VA secretary denies cover-up of suicide rates
Veterans groups sue to improve department's procedures

By Jill Coley (Contact)
The Post and Courier
Tuesday, April 29, 2008



The Department of Veterans Affairs is facing accusations that it covered up veteran suicide rates. Two veterans groups are suing the VA claiming that veteran suicides are rising at alarming rates, in large part because of VA failures.

The groups — which the Los Angeles Times reported are Washington-based Veterans for Common Sense and Santa Barbara, Calif.-based Veterans United for Truth — want the VA ordered to improve application processing speed and delivery of mental health care.


The Post and Courier

Secretary of Veterans Affairs James B. Peake
Dr. James Peake, secretary of Veterans Affairs, visited Charleston on Monday to meet with officials from Ralph H. Johnson VA Medical Center and the Medical University of South Carolina.

"The notion we're not trying to get the truth out there is erroneous," Peake said.

The secretary told Congress in a Feb. 5 letter that 144 combat veterans of Iraq and Afghanistan committed suicide between October 2001 and December 2005.

But a lawyer representing the veterans' groups produced internal VA e-mails that contended 18 veterans a day were committing suicide. The e-mails were written by Dr. Ira Katz, the agency's mental health director.

Ronald Maris, a University of South Carolina sociology professor, testified last week in the trial, being held in San Francisco.

"Every time you do a study, you have different samples," Maris said in a phone interview. "Each study looks at different populations. Samples are often not complete."

"We make sure we're working off the same set of numbers," Peake said Monday. Maris and Peake are scheduled to testify May 6 before the U.S. House Committee on Veterans' Affairs.

Those numbers say veterans commit suicide at a rate that varies from 2 times that of the general population up to 7.5 times, Maris said. The bottom line, he said, is "Everybody agrees the veterans' rate is higher. What are we going to do about it?"

Maris takes issue with the VA's mental health screening. Veterans are asked two questions: whether they've felt hopeless or depressed in the last two weeks and whether they've thought of hurting themselves in the same time period.

If a person says no, the questions stop, Maris said. "That's a serious problem in my judgment," he said. Maris would prefer to see standardized paper and pencil tests with 15 to 20 questions. "We need to be concerned about the whole panorama of self-destructive behaviors."

Peake also met with Tom Mikolajcik, a retired Air Force general and former commander of Charleston Air Force Base. Mikolajcik was diagnosed with Lou Gehrig's disease about five years ago.

Mikolajcik urged Peake to grant all veterans with the disease, also called amyotrophic lateral sclerosis, a service-connected disability. Currently only Gulf War veterans are covered, Mikolajcik said. "My comrades in arms don't get the same benefits, and it's not fair," he said.

For unknown reasons, veterans have a 60 percent higher chance of developing ALS.

The retired general described the meeting as "very personable." "Now we just wait and pray," he said.


The Associated Press contributed to this report. Reach Jill Coley at jcoley@postandcourier.com or 937-5719.



http://www.charleston.net:80/news/20...cide_rat38941/

Findings on the Nature and Causes of Gulf War Syndrome
and Plans to Extend the Research

Testimony of

Robert W. Haley, M.D.

University of Texas Southwestern Medical Center Dallas, Texas

Before the Subcommittee on National Security,
Veterans Affairs and International Relations, Committee on Government Reform,
United States House of RepresentativesWashington, D.C.

January 24, 2002

I want to thank you for the opportunity to speak to you about the research on the nature and causes of Gulf War syndrome, conducted and coordinated by my group at the University of Texas Southwestern Medical Center in Dallas. Our research began in 1994 under initial funding support from the Perot Foundation of Dallas and has been continued under a 1997 cooperative agreement with the Office of the Secretary of Defense administered through Ft. Detrick. We are presently negotiating a new cooperative agreement for funding a new phase of our research.

Initial Findings

Our initial studies focused on 249 members of a Reserve Naval Mobile Construction Battalion, or Reserve Seabees. In that work, we made four important observations.

First, we found strong evidence of a single Gulf War illness with three variants.

Second, those with the illness have more abnormal brain function by objective tests than well veterans, suggesting a brain injury or illness.

Third, the sick veterans were 4 to 32 times more likely to report exposure to combinations of certain chemicals in the war, specifically sarin nerve gas, side effects from pyridostigmine, highly concentrated government-issue DEET insect repellant, and pesticides in flea collars.

