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Townsend Letter for Doctors

 -­‐  Quantum  Medicine  Update  Aug-­‐Sept  2010–  Paul  Yanick,  Jr.  Ph.D.  ©2010                            1  

Colonization Resistance of Barrier Microflora in Carcinogenesis


& Allergic Patients
Paul Yanick, Jr. Ph.D. - American Academy of Quantum Medicine www.aaqm.org
       The astounding degree of microbial diversity in the gut indicates a multitude of
ecological niches, which are generated through the development of complex food
webs (niche construction) whereby beneficial colonization leads to commensalism,
symbiosis and immunological competence.1-10
Over the past two decades, my research has focused on acquiring an understanding of gut
microflora composition, loops and processes such as intestinal adherence, colonization,
translocation, and immunological reciprocity and competence. Recently, an independent study by
a group of 24 scientists has scientifically validated my earlier work on commensal colonization
resistance. These researchers state, “It has been estimated that the microbes in our bodies
collectively make up to 100 trillion cells, tenfold the number of human cells, and suggested that
they encode 100-fold more unique genes than our own genome. The majority of microbes reside
in the gut, have a profound influence on human physiology and nutrition, and are crucial for
human life. Furthermore, the gut microbes contribute to energy harvest from food, and changes
of gut microbiome may be associated with bowel diseases or obesity.”1
Four decades of my clinical research on thousands of patients has taught me that colonization
resistance of commensal cell microflora causes digestive symptomatology, opportunistic
infections, and carcinogenesis. Human and commensal cell polarity deficits are the prime force
behind these ecosystem disruptions. Cell polarity involves signaling networks; transcription
factors, membrane-trafficking pathways, and quorum cell-to-cell communication, all of which
need to be restored in order to properly colonize the human ecosystem. 11,12
Viewing the gut as a complex ecosystem with a diverse assemblage of commensal cell
microflora possessing a rich genetic diversity can help us realize that these cells can produce all
sorts of anti-allergic, anti-cancer, anti-inflammatory and anti-viral compounds. Our consortium of
gut microbes (microbiome) possesses at least a hundred times more genes as the mere 20,000 in
the human genome. Since human rely on their microbiome for digestion, detoxification and a
wide spectrum of immunological functions, we can be thought of as a “superorganism” nourishing
and restoring the quorum language and teamwork of our commensal cell microbiotica.1,65
Scrutinizing popular health claims can provide a new window onto our clinical worlds and
enable us to make better decisions in detoxifying our patients of carcinogens. Since cells need to
have the proper polarity to clean house, the challenge in today’s toxic world is to find ways to
eliminate man-made chemicals with a positive ionic charge that disrupt colonization. This
aberrant cell physiology has it primary effect by depolarizing hepatocytes. When this happens,
hepatobiliary stagnation with diminished bile production, has the tendency to induce and promote
allergic, respiratory and inflammatory reactions that induce and promote carcinogenesis.11-14
Irwin M. Arias, MD of the Unit of Cell Polarity at Tufts University School of Medicine stated,
”Polarization of hepatocytes critical for hepatocyte production of bile. A lack of hepatocyte polarity
can impair biliary secretion resulting in cholestasis (i.e., bile secretory failure).” Dr. Arias and
other scientists have used live-cell fluorescent, biochemical, genetic, and molecular techniques to
study mechanisms responsible for trafficking of proteins selectively to the apical domain of
hepatocytes and other polarized cells to confirm my original hepatobiliary research.11-30
Cell polarity deficits cause liver detoxification deficits, which, in turn, cause prolonged
inflammation in the gastroduodenal excretion channel so allergens and carcinogenic toxins cannot
be safely excreted out of the body. Enhancing bile production has the potential to play an
important clinical role in providing relief in allergic patients and in restoring innate immunological
integrity in cancer patients. But, the war on microbes and the simplistic nuke-the-microbe
mindset has caused a rising incidence of human ecosystem disorders like multiple chemical
sensitivity (MCS), asthma, and all sorts of allergic disorders. For this reason, caution needs to be
exercised with the excessive clinical use of natural anti-infective herbs, colloidal silver and anti-
microbial compounds like allicin from garlic or oregano oil.
