Article: Gulf war syndrome research reveals present danger

Discussion in 'Fibromyalgia Main Forum' started by JaciBart, Mar 27, 2003.

  1. JaciBart

    JaciBart Member

    Gulf war syndrome research reveals present danger

    19:00 26 March 03

    Exclusive from New Scientist Print Edition

    A week into the invasion of Iraq and news networks are beaming home images of American and British soldiers donning gas masks and body suits to protect themselves from potential chemical weapons attack.

    The troops have practised the drills, and are carrying the best high-tech chemical detectors an army can buy. The US marines even have a brand new piece of kit: pigeons, which act like canaries in a 19th-century coal mine. The birds are so sensitive to nerve agents such as sarin and VX that they fall ill at a whiff of danger.

    What the soldiers have not been told is that about one in 10 of them are almost as sensitive to nerve agents as the pigeons. There is now mounting evidence that exposure to minuscule amounts of these chemicals can cause permanent brain damage in susceptible people, and that is exactly what happened 12 years ago when thousands of troops returning from Kuwait started to complain of debilitating symptoms.

    Repeated surveys find 30 per cent more sick people among Gulf veterans than in comparable groups who did not serve. But the official position in Britain, Canada and the US is that Gulf war syndrome is not a specific medical condition.

    All accept something is wrong with the 1991 veterans, but official research has focused on post-traumatic stress. The US has paid disability compensation to more than 110,000 of the 696,000 troops who fought in that war.

    Neural damage

    Then in October 2002, the US Department of Defense admitted there is "increasing evidence" that neural damage is affecting the ex-soldiers. It doubled research funding, including work on protective treatments. Veterans called it a "stunning reversal".

    Part of the problem has been that veterans report a variety of symptoms which, though serious and chronic, are often vaguely defined. But in September 2002, researchers at the Gulf War Illnesses Research Unit at King's College in London showed that stress cannot explain symptoms displayed by British veterans.

    At the same time, a medical team in the US identified three distinct syndromes among US Gulf war veterans. Han Kang and his team at the US Department of Veterans Affairs used a statistical technique called factor analysis that reveals unusual clusters of symptoms. They found syndromes that matched those seen in a smaller group by Robert Haley of the University of Texas Southwestern Medical Center in Dallas, who pioneered the investigation.

    Syndrome 1 involves symptoms such as sleep and memory disturbance, while people with syndrome 3 have joint and muscle pain. The most serious is syndrome 2, whose symptoms include confusion and dizziness.

    When Haley's team used magnetic resonance spectroscopy (MRS) to study veterans with syndrome 2 they found that they had lost nerve cells in the basal ganglia, structures involved in the brain functions disturbed in those with the syndrome. Veterans with other syndromes had also lost neurons in brain areas that fitted their symptoms. The finding was confirmed in another group by MRS expert Michael Weiner at the University of California at San Francisco.

    Chemical weapons alerts

    But what caused the damage? Haley found that syndrome 2 veterans are eight times as likely as healthy veterans to have been present when chemical weapons alarms sounded in the Gulf: for example, in January 1991, when Czech experts using sensitive Russian-made equipment detected nerve agent near a US army camp in Saudi Arabia.

    Military authorities have denied that any soldiers were damaged by chemical weapons during Desert Storm, as none ever showed symptoms of acute nerve gas poisoning. But Jonathan Tucker of the US Institute of Peace, a congressionally funded think tank in Washington DC, has found dozens of reports of low levels of chemical weapons being detected near troops. These could have been released when allied forces bombed Iraqi arms depots or factories.

    Syndrome 2 veterans were also around eight times as likely as healthy comrades to have reacted badly to pyridostigmine, a drug given to soldiers in the Gulf, then and now, to protect against nerve agent attacks. In troops who were both exposed to nerve agent and showed side effects to the drug, the risk of long-term ill effects was five times the risk conferred by each factor separately.

    The link, says Haley, is that chemical weapons, and the drug that protects against them, affect the same physiological pathway. Nerve gas sends muscles into fatal spasm by blocking an enzyme that destroys acetylcholine, the neurotransmitter that makes muscles contract. In theory, pyridostigmine protects by blocking the enzyme for a short time, keeping nerve agents from binding to it permanently.

    But some people may not be able to cope with having the enzyme blocked at all. Animal experiments show that exposure to enzyme blockers at levels too low to produce acute toxic effects can subtly change acetylcholine activity in the brain, and the animals' long-term behaviour.

    Memory and cognition

    Rogene Henderson of the University of New Mexico reported in 2002 that low doses of sarin change the distribution of acetylcholine receptors in rats' brains. Affected regions include those used for memory and cognition - which are the functions disturbed in Gulf war veterans.

    The effect is more marked in stressed animals, which may explain why soldiers who saw combat show more severe symptoms. Other groups have also shown that nerve agents cause basal ganglion damage in animals.

    Why are all soldiers not equally affected by the exposure to nerve agents? Pigeons make good detectors because they do not produce the enzyme paraoxonase which destroys nerve gas. Haley has found that syndrome 2 victims have very low levels of the form of human paraoxonase that is most effective against nerve agents, an observation repeated by Department of Veterans Affairs researchers in New Jersey in a study yet to be published.

