Dear Medical Friends,
This study of viruses and bacteria just keeps getting “funner and funner”. Cancer is beginning
to make perfectly good sense. (Of course, like everything else, it is a good news, bad news thing. The good news
is that we can do something about it.)
After looking into the natural roles of viruses and repeating the process with intracellular bacteria (L-forms
and mollicutes) and having read a sizeable number of scientific, more-facts-than-needed types of articles, I have
made these discoveries and come to these conclusions:
1) Viruses and bacteria are natural
inhabitants of our bodies. (This is a given)
2) Both viruses and bacteria mutate
to suit their environment and the challenges they sustain. (Another given)
3) Some viruses (e.g. retroviruses)
incorporate their genetic information into the nuclear DNA of cells while many intracellular bacteria exchange their
genetic information with that of the mitochondrial DNA. (Scientific fact)
4) Mitochondria are not only the “powerhouses
of the cell” but are also involved in cell differentiation, cell death, and cell division through their own independent
machinery used in protein synthesis, including DNA, messenger and transfer RNAs, and ribosomes. (Scientific fact)
5) In pathology we have benign and malignant
tumors, “precancerous” lesions, and granulomatous diseases. Among neoplasms, we have a range of well-differentiated
to poorly differentiated tumors. (Scientific fact)
6) Among those tumors that can occur
in the skin and in the mouth (e.g. melanoma, squamous cell carcinoma), those in the mouth are typically much worse
(behaviorally more malignant). We have typically explained this difference by their rich blood supply but is that so? Cancer
doesn’t like oxygen anymore than the individual components (viral and bacterial) that cause that cancer. So, what is
the biggest difference between a melanoma sitting on the skin of the muzzle and one on the inside the mouth invading the gum?
One answer is the presence of bacteria.
7) Conclusion: The difference between
granulomas (e.g. sarcoidosis), benign tumors and malignancies is the presence or absence of one of the two main entities-
the virus and the intracellular bacteria. In granulomas, the action is governed by the intracellular bacteria through
their influence in the mitochondrial DNA. In benign tumors, the action is governed by the presence of a virus
in the nuclear DNA. But in (some/many/all) malignancies, the action is governed by both. Could malignancies
be a viral tumor that is “secondarily infected” with bacteria, just like other disease processes we see (e.g.
IBS, atopic pyoderma, asthma, etc.)? This would help to explain “premalignant” lesions and conditions like
sebaceous adenomas and perianal gland tumors in which the vast majority are benign…until a malignancy finally pops up.
And speaking of perianal gland tumors (and mast cell tumors of that area), is there an area of skin subject to more potentially
virulent bacteria on the body other than around the mouth? (Speaking of bacterial influence, how many benign intestinal tumors
do we see?)
I had a case of a very strange malignancy in the foot of a Labrador retriever last year. It was never definitively
diagnosed by Antech except for being a highly undifferentiated sarcoma. It occurred after what appeared to be a stab wound
between the toes. The owner thought he had stepped on glass in the backyard and that’s just what it looked like. But,
the lesion that appeared a month later continued to grow, leading the biopsy. We tried some medications and natural remedies
but it continued to grow, leading to amputation of the leg. What got in there? A new virus, a new bacteria, or both? Did a bacteria
enter an area where a virus already resided?
Is this what happens in other cancers? Do mycoplasma do this? Are mycoplasmal vaccine contaminants (which
we know occur) part of the process of vaccine-induced sarcomas or is it just the adjuvant activating a residential virus?
Could a secondary infection with intracellular bacteria be the thing that decompensates the FeLV, FIV, or HIV individual,
knowing that L-forms and mollicutes invade white cells (as well as platelets and RBCs) and compromise their vitamin D receptors, creating a state of immunodeficiency
within that cell?
It has been postulated for years that viruses and mycoplasma work in concert. These viruses and intracellular
bacteria both reside inside the cell, working in different areas as described above. They are both part of our adaptive system,
reacting to toxins, lectins, and other challenges. It’s cool to see that there is something alive inside the
cell reacting to challenges being made to that cell (not that DNA and RNA are not “alive”). Could it be that viruses
are the main adaptive force and bacteria take it to a whole new level when things get really serious??? That’s
kind of what happens in the gastrointestinal tract, isn’t it?
It is clear that we lose the battle mainly when our immune system takes a nose dive. We spend our lives before
then being benefitted by the constant action of these guys (except for the ones that have been altered by man), who serve
to signal the immune system that we have done something wrong, bringing on a variety of signs and symptoms. A healthy immune
system is the governor and keeps these "helpers" from getting too powerful. They need a foreman. But, when the
immune system crashes and we continue to insult these guys (kick their ant bed), these guys run rampant, including carrying
their proclamations to distant locations (metastasis, scleroderma, “rheumatoid arthritis of the lungs”, sarcoidosis).
We lose our grip on them and they take over, all in the name of their own survival. They never wanted to hurt us. They were
simply reacting to what we were doing to them. In fact, they’re running scared. But make no mistake: They have no
conscience and they will do what it takes to survive, even if it means killing the host. And when that occurs,
these viruses and bacteria don’t know they are committing suicide. But we should.
Lemme know what you think,
John B. Symes, DVM (aka "Dogtor J")