Commensals are immunological peacekeepers and the strong arm of immune defenses that
promote the proper digestion of food and the excretion of toxins. Indeed, two Nobel laureates
reported that commensal flora is a realistic therapeutic strategy for infectious, inflammatory and
Townsend Letter for Doctors  -­‐  Quantum  Medicine  Update  Aug-­‐Sept  2010–  Paul  Yanick,  Jr.  Ph.D.  ©2010                            2  

neoplastic disorders.30-33 Studies reveal that commensals are essential health assets that confer
protection against infections, prime mucosal immunity, produce a rich repository of nutrients and
metabolites, and have efficacy in acute enteric infections, post-antibiotic syndromes, colitis, and
irritable bowel syndrome. 31-43
Clinically, when we fail to address colonization resistance and barrier function, we may
inadvertently induce efferent-generated cytokine inflammation and carcinogenesis, which results
in an inability of the body to maintain stable ecological niches and quorum cell-to-cell
communication. The complex, dynamic and spatially diversified microbiotica and its microbiome of
collective genomes have been studied via culture-based assays, and a variety of molecular
methods that include fluorescent in situ hybridization, terminal restriction fragment length
polymorphisms, microarrays, and direct sequencing. These studies offer hope and help for
patients with allergic conditions or cancer as proper 8-strain commensal colonization can help
detoxify the body, fight inflammation, employ innate immunologic weaponry with greater force
and nourish afferent neurons that regenerate the body.48-61

In summary, we need to view commensal microbiotica as our close allies and consider
employing effective colonization techniques to restore this vast, complex, and dynamic
consortium of cells. A recent editorial in Medical Hypothesis says, “this symbiont provides us, the
host, with metabolic functions far beyond the scope of our own physiological
capabilities…imbalances of this intestinal microbial community structure have the potential to
cause many debilitating conditions such as Crohn’s disease, inflammatory bowel disease, allergy,
obesity, and even cancer.”65 Clearly, the body’s commensal weaponry can outperform any we
can do or prescribe for our patients. When we restore colonization lost by antibiotics or natural
anti-infective agents, we restore homeostasis and our “superorganism” potential.65
Finally, studies show that colonization patterns are influenced by physicochemical properties
and by the health of the gut mucosa and fulfilling a niche.60-64 In keeping up with the steady pace
of scientific change, clinicians need to understand how to overcome colonization resistance and
realize that the prospects for clinical success with current fragmented approaches are limited
because the body cannot detoxify and cleanse itself completely without the hundreds of
thousands of nanoscale, synbiotic nutrients produced by commensal cells.15-22, 58-61
To Learn More – www.quorumnutritionllc.com
REFERENCES
1. Quin,  J  et  al  A  human  gut  microbial  gene  catalogue  established  by  metagenomic  sequencing,  Nature  2010:  464,  59-­‐65.  
2. Day,  R  et  al:  Rethinking  adaptation:  the  niche-­‐construction  perspective.  Perspect  Biol  Med  2003:46,  80-­‐95.  
3. Ley,  R  et  al:  Ecological  and  evolutionary  forces  shaping  microbial  diversity  in  the  human  intestine.  Cell  2006:124,  837-­‐48.  
4. Backhed,  F  et  al:  Host-­‐bacterial  mutualism  in  the  human  intestine.  Science  2005:  307,  1915–20.  
5. Hooper,  LV  et  al:  How  host-­‐microbial  interactions  shape  the  nutrient  environment  of  the  mammalian  intestine.  Annu  Rev  Nutr  
2002:22,  283–307.  
6. Ley,  RE  et  al:  Microbial  ecology:  human  gut  microbes  associated  with  obesity.  Nature  2006:444,  1022–23.  
7. Turnbaugh,  PJ  et  al.  An  obesity-­‐associated  gut  microbiome..increased  capacity  for  energy  harvest.  Nature  2006:  444,  1027–1031.  
