Some might rememer my series of posts on inflammation. The first was "Inflammation. [1] Neutrophil-to-Lymphocyte Ratio [NLR]" [2].
The gist of the series was simply this: while countless studies now see subclinical inflammation markers as having prognostic value, I see them as pointers for intervention.
Chronic inflammation, whether it be associated with cancer or conditions such as rheumatoid arthritis, is always due to chronic activation of nuclear factor-kappB [NF-kB]. NF-kB creates a large number of cell survival proteins, but notably, the COX/LOX enzymes that act on the arachidonic acid in the cell to create inflammatory metabolites that promote cell division.
We can take the heat out of these medical conditions by inhibiting NF-kB. All of the polyphenols I have written about are NFkB inhibitors.
Tom Gilmore at Boston U. has a nice NF-kB site. It contains a page on inhibitors [3].
How can we monitor success? By re-testing the markers & increasing dosage if necessary. Elimination of inflammation will extend life.
In the new study:
"... analyses showed that NLR, PLR, and ELR ... were significantly associated with upgrading (ORs ranging from 2.13 to 4.13)"
NLR is neutrophil to lymphocyte ratio (see [2])
PLR is platelets to lymphocyte ratio (see [4])
ELR is eosinophil to lymphocyte ratio
Inflammation = fast-track disease.
There isn't a lot about PLR in the PCa literature, but here is a meta-analysis from October [4]:
"This meta-analysis showed that a high PLR was correlated with poor DFS {disease-free survival} and OS {overall survival} in patients with prostate cancer."
***
Other old posts:
"Inflammation. [2] Albumin & C-Reactive Protein [CRP]" [5]
May people who shun cooking fats high in omega-6, do so because linoleic acid [LA] can convert to arachidonic acid [AA].
In fact, there is a limit to the amount of AA that the body will produce. AA ia a conditionally essential fatty acid, so elimination of LA & AA from the diet is not a good idea. There is AA in eggs, but I do not live in fear of the occassional egg.
One problem for many people is the ratio of omega-3:6 in the diet. & so, the lipid rafts in cells have high amounts of AA & low amounts of EPA/DHA. The cells end up with an inflammation hair trigger. (& don't think that omega-3 eggs are the solution).
But even if we can get the ratio right, NF-kB has to be dealt with.
For those who have low EPA/DHA intakes, there will be more AA in the rafts & more inflammatory metabolites.
Interestingly, PCa tissue samples usually show low amounts of AA because it is rapidly metabolized to inflamatory elements when NF-kB is activated.
Patrick you rock. You just overloaded me with highly relevant information. Earlier, I came to a conclusion that my aggressive PCa at young age is most likely due to systemic inflammation as a result of ankylosing spondylitis I've been battling for over 25 years. With all this in mind, targeting NF-kb is another potential approach to put the brake on cancer progression in addition to COX-2 inhibitors I've been taking lately.
I wonder, why many oncologists ignoring the fact that many of their patients with aggressive cancer may have another systemic inflammation disease? I thought the link between inflammation in cancer has been established already. cancer.gov/about-cancer/cau...
As long as inflammation is merely seen as prognostic & not a call to action, doctors will not address it.
I'm reminded of the link between cancer & blood clots. Do doctors test for out-of-whack coagulation factors? No - because they lack a protocol to act before a clot appears. At that point they know what to do.
One day, new PCa cases might get a script for a NF-kB inhibitor, a clot inhibitor & who knows what else.
Do you take polyphenols, nattokinase, and Serrapeptase via supplements? Or simply get these through your food intake i.e. your diet? I’m very interested in reducing my high-sensitivities CRP number but just not exactly sure how to do so.
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