Gulf War syndrome

	Gulf War syndrome

	*Gulf War syndrome - a real problem or a figment of a soldiers imagination?* Over the last six years, following the gulf war, a number of misterious conditions have appeared in a large number of the veterans who served in the gulf. Since then an intense debate has arisen over the seriousness of the problem and, perhaps more importantly, the exact cause of the problem. Are the gulf war veterans suffering reactions to toxic exposure or are they suffering from some form of war 'stress'? Scientists worldwide have been trying to answer this very question ... At the beginning of 1994, an advisory panel to the US National Institutes of Health (NIH) recommended that a health survey be carried out on the 700,000 veterans who served in the gulf war. In addition the NIH stated that the extensive variety of symptoms described by a number of gulf war veterans were not indicative of a single medical syndrome. These symptoms included skin rashes, headaches, loss of memory and extreme hypersesitivity to common everyday products. Many veterans had had extreme problems in finding employment but were unable to qualify for any form of disability benefits in 1994 because of the absence of a precise definition for Gulf War syndrome. In order to solve this problem, Major General Ronald Blanck, of the Walter Reed Army Medical Centre in Washington called for a complete definition of the Gulf War syndrome to be drawn up. Whilst the NIH rejected any claim of a single syndrome, it admitted that gulf war veterans were suffering real pain. John Spengler of the Harvard School of Public Health complained of the absence of any health records for the 700,000 veterans who served in the gulf. In May of 1994, over three years after the end of the gulf war, the Department of Veteran's Affairs was reported to stock complete health records for only 20,000 of the gulf war service men and women. In January of 1995 the US Institute of Medicine (IOM) made a statement condeming research into the Gulf War syndrome as badly designed and poorely coordinated. More specifically, the IOM crtiticised the methods used for data collection with experiments apparently lacking proper controls. According to the IOM, the lack of coordination between the two main government departments involved in Gulf War syndrome research, the Departments of Defense Veterans' Affairs and Health and Human Services, had seriously affected the quality of research into the Gulf War syndrome. Consequently, the IOM called for American Vice-President, Al Gore, to chair a meeting between these two government departments and leading American epidemiologists to improve coordination between different research groups. *Chickens lead the way in Gulf War syndrome research* In April of 1996 the US Department of Defence announced that an 80 million dollar study had failed to identify a specific disease that could account for the variety of symptoms observed in gulf war soldiers. However, a private study headed by Mohammed Abdou-Donia of Duke University and Robert Haley of the Texas Southwestern Medical School, had shown a rather different picture. A series of experiments carried out on chickens and hens showed that a combination of some of the drugs used by gulf war veterans caused damage to the central nervous system in these animals. Abdou-Donia claimed that some of the symptoms observed in the treated chickens and hens resembled those observed in veterans of the gulf war. The US Environmental Protection Agency stated that both chickens and hens were well suited for such a drug toxicity study since their nervous systems are highly sensitive to toxic damage. The Abdou-Donia and Haley experiments centred around three chemical compounds - the two pesticides DEET and Permethrin which were used to protect soldiers against insect-transmitted diseases such as Malaria, and Pyridostigmine, an anti-nerve gas agent. Treatment of hens with any one of these compounds had no apparent effects on health. However, combinations of these three compounds resulted in animals that were extremely weak and unable to fly. In some cases a loss of weight was observed together with tremors and frequent stumbling. According to the researchers, the enzyme Butyrylcholinesterase which is present in the blood circulation is, under 'normal' conditions, able to break down the three compounds tested. However, under certain conditions, the pyridostigmine saturates the butyrylcholinesterase thereby preventing the breakdown of DEET and permethrin. Consequently the DEET and permethrin can pass into the brain unchecked to exert toxic effects. Shortly after the US Defence Department's April announcement, Doctor Critchley at the Department of Neurology at the Royal Preston Hospital in the UK, mentioned similarities between symptoms observed in the Gulf War syndrome and those observed in the 1989 Botulism outbreak in the UK. In a letter to the medical journal The Lancet, Critchley pointed out that tablets containing botulinum toxoid had been administered to gulf war veterans. Moreover Critchley added that a number of unexplained symptoms had been experienced by Botulism patients following the acute phase of the disease which affected both physical and mental health. *Assessing levels of drug exposure during the Gulf war - Is Pyridostigmine Bromide the 'guilty' drug?