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home:pathogenesis:evidence_bacteria [09.21.2011] – [Notes and comments] paulalberthome:pathogenesis:evidence_bacteria [03.26.2016] – [Evolutionary evidence] swopped order last 2 sentence sallieq
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   * **Disease appearing in scars** – There are several case reports of sarcoidosis lesions forming within scars, which are especially susceptible to infection. That these granuloma often take long periods of time to be realized corresponds with the growth rate of the slow-growing chronic pathogens which the Marshall Pathogenesis implicates in chronic disease.(({{pubmed>long:17243430}})) According to one report, a patient developed sarcoid granuloma fully 50 years after his initial injury.(({{pubmed>long:19094856}})) Sorabee //et al// write(({{pubmed>long:15640432}})) that in addition to reactivation of scars obtained from previous wounds, scar sarcoidosis has been reported at the sites of previous intramuscular injections, blood donation venepuncture sites, scars of herpes zoster,(({{pubmed>long:10086879}})) sarcoidosis on ritual scarification,(({{pubmed>long:2917808}})) and at the sites of allergen extracts for desensitisation.(({{pubmed>long:1458650}}))    * **Disease appearing in scars** – There are several case reports of sarcoidosis lesions forming within scars, which are especially susceptible to infection. That these granuloma often take long periods of time to be realized corresponds with the growth rate of the slow-growing chronic pathogens which the Marshall Pathogenesis implicates in chronic disease.(({{pubmed>long:17243430}})) According to one report, a patient developed sarcoid granuloma fully 50 years after his initial injury.(({{pubmed>long:19094856}})) Sorabee //et al// write(({{pubmed>long:15640432}})) that in addition to reactivation of scars obtained from previous wounds, scar sarcoidosis has been reported at the sites of previous intramuscular injections, blood donation venepuncture sites, scars of herpes zoster,(({{pubmed>long:10086879}})) sarcoidosis on ritual scarification,(({{pubmed>long:2917808}})) and at the sites of allergen extracts for desensitisation.(({{pubmed>long:1458650}})) 
   * **Absence of an effect for most chemicals thought to be toxic** – In contrast to infectious agents, little evidence implicates typical doses of dietary chemicals as primary causes of human cancer. Paul Ewald, PhD has concluded that humans have evolved effective flexible enzymatic systems for degrading potentially carcinogenic chemicals.(({{pubmed>long:9255573}})) Even aflatoxins, which are one of the most carcinogenic of dietary constituents, may exert their negative effects largely in conjunction with viral infection.(({{pubmed>long:9270015}}))   * **Absence of an effect for most chemicals thought to be toxic** – In contrast to infectious agents, little evidence implicates typical doses of dietary chemicals as primary causes of human cancer. Paul Ewald, PhD has concluded that humans have evolved effective flexible enzymatic systems for degrading potentially carcinogenic chemicals.(({{pubmed>long:9255573}})) Even aflatoxins, which are one of the most carcinogenic of dietary constituents, may exert their negative effects largely in conjunction with viral infection.(({{pubmed>long:9270015}}))
 +  * **Difficulty distinguishing autoimmune disease from infectious disease** – Although they have identified a signature that distinguishes healthy individuals from sarcoidosis or tuberculosis patients, the biosignatures of both diseases are nevertheless very similar. According to the [[http://www.mpg.de/5771449/biosignatures_tuberculosis_sarcoidosis|Max Planck Institute]], it is almost impossible to distinguish between tuberculosis and sarcoidosis with just a single signature. A set of different biosignatures is better suited for distinguishing in a first step between diseased and healthy individuals and, in a further step, between the specific diseases.
  
  
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 If the common inflammatory diseases (including autoimmune diseases) were genetic, the only way they would manage not to be weeded out of the population would be if they conferred some sort of beneficial survival trait not related to the disease.   If the common inflammatory diseases (including autoimmune diseases) were genetic, the only way they would manage not to be weeded out of the population would be if they conferred some sort of beneficial survival trait not related to the disease.  
  
-To date, no such benefits have been identified in any chronic disease, schizophrenia being a good example.(({{pubmed>long:12878806}})) Schizophrenics have a high suicide rate, few children, and a high rate of abnormality in their children.(({{pubmed>long:10978869}})) (({{pubmed>long:8885043}})) Schizophrenic mothers are more likely than non-schizophrenics to have stillborn babies and children with congenital malformations.(({{pubmed>long:11448375}})) On the contrary, incidence of the disease is only escalating suggesting that bacteria are passed from generation to generation. This would mean schizophrenic mothers and fathers would be less likely to pass on a theoretical schizophrenic gene to their offspring.+To date, no such benefits have been identified in any chronic disease, schizophrenia being a good example.(({{pubmed>long:12878806}})) Schizophrenics have a high suicide rate, few children, and a high rate of abnormality in their children.(({{pubmed>long:10978869}})) (({{pubmed>long:8885043}})) Schizophrenic mothers are more likely than non-schizophrenics to have stillborn babies and children with congenital malformations.(({{pubmed>long:11448375}})) This would mean schizophrenic mothers and fathers would be less likely to pass on a theoretical schizophrenic gene to their offspring. On the contrary, incidence of the disease is only escalating suggesting that bacteria are passed from generation to generation
  
  
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 ===== Notes and comments ===== ===== Notes and comments =====
-TECHEDIT+
  
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home/pathogenesis/evidence_bacteria.txt · Last modified: 09.14.2022 by 127.0.0.1
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