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Alternative models for chronic disease

The evidence supporting a bacterial cause for chronic disease is strong. Still, there are other competing explanations including the acid/alkaline imbalance theory, autoimmune disease theory, the genetic predisposition theory, the single pathogen theory, and the spontaneous remission theory. Some have argued that viral co-infections are to blame for diseases of unknown etiology despite the evidence which has accumulated to the contrary.

Acid/alkaline imbalance theory

Main article: pH balancing

According to the acid/alkaline imbalance theory, disease is caused or exacerbated by an overly acidic environment and can be remedied by consuming alkali or alkali-producing substances. In reality, the pathogenesis of disease is much too nuanced to say “low pH leads to disease.” If it were true that an imbalance is an indication of disease, doctors would use pH as a catch-all diagnostic tool, and the vast majority do not.

Some patients have reported feeling better after hyperbaric oxygen therapy. As with any therapy that may cause short-term benefit, there is always the concern that it is inhibiting the immune response. According to the Marshall Pathogenesis, chronic disease patients must experience immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed. in order to resolve disease. Anything else is ultimately counterproductive, and in the case of hyperbaric oxygen therapy, somewhat dangerous.

Autoimmune disease

Autoimmune diseases are thought to arise from an overactive immune response of the body against substances and tissues normally present in the body. The autoimmune disease theory has yet to present a satisfactory reason, evolutionary or otherwise, why an immune system would attack human tissue.

Conversely, the Marshall Pathogenesis explains that so-called “autoantibodies” are merely antibodies generated in response to pathogenic bacterial cells that have been destroyed as a result of an active immune response – in essence, collateral damage.

At least forty different chronic diseases are suspected or accepted as being caused by an autoimmune response. According to Yehuda Shoenfeld, when it comes to autoimmune disease, “Everything is infectious until proven otherwise.”

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Environmental causation theory

Chronic inflammatory diseases have existed for at least thousands of years. Manifestations of both arteriosclerosis can be observed in mummies of ancient Egypt. Ötzi the Neolithic Iceman who lived around 3300 BC was found to have arthritis.

This relative consistency of disease prevalence suggests that a number of the proposed environmental causes for disease, like man-made toxins and junk food are not the exclusive cause.

It has been widely hypothesized that lifestyle factors, including a poor diet and a lack of exercise, are driving what the World Health Organization has termed “an obesity epidemic,” but even the most ambitious obesity intervention programs, which have gone to great lengths to increase rates of exercise and improve eating habits of a population, have been, for lack of a better term, failures.

In contrast to infectious agents, little evidence implicates typical doses of dietary chemicals as primary causes of human cancer, probably because humans have evolved effective flexible enzymatic systems for degrading potentially carcinogenic chemicals.

Co-infections / Viral infections

Main article: Co-infections

Related article: Microbes in the human body

A variety of bacteria, fungi, and viruses are commonly described as co-infections. These include: Bartonella, cytomegalovirus, Borellia, Babesia, Candida, Ehrlicha, Epstein-Barr virus, and Rickettsia. In the absence of a robust immune response, these microbes along with others proliferate inside the human body.

Because the Marshall Protocol activates the innate immune response, a system that is responsive to a range of microbes, there is a good chance the MP targets these infections. Patients on the MP experience an immunopathological reaction in eliminating any microbes including those labelled as co-infections.

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Genetic predisposition theory

Main article: Genetic predisposition

Many researchers have long argued that most chronic diseases are caused by humans' genetic predisposition for a condition. However, despite ambitious efforts, there is substantial evidence that chronic diseases are not caused by human genes. Studies of monozygotic (fraternal) twins are particularly damning. The high percentage of disease-discordant pairs of monozygotic twins demonstrates the central role of environmental factors (like microbes) in the cause of autoimmune diseases, to say nothing of similar data about other inflammatory diseases such as cancer.1)

According to the Marshall Pathogenesis, humans accumulate a plethora of pathogenic bacteria during their lifetimes, and it is the genetic mutations and disruption of key transcriptional pathways which result from active infection that play a major role in what is commonly thought of as “genetic susceptibility.”