8. Ley,  R.  E.  et  al.  Obesity  alters  gut  microbial  ecology.  Proc.  Natl  Acad.  Sci.  USA  2005:102,  11070–75.    
9. Eckburg,  PB  et  al.  Diversity  of  the  human  intestinal  microbial  flora.  Science  2005:  308,  1635–38.  
10. Ley,  RE  et  al:    Worlds  within  worlds:  evolution  of  the  vertebrate  gut  microbiota.  Nature  Rev.  Microbiol.  2008:6,  776–88.  
11. Johnson,  D  et  al:  A  genetic  hierarchy  controlling  cell  polarity.  Nature  Cell  Biology  2003:5,  12–14.  
12. Byrant  DL  et  al:  From  cells  to  organs:  building  polarized  tissue.  Nature  Reviews  Molecular  Cell  Biology  2008:  9,  887-­‐901.  
13. Iden  S  et  al:  Crosstalk  between  small  GTPases  &  polarity  proteins….  Nature  Reviews  Molecular  Cell  Biology  2008:  9,  846-­‐59.  
14. Nelson  J  et  al:  Coordinated  protein  sorting,  targeting  and  distribution  in  polarized  cells.  Nature  Reviews  Molecular  Cell  Biology  
2008:  9,  833-­‐45.  
15. Yanick,  P.  The  role  of  the  hepatocyte  &  commensal  cell  microbiotica  in  the  successful  detoxification  of  carcinogenic  toxins.  2007  
(December)  Townsend  Letter  for  Doctors.    
16. Yanick,  P  Functional  disturbances  of  the  Liver  and  Lymphatic  System.  1994  (October).  Townsend  Letter  for  Doctors,  1050-­‐56.    
17. Yanick,  P  Functional  Correlates  of  pH  in  accelerated  molecular  and  tissue  aging.  1995  .  Townsend  Letter  for  Doctors.    
18. Yanick,  P  Activating  the  Longevity  Gene  to  Restore  Insulin  Sensitivity  and  Immune  Reciprocity  in  Patients  with  Metabolic  
Syndrome.  2007  (May)  Townsend  Letter  for  Doctors,  146-­‐51.  
19. Yanick,  P  The  Neglected  Role  of  Hepatocyte  and  Commensal-­‐Probiotic  Cell  Physiology  in  Detoxification  Strategies.  2007.  Townsend  
Letter  for  Doctors.  
20. Yanick,  P.  Man-­‐made  Chemicals:  The  hidden  Role  in  the  Lymphatic  System  and  the  Genesis  of  Disease.  Townsend  Letter  for  Doctors  
2009  (April):  95-­‐97.    
21. Yanick,  P.  Restoring  Immunity,  the  ANS  and  Reciprocity  for  a  Fuller  Expression  of  Innate  Healing  in  Naturopathic  Medicine.  
Townsend  Letter  for  Doctors  2007  (April):  161-­‐7.  
Townsend Letter for Doctors  -­‐  Quantum  Medicine  Update  Aug-­‐Sept  2010–  Paul  Yanick,  Jr.  Ph.D.  ©2010                            3  

22. Yanick,  P.  Efferent-­‐Afferent  and  Microbiotica  Imbalances  in  MCS  and  Fibromyalgia.  Townsend  Letter  for  Doctors  2009  (November):  
99-­‐104.  
23. Ortiz  DF  et  al:  Identification  of  HAX-­‐1  as  a  protein  that  binds  bile  salt  export  protein  and  regulates  its  abundance  in  the  apical  
membrane  of  MDCK  cells.  J  Biol  Chem  2004:  279:32761-­‐70.  
24. Wakabayashi  Y  et  al:  Intracellular  trafficking  of  bile  salt  expert  pump  (ABCB11)  in  polarized  hepatic  cells:  constitutive  cycling  
between  the  canalicular  membrane  and  rab  11-­‐positive  endosomes.  Mol  Biol  Cell  2004:15:3485-­‐96.  
25. Wakabayashi  Y  et  al.  Rab11a  and  myosinVb  required  for  polarization  of  WIF-­‐B9  cells.  Proc  Natl  Acad  Sci  USA  2005:102:115087-­‐92.  
