Young Soldier Dies Weeks After Receiving Mandatory Vaccinations 5-3-03

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Young Soldier Dies Weeks After Receiving Mandatory Vaccinations 5/3/03

Dr. ph Mercola

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Young Soldier Dies Weeks After Receiving Mandatory

Vaccinations

A 22-year-old soldier died of a mysterious illness after

receiving several mandatory vaccinations, including anthrax and smallpox.

According to the girl’s father, doctors thought she had a cold

or a minor reaction to inoculations, but then her condition worsened and she

didn’t respond to treatment for pneumonia.

Two days before her death, she could not breathe unaided and

had an extremely high fever, weakness, headaches and nausea.

Although an Army spokesperson said there was no indication

that vaccines were involved in the girl’s death, her father was told that she

might have had the immune disorder lupus, which could have been caused by the

smallpox vaccination. The true cause of death will not be known until an autopsy

is performed.

Chicago Sun Times April 11, 2003

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DR. MERCOLA'S COMMENT:

As Dr. Tenpenny said last month:

Because the civilian casualties of the vaccination program

ranged in age from 43 to 55 years and all patients had some form of cardiac

problem in their medical histories--including hypertension and angina--the oft

repeated vaccination industry mantra, “temporal association does not prove

causality,” is once again being used to diminish the link between the smallpox

vaccine and the deaths it has caused. Why is it that a vaccine is never the

cause of a health problem?

What is truly sad is that these deaths never should have

happened, and not just because the vaccination is unnecessary. If the CDC were

to do its homework, it would discover that the connection between the smallpox

vaccine and death from cardiovascular disease is not conjecture. Nor is it

something that needs “further study.” The mechanism of action has already been

proven.

The smallpox vaccine is capable of causing death because it is

a live virus vaccine that induces a physiological state in the body called

“hypercoagulability.”

A “hypercoagulable state” is a condition in which a person has

an increased potential to develop a thrombosis, commonly known as a blood clot.

There are many causes of hypercoagulability, ranging from rare genetic

conditions and a variety of blood disorders, to surgical interventions, birth

control pills and cancer.

In addition, there is a long list of cardiovascular diseases,

including valvular defects, bypass surgery and hypertension, that can lead to

hypercoagulability.[1]

The physiology of the hypercoagulable state is complex. The

cascade of events begins when an irregularity develops on the endothelial wall,

or inside lining of a blood vessel. As the blood flows past this turbulent

surface, platelet cells are disrupted, causing the release of thrombin.

Thrombin is an enzyme that converts fibrinogen into molecules

called soluble fibrin monomers (SFM), generally referred to as fibrin. Strands

of this “sticky,” insoluble protein form a mesh that collects the other types of

blood cells involved in the formation of blood clots and scars.

However, the release of fibrin doesn’t necessarily result in

the formation of blood clots. As the body depletes its supply of circulating

fibrinogen to create fibrin, more and more fibrinogen is released into the

circulatory system. The combination of the additional fibrinogen and free,

non-polymerized fibrin fragments increases blood viscosity, meaning the blood

becomes “thicker and stickier.”

Over time, the excess “sticky” fibrin adheres to the walls of

capillaries in the microcirculation, resulting in narrowed blood vessels.

Tissues become compromised as oxygen and nutrients are blocked from entering the

cells. In the heart, this leads to ischemic heart disease and heart attacks. In

the brain, it can lead to strokes.

Cardiologists understand the phenomenon of hypercoagulability

and routinely recommend an aspirin a day and other drugs to “thin the blood.”

However, these medications are only treating the symptom and do nothing to

address what is causing the hypercoagulation in the first place.

Pathogens that can activate the fibrin-forming cascade include

a long list of bacteria, fungi, mycoplasma and viruses. Because these pathogens

are primarily anaerobes, they thrive in cells that are deprived of oxygen.

