The Role of an Infectious Disease(s) in the
InflammoThrombotic Immunologic Response (ITIR) Process - More than Just an Infection. Infections Can Produce Other Disease (ITIRD) Which Can Kill You!
Prior to the discovery of penicillin by Sir Alexander Fleming, PhD in 1928, the number 1 cause of death world wide was infectious disease.
​
Following that discovery and changes in how we lived and ate, a serious of chronic diseases would appear. These diseases are caused by outside influences acting upon our bodies resulting in an InflammoThrombotic Immunologic Response (ITIR) producing InflammoThrombotic Immunologic Response (ITIR) Diseases (ITIRD).
​
These ITIRDs include:
​
Heart Disease,
Cancer,
Diabetes Mellitus,
Obesity,
Hypertension - High Blood Pressure,
CVAs, RINDs & TIAs - Various duration strokes,
Autoimmune Disorders,
Et Cetera
​
​When I entered Medical College at the University of Iowa in 1981, the second statement made by our Dean surprised a number of students in our entering class.
​
He told us that "90% of what we would be taught would eventually turn out to be wrong." He continued to ask those of us with research experience to forgo the lucrative life of private practice and devote ourselves to research/academic medicine.
​
The following year in 1982, researchers Barry J Marshall and J Robin Warren discovered that gastritis, stomach and duodenal (first part of small intestine) ulcers were not the result of too much acid in the stomach; but rather, an ITIR to a bacteria that was present in the stomach of half of all people. A discovery which earned them the 2005 Nobel Prize in Physiology or Medicine.
​
In 1982-1983, we went from being taught about rare diseases like Kaposi's Sarcoma, to seeing it in our patients.
This once rare cancer of the skin and lymph nodes was now becoming common place as patients were presenting to our University Hospital - and elsewhere around the world - with a new infectious disease; human immunodeficiency virus (HIV). The virus, that would with other precipitating factors cause the ITIRD known as Acquired Immunodeficiency Syndrome (AIDS).
​
With this new virus would come the recognition that HIV contained the enzymatic genetic material - reverse transcriptase - to place its RNA into human DNA. An ability that resulted in HIV being able to evade the human immune system and in doing so, would result in multiple infections occurring within HIV infected patients.
​
These infections known as opportunistic infections (OIs) were made possible by HIV weakening our immune systems and they included Pneumocystis pneumonia (PCP), Cytomegalovirus (CMV), Tuberculosis (TB), Candidiasis, Toxoplasmosis, Herpes Simplex Virus 1 (HSV-1) and Salmonella.
While these infections were not unheard of, the prevalence and the combination of these infections altered our approach to medicine forever.
As a senior honor student doing research on hypertension and salt sensitivity, I also presented a symposium presentation on the new disease AIDS. The presentation, while an honor, was also a demonstration of how hard old ideas die.
The focus of my AIDS honors presentation was simple. AIDS and the transmission of HIV making AIDS possible would soon become a heterosexual, not merely a homosexual or IV drug abuse disease. I was told I did not know how to read research data and to come back in 10-years to be shown how ignorant I was in my proposal.
I did not return. I simply moved forward.
By 1994 following decades of research I presented what I then called the Fleming Unified Theory of Vascular Disease. My theory of what coronary artery disease (CAD) occurred was first presented at the 1994 American Heart Association Conference in Dallas, TX.
​
The first version of it is shown in the following hand drawn diagram.
By 1999, after several more presentations, the theory had become accepted by many as scientific fact and it was published the the Chang Textbook of Angiology.
​
While I have always contended that it removed some of the detail from my original drawing, I cannot disagree with the fact that it is undoubtedly easier to read.
During the release and publication of my theory, I continued working on correcting problems occurring during nuclear imaging.
​
As detailed here and [https://www.flemingmethod.com/], my efforts to quantify changes in isotope distribution and redistribution, resulted in the same types of criticisms I encountered with my HIV presentation, and while it took roughly the same amount of time to be proven right, the response has been the same - crickets by the critics who have attacked me and the science correcting the medical errors my dean called upon me (and others) to correct.