And fourth, in collaboration with researchers at Duke and Kansas State universities and the EPA, we experimentally produced brain and nerve damage in hens with combinations of some of these same chemicals, not previously thought to be neurotoxic.

In January 1997 this work passed rigorous peer review and was published in three scientific papers, appearing back to back in the Journal of the American Medical Association. A research group in India led by K. Husain, has extended these findings by demonstrating neurological damage from low-level sarin nerve agent in two animal species. These findings are also supported by published papers demonstrating chronic neurologic damage in survivors of the sarin attack in the Tokyo subway.

Most Recent Findings

Later in 1997 we submitted a $16 million proposal to extend and replicate our initial findings in a national survey, but it was not funded by the government peer review system administered by the Persian Gulf Veterans Coordinating Board. Later the Joint Chiefs and the Secretary of Defense conducted a special peer review of the proposal and granted us partial funding of $3 million through a cooperative agreement to begin further testing and plan a national random-sample survey to replicate our findings. With that funding, we have published five additional important observations.

First, we identified the same syndrome structure in the symptoms of a new group of mostly Army veterans from north Texas area. This was the first study to use the preferred method of structural equation modeling to demonstrate the same syndrome present in a second veteran population.

Second, we identified a gene, the PON1 gene, that appears to have predisposed soldiers to getting the Gulf War syndrome and appears to link the illness with low-level sarin nerve gas exposure.

Third, we demonstrated the site of brain damage with a new brain scanning test called Magnetic Resonance Spectroscopy (MRS). This brain scanning technique detected a lower level of a brain chemical in the deep brain structures of ill Gulf War veterans than well controls, indicating brain cell damage or illness.

Fourth, we found abnormal increases in the brain hormone dopamine in those veterans with the worst brain damage measured by the MRS scans. This indicates that the brain cell damage documented by the MRS scans is causing physiologic dysfunction of those brain structures and thus is a medically meaningful finding.

Fifth, we found that veterans with Gulf War syndrome satisfying our case definition are substantially more physically impaired than prior research had showed. Using the SF-36 questionnaire, the most widely validated measure of physical functioning, we showed that subgroups of the ill veterans were more impaired than the average civilian patient with emphysema, recent heart attack or clinical depression. The prior Iowa survey, using the SF-36 questionnaire, suggested only mild impairment, but by combining the sick veterans and well veterans their average impairment level underestimated that of the sick veterans.

Our study using a case definition to separate out the sick veterans has corrected the misconception.

All of the above findings were published in prominent peer-reviewed medical journals.

Along the way, I published important commentaries in peer-reviewed journals showing a) that the government studies pointing to stress as the cause of Gulf War syndrome were based on statistical errors that invalidated them and b) that the government findings of no excess mortality, hospitalization or death in the Gulf War veteran population were flawed by systematic errors that, when corrected, let to just the opposite conclusions.

Limitations of the Research

To put our research findings into proper perspective, it is important to realize that we have framed a theory or hypothesis which could explain the nature and causes of the Gulf War syndrome, but this theory is not thoroughly proven. Since our studies were the first to blaze this trail toward evidence of a physical basis for Gulf War syndrome, they were relatively small and focused in a single battalion and therefore might not be representative of what is true in the larger Gulf War veterans population. On the other hand, past CDC investigations that solved hundreds of epidemic mystery diseases in the past have traditionally been very similar to our studies on Gulf War syndrome. Epidemic diseases have unique characteristics that make these studies useful.

Consequently, our theory is in need of extension by us and replication by other researchers working independently but using the same methods as we have used in deriving the theory.

At present we have replicated parts of our work in a new group of Gulf War veterans recruited through the Dallas VA Medical Center, and an independent researcher in another state has replicated our MRS brain scanning finding in a small group of sick and well Gulf War veterans, as described below. Several other studies have questioned our theory, but none has actually tested our findings using the same methods. Scientifically, a replication requires use of the same methods.

Replication of our Findings by Others

Researchers in the VA Central Office have analyzed symptoms of approximately 10,000 deployed and 10,000 nondeployed Gulf War-era military personnel and found the same three syndrome variants that we reported; they found their second syndrome variant to be "neurologic" in character, like ours, and to be a A unique Gulf War syndrome. They also found their second syndrome to be approximately 7 times more common in veterans giving a history of exposure to chemical nerve agent in the war than in those without such a history, replicating our finding almost exactly. They reported these key findings at a national research meeting in 1998 but have not published them in a medical journal.

