Thanks to Olsen for turning us onto Dr. Paul Ewald. Note especially at the end what he has to say about dogma. This is the root of why we see so little progress in research. He is a gem! Not at all afraid to go public and call out scientists and doctors. What makes this disorder all the more frustrating is that ego stands in the way of progress for us. -Laura

How do the concepts of evolutionary biology support the idea that pathogens are to blame for most diseases?

When we consider the possible causes of disease, it’s important to make sure that at our starting point, we put all categories on the table. I believe the most useful way to do this is to think in terms of three main categories:

1. inherited genes
2. parasitic agents (this includes bacteria, viruses, fungi, protozoa
3. non-living environmental factors (too much or too little of a particular substance, radiation, exposure to a chemical etc.)

Once we have this spectrum of categories in mind we ask, “Have all three areas been investigated?

At this point scientists tend to make an error. They decide that if they have found enough evidence for categories 1 or 3, that category 2 is not playing a role. This is a fundamental problem that has led the medical community to misunderstand the cause of most debilitating chronic diseases.

So, which of the three categories is overlooked? Category 1 certainly isn’t – once scientists figured out the structure of DNA and the nature of mutations they were extremely eager to show their relationship to disease. Category 3 hasn’t been overlooked, largely because of the fact that we can sense environmental causes of disease. We suffer from a stomach ache after eating contaminated food or feel the pain from a sunburn.

But, if we look back at every decade, there has been a lack of research on category 2 relative to its actual importance in causing disease. Our track record shows that we have consistently failed to fully understand the role that pathogens play in causing disease and this trend has continued up until 2008.

There are many examples of how we have continually overlooked the category of infectious disease. I’m not talking about acute infection – researchers were essentially able to work out the mechanisms of acute infection from 1880 to about 1920. I’m talking about chronic infection, and thus the role of pathogens in causing chronic disease.

Take the case of peptic ulcers. The idea that bacteria cause peptic ulcers was first solidified in the 1940s, then independently investigated and solidified again by Marshall and Warren in the 1970s. It took over 20 more years before the relationship was finally accepted by mainstream medicine. Now, when people look back on previous theories about the cause of peptic ulcers they think, “Oh, isn’t it surprising that we didn’t understand the cause for so long!” or “We should have known better!” But when they proceed to hypothesize about the cause of other diseases, they go right back to the dogma. They haven’t learned the lessons from the peptic ulcer story.

Instead, they should think in an opposite fashion. If we find that one disease has an infectious cause, we should learn from that information and seriously consider the same possibility in other diseases.

Think about syphilis. In 1913, it was discovered that the disease resulted from infection with the bacterium Treponema pallidum. Soon, the disease was dubbed the “Great Imitator” because its symptoms often resembled those of other diseases, particularly in the later stages. I think syphilis should be called the “Great Illustrator,” because it’s a disease that imitates a whole spectrum of other diseases. This suggests that we should be actively looking for a pathogenic cause in these other diseases as well – especially since so many illnesses are still considered to be of unknown cause. Back in the day, the psychoses associated with syphilis and schizophrenia were grouped together into a single category of illness. But as soon as syphilis was found to have a bacterial cause, we separated syphilitic insanity from what is now called schizophrenia, and assumed that schizophrenia was not caused by infection. Rather than just separating the two diseases we should have actively pursued the hypothesis that schizophrenia also has an infectious cause. The information we can gain from these kinds of relationships is far more enlightening than any genetic data.

That’s one of the realities of medicine – researchers tend to deny associations. Denial plays a major role as scientists love to hold on to the current dogmatic explanation. This suggests that in order for pathogens to be fully tied to chronic disease we will have to wait until the current powerful people pass away and a sufficient number of young people entering the arena without these vested interests mature into positions of influence, to tip the balance of expert opinion. This is something that Charles Darwin, Max Planck, and Thomas Kuhn all agreed with.

