Aa
Research supported antifibrotics - do they exist?
The problems of treatment failure for SOC/IFN nonresponders and the possibility of reducing future supercombo-SVRchances by introducing archived resistance mutations when using "Pseudomonotherapy" - (that is here defined as using a single antiviral agent that is not protected against resistance development by its combo with an IFN/riba component (IFN by definition in this scenario is not sufficiently effective in reducing viral replication so that all the burden to tame the adaptive quasispecies evolution falls on the antiviral)) together with the 61% and 65% SVR rates for the latest triple modality in Geno 1s, have raised concern and the awareness for the need for alternate/additional treatment modalities in many HCV patients and their health care providers. Waiting for future antiviral developments is one route frequently recommended, but for the patients in current need, our repertoire of additional meaningful approaches needs to be carefully reevaluated. Using antifibrotics to halt fibrosis progression is one concept not proven in large trials but it might well be effective in many, because the mechanisms for fibrosis generation are not intrinsically linked to HCV persistence, but rather to secondary response mechanisms evoked in the chronically inflamed liver, with the stellate cell activation holding center stage in this scenario. The following is one of several possible add on modalities.
MEDICAL PROFESSIONAL
Here is your analysis:
The sum of improved metabolic lifestyle,
decreased intestinal toxicity/inflammation on liver and systemwide
and the combo of the various components of the liver protective antinflammatory and stellate system activation (TGFbeta and NFkappaB expression reducing) reducing supplements
will often lead to improved endothelial function as a welcome "side effect".
Endothelial function is a summary term for the various reactions of the endothelium to the stimuli that in normal physiology make it respond to demands in regional blood flow and other situations, like a damage to the vascular bed.
Of particular interest is the relaxation of arterial-vascular tone - by relaxing the smooth muscle ring inside the arterial wall- in response to increased peripheral demand like in the coronary system, the leg muscles when you run up a flight of stairs and -of particular interest to men with diabetes and hypertension- in response to sexual stimulation.
All these functions are achieved by the healthy, non dysfunctional endothelial cells releasing Nitrous oxide -NO- through activation of the endogenous nitrous oxide synthetase, provided all the pathways and molecular machinery is intact.
In endothelial dysfunctions many of the complex subsystems at play here work at suboptimal levels, leaving the patient with a nonrelaxing artery, so the heart and muscles etc. do not get enough blood flow increase, resulting among other problems, in the now so famous ( By TV commercials) ED. Hence the liver/lover connection/slip that I referred to.
The "seeming contradiction" that you are referring to , Goofydad is the fact that in advanced cirrhosis there exists a complex syndrome called "hyperdynamic circulation", which contributes to the portal hypertension by increasing the blood flow into the splanchnic ( gastroenteric=guts) circulation, delivering more blood to the liver (with a decreased capacity/increased resistance) , that makes the portal pressure even higher. In this situation there is
an increased overall production of NO,
not locally but systemically present,
by the inducible nitrous oxide synthethase, that reduces the bodywide vascular resistance
( but not in the liver!)
and leads to blood pressure reduction, cardiac minutevolume /output overload
and overall volume overload
and also sodium retention in response to that, so as to compensatory increase blood pressure/volume, by the renin/angiotensin system, ( this can lead to ascites and spontaneous peritonitis, all complications of advanced cirrhosis)
and often to renal vasoconstriction in response to the accumulation of blood in the splanchnic ( gut) vascular bed
which can lead to the lifethreatening "hepatorenal syndrome".
In this situation extra arginine means even more systemwide , nonphysiological NO production with aggravation of the syndrome as described.
This has little to do with the improvement in local endothelial function and local NO production, a vital part of normal human physiology often impaired in persons with obesity, diabetes, fatty liver, hypertension and chronic inflammation.
I think this is the dichotomy that you were hinting at. Not so easy to clarify that, but I did it as simple as possible.
The sum of improved metabolic lifestyle,
decreased intestinal toxicity/inflammation on liver and systemwide
and the combo of the various components of the liver protective antinflammatory and stellate system activation (TGFbeta and NFkappaB expression reducing) reducing supplements
will often lead to improved endothelial function as a welcome "side effect".
Endothelial function is a summary term for the various reactions of the endothelium to the stimuli that in normal physiology make it respond to demands in regional blood flow and other situations, like a damage to the vascular bed.
Of particular interest is the relaxation of arterial-vascular tone - by relaxing the smooth muscle ring inside the arterial wall- in response to increased peripheral demand like in the coronary system, the leg muscles when you run up a flight of stairs and -of particular interest to men with diabetes and hypertension- in response to sexual stimulation.
All these functions are achieved by the healthy, non dysfunctional endothelial cells releasing Nitrous oxide -NO- through activation of the endogenous nitrous oxide synthetase, provided all the pathways and molecular machinery is intact.
In endothelial dysfunctions many of the complex subsystems at play here work at suboptimal levels, leaving the patient with a nonrelaxing artery, so the heart and muscles etc. do not get enough blood flow increase, resulting among other problems, in the now so famous ( By TV commercials) ED. Hence the liver/lover connection/slip that I referred to.
The "seeming contradiction" that you are referring to , Goofydad is the fact that in advanced cirrhosis there exists a complex syndrome called "hyperdynamic circulation", which contributes to the portal hypertension by increasing the blood flow into the splanchnic ( gastroenteric=guts) circulation, delivering more blood to the liver (with a decreased capacity/increased resistance) , that makes the portal pressure even higher. In this situation there is
an increased overall production of NO,
not locally but systemically present,
by the inducible nitrous oxide synthethase, that reduces the bodywide vascular resistance
( but not in the liver!)
and leads to blood pressure reduction, cardiac minutevolume /output overload
and overall volume overload
and also sodium retention in response to that, so as to compensatory increase blood pressure/volume, by the renin/angiotensin system, ( this can lead to ascites and spontaneous peritonitis, all complications of advanced cirrhosis)
and often to renal vasoconstriction in response to the accumulation of blood in the splanchnic ( gut) vascular bed
which can lead to the lifethreatening "hepatorenal syndrome".
In this situation extra arginine means even more systemwide , nonphysiological NO production with aggravation of the syndrome as described.
This has little to do with the improvement in local endothelial function and local NO production, a vital part of normal human physiology often impaired in persons with obesity, diabetes, fatty liver, hypertension and chronic inflammation.
I think this is the dichotomy that you were hinting at. Not so easy to clarify that, but I did it as simple as possible.
Somewhere in this long thread - or a spin-off thread - HR made mention of the relationship between liver and lover. As I understand the comments, some of the suggested supplements are known to boost Niric Oxide. Can we talk about the implications, if any, of this NO boost and an underlying portal hypertension condition?
Here's an interesting link that suggests boosting NO would be a good thing....http://www.utsouthwestern.edu/utsw/cda/dept37389/files/245390.html
And this one seems to contradict...http://cat.inist.fr/?aModele=afficheN&cpsidt=2138722
HR, can you share more of your enlightened analaysis?
Here's an interesting link that suggests boosting NO would be a good thing....http://www.utsouthwestern.edu/utsw/cda/dept37389/files/245390.html
And this one seems to contradict...http://cat.inist.fr/?aModele=afficheN&cpsidt=2138722
HR, can you share more of your enlightened analaysis?
The $44 prices include shipping and handling. So I bet we are about the same.
Heppy Thanksgiving!!!
I googled the stuff and just picked one of the links and it has 2 sources for LEF PPC for $44 or so.
http://www.shopping.com/xCC-co900-price_range_30_90-softgels
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