Fibrin-narrowed vessels deliver less oxygen, allowing the pathogens to become

embedded in tissue and to propagate at the local level, creating tiny tissue

“abscesses” that fester and cause inflammation.[2]

This process is thought to be one of the causes of the muscle

aches seen in fibromyalgia, and why aerobic exercise seems to decrease pain.[3]

In addition, viruses create a self-perpetuating

hypercoagulable state by adhering to the blood vessel wall. When this occurs,

fibrin covers the virus to isolate it from the rest of the body. The result is

the formation of additional “bumps” on the inside of the blood vessels,

increasing the blood flow turbulence and continuing the

thrombin-fibrin-deposition cycle. [4]

The primary blame for narrowed blood vessels and clot

formation is placed on elevated cholesterol levels.

But it is the adherence of microbes to the endothelial lining

of the blood vessels and subsequent fibrin deposition that is the underlying

mechanism of action for cardiovascular disease.[5] In a word: heart disease is

an infection.

In fact, a recent edition of Critical Care Medicine describes

in detail the number of different types of viruses that can cause

hypercoagulability:

“Direct interaction between microorganisms and endothelial

cells can also occur, especially in the case of viral infections. Endothelial

cell perturbation [disturbance] is a common feature of viral infection and can

alter hemostasis in both a direct and indirect manner. Endothelial cells can be

directly infected by a number of viruses (e.g., herpes simplex virus,

adenovirus, parainfluenzavirus, poliovirus, echovirus, measles virus, mumps

virus, cytomegalovirus, human T-cell lymphoma virus type I, and HIV. In

particular, viral infection of endothelial cells has been demonstrated in

hemorrhagic fevers (e.g., Dengue virus, Marburg virus, Ebola virus, Hantaan

virus, and Lassa virus).”[6]

Even though vaccinia, the virus that is the active component

of the smallpox vaccine, is not specifically mentioned in this list, it should

be. The link between vaccinia and hypercoagulability is the reason why

cardiologists admit that the connection between the vaccine and cardiovascular

side effects is “biologically plausible.”

Smallpox vaccination causes a low-grade infection and

initiates the hypercoagulability cascade.[7] Researchers have documented that a

similar type of hypercoagulability is induced by the anthrax vaccine.[8]

It took many years for conventional medicine to identify the

bacteria, H.pyoli as the culprit in gastric ulcer disease. I wonder how many

years it will be before viral infections are routinely considered the cause of

cardiovascular disease.

Even if conclusive evidence existed that viruses were

responsible, the lack of a pharmaceutical answer to the problem would diminish

their role. Some investigators have been studying the connection between

Chlamydia and cardiovascular disease, but this hypothesis is being discarded.

In fact, a very recent study concluded that treating two

groups of patients with the antibiotic azithromycin (Zithromax) for two weeks

and three months respectively had “no effect” on the brachial artery response to

nitroglycerin.[9] It is difficult to imagine how an antibiotic could affect a

microbe buried beneath a layer of fibrin.

The CDC is deeply disturbed over highly publicized anxiety

surrounding the smallpox vaccine. Once the complications from this vaccine are

exposed, we are only one, small precarious step away from questioning the

unspoken impact that all vaccines have on health.

After all, the vast majority of vaccines are viral

vaccines--including measles, mumps, rubella, chicken pox and oral polio. Even

more, they are “live virus” vaccines, just like the smallpox vaccine.

It is my personal opinion that the impact of the viral load

caused by vaccines has been overwhelmingly underestimated and is creating

hypercoagulability problems in people of all ages. The virus-hypercoagulability

connection will eventually prove to be the “missing link” in connecting a myriad

of health problems to our one-size-fits-all mass vaccination policies.

It is good that the CDC is taking a cautionary stance

regarding the smallpox vaccine and those with a history of cardiovascular

disease. Many others have already been medically exempted from the vaccine.

It is estimated that at least 10 percent, or more than 28

million people in the United States, have eczema.[10] There are 184,000 organ

recipients,[11] 850,000 individuals with diagnosed and undiagnosed HIV infection

or AIDS,[12] and 8.5 million people with cancer.[13] The presence of these

health conditions constitutes a reason for avoiding the vaccine.

An even more extensive list of people at risk is the untold

millions who are taking immunosuppressive drugs such as corticosteroids.