* One major problem in assessing the levels of exposure to certain drugs during the gulf war is that the recommended levels of drug intake were often lower than the actual levels of intake by soldiers. This was particularly true for the drug pyridostigmine bromide (PB), a nerve gas protection drug which, according to Irving Cohen at the Veteran's Administration Medical Centre in Topeka, Kansas, was taken every day by some gulf war soldiers. PB and nerve gas have the same mode of action binding and inactivating the enzyme acetylcholinesterase. Such inactivation leads to the accumulation of acetylcholine which causes an overstimulation of the muscles. In the case of nerve gas, such muscle overstimulation leads to death since the binding of nerve gas to acetylcholinesterase is irreversible. By administering PB to gulf war soldiers, the effects of nerve gas can be avoided since nerve gas cannot bind to acetylcholinesterase that is already bound to PB. The US department of Defence defended its use of PB during the gulf war stating that it had previously been used for the treatment of patients suffering from the neurological disorder, Myasthenia Gravis without any side effects. However, the gulf war environment had possibly presented a 'stress' in the body causing physiological side effects which were not normally experienced under non-stressful conditions. The NIH panel also concluded that two other factors, post-traumatic stress syndrome and the parasitic disease, Leishmaniasis, could be contributing to some of the post war symptoms. The possible exposure to biological and chemical weapons was also not ruled out by the NIH panel following a report by the Czech government that soldiers had been exposed to biological and chemical warfare. *A possible genetic cause for some of the Gulf War symptoms?* In October of 1995 Loewenstein-Lichtenstein and his colleagues from the Hebrew University in Jerusalem, Israel, reported on an individual who had undergone treatment with pyridostigmine during the gulf war and had suffered neurological problems. Further studies showed that the individual was homozygous for a Butyrylcholinesterase mutation thereby rendering the Butyrylcholinesterase inactive. Since the Butyrylcholinesterase is responsible for 'mopping up' the effects of Acetylcholinesterase inhibitors such as pyridostigmine, these Butyrylcholinesterase mutations could lead to adverse effects in soldiers exposed to pyridostigmine during the gulf war. This study is therefore a clear indication that soldiers who served in the gulf war could have been geneticallty predisposed to adverse effects from the treatment of pyridostigmine. Marcello Lotti and Angelo Moretto at the Universita degli studi di Padova in Italy have criticised this study saying that the levels of pyridostigmine administered to the gulf war soldiers were too low for mutations in the Butyrylcholinesterase to really have adverse effects on the soldiers. *The effects of Gulf war 'stress'* In a paper to Nature Medicine, Alan Friedman and his colleagues in Israel have shown evidence that, under stress conditions, the effects of pyridostigmine on the Central Nervous System and the brain is enhanced. Thus whilst in peace time the pyridostigmine may not have detrimental effects, the stressful conditions of the gulf war may have increased the toxicity of pyridostigmine in Gulf War soldiers. *The British investigation into the gulf war syndrome targets reproductive health* In December of 1996, almost two years after the US had started studying the symptoms of gulf war syndrome in gulf war veterans, the British Ministry of Defence (MOD) announced the start of a similar study in the UK. The MOD allocated a total of 1.32 million pounds for these two studies which initially involved comparing 3000 gulf war veterans with 3000 service men and women who had not served in the gulf. The second study, led by Patricia Doyle at the London school of Hygiene and Tropical Medicine, was set up to investigate the reproductive health of service personnel and their children. The results of both of these studies will be published at the end of 1999. If the results indicate a link between the reported symptoms of ill health and service in the gulf war, it will be necessary to establish the precise causes of these symptoms. A number of potential causes of ill health have already been suggested including the use of delousing powder in Iraqi prisoners, protective treatments against biological and chemical weapons, smoke from burning oil refineries and the use of chemical and biological weapons themselves. The MoD's announcement came as Nicholas Soames the ex-mimister of the British Armed Forces told the house of Commons that he had been badly informed on the use of organophosphate insecticides during the gulf war. These were used by gulf war service personnel to protect against a number of insect-transmitted dieseases. Soames admitted that such insecticides had been widely used in contrast to previous government reports that their use was minimal. *American presidential panel heavily criticized for wrong conclusions on chemical exposure* In January of 1997, an American presidential panel made an announcement stating that the adverse symptoms being described by gulf war veterans was not due to any environmental exposure during the war. Whilst the presidential report criticized what it called 'a laxity' in the studies of the Gulf War syndrome, it also stated that no link could be drawn between a particular environmental exposure in the gulf and the variety of medical symptoms experienced by gulf