A leading brain imaging research group at the University of California at San Francisco and the San Francisco VA Medical Center has performed our MR Spectroscopy brain scanning protocol on 11 ill Gulf War veterans and 11 controls from the San Francisco area and found the same degree of brain cell loss or injury in the right basal ganglia in the Gulf War syndrome patients (Proc. Intl. Soc. Mag. Reson. Med. 2000;9:994).

chemical weapons researcher (C. A. Broomfield) at the U.S. Army research laboratory at Ft. Detrick, MD, analyzed the serum samples from the Gulf War veterans and controls studied in our paraoxonase study. He found markedly low hydrolytic activity against sarin and soman in the blood of the Gulf War veterans with Gulf War syndromes and normal levels in the well control veterans, thus corroborating and extending our original finding (La Du et al. Drug Metabolism and Disposition 2001;29:566-569).

Leading enzyme researchers in the U.K. have measured plasma paraoxonase enzyme concentrations in a large cohort of ill British Gulf War veterans and well controls and found it to be substantially reduced in the ill group, as we found (Biochem Biophys Res Comm 2000;276:729).

Current Research Proposal

Last summer my research team submitted a new proposal to extend and replicate our work.

We asked for grant funds to establish an independent Gulf War Illness Research Center to do the studies necessary to advance the findings substantially. Initial amounts were included in the 2001 and 2002 Defense Appropriation to support this center, and we are currently in negotiations on funding from USAMRMC at Ft. Detrick. Briefly, we proposed to:

1. Perform a national survey in random samples of Gulf War-era deployed and non-deployed veterans to compare the prevalence of the illness we have identified. DoD has already invested $500,000 in planning this survey, and it is virtually ready to go. An independent survey firm will carry out the survey to ensure objectivity.

2. Upgrade to the latest brain imaging technology to explore deeper into the nature of the brain cell damage and attempt to develop a cost-effective diagnostic test that could be widely applied to make objective diagnoses.

3. Extend our genetic studies to learn more about the genetic predisposition to Gulf War syndrome and chronic illness from low-level chemical nerve agent and pesticide exposure.

4. Extend our new laboratory animal model of Gulf War syndrome by testing for chronic behavioral effects of low-level sarin alone and in combination with pesticides and pyridostigmine.

5. Re-study veterans from our prior studies to determine whether they are getting better or worse or remaining the same over time.

6. Identify and test promising treatments and preventive measures, including a gene therapy technology to protect against nerve agent exposure.

For this new work to be successful, it will be important to receive funding under terms in the cooperative agreement that will give us an appropriate degree of independence to follow our own instincts on research directions and to accomplish the work in a timely manner. In addition, we will need the cooperation of the Department of Defense in providing the computer list of Gulf War-era military personnel for us to draw our national random samples, computerized background information such as plume exposures needed to analyze the survey, and research dilute solutions of sarin for our laboratory animal experiments.

List of Publications in Peer-Reviewed Scientific Journals

PRIMARY RESEARCH PAPERS

1. Haley RW, Kurt TL, Hom J. Is there a Gulf War syndrome? Searching for syndromes by factor analysis of symptoms. Journal of the American Medical Association 1997;277:215-222.

2. Haley RW, Hom J, Roland PS, Bryan WW, Van Ness PC, Bonte FJ, Devous MD, Mathews D, Fleckenstein JL, Wians FH, Wolfe GI, Kurt TL. Evaluation of neurologic function in Gulf War veterans: a blinded case-control study. Journal of the American Medical Association 1997;277:223-230.

3. Haley RW, Kurt TL. Self-reported exposure to neurotoxic chemical combinations in the Gulf War: a cross-sectional epidemiologic study. Journal of the American Medical Association 1997;277:231-237.

4. Abou-Donia MB, Jensen KF, Oehme FW, Kurt TL. Neurotoxicity resulting from coexposure to pyridostigmine bromide, DEET, and permethrin: implications of Gulf War chemical exposures. Journal of Toxicology and Environmental Health 1996; 48:35-56.

5. Abou-Donia MB, Wilmarth KR, Abdel-Rahman AA, Jensen KF, Oehme FW, Kurt TL. Increased neurotoxicity following concurrent exposure to pyridostigmine bromide, DEET, and chlorpyrifos. Fundamental and Applied Toxicology 1996; 34:201-222.

6. Hom J, Haley RW, Kurt TL. Neuropsychological correlates of Gulf War syndrome. Archives of Clinical Neuropsychology 1997;12:531-544.

