For a long time now, I have been flummoxed by my inability to get confirmation of underlying inflammation in my body. I have used 3 widely used markers of inflammation, and these are hsCRP (high sensitivity C-Reactive Protein), ESR (Erythrocyte Sedimentation Rate), and LDH (Lactate Dehydrogenase). There are other marker out there, but they are not as common, AFAIK, and many are just unaffordable and impractical if used regularly to monitor progress.
All these three markers I mentioned fail to tell me that I have inflammation. In fact, hsCRP and ESR are very low, and LDH is just barely above optimal range. [And the LDH is only above range because I have low blood volume, which would tend to make readings appear high than they really are, as many blood markers are based on a concentration per volume of blood. With low blood volume, whatever substance being measured in blood becomes more concentrated. Given that it's really the total quantity of that substance in the entire blood that's important, it makes sense to use concentration as a surrogate marker for total quantity only if the subject has normal blood volume.]
Yet I have high blood pressure, and I have strong indications to assume that the high blood pressure stems from immune complexes deposited in my kidney glomerulus that cause inflammation. The inflammation is noted by high wbc, neutrophil, and monocytes in my CBC, as well as the excretion of albumin in my urine, and confirmed by lower serum albumin. The neutrophils and macrophages (from monocytes that turn into macrophages when inside tissues) attack the immune complexes, which they consider antigens, and send inflammatory cytokines to the site. Coupled with the spillover ROS from the phagocytic action of neutrophils, a constant level of oxidative stress is generated that needs to be countered by the body's antioxidant system. This is why my serum uric acid is high, as it is needed as an antioxidant, and why my serum albumin, another antioxidant, is being oxidized. The oxidized albumin, having a positive charge, easily passes through the kidneys and is not reabsorbed, and is excreted. This loss of albumin is what causes my serum albumin to be low, and is what causes by blood volume to be low, as albumin agglomerates and holds on to sodium, and sodium attracts water from the interstitial fluids, and increases blood plasma and as a result blood volume increases. With low volume, I have high blood pressure (this is consistent with Ray Peat's findings but is contrary to conventional medical thought).
With that being the context of my discussion, I had been asking for a long time why all that inflammation is not being confirmed in the three inflammation markers I mentioned.
Then slowly I came to the realization that high blood pressure, through the sacrifice of albumin, had all along been saving me from having tissues destructed from the inflammation. While the oxidative stress is there constantly, my body has not been derelict in its duty to protect the surrounding tissues from damage because the antioxidant system of the body has been coming out in full force each time. It didn't act like Chris Wray and Bill Barr when the cities were burning from riots. It was never compromised in anyway and my tissues were never destroyed.
For the inflammation markers should actually be called tissue destruction markers - LDH, hsCRP and ESR. No tissue were being destroyed, so these markers were low. Yes, there was plenty of inflammation going on, but the oxidative stresses coming from them were being met equally with antioxidant action from the body's stores, and therefore no tissues were being destroyed.
So I should thank my body's antioxidant system for being there all the time for me, and allowing albumin to be sacrificed in place of tissues, and for the body to have the wisdom to compensate for the low blood volume (arising from low albumin due to the albumin loss) by increasing my blood pressure.
This is what I've come to conclude. I may be wrong. I may have no evidence for the "evidence-based" establishment guys. This is only a hypothesis. But for me, the person with the problem (or I should call it a condition - in a good way) of hypertension, this is good enough for now. Since no one, not a doctor for sure, can give me a coherent reason for this stupefying inconsistency, I will gladly settle for this.
This behooves me to ask "what's in a name?" In this case, I should stop fixating on these three markers as markers of inflammation. It may be that most of the time inflammation results in tissue destruction. And that calling them markers of inflammation is very well appropriate.
But it is high time to ask the question "When does inflammation not result in tissue destruction, even when the inflammation is chronic?"
All these three markers I mentioned fail to tell me that I have inflammation. In fact, hsCRP and ESR are very low, and LDH is just barely above optimal range. [And the LDH is only above range because I have low blood volume, which would tend to make readings appear high than they really are, as many blood markers are based on a concentration per volume of blood. With low blood volume, whatever substance being measured in blood becomes more concentrated. Given that it's really the total quantity of that substance in the entire blood that's important, it makes sense to use concentration as a surrogate marker for total quantity only if the subject has normal blood volume.]
Yet I have high blood pressure, and I have strong indications to assume that the high blood pressure stems from immune complexes deposited in my kidney glomerulus that cause inflammation. The inflammation is noted by high wbc, neutrophil, and monocytes in my CBC, as well as the excretion of albumin in my urine, and confirmed by lower serum albumin. The neutrophils and macrophages (from monocytes that turn into macrophages when inside tissues) attack the immune complexes, which they consider antigens, and send inflammatory cytokines to the site. Coupled with the spillover ROS from the phagocytic action of neutrophils, a constant level of oxidative stress is generated that needs to be countered by the body's antioxidant system. This is why my serum uric acid is high, as it is needed as an antioxidant, and why my serum albumin, another antioxidant, is being oxidized. The oxidized albumin, having a positive charge, easily passes through the kidneys and is not reabsorbed, and is excreted. This loss of albumin is what causes my serum albumin to be low, and is what causes by blood volume to be low, as albumin agglomerates and holds on to sodium, and sodium attracts water from the interstitial fluids, and increases blood plasma and as a result blood volume increases. With low volume, I have high blood pressure (this is consistent with Ray Peat's findings but is contrary to conventional medical thought).
With that being the context of my discussion, I had been asking for a long time why all that inflammation is not being confirmed in the three inflammation markers I mentioned.
Then slowly I came to the realization that high blood pressure, through the sacrifice of albumin, had all along been saving me from having tissues destructed from the inflammation. While the oxidative stress is there constantly, my body has not been derelict in its duty to protect the surrounding tissues from damage because the antioxidant system of the body has been coming out in full force each time. It didn't act like Chris Wray and Bill Barr when the cities were burning from riots. It was never compromised in anyway and my tissues were never destroyed.
For the inflammation markers should actually be called tissue destruction markers - LDH, hsCRP and ESR. No tissue were being destroyed, so these markers were low. Yes, there was plenty of inflammation going on, but the oxidative stresses coming from them were being met equally with antioxidant action from the body's stores, and therefore no tissues were being destroyed.
So I should thank my body's antioxidant system for being there all the time for me, and allowing albumin to be sacrificed in place of tissues, and for the body to have the wisdom to compensate for the low blood volume (arising from low albumin due to the albumin loss) by increasing my blood pressure.
This is what I've come to conclude. I may be wrong. I may have no evidence for the "evidence-based" establishment guys. This is only a hypothesis. But for me, the person with the problem (or I should call it a condition - in a good way) of hypertension, this is good enough for now. Since no one, not a doctor for sure, can give me a coherent reason for this stupefying inconsistency, I will gladly settle for this.
This behooves me to ask "what's in a name?" In this case, I should stop fixating on these three markers as markers of inflammation. It may be that most of the time inflammation results in tissue destruction. And that calling them markers of inflammation is very well appropriate.
But it is high time to ask the question "When does inflammation not result in tissue destruction, even when the inflammation is chronic?"