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    US Department of Defense

    US Department of Veterans Affairs

    Internal Medicine, UT Southwestern Medical Center

    Gulf War Veterans

    Conflict over Iraq, New Scientist

    In Britain, Bharti Mackness and her team at the Manchester Royal Infirmary have found that British veterans with Gulf war syndrome have half the paraoxonase activity of healthy colleagues.

    Evidence that this kind of physical damage underlies Gulf war syndrome has been mounting since 1997. But the US government did not begin to take it seriously until the Department of Veteran's Affairs appointed a new Research Advisory Committee on Gulf war veterans last year.

    The Department is now planning a national survey of Gulf veterans based on the newly defined syndromes, while Haley is building a more powerful MRS lab to observe brain damage more precisely. "We will then turn to finding treatments," he says. He has already shown that mice induced to make more paraoxonase are protected from a chemical similar to sarin.

    Such progress promises to shed more light on why so many Gulf veterans are sick, and stop it from happening again. But it has come too late to help soldiers exposed to chemical weapons during the current conflict.

    Debora MacKenzie

  2. dojomo

    dojomo New Member

    I'm confident that our illnesses will be attributed to exposure to toxic substances. Since no pathogen can be isolated, it makes sense that some predisposed people can have multiple system dysfunctions after contact with poisons......... in our air, food, water and pharmacueticals..(ie vaccines..ect.).........Thanks for posting............DJ
  3. dojomo

    dojomo New Member

    Found this new article and thought you would be interested.................

    [Lessons from macrophagic myofasciitis: towards definition of a vaccine adjuvant-related syndrome]

    [Article in French]

    Gherardi RK.

    Groupe Nerf-Muscle, Departement de Pathologie, Hopital Henri Mondor, Creteil.

    Macrophagic myofasciitis is a condition first reported in 1998, which cause remained obscure until 2001. Over 200 definite cases have been identified in France, and isolated cases have been recorded in other countries. The condition manifests by diffuse myalgias and chronic fatigue, forming a syndrome that meets both Center for Disease Control and Oxford criteria for the so-called chronic fatigue syndrome in about half of patients. One third of patients develop an autoimmune disease, such as multiple sclerosis. Even in the absence of overt autoimmune disease they commonly show subtle signs of chronic immune stimulation, and most of them are of the HLADRB1*01 group, a phenotype at risk to develop polymyalgia rheumatica and rheumatoid arthritis. Macrophagic myofasciitis is characterized by a stereotyped and immunologically active lesion at deltoid muscle biopsy. Electron microscopy, microanalytical studies, experimental procedures, and an epidemiological study recently demonstrated that the lesion is due to persistence for years at site of injection of an aluminum adjuvant used in vaccines against hepatitis B virus, hepatitis A virus, and tetanus toxoid. Aluminum hydroxide is known to potently stimulate the immune system and to shift immune responses towards a Th-2 profile. It is plausible that persistent systemic immune activation that fails to switch off represents the pathophysiologic basis of chronic fatigue syndrome associated with macrophagic myofasciitis, similarly to what happens in patients with post-infectious chronic fatigue and possibly idiopathic chronic fatigue syndrome. Therefore, the WHO recommended an epidemiological survey, currently conducted by the French agency AFSSAPS, aimed at substantiating the possible link between the focal macrophagic myofasciitis lesion (or previous immunization with aluminium-containing vaccines) and systemic symptoms.

    Interestingly, special emphasis has been put on Th-2 biased immune responses as a possible explanation of chronic fatigue and associated manifestations known as the Gulf war syndrome. Results concerning macrophagic myofasciitis may well open new avenues for etiologic investigation of this syndrome. Indeed, both type and structure of symptoms are strikingly similar in Gulf war veterans and patients with macrophagic myofasciitis. Multiple vaccinations performed over a short period of time in the Persian gulf area have been recognized as the main risk factor for Gulf War syndrome. Moreover, the war vaccine against anthrax, which is administered in a 6-shot regimen and seems to be crucially involved, is adjuvanted by aluminium hydroxide and, possibly, squalene, another Th-2 adjuvant. If safety concerns about long-term effects of aluminium hydroxide are confirmed it will become mandatory to propose novel and alternative vaccine adjuvants to rescue vaccine-based strategies and the enormous benefit for public health they provide worlwide.

    PMID: 12660567 [PubMed - in process]

  4. Mikie

    Mikie Moderator

    Interesting that the Univ. of Texas has been involved in research. They have a long history of working with the Dept. of Defense and experiments on Texas prisoners with chemical/biological weapons.


    Love, Mikie
  5. JaciBart

    JaciBart Member

    There are some people (from the click it news under emerging diseases website) who believe that the govt and the biolabs are responsible for hiv, anthrax, the new sars outbreak, etc. Interesting theory. We could all be part of a giant experiment, stranger things have happened. That would explain why so many docs roll their eyes when you mention mycoplasma. My old doc did.

    [This Message was Edited on 03/28/2003]