Prednisone and Medrol, given to both adults and children, are prescribed for

dozens of conditions including but not limited to: asthma, emphysema, allergies,

Crohn's disease, multiple sclerosis, herniated spinal discs, acute muscular pain

syndromes, and all types of rheumatoid arthritis and autoimmune diseases. All of

these patients would be at risk for serious complications from contact with a

smallpox vaccinated individual.

And now those with a history of cardiovascular disease are

being excluded from receiving the smallpox vaccine. Nearly 61 million Americans

(almost one-fourth of the population) live with cardiovascular disease, and

coronary heart disease is a leading cause of premature, permanent disability in

the U.S. workforce.[14]

When adding up the number of Americans who should not receive

this vaccine, it comes to more than 98.5 million people. Who is left? Perhaps

the rush to spend $780 million to develop this vaccine will turn out to be the

industry’s ultimate boondoggle.

(Sherri J. Tenpenny, D.O. is a nationally renowned and

respected vaccine expert. In August 2002, I hosted a timely and important

teleconference featuring Dr. Tenpenny to discuss the real dangers of vaccines

and how you can legally avoid them. " The Danger of Vaccines, and How You Can

Legally Avoid Them " audio tape, a professionally recorded 90-minute cassette

available in my " Recommended Products " section, presents that full conference.)

Related Articles:

Everything You Ever Wanted to Know About Smallpox

Bioterrorism

Smallpox Myths, Revisited

Safe Minds’ Assessment of the Thimerosal-Containing Vaccine

Study

When Your Doctor is Wrong: Hepatitis B Vaccine & Autism

--------------------------------------------------------------

References:

[1] Whiteman, T. Hypercoagulable States. Hematol. Oncol.

Clin. North Am. - 01-Apr-2000; 14(2): 355-77

[2] Marshall, C. MD, FRCSC. Inflammation, coagulopathy

and the pathogenesis of multiple organ dysfunction syndrome. Crit Care Med. Vol.

29; No. 7. July, 2001

[3] Berg, . Berg D, Berg LH, Couvaras J, on H.

Chronic fatigue syndrome & /or fibromyalgia as a variation of antiphospholipid

antibody syndrome (APS): An explanatory model and approach to laboratory

diagnosis. Blood Coagulation and Fibrinolysis 1999: 10 435-438.

[4]Arid, C., MD Endothelial cell dynamics and

complexity theory. Crit Care Med

Vol. 30; No.5; May, 2002

[5] Friedman, H.M. Virus infection of endothelial cells. J

Infect Dis. February 1, 1981; 143(2): 266-73

[6] Marcel Levi, MD. Endothelium: Interface between

coagulation and inflammation. Crit Care Med. Vol. 30, No. 5. May, 2002.

[7] http:// query.nytimes.com/ search/ restricted/ article?

res= F30B17FE3D5 D0C7B8EDDAA0 894DB404482

[8] Hannan KL. et al. Activation of the coagulation system

in Gulf War Illness: a potential pathophysiologic link with chronic fatigue

syndrome. Blood Coagulation and Fibrinolysis, 11(7);2000:673-678.

[9] T. Kuvin, MD et al. Effect of short-term

antibiotic treatment on chlamydia pneumoniae and peripheral endothelial

function. The American Journal of Cardiology. Vol. 91; No. 6 • March 15, 2003

[10] Diepgen TL. Is the prevalence of atopic dermatitis

increasing? In: HC, ed. Atopic Dermatitis: The Epidemiology, Causes and

Prevention of Atopic Eczema. New York: Cambridge Univ Pr; 2000:96-112.

[11] United Network for Organ Sharing (UNOS). All

Recipients: Age at Time of Transplant. www.unos.org

[12] Joint United Nations Programme on HIV/AIDS.

Epidemiological Fact Sheets on HIV and Sexually Transmitted Infections: United

States. http:// www.unaids.org/ fact_sheets/ index.html

[13] National Cancer Institute. CanQues. http://

srab.cancer.gov/ Prevalence/ canques.html

[14] CDC. Preventing Heart Disease and Stroke: Addressing

the Nation’s Leading Killers http:// www.cdc.gov/ nccdphp/ aag/ aag_cvd.htm

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