26. Arias,  IM  et  al:  Two  N-­‐linked  glycans  are  required  to  maintain  the  transport  activity  of  the  bile  salt  export  pump  (ABCB11)  in  MDCK  
II  cells.  Amer  J  Physiol  2007:292:G818-­‐28.  
27. Wakabayashi  Y  et  al:  Four-­‐dimensional  imaging  of  filter  grown  polarized  epithelial  cells.  Histochem  Cell  Biol  2007:127:463-­‐72.  
28. Wakabayashi  Y  et  al:  Transporters  on  demand:  intracellular  reservoirs,cycling  of  bile  transporters.  J  Biol  Chem  2006:281:27699-­‐72.  
29. Stieger,  B  et  al:  The  bile  export  pump.  European  J  Physiology  2007:453:  611-­‐20.  
30. Baier,  PK  et  al:  Zonation  of  hepatic  bile  salt  transporters.  Digestive  Diseases  and  Sciences  2006:  51:587-­‐93.    
31. Shanahan  F.  Pathophysiological  basis  and  prospects  for  probiotic  therapy  in  inflammatory  bowel  disease.  Am  J  Physiol  Gastrointest  
Liver  Physiol    2005;288:G417-­‐G421.  
32. Shanahan  F.  Host  flora  interactions  in  inflammatory  bowel  disease.  Inflamm  Bowel  Dis  2004;(Suppl  1);S16-­‐S24.  
33. Shanahan  F.  Probiotics  in  inflammatory  bowel  disease:  therapeutic  rationale  and  role.  Adv  Drug  Delivery  Rev  2004;56:809-­‐818.  
34. Elliott  DE  et  al:    Helminths  and  the  modulation  of  mucosal  inflammation.  Curr  Opin  Gastroenterol  2005;21:51-­‐58.  
35. Summers  RW  et  al:  Trichuris  suis  therapy  in  Crohn’s  disease.  Gut  2005;54:87-­‐90.  
36. Gill  HS  et  al:  Probiotics  and  human  health:  a  clinical  perspective.  Postgrad  Med  J  2004;80:516-­‐526.  
37. Senok  AC  et  al:  Probiotics:  facts  and  myths.  Clin  Microbiol  Infect  2005;11:958-­‐966.    
38. Floch  MH,  Montrose  DC.  Use  of  probiotics  in  humans:  an  analysis  of  the  literature.  Gastroenterol  Clin  North  Am  2005;34:547-­‐570.  
39. Allen  SJ  et  al:  Probiotics  for  treating  infectious  diarrhea.  Cochrane  Database  Sys  Rev.  2004;(2):CD003048.  
40. D’Souza  AL  et  al:  Probiotics  in  prevention  of  antibiotic  associated  diarrhea:  meta-­‐analysis.  BMJ  2002;324:1361.  
41. McCarthy  J  et  al:  Double  blind,  placebo  controlled  trial  of  two  probiotic  strains  in  interleukin  10  knockout  mice  and  mechanistic  
link  with  cytokine  balance.  Gut  2003;52:975-­‐980.  
42. Di  Giacinto  C  et  al:  Probiotics  ameliorate  recurrent  Th1-­‐mediated  murine  colitis  by  inducing  IL-­‐10  and  IL-­‐10-­‐dependent  TGF-­‐beta-­‐
bearing  regulatory  cells.  J  Immunol  2005;174:3237-­‐3246.  
43. Bjorksten  B.  Effects  of  intestinal  microflora  and  the  environment  on  the  development  of  asthma  and  allergy.  Springer  Semin  
Immunopathol  2004;25:  257-­‐70.  
44. Kalliomaki  M  et  al:  Role  of  intestinal  flora  in  the  development  of  allergy.  Curr  Opin  Allergy  Clin  Immunol  2003;3:  15-­‐20.  
45. Bäckhed,F  et  al:  The  gut  microbiotica  as  an  environmental  factor  that  regulates  fat  storage.  Proceedings  of  the  National  Academy  
of  Sciences,  2004,101:44,  15718-­‐23.  
