And Jesus answered and said to them, “See to it that no one deceives you” (Matthew 24:4)
As I shared in my book, Overcoming Lyme Disease, on March 7, 2013 during a Transvaginal Ultrasound and Doppler Limited Study, I was diaganosed with an intramaural fibroid, uterine prolapse, and adenomyosis. I was told eventially I would need surgery and ended up in the ER a few hours later and was diagnosed with Peripheral Edema (swelling of the legs). Needles to say, I ended up having surgery 12 days later. During surgery I was diagnosed with enterocele and surgery was performed to fix it. I was told my intestine had grown into my uterus.
“The cells of the uterine lining (endometrium) may grow, however, in an aggressisve fashion and invade the muscular portion of the uterus. This disorder is nonmalignant but is a serious and disabling disease called adenomysosis. THE REASON THIS OCCURS IS NOT KNOWN.”
Of course I never got better and was admitted into the hospital 12 days later and almost died from an infected abyscess hemotoma – unspecified! As my story goes, I kept going back to the doctor and saught other doctors as well to figure out why I am now so ill and why I can no longer function without pain.
During an ER run on May 15, 2013, even the dorctor on call said, and I quote, “She had a hysterectomy for fibroids and what sounds like adenomyosis and not endometriosis.”
Why would she say that, you may ask yourself? Well, during all my surgeries and my final surgery on November 4, 2013, my doctor kept calling it endometriosis?
The 4th and finaly surgery was to take out my now said bad ovaries because of NEW ovarian cysts that were growing rapidly on them, and not in them…my ovaries! Here is what the pathology report said:
BENIGN MUCINOUS CYSTOMA AND BENIGN MUCINOUS CYSTADENOMA.
Wait, I though the doctor said endometriosis? I guess he is uneducated?
NO ONE ever suggested that adenomyosis could be the cause of my legs swelling? I guess they were not educated?
Vascular endothelial growth factor gene polymorphisms are associated with the risk of developing adenomyosis https://onlinelibrary.wiley.com/doi/abs/10.1002/em.20455
No one warned me! “Conclusions Women with adenomyosis are at higher risks of endometrial and thyroid cancers, while women with endometriosis are at higher risks of endometrial and ovarian cancers.” https://www.sciencedirect.com/science/article/abs/pii/S1092913406001043
“Endometrial cancer arising from uterine adenomyosis may be difficult to diagnose. Awareness of this entity and careful ultrasonography are likely to reduce diagnostic delay.” http://www.irog.net/download/?magazine=83#page=67
“Adenomyosis appears to be associated with less aggressive tumor behavior of endometrial cancer, suggesting that it may have inhibitory effects on the progression of this disease.” https://link.springer.com/article/10.1245/s10434-014-3880-6
As my story goes, I went to doctor after doctor! I had breast, bone, and thryoid cancer scares and I finally understand why…adenomyosis causes Cancer or something similar? I was never diagnosed with thyroid issues from a medical doctor nor was on thryoid medications until after all of my surgeries…how bizarre…and..during another ER run..I was diagnosed with hypothyroidism, on June 8, 2014. (I documented all of my doctor visists and ER runs in my book, Overcoming Lyme Disease, if you want to see all the diagnoses I was given.)
As you can see, I have something attacking my thyroid!
So, if they don’t know about this disease, how are they going to treat it? More importantly, how many people are suffering and are not getting help?
I wrote about the Nagalase enzymes in my book, chapter 9, and how these enzymes are being put in needles which helps cause autism! Well, I guess that nagalase enzymes are not just causing autism… they can cause cancer as well. Why didn’t any of my doctors ask to run this simple test to help validate a pathogen attacking me?
Wait, I know why….I was also diagnosed with Lyme disease! I suggested to run a Lyme test after my holisitc doctor, Richard Easterling, said so. The non accurate Lyme test that I talk about in my book gave me 2 positive ELISA tests, so I was put on 2 weeks of antibiotics. The very last day of my antibiotic I started to throw up non stop for 9 days straight! I ended up at U of M ER while I was still waiting for Western Blot results. I was asked if anyone ever diagnosed me with COPD? I told them no, I was diagnosed with Lyme and I was needing to see if the antibiotics were working and that I needed a Western Blot test! I was informed that U of M does not diagnose nor treat Lyme disease in the ER, and as far as I am concerned, I was sent home to die! The next day my doctor office ordered the Western Blot test, but the labs in Michigan did not know how to run the test! It took about 20 minutes for the lab to figure out what test to acturally run! Of course the Western Blot came back negitive! (again, my story is in my book!)
So, I had an IGeneX test done after I was left for dead, and it came back IGeneX and CDC positive on IgM bands. Wait, my medical doctor said the Western Blot was negative? Hmmm…
I wonder why doctors are not warned about late stage Lyme disease? http://www.actionlyme.org/clinical-pathologic-correlations-of-lyme-disease-by-stage-Steere-Duray.pdf
Wait a minute, I grew up poor! Maybe I got this pathogen from my cheap high school physical, shortly after the Red Cross came to our school and took our blood? Here is the document!