That’s because powerful people tend to hang on to the opinions that made them powerful even if there is no longer sufficient evidence to support their views. It’s a social problem that relates to the weakness of the mind. Human beings didn’t evolve to be scientists. Instead they evolved to be competitive – to grab and hold onto what is theirs. Hence the name calling often observed among the medical community and the resistance among scientists to fund or support ideas other than their own, ideas that question the validity of current dogma.

http://www.healthcanal.com/brain-ner...s-protein.html

Viral infections like influenza and herpes increase the risk of developing neurodegenerative diseases such as Parkinson's and Alzheimer's later in life , according to a study led by Ole Isacson, professor of neurology at Harvard Medical School. The reason is that inflammation resulting from viral infections can initiate and propagate cellular damage in the brain, which over time could accumulate, and lead to neurodegenerative diseases.

A single bout of flu doesn't cause significant damage but contracting the infection regularly increases the risk of developing the debilitating brain diseases, Isacson said.
http://www.rttnews.com/1822819/flu-n...mpaign=sitemap

Journal issue devoted to infection and alzheimer's

http://www.j-alz.com/issues/13/vol13-4.html

Volume 13, Number 4, May 2008 - Special Issue "Chronic inflammation and Amyloidogenesis in Alzheimer’s Disease: The Emerging Role of Infection" (Guest Editors: Judith Miklossy and Ralph Martins)

Page 357
Judith Miklossy and Ralph Martins
Preface: Chronic inflammation and amyloidogenesis in Alzheimer’s disease: The emerging role of infection

Pages 359-369
Claudia Schwab and Patrick L. McGeer
Inflammatory Aspects of Alzheimer Disease and Other Neurodegenerative Disorders
Abstract: Alzheimer and a number of other neurodegenerative diseases are characterized by the presence of reactive microglia and reactive astrocytes in association with the lesions. The classic view that microglia exist primarily in either a resting or activated state needs to be broadened in view of recent results. Resting microglia are in constant activity sampling their surround. Activated microglia may be pro-inflammatory, releasing inflammatory cytokines and other inflammatory mediators, or anti-inflammatory, promoting the healing process. There is evidence that microglial phagocytosis is more powerful in the anti-inflammatory state. Activated astrocytes also have pro-inflammatory and anti-inflammatory properties. In the pro-inflammatory state they release inflammatory cytokines. In the anti-inflammatory state they release various growth factors. In AD and other neurodegenerative diseases, both microglia and astrocytes are in a pro-inflammatory state. From a therapeutic point of view it is desirable to find methods of tipping the balance towards an anti-inflammatory state for both types of glia.

Pages 371-380
Brian J. Balin, C. Scott Little, Christine J. Hammond, Denah M. Appelt, Judith A. Whittum-Hudson, Hervé C. Gérard, Alan P. Hudson
Chlamydophila pneumoniae and the etiology of late-onset Alzheimer’s disease
Abstract: Sporadic, late-onset Alzheimer’s disease (LOAD) is a non-familial, progressive neurodegenerative disease that is now the most common and severe form of dementia in the elderly. That dementia is a direct result of neuronal damage and loss associated with accumulations of abnormal protein deposits in the brain...

I just want to tell you that I agree with the virus issues as being a trigger for auto immune diseases. I fully believe that. I was 29, some virus put me in the hosptial ER. Flu it was labled. While labled and on the table receiving fluids, my body began to tingle. My hair stood on end, and I can remember thinking, that I was worried it would do something to my hair. Six weeks later my hair dropped out in clumps. I have alopecia universalis now since that age. I have added four other immune diseases. My diseases intensified in 2001 with type A Asian Flu, picked up on a cruise. All my conditions worsened after that episode. I have not had my health since my origional problem at the age of 29. I am now 60, and struggle with all the issues I have. The medical community is exploring this with monal clonal antibiodies. That is as far as I got with research when I quit a trial study. I do not have PD, but I do recognize that as being in the immune problem catagory. ginnie