we don't, we're in for more trouble. An example of just how reckless scientists have become can be seen in a new threat that has appeared. Not some "emerging" virus, stumbled upon during a trek through previously unknown environs, but in lung tissue from a soldier who died in1918 . During the late spring of that year a strange and lethal new disease began appearing at military installations across the US. By September this infection, known as Spanish flu, rapidly spread across the country and then to every corner of the world. It was over by year's end but with twenty million dead it became the deadliest plague the world has ever known. The virus that caused this pestilence has not been available for studying. But now, using modern techniques, the eighty year old lung tissue that sat undisturbed in Washington D.C. has revealed fragments of the virus, enough so that the DNA sequences may soon be known. The CDC is also planning a trip to Norway to study the remains of seven miners who also died of the Spanish flu. They hope to find an intact virus, but if successful they may unleash this possible pandemic. Is it worthwhile to take these kinds of risks? Regretfully, we will have no say in the matter; it's classified and beyond discussion by mere mortals.
The elimination of all bio-warfare research and testing, even if it is theoretically defensive in nature, should be the goal of the scientific community. The public can apply only so much pressure; it is the scientists themselves who must sever their connections to the growing menace of bio-warfare. The easiest way would be by refusing to work on secret science. There are no credible justifications to continue these explorations and only scientists have the prestige, influence and status to redirect the attitudes and practices of their fellow scientists.

  1. End Notes
  2. Ivan L. Bennett, Jr., former Deputy Director of the U.S Office of Science and Technology before a symposium on chemical and biological warfare, sponsored by the National Academy of Sciences. Proc. N.A.S. 1970; 65:250-279. Taken from Emerging Viruses: AIDS and Ebola.
  3. Lee Bowman, "America Gets a Taste of Chemical Terror", April 26, 1997 Scripps Howard News Service. A well written news report; one of the few I've read that tries to point out the significant danger of bio-warfare.
  4. Dr. Frederick A. Murphy Talks about the Ebola Virus—An Interview by Sean Henahan, Access Excellence: a WWW site that supplies information about emerging diseases and viruses.
  5. Dr. Garth Nicolson from a discussion recorded by Gustav Grossman, 7/28/97.
  6. This is from an interview I conducted, about a year ago, with Dr. Cantwell for my column in the Sonoma County Free Press. The Tuskegee syphilis experiment, funded by the Center for Disease Control, is well documented in Dr. Cantwell's writings and in numerous other sources as well. Dr. Cantwell has written two books on the genesis of the HIV: AIDS and the Doctors of Death and Queer Blood. Both are excellent. He has also written about the ability of bacteria to cause disease in the Cancer Microbe.
  7. This also is well documented information. Michael Gold's Conspiracy of Cells shows clearly the type of scientific errors that can occur on a regular basis, even in well run labs. Another look at scientific Snafus and downright skullduggery is the brilliantly researched "Emerging Viruses: AIDS and Ebola, Nature, Accident or Genocide?" by Leonard Horowitz. There is no need to distort or fabricate information concerning bio-warfare; the truth is there for all to see.
  8. I had previously researched the nature of mycoplasmas and spiroplasmas for an article I wrote on Transmissible Spongiform Encephlopathy : Mad Cows —Mad Scientists; FLATLAND #14 or Sonoma County Free Press. Mycoplasma type organisms are poorly understood, even by most scientists because they are so difficult to culture. They are often ignorantly discounted as the cause of disease. This could prove to be a fatal mistake for us all.
  9. From recorded conversations by Gustav Grossman 6/23/96. The Eight Myths of Operation Desert Storm—Gulf War Syndrome by Garth L. Nicolson, Ph.D., and Nancy L. Nicolson, Ph.D. The Institute for Molecular Medicine, P. O. Box 52470, Irvine, California 92619-2470 USA.
  10. From the introduction to Gene Wars: Military Control Over the New Genetic Technologies by Charles Piller and Dr. Keith Yamamoto.
  11. Much of the above information can be found in Gene Wars . This is an important look at our government's bio-warfare program, the rationale and motives. It is also a plea to their fellow scientists to take a long, hard look at the pitfalls of continuing this dangerous activity. Written in 1986, it predicts clearly the type of problems that might arise, just as they did four years later during the Gulf War. Too bad we didn't listen.