war veterans. The panel also came to the conclusion that some form of 'war stress' was responsible. *JAMA contradicts presidential panel* Immediately following the presidential panel's announcement, the editor of the Journal of the American Medical Association (JAMA) responded by revealing that three articles would be published that indicated the exact opposite. The gulf war controversy had yet again been thrown up into the air. These articles referred to three separate conditions which, according to one of the authors, Robert Haley, help to explain the symptoms being experienced by gulf war veterans. The first of these conditions, referred to as Impaired Cognition Syndrome, had possibly been caused by collars containing the pesticide Chloropyrifos which had been worn by some of the gulf war soldiers. Symptoms of Impaired Cogniton Syndrome include severe memory problems, depression and insomnia. The second of these conditions, referred to as Confused-Ataxia Syndrome, had possibly been caused by chemical weapons and carried the symptoms of reasoning difficulties and balancing problems. Finally Arthro-myo-neuropathy occurred most frequently in soldiers exposed to insect repellent containing the chemical DEET and produced severe muscular weaknesses. A member of the presidential panel, Phillip Landrigan, heavily criticised these articles saying that the researchers had used a very small number of soldiers in their studies adding that the results were not statistically representative of overall health problems experienced by veterans of the gulf war. *The American Society of Neuroscience sheds new light on possible causes of Gulf War Syndrome* In October of 1997, the 27th annual meeting of the American Society of Neuroscience revealed new findings in the study of potential causes of Gulf War syndrome. Neuropharmacologists Jerry Buccafesco, Mark Prendergast and Alvin Terry, at the Medical College of Georgia and the Veterans Administration Medical Centre in Augusta discussed results obtained using organophoshpates on an animal model of Gulf War syndrome. More specifically, it was shown that in rats exposed to organophosphates, there was a reduction in the level of Acetycholine receptors in the hippocampus region of the brain. These rats showed subsequent learning defficiencies which lasted for prolonged periods of time even after organophosphate exposure had stopped. The first indications of organophosphate mediated effects on the brain came in the 1960s when farmers and agricultural workers reported cognitive problems after low level exposure to organophosphates. Subsequent studies did not give any indication as to the long term effects of such exposure. Therefore the results of Buccafesco's, Prednergast's and Terry's work gave the first indication of the long term effect on the brain of organophosphate exposure. The tests carried out by Buccafesco's team involved injecting rats with the organophosphate DFP every day for two weeks. When these rats were placed in a Morris water maze, in which rats have to find a platform in a pool of water, the DFP-treated rats reportedly took up to 30% more time than untreated rats to find the platform. Moreover the cognitive defficiencies in DFP-treated rats continued for three weeks following the last treatment with DFP. Biochemical studies on DFP-treated rats showed that DFP caused a decrease in Acetycholine receptor levels in the brain and that these decreases were responsible for the observed cognitive defficiency in the DFP-treated rats. However Buccafesco admitted that these results must be considered with caution since neither his nor other people's experiments had succeeded in reproducing the precise conditions experienced by soldiers during the gulf war. *A British double vaccine treatment comes under fire* In November of 1997, the UK MoD admitted that it had not seriously considered warnings concerning the potential side effects of multiple vaccinations to the British service personnel in the gulf war. More specifically, the pertussis vaccine (whooping cough) had been administered to gulf war soldiers so as to 'speed up' the effects of a subsequent anthrax vaccine treatment. Such a pertussis vaccine pretreatment reduces the time for the anthrax vaccine to take effect from 32 weeks to 7 weeks. This double vaccine treatment was therefore ideal for quickly preparing soldiers before going out to the gulf. However, the MoD had received warnings from the National Institute for Biological Standards and Control (NIBSC) that such combined vaccine treatments could have severe health implications. The MoD had apparently ignored these warnings. So what conclusions can be drawn from the research results over the last six years ? Clearly the scientific community is in conflict over the precise nature of the gulf war syndrome and whether it can really be termed as a single syndrome. One of the severe problems in understanding the precise nature of the symptoms being suffered by gulf war veterans is obviously the impossibility of reproducing the precise conditions of the gulf war when carrying out experiments. Moreover it may be that the symptoms being experienced by the gulf war veterans result from a combination if not all of the causative factors described above. As research continues, it can only be hoped that a clear picture will develop of the nature of the gulf war syndrome so that potential therapies can be produced for the treatment of our suffering service men.