46. Savage,  DC:  Microbial  ecology  of  the  gastrointestinal  tract.  Annual  Reviews  in  Microbiology,  1977,31:107-­‐133.  
47. Xu  J,  Gordon  JL.  Honor  thy  symbionts.    Proceedings  of  the  National  Academy  of  Sciences,  2003,100:18,  10452-­‐59.    
48. Breitbart  M  et  al:  Metagenomic  analysis  of  an  uncultured  viral  community  from  human  feces.  Journal  of  Bacteriology.  2003,  
185:20,  6220-­‐23.  
49. Winter  C  et  al:  Impact  of  virioplankton  on  archael  and  bacterial  community  richness  as  assessed  in  seawater  batch  cultures.  
Applied  Environmental  Microbiology  70:2,  804-­‐13.    
50. Blassler,  BL.  How  bacteria  talk  to  each  other.  Regulation  of  gene  expression  by  quorum  sensing.  Current  Opinions  in  Microbiology.  
1999.  2:6,  582-­‐87.  
51. Whiteley,  M  et  al:  ID  of  genes  controlled  by  quorum  sensing.  Proc  National  Acad  Sciences,  1999,  96,  13904-­‐09.  
52. You,  YS  et  al:  Use  of  bacterial  quorum  sensing  components  to  regulate  gene  expression.  Plant  Physiology.  2006,  152:  1155-­‐67.    
53. Blaser,  M.  Ecology  of  H  pylori  in  the  human  stomach.  Journal  of  Clinical  Investigation.1997,  100:4,  759-­‐62.  
54. Merrell,  DS  et  al:  Frontal  and  stealth  attack  strategies  in  microbial  pathogenesis.  Nature.  2004,  430,  250-­‐56.  
55. Lederberg,J  Infectious  history.  Science  2000,  288:287-­‐93.  
56. Castagliuolo  I  et  al:  Saccharomyces  boulardii  protease  inhibits  Clostridium  difficile  toxin  A  effects  in  the  rat  ileum.  Infectious  
Immunology  1996;  64:  5225-­‐32.    
57. Czerucka  D  et  al:  Saccharomyces  boulardii  inhibits  secretagogue-­‐mediated  adenosine  3,5-­‐cyclic  monophosphate  induction  in  
intestinal  cells.  Gastroenterology  1994;  106:  65-­‐72.  
58. Bengmark,  S.  2001  Current  Opinions  of  Clinical  Nutrition  and  Metabolic  Care  4(6).  
59. Bengmark,  S.  2002:  Use  of  Pro-­‐,  Pre-­‐  and  Synbiotics  in  the  ICU  -­‐  Future  options.  In  Shikora  SA,  Martindale  RG,  Schwaitzberg  SD  
(eds):  Nutritional  Considerations  in  the  Intensive  Care  Unit  -­‐  Science,  Rationale  and  Practice.  Kendall/Hunt  Publishing  Company,  
Dubuque,  Iowa  USA.  Chapter  34:381-­‐399.  
60. Bengmark  S  2002:  Gut  microbial  ecology  in  critical  illness:  …a  role  for  pre-­‐,  pro-­‐,  and  synbiotics.  Current  Opinion  in  Critical  Care  
8:145-­‐151.    
61. Bengmark,  S.  2001  Current  Opinions  of  Clinical  Nutrition  and  Metabolic  Care  4(6).  
62. Penna,  JF  et  al:  Probiotics  and  mucosal  barrier  in  children.  Current  Opinion  in  Clinical  Nutrition  and  Metabolic  Care.  2008:  11.      
63. Cario,  E.  Therapeutic  impact  of  toll-­‐like  receptors  on  inflammatory  bowel  diseases:  A  multiple-­‐edged  sword.  Inflammatory  Bowel  
Diseases.  2008:4(3):411-­‐21.    
64. Finlay,  B  et  al:  Fulfilling  a  niche.  Cell  Host  &  Microbe.  2009:1,  1-­‐3.    
65. Editorial  -­‐  The  human  superorganism:  Of  microbes  and  men.    Medical  Hypothesis  2010:74;  214-­‐215.    

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