Capt Brad Fry USMM Med Ret

Discussion in 'Fibromyalgia Main Forum' started by Capt Brad Fry, Sep 15, 2014.

  1. Capt Brad Fry

    Capt Brad Fry Member

    I was born in 1957 in Norfolk Naval Hospital. For the first 12 years of my life I lived in or next to military bases that are all now EPA superfund sites which were part of the original Malaria Control in Wartime Areas act the predecessor to the CDC. One of the first directors came from the miskokee syphilis project and you know how caring those men were. These bases were first sprayed for vector control in about 1943. In 1972 I got mono and in 1974 Capt Inman Director of internal medicine at Balboa Naval hospital diagnosed me with immune suppression after problems with EBV. I then moved to Moffett Field NAS which is now an EPA superfund site. I enlisted in spring of 75. While serving at Moffett it was made known that the drinking water was contaminated with tetrachloromethylene which was pumped into deep wells by Lockeed Martin across the east fence. I had further exposures to Turco, an aircraft degreasing solution and type Two Otto fuel for torpedoes. I had lifelong lengthy periods of undiagnosed ME my entire life with no help except for family. My DDE level is 1 ppb. If this is looked at in a half life regression it could have meant DDT levels as high as 128 ppb and in ASTRA I found one report in over 150 that stated human immune suppression started at 27ppb. I was given the Oral Polio vaccine contaminated with Simian Virus and all the first generation vaccines for overseas deployments in 1963 thru to the first generation swine flu vaccine in 1976 in Misawa Japan. In 1993 after failing multiple attempts at local Colleges and the University of Hawaii and having worked as a Trauma Tech and completing three semesters of nursing rotations for clinical I had recuperated once again and embarked on a less stressful Merchant Marine career. In 1998 I received all the vaccines for employment in central America. Including the hep B vaccine and all others and was taking oral anti malarials. It started again. In 1999 I was experiencing arthralgias of the R knee Hip and spine worse than ever. Had plica removed(10 week gestational failure of mesenchymal remodeling of three chambers into one chamber) and begged Dr Allari at Santa Cruz Medical center for help. I had developed ataxia, worsening balance problems etc. He tested me for syphilis and of course I went away. On 9/11 I volunteered to serve with the Merchant Marine Expeditionary forces for Enduring Freedom and Iraqi Freedom. I worked 80 hours a week and once more received all the vaccines required for service. It was common to work 30 hrs straight. I came home and got no support from the local medical community in Medford/Grants Pass Oregon. I was handed off to the VA clinics close by and diagnosed with PTSD and told that all my pain was due to that. Dr Tomlinsen sent me to an outside physician and she diagnosed ME in 2004. I continued at the VA and was encouraged to take more psyc meds which I refused except for Wellbutrin. I continued with the most horrible symptoms including migrains with projectile vomiting and explosively high BP, IBS, neuropathies, arthralgia etc. I then found and read Myalgic Encephalomyelitis/Chronic Fatique Syndrome: clinical Working case Definition. I realized that Rnase L was the test to start with and that Montoya at Stanford had a protocol for antivirals. But the VA refused to help. My wife found the greatest and kindest Doctor named Robin Miller and she did the test and collaborated with Montoya. I started on Valtrex because I couldn't afford valcyte. I then found VC Lombardi and got into his study and started sending biopsies and blood. My th1/2 profile was done and I had TNF at ten times the normal mean and Il 8 at 8 times the mean. Il4 was lower and Il 10 was higher as in MS which my brother has. Other inflammatory markers were almost as high. Through out this I continued reading pier review at NCBI and obtained an API number for OMIM. I know that human monocytes produce decreased levels of Il 2 and therefore lower levels of Bcl 2 and decreased molecular weight 80 Rnase L under the exposure to DDT. I also know that you need to recognize the other DDT which is Dichrome Tauteramase, an analog to Macrophage colonizing factor. The NFkB is very important because there are two down stream outcomes. IFN 1 and the inflammatory cytokines or all other IFNs and no inflammatory cytokines. This is important because Interferon "W" will sleep the HERVs in the W group. Remember Lombardi and Montoyas paper that found Dentritic cells in the gut produced HERVs in an aberrant presentation by those Dentritic cells of very common bacteria that burrow into the interstitial spaces between mucosa and muscle. It has been recognized that this same thing happens in most nuero immune diseases as autoimmune dysfunction. So are the HERVs making us sick. Read another paper that found HERVs of a different code in healthy controls. Do the HERVs play a role in immunity to helpful bacteria as a marker when Th1 shifts permenantly to Th2? Even more data coming on OMIM on TLR 7/9 and don't forget heat shock protiens. So the protein complex uphill from NFkB possibly could be affected by antibodies to one of the protiens such as Myd 88, HS 60, Bcl 2, to be titrated to effect NFkB to produce only the interferons other than IFN1. But would the inactive unfolded protein be reabsorbed or get stuck in the kidneys? Such amazing science going on. The last big study that used all frozen older preserved specimens didn't show much in the way of elevations of inflammatory markers. Were the protocols in question? All I know is that Rnase L differentiates fibro from ME. My C reactive protein is higher than normal but not so high. My sed rates are 0. And in the past my Total protein has been high, an indication of hyperviscosity. Are my red blood cells slightly inflamed? Does the hypocirculation result from inflammation of cells themselves showing no interstitial inflammation? My Cyp 450 profiles show many polymorphisms for methylation and SOD, etc. I know DDT has 7 metabolites and all but one are estrogenic or antigenic but only one is neutral. I know I cant properly metabolize many medications or compounds. If DDT increases apoptosis and decreases Rnase L and as with resistant mosquetoes changes expression of VEGF and mitigates lysis as an alternative to apoptosis then there is the cellular inflammation as cells swell to dilute toxins in the absence of Rnase L. If your body is aware of every cell and the cells are dying then you don't need programmed cell death at a very high rate or you will run out of cells. If ME is a demyelination of a cell layer which is the basal layer and is to thin to see on MRIs it makes sense, just like the 10 week plicas of our other joints including the intervertebral joints. If fetal mesenchymal cell dysfuntion cuases the demylanation of the continuouse basal layers of the brain stem etc.If you remember that the viruses that love us mostly affect epithelium and endothelium and that the intermembranous Krebs cycle only produces two ATP and one AMP is lost thru this dysfunction then of course the channelopathys are caused by pump dysfuntion at any active site. Anyway G-d Bless you all and this is what I think and It cant be proven that DDT and other toxins are in part to blame because its a crime to do it to any one especially a fetus. One the other hand you cant disprove it either. This is the biggest liability our government has ever faced. There are 25 million people suffering from one form of neuroimmune disease or another to varying degres. I need to find other people like me. Born in military hospitals and spending 18 years as a dependent and then 4 or more years active duty then returning after 9/11. Please cant you help me do this. Capt Brad Fry
  2. Mikie

    Mikie Moderator

    Dear Capt. Fry,

    Could you please edit your post and insert some paragraph breaks. Many of us, like me, cannot read long posts without breaks. I would hate for people to miss your post simply due to lack of breaks. Thanks.

    Love, Mikie