Gulf War syndrome - a real problem or a figment of a soldiers imagination?
Over the last six years, following the gulf war, a number of misterious conditions have appeared in a large number of the veterans who served in the gulf. Since then an intense debate has arisen over the seriousness of the problem and, perhaps more importantly, the exact cause of the problem. Are the gulf war veterans suffering reactions to toxic exposure or are they suffering from some form of war 'stress'? Scientists worldwide have been trying to answer this very question ...

At the beginning of 1994, an advisory panel to the US National Institutes of Health (NIH) recommended that a health survey be carried out on the 700,000 veterans who served in the gulf war. In addition the NIH stated that the extensive variety of symptoms described by a number of gulf war veterans were not indicative of a single medical syndrome. These symptoms included skin rashes, headaches, loss of memory and extreme hypersesitivity to common everyday products. Many veterans had had extreme problems in finding employment but were unable to qualify for any form of disability benefits in 1994 because of the absence of a precise definition for Gulf War syndrome. In order to solve this problem, Major General Ronald Blanck, of the Walter Reed Army Medical Centre in Washington called for a complete definition of the Gulf War syndrome to be drawn up.

Whilst the NIH rejected any claim of a single syndrome, it admitted that gulf war veterans were suffering real pain. John Spengler of the Harvard School of Public Health complained of the absence of any health records for the 700,000 veterans who served in the gulf. In May of 1994, over three years after the end of the gulf war, the Department of Veteran's Affairs was reported to stock complete health records for only 20,000 of the gulf war service men and women.

In January of 1995 the US Institute of Medicine (IOM) made a statement condeming research into the Gulf War syndrome as badly designed and poorely coordinated. More specifically, the IOM crtiticised the methods used for data collection with experiments apparently lacking proper controls. According to the IOM, the lack of coordination between the two main government departments involved in Gulf War syndrome research, the Departments of Defense Veterans' Affairs and Health and Human Services, had seriously affected the quality of research into the Gulf War syndrome.

Consequently, the IOM called for American Vice-President, Al Gore, to chair a meeting between these two government departments and leading American epidemiologists to improve coordination between different research groups.

Chickens lead the way in Gulf War syndrome research
In April of 1996 the US Department of Defence announced that an 80 million dollar study had failed to identify a specific disease that could account for the variety of symptoms observed in gulf war soldiers. However, a private study headed by Mohammed Abdou-Donia of Duke University and Robert Haley of the Texas Southwestern Medical School, had shown a rather different picture. A series of experiments carried out on chickens and hens showed that a combination of some of the drugs used by gulf war veterans caused damage to the central nervous system in these animals. Abdou-Donia claimed that some of the symptoms observed in the treated chickens and hens resembled those observed in veterans of the gulf war. The US Environmental Protection Agency stated that both chickens and hens were well suited for such a drug toxicity study since their nervous systems are highly sensitive to toxic damage.

The Abdou-Donia and Haley experiments centred around three chemical compounds - the two pesticides DEET and Permethrin which were used to protect soldiers against insect-transmitted diseases such as Malaria, and Pyridostigmine, an anti-nerve gas agent. Treatment of hens with any one of these compounds had no apparent effects on health. However, combinations of these three compounds resulted in animals that were extremely weak and unable to fly. In some cases a loss of weight was observed together with tremors and frequent stumbling. According to the researchers, the enzyme Butyrylcholinesterase which is present in the blood circulation is, under 'normal' conditions, able to break down the three compounds tested. However, under certain conditions, the pyridostigmine saturates the butyrylcholinesterase thereby preventing the breakdown of DEET and permethrin. Consequently the DEET and permethrin can pass into the brain unchecked to exert toxic effects.

Shortly after the US Defence Department's April announcement, Doctor Critchley at the Department of Neurology at the Royal Preston Hospital in the UK, mentioned similarities between symptoms observed in the Gulf War syndrome and those observed in the 1989 Botulism outbreak in the UK. In a letter to the medical journal The Lancet, Critchley pointed out that tablets containing botulinum toxoid had been administered to gulf war veterans. Moreover Critchley added that a number of unexplained symptoms had been experienced by Botulism patients following the acute phase of the disease which affected both physical and mental health.

Assessing levels of drug exposure during the Gulf war - Is Pyridostigmine Bromide the 'guilty' drug?
One major problem in assessing the levels of exposure to certain drugs during the gulf war is that the recommended levels of drug intake were often lower than the actual levels of intake by soldiers. This was particularly true for the drug pyridostigmine bromide (PB), a nerve gas protection drug which, according to Irving Cohen at the Veteran's Administration Medical Centre in Topeka, Kansas, was taken every day by some gulf war soldiers.