If anything, we don't really know how to read the genome and it can't tell us very much right now. So what's the ethical debate about?… We couldn't even be certain from my genome what my eye color was. Isn't that sad? Everyone was looking for miracle 'yes/no' answers in the genome. “Yes, you'll have cancer.” Or “No, you won't have cancer.” But that's just not the way it is…. [The Human Genome Project has had] close to zero [medical benefit] to put it precisely…. We have, in truth, learned nothing from the genome other than probabilities. How does a 1 or 3 percent increased risk for something translate into the clinic? It is useless information.

J. Craig Venter, Der Spiegel interview

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Psychosomatic explanations for disease

Sigmund Freud and Jean-Martin Charcot were born 150 years ago, but their ideas about the effect of the subconscious on disease continue to resonate in the scientific community.2) Freud and colleagues argued that unconscious mental processes such as sublimated rage could manifest as physical symptoms. However, with the advent of superior technology, one by one, many diseases once supposed to be caused by psychological stress have since been attributed to other factors including infections.

According to the Marshall Pathogenesis, chronic fatigue syndrome, multiple chemical sensitivity and other chronic inflammatory diseases are likely caused by pathogens, yet many physicians consider these diseases to be “medically unexplained.” Medically unexplained diseases are widely prevalent3) but at the same time have few discernible markers or objectively measurable symptoms. While a lot of Freudian ideas have fallen out of favor, one legacy remains: difficult-to-explain diseases are still routinely attributed to psychological causes. The process by which patients supposedly manifest psychological problems as a disease has been named and renamed, classified and reclassified: hysteria, psychosomatic disorder, somatoform disorder, conversion disorder, functional disorder, etc. In each of these diagnoses, however, the stated origin of disease is unchanged: symptoms that cannot be explained are ultimately “all in a patient's head.”

While there is no denying the existence of some sort of “mind-body connection,” there is minimal compelling evidence that as the 19th century Swiss physician Georg W. Groddeck claimed: “Illness has a purpose; it has to resolve the conflict, to repress it, or to prevent what is already repressed from entering consciousness.”4) Despite the stark absence of evidence supporting these views, it is not unusual to read papers describing how patients with long-term so-called psychological illnesses may be subconsciously manifesting them, because it would allow them to have more “care, attention, disengagement, or even financial benefits.”5) Nor, is it uncommon for new theories to spring up along these lines. In one example, a 2008 continuing medical education publication taught physicians that when a celebrity becomes ill, healthy people are suggestible enough to develop long-term illnesses consistent with the celebrity's descriptions of their conditions. Such claims are recklessly speculative, harming patients and stalling needed research.

Treating patients who complain of so-called medically unexplained symptoms with cognitive behavioral therapy or, in the case of chronic fatigue syndrome, graded exercise therapy, may do more harm than good.6) The emergence of metagenomic technologies offers a more sophisticated set of tools for detecting and characterizing microbes in these disease states. Perhaps it is only the use of this technology that will finally relegate the notion of patient as attention-seeking victim to historical relic.

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Single pathogen theory

There are currently a range of diseases for which there is epidemiological evidence, evolutionary evidence, and other kinds of evidence strongly suggesting bacterial involvement. Koch's postulates stipulate that chronic diseases caused by infections must be caused by a single species of pathogen, yet the minority of chronic diseases have been shown to be caused by a single species of pathogen.

Take Crohn's disease as an example. The following types and species of bacteria have been found in patients with Crohn's: L-form bacteria7), Bacteroides fragilis8), Chlamydia trachomatis9), Listeria monocytogenes10), Mycobacterium avium, subspecies paratuberculosis11), Mycobacterium kansasii12), and Pseudomonas maltophilia13). Yet none of these species are found consistently in Crohn's.