Of course I did not remember this so it is not mentioned in my book!
What will you do with this information?
Proverbs 24:10-12
10If you faint in the day of adversity,
Your strength is small.
11Deliver those who are drawn toward death,
And hold back those stumbling to the slaughter.
12If you say, “Surely we did not know this,”
Does not He who weighs the hearts consider it?
He who keeps your soul, does He not know it?
And will He not render to each man according to his deeds?
May God bless you and keep you,
Jennifer Heath
New Evidence: Adenovirus 41 = spike,
Human adenovirus 41
: https://www.ncbi.nlm.nih.gov/protein/120153
Update:
TAXONOMY
https://www.ncbi.nlm.nih.gov/nuccore/?term=Lone+star+***
And, Googles Patent for Tracking: Methods of measuring human body frequencies or harmonics and treating conditions based on the resonance phenomenon between a product and a human body’s frequencies or harmonics:
https://patents.google.com/patent/WO2010039465A2/en
___
Breaking: Shit just hit the fan!
Almost 5 million adverse events reported by Pfizer’s own document: https://pharmafiles.substack.com/p/breaking-shit-just-hit-the-fan?r=fh3ja&utm_medium=ios&utm_campaign=post
___
Uterine Leiomyomata: https://www.ncbi.nlm.nih.gov/books/NBK546680/
‘Differential Diagnosis
Many other disease processes share the signs and symptoms of uterine leiomyomas, most of which are common etiologies of abnormal uterine bleeding (AUB) and pelvic pain. According to the Federation of Gynecology and Obstetrics (FIGO), the differential can be broken down into the classification system PALM-COEIN.[21][22] The mnemonic is grouped by structural and non-structural causes of AUB, which includes the following:
Polyps, adenomyosis, leiomyoma, malignancy, coagulopathy, ovulatory dysfunction, endometrial, iatrogenic, not yet classified.
Adenomyosis, in particular, has been shown to have a high rate of coexistence with uterine fibroids.[23] Unlike fibroids, adenomyosis tends to be more oval-shaped with indistinct margins on ultrasound. They do not typically display a mass effect.
It is essential to realize that leiomyosarcomas can present similar to leiomyomas. Brohl et al. concluded that sarcomas are diagnosed in presumed fibroids after surgery in 1 in 340 women. That number increases to 1 in 98 in women 75 to 79 years of age.[24] Although there is no reliable way to differentiate the two without biopsy, a few studies have identified factors that are associated with sarcoma which include but are not limited to postmenopausal status, a predominantly subserosal mass, solitary fibroid, rapid growth, and a T2-weighted signal heterogeneity on magnetic resonance imaging.[2][25]’
_____
Humoral Immunity to Borrelia burgdorferi N40 Decorin Binding
Proteins during Infection of Laboratory Mice: file:///C:/Users/abunc/Desktop/Humoral_Immunity_to_Borrelia_burgdorferi.pdf
SUNLIAN FENG,1 EMIR HODZIC,1 BRIAN STEVENSON,2
AND STEPHEN W. BARTHOLD1
*
Center for Comparative Medicine, Schools of Medicine and Veterinary Medicine, University of California, Davis,
California 95616,1
and Laboratory of Microbial Structure and Function, Rocky Mountain Laboratories,
National Institute of Allergy and Infectious Diseases, Hamilton, Montana 598402
Received 9 September 1997/Returned for modification 19 November 1997/Accepted 6 March 1998
A Borrelia burgdorferi N40 genomic expression library was screened with serum from actively infected mice
to identify gene products that elicit protective immunity. A clone that contained a putative bicistronic operon
containing two genes that encoded 20- and 22-kDa lipoproteins was identified and sequenced. These genes
showed homology with the genes encoding decorin binding proteins DbpB and DbpA, respectively, of B.
burgdorferi 297 and B31. N40-dbpA DNA hybridized with B. burgdorferi N40 DNA on a single 48-kb linear
plasmid. Homologous genes could be amplified under various degrees of stringency by PCR or hybridized by
Southern blotting from B. burgdorferi sensu stricto N40 and B31, and from B. burgdorferi sensu lato PBi and
25015, but not PKo. Recombinant N40-DbpB and N40-DbpA were reactive with antibody in serum from
infected mice, and serum was more reactive against N40-DbpA than against B. burgdorferi N40 recombinant
P39, OspC, or OspA. Sera from mice infected with B. burgdorferi sensu lato strains PKo and PBi were weakly
reactive against N40-DbpB and N40-DbpA, and sera from mice infected with 25015 were moderately reactive,
compared to sera from mice infected with B. burgdorferi N40. Hyperimmunization of mice with N40-DbpA, but
not N40-DbpB, induced protective immunity against syringe challenge with cultured B. burgdorferi N40. DbpA
may therefore be one of the antigens responsible for eliciting protective antibody known to exist in serum from
infected mice. DNA amplification and serology suggest that DbpB and DbpA are likely to have homologs
throughout the B. burgdorferi sensu lato family, but they are likely to be heterogeneous.
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