PB and nerve gas have the same mode of action binding and inactivating the enzyme acetylcholinesterase. Such inactivation leads to the accumulation of acetylcholine which causes an overstimulation of the muscles. In the case of nerve gas, such muscle overstimulation leads to death since the binding of nerve gas to acetylcholinesterase is irreversible. By administering PB to gulf war soldiers, the effects of nerve gas can be avoided since nerve gas cannot bind to acetylcholinesterase that is already bound to PB.

The US department of Defence defended its use of PB during the gulf war stating that it had previously been used for the treatment of patients suffering from the neurological disorder, Myasthenia Gravis without any side effects. However, the gulf war environment had possibly presented a 'stress' in the body causing physiological side effects which were not normally experienced under non-stressful conditions. The NIH panel also concluded that two other factors, post-traumatic stress syndrome and the parasitic disease, Leishmaniasis, could be contributing to some of the post war symptoms. The possible exposure to biological and chemical weapons was also not ruled out by the NIH panel following a report by the Czech government that soldiers had been exposed to biological and chemical warfare.

A possible genetic cause for some of the Gulf War symptoms?
In October of 1995 Loewenstein-Lichtenstein and his colleagues from the Hebrew University in Jerusalem, Israel, reported on an individual who had undergone treatment with pyridostigmine during the gulf war and had suffered neurological problems. Further studies showed that the individual was homozygous for a Butyrylcholinesterase mutation thereby rendering the Butyrylcholinesterase inactive. Since the Butyrylcholinesterase is responsible for 'mopping up' the effects of Acetylcholinesterase inhibitors such as pyridostigmine, these Butyrylcholinesterase mutations could lead to adverse effects in soldiers exposed to pyridostigmine during the gulf war. This study is therefore a clear indication that soldiers who served in the gulf war could have been geneticallty predisposed to adverse effects from the treatment of pyridostigmine.

Marcello Lotti and Angelo Moretto at the Universita degli studi di Padova in Italy have criticised this study saying that the levels of pyridostigmine administered to the gulf war soldiers were too low for mutations in the Butyrylcholinesterase to really have adverse effects on the soldiers.

The effects of Gulf war 'stress'
In a paper to Nature Medicine, Alan Friedman and his colleagues in Israel have shown evidence that, under stress conditions, the effects of pyridostigmine on the Central Nervous System and the brain is enhanced. Thus whilst in peace time the pyridostigmine may not have detrimental effects, the stressful conditions of the gulf war may have increased the toxicity of pyridostigmine in Gulf War soldiers.

The British investigation into the gulf war syndrome targets reproductive health
In December of 1996, almost two years after the US had started studying the symptoms of gulf war syndrome in gulf war veterans, the British Ministry of Defence (MOD) announced the start of a similar study in the UK. The MOD allocated a total of 1.32 million pounds for these two studies which initially involved comparing 3000 gulf war veterans with 3000 service men and women who had not served in the gulf. The second study, led by Patricia Doyle at the London school of Hygiene and Tropical Medicine, was set up to investigate the reproductive health of service personnel and their children. The results of both of these studies will be published at the end of 1999. If the results indicate a link between the reported symptoms of ill health and service in the gulf war, it will be necessary to establish the precise causes of these symptoms.

A number of potential causes of ill health have already been suggested including the use of delousing powder in Iraqi prisoners, protective treatments against biological and chemical weapons, smoke from burning oil refineries and the use of chemical and biological weapons themselves.

The MoD's announcement came as Nicholas Soames the ex-mimister of the British Armed Forces told the house of Commons that he had been badly informed on the use of organophosphate insecticides during the gulf war. These were used by gulf war service personnel to protect against a number of insect-transmitted dieseases. Soames admitted that such insecticides had been widely used in contrast to previous government reports that their use was minimal.

American presidential panel heavily criticized for wrong conclusions on chemical exposure
In January of 1997, an American presidential panel made an announcement stating that the adverse symptoms being described by gulf war veterans was not due to any environmental exposure during the war. Whilst the presidential report criticized what it called 'a laxity' in the studies of the Gulf War syndrome, it also stated that no link could be drawn between a particular environmental exposure in the gulf and the variety of medical symptoms experienced by gulf war veterans. The panel also came to the conclusion that some form of 'war stress' was responsible.

