Home

Differences

This shows you the differences between two versions of the page.

Link to this comparison view

Both sides previous revisionPrevious revision
Next revision
Previous revision
Next revisionBoth sides next revision
home:publications:proal_autoimmunity_2010 [06.15.2010] marysuehome:publications:proal_autoimmunity_2010 [06.15.2010] marysue
Line 60: Line 60:
  
 So - this is such a logical survival mechanism on the part of these microbes that it's almost certain that other less well-studied microbes have also evolved to slow VDR activity, or the activity of other receptors involved in controlling the immune response. So - this is such a logical survival mechanism on the part of these microbes that it's almost certain that other less well-studied microbes have also evolved to slow VDR activity, or the activity of other receptors involved in controlling the immune response.
- 
 ====#11 Successive infection==== ====#11 Successive infection====
  
-Well, these persistence mechanisms result in a snowball effect. When the immune system slows, and a person acquires one pathogen, then it becomes easier to acquire another pathogen.  Then the immune system acquires another pathogen.  These pathogens - they can each slow the immune system in turn. They can be viral, bacterial, fungal... and so on and so on. And this process is referred to as successive infection.+Well, these persistence mechanisms result in a snowball effect. When the immune system slows, and a person acquires one pathogen, then it becomes easier for them to acquire yet another pathogen.  And the immune system then acquires yet another pathogen.  And these pathogens each slow the immune system in turn. And the pathogens - they can be viral, fungal, bacterial... and so on and so on. And this process is referred to as successive infection.
  
 In the context of successive infection, an inflammatory disease state appears to result from the combined pathogenicity of the sum of microbes that any one person accumulates over the course of a lifetime. As human genes are upregulated or downregulated by components of these microbes, the human body shifts further and further away from its natural state of homeostasis. In the context of successive infection, an inflammatory disease state appears to result from the combined pathogenicity of the sum of microbes that any one person accumulates over the course of a lifetime. As human genes are upregulated or downregulated by components of these microbes, the human body shifts further and further away from its natural state of homeostasis.
Line 70: Line 69:
 ====#12 Epstein-Barr Virus (EBV)==== ====#12 Epstein-Barr Virus (EBV)====
  
-So, for example, over the past years, Epstein-Barr Virus has been detected in so many different proportions in so many disease states.  Here's just a sample of conditions associated with EBV. For almost the last century, these results have served as the source of such confusion.  But, if we view them through the lens of metagenomics and in the context of successive infection they make sense! Epstein-Barr Virus is just one component of a mix. In some cases it could be a precipitating factor for an autoimmune disease. Or, in other cases, it's just a pathogen that is acquired later on in the disease process, when the body's already dealing with the widespread immunsuppression that can be caused by the hundreds of bacterial pathogens that accumulate in the body. And we now understand that by altering nuclear receptor activity, viruses can aid the survival of bacteria and vice versa. +So, for example, over the past years, Epstein-Barr Virus has been detected in so many different proportions in so many disease states.  Here's just a sample of different diseases that've been associated with EBV. And for almost the last century, these results have served as the source of confusion.  But, if we view them through the lens of metagenomics and in the context of successive infection they make sense! Epstein-Barr Virus is just one component of a mix. In some cases it could be a precipitating factor for an autoimmune disease condition. Or, in other cases, it's just a pathogen that'acquired later on in the disease process, when the body's already dealing with the widespread immunsuppression that can be caused by any of the hundreds of bacterial pathogens that accumulate in the body. And we now understand that by altering nuclear receptor activity, viruses can aid the survival of bacteria and vice versa. 
 ====#13 Pathogens, aka "rascals"==== ====#13 Pathogens, aka "rascals"====
  
-With this in mind, a "one microbe/one disease" paradigm is no longer viable and treatments for autoimmune disease that aim to eradicate only a single microbe - such as say, our purple friend here (EBV) - will at best succeed in only reversing a very small part of the overall disease process.+With this in mind, a "one microbe/one disease" paradigm is no longer viable and treatments for autoimmune disease that aim to eradicate only a single microbe - let'say, only our purple friend here (EBV) - will at best succeed in only reversing a very small part of the overall disease process.
 ====#14 Co-morbidities among inflammatory diagnoses==== ====#14 Co-morbidities among inflammatory diagnoses====
  
-Well, it may also not be by accident that the uniqueness with which a patients' autoimmune disease symptoms develop parallels the incredible diversity of the pathogens that can persist in the human body. The following wheel shows how truly related chronic diseases are. Each “spoke” on the wheel represents a published study that's shown a significant statistical relationship between patients suffering from one disease and the next. And that is a lot of comorbidity and a lot of symptom overlap.+Well, it may also not be by accident that the uniqueness with which a patients' autoimmune symptoms develop parallels the incredible diversity of the pathogens that can persist in the human body. The following wheel shows how truly related chronic diseases are. Each “spoke” on the wheel represents a published study that's shown a significant statistical relationship between patients suffering from one disease and the next. And that is a lot of comorbidity and a lot of symptom overlap. 
 ====#15 Select bacterial genera detected in commonly smoked cigarettes==== ====#15 Select bacterial genera detected in commonly smoked cigarettes====
  
home/publications/proal_autoimmunity_2010.txt · Last modified: 09.14.2022 by 127.0.0.1
© 2015, Autoimmunity Research Foundation. All Rights Reserved.