lassesen 9:41 pm on September 18, 2016

Two interesting studies

While these studies are not dealing with CFS patients — they are interesting because some of the conclusions / observations may be relevant.

Feed a cold (viral infection), starve a fever (bacterial infection)

This was reported in a NewScientist news story on 2002. “Dutch scientists have found that eating a meal boosts the type of immune response that destroys the viruses responsible for colds, while fasting stimulates the response that tackles the bacterial infections responsible for most fevers.” This was also reported in Opposing Effects of Fasting Metabolism on Tissue Tolerance in Bacterial and Viral Inflammation [Cell Sept 2016] – so both human and mice studies found the same thing.

Impact for CFS:

If you have a flare — then one time:
- fast for 12 hours
- take food (or capsules) high in glutamine amino acid (i.e. milk, meat, nuts)

If fasting make you better, faster than food then a bacterial infection is likely a significant factor.

If food makes you better, faster than fasting, then a vial infection is likely a significant factor. – for example a viral re-activation.

Bacteria lurking in blood could be culprit in countless diseases

This NewScientist Sept 14, 2016 article reported “A molecule made only by bacteria has been found to change blood proteins in a way that is common to a score of “non-infectious” conditions, from heart attacks to Alzheimer’s disease….. They need iron ions to grow, and iron is bound up by proteins that keep free ions at vanishingly low levels in our blood.”

What is very surprising is the impact “Just one molecule of lipopolysaccharides (LPS). mixed with 100 million fibrinogen molecules was enough to trigger these changes (Journal of the Royal Society Interface, doi.org/bqh5).” Fibrinogen can lead to thick blood.

In terms of treatment, “There could potentially be a link to cancer, too. Inflammation is seen in cancer and the anti-inflammatory drug aspirin is known to lower cancer rates. The pill is also reported to bind free iron, which together may suggest bacteria have a hidden role in this disease too.”

Aspirin

Aspirin has been a bit of a mystery drugs — I recall reading several years ago, a Scientific American article on Aspirin stating that they do not understand how aspirin works. “Although many of ASA’s pharmacological actions are related to its ability to inhibit prostaglandin and thromboxane biosynthesis, some of its beneficial therapeutic effects are not completely understood.” [1995]

During my second remission, I took the maximum daily dosage of aspirin for 10 days to see if hypercoagulation was indeed part of CFS. I made a dramatic improvement. My MD was now willing to explore hypercoagulation. In hindsight, aspirin may have been doing multiple things that resulted in the improvement.

The influence of non-steroidal anti-inflammatory drugs on the gut microbiome [2016].
- “The bacterial composition of the gut varied with the type of NSAID ingested.”
- “Four OTUs (Prevotella species, Bacteroides species, family Ruminococcaceae, and Barnesiella species) discriminated aspirin users from those using no medication”
Non-steroidal anti-inflammatory drugs may modulate the protease activity of Candida albicans [2010].
- “In other hand, aspirin seems to reduce the secretion of aspartyl-proteases -related pathogenic behavior of candidal biofilms.”
Aspirin-associated iron loss: an anticancer mechanism even in the short term?[2013]
Antiviral activity of aspirin against RNA viruses of the respiratory tract – an in vitro study [2016]
- “These data demonstrate a specific antiviral activity of aspirin against influenza A virus and HRV. The mode of action against rhinoviruses is still unknown and requires further investigation, as does the possibility of aspirin being effective in vivo to treat the common cold.”
Aspirin inhibits hepatitis C virus entry by downregulating claudin-1. [2016]
Aspirin attenuates cytomegalovirus infectivity and gene expression mediated by cyclooxygenase-2 in coronary artery smooth muscle cells. [1998]
Aspirin inhibits a murine viral infection[1975].
- “it is possible that aspirin has previously unrecognized therapeutic effects in various clinical situations, such as in viral infections (when used as an antipyretic agent) and in atherosclerosis (when used as an antiplatelet agent).

http://www.heparinscience.com/biological_activities.html

There are under study at least four potential mechanisms explaining the anti-inflammatory effects of heparin. They are:

Binding proteins. There are more than 100 heparin-binding proteins. Heparin modulates the function and activity of a number of proteins, including acute phase proteins (i.e. proteins whose plasma concentrations increase or decrease in response to inflammation) and complement proteins (proteins forming the complement system). This property of heparin may explain the anti inflammatory activity of heparin. Researchers think that the binding of a cytokine to heparin-like molecules can protect the cytokine protein from proteolytic degradation. The glycosaninoglycan-cytokine interaction has potential therapeutic uses: heparin can attenuate ongoing tissue damage because it can bind and neutralize a wide range of mediators released from inflammatory cells. Heparin binds to many chemokines and cytokines therefore preventing these pro-inflammatory elements from interacting with their respective receptors.

Selectin-mediated cell adhesion. Heparin interferes with the adhesion of leukocytes to the endothelium (leukocyte adhesion and activation is key in the response to inflammation). Excessive leukocyte activation releases toxic oxygen radicals and proteolytic enzymes which in turn contribute to vascular and tissue damage. These findings further support the hypothesis that the ability to bind to P-selectin of heparin and heparin-like products is the reason why it can inhibit neutrophil adherence to activated endothelial cells, thus blocking severe inflammation.

Nuclear factor kappa B (NF-κB). Heparin blocks the NF-κB transcription factor. The blocking of this transcription factor can potentially reduce activation of inflammatory genes and regulate the gene expression and production of pro inflammatory cytokines, chemokines and adhesion molecules.

Apoptotic cell death. Heparin and related compounds have been proved to modulate the activity of Tumor Necrosis Factor and NF-κB, which are involved in apoptotic cell death. Therefore, future research should investigate therapeutic potential of heparin in this area. The use of heparin as an anti-inflammatory agent has been limited for the high bleeding risk at the doses where the anti-inflammatory activity is expressed. Consequently, during the last years research work has been focused on the discovery of non-anticoagulant heparin derivatives or mimics. Ongoing investigations must focus on elucidating the mechanisms of action of these non anticoagulant heparins in cellular and animal models of acute and chronic inflammation.

gse4joints 1:14 pm on September 19, 2016

Well, I think I will probably stop posting here. I’m tired of getting stymied by all the spam traps. Today, I’ve tried repeatedly to post about the “potent” anti-inflammatory action of heparin and though it has only one link (to PMC) it still gets trapped for some inexplicable reason. But the other comment I subsequently posted (from the non-authoritative heparinscience site) went right through first time. I had an interest here because I did a CME (continuing medical education) on novel anticoagulants a few years ago.

Bye, and good luck to everybody.
- melamine 12:27 pm on September 21, 2016
  
  Ketamine is the only thing that has helped me but I cannot afford treatment. Tested high chronic range: EBV, adenovirus and all coxsacki Bs.

CFS Remission

Striving for true remission of CFS, chronic Lyme, FM, IBS etc

Two interesting studies

Feed a cold (viral infection), starve a fever (bacterial infection)

Impact for CFS:

Bacteria lurking in blood could be culprit in countless diseases

Aspirin

Feed a cold (viral infection), starve a fever (bacterial infection)

Impact for CFS:

Bacteria lurking in blood could be culprit in countless diseases

Aspirin

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