In isolated cases of Crohn’s disease, dietary manipulations have produced what biologics and steroids have yet to document, permanent remissions/cures. The postulate introduced is that permanent remissions achieved through dietary manipulation are achieved by marked reduction of MAP antigen/pre-primed antibody interactions and by dietary immune system restoration/enhancement that may result in the destruction of the MAP-template driving the dysfunctional pro-inflammatory immune response.
Mycobacterium avium subspecies paratuberculosis (MAP) is a significant pathogen for milk-producing domestic animals. Infected animals have the ability to shed the mycobacterium into their milk [1,2]. MAP survives pasteurization [3,4]. USDA’s failure to address the growing prevalence of MAP in dairy herds has resulted in widespread dissemination of the mycobacterium particularly within milk-based food products . MAP has been identified in infant formula, powdered milk, milk, cheese, etc [6-13].
In contrast to their pathogenicity as replication pathogens in domestic animals, MAP and other atypical mycobacteria have limited pathogenicity for humans unless congenital or acquire immunodeficiency is present [14,15]. At birth, newborn infants lacking acquired immunity are analogous to a germ-free animal. Acquired immunity is central to establishing immunological governance over viral and mycobacterial infections. The Hruska postulate introduced the concept that, if a newborn becomes infected with MAP in its period of immunological vulnerability, the ability of its inherent immune system to abort mycobacterial replication could be severely challenged . Depending on the baby’s genetic profile, the magnitude of the infectious MAP inoculum, and the status of its developing acquired immunity, the baby’s inherent immune system can become so taxed that its TH1 pro-inflammatory response to MAP becomes fixed within immunological memory. Whenever the body is again presented with MAP’s antigenic array, rather than responding by exhibiting immunological tolerance, immunity re-initiates it’s original pro-inflammatory cytokine
responses and attacks MAP at its site of attachment and antigen processing. Fecal stasis concentrates MAP challenges in the ileoce
cum. The focal destruction of the gastrointestinal mucosa allows for penetration of the gastrointestinal microbiota into the lamina propria and underlying tissues [17,18].
Things happen for a reason. Isolated unstructured observations without implied mechanism of action are rarely published in the medical literature. Most cases of permanent resolution of Crohn’s disease through dietary manipulation are found in the lay literature. What is in the medical literature is the demonstration that dietary use of specific carbohydrates (the SCD diet) can produce demonstrable clinical amelioration in cases of pediatric Crohn’s disease [19,20]. While the SCD diet improved mucosal inflammation, healing could not be documented [21,22].
Central to re-establishing mucosal integrity is aborting antigen/antibody cytotoxicity at MAP’s sites of mucosal attachment. The pathogenesis of Crohn’s disease argues for the removal from diet of all foods that have the potential of having been adulterated by MAP, more specifically all dairy based products and red meat. By so doing, the number of cytotoxic antigen/antibody interactions within the gastrointestinal tracts are markedly reduced. Biologics act by dismantling the cytotoxic cytokine response to MAP. Dietary exclusions utilize prevention of, rather than immune response interference to achieve the same objective, reconstitution of mucosal integrity. Being nearly impossible to identify and/or
eliminate all MAP adulterated foods, dietary exclusion and biologics
are complementary to each other in re-establishing mucosal
How individual dietary constituents influence host immunity
is well documented in the medical literature. In Crohn’s disease,
the induced alterations of gastrointestinal structure and function
compromise the quantitative availability of vitamins, minerals
and selected amino acids essential to effective immune system
Zinc is a prime example of how deficiency of a single mineral
can undermine immune system integrity. The body has no specialized
system to store zinc . Individuals with Crohn’s disease
will have zinc deficiency impairment affecting a broad spectrum
of immune mechanisms owing to decreased absorption and increased
exogenous loss . Individuals with a diarrheal disease
will have high fecal loss. Zinc is important to the catalytic activity
of approximately 100 enzymes involved with immune system
function and DNA synthesis . Zinc deficiencies result in adverse
changes in cytokine production and T-cell subpopulations
. A side effect of zinc deficiency is anorexia which in itself can
create a negative feedback.
The vitamin C and E interactions are central to immune system
maintenance. Vitamin C regenerates vitamin E from its oxidized
form. The lipid soluble antioxidant vitamin E not only protects
the integrity of cell membranes, but functions synergistically with
other nutritional elements that beneficially influence cell-mediated
immunity. The salvage of vitamin E influences the immune
functions of selenium which in turn has a beneficial impact on
copper and zinc utilization.
Like zinc, vitamin C has limited storage within the human
body. Through its antioxidant effect, vitamin C plays a central role
in the containment of mycobacteria . The body’s need for vitamin
C dramatically increases with infection/disease .
The reason for acute therapeutic focus on vitamins, minerals,
and amino acids central to maintenance of optimal host immunity
is the postulate that the curing of Crohn’s disease is contingent
upon destruction of the MAP templates (spheroplasts) sustaining
the dysfunctional immune response that is characteristic of
The evidence relating to destruction of the MAP template
through specific enhancement of host immunity is derived in part
from a four-month study of a cow with near terminal Johne’s disease.
In an attempt to prolong her life in order to collect high-titer
anti-MAP serum, a specialized diet was designed that targeted
enhancement of cellular immunity. When finally necropsied four
months later, the cow had regained all her body weight. The serological
markers for MAP infection had dropped to near normal
status. No gross or histological evidence of Johne’s disease could
be identified . Evidence of acid-fast bacilli in diseased tissue
was totally absent. What was present was a clue as to how the
body can actually destroy mycobacteria . The significance of
this observation, which was supported by field trials in diseased
animals, provided insight as to how dietary manipulation had,
more likely than not, attained permanent remissions .
A secondary substantiation of MAP spheroplasts driving the
dysfunctional proinflammatory immune-mediate response comes
from the only other therapeutic regimen that has produced isolated
cures of Crohn’s disease: anti-mycobacterium drugs [32-
37]. As a general rule, anti-tuberculosis drugs have not produced
cures. When they have, the mechanism of action of one or more of
the compounds used involved disruption of RNA function. For an
antibiotic to destroy bacteria without a cell wall (spheroplasts),
the drug must act on the organism’s ribosomes.
Crohn’s disease is the consequence of two inter-related but
separate disease processes; a dysfunctional immune-mediated
response to MAP’s antigen array and polymicrobial bacterial
invasion of small bowel by the gastrointestinal microbiota .
Failure to appropriately negate the latter through comprehensive
antibiotic therapy will produce the late sequela of Crohn’s disease:
strictures, loop-to-loop anastomoses, peri-anal fistula, bowel perforations,
etc. [39-40]. Once in place, the curing of Crohn’s disease
may require surgical intervention.
To date, there is still no test that distinguishes human MAP
infection from Crohn’s disease. Delay in commitment to therapy
enhances the potential for structural damage to the ileocecum. Dietary
manipulation is a therapeutic tool with literally no indefinable
adverse consequence whose end-titration point is contended
to be cure destruction of the MAP templates.
Hruska K, Baros M, Kralik P, Pavlik I (2005) Mycobacterium avium subspecies paratuberculosis in powdered infant milk: paratuberculosis in cattle – the public health problem to be solved. Veterinarni Medicina 50: 327-335.
Prasad AS, Beck FW, Grabowski SM, Kaplan J, Mathog RH (1977) Zinc deficiency: changes in cytokine production and T-cell subpopulations in patients with head and neck cancer and non-cancer patients. Proc Assoc Am Physicians 109(1): 68-77.