​
The result of correcting nuclear imaging errors lead to the development of quantitative FMTVDM; allowing for measurement of not only the varying diseases of ITIRDs, but the ability to measure changes in these ITIRDs.
​
During the development of The Fleming Unified Theory of Vascular Disease, I realized two critical concepts.
​
First, that what I had really put together was an InflammoThrombotic Immunologic Response (ITIR) Diseases (ITIRD) Theory, explaining why our chronic diseases were appearing in ever increasing numbers.
​
While I first changed the theory to Inflammation and Heart Disease - using what was considered popular terminology at the time - I later modified this to InflammoThrombotic Response (ITR), only later incorporating all of its parts into the correct name to provide the full name InflammoThrombotic Immunologic Response (ITIR) Diseases (ITIRD) Theory.
​
The was more of an acquiescence to those who considered the name too long; but, as I thought more and more about the resistance I have encountered in correcting medical scientific errors, the more convinced I became that it was necessary to not dumb it down, but to elevate humanity's understanding.
​
People are not unable to learn - there are merely those people who would prefer that we not. I will not give these people that control over medical science, or over you.
​
Second, I realized with the inclusion of infectious disease into the ITIRD theory, that our future could look much like our past; meaning that infectious disease could once again become the number one killer of people - only this time it wouldn't be the result of a simple infection. This time it would be the result of an ITIR, producing ITIRD - like heart disease.
​
During my investigations I had noticed that people with infections and CAD would report more symptoms - more chest pain (angina), shortness of breath (dyspnea) and stomach irritation (nausea).
​
Was this merely the result of the infection wearing on the body of the people infected, or was it something else.
​
Were the infections, like Marshall and Warren discovered, doing something more?
Were the infections causing a measurable change in regional coronary flow reserve, which translated into measurable disease, and if treated, would there be evidence of
​
(1) resolution of the infection,
(2) improvement in symptoms, and
(3) improvement in the ITIRD known as CAD (heart disease) with measured improvement in flow reserve?
​
The answer these questions I began a series of investigations during the mid to late 1990s. Given the experience from Marshall and Warren, coupled with bacterial infections being reported by people, like the Hubble Telescope Deep Fields experiment, I looked where others had not. I selected three bacteria of interest including
​
Helicobacter Pylori (Stomach Ulcers),
Klebsiella Pneumonia (Pneumonia - Infection of Lungs), and
Streptococcus Pneumonia (Dental Infections).
​
The results of that research - available under the Before MAHA tab - showed that people with underlying heart disease who became infected with one or more of these bacteria showed worsening of the heart disease.
A problem I called Bacterially Aggravated Atherosclerosis (BAA), an InflammoThrombotic Immunologic Response (ITIR) Disease (ITIRD), made worse by the bacterial infection elsewhere in their body. Worsened of their atherosclerosis demonstrated by showing a reduction in their coronary flow reserve - i.e. blood flow to areas of their heart.
​
This worsening of coronary blood flow reserve improved with treatment of the infection.
​​
​
​
​
This series of investigations, confirmed by others, demonstrated that infectious disease agents including fungi, bacteria, mycobacteria, viruses, rickettsia, et cetera, can worsen underlying ITIRDs like heart disease by initiating their own in ITIRD, further altering homeostasis within the body.
​
Should the ITIRD be allowed to progress without treatment, something we saw repeatedly during the COVID pandemic, it would not be unexpected that further health problems would occur; including heart damage, neurologic damage, kidney damage, miscarriages, et cetera.
​
​Given this information and the understanding that infectious diseases can worsen underlying chronic ITIRD, I was ready to investigate the consequences of SARS-CoV-2 viral infections and their subsequent ITIRD known as COVID-19.
​
Including both the impact of the infection and determination of what treatment(s) might work to stop the ITIRD COVID.