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Scientists at Stanford and the Buck Institute have found a way to predict an individual's immunological decline as well as the likelihood of incurring age-associated diseases and becoming frail.
Sorry but I don't buy the hype and that comes after forty years of reading hype that failed to yield anything. It is rare to see any primary research end up having a significant role in the practice of medicine. There have been many research papers identifying chemicals in the blood tied to disease inclusive of new technology intended to detect those chemicals that never made it into clinical practice. The criteria that allows something into clinical practice falls on two things:Cost and does this new thing provide better clinical information compared to what we have now especially if it is cheaper doing it the old way.
There are periodic assessment of new tests that can impact coronary risk assessment and the clinical studies providing evidence for their inclusion. They must be independent risk factors in other words the information obtained is independent from other markers of being presently used for coronary risk. Any new test must be proven better than anything currently being used and can only be obtained by adding this new test. Mediators of inflammation like hs-CRP is already being used in situations to evaluate inflammation. CXCL9 will have to go through the same evaluation that oxidized cholesterol testing went through which I also think Stanford performed and never took off. It just wasn't better than what was being used today and never took off.
Clinical risk factors with regards to inflammation have already been incorporated into assessing coronary risk. The research they did is one of association between the clinical risk factor and a laboratory marker for inflammation. One may lead to another. For example if one is obese or if becoming obese causes an elevation of inflammatory markers then we say that obesity is an inflammatory state. Did the markers for inflammation lead one to become obese or did obesity make one elevate the inflammatory makers? Which is a better marker the clinical state or the laboratory marker? Right now we are using the clinical state of obesity and so the laboratory marker doesn't add much more. One also does not treat laboratory markers. It's easier to tell somebody to lose weight rather than telling somebody that they have to lower their CXCL9 levels. Nobody knows how to do that.
Sorry but I don't buy the hype and that comes after forty years of reading hype that failed to yield anything. It is rare to see any primary research end up having a significant role in the practice of medicine. There have been many research papers identifying chemicals in the blood tied to disease inclusive of new technology intended to detect those chemicals that never made it into clinical practice.
...or, that did make it into clinical practice, only to be eschewed -- like serum Homocysteine measurement.
Quote:
Originally Posted by Medical Lab Guy
Mediators of inflammation like hs-CRP is already being used in situations to evaluate inflammation.
Here too, I'm seeing clinicians being less & less interested in this measurement -- they're common response is "too many other things can influence hs-CRP levels". I disagree, but I'm just a layperson.
Quote:
Originally Posted by Medical Lab Guy
CXCL9 will have to go through the same evaluation that oxidized cholesterol testing went through which I also think Stanford performed and never took off. It just wasn't better than what was being used today and never took off
I was getting Ox-LDL tests back 6-7 years ago, my levels responded to low-dose statin therapy. My integrative MD is now more interested in Lp(a) levels...
...or, that did make it into clinical practice, only to be eschewed -- like serum Homocysteine measurement.
Here too, I'm seeing clinicians being less & less interested in this measurement -- they're common response is "too many other things can influence hs-CRP levels". I disagree, but I'm just a layperson.
I was getting Ox-LDL tests back 6-7 years ago, my levels responded to low-dose statin therapy. My integrative MD is now more interested in Lp(a) levels...
With regards to hs-CRP, I used that example if a doctor wished to assess inflammation within a coronary risk assessment framework. Doctors have classically used the regular CRP for assessing classical inflammation. Most do not order hs-CRP and it isn't a high volume test. There are many laboratory markers for inflammation and that been used on people admitted with COVID for example. With regards to coronary risk, rather than inflammatory laboratory markers, clinical markers such as obesity, diabetes and metabolic syndrome, renal failure are being used.
So we are on the same page without going into pages and pages of detail. It is always best to have a person educate themselves like you have in order to have optimum care so I salute you on that.
Yes, there is a ebb and flow on test utilization and it happens at each institution and more so at teaching research large centers. Part of the workflow is directly related to the research. There's often new tests or simply old tests with new usage that is being researched. There might be positive indicators found on research and when the research is over it slowly starts to decline on test usage. After years then it falls off a cliff and nobody orders it anymore. That happened with Vertical auto profile that ended up in disfavor. It's a fad and then it dies out after usage.
Usually Lp(a) levels are ordered after a coronary event to investigate early causes for events in the young and with family history of AMI at young age. Those are genetically determined levels and atherogenic. I have never performed one but if my recollection is correct there was some discord about the correlation of methodologies in order to find true and accurate levels.
Hyperhomocyteinemia is also a genetic disorder that even though one can lower it with folate and B12 vitamins the risk does not go away indicating that it is solely a marker for that genetic condition and not causative.
Sorry but I don't buy the hype and that comes after forty years of reading hype that failed to yield anything....................
We have ALL been "reading hype" - some of it thousands of years old. We were told the chest would forever be closed from surgery, assured that hearts could never be transplanted, told that cataracts resulted in blindness and thousands upon thousands of other things that later proved untrue.
I read some "hype" about 20 years ago that claimed a company had figured out a way to separate a pregnant mother's DNA from her baby's DNA, just by taking a blood sample, and THEN determine the health of baby! ....... Today, Non Invasive Prenatal Testing is as common as pregnancy itself.
Thomas Edison is said to have experimented thousands of times before ........ never mind.
The term "inflammatory age", in itself, is intriguing.
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