JAMA contradicts presidential panel
Immediately following the presidential panel's announcement, the editor of the Journal of the American Medical Association (JAMA) responded by revealing that three articles would be published that indicated the exact opposite. The gulf war controversy had yet again been thrown up into the air.

These articles referred to three separate conditions which, according to one of the authors, Robert Haley, help to explain the symptoms being experienced by gulf war veterans. The first of these conditions, referred to as Impaired Cognition Syndrome, had possibly been caused by collars containing the pesticide Chloropyrifos which had been worn by some of the gulf war soldiers. Symptoms of Impaired Cogniton Syndrome include severe memory problems, depression and insomnia. The second of these conditions, referred to as Confused-Ataxia Syndrome, had possibly been caused by chemical weapons and carried the symptoms of reasoning difficulties and balancing problems. Finally Arthro-myo-neuropathy occurred most frequently in soldiers exposed to insect repellent containing the chemical DEET and produced severe muscular weaknesses.

A member of the presidential panel, Phillip Landrigan, heavily criticised these articles saying that the researchers had used a very small number of soldiers in their studies adding that the results were not statistically representative of overall health problems experienced by veterans of the gulf war.

The American Society of Neuroscience sheds new light on possible causes of Gulf War Syndrome
In October of 1997, the 27th annual meeting of the American Society of Neuroscience revealed new findings in the study of potential causes of Gulf War syndrome. Neuropharmacologists Jerry Buccafesco, Mark Prendergast and Alvin Terry, at the Medical College of Georgia and the Veterans Administration Medical Centre in Augusta discussed results obtained using organophoshpates on an animal model of Gulf War syndrome. More specifically, it was shown that in rats exposed to organophosphates, there was a reduction in the level of Acetycholine receptors in the hippocampus region of the brain. These rats showed subsequent learning defficiencies which lasted for prolonged periods of time even after organophosphate exposure had stopped.

The first indications of organophosphate mediated effects on the brain came in the 1960s when farmers and agricultural workers reported cognitive problems after low level exposure to organophosphates. Subsequent studies did not give any indication as to the long term effects of such exposure. Therefore the results of Buccafesco's, Prednergast's and Terry's work gave the first indication of the long term effect on the brain of organophosphate exposure. The tests carried out by Buccafesco's team involved injecting rats with the organophosphate DFP every day for two weeks. When these rats were placed in a Morris water maze, in which rats have to find a platform in a pool of water, the DFP-treated rats reportedly took up to 30% more time than untreated rats to find the platform. Moreover the cognitive defficiencies in DFP-treated rats continued for three weeks following the last treatment with DFP.

Biochemical studies on DFP-treated rats showed that DFP caused a decrease in Acetycholine receptor levels in the brain and that these decreases were responsible for the observed cognitive defficiency in the DFP-treated rats. However Buccafesco admitted that these results must be considered with caution since neither his nor other people's experiments had succeeded in reproducing the precise conditions experienced by soldiers during the gulf war.

A British double vaccine treatment comes under fire
In November of 1997, the UK MoD admitted that it had not seriously considered warnings concerning the potential side effects of multiple vaccinations to the British service personnel in the gulf war. More specifically, the pertussis vaccine (whooping cough) had been administered to gulf war soldiers so as to 'speed up' the effects of a subsequent anthrax vaccine treatment. Such a pertussis vaccine pretreatment reduces the time for the anthrax vaccine to take effect from 32 weeks to 7 weeks. This double vaccine treatment was therefore ideal for quickly preparing soldiers before going out to the gulf. However, the MoD had received warnings from the National Institute for Biological Standards and Control (NIBSC) that such combined vaccine treatments could have severe health implications. The MoD had apparently ignored these warnings.

So what conclusions can be drawn from the research results over the last six years ? Clearly the scientific community is in conflict over the precise nature of the gulf war syndrome and whether it can really be termed as a single syndrome. One of the severe problems in understanding the precise nature of the symptoms being suffered by gulf war veterans is obviously the impossibility of reproducing the precise conditions of the gulf war when carrying out experiments. Moreover it may be that the symptoms being experienced by the gulf war veterans result from a combination if not all of the causative factors described above. As research continues, it can only be hoped that a clear picture will develop of the nature of the gulf war syndrome so that potential therapies can be produced for the treatment of our suffering service men.

© 1998 Roberto Deyes. Printed with Permission.
The Mad Scientist Network
Washington University School of Medicine
St. Louis, Missouri, USA

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