For a 19th century researcher, Robert KochAuthor of Koch's postulates, a set of rules for establishing a relationship between a causative microbe and a disease. Koch's belief that only one pathogens causes one disease has now been called into question as multiple postulates are increasingly considered out of date. had a strong, even visionary, grasp of molecular biology, but he did not have access to molecular tools. Koch might be shocked to learn the extent to which different species engage in horizontal gene transfer, to the point where the very definition of “species” may have to be reconsidered.14)

The best way to resolve this inconsistency is to say simply that Koch was wrong and that chronic diseases are caused by a multitude of species and forms – a metagenomic microbiota.

Spontaneous remission theory

Main article: Spontaneous remission

The chronic inflammatory diseases treated by the Marshall Protocol (MP) almost never go away on their own. It’s not that patients with Th1 disease can’t and won’t go through periods where they might feel better. Unfortunately, these periods are usually a sign that the immune system has become severely compromised.

Whether temporary “remission” is driven by immunosuppressive drugs like corticosteroids, a high intake of vitamin D, excessive sun exposure, or simply the accumulation of a bacterial load that is so high that the VDR is almost completely shut down by bacterial ligands – these periods are times when the Th1 pathogens are alive and well, spreading, and surely infecting other tissues. This unchecked infection leads to illnesses that will only be discovered later in life such as arthritis, heart disease, decreasing kidney function, diabetes, cancer and even the diseases of aging. But during the “remission period,” when the immune system is not capable of killing the pathogens, there is no corresponding inflammatory response that would be occurring if the body was mounting a defense against the infection. This causes t'he patient to feel a sense of temporary relief during immune suppression that is often mistaken for “wellness.”

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References

1)
Infections and autoimmune diseases.
Bach JF
J Autoimmun25 Supplp74-80(2005)
2)
Reasons for the Freudian revolution.
Friedman L
Psychoanal Q46p623-49(1977)
3)
Medically unexplained symptoms: an epidemiological study in seven specialities.
Nimnuan C, Hotopf M, Wessely S
J Psychosom Res51p361-7(2001 Jul)
4)
Webster, R. 1996. Why Freud was wrong: sin, science and psychoanalysis. London, HarperCollins.
5)
Functional somatic syndromes.
Barsky AJ, Borus JF
Ann Intern Med130p910-21(1999 Jun 1)
7)
Bacterial L-form isolation from inflammatory bowel disease patients.
Belsheim MR, Darwish RZ, Watson WC, Schieven B
Gastroenterology85p364-9(1983 Aug)
9)
Antibodies against Chlamydia of lymphogranuloma-venereum type in Crohn's disease.
Schuller JL, Piket-van Ulsen J, Veeken IV, Michel MF, Stolz E
Lancet1p19-20(1979 Jan 6)
10)
Immunocytochemical evidence of Listeria, Escherichia coli, and Streptococcus antigens in Crohn's disease.
Liu Y, van Kruiningen HJ, West AB, Cartun RW, Cortot A, Colombel JF
Gastroenterology108p1396-404(1995 May)
11)
Detection and verification of Mycobacterium avium subsp. paratuberculosis in fresh ileocolonic mucosal biopsy specimens from individuals with and without Crohn's disease.
Bull TJ, McMinn EJ, Sidi-Boumedine K, Skull A, Durkin D, Neild P, Rhodes G, Pickup R, Hermon-Taylor J
J Clin Microbiol41p2915-23(2003 Jul)
12)
Mycobacteria as a possible cause of inflammatory bowel disease.
Burnham WR, Lennard-Jones JE, Stanford JL, Bird RG
Lancet2p693-6(1978 Sep 30)
13)
Bacterial variants: etiologic agent in Crohn's disease?
Parent K, Mitchell PD
Gastroenterology71p365-8(1976 Aug)
14)
Fuzzy species among recombinogenic bacteria.
Hanage WP, Fraser C, Spratt BG
BMC Biol3p6(2005 Mar 7)
home/alternate.txt · Last modified: 01.03.2012 (external edit)
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