7. Haley RW, Billecke S, La Du BN. Association of low PON1 type Q (type A) arylesterase activity with neurologic symptom complexes in Gulf War veterans. Toxicology and Applied Pharmacology 1999; 157:227-233.

8. Roland PS, Haley RW,Yellin W, Owens K. Vestibular dysfunction in Gulf War syndrome. Otolaryngology--Head and Neck Surgery 2000;122:319-329.

9. Haley RW, Marshall WW, McDonald GG, Daugherty M, Petty F, Fleckenstein JL. Brain abnormalities in Gulf War syndrome: evaluation by 1H magnetic resonance spectroscopy. Radiology 2000;215:807-817.

10. Sinton CM, Fitch TE, Petty F, Haley RW. Stressful manipulations that elevate corticosterone reduce blood-brain barrier permeability to pyridostigmine in the rat. Toxicology and Applied Pharmacology 2000;165:99-105

11. Haley RW, Fleckenstein JL, Marshall WW, McDonald GG, Kramer GL, Petty F. Effect of basal ganglia injury on central dopamine activity in Gulf War syndrome. Archives of Neurology 2000;57:1280-1285.

12. La Du BN, Billecke S, Haley RW, Broomfield CA. Serum paraoxonase (PON1) isozymes: the quantitative analysis of isozymes affecting individual sensitivity to environmental chemicals. Drug Metabolism and Disposition. 2001; 29:566-569.

13. Cowan J, Sinton CM, Varley AW, Wians FH, Haley RW, Munford RS. Gene therapy to prevent organophosphate intoxication. Toxicology and Applied Pharmacology 2001;173:1-6.

14. Haley RW, Luk GE, Petty F. Use of structural equation modeling to test the construct validity of a case definition of Gulf War syndrome: invariance over developmental and validation samples, service branches and publicity. Psychiatry Research 2001 102:175-200.

15. Haley RW, Maddrey AM, Gershenfeld HK. Severely reduced functional status in veterans fitting a case definition of Gulf War syndrome. American Journal of Public Health 2002;
2:46-47.

16. Haley RW, Maddrey AM, Gershenfeld HK. Severely reduced functional status in veterans fitting a case definition of Gulf War syndrome. American Journal of Public Health 2002; 92:46-47.




REVIEW ARTICLES AND META-ANALYSES

17. Haley RW. Is Gulf War syndrome due to stress? The evidence reexamined. American Journal of Epidemiology 1997;146:693-703.

18. Haley RW. Point: Bias from the "healthy-warrior effect" and unequal follow-up in three government studies of health effects of the Gulf War. American Journal of Epidemiology 1998; 148:315-323. (With counterpoint replies by three government authors and a countercounterpoint rejoinder by Dr. Haley).

19. Kurt TL. Epidemiological association in US veterans between Gulf War illness and exposures to anticholinesterases. Toxicology Letters 1998;102:103:523:6.

20. Marshall WW, Haley RW. Use of a secure Internet Web site to collect data in collaborative medical research. Journal of the American Medical Association 2000;284:1843-1849.



SCIENTIFIC LETTERS

21. Haley RW, Kurt TL, Bryan WW, et al. The authors reply [Letter]. Journal of the American Medical Association 1997;277:385-386.

22. Haley RW. Is the Gulf War syndrome due to stress? The evidence reexamined, the author replies [Letter]. American Journal of Epidemiology 1998:148:405-406.

23. Haley RW. Re: Chronic multisystem illness in Gulf War veterans [Letter]. Journal of the American Medical Association 1999; 327:328-329.

24. Haley RW. The Gulf War syndrome controversy: Dr. Haley replies [Letter]. American Journal of Epidemiology 1999;150;216-7.

25. Haley RW. Re: Is there a Gulf War syndrome? [Letter] The Lancet 1999; 354:1645-6.

26. Haley RW. PON1 and low-Dose sarin in marmosets [Letter].
Journal of Psychopharmacology 2000;14:87-88. 27. Haley RW. Gulf War syndrome: another side of the debate [Letter]. Mayo Clinic Proceedings 2000; 75:1221-1222.

28. Haley RW. Re: A Factor analysis of self-reported symptoms: does it identify a Gulf War syndrome? [Letter]. American Journal of Epidemiology 2000; 152:1204-1206.

29. Haley RW. Will we solve the Gulf War syndrome puzzle by population surveys or clinical research? [Letter]. American Journal of Medicine 2000; 109:744-745.

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